Advances in Veterinary Antimicrobial Therapy and Forensic Toxicology

RATIONAL MEANS OF ANTIMICROBIAL SELECTION IN
VETERINARY PRACTICE
M.VIJAY KUMAR
The choice of antimicrobial agent in the clinical practice should be based upon
susceptibility of the infecting organism to the drug concentrations achieved in the tissue
and pharmacokinetic characteristics of the drug and its dosing protocol. Although, several
class of antimicrobials are readily available, the clinical cure may not be always
successful and its partially attributable to lack of culture and sensitivity tests under field
conditions. Therefore, atleast, one can bank upon certain pharmacokinetic principles in
the routine clinical practice as well as in serious infections like meningitis, endocarditis
and in immuno-compromised hosts.
Pharmacokinetics:
Pharmacokinetics deals with absorption, distribution, metabolism and excretory pattern of
a given therapeutic agent. Selection of antimicrobial agent based on its pharmacokinetic
characteristics aid in achieving optimal concentration at the desired site. For example, the
location of infection can have a major influence on the drug concentration achieved there,
as some sites (eg: CNS) are protected by barriers to drug penetration, while others (eg.
mammary gland, urinary tract) local pH may favour drug accumulation. Knowledge of
pharmacokinetic data is also useful to avoid possible toxicity in a given species as well to
take necessary precautions during physiological stress (eg. pregnancy, lactation) or
pathological conditions (eg: hepatic failure, renal dysfunction). The probable
antimicrobial agent that can be employed in the clinical practice should be selected after
giving due considerations to following issues:
 organ/s is/are involved
 Most likely pathogen
 Antibiotic likely to be effective
 Drug concentrations at the site of infection
 Drug/route likely to achieve that concentration
Absorption: The absorption and disposition of antimicrobial agents in the body

arelargely governed by their chemistry and certain physiochemical properties as well as
status of the animal (Fig.1). The various antimicrobials are basically grouped into weak
KVC Sponsored CVE training programme on “Advances in

Chemotherapy and Forensic Toxicology” organized by the Dept.of
Pharmacology &Toxicology,Veterinary College,Bidar,from 31st January
to 5th February, 2011
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organic electrolytes (acids/bases), amphoteric or neutral compounds. The absorption is
primarily dependent on extent of lipid solubility and degree of ionization,
which are determined by pKa of the drug and pH of the biological fluid in question.
These factors also determine the extent of distribution and elimination process for
antimicrobials. Only non-ionized forms of drugs are passively diffuses across GIT or can
pass across blood-brain or blood-milk barrier. For acidic drugs, a fall in 1 pH unit results
in a 10 fold increase in the concentration of the non-ionized form and converse applies for
organic bases.
Distribution and elimination: Some of the lipophilic antimicrobials listed below enter
most tissues of the body and penetrate cellular barriers and can generally reach infection
foci. Chloramphenicol,Trimethoprim,Erythromycin,Metronidazole,3rd generation
cephalosporins like moxalactam,Fluoroquinolones:Enrofloxacin, Pefloxacin, Ofloxacin,
Norfloxacin.These antimicrobials are eliminated mainly by hepatic metabolism and/or
carrier mediated biliary exertion. This rate of elimination varies with species, but obeys
first order kinetics when therapeutic doses are administered.
Tetracyclins: The lipid solubility of tetracyclins varies with the compound but enter most
tissues and body fluids except CSF. The more lipophilic number, minocycline attain
effective concentration at relatively inaccessible infection site, such as the prostate. As a
result of chelation with calcium, tetracyclins become bound at active sites of ossification
and in developing teeth. Long acting tetracyclins (doxycyline, minocycline) undergo
biliary excretion and may adversely affect indigenous microbes in the caecum/colon of
horses. However, they are suited for biliary and upper intestinal tract infection in farm
animals. Oxytretracyclin in 2-PVP base (IM only) exert long duration of action over
propylene glycol base. Because of poor water solubility, oxytetracyclin dihydrade must
be given in much higher dose (50 mg/kg) than the hydrochloride salt to produce
equivalent tissue concentration.
Sulfonamides: Most of the sulfonamides predominantly non-ionized in biological fluid of
pH below their pKa value (sulfisoxzole = 5; sulfonilamide = 10.4). Commonly used
compounds like sulfamethazine (pka = 7.4) and sulfadimethoxin (pKa = 6.1) enter most
tissues of the body and eliminated by a combination of metabolic reactions (acetylation)
and renal exertion (filteration and pH - dependent passive tubular reabsorption). Cats are
poor acetylators and therefore sulfonamides are contraindicated. Sulfisoxazole (pKa =
5.0) is more ionized in the plasma and widely distributed and eliminated mainly by
glomerular filtration (best suited for UTI), but their exerction is dependent on urinary pH.
Penicillins: Distributions of penicillin are limited due to high ionization and they attain
low concentration in cells and do not penetrate well into transcellular fluids. Protein
binding varies among penicillin over a wide range (80%-cloxacillin, 22%-ampicillin) and

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this is responsible for low extra-vascular distribution. However, penicillin and/or in
combination with streptomycin is best suited for lower respiratory tract infection
(unknown pathogen) with exudation. Penicillins are rapidly eliminated by kidney.
Probencid compete with their excretion (for tubular excretion) and delays penicillins
excretion.
Antibiotic Desired environment for optimal action
Penicillins,Hexamine(only UTI) Acidic pH
Nitrofurazones,Cephalosporins
Tetracyclins,Fluoroquinalones,Aminoglycosi Alkaline pH
des
Ampicillin, amoxicillin and naficillin undergoes enterohepatic circulation and
therefore their half-lives are longer than penicillin-G. Penicillins and cephalosporins
(beta-lactams) are highly active during logarithmic phase of bacterial growth (time
dependent action). Dosing of beta-lactams should be aimed to keep serum concentration
over MIC to prevent regrowth. Penicillins retains their activity even in the presence of
fibrin and abscess formation.
Antibiotic Factors decrease their action
Sulfonamides Pus, blood clot
Penicillin,Cephalosporins,Aminoglycosides Intracellular organisms
Gentamicin,Polymyxin Pus
Aminoglycosides DecreasedpH,anaerobiasis, hyperosmalarity
Aminoglycosides :
Aminoglycosides does not attain therapeutic levels in CSF and ocular fluid. Poor
diffusibility is attributed to this low degree of lipid solubility. Hafl-lives are short (1-2 hr)
in domestic animals. Inspite of limited distribution, selective binding to renal tissue
(cortex) occurs. Their bacteriocidal action is rapid but killing of Gm-ve aerobes is
concentration dependent and produce a prolonged post-antibiotic effect. Due to this
biphasic mode of action, serum concentration continuously exceeding MIC are not
required unlike penicillins. Loop diuretics and impaired renal function delays their renal
excretion and it is necessary to adjust maintenance dosage to prevent ototoxicity and
nephrotoxicity. One should not administer large IV dose or multiple injections in
dehydration or ureamic conditions. Intravenous eg: neomycin) must be restricted to one
or two occasions only. Systemic administration does not give satisfactory levels in milk
and therefore local (intramammary) route should be employed in mastitis cows.

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Chloramphenicol: In pre-ruminant calves, chloromphenicol is well absorbed from GIT
following systemic administration. The drug readily pass through cellular barriers and
attain sustained concentration in CSF and aqueous humor. The drug can readily cross
placenta. Penetration of the blood: prostate barrier is relatively poor. Due to lipophilic
nature, the apparent volume of distribution is large (> 1L/kg) in all species and its
distribution is independent of pH. It possess short half-lives in most species except cat
(poor in conjugation with glucoronic acid). Due to short of half-life chloromphenicol
(sodium succinate) at the rate of 50 mg/kg (priming dose) followed by maintenance doses
of 25 mg/kg at 8-12 interval is suggested in ruminants.
Fluoroquinolones:
These are amphoteric compounds and having low degree of ionization. Therefore, their
distribution is widespread and even penetrate well into CSF (>50% serum levels in
meningitis), bronchial secretions, bone and cartilage and prostatic tissue. Partially
metabolised in liver and bile concentrations are 2-10 times the serum levels and even
enterohepatic circulation may occur. Plasma half-lives varies with species and urinary
concentration exceed serum concentration by several hundred times and remain high for
24 hr after administration. Clearance of certain drugs like theophylline get reduced
leading to adverse effects and one should not administer concurrently. They have affinity
for weight bearing cartilages and therefore do not administer to puppies (before 8 months
of age) or foals (below 1 year of age). Reduction of dosage is required in animals with
impaired renal function.
Antimicrobial combinations and their effect
Bacteriostatic (systemic) + bacteriocidal (systemic) Antagonistic

Bacteriostatic (local) + bacteriocidal (systemic) Antagonistic
Bacteriocidal (local) + bacteriostatic (systemic) Antagonistic
Chloramphenicol + Aminoglycosides Antagonistic
Macrolid + Chloramphenicol Antagonistic
Conclusion:
The antimicrobial chemotherapy particularly in the absence of antibiotic sensitivity
testing facility under field conditions is a difficult task. In the routine clinical practice as
well as in the absence of microbial sensitivity pattern, one can adopt certain
pharmacological principles discussed here so as to obtain clinical and/or bacterological
cure. The veterinarian must update their knowledge pertaing toclinical pharmacology of
newer antimicrobials released in to market.

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*****

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AN UPDATE IN VETERINARY BIOLOGICALS
Y.HARI BABU
Vaccine is preparation of processed, innocuous specific antigen sometimes

together with adjuvants. This preparation when introduced in to animal system
(preferably) parenterally induces production of specific proteins called antibodies
(Immunoglobins).
Presence of these antibodies in the circulating blood system confers high degree of
immunity in the host body, against pathogens in the events of real infection. Obviously
the antigens mentioned above are proteins derived from pathogens or disease causing
organism. These proteins neutralize the pathogens invitro and prevent their growth.
Vaccination is something like Army exercise, mock war, war games to keep the
body in readiness to take on any infection. The body has a wonderful mechanism of
Anamnesis (remembering) and would switch on production of specific antibodies in short
time.
The antigens are of great help in:
• Inducing immunity in host.

• Providing diagnostic reagent for detecting the disease. Since the days of Jenner, a
vaccine has become life saving preparation and constitutes the main weapon against
infections and contagious diseases. Vaccines are available against almost all
infectious agents.
Types of vaccine:
Obviously the vaccines and vaccinations have brief history. The early vaccine
were prepared out of material contents from wounds, lesions etc., of the affected
individual. The material thus collected would be processed to remove accessory adhesions
and impurities. The material would be rendered innocuous enough to be safe for .Then it
used to be administered in prescribed doses.
Now the vaccines are produced on large scale, freezes dried and are preserved
safely- ready for use in moments notice. Instead of whole organisms being included in
vaccine preparation, only specific proteins responsible for ‘Antigenicity’ are being
included in the vaccines. This procedure reduces all sorts of risks posed by the presence
of extraneous materials. Today most of the diseases are controlled. For this credit goes to

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vaccines, which were evolved over a period of time. Best example of vaccine utility is the
elimination of pox from globe. Recent success of total containment or RinderPest in A.P.
and Karnataka only reflect the glory of these vaccines. We have following kinds of
vaccines today in market.
• Killed vaccines
• Live vaccines
• Attenuated vaccines
• vector vaccines
• Subunit vaccines
• Very soon we will have transgenic vaccines.
• Other classification is:
• Bacterial vaccines
• Viral vaccines
• Protozoan vaccines
• Antitoxin
• Anti venom (snake etc.)
Vaccine failure in animals and birds:
Failures in vaccination are a common phenomenon which is being encountered by

the veterinarian in the field, either in case of animals or birds. It is more so in poultry
which, has become a challenge to both the field Veterinarian a well as to the biological
manufacturers. To arrive at a proper conclusion about where actually the vaccinations
have failed and how to correct it, one has to know, various ways in which a vaccine may
fail to protect an animal and birds.
There are many reasons why a vaccine may not confer protective immunity on an
animal. These can be discussed in brief hereunder.
Animal and Birds
1. Immunosuppressed
2. Passive immunization
3. Parasitic immunization
4. Biological variation
Vaccine:
1. Death of live vaccine

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2. Defect in storage vaccine
3. Cold chain failure for live vaccines.
Vaccination:
1. Inappropriate route of administration

2. Administration of passively protected animal/bird
3. Inadequate vaccine
4. Vaccine given too late to animal/bird already infected
5. Wrong strain or organism used
6. Non-protective antigen used.
Now we will discuss about the aforesaid factors in brief
ANIMAL /BIRDS
Animal or birds which are immunosuppressed:
This type of vaccine failure is very common in poultry, occurs when the normal immune
response is suppressed. For example, malnourished animals may be immunosuppressed
and should not be vaccinated. Some viral infections like infectious bursal disease (IBD or
Gumboro disease) induce profound immunosupression.
Stress in general including pregnancy, extremes of cold, heat, fatigue, may reduce a
normal immune response. Probably because of increased steroid production.
Passive immunization:
The most important cause of vaccine failure is the presence of passively derived maternal
immunity in young animals.
In case of chick; serum immunoglobulin are readily transferred from hen serum to
yolk while the egg is still in the ovary. In this fluid phase of yolk, IgG is therefore found
at level equal to those in hen serum. In addition, as the egg passes down the oviduct, IgM
and IgA from oviduct secretions are acquired with the albumin. As the chick embryo
develops, it absorbs some of the yolk IgG which then appears in its circulation. The
maternal IgM and IgA from the albumin diffuse in to the amniotic fluid and are
swallowed by the embryo, so that when the chick hatches. It posses IgG in its serum and
IgM and IgA in its intestine. The newly hatched chick doses not absorb all its yolk sac
antibody until about 24 hrs after hatching. These maternal antibodies effectively prevent
successful vaccination until they disappear between 10 and 20 days after hatching.
In case of animals, the maternal antibodies reach the fetus through the placenta,
and it is determined by the structure of placenta. The placenta of ruminants as

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syndesmochorial; that is, the chorionic epithelium is in direct contact with uterine tissue.
In animal with these types of placenta, the transplacental passage of Ig is prevented and
the newborn of these species are thus entirely dependent on the antibodies secured
through the colostrums.
Parasitic infestation:
Immune response is also suppressed in heavily parasitized animals or birds. Thats why,
to induce proper immune response in birds against vaccination, it was suggested to
deworm the bird against antihelmintics prior to vaccinations.
Biological variation:
The immune response, being a biological process never confers absolute protection and is
never equal in all members of genetic and environmental factors, the range of immune
responses in large random population of animal tends to follow a normal distribution.
This means that most animals respond to antigen by mounting an average immune
response, a few will mount an excellent response and a small proportion will mount a
very poor immune response. The group of poor responders may not be protected against
infections in spite of having received an effective vaccine. Therefore, it is impossible to
guarantee 100% protection in random population of animals by vaccination.
VACCINE
Sometimes, the quantity of vaccine, handling of vaccine also affect the failure of immune-
response against vaccination.
Death of live vaccine:
In some cases, the vaccine may actually be ineffective. This could be because it contains
the wrong strain of organism or wrong antigens. The method of production may have
destroyed the protective epitopes, or there may simply be insufficient antigen in the
vaccine, of much greater importance is the failure of an effective vaccine to stimulate
protective immunity. A live vaccine may have died as a result of poor storage, the use of
antibiotics in conjunction with live bacterial vaccines, the use of chemicals to sterilize
syringes or excessive use of alcohol while swabbing the skin.
Death in storage of vaccine:
The storage of vaccine is important in order to maintain the quality of vaccine. It holds
good both for bacterial as well as viral vaccines even though it needs exacting low

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temperatures to store the vaccines. It is a common phenomenon in the field especially the
storage of vaccines is concerned.
Cold chain failure for the live vaccines:
There are many live vaccines needed to be vaccinated to either birds or animals.
Transport of such vaccines from the point of production to the institute or hospital and
then to the point of vaccination needs the cold chain, as most of the live vaccines get
destroyed in absence of cold atmosphere. This is one of the most important aspects to be
observed and followed strictly in field to ascertain effective results out of vaccinations.
Vaccine Production defect:
It is not uncommon, that there arise doubts about the quality of vaccine many times in the
minds of the field veterinarian. It is true and problems of this type are uncommon and can
generally be avoided by using only vaccines from reputable manufacturers.
VACCINATIONS
Finally much of the task of making successful vaccination programme lies with the
Veterinarian or Para veterinarian who is administering the vaccines. As the aforesaid
aspect is limited involvement of the expertise of the Veterinarian, the methodology of
vaccination, choosing of the vaccine, time of vaccination etc., which are discussed
hereunder falls within intelligentsia of field worker or veterinarian.
Inappropriate route of administration:
Inappropriate route of administration is of much greater significance in the failure of an

effective vaccine to stimulate protective immunity. In many cases, this is due to
unsatisfactory administration. Inappropriate route of administration if vaccines to animals
or birds lead to vaccination failure.
Administration of passively protected animal/bird:
As it has been discussed earlier, that the maternal antibodies that are present in the
animals or birds will hamper the vaccination processes, by effectively neutralizing the
vaccine antigens and making the vaccination ineffective. And hence, here it is stressed
that before the vaccination, it has to be ascertained whether the maternal antibodies are
still present or not .For this, simple laboratory techniques are available or even history of
the animal also reveals the required information.
In-adequate vaccine:

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Sometimes, animals/birds given vaccines by unconventional routes may not be
protected. When large flock of poultry as to be vaccinated, it is common to administer the
vaccine eighter as an aerosol or in drinking water. If the aerosol is not evenly distributed
throughout a building or if some animals do not drink may receive insufficient vaccine.
Animal/birds that subsequently develop disease may be interpreted as cases of vaccine
failure.
Vaccine given too late to animal/bird already infected:
Even animal given an adequate dose of an effective vaccine may fail to be protected.
If the vaccinated animal was incubating the disease before inoculation, the vaccine may
be given too late to affect the course of the disease. In such cases, more commonly, the
animal/birds may fail to mount an immune response.
Wrong strain or organism used and Non-protective antigens used
The size of unreactive portion of the population will vary between vaccines, and its
significance will depend on the nature of the disease. This for highly infectious diseases
against which herd immunity is poor and in which infection is rapidly and effectively
transmitted, such as foot and mouth disease, the presence of unprotected animals could
permit the spread of the disease and would thus disrupt control programmes.
*****

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AN UPDATE IN DISEASE INVESTIGATION AND
DIAGNOSIS
K.C. Mallinath
INTRODUCTION:
In recent years disease diagnosis and disease management have become a highly
specialized science. There was a time when people used to focus attention on a fewer
diseases of livestock. Now, the scene is different, importation of highly productive
germplasm, intensive cross breeding, extensive and intensive rearing of livestock,
composite farming, extensive use of biologicals either imported or unwittingly smuggled
from unknown sources have totally changed the disease scenario. Each species of
domestic livestock now have a long list of diseases to be handled, some of them go
unrecognized; a few have identical symptoms, some with confusing clinical signs.
Normally a field officer recognizes a disease based on classical clinical signs and
deals with such a disease at his level. In the changed scenario as mentioned above where
the clinical signs are confusing he has to depend on the referral diagnostic laboratory.
This confirmation process surely depends on the clinical samples made available
to the laboratory. Therefore, the clinical material becomes a very valuable raw material
for the success of the mission of disease diagnosis. Proper collection of relevant material
and dispatching it to the laboratory in proper condition should be done with utmost care.
Any negligence in this exercise may lead to faulty diagnosis leading to loss of valuable
life of vulnerable livestock population and loss of precious time in dealing with field
outbreaks.
A. COLLECTION OF SAMPLES
Before collection of samples, careful consideration should be given to the purpose for
which they are required. This will determine the type and number of samples needed to
provide valid results. The samples should be collected aseptically, and care should be
taken to avoid cross contamination between samples.
When samples are taken from live animals, care should be taken to avoid injury or
distress to the animal or danger to the operator and attendants. It may be necessary to use
mechanical restraint, tranquilization or anesthesia. Whenever handling biological
material, from either live or dead animals, the risk of zoonotic disease should be kept in
mind and precautions taken to avoid human infection.

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Post-mortem examinations should be carried out under as aseptic conditions as is
practicable. Care should be taken to avoid environmental contamination or risk of spread
of disease through insects or fomites. Arrangements should be made for appropriate safe
disposal of animals and tissues. The samples collected should be representative of the
condition being investigated and the lesions observed. Frequently, a combination of blood
samples for serology and tissues from dead or culled animals for microbiological culture
and pathological examination will be required.
For diagnostic purposes various types of specimens may be collected from live,
dead animals and environment.
1. Sample collection from live animals:
a) Blood:
Blood samples may be taken for hematology or for culture and / or direct
examination for bacteria, viruses or protozoa, in which case it is usual to use
anticoagulants, such as ethylene diamine tetra-acetic acid (EDTA) or heparin. They may
also be taken for serology, which requires a clotted sample. Blood plasma is also used for
some procedures.
A blood sample is taken, as cleanly as possible, by venipuncture. In most large
mammals, the jugular vein or a caudal vein is selected, but brachial veins and mammary
veins are also used. Vena cava veins are also used in pigs. In birds, a wing vein (brachial
vein) is usually selected.
Blood may be taken by syringe and needle or by needle and vacuum tube (not
easy in delicate veins but convenient in strong veins).Ideally the skin at the site of
venipuncture should first be shaved (plucked) and swabbed with 70% alcohol and allowed
to dry.
For samples that are collected with anticoagulant, thorough mixing, using gentle
agitation only, is necessary as soon as the sample has been taken. It may also be necessary
to make a smear of fresh blood on a microscope slide; both thick and thin. For polymerase
chain reactions, EDTA is the preferred anticoagulant. For serum samples, the blood
should be left to stand at ambient temperature (protected from excessive heat or cold) for
1–2 hours until the clot begins to contract. The clot can then be ringed round with a sterile
rod and the bottles placed in a refrigerator at 4°C. After several hours, or overnight, the
sample can be centrifuged at about 1000 g for 10–15 minutes and the serum can be
decanted or removed with a pipette.Chemical preservatives viz., Thiomersal or
Merthiolate or Sodium Azide can be used for longer storage of serum sample. In order to
establish the significance of antibody titres, paired serum samples will
often need to be collected 7–14 days apart.
b) Faeces:

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Freshly voided faeces of suitable quantity (at least 10 g) should be collected.
Faeces for parasitology should fill the container or topped up with sterile water and be
sent to arrive at the laboratory within 24 hours. If transport times are likely to be longer
than 24 hours, the sample should be sent on ice or refrigerated to prevent the hatching of
parasite eggs.
Screw top containers or sterile plastic bags should be used for shipment; avoid
tubes with rubber stoppers as gas generated can result in blowing the stopper off the tube,
ruining the integrity of the sample and contaminating other samples in the package. An
alternative and sometimes preferable method is to take swabs from the rectum (or cloaca),
taking care to swab the mucosal surface. However, samples collected with a swab are
inadequate for parasitology. Swabs should be transported in appropriate transport
medium. Faeces are best stored and transported at 4°C.
c) Skin:
In diseases producing vesicular lesions, collect, if possible, 2 gm of affected
epithelial tissue as aseptically as possible and place it in 5 ml phosphate buffered glycerin
or Tris-buffered tryptose broth virus transport medium at pH 7.6. Plucked hair or wool
samples are useful for surface-feeding mites, lice and fungal infections. Deep skin
scrapings, using the edge of a scalpel blade, are useful for burrowing mites.
d) Genital tract and semen:
Samples may be taken by vaginal or prepucial washing or by the use of suitable
swabs. The cervix or urethra may be sampled by swabbing. Samples of semen are best
obtained using an artificial vagina or by extrusion of the penis and artificial stimulation.
The sperm-rich fraction should be present in the sample and contamination by antiseptic
washing solutions should be avoided. Specific transport media and conditions are often
required.
e) Eye:
A sample from the conjunctiva can be taken by holding the palpebra apart and the
swab is then taken into the transport medium. Scrapings may also be taken on to a
microscope slide. The
handles of metal-handled swabs are useful for this, to ensure that sufficient cells are
removed for
microscopic examination.
f) Nasal discharge:
Samples may be taken with dacron, cotton or gauze swabs, preferably on wire
handles as wood is inflexible and may snap. It may be helpful if the swab is first
moistened with transport medium. The swab should be allowed to remain in contact with
the secretions for up to 1 minute, then placed in transport medium and sent to the
laboratory without delay at 4°C.

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g) Milk:
Milk samples should be taken after cleansing and drying the tip of the teat and the
use of antiseptics should be avoided. The initial stream of milk should be discarded and a
tube filled with the next stream(s), a sample of bulk tank milk can be used for some tests.
Milk for serological tests should not have been frozen, heated or subjected to violent
shaking. If there is going to be a delay in submitting them to the laboratory, preservatives
can be added to milk samples that are being collected for serological testing.
h) Urine:
Urine samples should be collected with the help of a sterile catheter and
dispatched in screw cap tube. Boric acid may be added as a preservative
2. Sample collection at post-mortem:
Samples of tissue from a variety of organs can be taken at post-mortem. It is
unusual to take biopsy samples of tissues in veterinary practice however are done in
certain circumstances, using appropriate surgical techniques.
Animal health personnel should be trained in the correct procedures for post-
mortem examination of the species of animals with which they work. The equipment
required will depend on the size and species of animal. Normally a knife saw cleaver,
scalpel, forceps and scissors, including scissors with a rounded tip on one blade will be
required. A plentiful supply of containers and tubes of transport media appropriate to the
nature of the sample required should be available, along with labels and report forms.
Containers should be fully labeled with the date, tissue and animal identification. Special
media may be required for transport of samples from the field. The operator should wear
protective clothing,overalls, washable apron, rubber gloves and rubber boots.
Additionally, if potential zoonotic diseases are being investigated, the post-mortem
examination should be conducted in a biological safety cabinet; if this is not possible, an
efficient face mask and eye protection should be worn. If rabies or transmissible
spongiform encephalopathies (TSEs) are suspected, it is usual to detach the animal’s
head.
Tissues may be collected for microbiological culture, parasitology, biochemistry,
histopathology and/or immunohistochemistry, and for detection of proteins or genome
nucleic acids. In addition buccal, oropharyngeal or rectal (cloacal) swabs may be
collected. The person conducting the post-mortem examination should have sufficient
knowledge of anatomy and pathology to select the most promising organs and lesions for
sampling. Each piece of tissue should be placed in a fully labeled separate plastic bag or
sterile screw-capped jar. Swabs should always be submitted in appropriate transport
media. Disinfectants should not be used on or near tissues to be sampled for bacterial
culture or virus isolation.

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After collection, the samples for microbiological examination should be
refrigerated until shipped. If shipment cannot be made within 48 hours, the samples
should be frozen; however, prolonged storage at –20°C may be detrimental to virus
isolation. For histopathology, blocks of tissue not more than 0.5 cm thick and 1–2 cm
long are cut and placed in neutral buffered 4–10% formalin, which should be at least ten
times the volume of the tissue sample. The tissues may be sent to the laboratory dry or in
bacterial or virus transport medium, depending on the type of
specimen and the examinations required.

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3. Environmental and feed sampling:
Samples may be taken to monitor hygiene or as part of a disease enquiry.
Environmental samples are commonly taken from litter or bedding and voided faeces or
urine. Swabs may be taken from the surface of ventilation ducts, feed troughs and drains.
This kind of sampling is particularly important in hatcheries, artificial insemination
centres and slaughter houses in which specialized equipment is maintained. Samples may
also be taken from animal feed, in troughs or bulk containers. Water may be sampled in
troughs, drinkers, header tanks or from the natural or artificial supply.
B. SELECTION OF SAMPLE
Considerable skill and care are required to decide on the correct samples to be sent
to the laboratory. The experimental or field condition will suggest in good part about the
appropriate sample and method of collection for microbiological study. However there are
number of factors which will determine the effectiveness of sample collection. Among
these are 1) Time of collection 2) Tissue selected 3) Handling and storage of the samples.
It is best to obtain sample from an animal as early as possible in the course of the
disease. Avoid waiting to take sample until an animal moribund and near to death. The
site of multiplication may be so destroyed as to no longer yield the viable organisms.
Wherever possible specimen should be collected over a period of time. The specimens
collected should be representative of the condition/population/organ. Proper quantity of
sample collected as per the need.
C. INFORMATION TO BE SENT WITH SAMPLES
It is essential that individual samples be clearly identified using appropriate
methods. Marking instruments should be able to withstand the condition of use, i.e. being
wet or frozen (use indelible marking pen). Pencil has a tendency to rub off containers and
labels attached to plastic will fall off when stored at –70°C. Information and case history
should always accompany the samples to the laboratory, and should be placed in a plastic
envelope on the outside of the shipping container. The information should include the
following points.
i) Name and address of owner with telephone and fax numbers.
ii) Diseases suspected and tests requested.
iii) The species, breed, sex, age and identity of the animals sampled.
iv) Date samples were collected and submitted.
v) List of samples submitted with transport media used.
vi) A complete case history would be beneficial for the laboratory and should be included
if possible. Some of the components of the history are:
a) A list and description of the animals examined.
b) The length of time sick animals have been on the farm; if they are recent arrivals,
from

134
where did they originate.
c) The date of the first cases and of subsequent cases
d) A description of the spread of infection in the herd or flock.
e) The number of animals on the farm, the number of animals dead, the number
showing
clinical signs,and their age, sex and breed.
f) The clinical signs exhibited by the affected animals and manage mental practices
followed
in the farm
g) Any medication given to the animals, and when given.
h) Any vaccines given, and when given.
i) Post mortem lesions recorded.
D.TRANSPORTATION OF SAMPLES
1. Approval to ship specimens:
The laboratory that is going to receive the samples should be contacted to ensure
that it has the capability to do the testing requested and to see if there are any special
packaging or shipping requirements. It is essential to contact the receiving laboratory
when material is sent to another country. A special import license will usually be required
for shipment of any biological material to other countries and must be obtained in
advance. This license should be placed in an envelope on the outside of the parcel.
Shipments must be made in accordance with the Dangerous Goods Rules (DGR)
for the particular mode of transport. For air transport it is the International Civil Aviation
Organization (ICAO) technical instructions for the safe transport of dangerous goods by
air.
2. Transportation of specimens:
Samples referred to as diagnostic specimens in official regulations must carefully
be packed to avoid any possibility of leakage or cross contamination.
The specimens should be forwarded to the laboratory by the fastest method
available. If they can reach the laboratory within 48 hours, samples should be sent
refrigerated.
E. PRESERVATION OF SAMPLES FOR PROLONGED STORAGE
Establishing a collection of samples for future studies can be very useful. This can
include cultures for comparison with future isolates, tissue or serum samples that can be
used for the validation of new tests and a collection of fixed tissues, or paraffin blocks, for
future histological examination. Possibly the most useful collection is the storage of
serum samples. These samples may be useful if a retrospective investigation is carried out
to compare the present disease status with that of earlier times. The different methods of
preserving the clinical samples are:

134
1) Short term storage (upto 24 hrs) at refrigeration
2) Long term storage:
a) Freezing the sample at -20o C/-60o C/-80o C/ -196 (LN2) can preserve up to 1 year
without
any alteration in the clinical material.
b) Lyophilisation (Freeze drying) The water content of clinical material (specially viral
origin) is removed and kept in powder form. This is the common method used for
vaccines stored at 40 C.
The nature of samples recommended for Bacterial, Viral, Fungal, Parasitic & other
diseases are as follows:
Name of the Disease Samples to be collected
Bacterial and Fungal Diseases
• Hemorrhagic Septicemia : Fixed smears of blood/throat swelling in ailing

animals Smears of heart blood & liver, heart blood, lymph node & spleen in
dead animals
• Anthrax : Flame fixed blood smears of cattle & sheep, swabs of blood from
ear vein for cultural examination from dead animals or small piece
from tip of ear/muzzle in saline
• Black Quarter : Impression smears from the affected muscle tissue or
exudates
• Enterotoxemia / Contents of small intestine with and without chloroform
separately on ice, Kidney, Urine
• Brucellosis : Paired serum sample, blood and abomasal contents of aborted
foetus, placenta with 2-3 cotyledons/vagina swabs in PBS
• Johne’s disease Rectal pinch smears, Bowl washings preserved in 10%
formalin & in dead animals terminal portion of ileum with ileocaecal
valve, mesenteric lymph node in 10% formal saline
• Glanders : Exudate from skin & lung lesions / its smears
• Tuberculosis : Cough material in sterile tube in live animal or milk sample in
sterile tube /smears from suspected lesions and lymph glands or lung lesions
in sterile tube & in 50% buffered glycerin.
• Leptospirosis : Blood serum, Pieces of liver in 10% formalin or milk or urine
in vials adding 1 drop of formalin/ 20 ml
• Salmonellosis : Intestinal swab, heart, blood, bile in sterile container on ice
• Actinomycosis /Actinobacillosis :Smears from pus lesions, pus in vial on ice
and formalin preserved material from affected muscle

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• Listeriosis : Aborted foetus, brain, placenta and all internal organs in 10%
formalin on ice
• CCPP/CCBP/Coryza : Swab from nasal or vaginal cavity in PBS and pieces of
lung formalin and paired sera
• Chlamydia/Psittacosis : Nasal swab, lung pieces in sterile tube and fixed
smears from liver, lung & foetus
• Mycotic Infections : Deep skins scrap in sterile vials
• Skin Diseases : Skin scrapings for identification of ecto-parasites & fungus
Viral Diseases :
• RP/PPR/BVD: Anticoagulant blood at height of temperature/ Pre-scapular lymph

node, spleen on ice and lung liver spleen or tonsils in 10% formalin or eye,
mouth and rectal swabs in PBS on ice and pieces of
intestine on ice
• FMD: Vesicular fluid from unruptered oral vesicles and epithelial tissue from
fresh lesions, oesophanrygeal fluid in 50% Phosphate Buffered Glycerin and
Blood serum
• Rabies: Hippocampus and brain in 50% Buffered glycerin and 10%
formalin separately
• Pox : Scabs in 50% Buffered glycerin and formalin separately
• Swine Fever : Heparinized blood from live animal or heart blood, pieces of spleen,
lymph node, pancreas in 50% Buffered glycerin BT or Septicemic blood in
heparin/EDTA
• Canine Distemper : Impression smears from liver and pieces of liver/spleen on ice
in 10% formalin
• ICH : Impression smears of liver fixed in methanol spleen, liver in sterile tube on
ice and liver & kidney in10% formal saline
• Canine Parvovirus Rectal swab in PBS or pieces of intestine,heart on ice and all
internal organs in 10% formalin
• Ranikhet Disease : Fresh dead/moribund bird on ice or portion of liver spleen
trachea bronchi & lung in 50% Buffered glycerin or Proventriculus in 10% formal
saline
• Mareks Disease : Live bird in acute disease /Feather follicles from chest & neck
intransport medium /Paired sera sample /portion of peripheral nerve, trachea,
ovary, liver & spleen in 10% formalin
• IBR : Live affected bird /Bursa in transport medium and in 10%
Formalin / Paired sera sample(IB : Swab from the exudates lung and paired sera
Parasitic Diseases

134
• Protozoan Diseases : Blood smears/ anticoagulated blood
• Gastro-Intestinal parasites: Faecal sample in 10% formalin/in dead animals’
(Round Worms 70% formalin) for identification and all internal organs in10 % in
formalin
*****

134
ADVANCES IN ANTIMICROBIAL THERAPY OF OCULAR
AILMENTS
M.VIJAY KUMAR
Corneal epithelium is the main site of resistance to drug penetration.. As a result, the
epithelium and endothelium are relatively impermeable to electrolytes but are readily
penetrated by fat-soluble substances. Drugs that have the ability to exist in equilibrium in
solution as ionized (water soluble; polar) and unionized (lipid soluble;nonpolar) forms are

134
ideal for topical use, i.e., chloramphenicol, fluoroquinolones. Topical administration is
used for treatment of eyelids, conjunctiva, cornea, iris, and anterior uvea. Following
which , up to 80% of the applied drug(s) is absorbed systemically across the highly
vascularized nasopharyngeal mucosa. Because absorption via this route bypasses the
liver, there is no large first-pass metabolism seen after administration PO.
2. Subconjunctival (bulbar conjunctiva): This technique requires only topical

anesthesia and a tuberculin syringe with a 25- or 27-gauge needle. Volumes should not
exceed 0.25 ml in cats and dogs and 1.0 ml in horses and cows. Subconjunctival
medication reaches the cornea by slowly leaking out of the injection site. Intraocular drug
levels are attained by diffusion through the cornea and sclera. This is used for diseases of
the cornea, anterior, uvea, anterior vitreous, and sclera.Drugs with low solubility such as
corticosteroids may provide a repository of drug lasting days to weeks. Appropriate
amounts must be used, as large amounts, especially of long-acting salts, can cause a
significant inflammatory reaction. For sub-Tenon’s injections, 0.5 ml/site is usually safe
and effective in small animals and ≤1 ml in large animals such as the horse and cow.
3.Retrobulbar medications:are used infrequently for therapeutics. In cattle, the

retrobulbar tissues can be anaesthetized with local anesthetic (lidocaine) for enucleations.
Whenever any medication is placed into the orbit, extreme care must be taken to ensure
that the medication is not inadvertently injected into a blood vessel, the optic nerve, or
one of the orbital foramen. Retrobulbar injection has a high risk of adverse effects and
should not be used unless the clinician is experienced and the animal is appropriately
restrained.
4. Intravitreal-used infrequently: Antibiotics,antifungal drugs have been effectively used

in microgram dosages. Generally injected at the pars plana for infectious endophthalmitis.
5. Systemic-P.O., I.V. or I.M: Systemic administration is required for treatment of

diseases of the retina, optic nerve, and vitreous., for posterior segment therapy and to
complement topical therapy for the anterior segment. The blood-ocular barriers can limit
absorption of less lipophilic drugs, but inflammation initially allows greater drug
concentrations to reach the site. As the eye starts to heal, these barriers become more
effective and can limit further drug penetration. This should be considered when treating
posterior segment disease, eg, blastomycosis in small animals with hydrophilic drugs such
as itraconazole.
Ocular dosage forms : Topical ophthalmic drugs are formulated as ointments,

suspensions and solutions. Deciding which formulations to be used depends on the
several practical considerations.Ocular contact time of ointment is longer than solutions

134
or suspensions,so they are more practical when the owner cannot follow a frequent
administration regimen.avoid ointments on penetrating wounds or descemetocele,and
prior to intraocular surgery,as their petroleum base elicits severe granulomatous reaction
when in direct contact with intraocular tissue. The frequency of topical application
depends on disease and formulation.One drop of an antimicrobial solution applied four
times daily is usally sufficient in uncomplicated corneal ulcers and bacterial
conjunctivitis.When ointment is used a , 5mm strip is applied to the conjunctiva a
minimum of three times a day. If more than one drug is involved in the therapeutic
regimen,then 3 to 5 minutes should be allowed between application of each medication to
avoid dilution or chemical incompatability.antimicrobial therapy is typically continued for
seven days or until the ocular infection is resolved.
Antibacterial ocular drug therapy
Topical antibiotics are indicated for the treatment of corneal ulcers, corneal perforations,
conjunctivitis,and blepharitis.. Ideal choice of appropriate therapy begins with
identification of the organism and its sensitivity. Culture or cytologic examination of
material from the affected area is necessary.Minor bacterial conjunctivitis infection may
not justify routine culture and may be amendable to initial therapy with broad spectrum
antibiotics. Normal ocular flora is predominantly gram positive;a predominance of gram
negative organisms is indicative of an abnormal condition.
Chloramphenicol: Broad spectrum, bacteriostatic. Soluble in both water and fat so it

penetrates intact cornea with topical administration-thus may be considered for initial
treatment of intraocular infections (penetrates the cornea).it is good first choice
antimicrobial for corneal ulcers and bacterial conjunctivitis.it is having poor efficacy
against gram negative bacteria and pseudomonas spp.Frequency of administration- q4
hours for full therapeutic levels. Toxicity- risk of aplastic anemia
Aminoglycosides: a.. Neomycin: Usually found in combination with other antibiotics.

Broad spectrum-bacteriocidal impairs protein synthesis.Frequency of administration-BID-
TID. Toxicity- Topical-localized sensitivity; conjunctival irritant.Systemic-ototoxicity-
possible head tilt. b. Gentamicin: Broad spectrum bactericidal activity including
Streptococcus, Staphylococcus, Proteus spp, and Pseudomonas aeruginosa. Effective
topically and subconjunctivally for external ocular infections. It is available as solution
and ointment because of its chemical characteristics does not readily cross lipid
membranes,but readily enters the stroma when the corneal epithelium is damaged. Renal
toxicity with concurrent oral therapy, may be toxic to surface epithelium. c.
Tobramycin.: Two to four times more effective against Pseudomonas spp. and

134
betalactamase producing staphylococci than gentamicin and effective against gentamicin-
resistant microbes.
Polypeptides:a.Bacitracin: Bactericidal, active against gram positive microorganisms.

Used in combination with other antibiotics. Poor corneal penetration. b. Polymyxin B:
Poor penetration. Bactericidal. Effective mainly against gram-negative bacilli and
Pseudomonas spp. Should not be given subconjunctivally.
Cephalosporins: a.Cefazolin: Broad spectrum, first generation cephalosporin.Topical

use for gram + cocci resistant to other antimicrobials. Can be administered
subconjunctivally-does penetrate intact cornea. Usually diluted to 50 - 100 mg/ml
concentration. Mix with artificial tears to a concentration of 33 mg/ml for treatment of
meibomitis
Fluoroquinolones: Eg: Ciprofloxacin ,Levofloxacin, Ofloxacin etc. Broad spectrum,

active against gram positive and gram negative microorganims. Drug of choice for
betalactamase producing staphylococcus and aminoglycoside resistant pseudomonas spp.
Generally preferred in corneal, conjunctival, and intraocular infections. Excellent corneal
penetration.not effective against streptococci spp. Because of their spectrum of activity
these agents should never be used as empirical treatment.
Antiviral ocular drug therapy
The topical antiviral agents are static in action and topically irritating,so frequent
dministration is necessary and client compliance and patient tolerance are issues.
Idoxuridine: Frequency of administration is 1 drop every 4hrs until corneal re-

epithelialization occurs. Doesnot penetrate the cornea unless the epithelial barrier is
broken. Acts by altering the viral replication by substituting for thymidine in the viral
DNA chain therefore prolonged or too frequent administration may damage the corneal
epithelium and prevent the ulcer healing.
Vidarabine: 3%Ointment-it is poorly lipid soluble,so corneal penetration is minimal

unless ulceration is present.Penetrates the cornea better than Idoxuridine. Frequency of
administration is to apply small amount of ointment 5 times daily until corneal re-
epithelialization is complete,the every 12 hours for 7 days.
Trifluridine: 1%Solution-Current drug of choice for feline herpetic keratitis. Antiviral

potency reported as over twice that of idoxuridine and 5 times greater than Vidarabine.
s.penetrates the intact cornea,and ulceration and uveitis increase its intraocular
penetration.; administered 4-8 times/day for 2 days, and reduced over next 2-3 weeks.

134
Antifungal ocular drug therapy
Topical antifungal agents are used more commonly to treat fungal keratitis in horses than
in small animals. Penetration of the intact cornea is poor with all antifungals.
Polyenes : Natamycin : Used against Candida spp. and Fusarium spp. Amphotericin B:
Fungistatic. Generally used systemically for fungal endophthalmitis. May be given as an
intravitreal injection in mcg dosages.
Imidazoles. Miconazole 1%: the drug of choice for most veterinary fungal
keratitis.Tolerated well as subconjunctival injection. 1 ml SID x 3-5 days if tolerated.
Treatment frequency of a fungal keratitis may warrant 1 to 4hour treatment
intervals.lotions or sprays that contain ethyl alcohol should not be applied to the
eye. .Fluconazole is the synthetic triazole, fungistatic.currently drug of choice for topical
use, subpalpebral lavage unit, and intracameral (100 μg) injection. Treatment for fungal
keratitis may warrant 2 to 4hour treatment intervals.
Anti-inflammatory ocular drug therapy:
Corticosteroids: Subconjunctival injection of corticosteroids provide a greater local anti-

inflammatory effect than can be achieved by topical or systemic administration. Posterior
segment inflammation requires systemic corticosteroid therapy. In general, topical
therapy should be continued two weeks beyond resolution of clinical signs. Local side
effects of corticosteroid use include delayed corneal healing, increased corneal
collagenase activity, and an increased incidence of bacterial and mycotic keratitis. In
addition, topical corticosteroids may result in systemic changes. These include reduced
baseline cortisol levels, suppression of the adrenocorticotropic hormone response curve,
and altered carbohydrate metabolism. Frequency of administration-dependent on clinical
signs and the type of steroid used..
Nonsteroidal anti-inflammatory ocular drugs : Some degree of GI intolerance may

occur such as gastroduodenal ulceration and hemorrhage-when NSAIDs are used
systemically.
Aspirin: dog-10 to 20 mg/kg, BID; cat-10 mg/kg, q 48 hours. Carprofen :. May have
fewer side effects.Do not use in Labrador retrievers - may cause liver disease. Dosages:
2.2mg/kg BID. Not approved for use in cats. Etodolac :: dog-10 - 15 mg/kg, PO SID.
Should not be used in dogs < 5 kg in the horse and dog , although not currently approved
for use in dogs.: dog-0.75 to 1.20 mg/kg, IV, SID, not to exceed 2 days. Commonly given
30 minutes prior to surgery to minimize postoperative swelling and inflammation .; Not to
be used. In cat. Flurbiprofen: Used topically preoperatively to stabilize the blood-

134
aqueous barrier in inflammation (in diabetes mellitus), decrease production of ocular
prostaglandins and maintain pupil size. Used to treat anterior uveitis and in the presence
of corneal ulceration.
Ocular topical Anesthetics : To be effective, local anesthetics must have properties

similar to drugs that penetrate the cornea. They must be capable of existing in ionized
(water-soluble) and nonionized (lipid soluble) forms. Local anesthesia is less effective in
inflamed tissue which has more acidic pH than normal. Most topical anesthetics are
effective within 30 seconds to 3 minutes to facilitate procedures such as tonometry,
corneal and conjunctival scrapings, and subconjunctival injections. Microbial cultures
should be taken prior to application of topical anesthetics as inhibition of microorganisms
has been attributed to topical anesthetic agents. The agents used are Proparacaine -
0.5%, . Tetracaine - 0.5% to 2%.. Topical anesthetics should not be used on a regular
basis with painful eyes because: Animal may scratch off corneal epithelium (feels no
pain) and may inhibit mitosis (thus healing) in corneal cells.
a. Osmotic Agents (topical) : 2-5% NaCl (hypertonic saline). Indicated primarily for
treatment of severe chronic corneal edema originating from superficial epithelial
disruption and for severe cornea bullae formation. Side effect-localized irritation.
b.Tear Film Supplements : Many tear film supplements currently exist today. All are
indicated to control keratitis sicca. May provide temporary comfort to corneal irritation
resulting from distichia, entropion, or sutures, and as a vehicle for delivery of
medications. Tear supplements are available in solution and ointment form and are
intended to replace the aqueous or lipid layer of the tear film. Preservative-free products
generally recommended.
c.Lacrimogenics: These are drugs potentially capable of stimulating tear secretion.
1. Pilocarpine: May be effective in the rare case of neurogenic KCS. Prescribed as 2

drops of 2% Pilocarpine per 4.5kg body weight added to the food twice daily.
2. Cyclosporine A 0.2% ointment : Cyclosporine is a potent suppressor of T-cell growth

factor and of the cytotoxic T-cell response to this growth factor.
3. Tacrolimus 0.02%, 0.03% ointment or solution : Effective alternative to

cyclosporine. T-cell surpressor with a distinct receptor site to cyclosporine.
Anticollagenase/Mucolytic Agents :Collagenase inhibitors are indicated for the

treatment of melting corneal ulcers. Acetylcysteine : Diluted from 10 to 20% with

134
artificial tears to a 5 to 8% concentration. Administered every 1 to 4 hours until desired
effect is achieved.
*****

134
CLINICAL PHARMACOLOGY OF BETA- LACTAM AND
AMINOGLYCOSIDE ANTIBIOTICS
U.SUNILCHANDRA
The group of beta lactam of antibiotics includes Penicillins, Cephalosporins,

Carbapenems and Monobactams.
PENICILLINS
Narrowspectrum penicillins : Acid labile penicillin(crystalline penicillin G / benzyl

penicillin) and Acid resistant penicillins( penicillin V/phenoxymethyl penicillin and
phenethicillin (phenoxy ethyl penicillin) are active specifically against gram-positive
aerobes, facultative aerobes and obligate anaerobes. These can be still the drug of choice
in infections : clostridial, listerial, actinomycosis, anaerobic infections (abscess, wound,
pyothorax) and β-hemolytic streptococcal infections.
Penicillin G is complexed with sodium or potassium salts for parenteral administration,
which gives high concentrations of short duration with IV administration and lower
concentrations of longer duration after IM administration. Penicillin G is complexed with
procaine or benzathine for IM administration. Penicillin G procaine (PAM; aluminum
monostearate- adjuvant used) by IM injection is more slowly absorbed than Penicillin G
sodium salt. (An injection of 300,000 IU-adequate plasma levels for 24 hours).
Benzathine Penicillin G, by IM route has the slowest rate of absorption. (frequency once
in 72-96 hours). The availability of penicillin from procaine formulations is greater than
from benzathine formulations. Plasma and tissue concentrations with procaine penicillinG
are satisfactory for 12–24 h for most penicillin-sensitive organisms.
Antistaphylococcal penicillins (Cloxacillin, dicloxacillin, temocillin, nafcillin

flucloxacillin, methicillin, oxacillin) have similar spectrum though with lesser potency,
except that they are resistant to staphylococcalβ-lactamase. They are preferred in
Staphylococcal skin infections in dogs, surgical prophylaxis, especially for orthopedic
procedures and osteomyelitis
Broadspectrum penicillins: i) Aminopenicillins-ampicillin,amoxicillin(amoxycillin)and

ampicillin prodrugs/precursors (bacampicillin, pivampicillin, hetacillin , talampicillin ii)
Amidopenicillins eg: mecillinam (amidinopenicillin)
These have decreased activity against most of the gram positive species which are
covered by the natural penicillins . They are slightly less active against gram-positive and
anaerobic bacteria than penicillin G but have greater activity against gram-negative

134
bacteria. These are not active against penicillinase-producing Staphylococcus or gram
negative bacteria that produce β-lactamases.They are used for soft tissue infections (non
Staphylococcal)in dogs, cats and uncomplicated urinary tract infections.Aminopenicillins
may not be used for surgical prophylaxis as Staphylococcus are common pathogens.
Their spectrum of activity is extended to include some Gram negative bacteria, most
notably: Hemophillus influenzae, Escherichia coli and Proteus mirabilis. They retain
good activity against Neissaria species.
Extended spectrum Penicillins: (Antipseudomonal penicillins): Carbenicillin and
ticarcillin, in addition to gram negative coverage of aminopenicillins; have action against
Pseudomonas, Enterobacter and Proteus species. Azlocillin, mezlocillin, and
piperacillin,in addition, have spectrum against Klebsiella species. These (ticaricillin and
piperacillin) are indicaited in the topical treatment of otitis externa due to P.aeruginosa
resistant to other drugs and systemic treatment infections by Pseudomonas spp, usually
in combination with an aminoglycoside .
Active secretion of penicillins can be blocked by probenicid, an uricosuric agent; which

delays the excretion of penicillins, enhancing the duration of action.
Adverse Effects and Interactions: Hypersensitivity: Anaphylaxis (anaphylactic shock)

– manifested by skin rash, hives, itching, difficulty breathing, shock, and
unconsciousness. GI disturbances: diarrhea. nausea, vomition . Penicillins bind to and
inactivate aminoglycosides, a form of chemical antagonism.They should never be
administered simultaneously through the same I.V. line or through the same syringe.
Carboxy- or Ureidopenicillins and aminoglycosides are synergistic in their anti-
pseudomonas activity. Penicillin is synergestic with streptomycin. Antibacterials,
bacteriostatic, such as: Chloramphenicol or Tetracyclin are antagonistic with penicillins.
CEPHALOSPORINS
Thee are wide-spectrum bactericidals exhibiting time-dependent efficacy .The agents

are classified in to four generations, based on spectrum of antibacterial
First generation: Oral: cephalexin, cefadroxil, cefadrine, cephradine, cephaloglycin;

Parenteral: cefazolin, cephapirin, cefalonium, cephalothin, cefacetrile, cefapirin,
cefatrizine.
Characterestic Features: High activity against gram positive,Moderate activity against

gram negative. Absorption being highly erratic in ruminants, thus being used only in
preruminant calves and small animals. poor penetration across barriers (such as blood
brain barrier)

134
Cephalexin, cefadroxil and cefazolin : indicated for skin and soft tissue infections such
as pyoderma caused by streptococci and Staph. Aureus. Cefazolin is used to treat bone
and joint infections in the treatment of open fractures, lymphadenitis, abscesses,
pharyngitis
Second generation: Oral: Cefamandole, cefotiam, ceforanide, cefonicid, cefmetazole,

cefacetrile, cefotiam, cefranide, loracarbef, cefoxitin* cefotetan* (*-cephamycins);
Parenteral: cefaclor, cefuroxime axetil, cefprozil, cefuroxime
Their use is reserved for infections, resistant to first-generation agents. Less efficacious
than 1st generation against gram-positive pathogens; greater gram-negative spectrum of
activity Relatively more resistant than first generation ,to β-lactamases, Poor penetration
of the barrier. Cefoxitin and cefotetan (cephamycins): effective against gram negative
anaerobes, are used in aspiration pneumonia, bite infections, ruptured intestine gangrene,
peritonitis and pleuritis.
Third generation: Oral: cefsulodin, ceforanide, cefpodoxime proxetil, cefixime,
ceftibuten, cefdinir, cefmenoxime, cefditren pivoxil, cefodizime, cefetamet; Parenteral:
ceftiofur, cefotaxime, cefmenoxime, ceftriaxone, ceftizoxime, ceftazidime, cefovecin,
cefoperazone, latamoxef* (moxalactam) , (* -cephamycin)
They exhibit high antibacterial activity; broader resistance to β-lactamases, though show
moderate activity against gram-positive and are inferior in activity against Staphylococci.
Ceftriaxone, ceftizoxime, cefotaxime and ceftazidime are effective in therapy for
bacterial meningitis. Cefpodoxime has been used in skin infections of dogs
Ceftazidime,ceftriaxone and ceftizoxime and Cefoperazone are Antipseudomonal.
Cefovecin is given as a single injection (SC), has about five days of elimination half life;
used in dogs and cats to treat skin and soft tissue infections and urinary tract infections.
It should not be used in less than 8 weeks old, renal dysfunction,breeding animals,
pregnant and lactating dogs. Ceftiofur is indicated in bronchopneumonia of cattle
(Pasteurella)
Fourth generartion: Oral:. Cefmetazole, cefditoren; Parenteral: cefepime, cefpirome,
cefquinome cefclidine, cefluprenam cefozopran
They have extended spectrum of activity against both gram positive and gram negative
organisms ,greater stability against hydrolysis by beta lactamases. With excellent
penetration ability in to CSF..
Adverse Effects: Gastrointestinal disturbances : Anorexia, vomiting and diarrhoea.
Hypersensitivity reaction : manifested as urticarial rashes, fever, eosinophilia,
angioedema and lymphadenopathy. ; avoided or used with caution in penicillin allergic
individuals. Bleeding disorders: cefotetan, ceftazidime,cefamandole and cefoperazone :

134
increased risk of bleeding due to a decrease in prothrombin activity and anti- vitamin K
effects.Prophylactic vitamin K therapy is recommended if to be used for prolonged
periods in malnourished patients.
Most of the the cephalosporins are synergistic with aminoglycosides. Antacids and H2-
receptor antagonists: decrease the absorption of cephalosporins ; thus to be
administered at two hours intervals. Nephrotoxic medications:, such as loop diuretics,
especially in patients with pre-existing renal function impairment and Platelet
aggregation inhibitors: (NSAIDS) may increase risk of hemorrhage if used
concurrently with cephalosporins
PENEMS (CARBAPENEMS)
The carbapenems are more rapidly bactericidal than the cephalosporins and less likely to
induce release of endotoxin in an animal from gram-negative sepsis. Examples:
imipenem, meropenem faropenem.
Imipenem is a broad-spectrum antibiotic with excellent activity against gram positive and
gram negative organisms (both aerobic and anaerobic), by comparison to third and fourth
generation cepahalosporins.. It is resistant to most forms of beta-lactamase including that
produced by staphylococcus. They are indicated in multiple-resistant gram negative or
mixed aerobic and anaerobic infections, including those in immunocompromised hosts.
Adverse effecst: GI disturbances, hypersensitivity reactions, seizures with high doses,
renal failure or underlying neurological abnormality,infusion reactions such as
thrombophlebitis after rapid infusion. They are synergistic with an aminoglycoside. and
antagonistic with other β-lactam antibacterials, chloramphenicol .They are indicated for
intra-abdominal infections, severe lower respiratory tract infections, septicemia ,bacterial
meningitis ,osteomyelitis and life threatening soft tissue infections.
Dose: Imipenem-dogs ,cats- 5-10mg/kg, IV , IM, q 8 h; horse : 10-20mg/kg, IV, q 6 h .;

Meropenem: dog- 2-5mg/kg, slow IV (with IV fluids) , q 6 h; 5 -10mg/kg, deep IM q 8 h
or 8-12 mg/kg SC, q 8 -12 h.
MONOBACTAMS
Monobactams (Eg: aztreonam, tigemonam) are very beta-lactamase stable, with very
narrow spectrum, only against aerobic gram negative organisms, can be used instead of
aminoglycoside drugs with less nephrotoxic side-effect . These do not cause GI
disturbances Their inactivity against gram positive bacteria may lead to superinfection
with yeasts and gram positive aerobes including Enterococcus spp.and S.aureus . Dose
30-50mg/kg,IV q8 h; indicated in wide variety of UTI. RTI, Septicemic infections.

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BETA LACTAMASE INHIBITORS
Eg: Clavulanic Acid ( potassium clavulanate), tazobactam and sulbactam These drugs
themselves have no antibacterial activity. They irreversibly inactivate bacterial beta
lactamases, thereby enhancing the spectrum of activity of antibiotics used in combination
with them. (amoxicillin ampicillin , piperacillin, ticarcillin and some cephalosporins).
hese are often the drug of first choice for severe infections in skin,soft tissue and urinary
tract and for surgical prophylaxis. Clavulanate is highly moisture sensitive, so precaution
is to be taken to ensure the dryness of syringes for injection. Amoxicillin-clavulanic acid
injection is not compatible with and should neither be reconstituted or mixed with
dextrose / sodium bicarbonate solution nor it should be mixed with any other medication.
The combination of tazobactam plus piperacillin has the broadest antoibacterial activity of
the penicillins.
AMINOGLYCOSIDES
A post-antibiotic effect, i.e., residual bactericidal activity persisting after the serum
concentration has fallen below the minimum inhibitory concentration (MIC), is a
characteristic of aminoglycoside antibiotics; the duration of this effect also is
concentration dependent. These properties usually makes the once-daily dosing regimens
of aminoglycosides.
Narrow-spectrum : streptomycin and dihydrostreptomycin-against aerobic gram-

negative bacteria; Expanded-spectrum : Neomycin, framycetin (neomycin B),
paromomycin (aminosidine) and kanamycin have broader spectra than streptomycin that
often include several gram-positive as well as many gram-negative aerobic bacteria.
In potency, the spectrum of activity and stability to enzymes of plasmid-mediated

resistance is: amikacin > tobramycin ≥ gentamicin > neomycin > kanamycin >
streptomycin.
Amikacin has the broadest spectrum of activity among the aminoglycosides, particularly
important intreating serious Pseudomonas and other Gramnegative infections in
immunosuppressed patients. It can be administered for 2–3 weeks at recommended doses
with less risk of nephrotoxicity than with gentamicin.These aminoglycosides with
broader spectra that include P aeruginosa are often highly effective against a wide
variety of aerobic bacteria and have no activity against anaerobic microorganisms/ in
anaerobic conditions. Their action against most gram-positive bacteria is limited, and they
should not be used as single agents to treat infections caused by gram-positive bacteria. In
combination with a cell wall-active agent, such as a penicillin or vancomycin, an
aminoglycoside (streptomycin and gentamicin most extensively) produces a synergistic

134
bactericidal effect. Examples include septicemia; tracheobronchitis; pneumonia;
osteoarthritis; and infections of the urinary tract, GI tract, and skin and wounds. Several
aminoglycosides are used topically in the ears and eyes.
The treatment interval should be increased in neonates (especially puppies and foals), in
renal failure, and in obese animals. Doses may be increased in animals with edema,
hydrothorax, or ascites, provided their renal function is unimpaired. Because of their polar
nature, they do not penetrate into most cells, the CNS, and the eye. High concentrations
are found only in the renal cortex and the endolymph and perilymph of the inner ear; the
high concentration in these sites likely contribute to the nephrotoxicity and ototoxicity
caused by these drugs
Indications: Local and systemic infections caused by susceptible aerobic bacteria

(generally gram-negative): bacteremia ,septicemia, bone and joint infections, enteritis
(Neomycin sulfate: for enteritis caused by E. coli), respiratory tract, skin and soft tissue
and urinary tract infections.
Dosages:
AMINOGLYCOSIDES:Kanamycin12-15mg/kg,IMorSC,SID-BID;
Streptomycin/dihydrostreptomycin7.5-12.5 mg/kg, IM or SC, BID; Netilmicin3-6 mg/kg,
IM or SC, SID- BID; Neomycin15 mg/kg, PO, SID- BID0.5-1 g/quarter, intramammary, SID ;
Amikacin -IV, IM, SC 5-10 mg/kg q.12 h; Gentamicin IV, IM, SC 3-6 mg/kg q.24 h;
Neomycin PO 10 mg/kg q.6 h; Streptomycin POIM, SC; 20 mg/kg q.6 h; 10 mg/kg q.12
h; Tobramycin IV, IM, SC 1–2 mg/kg q.8 h
PENICILLINS: Narrow spectrum: penicillin G, Na, K IV, IM, SC 20,000–40,000
U/kg q.6–8 h; Penicillin G, procaine IM, SC 20,000 U/kg q.12–24 h Penicillin G,
benzathine IM 40,000 U/kg every 3–5 days Penicillin V PO 10 mg/kg q.8 h
Antistaphylococcal: Cloxacillin, flucloxacillin PO 10–40 mg/kg q.6–8 h Dicloxacillin
PO 10–40 mg/kg q.8
Aminopenicillins: Amoxicillin PO, IV, IM, SC 10–20 mg/kg q.8–12 h; Ampicillin IV,
IM, SC, PO 10–20 mg/kg q.6–12 h; amoxicillin-clavulanate : PO, IM, SC 12.5–25 mg/kg
q.8–12 h .Antipseudomonal : Carbenicillin IV, IM, SC 50 mg/kg q.6–8 h Ticarcillin IV,
IM, SC 50–75 mg/kg q.6–8 hInfusion: 15–25 mg/kg given over 15 min, then at constant
rate of7.5–15 mg/kg/h Ticarcillin-clavulanate: IV Dogs: 40–110 mg/kg IV q.6–8 h; Cats:
40–75 mg/kg IV q.6–8 h
CEPHALOSPORINS: First generation Cefachlor PO 10–25 mg/kg q.8–12 h;

Cefadroxil PO 10–30 mg/kg q.8–12 h Cefalexin PO Dogs: 20–40 mg/kg q.8–12 h; Cats:
22–50 mg/kg q.8–12 h; Cefazolin IV, IM 10–30 mg/kg q.4–8 h; Cefapirin IV, IM, SC,

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10–30 mg/kg q.6–8 hSecond generation: Cefotetan IV 30 mg/kg q.6–8 h; Cefoxitin IV,
IM, SC 10–30 mg/kg q.6–8 h; Cefuroxime IV, IM, SC 20–50 mg/kg q.8–12 hThird
generation: Cefi xime: PO 5–12.5 mg/kg q.12 h; Cefotaxime: IV, IM, SC 20–80 mg/kg
q.6–8 h; Cefovecin- SC 8 mg/kg (repeated every 14 days depending on indication);
Cefpodoxime proxetil : PO 5–10 mg/kg q.12–24 h; Ceftazidime: IV, IM 20–50 mg/kg
q.8–12 h; Ceftiofur : SC 2.2–4.4 mg/kg q.12–24 h; Ceftriaxone: IV, IM 15–50 mg/kg
q.12–24 h Antipseudomonal: Cefoperazone: IV, IM 22 mg/kg q.6–12 h
*****

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AN UPDATE ON MACROLIDES AND TETRACYCLINES
U.SUNILCHANDRA
The clinical pharmacological aspects of tetracycline, chloramphenicol, macrolide

and lincosamide group of antibacterisla are briefed in this article.
TETRACYCLINES: are broad spectrum antibiotics,effective against organisms: which

comprises- aerobic and anaerobic gram-positive and gram-negative, mycoplasmas,
rickettsiae, chlamydiae, and some protozoa (amebae, babesia, theileria).
1.Short acting (half life 6 hours)-Tetracycline, chlortetracycline, oxytetracycline

2.Intermediate acting-half life 16 hours-demeclocycline Newer ones : 3.Long acting –half
life-18-24 hours-doxycycline and minocycline. Tigecycline is the -newest, longest acting
–half life-36 hours2
The tetracyclines are used to treat both systemic and local infections. General organ
infections include bronchopneumonia, bacterial enteritis, urinary tract infections,metritis,
mastitis, prostatitis, and pyodermatitis. infectious keratoconjunctivitis in cattle,
chlamydiosis, anaplasmosis, actinomycosis, actinobacillosis, nocardiosis (minocycline),
ehrlichiosis( doxycycline), eperythrozoonosis, and haemobartonellosis. . As additives in
animal feeds, they serve as growth promoters.
Adverse effects: High doses (PO) in ruminants disrupt microflora, eventually producing
stasis. Elimination of the gut flora in monogastric animals reduces the synthesis and
availability of the B vitamins and vitamin K from the large intestine. Tetracyclines chelate
calcium in teeth and bones; they become incorporated into these structures, inhibit
calcification (eg, hypoplastic dental enamel), and cause yellowish then brownish
discoloration. At extremely high concentrations, the healing processes in fractured bones
is impaired. Rapid IV injection of a tetracycline can result in hypotension and sudden
collapse. This effect can be avoided by slow infusion of the drug (>5 min) or by
pretreatment with IV calcium gluconate. The IV adm. of undiluted propylene-glycol-
based preparations leads to intravascular hemolysis, which results in hemoglobinuria, and
other reactions such as hypotension, ataxia, and CNS depression The combined use with
glucocorticoids leads to weight loss, particularly in anorectic animals . The tetracyclines
are potentially hepato and nephrotoxic and are contraindicated (except for doxycycline)
in renal insufficiency.
Interactions: The absorption from the GI tract is decreased by milk and milk products,
antacids, kaolin, and iron preparations. Tetracyclines gradually lose activity when diluted

134
in infusion fluids and exposed to ultraviolet light. B-complex Vitamins , especially
riboflavin, hasten this loss of activity in infusion fluids. Tetracyclines bind to the calcium
ions in Ringer’s solution.. The tetracyclines are less active in alkaline urine, and urine
acidification can increase their antimicrobial efficacy
Tigecycline: is a glycylcycline.; broad antimicrobial spectrum; effective against many

tetracycline resistant organisms: Staph, MRSA, vancomycin intermediate and
ncomycinresistant strains, G+ve rods, enterobacteriaceae, multidrugresistant
acinetobactersp, anaerobes (G+ve, G-ve), atypical agents, ricketisiae, chlamydia,
legionella, rapidly growing mycobacteria.Used in multi drug resistant nosocomial
pathogens (MRSA, beta lactamaseG –sp) and skin and intraabdominal infections. Not
indicated for urinary tract infections.
CHLORAMPHENICOL: Broad spectrum bacteriostatic. With specific activity against

a wide variety of organisms (gram +ve and –ve and anaerobes gram-positive cocci and
clostridium species;gram-negative rods ,. staphylococci and streptococci;some gram-
negative organisms, such as Bordetellabronchiseptica, Escherichia coli, and Salmonella
species;anaerobic bacteria; and rickettsiae Adverse effects: Hematological toxicity
(aplastic anemia: leukopenia, thrombocytopenia, bone marrow depression). Indications:
Anaerobic infection-meningitis,Brain abscess-used together with penicillin. ; Intraocular
infection-Topical use in conjunctivitis, and external ear infections; as second choice drug
in: rickettsial infection and brucellosis. Dose: Dogs:, 45- 60 mg / kg body
weightPO,IM,IV,SC q8h; cats- 13 to 20 mg/ kg,PO,IM, q12h
MACROLIDES: are bacteriostatic,(bactericidal at high concentrations.). In general,

they have a spectrum similar to that of the penicillins and are often used as penicillin
substitutes for the treatment of streptococcal and staphylococcal infections.In
addition,against Mycoplasmae, Chlamydiae, Legionellae, Rickettsia spp. gram positive
anaerobes etc..
Interactions: Macrolides should not be used with chloramphenicol or the lincosamides.

Activity of macrolides is depressed in acidic environments. Macrolide preparations for
parenteral administration are incompatible with many other pharmaceutical preparations.
Erythromycin and troleandomycin are microsomal enzyme inhibitors that depress the
metabolism of some drugs like warfarin, theophylline, carbamazepine and methyl
prednisolone. terfinadine, azole antifungals, cisapride
Tilmicosin is used treatment of pneumonia in cattle, sheep and pigs, associated with
Pasteurella haemolytica, P. multocida, Actinobacillus pleuropneumoniae, mycoplasma
species Tilmicosin phosphate has been effective for treating: .bovine respiratory disease

134
(as effective or more effective than other established treatments: ceftiofur,
oxytetracycline, or florfenicol). Injections to horses, goats, swine, or nonhuman primates
can be fatal. heart ,the target of toxicity via depletion of cardiac intracellular calcium,
resulting negative inotropic efect. As a feed additive , it is effective for controling
pneumonia in swine. When injected in swine, tilmicosin has caused toxic reactions and
death due to cardiovascular reaction. Dose: Cattle and sheep: 10mg/kg, SC, every 72
hours; Pigs: 200-400g/tonne feed
Tylosin is therapeutically used to treat: swine dysentery, pleuropneumonia, colitis in

dog, other infections in cats, chickens Mycoplasma canis and Mycoplasma haemocanis
infection in dog,cattle Tylosin is alos used for growth promotion in pigs, cattle, and
chickens. Dose: Dogs: 40mg/kg,PO,tid; cats 4mg/kg,IM,sid; Cattle: 10-20mg/kg,IM,bid;
Pig: 10mg/kg, IM, bid,25g/100litres drinking water,100g/tonne feed;Poultry: 10 mg/kg,
IM, sid-bid 7-10 mg/kg, PO, tid ; 50g/100litres drinking water
Clarithromycin possess broad spectrum bactericidal activity ,with more activity

against mycobacterial avium complex and post antibiotic effect with very good activity
against opportunistic infections in Toxoplasmosis, Cryptosporidiosis; H.pylori in peptic
ulcer. High concentration in the alveolar macrophages, lung tissue and tonsillar tissue
show high penetration of the drug into the respiratory tract cells, a feature that enhances
efficacy against typical and atypical pathogens causing pneumonia It is more acid stable,
more active against mycobacterium avium complex with lower frequency of GI
intolerance. Dose: Dogs and cats: 5-10mg/kg,PO, bid
Azithromycin is slightly less active than erythromycin against staphylococci and
streptococci and slightly more active against Haemophilus influenzae.; good activity
against many intracellular organism. (Chlamydia, Toxoplasma) , mycobacteria
,mycoplasma ; but not against enteric gram-negative bacteria or Pseudomonas. The
features: better oral absorption,better tolerance,longer half-life ,higher tissue
concentration, broader spectrum of activity and lesser drug interactions . Dose: Dogs : 5-
10mg/kg,PO, sid ; cats: 5mg/kg.PO, once daily or every alternate day. Roxithromycin is
a longer acting and more stable: Dogs : 15mg/kg,PO, sid
Tacrolimus is a macrolide ; is an immunosuppressive with similar mechanism of action

as another immunosuppressant, cyclosporine to inhibit T lymphocyte proliferation. It has
topical anti inflammatory effects without the atrophogenic effects and metabolic effects
of topical GC. It is used topically for the treatment of atopic dermatitis,psoriasis ,
alopecia areata and effective in canine perianal fistula and localized lesions in diseases
like discoid lupus erythematosus, pemphigus erythematosus, pemphigus foliaceous.

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LINCOSAMIDES: bacteriostatic/ bactericidal depending on the concentration/;
particularly active against grampositive,mycoplasma, and anaerobes(most aerobic gram-
negative bacteria are resistant). The agents are lincomycin and clindamycin. The
antimycoplasmal activity of the lincosamides(clindamycin > potent) is similar to that of
erythromycin but less than that of the other macrolides. In horses,rabbits, chinchillas,
guinea pigs, neonates and hamsters: these are contraindicated due to risk of
gastrointestinal adverse effects like serious fatal enterocolitis and diarrhoea. Ruminants
exposed to oral lincomycin : anorexia, ketosis, and severe diarrhoea.
Interactions: Additive neuromuscular effects with anesthetic agents and skeletal muscle
relaxants. Antidiarrheals,adsorbent (kaolin/astringent) significantly decrease absorption..
Indications: lincomycin HCl: respiratory tract, skin and soft tissue,dental infections,
osteomyelitis (cats, dogs) ; swine dysentery, joint infections (pig); necrotic enteritis
(chicken); clindamycin: severe anaerobic,respiratory infections . Dose: Lincomycin: 10
mg/kg, IM, bid- Cattle,pig,cats; 20 mg/kg, PO, sid- dog.; Clindamycin: 5-10 mg/kg, PO,
bid- Dogs, cats
*****

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ADVANCES IN ANTIMICROBIAL THERAPY OF MASTITIS
N.A. PATIL
Bovine mastitis is internationally recognized as one of the most economically

important disease confronting the dairy industry. The disease not only decreases the
quantity, but also reduces the quality of the milk, thus resulting in significant losses to the
dairy farmer. The loss is further enhanced by the cost of the treatment and culling of
animals due to permanent damage of quarters in certain cases. The key to combat losses
due to mastitis is the early detection, accurate diagnosis, treatment and suitable control
measures are to be undertaken.
Diagnosis : The various diagnostic tests that can be employed for detection of
mastitis are
1. Strip cup plate test
A black surface strip plate is invariably used. Although, flakes and clots may be
palpable or obvious on other surfaces, serum like or watery milk is appreciated on a black
surface stripped plate.
2. PH indicator strips
Determination of milk pH is done by using specially prepared filter papers

containing bromothymol blue, bromocresol purple etc. Mastitis is characterized by a
change in pH towards alkalinity, though this change may not be present in the early stage
of mastitis. Normal PH is 6.5 to 6.7 or 6.0 to 6.4 in colostral milk. It is around 6.0 in
gangrenous mastitis and greater than 6.9 in other forms of mastitis.
3 White side test
Five drops of milk are mixed with 2 drops of sodium hydroxide solution on a
microscope slide. If the milk is normal and has a normal cell count, homogenous turbidity
develops within 2 - 3 seconds. If the cell count is high, flakes form and the mixture
become stringy.
4. California mastitis test

134
Two ml of milk from each quarter are placed in the four dishes of a black or
white test plate. 2 ml of the reagent is added to each dish and the contents are mixed by
slow circular movements. The results are read after 10 seconds.
Negative Mixture remains liquid. No precipitates
Trace Precipitates tends to disappear with movement of paddle
1+ Distinct precipitates. No gel formation
2+ Gel becomes thick and lumpy
3+ Gel adheres to the bottom of the paddle
The principle of the test is the ability of surface active substances to dissolve
leukocytes and their nuclei, liberating DNA from the latter. The DNA forms a complex
with the reagent that appears as a gel.
5. Chloride test
In a normal milk chloride level varies from 0.08 to 0.14 per cent. Due to
inflammatory exudate, abnormal milk have high chloride levels. The chloride level may
be estimated by addition of 5 ml of 0.134% silver nitrate solution and 2-3 drops of
10% potassium chromate solution. Yellow color indicates chloride level more than
0.14% and brownish red color indicates less than 0.14% level.
6. Catalase test : examined by evolution of oxygen on adding 1 ml of 3% H2O2 to 9

ml of milk.
7. Electrical conductivity
The test which has received more attention is based on increase in sodium and
chloride ions in mastitis milk and thereby increase in electrical conductivity. Electronic
sensors with shielded electrodes are used and hand held devise with a built in cup into
which milk is squirted
8. Serum albumin concentration in milk
This test set out to access the integrity of mammary mucosa. Radial
immunodiffusion test (RID) called as mono mast test is employed.
9. NAGase test

134
This test is based on measurement of cell associated enzyme ( N-acetyl-beta D-
glucosaminidase) in the milk. High level of the enzyme indicates high cell count and it is
the most accurate as somatic cell count and they are high at the beginning and end of
lactation.

134
10. Antitrypsin test
This test measurers trypsin inhibitor capacity of milk. This is high at the beginning
of lactation due to antitrypsin activity of colostrums, but after the first month of lactation
this activity is due to solely to serum antitrypsin activity which has leaked through
damaged epithelium.
Treatment
Clinical judgment to distinguish between mastitis caused by Gram positive or

Gram negative pathogens are not accurate. To select cows for antimicrobial therapy on
the basis of bacteriogical culture is costly and delays treatment, clinical judgment
would still be necessary because bacteria are not isolated from 15-40% of milk
samples from cows with clinical mastitis. The first decision to make whether to treat
parenterally or by intramammary infusion or both or not at all.
Parenteral antimicrobial therapy should be considered in all cases of mastitis in

which there is a marked systemic reaction and swollen udder in which intramammary
infusions are unlikely to diffuse to all parts of the glandular tissue. To achieve therapeutic
levels of an antimicrobial in the mammary gland, it is necessary to use higher than
normal dose rates daily for 3-5 days
Udder infusions are preferred because of convenience and efficiency. Cure rates
are very high with infusions in cases of mastitis caused by Str. agalactiae. The degree
of diffusion in to glandular tissue is the same when either water or ointment is used as
a vehicle for infusion. Strict hygiene is necessary during treatment to avoid the
introduction of bacteria, yeast and fungi in to the treated quarters. Use only a short canal
that can just penetrate the external sphincter. Complete emptying of the quarter by the
parenteral injection of oxytocin followed by hourly hand stripping of affected
quarters before infusion is advisable in case of clinical mastitis.
Selection of antibiotics:
The Selection of antibiotics for therapy has been the basis of important criteria of
sensitivity of the pathogens and the pharmacokinetic properties of the drugs. It is
necessary to know something about their diffusion in to mammary tissue, the degree of
binding of a drug to mammary tissues and secretions, the ability to pass through the lipid
phase of milk and the degree of ionization. For lactating cows the preferred treatment is
one which maintains a minimum inhibitory concentration (MIC) for 72 hours without
the need for multiple infusion and without prolongation of the withdrawal time

134
The aminoglycosides neomycin and framycetin, ampicillin and amoxicillin and
especially newer generation of cephalosporins are the drug of choice for use in cases in
which infection may be caused by either a gram positive or gram negative organism.
Penicillin is favoured for Gram positive infections. The drugs which have the best
record of diffusion through the udder after intramammary infusion are ampicillin,
amoxicillin, erythromycin and tylosin. Medium performance are pencillin G, cloxacillin
and tetracyclines. Poor diffusers, which do have a longer half life in the udder because
they bind to protein include streptomycin and neomycin.
In coliform mastitis antibiotics like gentamycin, amikacin, cephalothin,

trimethoprim plus sulfadoxine, amoxicillin plus clavulanic acid is recommended as these
have been claimed to be more effective.
Non steroidal anti-inflammatory ( NSAIDS) have the beneficial effects on the

severity of clinical signs such as body temperature heart rate, size of the udder and pain
associated with the mastitis. Meloxicam, flunixin meglumine (2.2mg/ Kg), flurbiporfen
(2mg/kg, I/V) and Dexamethasone (1mg/kg, I/V) can be used as anti-inflammatory
agents.
Supportive therapy including balanced electrolyte solutions containing 5%

glucose at the rate of 100-150 ml/kg body weight per 24 hours by continuous
intravenous infusion is indicated in cases where extensive tissue injury and severe
toxemia are present. Antihistamines may be used to reduce toxaemia. Application of
cold (crushed ice) in a canvas bag suspended around the udder may reduce the absorption
of toxins. Injection of selenium and vitamin E may enhance the resistance of the
mammary gland to infectious agents. Tri-sodium citrate given at the rate of 30mg/kg
orally once a day for 10 days has been claimed to be effective in treatment of mastitis.
Control :The specific components of mastitis control program must be devised to fulfill
three basic principles
• Elimination of existing infections by detection and treatment of infected quarters

during lactation and dry period and culling of chronic cases.Prevention of new
infections achieved by good managemental practices,administration of vitamin E-
3000mg of 5 to 10 days prior to calving, in diet at the rate of 4000 I.U. During last
14 days and 2000 IU during lactation decrease the incidence of infection.
• Monitoring udder health status: To reduce the new infections dipping of all teats
after each milking should be done. Environmental and nutritional management have
also become important for the prevention of new infections.

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*****

134
CHEMOTHERAPUETIC PROTOCOLS IN HEPATIC
AILMENTS
M. VIJAY KUMAR
Liver has very complicated functions and one of the most important function is
the detoxification of drugs such as antibiotics and its metabolites. Some antibiotics can
cause allergic reactions while others can cause direct damage to their liver, which can be
quite severe in patients with chronic liver disease. For patients with a pre-existing liver
disorder, the detoxification function of the liver is already compromised and substances
that would normally be metabolized could actually accumulate in the liver or in the
bloodstream.Liver disease may have a variable effect on drug clearance. There are no
tests for hepatic function that will reliably predict drug clearance.
Antibiotics that accumulate in this manner could become toxic to the body and its
functions can change drastically from its original purpose. For the most part in treating
patients with preexisting liver disease who develop infections outside the liver, one
should use caution in prescribing drugs known to be dependent on liver for inactivation or
excretion. Usually a safer substitute drug can be found. If a potentially toxic drug must be
used, blood levels can be useful in monitoring the dose to within safe limits. One should
also take care to avoid use of hepatotoxic non-antibiotic drugs concomitantly. On the
other hand, drugs metabolized and/or excreted by the liver are theoretically ideal for
treatment of acute infections of liver and biliary tract. Each one of the ollowing
antibiotic is ordered according to their potential harmful effects on the liver, the top group
being the most potentially harmful and the last group being the least.
Tetracyclines: Used in larger doses, cause jaundice, fever, and fatty liver. Hepatitis
patients should not be administered with these agents. All tetracyclines are concentrated
in liver and excreted via bile into intestine, where they are reabsorbed. Variable amounts
of each member of this drug family are thereafter eliminated in urine.; have prolonged
half-lives in the serum because of slower renal clearance than that of tetracycline or
oxytetracycline. With excess parenteral dose, liver toxicity progresses to acidosis, shock,
coma and death.Other organs which may suffer simultaneous toxicity are pancreas,
kidneys and brain. Pregnancy and chronic renal disease seem to predispose patients to this
type of hepatotoxicity. Dosage adjustment is necessary, avoid exceeding a blood level of
10mcg/ml. Tetracyclines have adverse effects on several hepatic enzymes. Inactivated
chlortetracycline causes same toxic hepatic changes as the active drug, so hepatic toxicity

134
appears not related to antibacterial activity; thus to be avoided completely in liver
disease
Macrolides : Erythromycin: It causes damage to the liver via cholestasis (bile

retention) and jaundice. The harmful effects usually start to show after 10 to 14 days use
and the incidence rate is approximately 5 to 10%. Clinically, patients may develop
abdominal pain, nausea, vomiting, jaundice, and elevation of liver enzymes. These
conditions are often considered allergic reactions since the incidence rate is not very high
Liver toxicity is caused by only estolate form. Avoid estolate form in liver disease and
other forms in usual dosage. Estolate-induced hepatitis is a dose dependent.
hypersensitivity reaction.
Lincosasmides: Lincomycin: is excreted and re-excreted via enterohepatic circulation.

Bile levels are high upto 10-20x the serum level. Occasional jaundice and/or abnormal
liver function tests which clear rapidly, sometimes even while drug is continued. Half-life
of drug is doubled in liver disease accordingly drug dose should be reduced, or drug
avoided entirely.
Kanamycin : Not Metabolised by liver.No change in dose in case of parenteral liver

disease.in case of oral dose kanamycin at 8 Gm/day eventually builds serum levels to
therapeutic range. This effect is even greater with hepatic disease and azotemia.
Accordingly, such patients on gut sterilization with kanamycin should be watched for
deafness and increasing nephropathy. Neomycin: Not metabolised by liver. No more than
6 Gm P.o in liver disease for gut sterilization. If azotemia also present,kanamycin is
preferred.
Chloramphenicol: When metabolized in the liver, they combined with glucoronic acid
and lose their anti-microbial effects. This combination of antibiotics and glucoronic acid
can accumulate in the bloodstream, which can cause bone marrow inhibition. As a result,
WBC and RBC counts can drop and patients with hepatitis should try to avoid this group
if they can. Metabolism by liver. 85-95% is conjugated in liver to monoglucuronide and
3% is further converted to aryl amines and aryl nitro derivatives.Most of above is secreted
then by kidney tubules. Significant concentration in liver tissue levels and average bile
levels,that of plasma. Liver toxicity is rare. Use with caution in liver disease. If ascites or
jaundice is present, use under 25 mg/kg/ day or another drug. Newborns are vulnerable to
"grey syndrome"due to immature hepatic and renal function.
Penicillins: These antibiotics cause the least liver damage and only patients who are
allergic may experience some side effects. Generally, antibiotics in the penicillin family
are the most "liver friendly" and safe for chronic hepatitis patients to use.

134
Penicillin G: . Metabolism by liver: Only minor fraction is ordinarily handled by liver,
but in impaired renal function the liver may be a major excretion route via bile. Attains
significant liver tissue levels and also bile levels.Liver toxicity is rare, as part of a
generalized hypersensitivity reaction. No change in dose in liver diseases if renal
function is good and reduce dose in circumstances of combined kidney and liver disease.
Generally the information for penicillin G applies also for Alpha-phenoxy-

peniclllins Methicillin., Oxacillin methicillin. Cloxacillin and broad spectrum penicillins:
ampicillin, hetacillin, carbenicillin and nafcillin.
Streptomycin and Dihydrostreptomycin: Metabolism by liver.Small fraction is secreted

into bile. Bile levels up to 10-20mcg/ ml on high doses. Liver toxicity is rare and also
may aggravate existing liver disease. No change in dose in liver disease.
Cephalosporins: Cephalothin: Metabolism by liver, 70-80% usually excreted

unchanged in urine. However, it can be inactivated by deacetylation (presumably in liver),
then excreted in urine. Advisable to decrease in presence of combined renal-hepatic
disease.
Nitrofurantoin: Metabolism by liver: 50-60% is metabolized at unknown site. Rarely,

causes a hypersensitivity hepatitis with cholestasis, focal necrosis, infiltrates,eosinophils.
Sulphonamides: Metabolism is significantly, but not solely by liver (acetylation,

glucuronidation, and/or oxidation), then excreted into urine. Not influenced by dose:
direct hepatotoxicity and hypersensitivity. Either may go on to acute yellow atrophy. Best
to avoid dose in liver disease. Pre-existing nutritional liver disease may predispose to
sulfonamide hepatotoxicity. Kidneys appear to be more susceptible to damage by sulfas in
patients with chronic liver disease.Neonate require less dose for therapeutic blood levels.
Metronidazole and related drugs (tinidazole, ronidazole): are sometimes used in patients
with hepatic disease because of the anaerobic spectrum. The most serious problem caused
by high dose of metronidazole has been attributed to CNS toxicity and include seizures,
ataxia, nystagmus, tremors, and rigidity.4 These signs have been attributed to inferring
with the inhibitory neurotransmitter GABA. Because animals with hepatic disease also
may be prone to CNS disorders that also share these clinical signs, veterinarians should
understand the risks of metronidazole, and become familiar with the signs associated with
toxicity.
Fluoroquinolones: The fluoroquinolones (enrofloxacin, marbofloxacin, orbifloxacin,

difloxacin) have had a good safety record and increased risk of toxicity in animals with
hepatic disease has not been documented. Although some of these drugs are metabolized,

134
the clearance is low and probably not affected unless there is substantial loss of hepatic
function. These drugs are also cleared by the kidneys
A common dilemma for veterinarians is which nonsteroidal antiinflammatory drug

(NSAID) to administer to a patient with hepatic disease. The six approved NSAIDs for
dogs: carprofen, etodolac, Meloxicam (cats), tepoxalin, deracoxib, and firoxixib. Because
studies have not been conducted in animals with hepatic disease, there is no single drug
shown to be safer than another. However, All NSAIDs have the potential to: (1) induce
liver injury. (2) Pre-existing elevations in liver enzymes has not been shown to increase
an animal’s risk for NSAID-induced liver injury, but a sharp increase in liver enzymes
and/or bilirubin after instituting NSAID therapy is cause for alarm. (3) cause
gastrointestinal injury, including erosions, ulcers, and bleeding. Patients with hepatic
disease have an increased risk of these problems. (4) There is no NSAID yet to be shown
safe for long-term administration for cats and hepatic reactions have been one of the
problems associated with NSAID administration in cats. Tramadol and opiate analgesic
drugs have high clearance and their metabolism is not likely to be affected by a loss in
hepatic function or changes in hepatic enzymes. These drugs have a high safety margin
and can be used safely in patients with hepatic disease.
*****

134
ADVANCES IN THERAPEUTIC PROTOCOLS IN
VETERINARY ONCOLOGY
B.V.SHIVA PRAKASH
The effectiveness of a chemotherapeutic agent is measured in terms of

concentration and exposure time. Routes of administration and absorption may influence
the efficacy of an administered drug.The chemotherapeutic agents can be administered
orally, subcutaneously, intramuscularly and intravenously for systemic effects.Local
effects can be obtained by topical,intrapleural/peritoneal ,intra cystic/intrathecal into the
CSF.All the chemotherapeutic agents can not be given by each and every route hence
proper selection of route of administration can maximize the efficacy . Biotransformation
of the drug also should be taken into consideration in chemotherapy.Prednisone used in
chemotherapy has to be converted into prednisolone by the liver to be effective.
Distribution of drugs partially determines its effectiveness. If the drug donot reach to the
tumour,the exposure of tumour cells to chemotherapeutic agent will be nil. Some drugs
will be effective during first time administration while they may not be so effective during
their subsequent administration Drug resistance may develop by several means such as
acquired resistance of the tumour may occur owing to decreased activation or increased
deactivation of drug reducing its effective contact time..Toxicity: GI toxicity,
bonemarrow suppression and immunosuppression.
Principles of combinations of chemotherapy: 1. Effective single agent used. 2. Two

drugs with different mechanisms of actions should be used. 3. Intermittent treatment
schedule
Guidelines for chemotherapy: Thorough clinical examination, history collection and

appropriate data base are necessary for chemotherapy.
1. Histological diagnosis of tumour is must to know whether it is begnin or malignant
2. Biological behavior of tumors should be understood
3. Drug toxicities,dose level ,species limitations should be understood.
4. Monitoring of toxicities is essential.
5. Therapy should be undertaken with properly explaining the pros and cons to the
owners.

134
Chemotherapeutic agents can be classified as : 1. Alkalyting agent’s 2.Antimetabolites
3.Plant alkaloids 4. Antibiotics 5.Hormones 6.Miscelaneous
1. Alkalyting agents: These are the compounds that substitute an alkyl radical (R-CH2-
CH2+) for hydrogen atom on some organic compounds. These agents interfere with DNA
replication and RNA transcription.There are five class of alkylating agents
a) Nitrogen mustard derivatives: Methchloethamine,Cyclophosphamide,Chlorambucil

and Melphalan; b) Ethenimine derivatives:Triethylenethiophospharamide; c)Alkyl
Sulfonate:Busulfan d) Triazene derivatives:Dacarbazine; e) Nitrosoureas: Carmustine,
Lomustine, and Somustine
Cyclophosphamide is the most commonly used alkylating agent in Veterinary practice.It

is used for lymphoreticular neoplasms,carcinomas,mast cell
tumour,TVT,Cyclophophamide requires activation to its active metabolite 4-hydroxy
Cyclophosphamide by liver.Dose 50mg/ M2 per orally or weekly once for four times
intravenously. Chlorambucil is used in canine lymphosarcoma.Dose rate is 2mg/ M2 Per
orally or at weekly intervals for two to four weeks.
2. Antimetabolites: The antimetabolites are structural analogues of normal metabolite

required for cell function and replication.They damage cells by interacting with cell
enzymes (1).By substituting for a metabolite needed in key molecule,rendering it
functionally abnormal (2.)By competing successfully with a normal metabolite that acts at
an enzyme regulatory site to alter the catalytic rate of a key enzyme.
The important antimetabolite drugs are Methotrixate, 6-Mercaptopurine,)5-Flurouracil

and Cytosine Arabinoside. The antimetabolite drugs are S-phase specific.
Methotrixate acts in S-phase to inhibit dihydroxy foliate reductase compitatively and

interferes with both DNA and RNA synthesis.The folic acid antagonists are used in the
treatment of lymphoreticular neoplasms,myeloproliferative disorders,transitional
metastatic cell tumours,TVT,sertoli cell tumour and ostesarcoma.Methotrixate dose
2.5mg/ M2 per orally daily until response or toxicity.
3.Plant alkaloids: Vincristine and Vinblastine are the alkaloids extracted from the
periwinkle plant.Vinca Rosea.They act specifically in M phase by binding with
microtubular protein tubulin and blocking mitosis by interfering with chromosomal
separation in metaphase.Both the drugs are used in the treatment of lymphoreticular
neoplasms Vincristine is the treatment of choice for TVT and has been used for the
treatment of carcinomas and mast cell tumour.

134
4.Antibiotics : They are derived from soil fungus( Streptomyces).They are cell cycle non
–specific drugs.They damage the DNA.Inhibit DNA or RNA synthesis.Doxorubicin is a
cytotoxic drug.Vomiting,diarrhea,myelosuprression,cardiac toxicity are the side
effects.Doxorubicin must be given slowly when given intravenously.Pretreatment with
histamine helps in avoiding complications.Dose:30mg/ M2 at three week interval for
TVT,lymphosarcoma,carcinoma.
5.Hormones: Peptide hormones convert ATP to c-AMP(cyclic AMP).c-AMP is a

secondary messenger to deliver and amplify signals to intracellular site.Steroid hormones
enter cell and bind to specific receptor protein. “Transformation” (activation) of this
newly formed complex allows it to pass the nuclear membranes where it binds to
DNA.This binding alters transcription of cell messenger RNA,resulting in synthesis of
new protein.Steroid induced increase in fatty acids may cause dissolution of the nuclear
membrane,leading to cell death.
Adrenal corticoids are used for treatment of lymphosarcomas and mast cell tumours.Sex
hormones are used in the treatment of mammary ,prostate and perineal gland
tumours.Hormones have valuable role in replacement therapy following abalation
surgery,in the management of some metastatic problems.Prednisolone 60 to20mg/ M2 per
orally every 48 hours used in Lymphoreticular tumors mast cell tumour,and CNS
tumours.Diethyl Stilbestrol 1.1mg/kg (not more than 25mg)- used for perianal adenomas,
prostatic tumours.
6. Miscellaneous agents: examples: L-Asparginase o,p-DDD. L-Asparginase enzyme

preparation is derived from the bacteria.L-asparginase deprives the neoplastic cells that
lack the ability to synthesise L-asparginase of extracellular source there by inhibiting
protein synthesis.L-asparginase acts against cells in G1 phase.Used for the treatment of
lymphoreticular neoplasms @20,000units/ M2 intraperitoneally.Side effects are
anaphylaxis and leukaemia. o,p-DDD: Directly suppresses normal and neoplastic
adrenocortical cells,used in adrenocortical insufficiency @50mg /kg PO, to effect.
Drugs used in Chemotherapy:Chemotherapeutic agents dose is expressed in terms of

mg per square meters of body surface area.This is physiologically more accurate method
of determining the dose.Weight in grams is converted to body surface area(meter square)
as follows: M2 = Km xW2/3 / 104; wherein: M2 - Body surface area in square meters; W-
Weight in grams; Km- Species specific constant (10 for cats and 10.1 for dogs).The
relation of body weight to surface area in square meters for dogs is given in this table:

134
m2 m2 m2
Kg
Kg kg m2 Kg kg m2
0.5 0.06 6 0.33 12 0.52 18 0.69 24 0.83
1 0.10 7 0.36 13 0.55 19 0.71 25 0.85
2 0.15 8 0.40 14 0.58 20 0.74 26 0.88
3 0.20 9 0.43 15 0.60 21 0.76 27 0.90
4 0.25 10 0.46 16 0.63 22 0.78 28 0.92
5 0.29 11 0.49 17 0.66 23 0.81 29 0.94

134
134
DRUGS MAJOR INDICATIONS Dose& Route of Admn.
Cyclophosphamide Lymphoma,sarcomas, mammary 60mg/kgBW daily oral

adenocarcinoma,lymphocytic leukemia
Melphalan Multiple myeloma 150mcg/kgBW/day or

250mcg/kgBW daily 4 weeks
oral
Chlorambucil Chronic lymphocyticleukemia, 100mcg/kgBW daily oral

lymphoma
Carboplastin CNS neoplasm,GI carcinomas 300-360mg/m2 BSA by IV
Dacarbazine Lymphoma 2-4.5mg/kgBW for 10 days

IV10-15mg/day for 4-8days
oral
Busulfan Chronic myelogenous leukemia, 60mcg/kg BW daily oral

polycythemia vera
Methotrexate Lymphoma, Sertoli cell tumor, 10-15mg/day for 4-8 days oral
osteosarcoma, metastatic TVT
Fluorouracil GI, lung, liver, and mammary 15mg/kgBW once a week

carcinomas (systemic); cutaneous oral15mg/kgBW in 500ml
carcinomas (topical) DNS
Dactinomycin Choriocarcinoma, testicular carcinoma, 15mcg/kgBW per day or400-

(Actinomycin D) rhabdomyosarcoma, lymphoma 600 mcg/m2 BSA IV
Doxorubicin Lymphoma, acute lymphocytic 60-75mg/ m2 BSA IV

granulocyticleukemia, sarcomas
carcinomas
Bleomycin Carcinomas (testicular, squamous cell – 15,000IU thrice a week IM/IV

head,neck,seminoma,malignant
teratoma
Vinblastine Lymphoma and leukemias, 0.1-0.5mg/kgBW IV

mastocytoma
Vincristine TVTs, lymphoma and leukemias,CNS 25-75 mcg/kg or 1.4mg/m2

tumors, mammary carcinoma
IV
Cisplatin Osteosarcoma, carcinomas (transitional 50-120mg/m2 BSA with % NS,

cell, testicular, squamous cell of head IV
and neck, ovarian, cervical, bladder
L-Asparaginase Acute lymphocytic and lymphoblastic 1000units/kg BW/10days with

leukemia and lymphoma NSor Dextrose 5%
Hydroxyurea Polycythemia vera, mastocytoma, 20-30 mg/kgBW oral

granulocytic and basophilic leukemia,
thrombocythemia
Pharmacology &Toxicology,Veterinary
Prednisolone College,Bidar,from
Lymphoma, mast cell tumors, 31st January
palliative 60mg/m2 IM,IV
treatment of brain tumors
to 5 February, 2011
th
Tamoxifen Estrogen-receptor-positive mammary 20mg/day single dose oral 134

carcinomas
Flutamide Testosterone-receptor-positive prostatic 250mg TID oral

tumors; surgical castration preferred
*****

134
CHEMOTHERAPEUTIC MANAGEMENT OF PROTOZOAL
AND RICKETTSIAL DISEASES
B.G. RAVINDRA
Protozoan and Rickettsial diseases are responsible for considerable mortality and
morbidity in animals leading to devastating losses. Protozoan parasites are unicellular,
eukaryotic organisms present in blood cells, tissues, skin and intestines. The Rickettsial
organisms are minute, lack cytoplasm and are present in blood cells. Attempts to develop
vaccines aginst these have been greatly handicapped due to complexity of different
parasitic stages and their life cycle. Few vaccines are available against these diseases.
Drugs currently available are effective, if they are used specifically with proper dose,
route and course of treatment. Integrated method of control is very important by using
vaccines, drugs and other managemental practices.
PROTOZOAL DISEASES
BABESIOSIS (PIROPLASMOSIS, RED WATER FEVER): The viable protozoa are

present in blood stream of animals only in active stages of infection. Ticks (Boophilus
spp.) are natural vectors in which transovarial transmission occurs.Contaminated needles
and surgical instruments can physically transmit the infection.
Clinical signs: acute syndrome- high fever (up to 106oF), anorexia, depression,
weakness, suspension of rumination, decrease in milk yield, increased heart and
respiration rates. Conjuctiva brick red but soon changes to extreme pale due to severe
anaemia. In terminal stages, severe jaundice, urine dark red/ brownish and produces stable
froath. Many severely affected animals die after 24 hours and which survive febrile
reaction last for week; pregnant animals often abort, course of disease is 3 weeks. In
subacute infection- mild fever, hemoglobinuria absent
.B. bigemina- cerebral babesiosis- incoordination, posterior paralysis, mania, convulsions
and coma. High mortality inspite of treatment in cerebral form.
B. divergens- additional sign is spasm of anal sphincter and feces expelled with greater
force in long thin stream referred to as “pipe-stem feces”.
Dogs: Signs vary from mild fever lasting for several days to sudden high fever, marked
anemia, hemoglobinuria and jaundice.There may be cerebral form (hyperexcitability),
alimentary form (stomatitis, gastritis, enteritis), respiratory form (dyspnea), circulatory
form (edema), ocular form (keratitis, iritis) and muscular form (muscular weakness).

134
Therapy: a) Quinoronium sulphate derivatives- Acaprin (@ 1ml/50 Kg BW s/c,
maximum dose 6ml otherwise salivation, panting, diarrhoea), Babesan, Piroparv,
Piroplasmin. b) Acridine derivatives- Acriflavin (50-100ml i/v as 1% solution),
Gonacrine, Trypan blue, Euflavine c) Aromatic diamidines- Diminazine aceturate
(Berenil- 0.8-1.6 gm/100 Kg BW deep i/m), Stilbamidine, Propamidine, Phenamidine. d)
Imidocarbs- Imizole @ 1mg/Kg BW s/c. (Imidocarb hydrochloride and Imidocarb
dipropionate)
In horses- Berenil @ 11mg/Kg BW deep i/m.; Imidocarb- most favoured drug. B.equi- @
4mg/Kg BW four IM injections of 10% solution at 72 hour interval. B.caballi- @ 2mg/Kg
BW two injections at 24 hour interval. In donkeys- maximum @ 2mg/Kg BW.;
Buparvaquone @ 4-6mg/Kg BW to control B.equi infection.In sheep- Berenil @
3.5mg/Kg BW on two successive days or 12mg/Kg single dose. Supportive treatment-
blood transfusion, Vitamin B complex.
Theilieroisis: Theileria parva, T. annulata- tropical theileriosis, T. mutans- less

pathogenic, T. ovis, T. hirci- sheep and goat.T. camelensis- camel. Mainly transmitted by
Hyalomma spp ticks; the organism pass trans-stadially through stages of larva, nymph
and adult. No transovarian transmission.
Clinical signs: Initial sign- enlargement of superficial lymph nodes (prescapular,

prefemoral, parotid) within 7-10 days of tick attachment. After 1-2 days, fever (105-
106oF), depression, anorexia and decrease in milk yield. In later stages- nasal and ocular
discharges, dyspnea, generalized lymph node enlargement and splenomegaly. In severe
cases- emaciation, weakness and recumbency followed by death due to asphyxia.
Ocassional cerebral theileriosis- circling, tremors, convulsions, profuse salivation and
head pressing. T. annulata infection- additional signs of anemia and jaundice.
Treatment: a) Halofuginone lactate- coccidiostat but also has schizonticidal effect @

1.2-2.0 mg/Kg orally for two days. Higher doses may be toxic- salivation, diarrhea,
conjunctivitis, subnormal temperature and even death. b) Parvaquone @ 10 mg/Kg, may
be repeated after 48 hours. c) Buparvaquone (Butalex) @ 2.5 mg/Kg i/m, may be
repeated after 48 hours. d) Tetracyclines, Nivaquine act only on the piroplasm stages. e)
Supportive treatment- blood transfusion, liver tonics, diuretics (to check pulmonary
edema).
Trypanosomiasis (surra): Trypanosoma evansi- highly pathogenic, produce surra/

murrina/ mal de caders affect cattle, buffalo, sheep, goat, horse, camel and dogs. Horses
and dogs most commonly affected, camel are carriers (chronic disease- Tibersa in camels-
3 year sickness). Transmission is through biting flies- Tabanus, Stomoxys, Lyperosia,

134
Glossina, Hematopota even vampire bats help in transmission from one animal to
other.Dogs may contract disease by eating infected meat (after 20 days of eating placenta
of affected cattle).
Clinical signs: i) Peracute form- sudden death within 2-3 hours, animal dies showing
some convulsions. Ii) Acute- Intermittant fever (103-105oF), animal dull and depressed,
eyes are starring and wide open, breathing hard and noisy, staggering gait, circling
movements, cattle stretches the rope to which it is tied, animal strikes head against wall or
manger, stamping of feet, apparent blindness, frequent micturition, profuse salivation,
muscular twitching followed by stage of comma and death within 6-12 hours. iii)
Subacute/chronic- dullness, lacrimation, animal show progressive emaciation, rapid pulse,
intermittent fever, edema of legs, wasting of muscles, loss of weight, occasionally
diarrhea, some animal remain standing with neck extended even throughout the day.
Dogs: may be acute form of disease, intermittent fever, anemia, edema and corneal
opacity.
Camel: in chronic form and may last for 3 years, first sign is weakness of all quarters,
eyes dull, alopecia, mucus membranes pale and show petechial hemorrhages, edema of
legs, abortion common, mange is frequently seen in surra affected cases.
Treatment: a) Quinapyramine sulphate (Antrycide) curative @ 5mg/Kg BW;
Quinapyramine sulphate and chloride (Antrycide prosalt); prophylactic @7.4 mg/Kg BW.
In horses- give injection at 2-3 sites, in weak animals there may be salivation, restlessness
and muscular tremors. b) Suramin @ 10mg/Kg BW i/v as 10% solution in horses and
camels. c) Diminazine aceturate- against T.vivax and T.congolense @ 3.5-7.0 mg/Kg,
toxic to horses and camels. d) Homidium- bromide and chloride salts @ 1mg/Kg BW. e)
Isometamidium @ 0.25-1.0mg/Kg BW. f) Pyrithidium bromide @ 2mg/Kg BW.
Coccidiosis: Eimeria bovis and Eimeria zurnii are the common species, transmited by
Feco-Oral route .Sub-clinical coccidiosis occur in 95% of the cases of ruminants. The
other 5% are clinical cases.Anorexia, Diarrhoea (may or may not contain blood),
dehydration, weakness, depression, weight loss, cachexia, Anaemia and death, Nervous
coccidiosis-muscle tremors, staggering, convulsions and occasionally blind nes.
Amprolium @ 10 mg/Kg BW for five days, 1.25% crumble, 9.6%solution, 20% soluable
powder ; Sulphaquinoxaline @ 8-70 mg/ kg BW for five days, as soluable powder or feed
alternative; Monensin @ 1 mg/ kg daily for 30 days, as feed additive is effective.
Giardiosis: It is a chronic protozoal disease, common in dogs caused by Giardia canis

and characterized by diarrhea, dysentery and abdominal pain. Treatment is with:
Chloroquin or Metronidazole 250 mg/kg for 10 days are effective.

134
Balantidiosis: Balantidium coli exist as a commensal in the large intestine of pigs.
Infection of cattle occurs by ingestion of the cysts. The organisms cause ulceration of the
mucosa and diarrhea. Diagnosis is based on the detection of cysts/trophozoites in the
faeces. Tetracyclines and Metronidazole are effective.
Toxoplasmosis: It is contagious disease of all species including man and is manifested

by abortions and stillbirths in ewes and in all species characterized by encephalitis,
pneumonia and neonatal mortality.
Clinical signs: cattle: in acute form marked by fever, dyspnoea, ataxia, hyperexcitability
in early stages followed by extreme lethargy, stillborn or weak calves die soon after birth.
The parasite plays no significant role in bovine abortion. Congenitally affected calves
show fever, dyspnoea, sneezing, coughing, nasal discharge, clonic convulsions and
grinding of teeth. The death may occur after 2-6 days.; Pigs: highly susceptible, all ages
affected. Adults show debility, weakness, incoordination, coughing, tremors and diarrhea
but no fever. In young pigs, high fever, diarrhoea, dyspnoea, coughing and ataxia. The
pregnant sows abort and piglets are premature or stillborn; Sheep: abortion at last 4 week
of gestation and neonatal death. is fever, dyspnoea and generalized tremors whereas
lambs show fever and dyspnoea. Goats: abortion and stillbirths; Horses- mainly nervous
signs including ataxia, circling movement, paresis, myeloencephalitis that may be positive
factor for Wobbler syndrome.
Treatment: a) A combination of sulpha drugs @200 mg/Kg BW i/v for 3-5 days
(sulphadiazine, sulphadimidine, sulphamerazine, sulphapyrazine) and pyrimethamine @
1-2 mg/Kg BW orally is quite effective b) Sulfomoyl diamino diphenyl sulphon (SDDS)
tried in pigs only @ 5 mg/Kg BW, not used clinically.c) Linomycin and Clindamycin are
reported to be quite effective. D) Treatment of anemia as there is blood loss.
Bovine trichominiasis: It is a non-febrile protozoal disease of cattle leading to irregular

estrus intervals, early fetal deaths and cases of pyometra.Trichomonas (Tritrichomonas)
fetus, the etiological agent. Clinical signs: The parasite normally persists for 3 months in
female genital tract after infection and a mild vaginitis is seen after the infective
coitusThere is death of fetus within 2-4 months of conception leading to cases of repeat
breeding and infertility.Abortions are usually not detected and main feature is failure of
animals to hold to service.In bulls, infection is confined to penile and prepucial surface
and cause mild inflammatory response.
Treatment: a) The majority of infected cows recover and clear the infection within 3
months so not normally treated. In bulls- douches of prepuce and penis with acriflavin.
Dimetridazole @ 50 mg/Kg/day orally for five days is quite affective. Ipronidazole can be

134
administered IM but priorl, bulls should be treated with broad spectrum antibiotic to
reduce preputial commensal bacteria which might inactivate the ipronidazole.
RICKETTSIAL DISEASES
Anaplasmosis (gall sickness) : A non-contagious disease of ruminants caused by

obligate intraerythrocytic parasites: Anaplasma marginale, A. centrale, A. ovis. Mainly
transmitted by ticks: Boophilus spp., Dermacentor spp, tabanid flies; infected hypodermic
needles, blood transfusions
Clinical signs: Subacute (in younger ones): Temperature rises slowly up to 105oF-
remain elevated or fluctuate, partial anorexia, animal may die at this stage or survive in an
emaciated condition- mucous membranes become pale, urine may be brown but no
haemoglobinuria. Peracute cases: sudden onset of high fever, anemia, jaundice, severe
dyspnea and death within 24 hours; animals become hyperexcited and may attack
pregnant animals may abort. Recovered bulls- testicular function depressed for several
months. Sheep and Goat- usually subclinical infection but sometime severe anaemia in
goats.
Treatment: a) Oxytetracycline @ 6-10 mg/Kg BW for three days or single injection of

long acting oxytetracycline @ 20 mg/Kg BW i/m. b) Imidocarb @ 3 mg/Kg BW s/c.
The problem of carriers can be avoided by using tetracycline @ 10-30 mg/Kg BW i/m
daily for 10-15 days or 22 mg/Kg BW i/v daily for 5 days or long acting tetracycline @
20 mg/Kg BW i/m weekly for 2-4 times or two injections of imidocarb @ 5 mg/Kg BW
i/m or s/c. The oral use of chlortetracycline @ 11 mg/Kg BW for 30-60 days or 1.1
mg/Kg BW for 120 days also eliminates carrier animals. c) Supportive treatment- blood
transfusion if PCV less than 15%.
Ehrlichiosis: Ehrlichia canis, Ehrlichia bovis are the etiological agents, commonly
transmitted by ticks: Rhipicephalus sanguineus. Clinical signs: Anorexia, fever,
incordination and enlargement of lymphnodes. The disease is of low significance in
indigenous cattle, however it is serious problem in imported and newly introduced cattle.
In dogs: Anorexia, fever, respiratory distress, Limb oedema, enlargement of lymphnodes,
bleeding tendacy (epistaxis, hematuria), and petichial haemorrhages on mucus membrane,
Progressive weight loss and Neurological disorder may be seen.
Treatment: Doxcycline @ 5-10 mg/Kg BW per oral for about 10-14 days for four days ;
Oxytetracycline @ 5-10 mg/Kg BW for four days ; Chloromphenicol, @ 5 mg/Kg BW
for four days, Enrofloxacin @ 2.5-5 mg/Kg BW for four days may also be effective
*****

134
ANTIMICROBIAL THERAPY OF FUNGAL SKIN
INFECTIONS
SANTOSH .P. SARANGAMATH
The ideal antifungal agent would be one that targets structures present in
fungal pathogens that are absent in other eukaryotic cells. The fungal cell wall, a structure
that is both unique and essential to fungi, would seem to be such a target. The vast
majority of traditional antifungal drugs selectively target ergosterol, an essential
component of the fungal cell membrane, with greater affinity than for cholesterol in the
mammalian cell membrane. New antifungals have evolved especially azoles and triazoles,
which selectively target fungal cell wall with least toxic effect on the body. Compounds
that interfere with the synthesis of important fungal cell wall components such as glucan,
chitin and mannoproteins have become a focus in the development of new antifungal
agents.
Among the cutaneous diseases fungal diseases involving skin and appendages
(Dermatophytosis) i.e cutaneous mycosis are commonly encountered as compared to the
deep mycosis involving deeper organs of the body. Fungal infections involving the
keratinized layers of the skin and its appendages like hoof, nails, and horns caused by
group of mycelial keratinophilic fungi are called dermatophytes, The term
dermatophytosis indicates the relationship of the disease with dermatophytes as
etiological agents. Dermatophytes of dog and cats mainly belong to T. mentagrophytes,
M. canis, M. gypseum.
The clinical signs of dermatophytosis are extremely variable; lesions are circular,
irregular and vary from scaly patches of alopecia to inflammed to nodular erythematous
patch of alopecia. Hairs partially broken/ fallen with bran like scales and crusts, signs like
erythema, scales, crusts, thinning of hairs frequently in the form of broken hairs with
secondary folliculitis with pruritus are usually observed.
Diagnosis is based on clinical signs, skin scraping examination, examination of
hairs by wood’s lamp, and finally by fungal culture on saborauds dextrose agar or
dermatophyte test medium. The gold standard for diagnosis is a fungal culture. Wood's
light examinations are only screening tools, and direct hair examinations, although
inexpensive, are only practical when infected hairs fluoresce on Wood's light
examination. Finding these hairs allows rapidly diagnosing the infection and starting
therapy. However, if the hairs are not present, this tool is time-consuming and not cost-
effective in practice.

134
Another type of fungal or yeast disease is malassezia dermatitis; the clinical
signs of which may be localized or generalized. Involving the external ear canal,
interdigital skin, ventral neck, axillae, and inguinal region. Affected areas are
erythematous, alopecic and often lichenified with or without hyperpigmentation. The
lesions surface is often greasy and affected dogs have musty or malodour.
Diagnosis of malassezia dermatitis is by cytological examination or acetate tape
impressions, stained with methylene blue which will be examined for the presence of
round to oval monopolar budding yeasts.
ANTIFUNGAL THERAPY
Dermatophytosis will spontaneously resolve in most healthy cats, but treatment is

recommended as the disease is zoonotic and highly contagious. The end point of therapy
will go up to the achievement of mycological cure as well as decontaminated environment
but not the clinical cure on the animal itself so as to prevent re-infection. A mycological
cure is defined as two or three consecutive negative fungal culture results at weekly or
biweekly intervals, and treatment should continue until all these negative culture results
are obtained.
Treatment recommendations:
1) Clipping the coat:. Clipping the coat removes infected hairs , minimizes continued
shedding of hair fragments and spores; also makes topical therapy application easier and
allows for more thorough penetration of topical antifungal agent. In addition, clipping
helps shorten the duration of therapy and ultimately decreases the cost of treatment. It
may temporarily worsen the infection by causing microtrauma to the skin. Also, it may
result in environmental contamination if appropriate efforts to capture infected hairs and
spores are not taken.Dipping is required in pets that live with children and elderly or
immunosuppressed people, as well as in shorthaired breeds with generalized lesions and
in longhaired cats regardless of lesion severity
2) Administering topical antifungal therapy twice weekly: The most effective topical
antifungal agents are lime-sulfur, enilconazole, and miconazole. Lime-sulfur is suitable
for sole therapy; combined topical and systemic therapy is the treatment of choice. It is
important to note that fungicidal efficacy does not imply that one application of any of
these products is 100% fungicidal. These products are fungicidal with repeated
application. Lime-sulfur (8 oz/gal water ) has been used as the topical therapy of choice,
and in some cases as the sole therapy. Enilconazole topical solution 10% concentrated
solution (100 mg/ml) is effective against M. canis. It is associated with hypersalivation,
anorexia, weight loss, emesis, idiopathic muscle weakness, and slightly elevated serum
alanine aminotransferase activity. Miconazole, as a sole therapeutic agent or in

134
combination with chlorhexidine, the shampoo needing a contact time of 10 minutes for
the therapeutic effect. This product can be irritating to the eyes and can cause skin
irritation. Other dips like povidone-iodine, chlorhexidine have been consistently found
to be ineffective against M. canis.
3) Administer systemic antifungal therapy - Systemic therapy is the treatment of
choice for feline dermatophytosis. The efficacy of griseofulvin, itraconazole, terbinafine
hydrochloride, and lufenuron alone or in combination with other therapies showed that
griseofulvin, itraconazole and terbinafine are most effective agents
Griseofulvin : is fungistatic that inhibits nucleic acid synthesis and cell mitosis
metaphase by interfering with function of spindle microtubules.Its absorption is enhanced
by administering it with fatty meal or by using formulations containing polyethylene
glycol.
It is teratogenic and should not be given to pregnant animals. also may interfere with
spermatogenesis, so it is best avoided in breeding males. Anorexia, vomiting, and diarrhea
are seen, which can be managed by dividing the dose into twice-daily administrations.
Bone marrow suppression and neurologic side effects are most likely idiosyncratic
reactions. Do not use griseofulvin in cats that have feline immunodeficiency virus (FIV)
infections, because severe neutropenic reactions have been seen in cats with FIV.
The most commonly used dosing regimen is daily: griseofulvin microsize at a
dosage of 25 to 50 mg/kg given orally once a day or divided twice a day; griseofulvin
ultramicrosize at a dosage of 5 to 10 mg/kg given orally once a day or divided twice a
day. Higher doses may be needed in refractory cases.
Ketoconazole : is administered at the rate of 5 to 10 mg/kg b.wt. orally once daily for 21
days. Available in the form of tablets or shampoos, this will be useful for topical as well
as systemic use. This drug is also tolerated in dogs, but long term therapy may involve the
potential risk of causing liver as well as renal damage.
Itraconazole : is a triazole derivative that alters fungal cell membrane permeability by
inhibiting ergosterol synthesis; is fungistatic at low doses, fungicidal at higher doses.It is
well-tolerated in cats and dogs, with vomiton, anorexia being most common adverse
effects a) Daily dosing: 10 mg/kg orally once a day; b) Combined continuous/pulse
therapy: 10 mg/kg given orally once day for 28 days and then on an alternate week
regimen (one week off and one week on) . c) Short-term cycle therapy: 10 mg/kg given
orally once a day for 15 days, followed by fungal cultures 10 -15 days later, this cycle is
repeated until the cure. . It has replaced griseofulvin as the drug of choice for treating
dermatophytosis
Terbinafine : is the newest systemic antifungal agent to be used in treating
dermatophytosis. It is an allylamine antifungal agent that suppresses the biosynthesis of

134
ergosterol by inhibiting the fungal enzyme squalene epoxidase.31 The drug is considered
to be fungicidal against dermatophytes.
Fluconazole : Fluconazole is also hepatotoxic and nephrotoxic, but its elimination from
the stratum corneum is approximately 2 to 3 times slower than the plasma. Also, due to its
rapidity in accumulation the skin after oral ingestion makes the drug to be administered
once a week or daily for 2 to 4 weeks will help in improvement of the condition. This is
administered safely at a dosage of 5 mg/kg/day which is well tolerated in both dogs and
cats.
Lufenuron : is a benzoylphenylurea drug that disrupts chitin synthesis and is used for
flea control. Chitin is a critical component of the outer cell wall of fungi, and it is possible
that drugs that disrupt chitin synthesis might also have antifungal activity. One report
suggested it is useful in treating variety of fungal diseases including dermatophytosis. But
still, lufenuron has been a widely debated topic in veterinary practice.
4) Considering Fungal vaccines: Intense interest in developing a fungal vaccine to
prevent and possibly treat dermatophytosis continues. Fungal vaccines as sole therapy are
not effective in treating dermatophytosis, but they may be a useful adjuvant therapy when
combined with appropriate topical and systemic therapy and environmental control or a
practical alternative to topical therapy in situations in which topical therapy cannot be
used.
*****

134
NEWER ECTOPARASITICIDALS AND MISCELLANEOUS
ANTIBACTERIALS
MEERA V.C.
Milbemycins
These are (eg:Moxidectin,Nemadectin,Milbemycin oxime,MilbemycinD) endecticidal

macrocyclic lactones, similar to avermectins, active against all stages of nematodes
including GI and lung nematodes,eye worms, schistosomes and ectoparasites- tick, flea.
mite, horn flies, warbles,maggot fly bots.Wide safety index, (greater margin of safety in
ivermectin sensitive collies) with no embryotoxic/teratogenic effects and safe for use in
breeding and pregnant animals. But Abamectin and Moxidectin are contraindicated in
calves and foals (< 4 month old). Dose:Moxidectin-200µg/kg,PO,IM;Pour on-500µg/kg,
Milbemycin oxime-0.5-.99mg/kg-dog; 2mg/kg-cats); recently has been combined with
lufenuron in a tablet formulation for the simultaneous prevention and control of flea
infestations and nematodes
Insect growth regulators and insect development inhibitors :
These do not kill the target parasite directly, but interfere with growth and development.
They act mainly on immature parasite stages and are not usually suitable for the rapid
control of established adult parasite populations. Where parasites show a clear seasonal
pattern, insect growth regulators can be applied prior to any anticipated challenge as a
preventive measure.
Lufenuron is administered PO to dogs (once monthly at a dose of 10mg/kg ) or cats
( 30mg/kg ) or by injection to cats. suppress the growth of adult fleas up to 32 days
Cyromazine is effective against blowfly larvae on sheep and lambs and also against other
Diptera such as houseflies and mosquitoes in poulktry sheds, commonly given a spremix
in feed.
Methoprene (and Pyriproxyfen ) is used as a feed-through larvicide for hornfly (

Haematobia ) control on cattle. Fenoxycarb usually formulated in collar or spray with
either pyrethroid (permethrin) or OPC (chloropyrifos) as an adulticide
Imidacloprid and nitenpyram are nicotinoids are modeled after natural nicotine.
Imidacloprid is applied as a 10% spot-on topical product and is used primarily to control
fleas on both dogs and cats. It also has excellent activity against lice. Nitenpyram is
administered PO in pill form to kill fleas in both dogs and cats.

134
Fipronil a broad-spectrum acaricidal against fleas, ticks, mites, and lice.;effective
against insects resistant or tolerant to pyrethroid, organophosphate and carbamate
insecticides.
Spinosad works as both contact poison and by ingestion to external parasites. It
should not be used in puppies under age 14 weeks and in pregnant or nursing females. It
is given once a month to kill fleas in dogs only, at a dose rate of 30-60mg/kg .
Metaflumizone presented in combination with amitraz as spot on solution; dose is 20
mg/kg, equivalent to 0.133ml/kg bodyweight. It is contraindicated in puppies under 8
weeks of age., sick or debilitated dogs or dogs suffering from heat stress, pregnant and
lactating animals.
MISCELLANEOUS ANTIBACTERIALS
Polymyxins: Colistin (Polymyxin E; available as sulphate for oral and topical use) and
Polymyxin B.The spectrum is gram negative bactericidal. They are synergistic with
sulfonamide and trimethoprim against variety of enterobacteriaceae. Colistin is
synergistic with rifampin against multidrug resistant P.aeruginosa and is employed in
coliform mastitis.They are indicted topically for Infections of skin, mucous membranes,
eye and ear.
Bacitracin: Activity against gram-positive organisms , used topically alone or with

neomycin or polymyxin for: infected eczema, infected dermal ulcers. and ophthalmic
applications: suppurative conjunctivitis. infected corneal ulcer.
Vancomycin: (and Teicoplanin) : The spectrum is gram positive bactericidal. Dogs-3
mg/kg PO, bid;10-20 mg/kg IV,tid. Ototoxicity, nephrotoxicity, and thrombophlebitis
-adverse effects. Administration with aminoglcosides to be avoided.Indicated in
MRSApneumonia, empyema, endocarditis, osteomyelitis and soft tissue abscesses and in
severe Staph. infection
Fusidic acid (Sodium fusidate) : is bacteriostatic effective only on gram-positive
bacteria such as Staph. and Corynebacterium. It is used topically for minor local skin
infections, wounds. It should not be used with quinolones, with which they are
antagonistic
Methanamine (Hexamine) : a urinary antiseptic is bacteriostatic agent, becomes cidal
in acidic urine. Active against both gram positive & negative organisms.Methamine
mandalate – Dogs:10-20 mg/kg PO, bid.GI disturbances ,painful micturation, albinuria,
hamaturia, cystitis, CNS symptoms produced occasionally. Use of urinary alkanizers: Na
bicarbonate and Sulphonamides antagonise its action.Concurrent use of urinary
acidifires such as ascorbic acid, methionine enhances its action.

134
Tiamulin: gram positive bacteriostatic ,including Mycoplasma spp., Spirochaetes and
obligate anaerobes. It is used for enteric pneumonia complex-Pigs-15 mg/kg IM, sid; for
3 days ; 8.8 mg/kg PO.sid. Overdose: transient salivation, vomiting and CNS
depressions . It should not be administered to feeds in combination with ionophore
antibiotics (monensin, lasalocid, salinomycin) as toxicity may occur.
Virginiamycin: broad spectrum, bactericidal against a wide range of organisms

including staphylococci, streptococci and enterococci. It is commonly used as feed
additive Overdose may result in gastric disturbances, dyspnea, emesis, tremor and ataxia.
Novobiocin: Spectrum mainly gram positive;.Dogs: 10 mg/kg q8h PO; Cattle:For

treatment of mastitis in dry cows:. For treatment of mastitis in lactating cows-using the
penicillin/novobiocin.
Quinupristin/dalfopristin: Streptogramins; Antibacterial spectrum:G+ve cocci .Given

by IV infusion. Inhibitor of CPY3A4 enzyme-increased levels of certain drugs like
diazpam, warfarin, protease inhibitors.
Linezolid: oxazolidinone derivative; gram+ve organisms:. Primarily bacteriostatic,

except for Strep for which it is bactericidal. Active against mycobacterium tuberculosis.
Indictaed in vancomycin-resistant infections and multidrugresistant gram +ve bacterial
infections.
Mupirocin: gram positive bactericidal spectrum;used topically for staphylococcal and

streptocococcal skin infections, wounds, burns etc.
Metronidazole : It is the the prototype of the group, Nitroimidazoles ( examples -

tinidazole, secnidazole, ornidazole, satranidazole, nimorazole etc), has both antiprotozoal
and antibacterial activity. Bactericidal against anaerobic bacteria, protozoas ; anti-
inflammatory in bowel.
Indications : Various tissue protozoal diseases(amoebiasis, giardiaisis, trichomoniasis

etc), in anaerobic and mixed bacterial infections : abdominal abscesses,
pleuropneumonia,peritonitis, empyema, genital tract infections, , otitis media, stomatitis,
osteomyelitis, soft tissue infections(topical) osteitis, arthritis, meningitis and sepsis.
Dose: dogs : 44 mg/kg, PO, followed by 22 mg/kg, qid for anaerobic infections; 25
mg/kg, PO, bid for giardiasis; and 66 mg/kg, PO, sid for trichomoniasis. Courses of
therapy are generally 5-7 days. Cats: 22-25 mg/kg, q 12h ; Cattle-75mg/kg,IV,q 12h for 3
doses. Tinidazole-15mg/kg,PO,q24h; Ronidazole- 30mg/kg,PO,q24h; Carnidazole-
20mg/kg,PO,q24h.

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Contraindications: first trimester of pregnancy, young puppies, kittens, lactating animals
*****

134
CHEMOTHERAPEUTIC PROTOCOLS OF PARASITIC
INFESTATIONS
PUTTALAKSHMAMMA
Chemicals/Drugs used to treat helminthic infections are called Anthelmintics; are

classified in to antitrematodal, anticestodal and antinematodals. The Ideal drug should be
active against all stages, least toxic to host, have wide therapeutic index, economical and
environment friendly. The principle sites of drug action in parasite include neuromuscular
system, biochemical reactions involved in energy metabolism and those related to
reproduction.
A. Antitrematodal drugs: Drugs used against liver flukes, rumen flukes, lung flukes and
Blood flukes
1. Carbon tetrachloride : Effective against mature Fasciola hepatica but not against
Dicrocoelium dentriticum. Sheep – 3 ml P.o or S.c. Cattle 20 ml S.c. or 5 ml P.o.
This drug is hepatotoxic. Hyperaesthesia, convulsions and coma may occur. More
toxicity in hypocalcemic animals. In toxicity, give calcium compounds and reduce
the protein intake.
2. Hexachlorethane: Effective against mature Fasciola sp Haemonchus sp and
Trichostrongylus sp. The dose is 20 gm/100 kg. Monthly dosing in areas of
repeated infestations.
3. Hexachlorphene : 10 mg/kg
4. Triclabendazole : Acting on both mature and immature liver flukes. Cattle –
12mg / kg, Sheep and goat 10 mg/kg.
5. Nitroxynil : Active against mature and immature stages (4 to 6 wks) of Fasciola sp
and gape worms in birds. Reaction at the infection site is common. Induce yellow
staining of the skin and wool. It is not used in lactating cows.
6. Rafaxanide : Effective against mature and immature flukes, oetsum ovis larva
and Haemonchus contortus. 10 mg/kg P.o. Toxicity rare but not used lactating
cows.
7. Oxyclozanide : 10 mg/kg. P.o. Safe for lactating, young and pregnant animals.
Toxicity: Transient diarrhoea and hypogalactia. Others from this group for
subacute and chronic fascioliasis are brotianide (22.5 mg+ thiophanate 200
mg/ml) closantel – 5 mg/kg I. M or 15 mg /kg. P.o. Effective against flukes,
Haemonchus sp, larval flies & ticks.

134
8. Diamphenithide : 180 mg/ml susp. 100 mg/kg against mature and immature
flukes
9. Bithiona : 50 mg/kg in divided doses on alternate days for 3 or 4 weeks is
effective against paragonimiasis, fascioliasis and clonorchiasis, taeniosis and
Diphyllobothrium latum
10. Chlorsulon : A sulphonamide 100 mg + Ivermectin 10 mg/ml inj. S.c.
Good for biliary fascioliasis in lactating cattle
11. Resorantel : 65 mg/kg P.o. in cattle and sheep against only intestinal
paramphistomes.
12. Albendazole : 7.5 mg/kg in cattle, sheep and goat, for the control of
Fasciola sp 15 mg/kg b.wt for the treatment of Dicrocoelium dentriticum in
sheep.
13. Lithium Antimony thiomalate 6%. Cattle 15-20 ml i.m 2-3 doses at
weekly intervals against nasal schistosomiosis.
14. Praziquantel : used in human schistosomiosis, clonorchis sinsensis and
opisthorchis viveroni.
B. Anticestodals
1. Natural compounds : The earliest anticestodal drugs used were of plant origin, like
minced pumpkin seeds, powdered rhyzome of male fern, kamala and Arecholine
2. Inorganic Compounds : a) Tin compounds were used against human, dog and poultry
tapeworms. Stannous chloride – man, dog-0.5 gm daily for 8 days. b) Di-n-butyl tin
dilaurate : 1ml for poultry c) Lead arsenate : used for treating Moneizia in lambs and
calves.
3. Synthetic organic compounds : i). Hexachlorophene : 100 mg tab
ii). Bunamidine hydrochloride : Used against Echinococcus granulosus : second dose

after 6 weeks to eliminates those which were immature, Also, effective against
Dipylidium caninum and moniezia expansa.
iii) Dichlorophen : Dogs : 300 mg/kg ,Cats : 100-200 mg/kg
iv) Niclosamide : Dogs & cats: 100-157 mg/kg ,Cattle : 50 mg/kg ,Sheep, Goat,
rabbit and monkey : 100 mg/kg
v). Paramomycin Sulphate :
vi) Praziquantel : 2.5 to 7.5 mg/kg P.o or S.c against Diphyllobothrium latum,
Hymenolepis nana, Taenia saginata etc. Dipylidium caninum, Taenia sp, E. granulosus

134
Spirometra, Side effects: Malaise, dizziness, headache, abdominal discomfort with or
without nausea. Not used in puppies or kittens younger than 4 wks.
vii). Nitroscanate : 50 mg/kg used against Dipyllidium caninum, Taenia
viii) Benzimidazoles : a) Mebendazole b) Albendazole c) Fenbendazole

d) Oxfendazoel e) Febantel etc are effective against tapeworms.
C. Antinematodals
1. Phenothiazine : 10 gm/45kg used in strongyles, Triodontophorus, Haemonchus,

Ostertagia and Trichonema. On exposure to light, it causes photosensitization keratitis
manifested by ulceration of the cornea. So, avoid sun for 2-3 days.
(a) Piperazine : 75 mg/kg P.o. for mammals ,3g/bird in water for 3d in poultry
(b) Bephenium hydroxynaphthoate : irritant and poor absorption from the gut. 80%.
Cure of Trichostrongylus in man, Ancylostoma in man and dogs and nematodirus in
ruminants.
(c). n-Butyl chloride : 90% effective against ascarids and 60% against hookworms.
(d) Toluene : 0.2 ml/kg P.o. 98% effective in ascarids and hookworms in dogs and cats,
Emesis, tremors and ataxia in pups and kitten.
(e) Tetrachloroethylene : Removes 90% hookworms. To prevent toxicity give fat free
diet 48h before dosing. It is hepatotoxic, causes dizziness, inco-ordination and death.
Contraindicated in tapeworm infection as the tapeworms may ball up due to irritation and
occlude the intestinal passage.
(f) Methyridine : 200 mg/kg P.o., S.c, or I.P. Twice the normal dose is toxic.
Diethylcarbamazine potentiates toxicity.
(g) Diethyl Carbamazine citrate: 6 mg/kg P.o or S.c in dogs in Spirocerca lupi, human
wucheria bancrofti or Loa loa, onchocerca volvulus, cutaneous larva migrans and tropical
eosinophilia. 22 mg/kg i.m for 3 days in early cases of Dictyocaulus viviparous infection
in cattle, 5mg/kg daily or alternate day commencing before exposure and continuing 60
days after exposure.
(h) Disophenol : 10 mg/kg P.o., S.c. or i.m. Effective against hookworms and spirocerca
lupi of dogs, syngamus trachea in turkeys. It causes pyrexia, tachycardia, polypnoea,
corneal and lens opacity in dogs which regress within 7 days. Non blood sucking and
histotropic parasites are unaffected, orally administered drug is more toxic.

134
(i) Phtholofyne : 200 mg/kg for whip worm. 24hour fast followed by light meal after
dosing. Toxicity leads to emesis, ataxia, and death.
(j) Hygromycin-B : An antibiotic in feed for swine and poultry against ascarids,
capillaria, oesophagostomum and Heterakis gallinarum. Feed 6 weeks prior to farrowing
in swine.
3. Tertrahydropyrimidines : Less active against larval stages and have minimal action
on hypobiotic larvae. Not ovicidal.
a) Morantel citrate : Not effective against adult lung worms. 10 mg/kg P.o in cattle
& sheep
b) Pyrantel pamoate : used for round worms in horses, dog and man. Due to mutual
antagonism, piperazine and pyrantel compounds should not be combined.
c) Oxantel : Specific single dose treatment of Trichuriasis in dog at 55 mg/kg.
4. Benzimidazoles :Benzimidazoles have a high therapeutic index, but not to be used in
the first month of pregnancy (teratogenic).
a) Thiabendazole : Not widely used now

b) Mebendazole : Generally not used in cattle, sheep and horse 10 mg/kg. 25-50
mg/kg twice daily for 5 days for round worms and tapeworms in dogs.
c) Parbendazole : 30 mg/kg P.o
d) Albendazole : It is used in the treatment of roundworms, tapeworms and flukes. 5
mg/kg for roundworms and 7.5 mg/kg for flukes in sheep and goats .7.5 mg/kg for
round worms and 10 mg/kg for flukes in cattle. 5 mg/kg in horses
e) Fenbendazole : In addition to important roundworms, it is effective against
hypobiotic larva and also on tapeworms in sheep, Goat and dogs.
f) Oxfendazole : Active against round worms, their inhibited larva and tapeworms
4.5 mg/kg P.o as a single dose to cattle, sheep and pig. 10mg/kg daily for 3 days in
horses and dogs
g) Oxibendazole : Effective against roundworms and lung worms in horses 10
mg/kg P.o.
h) Flubendazole : 5 mg/kg P.o. mainly used in pigs against round worms
i) Luxabendazole : Effective against round worms and flukes .7.5 mg/kg for round
worms
5. Benzimidazole pro-drugs.These are converted in vivo to benzimidazoles. The drugs
are ovicidal, larvicidal and affect adults including some tape worms (Taenia sp)
a) Febantel : Converted to fenbendazole and oxfendazole, 7.5 mg/kg in cattle and 5

mg/kg in sheep

134
b) Thiophanate : Converted to lobendazole 50 mg/kg
c) Netobin : Converted to albendazole 7.5 mg/kg P.o in cattle & sheep
6. Imidazothiazoles :
a) di-Tetramisole b) Levamisole (1-Tertramisole) : Effective against larvae (but not

hypobiotic and not ovicidal) and adults. anthelmithic dose is immunostimulant. The drug
is non-teratogenic and hence can be used in pregnant animals. The dose is 7.5 mg/kg
Antidote is Atropine
7. Macrolides (macrocyclic lactones)
a) Ivermectin : 0.2mg/kg single oral or P.o.Effective against nematodes and

ectoparasites. Used at 6 ug/kg at one month intervals for prevention of Dirofilaria immitis
infestation in dogs. Other macrolides includes Doramectin, milbomycin-D, milbomycin
oxime, Eprinomectin, Moxidectin and selamectin.
8. Organophosphorus compounds : The use is restricted to the treatment of

round worms of dogs, cats, pigs and especially horses where they also control the stomach
bots.
a) Dichlorovos : 20 -40 mg/kg in horses ,30-40 mg/kg in pigs,27-33 mg/kg in Dogs.

They may be incorporated into polyvinyl chloride resin pellets for slow release
and safety
b) Coumaphos : 2 mg/kg/day for 6 days in feed
c) Trichlorofon : A prodrug of dichlorvos used in horses at 40 mg/kg
d) Napthalofos : Narrow margin of safety
e) Crufomate: used for warble fly control.
Broad Spectrum Combinations
1. Clorsulon and Ivermectin : For use in cattle 1 ml/50 kg. S.C.

2. Dichlorophene and Toluene: used in dogs against cestodes and nematodes
3. Diethylcarbamazine and oxibendazole : used in dogs for prevention of infection
with D. immitis and A. caninum, and for the removal of T. canis and T.vulpis
4. Febantel, praziquantel, and pyrautel: A single dose is given to dogs to remove
D. caninum, T. pisiformis, E.granulosus, A. caninum, U. stenocephala, T. canis, T.
vulpis
5. Milbemycin oxime and Lufenuron :This is given once every mouth to remove G
I worms and control of flea population
6. Praziquantel and pyrantel : A single dose is given to cats and kittens to remove
D. caninum, Taenia sp Ancylostoma sp and T. cati

134
7. Ivermectin and pyrantel pamoate : This is given orally to dogs every 30 days to
prevent D. immitis and for the treatment & control of T. canis, T. leonina,
*****

134
CHEMOTHERAPEUTIC PROTOCOLS OF IMPORTANT
ZOONOTIC DISEASES PRADEEPKUMAR
The antimicrobial therapy of important diseases of zoonotic importance are

discussed in brief in this article.
Anthrax:Penicillin, the drug of choice for years other drugs from penicillin family such
as amoxicillin should be equally effective. Doxycycline, one of the tetracyclines, most
recently listed as the drug of choice in treating anthrax. Ciprofloxacin, one of the
quinolone antibiotics and is also effective. is recommended as the first drug to use until
the sensitivities of the organisms are known Lung infections may be treated with IV
antibiotics.If untreated, cutaneous anthrax may result in death. Untreated inhalation
anthrax always results in death.
Brucellosis: Use of surgical hand gloves is recommended during vaccination and yhe
vaccine should be handled properly. Vials, syringes, needles and gloves used during
vaccination should be discarded by suitably disinfecting them.Streptomycin is the drug of
choice. Doxycycline (per oral dosage) is also effective. Flouroquinolones can also be
used.
Tuberculosis: Tuberculosis is curable only with a combination of chemotherapy, in

which a medley of three or four anti-tubercular drugs is administered. The first line drugs
are Isoniazid, Rifampicin, Ethambutal, Pyrizinamite, and Streptomycin. The treatment is
streamlined over a period of 6-9 months.Azithromycin, clarithromycin, ciprofloxacin are
the second line agents, used in cases of resistance and toxicity tio first line drugs.
Toxoplasmosis: From acute maternal infection during pregnancy; incidence/severity

related to trimester of infection; may cause abortion, stillbirth, and premature birth.
Manifestations varied: if not evident at birth, usually develop in later life (85%) and may
include: microcephaly, hydrocephaly, neurologic disease/mental retardation, ocular
disease, pneumonitis, hepatomegaly, splenomegaly, icterus, anemia, thrombocytopenia.
Clindamycin; sulfa trimethoprim; monitor for evidence of bone marrow suppression. Do
not feed raw or undercooked meat to cats, keep cats inside and do not let them hunt.
Plague (bubonic, pneumonic, and septicemic): The etiological agent is: Yersinia
pestis (gram-negative coccobacillus); Rodents (dog, ground squirrel, rock squirrel) are the
major reservoirs. Bubonic form (most common; 80 - 90% of cases): enlarged, painful
lymph nodes (axillary, cervical, inguinal), fever, chills, weakness, GI signs, headache,

134
myalgia. Septicemic: septic shock, meningitis, coma, .Pneumonic (least common: severe
pneumonia, fever, dyspnea, and hemoptysis). Aminoglycosides, fluoroquinolones, are
effective agents with supportive care.Insect repellent, appropriate clothing, flea control
for pets and environment, rodent control. Avoid contact of cats with reservoir hosts.
Ringworm: Patchy pruritic dermatitis that may be multifocal. Many possible etiologies in
people (zoophilic, geophilic, anthrophilic dermatophytes); M. canis most common
zoophilic dermatophyte and infections are from cats. Keeping the affected part of the
body dry and clean and antifungal agents like griseofulvin, terbinafine, miconazole,
ketoconazole are used.
Cryptosporidiosis : Cattle, rodents, dogs, cats, birds, raccoons are the reservoirs.
Immunocompetent ones: Self-limited acute watery diarrhea, epigastric pain, nausea,
anorexia requiring fluid therapy. Immunocompromised: chronic profuse watery diarrhea,
fever, epigastric pain, nausea, anorexia. Gall bladder infection possible. Respiratory tract
infection may occur. Azithromycin may be effective. Evaluate for concurrent
immunosuppressive conditions if prolonged treatment needed. Clean and disinfect
environment (100% ethanol or 50% bleach with 30 minutes of contact effective after
removal of organic matter)
Q-fever : Coxiella burnetii is the etiological agent. Cattle, sheep, and goats are the
primary reservoirs. Inhalation of organisms from air that contains airborne barnyard dust
contaminated by dried placental material, birth fluids, and excreta of infected herd
animals. Outbreaks occur mainly from occupational exposure involving veterinarians,
meat processing plant workers, sheep and dairy workers, livestock farmers, and
researchers at facilities housing sheep.
Acute: high fever (up to 104-105° F), severe headache, general malaise, malign,
confusion, sore throat, chills, sweats, non-productive cough, nausea, vomiting, diarrhea,
abdominal pain, hepatitis and chest pain. 1-2% mortality in humans.
Chronic: Endocarditis, generally involving the aortic heart valves, less ommonly the
mitral valve. Patients who recover can develop lifelong immunity. Incubation period: 2-3
weeks. Doxycycline is the treatment of choice for acute Q fever. Antibiotic treatment is
most effective when initiated within the first 3 days of illness. A dose of 100 mg of
doxycycline taken orally twice daily for 15-21 days is a frequently prescribed therapy.
Quinolone antibiotics have demonstrated good in vitro activity against C. burnetii and
may be considered.
Influenza : Two antiviral agents: zanamivir (TN: Relenza) and oseltamivir (TN: Tamiflu)
are used to prevent or reduce influenza A and B symptoms. These should not be used
indiscriminately, because viral resistance to them can and has occurred. Also, they are not

134
recommended if the flu symptoms already have been present for 48 hours or more. Severe
infections in some patients may require additional supportive measures such as ventilation
support and treatment of other infections like pneumonia that can occur in patients with a
severe flu infection.
General precautions to prevent zoonotic infections:
Hand hygiene: Consistent thorough hand hand washing with plain (nonantimicrobial)
soap and running water mechanically removes organic material and reduces the number
of transient organisms on the skin, whereas antimicrobial soap kills or inhibits growth of
transient and resident flora.To reduce the opportunity for cross-contamination, liquid or
foam soap products should be selected rather than bar soaps. Hands should be washed
between animal contacts and after contact with feces, blood, body fluids, and exudates.
Alcohol-based hand rubs are highly effective against bacteria and enveloped viruses and
may be used if hands are not visibly soiled.
Use of gloves and sleeves: reduce the risk of pathogen transmission by providing barrier
protection; though, wearing gloves is not a substitute for hand washing. Gloves are
available in a variety of materials. Choice of gloves depends on their intended use. If
allergic reactions to latex are a concern, acceptable alternatives include nitrile or vinyl
gloves.
Facial protection: prevents exposure of mucous membranes of eyes, nose, and mouth to
infectious materials. Whenever exposures to splashes or sprays are likely to occur, such as
those generated during lancing of abscesses, flushing wounds, dentistry, suctioning,
lavage, and necropsy, facial protection- surgical mask worn with goggles or a face shield
is used..
Respiratory tract protection: designed to protect the airways of the wearer from
infectious agents that are transmitted via inhalation of small particles.It may be
appropriate in certain situations, such as during investigations of abortion storms in small
ruminants (Q fever), high mortality rates among poultry (avian influenza),positive herd
(bovine tuberculosis), and avian chlamydiosis. Disposable particulate respirators often
resemble surgical or dust masks but fit closely to the wearer’s face and are designed to
filter smaller particles (surgical masks are not designed to prevent inhalation of small
particles).
Protective outerwear: a. Nonsterile gowns: Gowns provide better barrier protection than
laboratory coats. Permeable gowns- used for general care of animals in isolation.
Impermeable gowns should be used when splashes or large quantities of body fluids are
present or anticipated.. b. Footwear: Footwear should be suitable for the specific working
conditions (eg, rubber boots for farm work) and should protect personnel from exposure
to infectious material as well as from trauma. Recommendations include shoes or boots
with thick soles and closed-toe construction that are impermeable to liquid and easy to

134
clean.. d. Head covers: Disposable head covers provide a barrier when gross
contamination of the hair and scalp is expected.
*****

134
STEROIDS AND ANTIHISTAMINICS OF VETERINARY
CLINICAL IMPORTANCE - AN OVERVIEW
U.SUNILCHANDRA
The class of steroids include sex steroids, corticosteroids (glucocorticoids) and

anabolic steroids. The clinical pharmacological aspects of glucocorticoids, anabolic
steroids and antihistaminics of veterinary relevance have been outlined in this article.
Glucocorticoids (GC) potentially affect every cell in the body and produce a wide
spectrum of effects depending on tissue concentration and cell type.
Classification: 1. Short acting (duration of action < 12 hours) eg: cortisone,
hydrocortisone (1 *) 2. Intermediate acting (duration of action: 12–36hours) eg:
prednisone(4*),prednisolone(4*), methylprednisolone(5*), isoflupredone(50*) and
triamcinolone(5 *) 3.Long acting (duration of action > 48hours)eg: dexamethasone (30*),
betamethasone (30*),, paramethasone (120*), and flumethasone (120*) *
Antiinflammatory potency as determined by comparison to a cortisol a value of 1.0.
Injectable glucocorticoids: To treat shock, doses of GC are 50 to 100 times the
physiological level.; phosphate and succinate esters are used IV. .To suppress the immune
system, doses are about 20 times the physiological level; solutions of free steroid alcohols
administered IVor IM; Egs include: Dexamethasone, Flumethasone
To inhibit inflammation, doses are 10 times the physiological levels.Preparations are
acetate and acetonide esters; given IM,SC or intra-articular (into the joint).Egs of long-
acting formulations include:methylprednisolone acetate, triamcinolone acetonide,
isoflupredone acetate, betamethasone dipropionate. Isoflupredone acetate is 14 and 4 time
times more potent than hydrocortisone and prednisolone respectively as anti-
inflammatory.
Topical corticosteroids: the potencywise classification:
Mild: e.g. hydrocortisone prednisolone, dexamethasone ; Moderate: e.g. betamethasone
valerate triamcinolone acetonide fluocinolone acetonoide.;Potent: e.g. betamethasone
dipropionate betamethasone valerate, diflorasone diacetate;Very potent: e.g. clobetasol
propionate, halobetasol propionate,, betamethasone Topical agents alone or in
combination with antibiotics are used to treat chronic superficial keratitis, conjunctivitis
or minor cuts, scratches, hot spots, or inflammation due to contact dermatitis, allergies,
ear infections or inflammations
Clinical Indications of GCs: 1.Adrenocortical insufficiency (acute,chronic): (Addison’s
disease).A rapidly acting parenteral corticosteroid with the most mineralocorticoid effect
administered in conjunction with vascular volume expander-isotonic saline.
Relativemineralocorticoidpotency:hydrocortisone>prednisolone/prednisone>methylpredn

134
isolone > dexamethasone 2.Allergic disorders: Dexamethasone , methylprednisolone
acetate, prednisolone sodium succinate, triamcinolone acetonide injectables are indicated
in the treatment of allergic conditions such as bee stings, drug allergy, pruritic
dermattose,allergic lung (rhinitis, astma). In acute case of atopic/flea allergy dermatitis
the lowest dose necessary or, if possible, alternate day therapy with either prednisolone,
methylprednisolone, or triamcinolone is instituted.. 3. Ocular and Aural
Inflammtion(otitis externa) : Topical steroids -for conditions of the anterior chamber;
systemic steroids for posterior chamber. Contraindicated in viral infections, fulminant
bacterial infections, fungal infections, injuries (ulcers) and glaucoma. 4.Musculoskeletal
Inflammation,: osteoarthritis, bursitis, tendonitis, immune mediated rheumatoid arthritis,
myositis; used in conjunction with therapies that target the underlying cause 5. Adjunct
therapy of cardiogenic and hemorrhagic shock: The primary treatment is the
administration of large volumes of crystalloid solutions.Dexamethasone sodium
phosphate and prednisolone sodium succinate are recommended. The primary treatment
of septic shock (endotoxaemia) is antimicrobial therapy and supportive parenteral fluid
therapy 6. As immunosuppressive in immune mediated haematopoietic and skin diseases:
immune-mediated:hemolytic anemia,thrombocytopenia,neutropenia(Dexamethasone,
prednisolone, and prednisone) skin diseases like Systemic lupus erythematus, pemphigus
complexus and myasthenia gravis.7.Respiratory conditions: in acute respiratory distress
syndrome in cattle, chronic obstructive pulmonary disease in horses, feline asthma
syndrome, aspiration pneumonia, pulmonary oedema from drowning, inhalation injury etc
8. Malignancies/Neoplasia: As a component of most combination regimens for
malignancies, in acute lymphocytic leukaemias, CNS tumors, lymphosarcoma, mast cell
tumor, multiple myeloma. 9. Termination of pregnancy/ Induction of abortion:
Dexamethasone injection ,after the 100th to 150th day of gestation, in conjuction with
prostaglandins. Mummification, retained placentas, metritis or dystocia are the possible
complications 10.Induction of Parturition : Dexamethasone,betamethasone and
flumethasone have been used; generally in conjunction with a prostaglandin.Parturition
may be induced in the last few weeks of gestation involves much less risk to the fetus
than earlier termination of pregnancy. 11. Cerebral oedema/ Hydrocepahlus due to CNS
neoplasms/parasites, sarcoidosis, spinal cord injury due to acute trauma:
Methylprednisolone sodium succinate administered 12.Intervertebral disc
diseas.:Dexamethasone, within 8 hours of an acute spinalcord injury.
flumethasone,Methylprednisolone,prednisolone, administered at an anti-inflammatory
dosage, are indicated as supportive therapy in intervertebral disk disease (Hansen
type:1).13.Ketosis in Cattle: Dexamethasone,flumethasone,isoflupredone acetate and
prednisolone acetate injectable suspension - more effective when administered with IV
glucose solutions. .A significant decrease in milk production is expected in lactating

134
cattle. 14. Mastitis: Dexamethasone is used as adjunctive therapy in the treatment of
selected cases of acute coliform mastitis to relieve some of the systemic signs (due to
endotoxin) and mammary gland inflammation; administered in conjunction with IV fluids
and antimicrobials
Side effects : of GC are mainly due to two types: from abrupt withdrawal or after
chronic therapeutic use of high doses. The longterm use of supraphysiologic doses. may
lead to iatrogenic Cushing’s syndrome, characterized by polyuria, polydipsia, bilaterally
symmetric alopecia, increased susceptibility to infection, peripheral myopathy and muscle
atrophy, and redistribution of body fat. Longterm suppression of HPAA may cause
adrenal gland atrophy and resultant iatrogenic secondary hypoadrenocorticism (acute
adrenal insufficiency/ Addisons disease).-lethargy, weakness, vomiting, and diarrhea
particularly in dogs and horses. Other adverse effects: flare up of underlying diseses,
fluid and electrolyte disturbances (potassium loss, sodium retention, and fluid retention),
inhibition of bone growth, collagen synthesis ,decreased growth rate, delayed wound
healing, gastrointestinal irritation/ulceration/perforation. hematopoietic changes;weight
gain or weight loss, precipitation of diabetes mellitus, increased susceptibility to
infections,immune response suppression,osteoporosis, myopathy, cataracts etc.
Contraindications: Infectious diseases,GIT/ peptic and corneal ulcers, diabtes mellitus,
demodicosis, osteoporosis, epilepsy, CHF, renal failure, late pregnancy, recent major
surgery , hypertension, ulcerative colitis and pancreatitis
Principles of GC therapy
1. Administered at the lowest dose known to be effective or the smallest dose that
achieves the desired effect. Drugs with primarily GC activity and minimal dose to
achieve the desired effect is chosen. Topical or local therapy is preferred whenever
possible. Once-daily dosing is usually preferred Large steroid doses are administered
in divided doses to reduce local GIT effects.
2. Animal should not have been vaccinated several weeks before/ after GC therapy. In
order to mimic the normaldiurnal cycle and reduce the risk of adrenal suppression, GC
should be given in morning between 6–10AM
3. Alternate day therapy: every other day treatments are used to maintain remission
without side effects of daily or twice daily administration such as HPAA suppression.
4. Pulse therapy: parenteral administration of supra pharmacological doses of short
acting steroids for shorter periods of time
5. Short term therapy: ( <2weeks) : short acting steroids, administered in divided
doses ,bid, till the condition is controlled (4-7days) and discontinuing therapy once
the condition is controlled
6. Long term therapy: Starting as above for 2 weeks, then bringing the dosage to the
lowest possible single dose per day or doubling the dose and give every other day.

134
Giving adjunctive therapy like antihistaminics,to keep steroid dose as low as possible.
Tapering the dose and gradually withdrawing before stopping therapy in order to
avoid iatrogenic hypoadrenocortisism.
Dosages: Hydrocortisone: adrencocortical insufficiency- dogs: 0.5mg/kg.PO.bid;
adjunctive therapy of shock- dogs and cats: 50mg/kg,IVq3-6h;antiinflammtory activity-
dogs and cats: 5mg/kg,PO,bid, IV,IM(sid); adjunctive in photosensitization-cats: 100-
600mg(total) in 1 L 10% dextrose saline,IV. Isoflupredone acetate: cattle-10-20mg total
dose, q24h, IM; Pig-0.036mg./kg/day,IM; dog-0.125-0.25mg/kg/day,IM
Cortisone: Dogs and cats: 1mg/kg.PO,IM,sid.Prednisolone: chronic/subacute
adrencocortical insufficiency- dogs: 0.2-0.4mg/kg.PO.sid;acute adrencocortical
insufficiency- dogs: 4-20mg/kg.IVq6h; adjunctive therapy of shock- dogs and cats: 5-
10mg/kg,IVq3-6h; for antiinflammtory activity-dogs and cats: 0.5-2mg/kg,PO,sid,IM;
dermatological /immune mediated disorders- dogs: 1-2mg/kg,PO,bid for 7-10 days,-cats:
2-4mg/kg,PO, q48h 100-600mg(total) in 1 iL 10% dextrose saline,IV.
Methyl prednisolone: anti inflammtory action -dogs and cats: 0.25-1mg/kg,PO;
Methyl prednisolone acetate(depot preparation)-dogs: 1mg/kg,SC,IM,cats-2-
5mg/kg,SC,IM for CNS trauma, spinal cord injury: dogs: 30mg/kgIV
Triamcinolone:dogs,cats:0.11-0.22mg/kg,PO,sid;cattle:0.02-0.04mg/kg,IM;horse-0.1-
0.2mg/kg,IM
Dexamethasone: adjunctive therapy in shock-dogsand cats:4-6mg/kg,IVq3-6h;
antiinflammtory -dogs and cats: 0.05-0.125mg/kg,PO,sid,IM; cattle- 0.06-
0.1mg/kg,IM.sid; swine-1-10mg(total) IM,IV;induction of parturition- cattle: 20-
30mg(total),IM single dose; sheep-8-16mg(total); termination of pregnancy- cattle:
25mg(total),IM,slow IV, bovine ketosis: 5-20mg(total)
Betamethasone: antiinflammtory acion-dogs and cats: 0.025mg/kg,PO,sid, all species-
0.04-0.08mg/kg,IM,IV; for induction of parturition- cattle: 20-30mg(total),IM single
dose; for bovine ketosis: 0.04-0.08mg/ kg,IM,IV
ANABOLIC STEROIDS
Anabolic (androgenic )steroids are synthetically produced variants of the naturally
occurring male hormone testosterone. The anabolic effects of the drugs promote the
growth of skeletal muscle, and the androgenic effects promote the development of male
sexual characteristics, which is responsible for the majority of the side effects of steroid
use. Nandrolone and Stanozolol are two agents commonly used in animals.
Clinical Indications: 1) Convalescence: Following surgical operations and febrile
diseases; .
Debilitating, wasting diseases, catabolic states, in major acute illness, immunosuppressive
state sand diseases, severe trauma, -conditions where there is negative nitrogen balance
2) Bone metabolism conditions – osteoporosis in elderly, to remove tissue depleting

134
processes in young ones , in diseases like CD, heavy parasitism, hypoproteinaemia etc. 3)
To hasten the tissue repair (tendon, bone damage) after major surgery and to promote the
healing and reunion in fracterous conditions. 4) To counteract glucocorticoid induced
catabolism and negative effects 5) To stimulate erythropoiesis in conditions of
hypolplastic, hemolytic anemia and malignancy conditions 6) Testosterone deficiency
conditions – male hypogonadism, andropause
Nandrolone decanoate (laurate): Dose : 1 mg/kg bodyweight,IM,SC at three week
intervals, monthly up to 50 mg (Dogs); 25mg (cat); 200mg(horse). Stanozolol : has
appetite stimulant action especially in cats. Dose: 0.25-3 mg/kg, PO, SID; 2-10 mg/kg,
IM, once weekly
Contraindications: Pregnancy, prostate or breast carcinoma in male.They may improve
glucose tolerance and decrease the need for insulin or other antidiabetic medicines in
diabetics.
Side Effects: Hypertension, acne, fluid retention, gynaecomastia, increased aggression,
epistaxis, withdrawal depression, reduced sperm count,prostate enlargement,sterility(long
term), reproductive failure, suppressive effect on sexual development in young male
animals, libido reduction, appetite stimulation, benign prostate enlargement acne and hair
loss; In female: Masculinisation of a female foetus, growth of facial hair, male-pattern
baldness, changes in or cessation of the menstrual cycle, enlargement of the clitoris,
deepened voice
ANTIHISTAMINES
Antihistamines are a) H1-receptor antagonists: that provide symptomatic relief of allergic

signs caused by histamine release, including pruritus and anaphylactic reactions and b)
H2 -receptor antagonists that mainly control overproduction of gastric parietal cell
mediated acid secretion.
H1-RECEPTOR ANTAGONISTS
Conventional antihistaminics, are categorized as First generation
(Sedative,withanticholinergiceffects:Eg:clemastine,dimenhydrinate,diphenhydramine,dox
ylamine,pheneramine,chlorpheneramine,pyrilamine,tripelennamine,cyproheptadine,prome
thazine,alimemazine,hydroxyzine,bromopheniramine and the behavior-modifying
tricyclic antidepressants: amitriptyline,clomipramine, doxepin) and Second generation
(Nonsedative,with non anticholinergic, lesser antiprutitic action; Eg:oxatomide
terfenadine, azatadine cetirizine, loratadine, astemizole) antihistamines.
Clinical Applications and Interactions : Responses to antihistamines vary
considerably, and several may need to be tried to find one that is effective for an animal

134
• As adjunct therapy for the management of systemic anaphylaxis ( allergens, insect
stings, drug induced), to control ongoing mediator release following the acute therapy
of circulatory collapse . with adrenaline and fluids.
• In the management of pruritus, generally given in conjunction with glucocorticoid, and
when pruritus is controlled (generally within 5 days) the glucocorticoid is withdrawn
and antihistamine therapy maintained to prevent recurrence of pruritus.
• Act synergistically with NSAID, glucocorticoids and ω-6/ω-3 (omega-6/3) fatty acid
supplements and may allow dosages of these agents to be reduced in some cases
• Used in acute septic gangrenous mastitis, septic metritis, retained placenta,
myoglobinuria, ruminal atony conditions in ruminanants.
• Some ( eg: promethazine,meclizine,cyclizine, diphenhydramine) are used as antiemetic
during travelling (motion sickenss) proheptadine has been indicated as the appetite
stimulant in dogs and cats
• Used for anxiety disorders in dogs and cats like inappropriate urination associated
with anxiety, excessive unexplained nocturnal activity such as pacing and vocalization
and pruritus associated with anxiety .Doxepin, has proved more useful than other
antihistamines for the treatment of anxiety-related pruritus and self-mutilation.
Adverse effects
• CNS depression (lethargy, depression, drowsiness,somnolence) which may resolve after

3–7days, even if antihistamine administration is continued. Anticholinergic effects (dry
mouth, throat, noseand eyes; urinary retention or dysuria; intestinalatony) An increase in
pruritus has occasionally been recognized in dogs treated with with higher dosages of the
drugs
• Overdosage-Excitement (restlessness, nervousness, tremors,hyperactivity), due to reduced
seizure threshold;Gastrointestinal effects (anorexia, vomiting, diarrhea,constipation)
which may be prevented if the drugs are givenwith food; Cardiovascular effects
(tachycardia, arrhythmia,hypertension) after overdosingwith some antihistamines.
Contraindications and Precautions: include avoiding the concurrent administrationof :

monoamine oxidase inhibitors (e.g.selegiline,amitraz), or CNS depressans.; Astemizole or
terfenadine with ketoconazole, itraconazole, fluconazole,clarithromycin; phenothiazine
antihistamines, diphenhydramine with antidiarrheal mixtures (e.g.kaolin/pectin),antacids,
adrenaline. Not recommended in animals with hepatic,cardiovascular disease, glaucoma,
hyperthyroidism , history of seizures,urinary retention , intestinal atony. There is no
detailed information on the safety of administration during pregnancy or potential effect
of milk. Treatment of antihistamine toxicosis: primarily symptomatic and supportive.

134
Induction of Emesis, Activated charcoal, useful for recent ingestion. Diazepam to control
seizures Physostigmine to counteract the CNS anticholinergic effect .
Dose: Amitriptyline:1–2 q.12 h (dog); 5–10 q.12–24 h (cat); Astemizole : 1mg/kg q.12–
24 h (dog); Azatadine- 1 mg/dog q.24 h (dog); Brompheniramine- 0.5–2, q.12 h (dog);
Cetirizine- 0.5–1, q.24 h(dog);Chlorpheniramine-0.2–2 q.8–12 h (dog)2–4,q.12–24h(cat);
Clemastine-0.05–1.5 q.12 h(dog);0.68 q.12 h (cat);Clomipramine 1–3, q.24 h;
Cyproheptadine- 0.1–2, q.8–12 h(dog) 2q.12 h (cat); Dimenhydrinate-8,q.8 h
(dog);Diphenhydramine- 1–4q.8 h (dog)2–4,q.12h(cat);Doxepin-0.5–1 ,q.8–12 h(dog);
Doxylamine-1–2, q.8 h(dog); Hydroxyzine 2–7 q.8 h (dog); 5–10 q.8–12 h; Ketotifen- 2–
4 mg/dog q.12 h; Loratadine -0.5 q.24 h(dog);
Oxatomide 0.5–2 q.12 h (dog) ,15–30 q.12 h (cat); Promethazine 1–2.5 q.12 h(dog)5
q.24 h (cat); Pyrilamine 1–2 q.8–12 h(dog); Terfenadine 0.25–10 q.12–24 h (dog);
Trimeprazine 0.5–5 q.8–12 h(dog); tripelennamine 1 q.12 h (dog).
H2 RECEPTOR ANTAGONISTS (H2 BLOCKERS)
They are competitive inhibitors of histamine at the gastric parietal cell H2 receptor by
blocking the H2 receptor; thus effectively blocking the gastric acid secretion .They
strengthen gastric mucosal defenses against ulceration, enhances cytoprotection.
Cimetidine, ranitidine, nizatidine and famotidine are the common ones.Cimetidine
reduces the metabolism of other drugs by inhibiting hepatic microsomal enzyme systems.
Potencywise:Famotidine> nizatidine >Ranitidine >cimetidine. Food delay the absorption
of cimetidine, has minimal effect on ranitidine, and enhances absorption of famotidine .
Indications: 1.Peptic Ulcer, Gastroesophageal Reflux,Dyspepsia,in monogastrics

2.Gastric ulcers in canines, foals, and pigs. 3. Prolonged inappetence in ruminants 4.
Abomasal ulcers in cattle and calves. Abomasal ulcers are common in high-producing
cows within the first 6 wk after parturition. The most likely cause is prolonged
inappetence, which results in sustained periods of low abomasal pH. The adverse effects
of cimetidine include: hypotension. , dizziness, confusion, diarrhea, constipation, and
rash, gynaecomastia in males, loss of libido, impotence,( antiandrogenic) which are
reversible upon discontinuation
Interactions: Antacids reduce the absorption; are to be administered at least 1 hour

interval . Cimetidine inhibits hepatic microsomal enzymes and may may increase the
serum concentrations to toxic levels of drugs like: theophylline, phenytoin, lidocaine, ,
propranolol,tricyclic antidepressants, benzodiazepines, sulfonylureas, metronidazole.
Contraindications : neonates, hepatic,renal insufficiency
Dose: Cimetidine-Dogs: 5-10 mg/kg, PO, QID Horses: 4 mg/kg, IV, BID; 18 mg/kg,
PO,BID; Raniitidine-Dogs, cattle : 0.5 mg/kg, PO, SC, or IV, BID Horses: 1.3 mg/kg, IV,

134
BID; 11 mg/kg, PO, BID Famotidine-Dogs: 0.5-1 mg/kg, PO, IV, SID Horses: 0.4 mg/kg, IV,
BID; 3 mg/kg, PO, BID
*****

134
ADVANCES IN CHEMOTHERAPEUTIC PROTOCOLS IN
POULTRY
Sandeep Halmandge
Disease is deviation from the normal state of health; it could be due to bacteria,
Viruses, Fungi, Protozoa, Parasites or nutritional or other causes. In poultry industry
productivity, profitability is enhanced by application of principles of bio-security,
vaccination, management and understanding and prevention of emerging diseases of
economic importance. Improved bio security and appropriate vaccination reduces the risk
of disease. There are several diseases which causes severe economic losses to this
industry either in the form of decreased egg production, meat production or from
mortality.
Some of the important diseases of poultry which are of economic concern are listed here.
Disease Transmission Clinical Pathology Diagnosis Treatment and

Name & Appearance Prevention
Etiology
BACTERIAL DISSEASES
Pullorum / Vertical Depressed, Spleenomegaly Isolation Treatment is of

Bacillary transmission Anorectic and and not much helpful
White tend to huddle Hepatomegaly Identificati only it reduces
Diarrhea (Trans under brooder, on of the the severity of the
ovarial Inflammation
Cupious white bacteria by disease.
Etiology : route), of the naval
diarrhea which culturing Sulphadiazine /
Salmonella Horizontal will be adherent Sulphaguinadine
( omphalitis )
pullorum Transmission to the plumage at 0.5-0.75 %
and focal
by direct surrounding conc. in feed or 1
abscess on
contact with vent, stunted gr/1 Ltr of water
heart, lung and
affected growth and for 5 days.
liver
birds, lameness due to
indirect arthritis, and Chloramphinicol
contact with huge mortality ( 0.5 % ) in feed
equipments at 2-3 weeks of for 10 days or 1
age. gr per 5 Ltr of
water.
Chlortetracycline

134
-200 mg/kg i.m
Enrofloxacin –
10 mg/kg i.e 1 ml
per 1 ltr of water.
Fowl Vertical Peak mortality Spllenomegaly Isolation Sulphamerazine

Typhoid Transmission at 2-3 weeks and -0.2 %conc. in
after outbreak, Hepatomegaly Identificati feed for 5 days
(Trans affected bird on of the ror 1-2 gr / Ltr of
ovarial Inflammation
are sleepy, poor bacteria by water.
Etiology: route), of the ovary,
growth, Sudden culturing
Salmonella Horizontal peritonitis, Furazolidone
drop in feed
gallinarum Transmission greenish bronze -0.01- 0.04 % in
intake,
by direct sheen on the feed for 10 days
Diarrhea,
contact with liver surface or 2 gr per tonne
depression,
affected upon exposure of feed or 1 gr/ ltr
Decreased egg
birds, to air and focal of water.
production ( but
indirect abscess on
these signs are heart, liver. and Enrofloxacin-5
contact with not of
equipments liver mg/kg, i.e. 1 ml
diagnostic) per 2 ltr of water.
Vaccination at 8
and 10 week of
age
Avian Vertical High chick Hepatomegaly, Conformati Sulphadiazine /

Paratyphoi Transmission mortality, Spleenomegaly on is by Sulphaguinadine
d huddling with isolation & at 0.5-0.75 %
(Trans profuse watery Inflammation identificati conc. in feed or 1
ovarial diarrhea of the ovary, on of gr/ltr of water.
route), peritonitis, organism,
Etiology : Horizontal focal abscess Chloramphinicol
lesions,
Transmission on heart, liver. ( 0.5 % ) in feed
S.typhimuri
by direct Specific for 10 days
um
contact with ELISA Kits
affected are Chlortetracycline
S.virchow
birds, available -200 mg/kg i.m
S.agona indirect for Furazolidone at
contact with detecting
S.enteritidi 0.04 % conc. in
equipment Anti bodies
s feed for 2 weeks
against or 1 gr/ ltr of
S.enteritidi

134
s water.
will suppress the

mortality but not
eliminate
infection.
Avian Direct Incidence is Spleen and Clinical Tetracycline

Pasturellos contact with more when liver signs -0.02 to 0.04 %
is/Fowl infected birds attain enlargement in feed or 5 gr
cholera/ birds, maturity with with PM lesions per 4.5 ltr of
Avian HS rodents, wild high mortality hemorrhages on water will reduce
Isolation
birds. and morbidity. viscera, heart the mortality and
and
Indirect by Sudden death and Ovary. clinical signs.
identificati
Contaminate without any Yolk material
Etiology: on of the Chlor
d feed and signs, poor in the
Pasturella bipolar tetracycline-40
water, saliva, appetite, peritoneal
multocida organism mg/kg i.m
feces. Mucous cavity. from liver
discharge from Hemorrhagic impression Erythromycin-1
eye, nostrils lesions in the smears and lb/ 500 gallon of
and mouth, respiratory lab. Animal water
diarrhea, tract. inoculation
cyanosis of Chloramphinicol-
test.
comb and 20 mg/kg i.m or 1
wattle, swollen gr in 5 ltr of
foot pads, water.
tracheal rales
and torticolis Vaccination at 6-
due to otitis 8 weeks of age.
interna. Repeat at 14-16
weeks of age.
Staphyloco Staphylococc a) Swollen a)synovial Clinical Chortetracycline

ccal al species hock joint, membrane of signs -40 mg/kg i.m
infection lameness, joint/ tendon
arthritis of sheath is thick PM lesions Streptomycin-
a) Arthritis/ phallengial and edematous 150 mg/bird
Isolation of
joints with fibrin
Tenosynovi the Sulphaquinnalon
deposit
tis organism e-0.05% in
b) lesions drinking water
are dark, moist
and Ampicillin –
gangrenous in 1gr/ltr of water

134
appearance for 4 -5 days.
c)
b) b) All age of Doxycycline – 1
gangrenous birds are gr/ltr of water for
dermatitis affected, wing d) Promin 3 -5 days.
tip and dorsal ent with
pelvic region necrotic naval, Enrofloxacin – 5
most affected inflamed, -10 mg/kg b.wt.
c) Sub for 3-5 days.
c) Affects more unabsorbed
dermal
mature birds/ yolk sac with
abscess
heavy breeds, yolk abnormal
( bumble undersurface of in color.
foot the foot is
disease) affected.
d) High chick
d) yolk sac mortality, yolk
infection sac infection,
distended
( mushy
abdomen,
chick
huddling
disease)
tendency
Infectious Direct Seromucoid Severe Isolation of Tetracycline

Coryza/ contact with nasal discharge, conjunctivitis organism -0.04 % in water
fowl affected conjunctivitis, with edema of from sinus or 5 grper 4.5 ltr
coryza birds, edema of the the face and swabs/ of water.
indirect face, swollen inflammation nasal
contact with wattles, of periorbital discharge. Chlortetracycline
equipment, decreased egg fascia, sinusitis And from – 40 mg/kg i.m
personal. production
Clinical For immature
Etiology : Aerosol
signs birds-
Haemophillus transmission sulphamethaxazo
paragallinar le-0.5% in feed
um for 5 days or 1-2
gr per ltr of
water.
VIRAL DISEASES

134
Marek’s Horizontal 5 to 35 weeks Enlargement of Neural Day old chick
disease transmission of birds are feather follicles lesions are vaccination.
-infected affected with on the skin diagnostic,
birds feather mortality may histological
dust reach as high as Enlargement of examinatio
contaminate 50 %. peripheral n of nerves
with virus, Weakness of nerves of will show
Etiology:
maybe legs which lead sciatic and lymphocyti
herpes
distributed to paralysis of brachial plexus c
virus
by wind, legs, wings. infiltration
equipment/pe Depression,
rsonal also ataxia,
by inhalation blindness, pupil
is irregular and
will be small
pin point
opening,
impaction,
diarrhea,
torticolis
Infectious Direct Variable Muscular Bursal No treatment

Bursal contact of morbidity and hemorrhages in changes are
disease/ young birds mortality in the dead birds, diagnostic, Vaccination at
Gumboro with infected young chicks of enlargement o by 18- 21 days of
disease birds. up to 6 weeks bursa of symptoms age by drinking
Indirect of age, whitish fabricius which and lesions, water repeat at 7
contact with watery is surrounded and by week.
contaminated diarrhea, by gelatinous virus
Etiology :
equipment, depressed, exudates isolation
RNA virus/
houses, recombancy,
avibirna
clothing and ruffled feathers.
virus
personal
strains
Causes high
morbidity and
New castle Inhalation high mortality. Hemorrhages
disease/ and ingestion on digestive
Ranikhet of Velogenic tract especially Symptoms, No treatment.
PM lesions,

134
disease contaminated Viscerotropic on Isolation of Vaccination:
feed and virus – causes proventriculus. virus from
water acute onset, Severe trachitis, lung, F-strain ( lasota)
cessation of pulmonary spleen, to day old to 7
respiration, congestion. trachea, day of age
Etiology : respiratory and chloacal R2B
Avian nervous signs swabs. (Mukteshwar
paramyxovi with high Conjunctivitis, strain) at 8 – 10
rus type 1 mortality (100 with mild week of age.
%) hemorrhagic
trachitis.
Mesogenic
virus – nervous
and respiratory
signs with less
lethal disease.
Decrease egg
production
Lentogenyc
virus – mild
respiratory
infection with
high morbidity
Infectious Inhalation, Sudden onset of Hemorrhagic Symptoms No treatment

Laryngeot direct contact respiratory tracheitis with and lesions. because of
racheitis with infected signs like blood clots, Isolation existence of
birds, caecious and carrier state. Only
indirect (snicking/gurgli exudates in the identificati symptomatic
contact with ng), Stretched trachea on of virus therapy with
contaminated neck with open from the antibiotics will
equipment mouth tracheal reduce the
Etiology :
and personal breathing, contents. severity.
Herpes
dyspnoea,
virus
conjunctivitis, Vaccination at 10
swollen head, -16 week of age
expelled cough

134
material
contaminated
with blood or
blood clots
Avian Direct Decreased egg Red Symptoms No treatment

infectious contact of production with discoloration of and lesions.
bronchitis young birds malformed trachea and Vaccination with
with infected shells, low accumulation Isolation Massachusetts /
birds. flock mortality, of mucus in and Connecticut
Indirect sneezing, nasal cavity identificati strain, at 2 – 3
contact with respiratory on of virus weeks of age and
contaminated rales (gurgling) by egg repeat at 4 – 6
Etiology :
equipment, with ocular inoculation. weeks of age.
Corona
virus houses, discharge.
clothing and
personal
Avian Indirect High Pathogenic Subcutaneous Isolation No treatment

Influenza infection Avian hemorrhages and
occurs by Influenza and odema of identificati Slaughter and
Etiology : moving (HPAI) result the head. on of the disposal of the
Type A flocks, in sudden Vesicles on the virus using affected flocks.
orthomyxo equipments, decline in egg comb/wattle. serum virus Quarantining of
virus and personal production with Hemorrhages neutralizati the affected area,
having and by wind rapid increase on respiratory on. ELISA restriction of the
dispersal in mortality tract and lymph Kits are movement of the
Haemagglu flocks, products
(aerosol). along with nodes of the available
tinating from the area of
respiratory and intestine. for sero-
(HA) and Direct infection.
nervous signs. surveillanc
Neuraminid infection Sneezing, e of
ase (N) occurs coughing, rales, antibodies.
antigen on between cyanosis of
the surface. infected comb and
carrier and wattle, edema
susceptible of head/face are
flock. commonly
noticed.

134
PROTOZOAN DISEASES
Coccidiosis Sporulated Sudden onset, Hemorrhages Signs of Sulphaqunaxline

oocyst can be depression, on intestine diarrhea at conc. 0.1% for
transmitted ruffled especially and 3 -5 days. Or 30
mechanically feathers/plumag duodenum and dysentery. gr in 20 ltr of
Etiology:
by personal, e, diarrhea, pale jejunum, white Microscopi water
Various
contaminated comb and foci/lesion on c
Eimeria Amprollium
equipment. wattle and the serous examinatio
Sps soluble powder
Also blood mixed surface of the n for the
ingestion of caecal intestine. demonstrati 0.012 – 0.024 %
E.acervulin
contaminated droppings Intestinal on of for 3- 5 days. Or
a
feed and (Dysentery ) contents are oocyst. 30 gr in 25 ltr of
E.mivati water mixed with water.
blood and
E.nicatrix Nitrofurazone
mucus. and furazolidone
E.maxima combination- 1
gr/ltr of water.
E.tenella
E.brunetti
ENDOPARASITIC INFESTATION
Ascardias Ingestion of Reduced egg Easily seen Fecal Piperazine -50-

contaminated production, upon PM examinatio 100 mg per bird.
is feed and Death may examination., n for the
water, also occur due to catarrhal egg Levamisole- 5
Etiology : gr/100 birds.
intermediate intestinal enteritis.
A.galli hosts like obstruction.
cockroaches,
Heterakis earthworms. Stunted/debilita
gallinnaru ted birds.
m
Cestodal
Infestation
Tape worms are
Etiology: readily seen,
Ingestion of Niclosamide 0.5

134
Hymenolep intermediate Decreased catarrhal Fecal gr/kg
sis spp hosts like weight gain, enteritis with examinatio
ants, beetle diarrhea with fluidity is n for the
Raillietina and flys. mucosal shreds. observed in the egg
spp Dichlorophen –
intestinal lumen 0.3 gr/kg orally
Vaccination Schedule in Poultry:
Vaccination involves administration of an antigen to stimulate the immune system to

produce specific antibodies against viral, bacterial and protozaol disease. Vaccination programme
should be based on these following considerations:
Disease prevalent in the area, risk of exposure, immune status of flock, cost of acquisition of
vaccine, availability of specific vaccines, cost to benefit ratio associated with vaccination taking
into account the risk of infection and financial losses from the disease.
Vaccination schedule for Layers:
Disease Vaccine Age (weeks) Dose & route
1. Marek’s disease HVT vaccine Day old 0.2 ml im or sc
2. Ranikhet disease Lasota vaccine 1st 1 drop in eye/nostril
3. Gumboro disease Gumboro (live) 2 - 3rd 1 drop in eye/nostril
4. Infectious bronchitis IB live Massachusetts 4th Drinking water
strain vaccine
5. Ranikhet disease Lasota vaccine 4 – 5th Drinking water
6. Fowl pox Fowl pox vaccine 6th Wing web prick
7. Ranikhet disease R2B vaccine 8th 0.5 ml im or sc
8. Infectious coryza Infectious coryza killed 8th 0.5 ml im or sc
9.Fowl Cholera Fowl cholera killed 8th 0.5 ml im or sc
10. Infectious coryza Infectious coryza killed 12th 0.5 ml im or sc

134
11.Fowl Cholera Fowl cholera killed 12th 0.5 ml im or sc
12. Fowl pox Fowl pox vaccine 14 - 16th Wing web prick
13. Ranikhet disease R2B vaccine 18th 0.5 ml im or sc
14. Gumboro disease Gumboro (killed) 18 – 20th 0.5 ml im or sc
*****

134
CLINICAL ASPECTS OF ANTIMICROBIAL DRUG
INTERACTIONS
SUNILCHANDRA.U
Drug interactions can reduces the effect of the ‘ primary/target drug” (the drug
already there) or increases the toxicity of the target drug – often perceived as an
adverse effect of one of the drugs because of increased drug concentrations and on
very few occasions these drug interactions may be beneficial in increasing the
overall activity.
Incompatibility: Mixing of certain drugs together in the same syrienge or with
intravenous fluids may lead to physical incompatibility (change in turbidity or
colouration) or chemical reactions (viz; hydrolysis, oxidation, reduction or complex
formation) and thereby loss of pharmacological activity. The vehicle/ stabilizers
/preservations used in the product may also cause drug interaction
Solutions may be incompatible with other solutions because of ionic interactions. For
example sodium bicarbonate will react with calcium-containing solutions, forming
calcium carbonate.
Fluoroquinolones should not be mixed with cation-containing fluid solutions, when
given by intravenous route. Admixing tetracyclines with calcium-containing solutions
will result in precipitation. It is not advisable to mix salts of hydrochloric acid (HCl)
(e.g., dobutamine HCl, dopamine HCl, and epinephrine HCl) with alkaline solutions.
Vitamin B1 (thiamine hydrochloride) is unstable in alkaline solutions and should not
be mixed with alkalinizing solutions, carbonates, or citrates. Caution to be exercised
in administration of fluids, especially those containing sodium ions, to patients
receiving corticosteroids
Potassium containing solutions should be used with caution in the presence of cardiac
disease, particularly in digitalized patients or in the presence of renal disease.
Solutions containing lactate ions should be used with caution as excess administration
may result in metabolic alkalosis. The solution has to be clear and container
undamaged. It is always better to discard unused portion of the solution.
Incompatibility may result in failure to get desired response, untoward responses
like febrile response, venous thrombosis ,phlebitis, extravasation and hypervolemia.
Normal saline, comparatively appears to be the most compatible intravenous fluid
among all, for most of the antimicrobial drugs. The admixture of any drug with other

134
medications in the same syrienge or intravenous fluid bottle is generally not
recommended as it may result in substantial mutual inactivation and drugs should not
be mixed in infusion or syrienges unless the componments are of known
compatibility.
Antibacterial drugs can be classified by their action as time-dependent or
concentration-dependent. If the drug is concentration-dependent, usually a once-
daily regimen can be administered effectively as long as a sufficiently high dose is
administered. When treating a pathogen for which emergence of resistance is a
concern, a higher dose may be justified, but the interval remains the same (e.g., once-
a-day). A time-dependent antibiotic, on the other hand, does not produce better
bacterial killing with higher concentrations. Activity is improved with longer
exposure. Therefore, for these drugs, a long half-life is beneficial. If the drug has a
short half-life (e.g., a cephalosporin or penicillin a constant rate infusion may improve
therapeutic success
Examples of antimicrobial interactions of veterinary importance
Drug Interacting agent (drug) Result/adverse effect
Fluoroquinolones Na+ and Cl-. Aluminum, Iron, Decrease absorption
calcium, and Mg+2 , antacids
CNS stimulation-Convulsions
Theophylline(methyl xanthines)
Increased risk of seizures
NSAIDS
CNS Depressants Antihistamines, opioid analgesics, Enhanced depressant effets
Phenothiazine derivatives
Tetracyclines Antacids , Calcium supplements, Chelation and reduced
(oral) Milk, Iron supplements, Magnesium- tetracycline absorption
containing laxatives, Sodium
bicarbonatePhenobarbital or
Microsomal enzyme inducers, Reduce efficacy
Digitalis Phenolphthalein (laxative), Abnormal rhythmicity

antihypertensives
Acid labile drugs Anticholinergic drugs (eg: atropine) Decrease absorption
like erythromycin
Linocomycin Antidiarrhoeals-kaolin, pectate Decreased absorption
Chloramphenicol, erythromycin, Antagonistic-reduced efficacy
neostigmine Opioid analgesics
Potentiate respiratory depression
Antibiotics Large dose of atropine Decreased bioavailability
administered per
os in ruminants

134
Aminoglycoside Cephaloridine, cephalothin Nephrotoxicity, neuromuscular
polymixins, furosemide, curare like blockade
drugs, anaesthetics, amphotericin
Chloramphenicol Dicoumarol, barbiturates Prolonged anesthesia,
Cyclophosphamide Phenytoin, anticoagulation/ bleeding
Salicylates
Griseofulvin Dicoumarol, barbiturates Reduced anticoagulant effect
Monensin Tiamulin Neurotoxicity
Rifampin Theophylline Enhanced theophylline clearance
Sulfonamides Oral anticoagulants Prolonged anticoagulation effect
Oral Salicylates ,Chloramphenicol Severe hypoglycemic effect
hypoglycaemics(e Phenylbutazone, long acting sulpha
g: tolbutamide) drugs
Corticosteroids Acetazolamide Increased hypokalemic risk
Antagoniosm of hypoglycaemia
Antidiabetic drugs
Increased risk of hypokalemia
Barbiturates
Antagonism of diuretic effect,
Diuretics
Aggression
Metoclopramide
Risk of GIT ulceration
NSAIDS
Phenobarbitone Barbiturates Chloramphenicol Cross tolerance can exist
Corticosteroids Progesterone between many of them
Testosterone
Thyroxin,Griseofulvin,Phenytoin
Phenylbutazone Cyclophosphamide
Warfarin phenylbutazone,phenytoin Increased warfarin toxicity
salicylate,sulphinpyrazone
Decongestants in Diuretics Aggravate high blood pressure
cold and cough
(antihistaminics)
Antihistamines Barbiturates, tranquilizers, CNS Increased sedative effects
used for allergies depressants
and colds,
NSAIDS Anticoagulants, corticosteroids Risk of excessive bleeding
Diuretics,beta blockers,ACE Reduced antihypertensive effect
inhibitors Sulfonylureas
Increased hypoglycaemic effect
Ketoconazole Antacids , H2 receptor antagonists
,Sucralfate Omeprazole,Isoniazid
Reduced absorption and efficacy
Rifampin, Phenytoin ,

134
Carbamazepine Phenobarbital
Antidiarrhoea tranquilizers (e.g., diazepam), increased effect of tranquilizers,
l medication sedatives sedatives
(e.g.,
diphenoxylate
)
Fat-soluble Mineral oil Reduced absorption of the
vitamins vitamins
Cephalospori Antacids, H2 recpetor amatagonists Reduced efficacy
ns
Nephrotoxci mediactions- Potentiate nephrotoxicity
Aminoglycosides, Diuretics
Potentiate bleeding
anticoagulants
Macrolides(eg Chloramphenicol , Florfenicol, Antagonistic: - Reduced efficacy
: Lincosamides, penicillins
azithromycin
xanthines
eryhthromyci Increased toxicity
n)
Penicillins Chloramphenicol, tetracyclines , Antagonistic: - Reduced
sulfonamides; phenyl butazone efficacy; reduced distribution
Oral- Antacids Decrease absorption
Levamisole Organophosphorous compounds, Enhanced toxicity
diethylcarbamazine
Metocloprami Antimuscarinic drugs, opioid Antagonism
de analgesics,
butyrephenones, phenothiazines,
Increased CNS signs
corticosteroids
Increased absorption
aspirin, paracetamol
Zinc salts Iron salts, tetracyclines Reduced absorption
Bacteriostatic Bactericidal antibacterials
antibacterials
Penicillins, cephalosporins, Bactericidals action will be
Tetracyclines, aminoglycosides, monobactams,
Ineffective
sulphonamide carbapenems, fluoroquinolones,
s, metronidazole etc
chlorampheni
Tetracycline with
col,
macrolide, Inhibitors of protein synthesis:
spectinomyci Macrolide, clindamycin, Interfere with one another’s
n, chloramphenicol , spectinomycin action against bacteria reducing
trimethoprim, dalfoprostin, lincosamides the net effcet
clindamycin,
fusidic acid,

134
lincosamides
*****

134
AN UPDATE ON HERBAL ANTIMICROBIAL AGENTS
Dr.Sagari Ramdoss
Anthra, an organization of women veterinary scientists working in the field of

livestock production and development, has been involved since 1996 in a Research
Project to document and validate local ethno -veterinary and animal management
practices carried out by livestock rearing communities in different parts of the states of
Andhra Pradesh and Maharashtra in India. Communal knowledge and innovations are an
integral part of the day to day healing and management practices of farmers in all areas
and over 80% farmers continue to use these because they are easily and quickly
available, especially in remote villages. However this knowledge is today being rapidly
lost. Farmers, both men and women, have expressed a keen desire to increase their own
knowledge of these systems. This paper outlines the validation framework evolved by
ANTHRA wherein farmers using these medicines are actively participating in an
evaluation process. Major findings are that local practices are effective, participating
farmers use them confidently and other farmers are keen to use and increase their
knowledge of them.
In 1996 Anthra had initiated an action research on Documnetation of
ethnoveterinary practices from six different regions of Andhra Pradesh and Maharashtra
initiated a process of reclaiming their indigenous knowledge systems with respect to
animal health. The entire process, which evolved through several stages, which can
roughly be classified into stages of learning and documentation, community prioritization
and social validation, wide spread dissemination, use and continuous innovation and in-
situ conservation of IK related plant and animal genetic resources, was facilitated by
Anthra, and has been widely described in several publications (Anthra, 1998; Anthra,
2006; Anthra 2008, 2009; Ghotge et. al, 2002; Ghotge N. 2004; Ramdas et. al., 2004,
Ramdas et. al., 2009, Ramdas, 2009). The knowledge was fast disappearing and eroding,
primarily due to a breakdown of the systems of oral transmission of knowledge couple
with a loss of the genetic resources. We would like to reiterate and focus on the pro-active
and preeminent role-played by women at every step of the process of taking back control
over the knowledge system, from its inception to today.
The process began with young members of the community, of whom half were
young women, apprenticing with knowledgeable elders and healers-both women and men,
from whom they learnt-. They documented the knowledge in different ways- written,
visual, photographic, stories, as also learnt practically. A total of 126 disease
conditions/symptoms in Maharashtra and 61 disease conditions in Andhra Pradesh

134
affecting livestock (large ruminants, small ruminants, camels, donkeys, pigs, poultry)
were documented. Diseases ranged from contagious diseases, diseases of the digestive,
respiratory, reproductive and urinary systems, to skin diseases and simple surgical
conditions. While a number of home remedies were known to farmers--men and women,
certain remedies were known exclusively to specialist healers. A total of 1223 treatments
in Maharashtra and 1186 treatments in Andhra Pradesh were documented. The same
treatments for the same disease were cited by more than one healer/farmer, and there were
numerous common treatments documented from all six regions. There were single and
mixed-plant treatments as also animal-based and chemical ingredients used in treatments.
Numerous plants were used for multiple purposes. Trees, herbs, climbers, shrubs, grasses,
legumes were used in treatments. The stem bark was the most commonly used part,
followed by leaves, seeds, roots, fruits and flowers (Anthra, 2006).
Women were key in the subsequent phase of “social validation”, where over 32
women from their communities, used the practices of their mentors- who were the
traditional healers and elders, to prevent and treat a variety of disease conditions. Of the
total diseases documented, 20% of the diseases were prioritized for further validation. The
treatments for these prioritized diseases constituted 25% or one-fourth of the total
documented treatments. One hundred twenty treatments (20%) were categorized as A,
372 (64%) as B treatments and the remaining 15% treatments were in the C category.
Forty-four per cent or 165 of category B treatments were used in field trials between
2000-2003. Nine hundred ruminant cases were treated. Of these, an average 92% of the
cases were cured and 8% were not cured. Similarly, 1777 poultry were treated with a
success rate of 100 per cent. Finally, a total of 20 treatments for 10 disease conditions in
ruminants and poultry in Andhra Pradesh, and 14 treatments in 8 disease conditions in
Maharashtra met the set criteria and have been socially validated and were widely
disseminated to farmers in the community for their further use (Anthra, 2006).
Women played a similar key role in the validation of traditional fodders. Women
continued to play a key role in taking the knowledge back to the community- through
sharing the practices with the village level women’s groups, sharing the information and
approach with communities in other areas, becoming trainers who in turn trained new
community volunteers and sharing experiences through jatras and campaigns. Anthra,
was able to make the knowledge accessible to the younger generations with literacy skills,
through low-cost publications in local language, school textbooks, and audio-visual
learning materials.
In the context of Anthra’s work with communities, the impetus to study

ethnoveterinary medicine came particularly from women farmers, who have historically
been denied access to many aspects of this body of knowledge, since practices have been

134
primarily transmitted from father to sons and only rarely to daughters. They wished to
know remedies that are easy to prepare, effective, readily available, inexpensive and
which could be used confidently. They also wanted to learn to recognise conditions that
cannot be treated with local remedies but need other kinds of management.
Some of the key findings with respect to ethno-veterinary practices were:

• While indigenous knowledge and practices exist in every area and over 85% of
farmers –both women and men in all regions prefer ethno-veterinary treatments as the
first choice for treating their animals, it is becoming increasingly difficult for them to
use it mainly due to the absence of healers, breakdown of traditional systems of
knowledge transmission, rapid depletion of local bio-resources on which this
knowledge depends and emergence of new “problems” for which local innovations
alone are inadequate. No single person or individual has access to “all components of
the communities knowledge”. While the majority of members within the community
universally shared parts of this body of knowledge, other information was known to
only a few.
• In quite a few areas, people were scared to discuss their practices, as they believed the
government had banned its use.
• Ethno-veterinary practices documented in each area are almost entirely linked to the
local flora and fauna of the area. Regions that shared similar agro-ecological features
and thus flora type- share a greater number of common etho-veterinary practices than
those that were agro-ecologically very different.
• While women perform between 50-90% of all day to day activities related to the care
and management of livestock and poultry, they have been effectively excluded from
the vast body of ethno-veterinary practice. 99% of all specialized healers are men and
transmit information only to sons. Women however are seen to have developed
expertise and knowledge on ethno-veterinary management practices specifically for
the young, pregnant, lactating animals and poultry.
• Farmers - especially women are keen to obtain guidelines for the proper use of ethno
veterinary treatments, as they observe that some treatments are effective and others
are not.
• With loss of bio-resources required for ethno-veterinary remedies- there is a growing
body of “new and dangerous practice” which are a crude mix of modern harmful
drugs and chemicals that are readily available in today’s rural market with some
“traditional” ingredients. Typical examples are using crop pesticides such as
“Endosulfan with turmeric or naphthalene balls/gammexane to clean maggot

134
wounds”.
The field validation commenced in June 1999. As of December 1999, AHW’s
have been trained in the diseases that have been selected for validation. Select “B”
category treatments are being used in the field since May 1999 (about 6 months).
Treatments that have been categorized as “A” have been compiled in the local languages
and disseminated to the communities in the project areas.
While it is still in its initial period, preliminary analysis indicates a virtual 100%
success rate in the effect of the “B” treatments (Table 5.a & b), in a sense reconfirming
our decision to place priority on empirical information while formulating a protocol for
validation. Women, who knew nothing about treating animals, are today confidently using
these simple and readily available remedies to treat cases. Where once healers were rigid
about teaching this knowledge to women, today these very same healers look upon the
women AHW’s as their partners- and jointly together are breathing new life into this
knowledge system which was threatened with extinction.
In this model of social validation where farmers are actually actively participating
in the validation process there remain many unanswered questions. For instance the wider
academic community still insists upon “statistical significance “to prove the “validity” of
a treatment. They may question the bias within this model of “in-situ” validation.
We are still trying to address the issue of “statistical significance”. On the one
hand all the treatments have histories dating back hundreds of years. Under this protocol
of validation the efficacy of these age-old treatments on sick animals; are being recorded
“real-time”, possibly for the first time. There are some treatments that have been used
and recorded under this current “social validation “ process maybe only 10 times, yet
have produced a positive cure each time. While this may not meet the “numbers”
required for statistical significance, the women who use these treatments are now so
confident about their effect, that they will use it and share the knowledge with others. At
a social level, the process of “personal use” convinces them of its “significance” and
validity.
Our attempt in evolving this model of social validation is also in a sense to challenge the
conventional paradigms of “validity” and put forth-new ones.
*****

134
HANDLING OF VETEROLEGAL POISONING CASES
M.VIJAY KUMAR
Every veterinarian will be encountered with diagnosing and treating the animals
exposed to toxicant / poisoning which may be either accidental or malicious in
origin.History, clinical signs and necropsy of the animals will assist in rapid tentative
diagnosis which will help in the treatment of other affected animals in case of accidental
poisoning. In case of malicious poisoning, which may turn up into veterolegal case, the
identification of the toxin/poison is a must to establish the cause of death. In all
poisonous/toxicological cases, chemical analysis of the biological specimens is essential
to know the cause of death or illness. For which proper collection and despatch of
toxicological specimens to the laboratory is necessary.
History of the case is of great importance in the diagnosis of poisoning. This includes the
number of animals in the farm, number of animals affected, and method of feeding,
regularity of feeding, recent changes in the rations or attendants, spraying of pastures with
pesticides or fertilizers, rodenticides, presence of poisonous plants in the farm
environment. The possibility of industrial effluents coming in contact with
grazing/watering sources etc.
Important aspect of Autopsies is to determine the date and time of death. Autopsists,
generally know the time and date of death from owner of dead animal or from the clinical
history forwarded by clinician or government farms. In Medicolegal (Veterolegal) cases,
Autopsist is to determine the exact time and date of death of animal during post-mortem
examination because police and court of law may like to know the time & date of death of
that animal.
Determination of time & date of death is difficult work. After a regular examination of a
good number of dead bodies, Autopsist will be able to gain experience to determine the
time of death. After gaining the experience of several post-mortem examinations,
determination of time of death becomes very easy. Do not send the material from
medicolegal / veterolegal cases to any of the institute directly - send through police only.
Some of the important points are mentioned below by which pathologist can determine
the time of death. Indications as to when death occurred are obtained from the presence or
absence of rigor-mortis, abdominal tympany, protrusion of rectum and an odour of
putrefaction of dead body. It is very essential to examine the carcass very carefully for

134
post mortem changes. If the dead body is very fresh and not showing any P.M. change
and blood clot is also of recent origin, it indicates that death has taken place 2 to 4 hours
earlier from time of examination. If there are P.M. changes in the dead body, then time of
death is determined on the basis of the presence of rigor mortis and on status of dead
body. Rigor-mortis is the shortening and contraction of muscles which occurs after death.
Due to Rigor mortis, body muscles become very hard, stiff and immobilize. Presence or
absence of rigor mortis helps in determining the time of death because rigor mortis
appears gradually in the body and also disappears in same order.
Rigor mortis first appears in the anterior portion of the cadaver (dead body) and progress
in the posterior direction. It usually appears first in head, then neck then fore limbs, then
trunk and finally in the hind limbs. It disappears in the same order. It disappears first head
then neck then from fore legs then trunk and finally from hind limbs. 'Whole body again
becomes loose. Rigor-mortis appears only once in the dead body. Appearance and
disappearance of rigor-mortis take certain time after death and this time intervals of
appearance and disappearance help in determining the time of death. These vary due to
high and low temperature of the atmosphere.
Appearance of rigor-mortis causes whole body stiff in which mouth cannot be opened and
joints of legs cannot be twisted. In the winter, rigor mortis appears in head within 2 to 8
hours after death but in the summer, it appears in the head in half to three hours after
death. Rigor mortis appears in head, neck and fore limb in about 12 hours and in the
whole body in about 15 hours after death. During autopsy if rigor mortis is present in the
whole body, That means death has taken place between 15 to 20 hours earlier from the
time of post-mortem examination. Disappearance of rigor mortis takes place in the same
order. After 20 hours of death, hind limbs are only found stiff and other parts are loose.
Disappearance of rigor mortis from whole body takes place in 24 to 30 hours and whole
body becomes loose but putrid or obnoxious smell is found in the dead body.
Decomposition or putrefaction is complete on the dead body after disappearance of rigor
mortis. Disappearance of rigor mortis depends upon the rapidity with which
decomposition occurs. The longer an individual has been dead the more advanced will be
the changes of decomposition. This occurs after 24 to 30hours of death. The carcasses
give obnoxious bad smell. Abdomen is distended with accumulated gas. Gas is produced
as a result of bacterial fermentation in the stomach and other parts of the body.
So when the carcass is completely putrefied, it means death has occurred more than 30
hours earlier from the time of P.M. examination. While determining the time of death of
an individual, atmospheric temperature and seasons are taken into account because the
appearance of rigor mortis and putrefaction are hastened by high external temperature,
violent exercise (racing, fighting or struggling) or when violent muscular contractions

134
have taken place as seen in death of tetanus or strychnine poisoning, likewise, rigor mortis
is retarded by low external temperature (winter). In emaciated animal animals, rigor
mortis appears very slowly. Sheep putrify more quickly than short coated animals, as the
fleece keeps the heat in the body. Fat animals retain heat owing to poor heat-conduction
property of adipose tissue.
Postmortem :
Necropsy by routine procedure is to be performed as soon as possible after the death of

animal. The animal should be examined externally for the presence of any incisions (for
sui poisoning, snake bite etc.,) on the skin or mucous membranes. The oral cavity is
examined for corrosive lesions (acids/alkali) or changes in colour of mucous membrane
(nitrate, co, cyanide poisoning). As most of the toxins gain entry through gut,
examination of gut mucosa, the contents, their smell, colour and pH (acids, alkali, urea) is
a valuable guide in diagnosing toxicoses. Poisoning by salts of heavy metals results in
significant post mortem lesions but poisoning by alkaloids like strychnine produces very
feeble lesions.
The natural orifices, sub-cutaneous fat tissue, muscles, bones and teeth (in fluorine
poisoning), body cavities, and internal organs should be examined. The stomach should
be punctured rather than cut open for examination to note the character of smell.
Puncture ensures greater accuracy and a longer time smell. Some of the poisons emit
characteristic smell like bitter almond in hydrogen cyanide poisoning, garlic odour in
phosphorus poisoning, rotten garlic or horse radish smell in selenium, tobacco odour in
nicotine, acetylene odour in zinc phosphide and ammoniacal odour in urea poiosoning.
The colour of stomach contents also to be examined as copper salts impart a greenish
blue colour whereas picric and nitric acid impart yellow colour to the contents.
The contents of the stomach, small intestine and large intestine vary from traces to flakes
of paints or lead objects, grains or baits, seeds etc. Blood should be examined for its
colour and clotting characters. Cyanide poisoning imparts cherry red colour, arsenic
imparts rose red colour and nitrate poisoning turns the blood to brown colour.
Examination of other visceral organs should be done in relation to their size, colour etc.
Spleen size is decreased and colour is changed to dark brown or black in copper
poisoning and spleen size is increased in mycotoxicoses. The description of
morphological changes should be noted clearly and absence of changes should be
notified.
Submission of specimens:

134
A complete set of tissues collected from PM examination should include the brain ,
eyeball, thymus, thyrioid, heart, lung, spleen, kidney, liver, urinary bladder, pancreas,
lymphnodes, various sections of the gastrointestinal tract, ovaries, placenta, testes etc. In
case of many animals being affected, sample from more than one animal should be used.
The following specimen samples are preferred to be sent for different suspected
poisoning/
Suspected
Sr. Specimen Amount
Xenobiotic Remarks
No. required required
for Analysis
Whole Blood or 5ml

serum Frozen or add 1-2
1. Ammonia/Urea drops of saturated
Urine 5ml mercuric chloride.
Rumen contents 100 g
Liver, kidney 100g
Whole blood 15ml
2. Arsenic Urine 50ml
Ingesta 100 g --
Feed 1-2 kg
Cerebrum Use only glass

½ containers
Chlorinated Fat
3. 100g Avoid aluminum
hydrocarbons
Liver, Kidney, foil for wrapping
100g
Ingesta specimens
Kidney, Liver 100g
Serum 2-5ml
4. Copper Whole blood 10ml
--
Feed 1-2kg
Faces 100g
Rush sample to
Forage /Ingesta 1-2kg
laboratory
Whole blood 10ml
5. Cyanide/HCN Frozen in air tight
Liver 100g bottle. Stomach
contents in 1%
mercuric chloride

134
Bone 20g
Water 100ml Ideal sample will
6. Fluoride be lesion seen in
Forage 100g organal bone
Urine 50ml
Treated weedy 1-2kg
Urine 50ml
7. Herbicides
Ingesta 500g --
Liver, Kidney 100g
Kidney 100g
Whole blood 10ml Heparinized, do
8. Lead, Mercury
Liver 100g not use EDTA
Urine 15ml
Forages, Feed 100g Airtight containers
sample, or plastic bags.
9. Mycotoxins
Liver, Kidney, Cloth bags for dry
Brain. 100g feeds
Forage/Ingesta 1kg
Ingesta in
Water 100ml chloroform or
10. Nitrate/Nitrite
Body fluids formalin filled air
10-
tight container
20ml
Feed 100g
Organophosph
ates and Ingesta 100g
11.
Organocarbam Liver 100g --
etes
Urine 50ml
Fresh forage 100g
12. Oxalates Fixed in formalin
Kidneys 100g
Brain 100g
Sodium Serum 5ml
13. Chloride
(NaCl) CSF 1ml --
Feed 1-2kg
Liver, Kidney 100g
14. Znc phosphide --
Gastric contents 100g

134
Packing:
1. Samples submitted to the laboratory should be individually packed and labelled so as

to avoid any confusion about specimen identification. Sample should be -wrapped in
foil to protect light sensitive compounds from degrading or frozen to prevent volatile
compounds from escaping o. All specimens should be double bagged ans submitted
in appropriate shipping containers to prevent leaking.
2. Following points to be taken in to consideration during packing the sample to be sent
for the investigation .
3. Samples must be placed in strong waterproof plastic bags or wide mouthed glass
container without adding any preservatives/fixative to the sample
4. The container tightly stoppered, properly sealed with paraffin sealing wax should be
kept kept in a larger wooden box which is sealed in cloth
5. All the specimens are to be taken in separate containers (polythene jars/covers),
securely tied, properly labelled with particulars of date, case number., organs
collected, species, name of preservative used etc.
6. A sample of the preservative used, brief history of the case along with treatment
given particulars should be sent
7. Details of the addresses of the sender and the address of the laboratory is written on
outside the box which can be sent either through a messenger or by post
8. The sample should not come in direct contact with any absorbent material like cotton
wool, gauze which will dry out the sample.
9. Empty used medicinal bottles, plastic mineral water bottles should not be used
10. Glass containers if used , must be well protected to prevent breakage in transit , by
packing with sufficient absorbent material like sawdust, newspaper etc
11. The containers should never be filled completely as fermentation may occur
particularly with stomach/ ruminal contents
12. The samples transported at ambient temperature or higher must be provided heat
seal, screw caps must be reinforced with tape.
13. In case of the samples being transported in refrigerated or frozen state using ice
pack/ waterproof frozen sachets, screw caps should not be used.
14. Rumen contents/vomitus is preferred to be sent to establish that the toxin has been
ingested.
15. Liver, spleen and blood are preferred to establish toxin/ poison absorption.
16. Kidney, urine and milk are preferred be sent for detecting toxin excretion.
17. A sample of preservative in a separate sealed container to be sent particularly in
veterolegal cases

134
18. The container with indelible pen / marker labelling must be sealed properly to
ensure that the original contents are not being tampered or so as to to provide proof
for being tampered especially in vetero legal cases .
19. In case of small animals (poultry, small dogs, lab animals) the cadavers are sent as it
is, in case of large animals the gastrointestinal contents are collected from the
vicinity of changes in the gastric/intestinal mucosa. If there are no changes, a
representative sample is collected, but in medium sized animals the stomach tied at
oesophageal and duodenal end, intestine tied at both ends and bladder with tied ends
is sent separately.
20. It is always preferable to send the specimens through a special messenger.
21. In medico legal cases, the specimens should be sealed in the presence of a witness
a sample of the preservative used should be sent.
22. It is always better to have a duplicate sample stored properly in a refrigerator for
future reference.
Preservatives :For visceral organs like pieces of liver, kidney, stomach, intestine,
contents of a stomach and intestine saturated solution of sodium chloride can be
used.Suspected plants or food can be sent to the laboratory without adding any
preservative Ice pack/ waterproof frozen sachets, are used in case of the samples being
transported in refrigerated or frozen state.Rectified spirit (95% ethyl alcohol) 1 ml/g of
tissue is the ideal preservative for toxicological specimens. ( except in alcohol,
phosphorous and carbolic acid poisoning conditions).Formaline should never be used for
toxicological analysis of specimen samples as it hardens the tissue without giving scope
for scraping and interferes in with the the analysis by making the extraction of poison
much more difficult. . Blood, urine and serum should be refrigerated and never be
frozen.The materials for histopathological examination can be kept in a fixative
preferably 10 percent formalin in a wide mouthed glass container with proper labelling
and well protected by cotton padding/ covering.
Labelling information:The samples being sent to the laboratory must be accompanied

by proper protected labelling with all the details regarding the case, including the
following information
1. Name and address of the doctor and the owner of the animal
2. Animal identification characteristics-species, colour, age, sex, breed etc.
3. Number of animals affected and number of animals dead
4. Date of onset of symptoms and the death
5. Clinical signs recorded by the doctor and symptoms noticed by the owner
6. Type and the quantity of samples sending
7. Post-mortem findings

134
8. Suspected poison/toxicant
9. Any other circumstantial fact or information which may assist the laboratory in
identifying the causative agent
10. In veterolegal cases, the label containing the details is placed inside the specimen
container and another label is pasted on the wooden box/cloth covering the
container. The sample is then sent to the forensic laboratory , with the forwarding
letter ,a copy of request letter from the police and a copy of the postmortem report
*****

134
CLINICAL MANAGEMENT OF POISONINGS OF
VETERINARY IMPORTANCE
B.KALA KUMAR
In veterinary field toxicities are often found as a result of ingestion of poisonous

substances while grazing or through water. Suspicion of poisoning is also aroused when
illness occurs in a number of previously healthy animals, all affected at a same time,
sharing the same signs, necropsy findings, to the same degree of severity. Poisoning in
most occasions is accidental in farm animals, but may occasionally be deliberate .
SOURCE OF POISONINGS
1. Insecticides:Insecticides are the major source of poisonings in livestock.. Most of the

insecticides are basically ‘neurotoxic’, hence they may share some of the clinical signs,
Insecticides can be classified in to following categories: 1. Organochlorines: Eg: Aldrin,
Endosulfan, Lindane, Dicofol etc 2. Oraganophosphates. Eg: Acephate, Malathion,
Parathion, Methyl parathion, Dimethoate, Phosphamidon,, Chlorpyriphos,
Chlorfenvinphos, Monocrotophos etc 3. Carbamates. Eg: Carbaryl, Metacil, Dimetan,
Pyramat etc. 4. Pyrethroids (Synthetic): Deltamethrin, Cypermethrin,Permethrin,
Allerthrin etc. 5. Miscellaneous: Chloro-nicotinic acid (nicotine), Arsenic
compounds,Captan
Organochlorines: By virtue of their high lipid solubility these agents can enter the
neuronal membrane with ease and therefore interfere with normal functioning of the nerve
membrane sodium channel. The clinical signs of toxicity can be broadly categorized in to:
Behavioural signs - Anxiety, aggressiveness, abnormal posturing, maniac symptoms like

jumping over inanimate objects, wall climbing etc. Neurological signs – Hypersensitive
to external stimuli, spasm and twitching of fre-and hind quarter muscles, fascicualtions of
facial and eye lid muscles and variations in body temperature (subnormal temperature to
hyperthermia, up to 116°F). Autonomic effects: Marked salivation (normally thick/ sticky
saliva), Mydriasis, frequent urination, defecation and lacrimation.
Organophosphates: Clinical essentially appears as a result of irreversible inhibition of

AChE, causing accumulation of acetylcholine in the neuro-muscular junction leading to
‘spastic paralyses. The cause of death is due to respiratory collapse. Muscaranic signs

134
(miosis, watery, drooling saliva, urination, colic and /or defecation, lacrimation are the
common signs followed by nicotinic effects (muscle fasciculations, tremors) and C.N.S
effects( ataxia, convulsions and later depression of respiratory and circulatory centers).
Hypotension, bradycardia and dyspnoea are observed in poisoned animals.
Carbamates: The inhibition of AChE enzyme by carbamates is ‘reversible’, therefore, on

most occasions animals recovers on own unless ingested large quantity of pesticide.
Synthetic pyrethroids: Although these compound process low insect: mammalian

toxicity ratio, treatment of poisoned animals may be a difficult task probably because of
multiple mechanisms involved in toxicity and variations among pyrethroid class (type-I &
type-II). Hypersalivation, lacrimation, mucoid nasal discharge, excitement, in-
coordination, extension of limbs are observed in deltamethrin toxicity in buffalo calves.
Few pyrethroids also cause contact dermatitis.
2. Rodenticides:.
Anticoagulant rodenticides: These include warfarin (less used now a days) and second
generation anticoagulant rodenticides viz: Bromadiolone , brodifucoum. The main source
of poisoning is the ingestion of residues of the rodenticides or baits intended for killing
rodents.. The poor coagulation mechanism cause massive internal haemorrhages over
aperiod of time. Normally after period of about 2-5 days clinical signs appears and these
include anorexia, pulmonary coughing (epitaxis, dyspnoea),hypothermia, haematuria,
stiffness of hind quarters and sudden death. Internal haemorrhage, blood in the
GIT(gastroenteritis), haemopericardium and menigeal/cerebral bleeding and
haemorrhages in joints are the pathological lesions one can observe during necropsy. The
affected animals should be shifted to quiet and warm place and the line of treatment
include Vitamin-K1 in physiological saline (Vitamin-K3 not recommended) and cardio-
vascular support.
Zinc phosphide/ Aluminium phosphide: It is one of the cheapest and quite effective
rodenticide. Monogastric species are more sensitive rather than ruminants. Clinical signs
include anorexia, lethargy, abdominal pain, bloat (in ruminants), deep respiration, ataxia,
prostration and dyspnoea, gasping, convulsions and death. Post-mortum lesions include
pulmonary congestion, edema, sub-pleural haemorrhages, congestion of liver and
kidneys. Acetylene odour may be detected in stomach. No specific treatment is possible,
however symptomatic and supportive care maybe given. Gastric lavage with 5% Sodium
bicarbonate, Calcium boro-gluconate injection, anticonvulsants and measures to prevent
shock can be undertaken as a life saving measure.

134
3. Herbicides & Fungicides:Dinitro-compounds: Dinitrophenol, DNP; dinitro-orthro
cresol, DNOC); are some of the commonly used as herbicides. Accidental ingestion of
foliage sprayed with these compounds may lead to toxicity in ruminants. These
compounds induce methaemoglobinemia (intravascular haemolysis),hyperthermia, dark
coloured blood and gastroenteritis. Rapid onset of rigor mortis, yellowish-green coloured
tissues/urine may be recorded during post mortem examination.
Zeneb & Thiram: Zeneb (Zinc-ethylene dithiocarbonate) and Thiram (Tetra-methyl

thiuron sulfide) are the two most commonly used fungicides in agricultural practice.
Although acute poisonings is less likely to observe in field, chronic toxicities may get
unnoticed. Zeneb can induce thyroid hyperplasia, hypothyroidism, degenerative changes
in myocardial, skeletal tissues and depletion of testicular germ cells. Thiram exposure
may cause conjunctivitis, rhinitis, bronchitis, abortion (ewes) and teratogenic effects.
4. Hydrocyanic acid (HCN) /Cyanide:The most prevalent form of HCN poisoning in

livestock is caused by various cyanogeneetc plants capable of producing hydrocyanic
acid. Such plants contain cyanogenetic glucocides (dhurrin in sorghum, amygdalin in
bitter almond etc.) which hydrolyzed in to HCN in ruminants. Wilted, drought affected,
injured (chopping, rinsing etc.) plants are more dangerous than fresh plants because of
their preformed HCN. Any plants possessing 20mg HCN per 100gm (wet wt.) may serve
as potential source of HCN poisoning. Other source of cyanide poisonings are: industrial
grade Na/K and calcium cyanide (also fertilizer) and effluents from vicinity of
electroplating/metal coating industries workshop.
Hyperoxygention of blood would lead to cherry red/ bright red colour of venous blood .
Intoxicated animals shows salivation (frothy), bradypnoea, mydriasis, ataxia,tremors,
epileptiform scizure, cardiac arrhythmia and clonic-tonic convulsions. Invariably loss of
conscious, coma and death with several jerky and convulsive movements if poisoned
animals are not attended with in a with in 1 hour after the appearance of clinical initial
signs. Odour of the breath is ammonical/ bitter almond due to benzaldehyde production
(often bloating, regurgitation is observed). Opening of rumen during post-mortem
examination impart similar odour. Animals suspected for HCN poisoning must be
differentiated from nitrite and other sr milar agents before initiating antidote therapy . In
addition to antidotes, per oral administration of Cobalt chloride(10 mg/kg)and glucose is
also indicated.
5. Nitrate/Nitrite:Drought is one of the root causes of nitrite toxicity in cattle/buffaloes.

Nitrates are reduced to nitrite in ruminates. Otherwise, pigs are most sensitive species for
nitrate toxicity. Contamination of drinking water with sewage, several plants species
(Amarantus sps,Palak etc.), plants grown in highly acidic soil, water logging and rich

134
nitrated fields / effluents zone, deep well water or pond water originated from leaching
of top soil (after -nitrate fertilizer application) are some of the common source of nitrite
poisonings. Water soaked/entry of moisture may also render paddy hays/ corn in to nitrite
rich within 18-22 hours. Frequent application of fields with non-toxic weed killer 2,4-D
and nitratic fertilizer favour accumulation of nitrtes in plants. Any forage that contains
over 1.5% nitrate (expressed as pot. nitrite) is considered relatively unsafe for livestock
and should be fed with extreme caution. Nitrite ions induce meth-haemoglobenaemia as
well as marked vasodilatation. Clinical signs include cyanosis, staggering gait, muscular
tremors, rapid pulse, dyspnoea and dilated pupil. Opisthotonus, polyurea, chocolate
brown colour of the blood and cyanotic mucous membranes are the characteristic features
of nitrite toxicity. Untreated animals die with out a struggle. Reducing agents like
Methylene blue or Ascorbic acid are the antidotes (see table 2 for details). Mineral oil or
mucilaginous substances and diluted vinegar (4-5 lt. in cold water, per os) must be
administered to counter GI irritation and further reduction of nitrates in the rumen
respectively. Cardiovascular support (vasoconstrictor); and stimulants to counter
prostration.
6. Poisonous plants: Toxicities/ death due to ingestion of poisonous plants are also often
being the etiology of poisoning in the farm animals. Commonly with plant poisonings
there are perplexing epidemiological features. For example, animal already grazing in the
dangerous field are often unaffected while recently introduced may be poisoned. Drought,
starved, ailing from pica, hungry, ravenous animals, curiously excited animals (often do
not eat), and young animals less discriminate plants with different texture (attraction).
Poisonous plants often show geographical limitations in their distribution, particularly
industrial enterprises may create ‘poison hazard’ in local areas (Ipomea carnea,
Amaranthus spinosus) and certain agricultural practices / soil type may also pose
toxicities (eg. Nitrite, Selenium). Severe drought followed by rain/moisture/humid
atmosphere favour accumulation nitrite in many plants. Similarly re-emergence of fresh
leaves following harvesting also contains dangerous levels of HCN.
Essentially the source of plant poisoning can be classified into: a. naturally occurring b.
Commercial crops/byproducts and c. Conventional and non-conventional fodders.
Immature sorghum, maize, flax (linseed); Manihot esculenta (tapioca) newly emerging
bamboo shoots and rubber leaves are the common source of HCN poisonings. Accidental
ingestion of castor bean, rotten beat roots, adult nicotine leaves,Mimosa invisa (used to
increase nitrogen fixation in soil) may become fatal.. Plants or foliage belonging to
Brassicaceae sps.(Cruciferae) family i.e kale, rape,turnip, cabbage,reddish plants and
mustard seeds or meal may elicit severe toxicities in animals when fed /ingested large
quantity due to the presence of glucosinolates in such plants..Digestive

134
disturbance(enteritis),goiter polioencephalomalacia (rape blindness), pulmonary
emphysema are the sequelae. Bloat, photosensitization is also observed. Affected animals
are to be treated symptomatically.
Feeding of urea treated straws in excess/or fed to un-acclimatized animals may lead to
urea poisoning, long term feeding of subabul may lead to hypothyrodism and feeding of
fungus infested straws (sorghum, paddy or leguminous fodders) may pose threat of
mycotoxicosis when fed relatively for a long period. Ficus tsjhela (Karnataka-Kerala
boarder, Western Ghats); Acccia leucopholea (HCN), Amaranthus spinosus (nitrite);
Jatropa curcus (purging nut); Crotalaria juncia (hepatotoxic pyrrolizidine alkaloids:
monocrotaline);Flax(linseed, HCN); Ipomea carnea (LSD alkaloid like effects, also
source of nitrite and cause photosensitization). Strychnous nux-vomica (coastal
Karnataka); Abrus precatorius (Gulaganji); marking nut, Calitropis gigantica (yakka),
croton oil and Yellow oleander are also some of the plant source of accidental poisonings
and/or recorded in case of malicious poisoning in animals.
Antidotes and supportive treatments for common poisonings in large animals
Poison/toxicity Antidote/ treatment Dosage and method of treatment
Hydrocyanic acid Sodium nitrite followed Administer 1% sodium nitrite @ 15-

(HCN) /Cyanide by Sodium thiosulfate 25mg/kg,i.v followed by 25% sodium
thiosulphate @ 1.25gm , slow i.v
Na nitrite + Na thiosulfateCattle:
3gm + 15gm in 20ml water, s.c;
Sheep/goats: 2gm+5gm in 15ml
water,s.c. Cobalt chloride @10.2
mg/kg, per os; Approx. 4 lt. vinegar in
10-20lt. cold water; A large dose of
vitamin B12 and anticonvulsants, if
necessary. Give cobalt chloride
10mg/kg per-orally. Fluid therapy with
dextrose-saline is ideal
Nitrate/nitrite Methylene blue 1% Methylene blue @ 8.8mg/kg, i.v

and repeat 30 min later and if
Or necessary administer at 6-8hr. interval
Broad spectrum antibiotics intra-
Ascorbic acid
ruminally; Administer 8-10L cold
water and give osmotic purgatives
Treat for hypotension/shock,
(vasoconstrictors like 1:1000, 0.5 ml

134
adrenaline, slow iv); Blood
transfusion, if possible
Heavy metals British anti- BAL: 3mg/kg as 5% mixture of 10%

Lewisite(BAL) benzyl benzoate in mineral oil. Give
(Arsenic,antimony, deep i.m injection every 4hr. on first
mercury) two days, every 6hr. on third day and
then b.i.d for next 10 days. In cattle
Arsenic/Mercurial
and horse sodium thiosulfate can also
insecticides)
be used @ 8-10gram in the form of 10-
20%solution (i.v) or 20-30gram per-
orally in 300ml water.
Arsenic poisoning
d-penicillamine Fluid therapy and other supportive
treatment as required. Administer @
30-40mg ,i..v + 60-80mg/kg; P.O,
b.i.d or t.i.d for 3-4 days
Urea No antidote Administer 20-30lt. water and drench

4-6lt. 5 % acetic acid ;
Reduce the rumen pH Anticonvulsants, if required
Strychnine Phenobarbital sodium Phenobarbitone sodium,30mg/kg,i.v
(Strychnous- nux Chloral hydrate Chloral hydrate @ 5g/45 kg, i.v

vomica)
Drench tannic acid and then purgative
Rest the animal in cool, noise free & in

dark room after a dose of purgative
Lead Calcium disodium EDTA Make 6.6% solution and administer @

73 mg/kg,i.v (repeat or two treatment
daily for 3 days if required).
Combined thrapy with thiamine HCl
@2-4mg/kg/day, s.c is more effective,
Anticonvulsants, if required
Warfarine Vitamin- K1 Vitamin-K1: 300-500mg, S.C,every 4-

6hr.Blood transfusion transfusion @
Bromodiolone 20ml/kg or plasma @ 9ml/kg body wt;
Sedatives/tranquilizer
Pyrethroids No specific antidote, but Diazepam: 0.5-2 mg/kg, i.vAtropine

SO4 as required

134
(Deltamethrin, Diazepam HCl + Activated charcoal (1-2kg), P.O Fluid
Atropine SO4 therapy
Cypermethrin etc.)
Carbamate insecticides Atropine sulphate 0.25mg-0.5mg/kg,give ¼ intravenously

and remaining ¾ by intra-muscular or
sub-cutaneous route
Organophosphates Atropine sulphate + Atropinization: 0.25mg-0.5mg/kg,give

¼ i.v,remaining ¾ by i.m or s.c for
2-PAM every 3-6 hours. Observe for papillary
dilatation and recovery symptoms and
Or
continue treatment as required.
DAM(diacetyl
2-PAM: 20%solution @ 25-
-monoxime)
50mg/kg,i.v or intra-muscualrly,
Activated charcoal,P.O
Fluid therapy and supportive care
Organochorines Pentobarbitone sodium 30mg/kg,i.v and supportive care

( D.D.T;, B.H.C & Or Chloral hydrate
endosulphan etc.,) 5g/45 kg ,i.v and supportive care
Dinitro-herbicides In ruminants only: Treat Methylene blue: 2-4%,8-10mg/kg,i.v

(Dinitro-orthocresol- for Methaemoglobinemia every 8hr. Or Ascorbic
DNOC & with methylene blue acid: 5-10mg/kg,i.v; every8hr. for first
Dinitrophenol-DNP) 24-48hr.Note: Do not give antipyretics
Or to control hyperthermia. Administer
saline purgatives. Fluid therapy with
Ascorbic acid
DNS
*****

134
CARE AND MANAGEMENT OF CRITICAL PATIENTS IN
CLINICS
VIVEK.R.KASARALIKAR
Critically ill patient is special challenge to the clinician because the underline
problem is not evident for about 24 to 48 hours after initial presentation. Expeditious
therapy in right time can be life saving, whereas delayed adequate therapy may be
ineffective therapeutic failure. Most common clinical conditions in ambulatory patients
are trauma with internal/ external hemorrhage, poisoning and post surgical complication.
In fact, specialized care of emergent patient begins with initial phone call from the owner
and instructions to be given regarding first aid and transport procedures. Level of
consciousness, breathing pattern and external hemorrhage should be enquired on priority.
The important first aid measures are:
• Immobility and transport on firm flat surface

• Mouth to nose resuscitation in critical patient which is unconscious and not breathing
(Ten to twelve times per minute)
• Pulsating arterial bleeding is controlled by digital pressure and pressure bandage
• Penetrating foreign objects should be left in place till specialized help is available
• Head elevated by 200 in altered mental status after head or spinal injury
Evaluation and initial treatment: Three important assessment criterion in emergency

patients are A, B and C by evaluating certain parameters .
A – Airway: Airway patency should be evaluated on priority. Noisy breathing without

need of stethoscope suggests Large airway problem e.g. trachea and bronchus, whereas,
inspiratory dyspnoea implies extra-thoracic airway compromise. Loud expiratory sounds
reflect towards pathology of intra-thoracic airway including bronchioles and lung
parenchyma.
B – Breathing: Sequence of respiratory compromise is increased in respiratory rate

initially, followed by change in respiratory pattern. Laboured open mouth breathing with
development of cyanosis suggests significant compromised pulmonary function.
In both the above conditions, immediate Oxygen administration is the priority. Intra-nasal
catheter is the best choice for compromised breathing patients, whereas slash tracheotomy

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with endotracheal intubation is preferred in unconscious and apneic patients (Nasal
Oxygen flow rate should be kept at 50 – 100 ml/kg/min).
C– Circulation: Hemodynamic and cellular changes that occur as a result of abnormality

in circulation is referred as shock or peripheral circulatory failure.; is clinically classified
in to four main categories.
 Hypovolemic: occurs due to atleast 15-25 % t deficit in circulatory blood volume

 Cardiogenic shock: occurs due to failure of heart to pump requisite quantity of
blood in to circulation
 Distributive shock: due to impaired distribution of circulatory blood volume as a
result of peripheral vasodialatation
 Septic shock: This is endotoxin mediated shock
Therapeutic management of critically ill patient:
1. Cardio-pulmonary Resuscitation (CPR):Hallmarks of Cardio-pulmonary arrest are

a) stage of apnea with cyanosis of visible mucous membranes b) absence of palpable
pulse c) absence of heart sounds and d) dilatation of pupils
Guidelines for Cardio-pulmonary resuscitation
a) Positioning of animal:Lateral recumbency on small animal examination table is

optimal position in small sized dogs (< 7 kgs), whereas dorsal recumbency is
preferred for large sized dogs.
b) Resuscitation:Chest compression coupled with mouth to nose ventilation should be

performed in patients in apneic stage.Compression rate should be 60 to 120 per
minute and the compression – ventilation ratio should be 15:2. It means for every 15
compressions 2 cycles of ventilation should be performed.
2. Management of shock: Assessment of shock is governed by these parameters

• Pale to cyanotic mucous membranes
• Tachycardia with weak pulse
• Significant fall in Systolic blood pressure (Below 60 mm of Hg)
• Central Venous Pressure (CVP) less than 5 mm of H2O
• Elevated level of Blood lactate (> 80 mg/dl)
• Significant increase in Capillary Refill Time (CRT)
Therapeutic management: Emphasis should be given to
 Fluid therapy:The main aim of fluid therapy is to restore circulation and improve the
tissue perfusion. Choice between crystalloid and colloidal solutions should be
determined. Crystalloid supplements fluid along with electrolytes, whereas colloidal

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solutions expand the plasma volume.Commonly used colloidal solutions are: Dextran
70, Hexastarch,Gelatin polymers, Frozen plasma, Packed cell component. Commonly
used crystalloids are: Normal Saline, Lactated Ringer’s solution, Dextrose Normal
Saline, 7.5 % Normal saline and Hypertonic dextrose solution
 Corticosteroids:Stabilization of cell membrane, blocking of arachidonic acid
metabolism and gluconeogenesis are few important roles of corticosteroids in the treatment
of shock
 Cyclo-oxygenase inhibitors:These decrease the prostaglandin synthesis and other
vaso-active amines.Eg; Flunixin Meglumin( 0.25 mg/kg); Ketoprofen(0.5- 2.2 mg/kg)
 Antibiotic therapy in septic shock: Broad spectrum antibiotic therapy has additional
advantage in endotoxin related shock. Anti-bacterials with synergistic action are also
preferred in septic shock. III to IV generation ceophalosporin like cefoperazone,
ceftrioxone and cefixim are frequently used in small animal practice.
 Control of hemorrhage and blood transfusion: Antifibrinolytic drugs are preferred
to counteract extensive hemorrhage. PAMBA (Para amino methyl benzoic acid), EACA
(Epsilon amino caproic acid) and Botropase have fast styptic activity
 Alpha Adrenergic agonist: These drugs help in improving cardiac output and thereby
improve tissue perfusion. Dopamine used @ 5 – 10 µg/kg/min as constant infusion has
positive ionotropic effect and increase the systolic pressure.
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MANAGEMENT OF TOXICITY OF COMMON HOUSEHOLD
SUBSTANCES
U. SUNILCHANDRA
Household products being formulated as complex chemical mixtures

with multiple active ingredients designed for specific applications may be hazardous to
pets and children with accidental exposure.The common route of exposure of the
household hazardous compounds may be dermal, oral, ocular or inhalational. Some of
the important indoor substancse with higher toxic potentiality are described especially
with reference to pets.
SOAPS AND DETERGENTS: This class include soaps,shampoos, spray cleaners,
dishwash liquids , powders, laundry products, disinfectants, fabric softeners and
sanitizers. Bath soaps and bar soaps usually have low toxic potential, causing mild
gastroenteritis with vomition, on ingestion. Demulcents and diluents: milk , rinsing with
water for dermal and ocular exposure; Induction of emesis if soap is non
alkaline( noncorrosive), if there is no spontaneous vomition within thirty minutes of
ingestion and, fluid and electrolyte therapy.
Nonionic detergents ( alkyl ethoxylate; sources: shampoos, dishwash detergents,laundry

detergents) generally have low order of 125oxicoses125 and toxicity, being non
corrosive. Anionic (alkyl sodium sulfonate, dioctyl sodium sulfosuccinate, sodium lauryl
sulfate; sources: shampoos, dishwash detergents, laundry detergents) and cationic
( benzalkonium chloride, ,cetirimide; sources: fabric softeners, germicides, disinfectants,
sanitizers) detergents (Quaternary ammonium compounds) are corrosive and highly toxic.
Ethanol and isopropanol, often found in cationic detergents ;enhance gastrointestinal
absorption and damaged skin favours percutaneous absorption.
Toxicity related clinical signs are vomition, diarrhoea, gastrointestinal

discomfort, intravascular hemolysis in impaired liver condition, dermal irritation, corneal
damage ; Oral-corrosive damage, salivation,muscle weakness, respiratory and CNS
depression, seizures, collapse, comapredominantly seen with cationic detergents.
Treatment involves dilution with milk, water, egg white, administering act.charcoal,
saline cathartics, fluids, antibiotic, analgesics and thorough washing the skin with soap
and water and eye lavage with isothermic isotonic saline for 20minutes.
CORROSIVES:. Acidic corrosive (Hydrochloric acid, sulfuric acid, nitric acid,

phosphoric acid, sodium bisulfite) product examples are antirust compounds, toilet bowl

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cleaners, automobile batteries, gun barrel cleaning fluid and swimming pool cleaning
agents. Alkaline (sodium hydroxide, potassium hydroxide, sodium carbonate, potassium
carbonate, ammonium hydroxide, potassium permanganate) product examples are drain
cleaners, washing products, liquid cleansers and toilet bowl products. On dermal and
ocular exposure: serious burns, extremely painful, corneal/conjuctival necrosis,
perforation and opacity. On ingestion: corrosive burns of mucosal membranes ( milky
white/ grey, turning to wrinkled black). Vocalization,depression,,panting, inability to
swallow.haematemesis, abdominal pain, polydypsia, respiratory distress, shock,
secondary pneumonia from aspiration of vapours, gastrointestinal bleeding, perforation
and fistula are the other signs observed depending on the severity. Oral dilution with egg
white , milk or water, skin and eyes thourghly flushed with copious water and sterile
saline respectively; therapy for shock: IV fluids, steroids within 48 hours, which reduce
the fibroblastic activity and inflammation, reduce the stricture from circumferential
alkaline burns. Analgesics and antibiotics prophylactically in animals with perforations.
Attempts to neutralize burns chemically(as exothermic reactions produce elevated local
heat and thermal burns), gastric lavage, induction of emesis are contraindicated. .
Charcoal is ineffective in binding to caustics.
DISINFECTANTS: found in cleanimg products include quaternary ammonium

compounds, phenol, pine oil, bleaches, alcohols; are more toxic than soaps and detergent
compounds
Phenols: highly reactive,corrosive contact poisons; denatures and precipitates cellular

proteins of all contacting cells. nephrotoxic, hepatotoxic and neurotoxic; rapidly absorbed
through ingestion, inhalation or skin. Cats are highly sensitive. Sources of phenolic
compounds: flooring materials, coal tar, creosote, tar paper. It results in intense pain,
areas of coagulative necrosis; treated by glycerol, polyethylene glycol washing, thorough
rinsing with water , dressings soaked in 0.5% soda bica. Also may cause corrosive
burns of mouth, oropharynx, oesophagus. Vomition, salivation,ataxia, panting, weakness,
tremor, coma, seizures, methhaemoglobinaemia, respiratory alkalosis, severe liver and
kidney damage. Demulcents-milk, egg white, gastric lavage and emesis(contraindicated
if severe damage) activated charcoal, saline cathartic, 1% methylene blue, 4mg/kg;IV;
ascorbic acid 20mg/kg,PO; N-acetyl cysteine 140mg/kgIV, 70mg/kg PO. Q,id for 3 days.
Ocular exposure is treated by sterile saline wash.
Bleaches: preparations contain sodium hypochlorite.Calcium hypochlorite and

trichloroisocyanuric acid are present in industrial strength bleaching solutions ,swimming
pool chlorine products and chlorine laundry bleaches. Non chlorine bleach preparations
or colorfast bleaches contain sodium peroxide, sodium perborate or enzymatic detergents.
Generally, the toxicity of bleaches is of lower degree, resulting in irritation of

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ropharynx, salivation, vomition and abdominal pain. Bleaching of hairs, pulmonary
irritation- coughing , dyspnoea and retching on inhalation may also be seen. Nonchlorine
bleach products, (sodium perborate, sodium peroxide) are alkaline and severe gastric
irritatants causing renal damage and CNS excitation, depending on the amount ingested.
Treatment: Milk and water orally; washing with soap and rinsing with abundant
water/sterile saline on dermal/ocular exposure. Induction of emesis and orogastric
lavage is contraindicated to avoid the risk of causing further oesophageal irritation. Milk
of magnesia (2-3ml/kg) can be administered and other clinical signs are treated
symptomatically.
Deodorants: composed of aluminum chloride and aluminum chlorohydrate; which have

moderate toxicity potential. Ingestion can cause oral irritation, necrosis, gastroenteritis
and nephrosis.; which can be treated by orogastric lavage, antiemetics and
gastroprotectant drugs.
SOLVENTS AND ALCOHOLS: The most commonly encountered solvent (acetone:

sources: nail polish remover, varnishes, glues )and alcohols include
isopropanol(perfumes,cologne, grooming products), methanol (antifreeze products,
automotive wind shield clesnser, consumer products) and alcohol (alcoholic beverages,
cosmetics, mouthwashes ,common baker’s and brewer’s yeast). Activated charcoal is
ineffective in binding to the alcohols, not to be used. Clinical signs noticed are CNS and
respiratory depression acidosis, ataxia, hypothermia, cardiac arrest, coma; which is
treated by emesis induction, (if < 2 hrs); IV fluid Ringers lactate/ saline solution with
NaHCO3(1-3mEq/kg). Ethanol reduce severity of methanol poisoning.
Petroleum distillates: The compounds include cyclohexane, alkanes and alkenes.

Sources: gasoline (petrol), kerosene, motor fuels, solvent paints and vehicles for
pesticides. Because of low surface tension, chance of aspiration is most common. Dermal
exposure may result in dermatitis. Oral exposure results in aspiration pneumonia, cough,
hyperthermia, cyanosis, CNS depression and pulmonary oedema.. Emetics and oily
purgatives are contraindicated, as they increase the risk of aspiration. Gastric lavage and
activated charcoal should be reserved for ingestion of large amount(2ml/kg) or when
other toxicants are present. Oxygen therapy, rest , flushing the skin and eyes with water
and IV fluids to maintain hydration and electrolyte balance is recommended. Other
solvents (eg: acetone, turpentine) or other hydrocarbons should not be used for removing
the petroleum distillates from skin.
BATTERIES : Automotive or dry cell batteries contain sulfuric acid, that can be
irritating on contact with eyes, skin and gastrointestinal tract., which is treated

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accordingly as with acid exposure.The sources of small disc/button batteries include
batteries used in calculators, cameras, hearing aids, watches , the content being mainly
mercuric oxide. The dry cell batteries , commonly used in toy flash lights, may contain
the alkaline ( NaOH, KOH; alkaline batteries) or acidic compounds (ammonium chloride,
manganese dioxide, heavy metals- Li, Ni, Zn, Ag, Cd) in them. On ingestion, most of the
intact batteries pass through digestive tract within 24 to 36 hours without producing any
major adverse effects, except for mechanical obstruction occasionally. Gastrointestinal
distress may occur resulting from retention and obstruction, which has to be diagnosed by
radiography and has to be corrected by endoscopy and surgery . If battery is chewed and
split apart, it may cause corrosive damage depending on the chemical content in it.
Timely surgical intervention together with the administration of saline cathartics,
enemas and appropriate chelation therapy with specific chelating agents if any (eg:
DMSA or D-Penicillamine as for Pb), can minimize the corrosive damage caused. Lead
is the major source of toxicity among the metals, resulting in acute or chronic toxicity
upon ingestion. The sources of lead are paints, batteries, solder, plumbing supplies,
lubricating material, ceramic containers, Pb pipes, toys, inks, dyes, used oil from vehicles
that burn leaded gasoline. The clinical signs noticed are Acute- CNS excitability signs,
convulsions, behavioural changes, ataxia, tremor, blindness. Chronic-gastrointestinal
disturbance signs, vomition, pica,diarrhoea, abdominal pain. Treatment is by
administering Ca disodium EDTA, 25mg/kg, q.i.d, SC diluted in 10% dextrose ,Oral D-
penicllamine, 110mg/kg/day, 1-2 weeks, Dimercaptosuccinic acid(DMSA),
10mg/kg,t.i.d.
CYANOACRYLATE ADHESIVES ( SUPERGLUE) : Uncured cyanoacrylate

adhesives form an almost instantaneous bond on contact with hair/skin resulting in
annoyance and frustration of the animal. Cured ones are nontoxic upon ingestion
.Dermal exposed areas are soaked with warm soapy water as quickly as possible. and
with acetone for several minutes, if area is away from face or eye. The hairs may be
clipped to reduce the tension on skin. The surfaces should not be pulled apart, with
direct opposing actions.Ocular : Eyelid/eyeball is thoroughly washed with warm water
and Elizabeth collar is applied to prevent self trauma. The animal will be able to open
eyes on its own with no residual tissue damage within 2-3 days and hence forceful
manipulation should not be done.
Methylxanthines: Sources: Coffee, tea, chocolates, cola/soft drinks, asthma,

analgesic,cold medications. Caffeine, 128oxicoses128is and theobromine are the primary
toxic agents. Clinical signs manifested by vomition, diarrhoea, polyuria, weakness,
hyperexcitability, tremors, seizures, coma and death resulting from cardiac
tachyarrhythmias. If ingestion is less than 2 hours, emetics administration followed by,

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activated charcoal and saline cathartic is indicated. Since methylxanthines undergo
enterohepatic recycling, charcoal should be administered every 3-6 hours until symptoms
disappear. Antiarrythmics (lidocaine, without epinephrine; 1-2mg/kg,IV- loading dose;
40-60mg/kg/min infusion rate, slow IV- as maintenance dose) or beta blocker
(metoprolol; 0.1- 0.3mg/kg,PO,tid) to control arrhythmia;Diazepam or phenobarbitol to
control seizures and fluid therapy to maintain hydration and electrolyte balance is
recommended. Corticosteroids and erythromycin should be avoided as they decrease
urinary excretion of methylxanthines.
Aspirin : Clinical signs of aspirin toxicoses in cats are dose-dependant and may include
CNS depression, anorexia, vomiting, gastric hemorrhage, 129oxicoses129is , toxic
hepatitis, anemia, bone marrow hypoplasia, hyerpnea and hyperpyrexia, hyperthermia,
hyperglycemia, and glycosuria. Treatment is by GI decontamination with emetics,
activated charcoal and cathartics, within 4 hours of ingestion. Acid-base imbalance is
corrected with a slow infusion of sodium bicarbonate, carefully monitored and adjusted
to avoid pulmonary edema being developed. The resulting hyperthermia should be
controlled by external cooling; the use of antipyretic drugs should be avoided.
Paracetamol: Toxicity Signs: Dirty brown colored gums, dyspnoea, haematuria,

jaundice ,facial and paw edema , cyanosis, hypothermia, and vomiting. Less common
signs include coma, generalized weakness, and death. If ingestion is less than 2 hours,
emetics, activated charcoal and saline or osmotic cathartic are indicated.. If severe
cyanosis is present, oxygen therapy should administered, and the animal should be subject
to as little stress as possible.IV Administration of acetylcysteine, 140mg/kg/hr for 7
hours; Ascorbic acid, 30 mg/kg orally to reduce methemoglobinemia to Hb. Supportive
care including fluid therapy for possible metabolic acidosis is also recommended.The
other drugs used for NSAID 129oxicoses include
ranitidine(2mg/kg,tid,IV,PO),omeprazole(0.7mg/kg,sid,PO),metoclopramide(0.2-
0.4mg/kg, tid,PO,IM), sucralfate (0.5-1g, bid,PO)and misoprostol(2-5µg/kg,tid,PO)
Xylitol: is a sweetener used in sugar free products/chewing gums;induces hypoglycaemia

by stimulating insulin secretion , resulting in weakness,m ataxia, seizures and collapse.
Therapy: Inducing emesis administering activated charcoal, 50% dextroseIV and liver
tonics
Amitraz: poisoning occurs commonly from ingestion of a tick collar. Clinical signs
include ataxia, bradycardia, CNS depression, vomition, diarrhoea, and seizures.
Treatment involves decontamination (emesis, activated charcoal, saline cathartic) and
repeated injections of yohimbine (0.1mg/kg.IV) or atepamizole to reverse its adrenergic
agonistic effects and atropine has to be avoided as it may increase the absorption.

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*****

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MANAGEMENT OF MYCOTOXINS AND ZOOTOXINS OF
M.VIJAY KUMAR
Mycotoxins are the toxic metabolites released by moulds under certain

conditions conducive for their growth. Acute or chronic toxicoses can result from
exposure to feed or bedding contaminated with toxins that may be produced during
growth of various saprophytic or phytopathogenic fungi or molds on cereals, hay, straw,
pastures, or any other fodder. The principles that characterize mycotoxic diseases: the
cause may not be immediately identified; they are not transmissible from one animal to
another; treatment with drugs or antibiotics has little effect on the course of the disease;
outbreaks are usually seasonal because particular climatic sequences may favor fungal
growth and toxin production and study indicates specific association with a particular
feed.
There are various types of mycotoxins and are classified as follows. Based on the
causative organism: Aflatoxins - Aspergillus flavus, A. parasiticus.;Rubratoxins -
Penicillium rubrum, P.purpurogenum.; T-2 toxins - Fusarium sp. F.gramaenareum and
F. roseum.; Ergotoxins – Claviceps purpurea and C. paspali.Among these most common
are aflatoxins. Aspergillus moulds grow rapidly when the moisture is <15%and the
temperature is 24-25ºC.They commonly affect GNC, CSC, coconut cake, sunflower cake,
wheat, sorghum, millets, soybean, peas and almonds.
Susceptibility:Ducks, rabbits, dogs, pigs, calves, chicken, cows, quail and sheep are
susceptible in the order of preference. Broilers are more susceptible than layers. Calves
are more susceptible than adult dairy cattle. Maximum allowable conc. in dairy cattle is
20 ppb (0.02 ppm)Depending on fluorescence aflatoxins are classified into B1, B2, and G1,
G2. B1 is most toxic and need to be converted into its active metabolites.Toxicity is
through ingestion of aflatoxin-contaminated feed. Aflatoxins are not accumulated to any
appreciable extent by animal tissues with the exception of milk.
Signs:Acute - sudden death or anorexia, depression, dyspnoea, coughing, nasal discharge,
anaemia, epistaxis, bloody faeces, possible convulsions and death. Subacute - jaundice,
hypoprothrombinemia, haematomas and haemorrhagic enteritis. Chronic - decreased feed
efficiency, decreased productivity and weight gain, rough hair coat, anaemia, enlarged
abdomen, mild jaundice, depression and anorexia. Abortions may occur.

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Postmortem Lesions: Wide spread heamorhages,Icterus,Gastroenteritis,Hepatic
necrosis,Massive centrilobular necrosis,fibrosis of bile duct,Enlarged liver,Hydrothorax,
Ascites,Oedema of Gall bladder wall,Pericellular cirrhosis
Diagnosis: based on History,Clinical signs,PM findings,Detection of Aflatoxin M1 in
milk & urine,liver, kidney,Serum liver enzymes SGOT,SGPT,ALP elevated,Reduced
prothrombin activity,Hyperbilerubinemia,Tlc,HPLC,RIA,ELISA
Differential diagnosis: Warfarin (haemorrhages), coal tar (mottling of liver)

Copper poisoning (haemoglobinuria, hemolysis); Pyrrozolidine alkaloids
(present in plants), CCl4, blue-green algae, crotalaria are hepatotoxic.
Treatment: 1. Avoidance of contaminated feed. 2. Hydrated sodium calcium alumino
silicate (HSCAS) adsorb aflatoxins @5kg /ton 3. Stanozolol (2 mg / kg) I/M decreases
hepatic necrosis 4. Oxytetracycline (10mg / kg) I/M decreases hepatic necrosis.( Never
administer oxytetracycline and stanzolol combination, they are mutually antagonistic) 5.
Activated charcoal 6.7 mg / Kg I/R as 30% W/V slurry in M/15, PH 7 PBS(Along with
charcoal,stanzolol/oxytetracycline(any one) ) 6. GSH Precursors Cysteine,methionine
@2.2mg/kgi/p 7. Multi vitamins Like E,K & Selenium 8. Feeding easily digestible and
low fat diet containing adequate protein
Sample collection : Samples can be taken at various stages:growing crops or during
transport or storage. Whenever possible, samples should be taken after particulate size has
been reduced (Ex: by shelling or grinding) and soon after blending has occurred (as in
harvesting, loading, or grinding).Most effective if small samples are taken at periodic,
predetermined intervals from a moving stream of grain or feed. These individual stream
samples should be combined and mixed thoroughly, after which a subsample of 10 lb (4.5
kg) should be taken.. A suggested method of probe sampling is to sample at 5 locations,
each 1 ft (30 cm) from the periphery of a bin, plus once in the center. This should be done
for each 6 ft (2 m) of bin depth. Thus, taller bins would require more samples, and the
total weight should be >10kg.
Dry samples are preferable for transport and storage. Samples should be dried at 176-
194°F (80-90°C) for > 3 hr to reduce moisture to 12-13%. If mold studies are to be done,
drying at 140°F (60°C) for 6-12 hr should preserve fungal activity.Containers should be
appropriate for the nature of the sample. For dried samples, paper or cloth bags are
recommended. Plastic bags should be avoided unless grain is dried thoroughly. Plastic
bags are useful for high-moisture samples only if refrigeration, freezing, or chemicals are
used to retard mold growth during transport and storage. Once a sample has been cooled
or frozen, warming may induce condensation and allow mold growth.

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Zootoxins :Out of 236 species of snakes in India, only 50 are venomous, However, the
common poisonous snakes of India that man and animal come into contact, are : Cobra,
Krait, Russel’s viper and Sea scaled viper, Apart from these, the other venomous snakes
found in India includes Sea snakes, Pit viper and King cobra.. In animals, many a time
incidence of snakes bite is near leg region and nostrils.
Sensitivity: Horse>Man>Sheep>Cattle>Goat>Dog>Pig>Cat
Venom composition: The venom compositions vary significantly among various class of
poisonous snakes. Therefore, the course of toxicity as well as well as cause of death
will be different, and obviously therapeutic approach will also vary. On most
occasions, the identification of snake is not available or doubtful. The nature of
toxicity of poisonous snakes are: Elapidae: Cobra , King Cobra, Krait- Neurotioxic;
Viparidae: Russel viper- Haemotoxic; Crotalidae: Pit Viper- Neutrotoxic
Haemotoxic. All the bites from venomous snakes do not lead to death due to “dry
bites” which means that no venom was injected. But, some snake venoms (krait) do
not have immediate effect even in a bad bite, it is wise to give veterinary/medical
care.
Cobra:. identified by their “defence display” by spreading their long bones to their
famous hood. ; are most active at dust, having along the wedges of agricultural fields in
search of rats/mice. For this reason they live mostly in cultivated area.. The cobra venom
is rich in enzymes, cardiotoxic, neurotoxic factors. The cobra venom is rich in enzyme
acetylcholinesterase. Therefore, rapid depletion of acetylcholine (ACh) at neuromuscular
junction occurs following envenomation. This leads to “muscular paralysis” (flacid
paralysis). In addition to it, the alpha-neurotoxin is a powerful cholinoceptor blocker
(nicotinic receptors). These factors hinder the function of muscles involved in respiration
and consequently death occurs due to “respiratory paralysis”. It is important to
identify the “big four” dangerous snakes. At first sight cobra looks like a non-venomous
rat snake, but, remember that the rat snake has a pointed head and larger eyes and it can
run faster.
Krait: The common krait has bluish-bluck body with white cross bands and the head is
short and blunt. Kraits venom is 10 times as powerful as that of the cobra and of all the
Asian snakes its venom is the most toxic (neurotoxic). Kraits are noctoural. They are
active at night and rest during the day. They are found throughout India and live mostly in
sandy soil in rat burrows. Their favarite hiding places are piles of wood (on bricks which
provide many pray to shelter in. They are canibalistic- eat snakes, rats, lizards and birds.
Famale lays eggs (10-15) and stays with them until hatch.

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Russel viper: is a fat and bulky snake, but it can move with surprising speed when in
danger. Its regular chain-like pattern and flat arrow shaped head make it easy to
recognise. Its fangs are along and curved.. Venom is rich in proteolytic enzymes,
hemolytic factors.
Pit vipers: are forest snakes and feed on frogs and lizards. Commonly found in coffee
and tea plantations in India. Pit vipes have a small “pits” between nostrils and eyes. They
are heat sensitive and can detect change in temperature when warm blooded animal
comes near. Venom is not powerful and seldom results in death.
First-Aid treatment: The first aim, in case of cobra/krait bite is to retard the absorption
of venom from the site of bite. ;done by applying a torniquet, provided site of bite is
suitable for that. Do not disturb/ or/excite the animal with little care incise the area (1/4)
and bleed. It is always better to avoid KMnO4 solution for wound wash and instead use
5% soap wash in 30 min. after bite. It is not advisible to apply torniquet in case of vipers
bite as this venom is rich in spreading factors (local tissue necrosis).
Hospital treatment: The nature of hospital treatment practically depends on identity of

the poisonous snake. Polyvalent antivenin is the drug of choce in the absence of identity.
It is better to avoid administration of antihistaminic as they are found to increase toxic
potential of certain vipers venom. Popularly, hospital treatment can be remembered as
“AAA”: A = Antivenin.; A = Antibiotic (broad spectrum) andA = Antitetanus / Gas
gnagrene antitoxins.
The antivenin (monovalent/polyvalent) should be administered IV at the rate of

100 ml. (small animals) or 10-50ml. (large animals). Administer antivenom with 1:00
epinephrine (0.5-1 ml. s/c) to avoid shock. Apply 1-2ml. of antivenin over the wound (site
of bite in case of viper bite. Monitor the cardio vascular activity constantly. Narcotic
analeptic is recommended in case of cobra bite to counteract intense pain. Epinephrine
and corticosteroid to overcome hypotension and shock. Employ plasma volume expander
(6% dextran-40) and calcium gluconate to reduce hemolysis. In case of viper bite, even if
the patient survive, amputation may be performed to avoid spread of local tissued
necrosis or gangrene formation.
Note: - Anitivenom should be stored at 40C. Do not administer if they are discoloured or
after the date of expiry.
*****

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A BRIEF NOTE ON ANTIDOTES OF VETERINARY
IMPORTANCE
U.SUNILCHANDRA
Acepromazine maleate: (Acetyl-promazine): Indicated in seizures associated with

amphetamine methamphetamine, 4-Methylimidazole, metaldehyde poisoning,usually
preceding use ofbarbiturate or other anticonvulsant. Contraindicated in organophosphate
or strychnine poisoning Dose: Dogs, Cats-0.03-0.05 mg/kg IV, IM;Swine-0.1-0.2 mg/kg
IV, IM;Cattle, Horses- 0.02-0.1 mg/kg IV, IM;Sheep-0.03-0.05 IV; Goats 0.03-0.1 mg/kg
Acetic acid (Dilute 4%-6%)/ : Indicated in Ammonia toxicosis; urea, carbon monoxide,
hydrogen sulfide, and opiate, metallic salts; arsenic, selenium, tin, thallium, antimony
Sheep, Goats-0.5-1 L/ animal/ PO Cattle, Sheep,Goats- 5-7 ml/kg of a dilute solution 1:4
or 1:5 with water or 20% DextrosePO
Aminophylline/ Theophylline: Respiratory stimulants, used in benzodiazepine type

poisonings: flurazepam, midazolam, forazepam. Dose: Horse- 4-15 mg/kg PO, IV; q8-12h
Dogs- 4-10 mg/kg PO, IV; q8-12h
Amyl Nitrite/ Isoamyl Nitrite/ Isopentyl Nitrite/: indicated in cyanide,

hydrogensulfide, acrylonitrile,chloroform, iodine,nitrates and strychnine poisonings.
Cattle,Horse -30-60 minute inhalation; Dogs- 1.5-5 minute inhalation
Activated Charcoal: (10%): Carbon absorbent which absorbs toxic substancesand

irritants, non-specific organics Not effectivefor minerals (elemental,acids, salts, alkalis),
nor oils. Cattle, Sheep, Goats-1.0-3.0 g/kg PO; Horses-0.5-1.65 g/kg PO; Dogs,Cats -2-8
g/kg PO
Atipamezole HCL: Indicated in medetomidine, xylazine,amitraz, midodrine, and

phenylepherine overdose poisoning and Dogs- 50 mcg/kg IM q3-4h . Yohimbine HCl is
alpha adrenergic antagonist with weak monamineoxidase (MAO) inhibition. Used in the
treatment of drug overdose and poisoning: Amitraz, Xylazine, Clonidine.
Ascorbic acid(Vitamin C): indicated for drugs, plants and metal poisonings;
copper,iron, selenium,chromium,cobalt,lead,arsenic,nitrate-nitrite,chlorates,aniline,
hydrazine,hydroquinones, benzocaine, phenacetin, potassium permanganate, quinines,
toluidine,sulfonamides, acetaminophen, ,Johnson Grass(Sorghum), Feed Grain plants that
have been stressed with drought or herbicide and thereby accumulate nitrates. Cattle,

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Horses - 7.5-15 mg/kgIV,IM,SQ,PO;Dogs,Cat10-25mg/kgIV,IM,,PO;Rabbits,
Rodents100mg/kgIV,IM,SQ,PO;
Swine,Sheep-5-10mg/kgIV,IM,SQ,PO;Goats-2.5-5mg/kgIV,IM,SQ,PO.
Atropine Sulfate (dl-Hyoscyamine): Indicated in Poisonings: carbamate and

organophosphate
pesticides:Aldicarb,Fumarate,Bromophos,Carbaryl,Chlofenvinphos,Chlorpyrifos,Diazino
n,Dicrotophos,Dioxathion,Disulfaton,Fensulfothion,Fenthion,Malathion,Methidathion,Me
thiocarb,Methomyl, Parathion,Profenphos, Propoxur,Terbufos, Tetraethyl, pyrophosphate,
Sarin, Soman, Tabun, Paraxon, Tacrine HCL,Baclofen, Bethanechol chloride, Bisprolol,
Chloroform, Nicotine,Mushroom,Carbolic Acid,
Phenol,Benzene,physostigmine,Nitrobenzene, Cyanides,Opium, Morphine, as well as to
treat poisoning associated bradycardia,hypotension. Dose: Cattle, Horse,Dog, Cat,
Swine,Sheep, Goats, Birds,Reptiles, Rabbits, Rodent -0.1-2.0 mg/kg administer ¼ dose
IV ;with the remainder SQ or IM
Calcium gluconate/ Calcium borogluconate: (Calcium chloride; Calcium lactate) :

Indicated in hypocalcemia and cardiac dysrhythmias associated with hyperkalemia:
Lead, Fluoride, Carbon tetrachloride, Ethylene glycol, Oxalic acid, Chlorinated
hydrocarbons, Hydrogen fluoride, Hydrofluric acid, Calcium channel blockers
(Nifedipine,Diltiazem),Phosphine, Hypermagnesemia, Oxalates. Dose: Ca gluconate:
Cattle, Horses, Sheep,Goats, Swine -150-250 mg/lg IVslowly, PO; Dogs, Cats 25-150
mg/kg IV slowly PO; Birds 50-100 mg/kg IV slowly ,PO Ca chloride: Cattle,Horses25-
125 mg/kg IV slowly PO; Sheep,Goats20-30 mg/kg IV slow,PO; Swine- 20-60 mg/kg IV
,Dogs, Cats 5-50 mg/kg IV slow; Ca lactate: cattle, Horses, Goat, Sheep- 40-250 mg/kg
PO ; Swine-40-500 mg/kg PO PRN; Dogs, Cats-30-150 mg/kg PO
Diazepam/ Methyl Diazepam: Anticonvulsant and Anxiolytic, indicated in the

treatment of seizures that may be caused bydirect toxic effects or secondary to hypoxia or
other metabolic or electrolyte disturbance; Isoniazid, Lithium, Salicylates,
Theophylline,Caffine, Theobromine, Amphetamines, Nicotine, Atropine,
Aminopyridine,Lead, Metaldehyde, Cyanides,
Fluoroacetate,Mycotoxins,Organochlorines,Organophosphates,Carbamates,TricyclicAnti
depressants,Strychnine, Cocaine, Opioids, Mefenamic Acid, Methylxanthines,
Phenylethylamines, Ergot Alkaloids . Dose: Cattle, Sheep,Goats -0.5-2.0 mg/kg IV, IM;
Horses -0.5-50.0 mg/kg IV, IM ; Swine- 0.5-10.0 mg/kg IV, IM; Dogs- 0.5-5.0 mg/kg
IV, IM; Cats-0.5-2.5mg/kg IV, IM; Rabbits- 0.5-10.0 mg/kg IV, IM; Birds -0.5-2.0
mg/kg IV, IM

134
Egg white: Natural clear colloidal protein (albumin) mass;denatures, coagulates, and is
heat sensitive, has good demulcentproperties. Indicated in thetreatment of
mercury,copper, tin, silver,hydrogen peroxide,phenol, picric acid,formaldehyde,
ether,alcohol, household cleaners and detergents, corrosive chemical poisonings. Dose:
Dogs, Cats, Calves, Foals, Lambs,Kids, Pigs11-2 egg whites/5-10 kg PO; Usually
administered with milk
Epinephrine/ Adrenaline: Positive inotrope,cardiovascular stimulantand

bronchodilator. Usedin the treatment of insect bite-induced anaphylaxis,insect bite
poisoning, drug-inducedanaphylaxis, drugpoisoning; beta-blocker poisoning,
chloroquine,vaccines, ants, Bees or honey bees. Dose: Cattle,Horses, Sheep, Goats,
Swine, Dogs, Cats 0.01-0.02 mg/kg (0.45-0.9 ml 1:1,000/kg) IM,SQ; 0.01-0.02 mg/kg
(1:10,000) IV.
Gelatin : Heterogeneous mixture of water-soluble proteins derived from natural collagen;

absorbent (absorbs 5-10 times its weight), demulcent, stabilizer, thickener, texureizer, and
hemostatic sponge. Used in the treatment of household chemical poisoning; aqueous
cleaners, bases and alkalis.Dose: Dogs,Cats, Foals, Lambs,Kids, Pigs. (2 tablsp/5-10
kg)3-6 g/kg PO
Sodium Nitrite: Used inconjunction with Amyl Nitrite and Sodium Thiosulfate in the
treatment of Cyanide,Hydrogen Sulfide and other poisonings: Cattle, Horses- 4.5-7.5
mg /kg IV, IP; Sheep, Goats- 10 mg/kg IV, IP; Dogs, Cats 16-22 mg/kg IV, IP Always
used in combination with Sodium Thiosulfate
Sodium thiosulfate: Used in the treatment of cyanide and some metal poisonings:
Cisplatin, Iodine, Arsenic, Chlorates, Cyanide, Eucalyptus (Eucalyptus), Acacia, Cherry,
Plum,, Sorghumand Johnsongrass (Sorghum), Contraindicated for Hydrogen Sulfide.
Dose: Cattle,Horses- 15-25 mg/kg IV, IP as25% solution; Cattle, Horses- 8.5-13.2 mg/kg
IV, IP as 25% solution when administered with or following Sodium Nitrite;
Sheep,Goats-20-60 mg/kg IV, IP as 25% solution; 10-30 mg/kg IV, IP as 25% solution
when administered with or following Sodium Nitrite; Swine- 10-20 mg/kg as 25%;
Dogs -50-200 mg/kg as 25% sol.
Sodium Bicarbonate/ Baking Soda : Short-acting, potent antacid. Systemic alkalinizer ,

used to correct metabolic acidosis and to alkalinize urine in poisonings and drug
overdose: Amitriptyline-Perphenazine, Amitryptyline, Doxepin, Ethylene Glycol,
Formaldehyde, Glycol Ethers,Imipramine, Metformin, Methanol, Nortriptyline,
Potassium Chloride, Propylene Glycol, Quinidine, Strychnine, Trimipramine Maleate,

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Ethanol, Salicylates, Chlorphenoxy Herbicides, Jimmyweed and Goldenrod (Isocoma),
Sugar Beet (Beta)
Dose should be equivalent to ½ of calculated dose administered by slow intravenous
infusion. Cattle-70-180 mg/kg PO ; Horses-40-120 mg/kg PO; Sheep, Goats-20-100
mg/kg PO ; Dogs-20-80 mg/kg PO ; Cats-20-150 mg/kg PO.
Phytonadione/Phylloquinone/Phytomenadione (Vitamin K1): promotes liver

biosynthesis and regeneration of clotting factors . Will not reverse the anticoagulant
effects of heparin. Used in the treatment of hypoprothrombinemia caused by drug
overdose, chemical, rodenticide and plant poisonings: Coumarin, Indandione, Quinidine,
Quinine, Salicylates, Sulfonamides, Brodifacoum, Bromadiolone, Chlorphacinone,
Hydroxycoumarin, Indanedione, Pindone, Dicumarol, Warfarin, sweet Clover
(Melilotus),Dose: Cattle, Horses, Sheep, Goats, Swine, Birds- 0.5-2.5 mg/kg SQ,
IMdaily; Dogs, Cats -2-5 mg/kg PO, SQ, IM daily in divided dose
Dimercaprol: Chelator of metal ions which form soluble sulfhydral group-ion complexes
that areeliminated in the urine; used for the treatment of gold, cobalt,
antimony,Contraindicated in Cadmium poisoning,arsenic (except arsine), copper,
mercury,bismuth, hromium,nickle, tungsten, zinc,and methyl bromide poisoning. and
much less effective in lead, selenium and thallium poisoning Dose: Cattle, Horses,
Sheep,Goats, Swine, Dogs,Cats- 1-2 mg/kg IM qid;Contraindicated in Cadmium
poisoning,
Neostigmine: competitive inhibitor of acetylcholinesterase. Used in the treatment of non-

depolarizing neuromuscular blocking agents. treatment of curare, atropine, ivermectin,
avermectins,tubocurarine, gallamine, atracurium, pancuronium , botulism (Cl.
Botulinum), and as a secondary agent in the treatment of Coral and Cobra (Naja) snake
bite and Tetrodotoxin poisoning from Porcupine Fish, Deadly Nightshade Atropa),
Jimson Weed (Datura), Henbane (Hyoscyamus), Mandrake (Mandragora), Jasmine .Dose:
Dogs- 0.001-0.05 mg/kg SQ, IM; Cats-0.01-0.04 mg/kg IM; Cattle, Horses- 0.02-0.4
mg/kg SQ, IV; Swine-0.03-0.06 mg/kg IM; Sheep, Goats-0.01-0.03 mg/kg
SQ;Corticosteroids may decrease effects.
*****

134
FORENSIC REGULATIONS-A DISCUSSION
PSI
BIDAR RURAL POLICE STATION
The following is a brief acts and sections that are commonly used at the site of crime
pertaining to the veterolegal cases commonly.
THE INDIAN PENAL CODE
[Act, No. 45 of 1860]1
[6th October, 1860]
Chapter: 1 – INTRODUCTION
Section 1 - Title and extent of operation of the Code
Section 2 - Punishment of offences committed within India
Section 3 - Punishment of offences committed beyond, but which by law may be tried
within, India
Section 4 - Extension of Code to extra-territorial offences
Section 5 - Certain laws not to be affected by this Act
Chapter: 2 - GENERAL EXPLANATIONS
Section 6 - Definitions in the Code to be understood subject to exceptions
Section 7 - Sense of expression once explained
Section 8 - Gender
Section 9 - Number
Section 10 - "Man", "Woman"
Section 11 - "Person"
Section 12 - "Public"
Section 13 - "Queen" [Repealed]
Section 14 - "Servant of Government"
Section 16 - "Government of India" [Repealed]
Section 17 - "Government"
Section 18 - "India"
Section 19 - "Judge"
Section 20 - "Court of Justice"
Section 21 - "Public Servant"
Section 23 - "Wrongful gain"
Section 24 - "Dishonestly"
Section 25 - "Fraudulently"
Section 26 - "Reason to believe"
Section 27 - Property in possession of wife, clerk or servant
Section 28 - "Counterfeit"
Section 29 - "Document"
Section 29A - "Electronic record"
Section 30 - "Valuable security"
Section 32 - Words referring to acts include illegal omissions
Section 33 - "Act", "Omission"

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Section 34 - Acts done by several persons in furtherance of common intention
Section 35 - When such an act is criminal by reason of its being done with a criminal
knowledge or intention
Section 36 - Effect caused partly by act and partly by omission
Section 37 - Co-operation by doing one of several acts constituting an offence
Section 38 - Persons concerned in criminal act may be guilty of different offences
Section 39 - "Voluntarily"
Section 40 - "Offence"
Section 41 - "Special law"
Section 42 - "Local law"
Section 43 - "Illegal", "Legally bound to do"
Section 44 - "Injury"
Section 45 - "Life"
Section 46 - "Death"
Section 47 - "Animal" The word "animal" denotes any living creature, other than a human
being.
Section 49 - "Year", "Month"
Section 50 - "Section"
Section 51 - "Oath"
Section 52 - "Good faith"
Section 52A - "Harbour"
Chapter: 3 - OF PUNISHMENTS
Section 53 - Punishments
Section 53A - Construction of reference to transportation
Section 54 - Commutation of sentence of death
Section 55 - Commutation of sentence of imprisonment for life
Section 55A - Definition of "appropriate Government"
Section 57 - Fractions of terms of punishment
Section 58 - Offenders sentenced to transportation how dealt with until transported
[Repealed]
Section 59 - Transportation instead of imprisonment [Repealed]
Section 60 - Sentence may be (in certain cases of imprisonment) wholly or partly rigorous
or simple
Section 61 - Sentence of forfeiture of property [Repealed]
Section 62 - Forfeiture of property in respect of offenders punishable with death,
transportation or imprisonment [Repealed]
Section 63 - Amount of fine
Section 64 - Sentence of imprisonment for non-payment of fine
Section 65 - Limit to imprisonment for non-payment of fine, when imprisonment and fine
awardable
Section 66 - Description of imprisonment for non-payment of fine
Section 67 - Imprisonment for non-payment of fine, when offence punishable with fine
only
Section 68 - Imprisonment to terminate on payment of fine

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Section 69 - Termination of imprisonment on payment of proportional part of fine
Section 70 - Fine leviable within six years, or during imprisonment-- Death not to
discharge property from liability
Section 71 - Limit of punishment of offence made up of several offences
Section 72 - Punishment of person guilty of one of several offences, the judgment stating
that it is doubtful of which
Section 73 - Solitary confinement
Section 74 - Limit of solitary confinement
Section 75 - Enhanced punishment for certain offences under Chapter XII or Chapter
XVII after previous conviction
Chapter: 4 - GENERAL EXCEPTIONS
Section 76 - Act done by a person bound, or by mistake of fact believing himself bound,
by law
Section 77 - Act of Judge when acting judicially
Section 78 - Act done pursuant to the judgment or order of Court
Section 79 - Act done by a person justified, or by mistake of fact believing himself
justified, by law
Section 80 - Accident in doing a lawful act
Section 81 - Act likely to cause harm, but done without criminal intent, and to prevent
other harm
Section 82 - Act of a child under seven years of age
Section 83 - Act of a child above seven and under twelve of immature understanding
Section 84 - Act of a person of unsound mind
Section 85 - Act of a person incapable of judgment by reason of intoxication caused
against his will
Section 86 - Offence requiring a particular intent or knowledge committed by one who is
intoxicated
Section 87 - Act not intended and not known to be likely to cause death or grievous hurt,
done by consent
Section 88 - Act not intended to cause death, done by consent in good faith for person's
benefit
Section 89 - Act done in good faith for benefit of child or insane person, by or by consent
of guardian
Section 90 - Consent known to be given under fear or misconception
Section 91 - Exclusion of acts which are offences independently of harm caused
Section 92 - Act done in good faith for benefit of a person without consent
Section 93 - Communication made in good faith
Section 94 - Act to which a person is compelled by threats
Section 95 - Act causing slight harm
Section 96 to 106 - Of the Right of Private Defence
Section 96 - Things done in private defence
Section 97 - Right of private defence of the body and of property
Section 98 - Right of private defence against the act of a person of unsound mind, etc.
Section 99 - Acts against which there is no right of private defence

134
Section 100 - When the right of private defence of the body extends to causing death
Section 101 - When such right extends to causing any harm other than death
Section 102 - Commencement and continuance of the right of private defence of the body
Section 103 - When the right of private defence of property extends to causing death
Section 104 - When such right extends to causing any harm other than death
Section 105 - Commencement and continuance of the right of private defence of property
Section 106 - Right of private defence against deadly assault when there is risk of harm to
innocent person
Chapter: 5 - OF ABETMENT
Section 107 - Abetment of a thing
Section 108 - Abettor
Section 108A - Abetment in India of offences outside India
Section 109 - Punishment of abetment if the act abetted is committed in consequence, and
where no express provision is made for its punishment
Section 110 - Punishment of abetment if person abetted does act with different intention
from that of abettor
Section 111 - Liability of abettor when one act abetted and different act done
Section 112 - Abettor when liable to cumulative punishment for act abetted and for act
done
Section 113 - Liability of abettor for an effect caused by the act abetted different from that
intended by the abettor
Section 114 - Abettor present when offence is committed
Section 115 - Abetment of offence punishable with death or imprisonment for life--if
offence not committed
Section 116 - Abetment of offence punishable with imprisonment--if offence be not
committed
Section 117 - Abetting commission of offence by the public or by more than ten persons
Section 118 - Concealing design to commit offence punishable with death or
imprisonment for life
Section 119 - Public servant concealing design to commit offence which it is his duty to
prevent
Section 120 - Concealing design to commit offence punishable with imprisonment
Chapter: 9 - OF OFFENCES BY OR RELATING TO PUBLIC SERVANTS

Section 161 - [Repealed]
Section 165A - [Repealed]
Section 166 - Public servant disobeying law, with intent to cause injury to any person
Section 167 - Public servant framing an incorrect document with intent to cause injury
Section 168 - Public servant unlawfully engaging in trade

134
Section 169 - Public servant unlawfully buying or bidding for property
Section 170 - Personating a public servant
Section 171 - Wearing garb or carrying token used by public servant with fraudulent
intent
Chapter: 10 - OF CONTEMPTS OF THE LAWFUL AUTHORITY OF PUBLIC
SERVANTS
Section 172 - Absconding to avoid service of summons or other proceeding
Section 173 - Preventing service of summons or other proceeding, or preventing
publication thereof
Section 174 - Non-attendance in obedience to an order from public servant
Section 175 - Omission to produce document or electronic record to public servant by
person legally bound to produce it
Section 176 - Omission to give notice or information to public servant by person legally
bound to give it
Section 177 - Furnishing false information
Section 178 - Refusing oath or affirmation when duly required by public servant to make
it
Section 179 - Refusing to answer public servant authorised to question
Section 180 - Refusing to sign statement
Section 181 - False statement on oath or affirmation to public servant or person authorised
to administer an oath or affirmation
Section 182 - False information, with intent to cause public servant to use his lawful
power to the injury of another person
Section 183 - Resistance to the taking of property by the lawful authority of a public
servant
Section 184 - Obstructing sale of property offered for sale by authority of public servant
Section 185 - Illegal purchase or bid for property offered for sale by authority of public
servant
Section 186 - Obstructing public servant in discharge of public functions
Section 187 - Omission to assist public servant when bound by law to give assistance
Section 188 - Disobedience to order duly promulgated by public servant
Section 189 - Threat of injury to public servant
Section 190 - Threat of injury to induce person to refrain from applying for protection to
public servant
Chapter: 11 - OF FALSE EVIDENCE AND OFFENCES AGAINST PUBLIC JUSTICE
Section 191 - Giving false evidence
Section 192 - Fabricating false evidence
Section 193 - Punishment for false evidence
Section 194 - Giving or fabricating false evidence with intent to procure conviction of
capital offence
Section 195 - Giving or fabricating false evidence with intent to procure conviction of
offence punishable with imprisonment for life or imprisonment
Section 195A - Threatening or inducing any person to give false evidence
Section 196 - Using evidence known to be false

134
Section 197 - Issuing or signing false certificate
Section 198 - Using as true a certificate known to be false
Section 199 - False statement made in declaration which is by law receivable as evidence
Section 200 - Using as true such declaration knowing it to be false
Section 201 - Causing disappearance of evidence of offence, or giving false information
to screen offender
Section 202 - Intentional omission to give information of offence by person bound to
inform
Section 203 - Giving false information respecting an offence committed
Section 204 - Destruction of document or electronic record to prevent its production as
evidence
Section 205 - False personation for purpose of act or proceeding in suit or prosecution
Section 206 - Fraudulent removal or concealment of property to prevent its seizure as
forfeited or in execution
Section 207 - Fraudulent claim to property to prevent its seizure as forfeited or in
execution
Section 208 - Fraudulently suffering decree for sum not due
Section 209 - Dishonestly making false claim in Court
Section 210 - Fraudulently obtaining decree for sum not due
Section 211 - False charge of offence made with intent to injure
Section 212 - Harbouring offender
Section 213 - Taking gift, etc., to screen an offender from punishment
Section 214 - Offering gift or restoration of property in consideration of screening
offender
Section 215 - Taking gift to help to recover stolen property, etc.
Section 216 - Harbouring offender who has escaped from custody or whose apprehension
has been ordered
Section 216A - Penalty for harbouring robbers or dacoits
Section 216B - Definition of "harbour" in sections 212, 216 and 216A
Section 217 - Public servant disobeying direction of law with intent to save person from
punishment or property from forfeiture
Section 218 - Public servant framing incorrect record or writing with intent to save person
from punishment or property from forfeiture
Section 219 - Public servant in judicial proceeding corruptly making report, etc., contrary
to law
Section 220 - Commitment for trial or confinement by person having authority who
knows that he is acting contrary to law
Section 221 - Intentional omission to apprehend on the part of public servant bound to
apprehend
Section 222 - Intentional omission to apprehend on the part of public servant bound to
apprehend person under sentence or lawfully committed
Section 223 - Escape from confinement or custody negligently suffered by public servant
Section 224 - Resistance or obstruction by a person to his lawful apprehension

134
Section 225 - Resistance or obstruction to lawful apprehension of another person Section
225A - Omission to apprehend, or sufferance of escape, on part of public servant, in cases
not otherwise, provided for
Section 225B - Resistance or obstruction to lawful apprehension, or escape or rescue in
cases not otherwise provided for
Section 226 - Unlawful return from transportation [Repealed]
Section 227 - Violation of condition of remission of punishment
Section 228 - Intentional insult or interruption to public servant sitting in judicial
proceeding
Section 228A - Disclosure of identity of the victim of certain offences etc.
Section 229 - Personation of a juror or assessor
Chapter: 14 - OF OFFENCES AFFECTING THE PUBLIC HEALTH, SAFETY,

CONVENIENCE, DECENCY AND MORALS
Section 268 - Public nuisance

Section 269 - Negligent act likely to spread infection of disease dangerous to life
Section 270 - Malignant act likely to spread infection of disease dangerous to life
Section 271 - Disobedience to quarantine rule
Section 272 - Adulteration of food or drink intended for sale
Section 273 - Sale of noxious food or drink
Section 274 - Adulteration of drugs
Section 275 - Sale of adulterated drugs
Section 276 - Sale of drug as a different drug or preparation
Section 277 - Fouling water of public spring or reservoir
Section 278 - Making atmosphere noxious to health
Section 279 - Rash driving or riding on a public way
Section 280 - Rash navigation of vessel
Section 281 - Exhibition of false light, mark or buoy
Section 282 - Conveying person by water for hire in unsafe or overloaded vessel
Section 283 - Danger or obstruction in public way or line of navigation
Section 284 - Negligent conduct with respect to poisonous substance
Section 285 - Negligent conduct with respect to fire or combustible matter
Section 286 - Negligent conduct with respect to explosive substance
Section 287 - Negligent conduct with respect to machinery
Section 288 - Negligent conduct with respect to pulling down or repairing buildings
Section 289 - Negligent conduct with respect to animal
Whoever knowingly or negligently omits to take such order with any animal in his
possession as is sufficient to guard against any probable danger to human life, or
any probable danger of grievous hurt from such animal, shall be punished with
imprisonment of either description for a term which may extend to six months, or
with fine which may extend to one thousand rupees, or with both.
Section 290 - Punishment for public nuisance in cases not otherwise provided for

134
Section 291 - Continuance of nuisance after injunction to discontinue
Section 292 - Sale, etc., of obscene books, etc.
Section 293 - Sale, etc., of obscene objects to young person
Section 294 - Obscene acts and songs
Section 294A - Keeping lottery office
Chapter: 16 - OF OFFENCES AFFECTING THE HUMAN BODY

Section 299 to 311 - Of Offences Affecting Life
Section 299 - Culpable homicide
Section 300 - Murder
Section 301 - Culpable homicide by causing death of person other than person whose
death was intended
Section 302 - Punishment for murder
Section 303 - Punishment for murder by life-convict
Section 304 - Punishment for culpable homicide not amounting to murder
Section 304A - Causing death by negligence
Section 304B - Dowry death
Section 305 - Abetment of suicide of child or insane person
Section 306 - Abetment of suicide
Section 307 - Attempt to murder
Section 308 - Attempt to commit culpable homicide
Section 309 - Attempt to commit suicide
Section 310 - Thug
Section 311 - Punishment
Section 312 to 318 - Of the Causing of Miscarriage, of Injuries to Unborn Children, of the
Exposure of Infants, and of the Concealment of Births
Section 312 - Causing miscarriage
Section 313 - Causing miscarriage without woman's consent
Section 314 - Death caused by act done with intent to cause miscarriage
Section 315 - Act done with intent to prevent child being born alive or to cause it to die
after birth
Section 316 - Causing death of quick unborn child by act amounting to culpable homicide
Section 317 - Exposure and abandonment of child under twelve years, by parent or person
having care of it
Section 318 - Concealment of birth by secret disposal of dead body
Section 319 to 338 - Of Hurt
Section 319 - Hurt
Section 320 - Grievous hurt
Section 321 - Voluntarily causing hurt
Section 322 - Voluntarily causing grievous hurt
Section 323 - Punishment for voluntarily causing hurt
Section 324 - Voluntarily causing hurt by dangerous weapons or means
Section 325 - Punishment for voluntarily causing grievous hurt
Section 326 - Voluntarily causing grievous hurt by dangerous weapons or means

134
Section 327 - Voluntarily causing hurt to extort property, or to constrain to an illegal act
Section 328 - Causing hurt by means of poison, etc. with intent to commit an offence
Section 329 - Voluntarily causing grievous hurt to extort property, or to constrain to an
illegal act
Section 330 - Voluntarily causing hurt to extort confession, or to compel restoration of
property
Section 331 - Voluntarily causing grievous hurt to extort confession, or to compel
restoration of property
Section 332 - Voluntarily causing hurt to deter public servant from his duty
Section 333 - Voluntarily causing grievous hurt to deter public servant from his duty
Section 334 - Voluntarily causing hurt on provocation
Section 335 - Voluntarily causing grievous hurt on provocation
Section 336 - Act endangering life or personal safety of others
Section 337 - Causing hurt by act endangering life or personal safety of others
Section 338 - Causing grievous hurt by act endangering life or personal safety of others
Section 339 to 348 - Of Wrongful Restraint and Wrongful Confinement
Section 339 - Wrongful restraint
Section 340 - Wrongful confinement
Section 341 - Punishment for wrongful restraint
Section 342 - Punishment for wrongful confinement
Section 343 - Wrongful confinement for three or more days
Section 344 - Wrongful confinement for ten or more days
Section 345 - Wrongful confinement of person for whose liberation writ has been issued
Section 346 - Wrongful confinement in secret
Section 347 - Wrongful confinement to extort property, or constrain to illegal act
Section 348 - Wrongful confinement to extort confession, or compel restoration of
property
Section 349 to 358 - Of Criminal Force and Assault
Section 349 - Force
Section 350 - Criminal force
Section 351 - Assault
Section 352 - Punishment for assault or criminal force otherwise than on grave
provocation
Section 353 - Assault or criminal force to deter public servant form discharge of his duty
Section 356 - Assault or criminal force in attempt to commit theft of property carried by a
person
Section 357 - Assault or criminal force in attempt wrongfully to confine a person
Section 358 - Assault or criminal force on grave provocation
Section 359 to 374 - Of Kidnapping, Abduction, Slavery and Forced Labour
Section 359 - Kidnapping
Section 360 - Kidnapping from India
Section 361 - Kidnapping from lawful guardianship
Section 362 - Abduction
Section 363 - Punishment for kidnapping STATE AMENDMENTS

134
Section 363A - Kidnapping or maiming a minor for purposes of begging
Section 364 - Kidnapping or abducting in order to murder
Section 364A - Kidnapping for ransom, etc.
Section 365 - Kidnapping or abducting with intent secretly and wrongfully to confine
person
Section 366 - Kidnapping, abducting or inducing woman to compel her marriage, etc.
Section 366A - Procuration of minor girl
Section 366B - Importation of girl from foreign country
Section 367 - Kidnapping or abducting in order to subject person to grievous hurt,
slavery, etc. Section 368 - Wrongfully concealing or keeping in confinement, kidnapped
or abducted person
Section 369 - Kidnapping or abducting child under ten years with intent to steal from its
person
Section 370 - Buying or disposing of any person as a slave
Section 371 - Habitual dealing in slaves
Section 372 - Selling minor for purposes of prostitution, etc.
Section 373 - Buying minor for purposes of prostitution, etc.
Section 374 - Unlawful compulsory labour
Section 375 to 376D - Sexual Offence
Section 375 - Rape
Section 376 - Punishment for rape
Section 376A - Intercourse by a man with his wife during separation
Section 376B - Intercourse by public servant with woman in his custody
Section 376C - Intercourse by superintendent of jail, remand home, etc.
Section 376D - Intercourse by any member of the management or staff of a hospital with
any woman in that hospital
Section 377 - Of Unnatural Offences : Unnatural offences
Section 420 - Cheating and dishonestly inducing delivery of property
Section 421 to 424 - of fraudulent deeds and dispositions of property
Section 421 - Dishonest or fraudulent removal or concealment of property to prevent
distribution among creditors
Section 422 - Dishonestly or fraudulently preventing debt being available for creditors
Section 423 - Dishonest or fraudulent execution of deed of transfer containing false
statement of consideration
Section 424 - Dishonest or fraudulent removal or concealment of property
Section 425 to 440 - Of mischief
Section 425 - Mischief
Section 426 - Punishment for mischief
Section 427 - Mischief causing damage to the amount of fifty rupees
Section 428 - Mischief by killing or maiming animal of the value of ten rupees
Whoever commits mischief by killing, poisoning, maiming or rendering useless
any animal or animals of the value of ten rupees or upwards, shall be punished
with imprisonment of either description for a term which may extend to two years,
or with fine, or with both.

134
Section 429 - Mischief by killing or maiming cattle, etc., of any value or any animal of
the value of fifty rupees
Whoever commits mischief by killing, poisoning, maiming or rendering useless,
any elephant, camel, horse, mule, buffalo, bull, cow or ox, whatever may be the
value thereof, or any other animal of the value of fifty rupees or upwards, shall be
punished with imprisonment of either description for a term which may extend to
five years, or with fine, or with both.
Section 430 - Mischief by injury to works of irrigation or by wrongfully diverting water

Whoever commits mischief by doing any act which causes, or which he knows to
be likely to cause, a diminution of the supply of water for agricultural purposes, or
for food or drink for human beings or for animals which are property, or for
cleanliness or for carrying on any manufacture, shall be punished with
imprisonment of either description for a term which may extend to five years, or
with fine, or with both.

134
DIAGNOSTIC TESTS FOR DETECTION OF COMMON
TOXICANTS
M.VIJAY KUMAR
Detection of Heavy metals: Place 10g of tissue (finely minced) in a beaker or test
tube.Add 10 ml of 10% HCl.Introduce a copper wire into the test tube Boil for 10-15 min.
(Do not inhale fumes) Remove the copper wire and place it on a filter paper Observe the
colour of the copper wire. Inference: Black coloration - Arsenic or Bismuth; Shining
silver deposit – Mercury; Dull white deposit – Silver; Dark colour with purple to blue;
violet green - Antimony.
Depending on the colour of copper wire the confirmatory test is conducted.If the deposit
is black it can be confirmed whether it is due to arsenic or bismuth by placing the copper
strip in 1-2 ml. of 10 % potassium cyanide. If the deposit is due to arsenic, it will dissolve,
but if it is due to bismuth or antimony, it will persist.In mercury, colour of the deposit
ranges grayish (50 mg) to shiny silver (100 mg).
Detection of lead: Mince the liver/kidney piece or collect a small amount of scraping
from stomach wall.Add a few drops of conc. nitric acid and heat gently till dry, (never
over heat the sample as it turns black making reading difficult). Add a few drops of water
and two drops of 10% pot. iodide solution.Development of yellow colour indicates
presence of lead.
Detection of Cyanide:
a) in biological material: Take 50 g of finely ground tissue or stomach contents in a 100

ml flask and acidify thecontents with tartaric acid. Take a filter paper previously
moistened with 10 % of guaiacol in alcohol and 0.1% of aqueous copper sulfate
solution.Plug the mouth of flask and warm gently. Allow it to stand for 30 minutes.
Observe the colour of paper. If cyanide is present, a blue colour develops.
b) in the plant sample: Preparation of sodium picrate paper-Dissolve sodium bicarbonate

5 g and picric acid 0.5 g in 100 ml of distilled water. Cut filter paper into strips of 2. x 6.
size. Dip the strips in the reagent and dry in cool place.
Take the given sample in a test tube and add a few drops of water and chlorofom. Plug the
test tube with cotton, hanging the dried picrate paper inside the test tube. The paper

134
should not touch the fluid in the tube. Heat the tube gently till fumes evolve. Observe the
colour of paper.If the colour of paper changes from yellow to brown it indicates that the
plant sampleis positive for cyanide.(The leaves and stomach contents are to be frozen
immediately after collection inpolythene bag as CN is likely to evaporate).
Detection of fluorides: To a small quantity (1-3 ml) of urine or stomach contents add 3
ml of sodium hydroxide solution in a glass or porcelain dish. Add a little quantity of
powdered glass and mix thoroughly. Apply moderate heat till dry. Add 10 ml of
concentrated sulfuric acid and cover the dish with a small plate from the under surface of
which is suspended a drop of 5% sodium chloride solution. Place a small piece of ice on
top of the plate to prevent evaporation of the drop. Heat gently for 3-5 min., carefully
remove the drop and examine under low power of microscope. If the given specimen
contains fluorides, silicon fluoride is formed which appears as small light pink hexagonal
crystals along the rim of the drop, whereas the crystals of sodium chloride are large and
square.
Detection of Nitrite:
a) Draw blood (10 ml) without anticoagulant from an affected animal and also from a
known normal animal in 20 ml capacity test tubes.Place them in boiling water bath for 45
minutes. Cool them.Observe the colour of the blood and the surface.Blood sample
containing nitrite is Salmon pink in colour, does not pull away fromthe side and the
surface is level or concave. Normal blood sample is chocolate brown,pulls away from the
side of tube and the surface is convex.
c) In a plant sample: Dissolve 0.5 g of diphenylamine in 20 ml of distilled water and

make up the volume to 100 ml with sulfuric acid. Store it in amber colored bottle.
This is a full strength solution and can be made into half strength by diluting with
equal parts of 80% sulfuric acid. To test a plant, place a drop of the reagent on the cut
surface of plant. Observe the colour.A green to blue colour indicates the presence of
nitrate.(A green to blue colour with a half strength solution indicates positive (++) for
nitrate, which could be toxic to animal).
*****

134
134
RATIONAL USE OF HORMONES IN ANIMAL
REPRODUCTION
M.K.TANDLE
The following is a brief description of various harmones used in animal

reproductive disorders
1. Oxytocin: The effect of oxytocin on uterus is to change the weak, spontaneous and
irregular contractions. Physiologically oxytocin has shorter half-life (about 2 minutes)
due to its cleavage in plasma by oxytocinase. Therapeutic response to oxytocin is always
better when administered as slow intravenous drip rather than given as a single bolus
dose. The binding of oxytocin to specific receptors present in mammary gland and
myometrium.stimulates smooth muscle contractions promoting uterine motility and
milk let down. The efficacy of exogenously administered oxytocin is more in estrogen-
sensitized uterus and the response to oxytocin is greatest when circulatory estrogen levels
are high.
Indications: Induction of parturition ( only in case of sufficient cervical dilation),

expulsion of last fetus in polytocous animal, post caesarian section- to speed up
involution and control bleeding after removal of fetus , as local infiltration,
expulsion of placental debris, uterine inertia and post repositioned uterine prolapse
( to reduce enlargement and facilitate contraction ).Dosage : Mare 75-125 IU ; Cow
75-100 IU ;Sow, Ewe 30-50 IU ;Bitch 5-25 IU;cat 5-10 IU. Route IM or IV
Precautions: Generally oxytocin preparations contain sodium sulfite as a preservative

therefore it should not be infused with solutions containing higher concentration of
dextrose to overcome possible drug interaction. Administration of oxytocin in dystocia
without sufficient cervical dilation is contraindicated. Intravenous administration may be
done by diluting oxytocin with distilled water in 1:10 ratio.Products: Inj. Pitocin (Parke –
Davis) 5 IU / 0.5 ml , Inj. Syntocinon (Novartis) 5 IU / ml
2. Prostaglandins :
a. Cloprostenol sodium (PGF2 α analogue) : It has potent luteolytic action that brings
about regression of corpus luteum (CL) and induces fertile estrus following luteolysis.

134
Indications: Cow, buffalo: sub estrum, luteal cyst, synchronized breeding, removal of
mummified fetus, chronic endometritis, pyometra and induction of parturition
Dosage: IM, IV, SC; Cattle, Buffalo: 2 ml IM, SC; 1.3 ml IV. Contra indicated in
pregnancy except for termination of pregnancy.Keep away from pregnant woman
veterinarian, persons suffering with asthma or other diseases of respiratory tract
Products: Inj. Juramate 263 µg / ml,2 ml (Vetcare); Inj. Synchromate 263 µg / ml, 4 ml
(Prima Vetcare), Inj Cyclix, Intervet, 2 mL and 20 mL vials ; Inj Clostenol, Sarabhai
Zydus. 2 mL
b. Luprostiol (PGF2α analogue) -Dosage: Cow 15 mg, heifer and Horse 7.5
mg;Products: Inj. Prosolvin 7.5 mg / ml 2 ml, 10 ml, 20 ml (Intervet)
c. Tiaprost (PGF2α analogue)-Products: Inj. Iliren 0.196 mg / ml, 10 ml (Intervet);

Dosage:Bovine 3.5 ml IV, 5 ml SC IM, Equine 3 ml IV, Caprine 1-1.5 ml SC
d. Dinoprost (PGF2 α analogue) : Dosage: Pyometra, chronic endometritis: Cattle 5 ml

IM’; Induction of parturition: Cattle 3.5 ml IV, Horse 3 ml IM, Pig 2-4 ml IM; MTP:
Cattle 3.5 ml IV .Products : Inj. Hormo P2α 5 mg / ml, 5 ml(BCAHP) ; Inj. Lutalyse
5 mg / ml10 ml (Novartis)
3. Estrogens: Natural estrogens include oestradiol, estrone and oestriols. They have
low bioavailability following postoperative administration. Simple esters of steroidal
estrogens such as benzoates or valerate are used in therapeutics as they release parent
molecule on hydrolysis. Potency of estrogen is enhanced adding ethinyl groups to the
molecule.
Indications: Misalliance, urinary incontinence in old, spayed bitches, uterine infections,

anal adenoma and to induce estrus in bitches. Dosage: Dog 1-3 mg daily orally / 0.5 – 1
ml, IM. Precautions: Polydypsia, polyuria, GI upsets, suppression of red cell production,
chronic use may lead to hypogonadism and cystic ovary in females. Products:Tab
Evalon,30s (Infar); TabProgynon-C30’s ;Inj. Progynon Depot 1 ml amp. (German
Remedies)
4. Conjugated estrogens: To prevent conception in small animal (misalliance) as it

delays transport of zygote from oviduct into the uterus. In uterine infections, estrogens
facilitate uterine drainage through cervix provided cervix is dilated.
Indications: Misalliance (within one week following breeding), urinary incontinence in

spayed / old bitches, anal adenoma, lactation, suppression and uterine infections .
Precaution: Pregnancy, feminization in male and large doses may cause aplastic anemia.

134
Products: Premarin (Wyeth lederle) Dosage: Dog, Cat 3 tabs daily for 3 days, 1 ml IM ,
Tab 0.625 mg; Inj. 25 mg / ml)
II. Hormones used to treat reproductive disorders :The choice of hormones and drugs
acting on reproductive system are important as therapeutic agents during reproductive
disorders like anoestrus, metritis, pyometra, repeat breeder, retention of fetal membranes,
delayed puberty, ovarian disorders etc. The dosage, route, frequency and indications of
hormones acting on reproductive system are mentioned in tabular form as below.
Note: Trade names mentioned by the authors are only examples and in any form
the author is not promoting or recommending any pharmaceutical products for
treatment.
Particulars Indications Dosage and Commercial

preparations
route in cow
and buffalo
DRUGS ACTING ON FEMALE GENITAL SYSTEM-OVARIES
Buserelin-GnRH Anoestrus, 2.5 mL, IM, IV Inj Receptal,

analogue Intervet
stimulates Delayed ovulation
follicular 0.0042 mg/mL,
development, Trueanoestrus,Follicular 5mL, IM, IV
estrus and cyst 10 mL vial
ovulation by
enhancing release
of FSH and LH
Gonadorelin- Cystic ovarian disease 100 mcg IM, IV Inj Cystorelin,

GnRH analogue BCAHP,50 mcg/ml,
stimulates Delayed ovulation,Repeat 250 mcg IM, IV 2 mL, 10 mL vials

follicular breeder,Improvement of
development, post partum fertility
estrus and
ovulation by
enhancing release
of FSH and LH
PITUITARY GONADOTROPINS
Follicle Superovulation in ETT 50 mg BID for 4 Inj Folltropin-V,

stimulating Vetrepharm Inc400

134
hormone days mg/vial + 20 mL
diluent
FSH induces
folliculogenesis in
mature female
ovaries
Luteinizing Anovulation 25 mg, IV Inj Lutropin-V,

hormone Vetrepharm Inc,25
Delayed ovulation mg vial + 5 mL
induces maturation, diluent
estrogen Cystic ovaries,Repeat
production and breeding
finally ovulation of
Graafian follicles
and also the growth
of CL
NON-PITUITARY GONADOTROPHINS
Human chorionic Repeat breeding 1500-3000 IU, IM Inj Chorulon,

gonadotrophin Intervet,1500 IU
Cystic ovaries 1500-3000 IU, IV vial
mimics the effect
of pituitary LH Inj Coriogan,
Delayed ovulation 1500-3000 IU, IM
causing ovulation. Intervet,250 IU/mL
repeat on day 8
It promotes the
formation and 1000 IU, 2000 IU
maintenance of CL Post partum lactation failure 1500-3000 IU, IM vials
, q 24 h with
Inj Corion,Win
synthetic oxytocin
Medicare,1000 IU,
Early abortion 1500-3000 IU /
2000 IU, 5000 IU
week for 4 weeks
vials
as IM
Pregnant mare Superovulation in ETT 1500-3000 IU Inj Folligon,

serum Intervet1000 IU vl;
gonadotrophin IM, IV Inj Synchro part
(FSH like action) 400, 500, 600,
induce follicular 700, 6000
growth in inactive IU,BCAHP
ovaries of mature
animals
Other To improve quality and Day 1, 6 mL Inj Ovaset, BCAHP

combinations yield of superovulation in BID ;Day 2, 5 mL
ETT n bovines BID;Day 3, 3 mL 9 mL vial FSH + 3
FSH 0.48 mg/9 BID;Day 4, 2 mL mL vial LH +12 mL
mL, LH 0.42

134
mg/3mL BID diluent
hCG 3000 IU, Cystic ovarian syndrome 1 vial as slow IV Inj Nymfalon,
Progesterone Intervet;hCG 3000
125mg/ vial IU, Progesterone
125 mg/ vial
Ovarian steroids
Hydroxy- Delayed ovulation,Post 500 mg, IM Inj Duraprogen,

Progesterone partum anoestrus Unichem;Inj
caproate Proluton Depot,
Cystic ovarian disease 500 mg, IM German Remedies
Stimulates luteal
action and cause Habitual abortion (late) 500 mg for 3 days Inj Uniprogestin
quieting of followed by 500 Depot, Foreva;Inj
myometrium, mg/week, IM Vetaprogen, Prima
enhances Vet care;Inj P-
endometrial Habitual abortions (early) 500 mg after 11/2 Depot, Sarabhai
glandular monthpregnancy, Zydus;Inj
secretions, thus repeat every 10 Dinolutin,
favour in days, IM ;Alved250 mg/ mL,
maintenance of 2 mL ampoule
pregnancy. At
lower doses it
induces ovulation
by its indirect
effects on LH
release
Progestagen Crestar implant,

Norgestomet- Intervet
Synthetic
Progestagen (Norgestomet 3 mg
Control/ induce/synchronize 3 mg implant SC + (estradiol valerate
Administered as ovulation in normal healthy on ear (to be kept 5 mg, Norgestomet
ear implant to animals for 9 days) + 2 mL 3 mg) per mL)
control/induce/ Inj IM
synchronize
ovulation in normal
healthy animals. In
conjunction with

134
estradiol act as a 6 mg implant SC Synchromate-B
strong negative on ear (to be kept implant, BCAHP
feed back complex for 9
on hypothalamic (Norgestomet 6 mg
hypophyseal days) + 2 mL Inj + (estradiol valerate
system preventing IM 5 mg, Norgestomet
final growth and 3 mg) per mL)
maturation of
follicles. Sudden
withdrawal of
Progestagen
releasing implant
lead to an increase
of LH pulse
frequency resulting
in estrus and
ovulation within 2-
3 days
Prostaglandins
Dinoprost- PGF2α Sub-estrum 5 mL, IM Inj Hormo P2α,

analogue BCAHP5mg/mL,
Luteal cyst
Potent luteolytic 5 mL vial;Inj
action by Timing and synchronization Lutalyse,
constriction of of estrus Novartis5mg/mL,
utero-ovarian 10 mL vial
vessels. It enhances
cervical dilation
and also has
selective
spasmogenic
action.
Luprostiol- Sub-estrus,Anoestrus, 15 mg, IM Inj Prosolvin,

PGF2α analogue Intervet.7.5mg/mL,2
Luteal cystPersistent mL, 10 mL,
It causes regression CL,Estrus synchronization
of CL followed by 20 mL vials
follicle growth,
estrus and
ovulation in sub-
estrus and
anoestrus.
Tiaprost- PGF2α Sub-estrus,Luteal cyst 3.5 mL, IV or Inj Iliren, Intervet

analogue
Estrus synchronization 5 mL SC/IM 0.196 mg/mL, 10

134
Luteolytic activity; mL vial
enhances cervical
dilation and has
selective
spasmogenic
action.
Estrogens Induction of estrus 1.5 mL on day1 Inj Progynon

and 1.5 mL after 3 Depot, Zydus
Natural steroidal Cadila,1 mL
estrogens- 3 mL amp,Inj Heatreg ,
estradiol, estrone, Induction of (di-ethyl stilboestrol
estriols. Low oral parturition,Pyometra,RFM 10 mg/mL),
activity, Potency is Novitech ,3 mL
enhanced adding ampoule
Ethinyl groups to
the molecules
Hydroxy Pre partum uterine/ vaginal 500 mg,alternate Inj Duraprogen,

Progesterone prolapse days for 3 times, Unichem
caproate IM
Inj Proluton
Progesterone acts Depot, German
Post partum prolapse 500 mg for 3
on the Remedies
days ; 500
endometrium mg/week for 3 Inj Uniprogestin
inhibiting
weeks, IM Depot, Foreva
myometrial activity
and thus quieting Prolapse due to pronounced 500 mg for 2
uterus Inj Vetaprogen,
heat days, repeat on 3rd Prima Vet care
day, IM
Inj P-Depot,
Habitual pronounced heat 500 mg at the Zydus AHL
beginning of
estrus, IM 250 mg/ mL,
2 mL ampoule
Miscellaneous drugs / products
Eazi Breed CIDR Post partum and suckling Inserted for 7 Eazi Breed CIDR,
anoestrus days; Saideep,
Cystic ovaries Inserted for 12 10,s

days
Silent estrus
Inserted for 10
Estrus synchronization days along with
estradiol benzoate
cap 10 mg or

134
insert for 7 days
and administer
PGF2α on 6th day
or at the time of
removal
*****

134
134
ANTIMICROBIAL THERAPY WITH MACROLIDES AND
LINCOSAMIDES
U.SUNILCHANDRA
Macrolides and lincosamides are antibacterials mainly employed in therapy of

respiratory infections and infections due to intracellular organisms and opportunistic
pathogens.
MACROLIDES:The macrolides (macrocyclic lactones)are bacteriostatic,(bactericidal at

high concentrations.) interfering with bacterial protein synthesis by reversibly binding to
the 50 S ribosomal subunit. In general, they have a spectrum similar to that of the
penicillins and are often used as penicillin substitutes for the treatment of streptococcal
and staphylococcal infections.In addition,they are active against Mycoplasmae,
Chlamydiae, Legionellae, Rickettsia spp. gram positive anaerobes etc.. They enter pleural,
ascitic fluids but not the CSF. The important agents are erythromycin, oleandomycin,
spiramycin, josamycin, tylosin, tilmicosin and newer ones: azithromycin,dirithromycin,
clarithromycin and roxithromycin The newer agents are effective in opportunistic
infections associated with toxoplasmosis, cryptosporidiosis etc, and also in the eradication
of H.pylori infection
Side Effects and Toxicity: Gastrointestinal disturbances: are the most common adverse
effect noticed. Vomiting, diarrhoea, anorexia, regurgitation and epigastric pain may be
observed .Horses are sensitive to macrolide-induced GI disturbances that can be serious
and even fatal. Some salts: Erythromycin estolate may be hepatotoxic and cause
cholestasis;
Hypersensitivity reactions occasionally been seen. Clinical signs include rashes, fever,
skin eruptions. Pain and swelling at the injection site . In pigs, tylosin may cause edema
of the rectal mucosa, mild anal protrusion with diarrhea, and anal erythema and pruritus.
Tylosin and Tilmicosin have a tendency to produce cardiac toxicity characterized by
tachycardia and decreased contractility. Tilmicosin is contraindicated in swine and
should not be used IV. Transcient auditory (hearing)impairments and super infections in
humans are the other unwanted side effects. They are contraindicated in patients
hypersensitive to them and should be used cautiously in patients with pre existing liver
dysfunction . Although they have not demonstrated teratogenic effect, they should be used
during pregnancy only when the benefits outweigh the risks.

134
Interactions: Macrolides should not be used with chloramphenicol or the lincosamides.
Activity of macrolides is depressed in acidic environments. Macrolide preparations for
parenteral administration are incompatible with many other pharmaceutical preparations.
Erythromycin and troleandomycin are microsomal enzyme inhibitors that depress the
metabolism of some drugs like warfarin, theophylline, carbamazepine and methyl
prednisolone. terfinadine, azole antifungals, cisapride
Erythromycin: The antimicrobial spectrum of is narrow, including mostly gram positive

organisms and a few gram negative organisms. It the drug of choice in corynebacterial
infections , respiratory , neonatal ocular inflammation, or genital chlamydial infections
In small animasl,pigs and poultry: used to treat pyoderma caused by staphylococci,

respiratory infection caused by Mycoplasma. The diarrhoea effect is self limiting, except
in adult horses it could be fatal. Rectal oedema and partial anal prolapse is seen in pigs.
Erythromycin is not recommended in adult horses (oral and systemic) and ruminants
(oral). Erythromycin estolate, can produce acute cholestatic hepatitis (fever, jaundice,
impaired liver function), probably as a hypersensitivity reaction.
Dose: Dogs and cats: 2-10mg/kg,PO,tid; cattle: 8-15mg/kg,IM,bid; Foals: 25mg/kg,PO or

IM, tid; Sheep and swine: 2-6mg/kg, IM,sid; Poultry: 25g/100litres drinking water.
Tilmicosin is used treatment of pneumonia in cattle, sheep and pigs, associated with
Pasteurella haemolytica, P. multocida, Actinobacillus pleuropneumoniae, mycoplasma
species Tilmicosin phosphate has been effective for treating: .bovine respiratory disease
(as effective or more effective than other established treatments: ceftiofur,
oxytetracycline, or florfenicol). Injections to horses, goats, swine, or nonhuman primates
can be fatal. heart ,the target of toxicity via depletion of cardiac intracellular calcium,
resulting negative inotropic efect. As a feed additive , it is effective for controling
pneumonia in swine. When injected in swine, tilmicosin has caused toxic reactions and
death due to cardiovascular reaction.
Dose: Cattle and sheep: 10mg/kg, SC, every 72 hours; Pigs: 200-400g/tonne feed
Tulathromycin is used in treatment of swine respiratory disease and bovine respiratory

disease,characterized by rapid absorption,high distribution and slow elimination. Dose:
cattle- 2.5 mg / kg body weight, SC,as a single dose.; Pig: 2.5 mg /kg,IM, single dose
Tylosin is therapeutically used to treat: swine dysentery, pleuropneumonia due to

Haemophilus parahemolyticus, colitis in dog, other infections in cats, chickens
Mycoplasma canis and Mycoplasma haemocanis infection in dog,cattle Tylosin is alos
used for growth promotion in pigs, cattle, and chickens.

134
Dose: Dogs: 40mg/kg,PO,tid; cats 4mg/kg,IM,sid; Cattle: 10-20mg/kg,IM,bid; Pig:
10mg/kg, IM, bid,25g/100litres drinking water,100g/tonne feed;Poultry: 10 mg/kg, IM,
sid-bid 7-10 mg/kg, PO, tid ; 50g/100litres drinking water
Clarithromycin possess broad spectrum bactericidal activity and post antibiotic effect
with very good activity against opportunistic infections in Toxoplasmosis,
Cryptosporidiosis; H.pylori in peptic ulcer. High concentration in the alveolar
macrophages, lung tissue and tonsillar tissue show high penetration of the drug into the
respiratory tract cells, a feature that enhances efficacy against typical and atypical
pathogens causing pneumonia It is more acid stable, more active against mycobacterium
avium complex with lower frequency of GI intolerance. Dose: Dogs and cats: 5-
10mg/kg,PO, bid
Azithromycin is slightly less active than erythromycin against staphylococci and

streptococci and slightly more active against Haemophilus influenzae.; good activity
against many intracellular organism. (Clamydia, Toxoplasma) , mycobacteria
,mycoplasma and Chlamydia; but not against enteric gram-negative bacteria or
Pseudomonas. The features: better oral absorption,better tolerance,longer half-life
,higher tissue concentration, broader spectrum of activity than erythromycin and lesser
drug interactions . Dose: Dogs : 5-10mg/kg,PO, sid ; cats: 5mg/kg.PO, once daily or
every alternate day. Roxithromycin is a longer acting and more stable than
erythromycin.Dose: Dogs : 15mg/kg,PO, sid
Tacrolimus is a macrolide ; is an immunosuppressive with similar mechanism of action

as another immunosuppressant, cyclosporine to inhibit T lymphocyte proliferation.. It has
topical anti inflammatory effects without the atrophogenic effects and metabolic effects
of topical GC. It is used topically for the treatment of atopic dermatitis,psoriasis ,
alopecia areata and effective in canine perianal fistula though at a lower rate than
systemic cyclosporine and localized lesions in diseases like discoid lupus erythematosus,
pemphigus erythematosus, pemphigus foliaceous.
LINCOSAMIDES: bacteriostatic/ bactericidal depending on the concentration/;

particularly active against grampositive,mycoplasma, and anaerobes(most aerobic gram-
negative bacteria are resistant). The agents are lincomycin and clindamycin. The
antimycoplasmal activity of the lincosamides(clindamycin > potent) is similar to that of
erythromycin but less than that of the other macrolides. Lincosamides, macrolides, and
chloramphenicol, although not structurally related, seem to act at this same site (50 S
subunit of bacterial ribosomes) and thus are antagonistic. Oral and IM absorption being
rapid (lincomycin- less well absorbed than clindamycin).They are widely distributed in
to respiratory tissue, soft tissue and, bones

134
In horses,rabbits, chinchillas, guinea pigs, neonates and hamsters: these are
contraindicated due to risk of gastrointestinal adverse effects like serious fatal
enterocolitis and diarrhoea. Ruminants exposed to oral lincomycin : anorexia, ketosis,
and severe diarrhoea.
Interactions: Additive neuromuscular effects with anesthetic agents and skeletal muscle
relaxants. Antidiarrheals,adsorbent (kaolin/astringent) significantly decrease absorption
oral lincosamides. Antiperistaltic agents, such as opiates, or loperamide /opioid receptor
agonist/ may prolong or worsen pseudomembranous colitis by delaying toxin elimination.
Indications: lincomycin HCl: respiratory tract, skin and soft tissue, dental infections,
osteomyelitis (cats, dogs) ; swine dysentery, joint infections (pig); necrotic enteritis
(chicken); clindamycin: severe anaerobic,respiratory infections . Dose: Lincomycin: 10
mg/kg, IM, bid- Cattle,pig,cats; 20 mg/kg, PO, sid- dog.; Clindamycin: 5-10 mg/kg, PO,
bid- Dogs, cats
*****

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CLINICAL ASPECTS OF CEPHALOSPORIN AND PENEM
GROUP OF ANTIBIOTICS
U.SUNILCHANDRA
Cephalosporins, penems (carbapenems), penicillins and monobactams are group

of antiobiotics classified under beta lactam antibiotics, sharing common chemical
properties and the bactericidal action of bacterial cell wall synthesis inhibition.
CEPHALOSPORINS: Cephalosporins are wide-spectrum β-lactum bactericidal

antibiotics exhibiting time-dependent efficacy as opposed to concentration-dependent
antibiotics (such as aminoglycoside and fluoroquinolones). Classified in to four
generations, based primarily on spectrum of antibacterial activity and resistance to β-
lactamases; the spectrum against gram negative organisms and the stability against β-
lactamase increase from first to fourth, along with same or reduced spectrum of activity
against gram positive organisms, except for 4th generation agents, which have enhanced
activity aginst gram positive pathogens.
First generartion: Oral: cephalexin, cefadroxil, cefadrine, cephradine, cephaloglycin;

Parenteral: cefazolin, cephapirin, cefalonium, cephalothin, cefacetrile, cefapirin,
cefatrizine, cephaloridine
They exhibit igh activity against gram positive bacteria including β-lactamase producing
S.aureus.Moderate activity against β-lactamase producing gram negative organisms.
Pharamcokinetic featurwes include Rapid absorption, high bioavailibility, unaffected by
the presence of food especially in monogastric animals; poor and highly erratic in
ruminants, thus being used only in preruminant calves. They show poor penetration
across physiological barriers (such as blood brain barrier)
Oral cephalexin, cefadroxil and parenteral cefazolin are the most commonly used ones,
primarily for skin and soft tissue infections such as pyoderma caused by streptococci and
Staph. aureus, and bacterial endocarditis caused by Streptococcus viridans and S .aureus.
Cephalexin used longterm (30days) in the treatment of chronic S.intermedius pyoderma,
is associated with increased resistane. Cefazolin is used to treat bone and joint infections
in the treatment of open fractures, lymphadenitis, abscesses, pharyngitis etc.
Second generartion: Oral:. Cefamandole, cefotiam, ceforanide, cefonicid, cefmetazole,

cefacetrile, cefotiam, cefranide, loracarbef, cefoxitin* cefotetan* (*-cephamycins);
Parenteral: cefaclor, cefuroxime axetil, cefprozil, cefuroxime

134
Their use is generally reserved for infections, resistant to first-generation cephalosporins.
They are less efficacious than 1st generation against gram-positive pathogens; primarily
against S. aureus and S. intermedius; show greater gram-negative spectrum of activity
against organisms such as H.influenze, Enterobacter aerogenes and Neisseria species.
They are relatively more resistant than first generation agents, to β-lactamases, with poor
penetration of the blood-brain barrier. Injections are painful, and may cause
thrombophlebitis when administered IV. The broad antibacterial activity may lead to
gastrointestinal disturbances and superinfection by resistant microorganisms including
yeasts
Cefoxitin and cefotetan (cephamycins): effective against gram negative anaerobes, are
used in aspiration pneumonia, bite infections, ruptured intestine gangrene, peritonitis and
pleuritis.
Third generartion: Oral:. cefsulodin, ceforanide, cefpodoxime proxetil, cefixime,
ceftibuten, cefdinir, cefmenoxime, cefditren pivoxil, cefodizime, cefetamet; Parenteral:
ceftiofur, cefotaxime, cefmenoxime, ceftriaxone, ceftizoxime, ceftazidime, cefovecin,
cefoperazone, latamoxef* (moxalactam) (* -cephamycin)
They exhibit high antibacterial activity; broader resistance to β-lactamases, though are
less effective than 1st and 2nd generation agents against gram positive bacteria. They are
most effective against antibiotic-resistant gram-negative aerobes effective against Proteus
vulgaris, Enterobacter species, Citrobacter species, Haemophilus species, Neisseria
species and Moraxella species. Moderate activity against Gram-positive bacteria and are
inferior in activity against Staphylococci. Ceftriaxone, ceftizoxime, cefotaxime and
ceftazidime, due to their ability to cross blood-brain barrier are effective in therapy for
bacterial meningitis. Cefpodoxime is part of a newer group of orally active
cephalosporins. that are absorbed in the form of a prodrug, cefpodoxime proxetil, which is
stable in presence of many beta-lactamase enzymes and has been used in skin infections
of dogs It also has activity including Moraxella spp,Haemophilus spp, and Klebsiella
spp. not active against most obligate anaerobes, Pseudomonas or enterococci.
Ceftazidime and Cefoperazone, are highly active against Pseudomonas aeruginosa
among all cephalosporins, compared to ceftriaxone and ceftizoxime, which also have
antipseudomonal activity to some extent. Cefoperazone is contraindicated in the
herbivore aspecies with an expanded bowel (horses). It has been used by intrmammary
route for treating coliform mastitis
Cefovecin is generally given as a single injection (SC), the effect lasting for up to14
days . It has about five days of elimination half life; used in dogs and cats to treat skin
and soft tissue infections; such as wounds, abscesses and pyoderma and urinary tract

134
infections. It should not be used in dogs,cats less than 8 weeks old, with severe renal
dysfunction,breeding animals ,pregnant and lactating dogs
Ceftiofur has broader activity against gram-positive and beta-lactamase–producing

strains as well as anaerobes. The injectable crystalline oil suspension formulation of
ceftiofur is administered subcutaneously in cattle, in the middle third of the posterior
aspect of the ear or in the posterior aspect of the ear where it attaches to the head ( base of
the ear), avoiding all the blood vessels. In swine, this is administered to the post auricular
region of the neck intramuscularly; the volume of injection at each site being a
maximum of 2ml. Ceftiofur is indicated for treatment of bronchopneumonia in cattle,
especially when caused by Pasteurella hemolytica or P.aeruginosa. Ceftiofur sodium
(50mg/ml powder vials for inj) and ceftiofur hydrochloride (50mg/ml sterile suspension)
are the formulations approved for use in dogs, horses, catlle,sheep, goats and swines.
Ceftiofur sodium: used intramammary for coliform mastitis as an extralabel use and
approved for treatment of urinary tract infections in dogs.
Fourth generartion: Oral:. Cefmetazole, cefditoren; Parenteral: cefepime,
cefpirome, cefquinome cefclidine, cefluprenam cefozopran
They have extended spectrum of activity than third, against both gram positive and gram
negative organisms ,greater stability against hydrolysis by beta lactamases. Generally,
they exhibit excellent penetration ability in to CSF. They are indicated in various
infections where resistance to β-lactum antibiotics is expected.Cefquinome, an extended
spectrum beta-lactam, is used for treating bovine respiratory disease and mastitis.
Pharmacokinetics: The absorption may be enhanced by formulatrion as prodrugs which
are metabolized to the active compound in the body. They distribute very well into most
of the body tissues and fluids. including bone, pleural fluid, pericardial fluid and synovial
fluid with poor penetration of blood-brain barrier, except some third-generation agents:
cefotaxime, ceftriaxone ceftizoxime and ceftazidime. They cross placenta with no
adverse teratogenic or fetotoxic effects, except a slight decrease in fetal weight( lab.
animals). Doses tobe adjusted in severe renal failure/insufficiency to guard against
accumulation and toxicity. Cefoperazone, cefamandole and ceftriaxone are eliminated
through bile into the feces; and are frequently used in patients with renal insufficiency
Adverse Effects: Gastrointestinal disturbances : Anorexia, vomiting and diarrhoea.
Hypersensitivity reaction : manifested as urticarial rashes, fever, eosinophilia,
angioedema and lymphadenopathy. ; avoided or used with caution in penicillin allergic
individuals. Bleeding disorders: cefotetan, ceftazidime,cefamandole and cefoperazone :
increased risk of bleeding due to a decrease in prothrombin activity and anti- vitamin K
effects. Critical illness, poor nutritional status, and presence of liver disease are risk

134
factors for hypoprothrombinemia and bleeding; as all cephalosporins can inhibit vitamin
K synthesis by suppressing gut flora. Prophylactic vitamin K therapy is recommended
when any of these medications is used for prolonged periods in malnourished or seriously
ill patients. Hepatic dysfunction: As cefotaxime, cephalothin, and cephapirin are majorly
hepatically metabolized before renal elimination, severe liver dysfunction can inhibit
their metabolism, indiating the dose to be reduced in these cases . Renal insufficiency :
Nephrotoxicity may occur in patients with renal insufficiency , receiving the full dosage
of cephalosporin; and thus dosage should be adjusted .Pain at the injection site:
Abscesses or other severe local tissue reactions (IM) and thrombophlebitis(IV) are
possible. Other adverse effects noticed in animals include anemia,(dogs:
ceftiofur);colic, diarrhoea, laminitis(horses: cefpodoxime proxetil,cefotaxime,cefazolin);
local ear swelling (cattle: ceftiofur).
Interactions : Food: Due to the adverse effects like diarrhoea and vomiting associasted
with most of the oral administered cephalosporins, , it may be desirable to administer
them along with food. Aminoglycosides: most of the other cephalosporins (except
cephalothin) demonstrate synergistic activity and are often combined in the treatment of
febrile illness in neutropenioc patients. Antacids and H2-receptor antagonists: decrease
the absorption of cephalosporins ; thus to be administered at two hours intervals.
Nephrotoxic medications: when used with other nephrotoxic medications, such as loop
diuretics, especially in patients with pre-existing renal function impairment Platelet
aggregation inhibitors: Hypoprothrombinemia and the gastrointestinal ulcerative or
hemorrhagic potential of NSAIDS increase risk of hemorrhage if used concurrently with
cephalosporins
CARBAPENEMS: Carbepenems are a new class of drugs which are structurally similar
to the penicillins. They currently have the widest activity of any antibiotics , being
highly active against a wide variety of gram positive and gram negative bacteria . The
agents are imipenem, faropenem,maropenem etc.
Imipenem is a broad-spectrum antibiotic with excellent activity against a variety of gram
positive and gram negative organism (both aerobic and anaerobic), by comparison to
third and fourth generation cepahalosporins.. The high activity of imipenem is attributed
to its stability against most of the β-lactamases and it's ability to penetrate porin channels
that usually exclude other drugs. The carbapenems are more rapidly bactericidal and less
likely to induce release of endotoxin in an animal from gram-negative sepsis.
Gastrointestinal disturbances: nausea and vomiting., seizures,hypersalivation and
vocalization indicating pain after IM amd SC administration in dogs was noticed.
Carbapenems are not absorbed after oral administration except a newer penem
faropenem. They are widely distributed to ECF throughout the body and reach

134
therapeutic concentration in most tissues Imipenem is rapidly hydrolyzed by the enzyme,
dihydropeptidase, which is found in the brush border of the proximal renal tubule. It is
always administered with cilastatin, (an inhibitor of dihydropeptidase) to decrease renal
tubular metabolism. The disadvantages of penems include induction of resistance and
high cost.
Dose: dogs and cats- 5-10mg/kg, IV or deep IM, q 8 h; horse : 10-20mg/kg, IV, q 6 h
Meropenem is as effective as cefotaxime or ceftriaxione in treatment of bacterial
meningitis It has lower incidence of adverse effects to the central nervous system, such as
seizures. The recommended empirical dose in dog is 2-5mg/kg, slow IV (with IV fluids)
, q 6 h; 5 -10mg/kg, deep IM q8 h or 8-12 mg/kg SC, q 8 -12 h. Individuals who are
allergic to the penicillins may demonstrate cross-reactivity with imipenem. Carbapenems
are synergistic with aminoglycosides against P.aeruginosa used for intra-abdominal
infections, severe lower respiratory tract infections, septicemia and life threatening soft
tissue infections
DOSAGES OF CEPHALOSPORINS
1. CATTLE SHEEP AND GOATS
Approved cephalosporin Dose (mg/ kg) Route Interval
(Hour)
Ceftiofur sodium 1.1-2.2 IM ,SC 24
Ceftiofur HCL, 50mg/ml 6.6 SC 24
Ceftiofur crystalline free acid suspension 15-20 IV,IM,SC 12
Cefazolin 10 IM
Cephapirin 200mg totaldose Intramamry 8
Cefoperazone 250mg total dose Intramamry 12
Cefuroxime 250mg total dose Intramamry Single dose
Cephacetrile 250 mg total dose Intramamry Single dose
Cephalothin 55 SC SD
Ceftriaxone 25-50 IM,IV 6
Cefadroxil 25 PO 24
Cephradine 7 PO 12
Cefetamet 10 PO 12
( calves) 20-40 IM 24
2. HORSES
Ceftiofur sodium 2.2-5.5 IM,IV 24
Cefotaxime 20-30 IM,IV 8
Cefadroxil 10-20 PO 8-12
Cefazolin 10-20 IV 6-8
Cephalexin 25-33 PO 6
Ceftriaxone 25-50 IM,IV 12-24
Cefamandole 10-30 IV,IM 4-8

134
Cefoperazone 30-50 IM.IV 6-8
Cefoxitin 20 IV,IM 8
Cephalothin 10-30 IM,IV 6
Cephapirin 20-30 IM,IV 8-12
Cefpodoxime 5-10 PO 8-12
Cefepime 2.2 IM 8
Cefpirome 11 IM 8
Ceftazidime 25-50 IV,IM 8-12
3. DOGS
Cefazolin 10-30 IV,IM,SC 6-8
Cefaclor 15-30 IV,IM, 6-8
Cefixime 5-10 PO 12-24
Cefoxitin 15-30 IM 8-12
Cefotetan 30 IV,IM,SC 6-8
Ceftazidime 25-50 IM,IV 8
Cefpodoxime 5-10 PO 8-12
Cephradine 15-30 PO 4-8
Cephalexin 10-25 PO 12
Cefadroxil 10-20 PO 8-12
Cefovecin 8 SC 14 Days
Cephaloglycin 10-20 IM,IV 6-8
Cephapirin 10-20 IM 6-8
Cefamandole 10-30 IM 8
Ceftriaxone 15-50 IM,IV 24
Cefoperazone 20 IM 6-8
Cefotaxime 20-40 IV,IM 8-12
Ceftiofur sodium 2.2 IM 24
Ceftizoxime 25-40 IV,IM 8-12
Cefuroxime 10-15 IV 8-12
Cefetamet 4-8 PO 12-24
4. CATS
Cephalexin 10-30 IV,IM, SC 6-8
Cefotaxime 20-40 IV,IM 8-12
Cefadroxil 10-20 PO 12
Ceftriaxone 15-50 IM, IV 24
5. PIGS
Ceftiofur(Free acid) 3-5 IM 24
6. POULTRY
Cephalexin 25-50 PO 8-12
Ceftiofur 1.3-2.6 IM 24
Cephalothin 100 IM 8-12
*****

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RECENT ADVANCES IN ECTOPARASITICIDAL THERAPY
VIJAY KUMAR.M
Ectoparasiticidals are formulated as Sprays, Dips, Pour-ons, Shampoos, Dusts or

powders, Foggers, Oral products, Spot-ons, Injectables, Granules, Jetting, Sponge on,
Collars etc. A brief introduction to the newer ectoparasiticidals for use in animls is
given in this article.
Insect growth regulators and insect development inhibitors: They represent a

relatively new category of insect control agents. They constitute a group of chemical
compounds that do not kill the target parasite directly, but interfere with growth and
development. They act mainly on immature parasite stages and are not usually suitable
for the rapid control of established adult parasite populations. Where parasites show a
clear seasonal pattern, insect growth regulators can be applied prior to any anticipated
challenge as a preventive measure. Examples: Cyromazine, pyriproxyfen, methoprene,
fluazuron, fenoxycarb, Lufenuron, Diflubenzuron, Novaluron, flufenoxuron.
Lufenuron interferes with polymerization and deposition of chitin, killing developing

larvae either within the egg or after hatching. It is administered PO to dogs (once
monthly at a dose of 10mg/kg ) or cats ( 30mg/kg ) or by injection to cats. Female fleas
feeding on treated animals are prevented from producing viable eggs or larvae. Suppress
the growth of adult fleas up to 32 days
Cyromazine, is effective against blowfly larvae on sheep and lambs and also against
other Diptera such as houseflies and mosquitos.
Methoprene is a terpenoid compound with very low mammalian toxicity that mimics a
juvenile insect hormone and is used as a feed-through larvicide for hornfly (
Haematobia ) control on cattle.
Fenoxycarb usually formulated in collar or spray with either pyrethroid (permethrin) or

OPC (chloropyrifos) as an adulticide
NEONICOTINOIDS : The nicotinoids are modeled after natural nicotine. Two

compounds in this category are currently available for veterinary use: imidacloprid and
nitenpyram .
Imidacloprid works by binding to postsynaptic nicotinic acetylcholine receptors in
insects. This inhibits cholinergic transmission, resulting in paralysis and death.

134
Imidacloprid is applied as a 10% spot-on topical product and is used primarily to control
fleas on both dogs and cats. It also has excellent activity against lice.
Nitenpyram is administered PO in pill form to kill fleas in both dogs and cats. It is
absorbed rapidly, with maximal blood concentrations reached within 1.2 hr and 0.6 hr in
dogs and cats, respectively. While imidacloprid is described as a paralytic, nitenpyram
produces hyperexcitability in fleas prior to death
PYRAZOLES: This group of compounds has broad-spectrum insecticidal and
acaricidal activity. The only member of this group currently available for use is
fipronil.
Fipronil : a broad-spectrum pesticide with activity against fleas, ticks, mites, and lice.
This is a long-acting poison for dogs and cats.. It kills adult fleas, cockroaches and ants. It
is the conventional barrier treatment for termites. Can be toxic to humans Fipronil is
absorbed and accumulates in the sebaceous glands, has very low solubility in water, and
has prolonged residual activity on both dogs and cats .It is also formulated as baits for
cockroaches, ants and termites. It is effective against insects resistant or tolerant to
pyrethroid, organophosphate and carbamate insecticides.
SPINOSYNS: Spinosad , the only agent must be ingested by the insect, therefore it has
little effect on sucking insects and non-target predatory insects. Spinosad works by
contact and by ingestion. Contact occurs either by direct application to the insect or by
movement of the insect onto a treated surface. Ingestion occurs as insects feed on treated
substrate (such as foliage). It is relatively fast acting. The insect dies within 1 to 2 days
after ingesting the active ingredient
The unique mode of action of spinosad, coupled with a high degree of activity on
targeted pests, low toxicity to non-target organisms (including many beneficial
arthropods) makes it an excellent new tool for integrated pest management. It should not
be used in puppies under age 14 weeks and in pregnant or nursing females. It is available
in chewable tablets (presently abroad only), given once a month to kill fleas in dogs only,
at a dose rate of 30-60mg/kg .
SEMICARBAZONE : Metaflumizone is a new small animal ectoparasitic compound,
with a different mechanism of action. It shows no incidence of resistance cross
resistance with other insecticides.It is rapidly distributed throughout the surface of the
body and do not work through a systemic effect, so there is minimal chance of any drug
interactions occuring. . Can be used in puppies from 8 weeks . Presently it is available as
a clear, yellow to amber spot-on solution, in combination with amitraz (Each ml contains
150 mg metaflumizone and 150 mg amitraz). It is contraindicated in puppies under 8
weeks of age., sick or debilitated dogs or dogs suffering from heat stress, pregnant and
lactating animals. The current available product(Not available in India, presently) is for
spot-on application only. Not to be administered orally or via any other route

134
*****

134
CONSIDERATIONS IN GLUCOCORTICOID THERAPY
U.SUNILCHANDRA
Glucocorticoids (GC) potentially affect every cell in the body and produce a wide
spectrum of effects depending on tissue concentration and cell type. GC act indirectly by
inducing lipocortin synthesis, which in turn inhibits phospholipase A2, the enzyme
responsible for cleaving arachadonic acid from damaged cell membranes. Therefore GC
inhibit both the lipoxygenase and cyclooxygenase pathways of inflammation, blocking
the formation the leukotrienes aswell as prostaglandins, prostacyclin and thromboxane.
Important Pharmacological effects.

1. Alteration of water and electrolyte balance: manifested by polyuria,polydipsia
2. Blood pressure increased, potentiate beta-adrenergic agonists actions
3. CNS effects : mood,behavioral changes, diminished response to pyrogens,
4. Decrease absorption of calcium and iron from GIT
5. Enhance lipolysis and mobilize fatty acids from adipose tissue; stimulates
hyperinsulinemia and results in lipogenesis, decrease in protein synthesis and an
increase in degradation,: muscle atrophy, thin skin, and delayed healing can result.
6. Inhibit osteoblasts and stimulate osteoclasts, thereby inhibiting bone healing;
reduce the proliferation connective tissue,slowing scar tissue production and
wound healing
7. Inhibit virus-induced interferon synthesis; diminish functional capacity of
monocytes, macrophages, and eosinophils through inhibition of interleukins
8. ACTH, beta-lipotropin, TSH, FSH, and growth hormone synthesis is suppressed.
9. Hypothalamo pituitary adrenal axis (HPAA) suppression: The suppression of the
inhibition of ACTH by the anterior pituitary gland, suppresses subsequent
stimulation of cortisol production depending on GC type, the dose, and duration
of therapy.; suppression lasting from one or two weeks to as long as several
months . Prevention of hypoadrenal crisis require gradual withdrawal of
medication. Animals at risk are generally considered to be those that were on
greater than physiological replacement dosing for more than 2 weeks,whose
treatment discontinued in the last 6 weeks, and that are under some form of
physiologic stress, such as surgery
Classification:
1. Short acting (duration of action < 12 hours) eg: cortisone, hydrocortisone (1 *)

134
2. Intermediate acting(duration of action: 12–36hours) eg: prednisone (4*)
prednisolone(4*),methylprednisolone(5*),isoflupredone(50*)and triamcinolone(5
*)
3. Long acting (duration of action > 48hours)eg: dexamethasone (30*),
betamethasone (30*),, paramethasone (120*), and flumethasone (120*)
* Antiinflammatory potency as determined by comparison to a cortisol a value of
1.0.
Injectable glucocorticoids: To treat shock, doses of GC are 50 to 100 times the
physiological level.; phosphate and succinate esters are used IV. .Eg:
Μethylprednisolone sodium succinate, Prednisolone sodium succinate,Dexamethasone
sodium phosphate
To suppress the immune system, doses are about 20 times the physiological level;
solutions of free steroid alcohols administered IVor IM; Egs include: Dexamethasone,
Flumethasone
To inhibit inflammation, doses are 10 times the physiological levels.Preparations are
acetate and acetonide esters; given IM,SC or intra-articular (into the joint). Absorption of
the drug into the systemic bloodstream occurs slowly, over days to weeks. Egs of long-
acting formulations include:methylprednisolone acetate, triamcinolone acetonide,
isoflupredone acetate, betamethasone dipropionate. Intra-articular GC should not be given
if infection is present, or if there is detectable structural damage or instability in the joint..
Surgery should not be performed on GC injected joints for two months following
injection
Oral corticosteroid formulations are well absorbed. Prednisone and prednisolone tablets
are the most commonly prescribed products and are frequently administered for long-
term therapy of adrenal gland insufficiency (hypoadrenocorticism) or immunemediated
diseases.
Duration of action (DOA) of steroid esters following IM administration is as follows.
1. Soluble short acting: sodium phosphate, sodium succinate;DOA is 30-120 minutes
2. Insoluble intermediate acting: acetate, undecanoate,phenyl propionate, pivalate:
DOA-2-14 days
3. Very insoluble long acting: acetonoide, adamantoate: DOA- several weeks
Topical corticosteroids : the potencywise classification of different topical GC:
Mild: e.g. hydrocortisone 0.5-1%, prednisolone, dexamethasone ; Moderate: e.g.
betamethasone valerate 0.02-0.05%, triamcinolone acetonide 0.02%, fluocinolone
acetonoide.;Potent: e.g. betamethasone dipropionate 0.05%,betamethasone valerate or
triamcinolone acetonide 0.1%, diflorasone diacetate ; Very potent: e.g. clobetasol
propionate, halobetasol propionate,, betamethasone dipropionate 0.05% in optimised
vehicle. Topical corticosteroids are used in ophthalmology to treat chronic superficial

134
keratitis Certain ophthalmic preparations combine antibiotics and a corticosteroid
(e.g.Neomycin-polymyxin B,bacitracin with hydrocortisone or dexamethasone) to treat
conjunctivitis. GC are also included in topical preparations (most of which contain
antibiotics) used to treat minor cuts, scratches, hot spots, or inflammation due to contact
dermatitis or allergies, ear infections or inflammations in which GC component helps
to decrease the itching.
Clinical Indications of GCs
1. Adrenocortical insufficiency (acute,chronic): acute adrenocortical insufficiency

(Addison’s disease).Hydrocortisone, methylprednisolone, prednisolone, and prednisone
produce minor mineralocorticoid effects in addition to their GC effects and may
adequately reverse electrolyte imbalances when administered in conjunction with IV
sodium chloride solution; however, methylprednisolone, prednisolone, and prednisone
are considered insufficient for long-term control of the potassium-retention or sodium
and chloride losing effects of most cases of primary adrenocortical insufficiency and a
mineralocorticoid-specific medication is generally indicated. In acute adrenocortical
insufficiency, a rapidly acting parenteral corticosteroid with the most mineralocorticoid
effect available should be administered in conjunction with vascular volume expansion
using isotonic saline. Relative mineralocorticoid effect from the most to the least
potency is hydrocortisone > prednisolone/prednisone > methylprednisolone >
dexamethasone
2. Allergic disorders: For anaphylactic reactions, corticosteroids play a secondary role

to epinephrine and fluid therapy.Dexamethasone injection, methylprednisolone acetate
injectable suspension,methylprednisolone tablets prednisolone sodium succinate,
triamcinolone acetonide injectable suspension and triamcinolone tablets are indicated in
the treatment of allergic conditions such as bee stings, drug allergy, pruritic
dermattoses and allergic lung (rhinitis, astma) and GI diseases. In acute case of
atopic/flea allergy dermatitis an initial anti-inflammatory dosages alleviate pruritus and
self trauma from scratching.. If continued, the lowest dose necessary or, if possible,
alternate day therapy with either prednisolone, prednisone, methylprednisolone, or
triamcinolone should be instituted. Repeated injections of acetate or acetonide
repository injections are not recommended for control of chronic skin disease because
of the risk of iatrogenic hyperadrenocorticism. Topical forms are commonly used for
allergic conditions like eczema, psoriasis, pemphigus
3. Ocular and Aural Inflammtion(otitis externa) : Topical steroids -for conditions of the
anterior chamber; systemic steroids for posterior chamber. Contraindicated in viral
infections, fulminant bacterial infections, fungal infections, injuries (ulcers) and
glaucoma.

134
4. Musculoskeletal Inflammation,: several musculoskeletal disorders including
osteoarthritis, bursitis, tendonitis, immune mediated rheumatoid arthritis, myositis;
should be used in conjunction with therapies that target the underlying cause
5. Adjunct therapy of cardiogenic and hemorrhagic shock: The primary treatment of

shock is the administration of large volumes of crystalloid solutions. High doses of GC
may aid in reversing some of the effects when administered in conjunction with IV
fluids. Dexamethasone sodium phosphate and prednisolone sodium succinate are
recommended Short-acting soluble steroids such as the succinate esters are routinely
used in the treatment of circulatory shock. When given IV in the early stages of shock,
GC and aggressive fluid therapy may improve hemodynamics and survival rates. The
use of GC in the treatment of septic shock (endotoxaemia) is controversial and the
primary treatment includes antimicrobial therapy and supportive parenteral fluid
therapy . High doses of a rapidly-acting GC, preferably of short duration, given in
conjunction with fluid and electrolyte therapy within a short period of time, possibly
less than 1 hour, after the onset of sepsis.
6. As immunosuppressive in immune mediated haematopoietic and skin diseases:

immune-mediated:hemolytic anemia,thrombocytopenia,neutropenia(Dexamethasone,
prednisolone, and prednisone) skin diseases like Systemic lupus erythematus,
pemphigus complexus and myasthenia gravis of dogs and cats that do not respond well
to anticholinesterase treatment, should initially be given GC at anti-inflammatory dose,
which may be increased to immunosuppressive levels over a 1-2 week period.
7. GIT diseases: Ulcerative colitis,inflammatory bowel disease, nonsuppurative

cholangitis,felinegingivitis, stomatitis- oral therapy with hydrocortisone/prednisolone
8. Respiratory conditions: in acute respiratory distress syndrome in cattle, chronic

obstructive pulmonary disease in horses, feline asthma syndrome, aspiration
pneumonia, pulmonary oedema from drowning, inhalation injury etc
9. In Organ transplantation: combined with other immunosuppressants(cyclosporine),

prednisolone/ methylprednisolone are preferred as they have an intermediate duration
of action,easily tapered or converted to alternate day regimens
10. Malignancies/Neoplasia: As a component of most combination regimens for

malignancies, in acute lymphocytic leukaemias, CNS tumors, lymphosarcoma, mast
cell tumor, multiple myeloma. Anti-inflammatory doses of GC provide the basis for the
palliative management of brain and spinal cord neoplasmsThey result in resolution of
signs; with a direct effect in reducing the size of some CNS tumors (e.g., lymphoma).

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11. Termination of pregnancy/ Induction of abortion: Dexamethasone injection generally
administered after the 100th to 150th day of gestation, in conjuction with
prostaglandins. Mummification, retained placentas, metritis or dystocia are the
possible complications
12. Induction of Parturition : Dexamethasone,betamethasone and flumethasone have been

used; generally in conjunction with a prostaglandin.Retained placentas are a common
sequale .Parturition may be induced in the last few weeks of gestation involves much
less risk to the fetus than earlier termination of pregnancy.Administration of GC more
than 1 month before expected gestation often leads to poor neonatal survival.
13. Cerebral oedema/ Hydrocepahlus due to CNS neoplasms/parasites, sarcoidosis,

spinal cord injury due to acute trauma : Considerable controversy exists concerning
the most appropriate management methods for acute spinal cord injury and cerebral
oedema as the functional outcome following spinal cord injury may be influenced by
management of systemic blood pressure and by use of methylprednisolone sodium
succinate administered within 8 hours of an acute spinalcord injury.
14. Infectious CNS disease: GC may contraindicated in infectious diseases affecting the
nervous system, but anti-inflammatory doses of corticosteroids have been
recommended for short periods at low doses when neurological signs are severe.
15. Intervertebral disc disease.:Dexamethasone and flumethasone injection;

Methylprednisolone, prednisolone, or prednisone, administered at an anti-inflammatory
dosage, are indicated as supportive therapy in intervertebral disk disease (Hansen
type:1;disk syndrome).However, acute paralysis due to intervertebral disk disease is an
emergency usually requiring surgery and/or higher anti-inflammatory dosages of GCs.
16. Ketosis in Cattle: Dexamethasone,flumethasone,isoflupredone acetate and

prednisolone acetate injectable suspension are likely to be more effective when
administered with IV glucose solutions.For secondary bovine ketosis, other therapies
for underlying disease, including local and systemic antibacterials to treat primary
bacterial infections is followed..A significant decrease in milk production is expected
in lactating cattle.
17. Mastitis: Dexamethasone is used as adjunctive therapy in the treatment of selected

cases of acute coliform mastitis to relieve some of the systemic signs (due to
endotoxin) and mammary gland inflammation. Itshould be administered in conjunction
with primary treatments, such as IV fluids, antimicrobials

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18. Other less common uses: The use of GC for snakebite may be inappropriate as it
may mask signs while not improving outcome. Though sometimes used for
stimulation of appetite especially in cats, debilitated animals do not show an increase
in appetite and other medications, such as cyproheptadine or a benzodiazepine, are
more accepted choices
Side effects : of GC are mainly due to two types: from abrupt withdrawal or after
chronic therapeutic use of high doses. The longterm use of supraphysiologic doses to
control inflammatory or immunologic disorders. may lead to iatrogenic Cushing’s
syndrome, characterized by polyuria, polydipsia, bilaterally symmetric alopecia, increased
susceptibility to infection, peripheral myopathy and muscle atrophy, and redistribution of
body fat. Longterm suppression of HPAA may cause adrenal gland atrophy and resultant
iatrogenic secondary hypoadrenocorticism (acute adrenal insufficiency/ Addisons
disease). characterized by lethargy, weakness, vomiting, and diarrhea particularly in dogs
and horses.
The other adverse effects: flare up of underlying diseses, fluid and electrolyte
disturbances (negative nitrogen balance, potassium loss, sodium retention, and fluid
retention), inhibition of bone growth, collagen synthesis ,decreased growth rate, delayed
wound healing, gastrointestinal irritation/ulceration/perforation. hematopoietic
changes;weight gain or weight loss, precipitation of diabetes mellitus, increased
susceptibility to infections,immune response suppression,osteoporosis, myopathy,
cataracts etc. The side effects of longterm (>2 wk) therapy can be diminished using an
alternate-day treatment regimen.
Contraindications: GC are contraindicated in : infectious diseases , GIT/ peptic and
corneal ulcers, diabtes mellitus, demodicosis, osteoporosis, epilepsy, CHF, renal failure,
late pregnancy ,recent major surgery , hypertension, ulcerative colitis and pancreatitis
Principles of GC therapy
7. GC are usually administered at the lowest dose known to be effective or the smallest
dose that achieves the desired effect in order to limit adverse side effects.
8. Drugs with primarily GC activity and minimal dose to achieve the desired effect is
chosen. Topical or local therapy is preferred whenever possible
9. Once-daily dosing is usually preferred Large steroid doses are administered in
divided doses to reduce local GIT effects.
10. Animal should not have been vaccinated several weeks before/ after GC therapy
11. In order to mimic the normal diurnal cycle and reduce the risk of adrenal
suppression, GC should be given in morning between 6–10AM
12. Alternate day therapy: every other day treatments are used to maintain remission
without side effects of daily or twice daily administration such as HPAA suppression.

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13. Pulse therapy: parenteral administration of supra pharmacological doses of short
acting steroids for shorter periods of time
14. Short term therapy: ( <2weeks) : short acting steroids, administered in divided doses
,bid, till the condition is controlled (4-7days) and discontinuing therapy once the
condition is controlled
15. Long term therapy: Starting as above for 2 weeks, then bringing the dosage to the
lowest possible single dose per day or doubling the dose and give every other day.
Giving adjunctive therapy like antihistaminics,to keep steroid dose as low as possible.
16. Tapering the dose and gradually withdrawing before stopping therapy in order to
avoid iatrogenic hypoadrenocortisism.
17. The antiinflammtory effect is palliative, routine use in inflammations should be
avoided.
18. Short/Intermediate acting GC : more flexible dosing schedules, potent GC effects,
lesser suppression of HPAA and less GIT irritation.
Dosages of commonly used GCs: Hydrocortisone: for adrencocortical insufficiency-
dogs: 0.5mg/kg.PO.bid; for adjunctive therapy of shock- dogs and cats: 50mg/kg,IVq3-
6h; for antiinflammtory activity-dogs and cats: 5mg/kg,PO,bid, IV,IM(sid); for
adjunctive in photosensitization-cats: 100-600mg(total) in 1 iL 10% dextrose saline,IV.
Cortisone: Dogs and cats: 1mg/kg.PO,IM,sid. Prednisolone: for chronic/subacute
adrencocortical insufficiency- dogs: 0.2-0.4mg/kg.PO.sid; for acute adrencocortical
insufficiency- dogs: 4-20mg/kg.IVq6h; for adjunctive therapy of shock- dogs and cats: 5-
10mg/kg,IVq3-6h; for antiinflammtory activity-dogs and cats: 0.5-2mg/kg,PO,sid,IM; for
dermatological /immune mediated disorders- dogs: 1-2mg/kg,PO,bid for 7-10 days,-cats:
2-4mg/kg,PO, q48h 100-600mg(total) in 1 iL 10% dextrose saline,IV.
Methyl prednisolone: for anti inflammtory action -dogs and cats: 0.25-1mg/kg,PO;
Methyl prednisolone acetate(depot preparation)-dogs: 1mg/kg,SC,IM,cats-2-
5mg/kg,SC,IM for CNS trauma, spinal cord injury: dogs: 30mg/kgIV
Triamcinolone: for various GC effects: dogs, cats: 0.11-0.22mg/kg,PO,sid; cattle: 0.02-
0.04mg/kg,IM; horse-0.1-0.2mg/kg,IM
Dexamethasone: for adjunctive therapy of shock- dogs and cats: 4-6mg/kg,IVq3-6h;
for antiinflammtory activity-dogs and cats: 0.05-0.125mg/kg,PO,sid,IM; cattle- 0.06-
0.1mg/kg,IM.sid; swine-1-10mg(total) IM,IV; for induction of parturition- cattle: 20-
30mg(total),IM single dose; sheep-8-16mg(total); ; for termination of pregnancy- cattle:
25mg(total),IM,slow IV.; for bovine ketosis: 5-20mg(total)
Betamethasone: for antiinflammtory aciony-dogs and cats: 0.025mg/kg,PO,sid, all
species-0.04-0.08mg/kg,IM,IV; for induction of parturition- cattle: 20-30mg(total),IM
single dose; for bovine ketosis: 0.04-0.08mg/ kg,IM,IV

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*****

134
CONSIDERATIONS IN SELECTION OF ANTISEPTICS AND
DISINFECTANTS FOR HOSPITAL SITUATIONS
U. SUNILCHANDRA
Antiseptics are used for the surgical sites, surgeon’s hands, traumatic wounds; as
antiseptics in soaps, teat dips and dairy sanitizers etc.. The agents are also used to
disinfect surgical instruments, apparel, hospital premises. home and farm premises, food
processing facilities, water treatment, and in public health sanitation, and, etc. The same
compound may act as an antiseptic or as a disinfectant, depending on the drug
concentration, conditions of exposure, usage and number of organisms etc.
Three factors are to be considered before selecting a particular

agent(antiseptic/disinfectant) for a given application: the type of microorganism the agent
has to eliminate(bacteria, virus, fungi or vegetative or spore forms), the environment in
which the agent will be used (living tissue/inanimate, presence or absence of dirt/debris)
and the characteristics of the agent(corrosiveness, cost and antimicrobial spectrum).
Alcohols: Ethyl alcohol (70% ethanol) and isopropyl alcohol (50% isopropanol) are used.
Isopropanol is slightly more potent than ethanol, used as a skin disinfectant and
rubefacient. Alcohol-based hand rinses have rapid-acting antiseptic effects,wide
germicidal activity,non corrosive, but-fire hazardous risk and limited residual activity
due to evaporation ; limited activity in the presence of organic matter and not effective
against bacterial or fungal spores
Acids and Alkalies: Strong mineral acids (HCl, H2SO4, etc) in concentrations of 0.1-1 N
used as disinfectants; corrosive action limits their usefulness. Acids are used as food
preservatives (eg, benzoic acid), antiseptics (eg, boric acid, acetic acid), fungicides (eg,
salicyclic acid, benzoic acid),. Acetic acid, 1%, used in surgical dressings and 0.25%
acetic acid is a useful antibacterial agent for irrigation of the urinary tract. At 5%, it is
bactericidal to many bacteria and has been used to treat otitis externa produced by
Pseudomonas, Candida, Malassezia, or Aspergillus spp. Hydroxides of sodium and
calcium used as disinfectants, their caustic property usually limits their application on
tissues. A 2% solution of soda lye (contains 94% sodium hydroxide in hot water) used is a
potent caustic . Calcium oxide, ie, lime (hydrated/ air-slaked lime) soaked in water is
used to disinfect premises.

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Chlorhexidine: has potent activity against gram-positive, some gram-negative bacteria
but not against spores; activity is enhanced by alcohols, quaternary ammonium
compounds, and alkaline pH, and is depressed by high concentrations of organic matter
(pus, blood, etc), hard water, and contact with cork. It is incompatible with anionic
compounds, including soap.. A 4% emulsion of chlorhexidine gluconate is used as a skin
cleanser, a 0.5% (w/v) solution in 70% isopropanol as a general antiseptic, and a 0.5%
solution in 70% isopropanol with emollients as a hand rinse. Chlorhexidine-alcohol
mixtures are particularly effective in that they combine the antiseptic rapidity of alcohol
with the persistence of chlorhexidine. Because of low potential for systemic or dermal
toxicity, chlorhexidine has been incorporated into shampoos, ointments, skin and wound
cleansers, teat dips etc
Hydrogen peroxide: (3%). The effervescent action (liberates oxygen when in contact
with catalase present on wound surfaces) helps to remove pus and cellular debris from
wounds; used for cleaning and deodorizing infected tissue. However, the antimicrobial
action is of short duration and is limited to the superficial layer of the applied surface
because there is no penetration of the tissue. Benzoyl peroxide can cause skin irritation;
has keratolytic and antiseborrheic activity, which makes it useful in treating pyoderma in
dogs
Potassium permanganate is an effective algicide (0.01%) and virucide (1%) for

disinfection, but concentrations >1:10,000 tend to irritate tissues. Staining of tissues is
disadvantage. Chocolate brown coloured old solutions indicate the loss of activity.
Iodine: Elemental iodine is a potent germicide with a wide spectrum of activity and low
toxicity to tissues. It is poorly soluble in water but readily dissolves in ethanol, which
enhances its antibacterial activity. Used as Tincture iodine (strong/weak). It has wide
germicidal activity including fungi and bacterial spores, characteristic odor and is
corrosive and has limited activity in the presence off organic matter
Iodophores (eg, povidone-iodine) slowly release iodine as an antimicrobial agent; do not

sting, stain; are nontoxic to tissues but may be corrosive to metals. They are effective
against bacteria, viruses, and fungi but less so against spores. They retain good
antibacterial activity even in the presence of organic matter, and often change color when
the activity is lost. Phosphoric acid is often mixed with iodophores to maintain an acidic
medium. They are used in teat dips, dairy sanitizers and for various dermal and mucosal
infections
Chlorine exerts a potent germicidal effect against most bacteria, viruses, protozoa, and
fungi (0.1 ppm), but much higher concentrations are required in the presence of organic

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matter.. It has a strong acid smell, is irritant to the skin and mucous membranes. It is used
to disinfect water supplies, inanimate objects (eg, utensils, bottles, pipelines) in dairies.
Inorganic chlorides include sodium hypochlorite (Dakin's solution) solutions (bleach) and
calcium hypochlorite. Chlorinated lime (bleaching powder): mixture of calcium
hypochlorite and calcium chloride; used for disinfection of water, livestock premises,
destruction and disposal of carcasses and elimination of pathogens from organic matter.
Phenol (carbolic acid) is bacteriostatic at 0.1-1%;s bactericidal/fungicidal at 1-2%. The

bactericidal activity is enhanced by warm temperatures and decreased by alkaline
medium, lipids, soaps, and cold temperatures; 5% solution is strongly irritating, corrosive
to tissues. Oral ingestion/ excess application to skin can cause systemic toxicity. Cresol:
2% solution of either pure or saponated cresol (Lysol) in hot water is a disinfectant for
inanimate objects
Formaldehyde: 1-10% solution of formaldehyde is commonly used as a disinfectant.

Glutaral (glutaraldehyde), a 1-2% alkaline solution (pH 7.5-8.5) in 70% isopropanol, is a
more potent germicide than 4% formaldehyde. is used to sterilize surgical and endoscopic
instruments and plastic and rubber apparatus.
Soaps are dipolar anionic detergents which emulsify lipoidal secretions of the skin and
remove, along with most of the accompanying dirt, desquamated epithelium and bacteria,
which are then rinsed away with the lather. The antibacterial potency of soaps is often
enhanced by inclusion of certain antiseptics, eg, hexachlorophene, phenols, carbanilides,
or potassium iodide. They are incompatible with cationic surfactants
Cationic detergents are quaternary ammonium compounds (eg, benzalkonium chloride,

benzathonium chloride, cetylpyridinium chloride, cetyl pyridinium bromide/cetrimide)
whose activity is reduced by porous or fibrous materials (eg, fabrics, cellulose sponges)
that adsorb them and are inactivated by anionic substances (eg, soaps, proteins, fatty
acids, phosphates). ; are of limited value in presence of blood and tissue debris. They are
effective against most bacteria, some fungi, protozoa but not against viruses and spores.
Aqueous solutions of 1:1,000 to 1:5,000 have good antimicrobial activity, especially at
slightly alkaline pH. When applied to skin, they may form a film under which
microorganisms can survive, which limits their reliability as antiseptics. Concentrations
>1% are injurious to mucous membranes
Chloroxylenols (Parachlorometaxylenol and dichlorometaxylenol) are broad-spectrum

with more activity against gram-positive than gram-negative bacteria.; Active in alkaline
pH; however, contact with organic matter diminishes their activity. 5% chloroxylenol
solution (in α-terpineol, soap, alcohol, and water) is diluted with water (1:4) for skin

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sterilization and (1:25 to 1:50) for wound cleansing and irrigation of the uterus and
vagina.
Preferred antiseptics i) with antifungal activity: phenols, chlorhexidine, iodine,

povidoneiodine, hypochlorite, cetrimide
;ii)with antviralactivity:isopropanol,ethanol,formaldehyde,glutaraldehyde,sodium
hyopochlorite,phenol,potassiumpermanganate,hydrogen peroxide, iodophors.
Recommended antiseptics/disinfectants for hospital conditions and instruments: All

the instruments have to be immersed for 30 mins and rinsed and autoclaved.
1. 2% sodium hypochlorite: for gloves, syrienges, needles , blood spills on floor, floor
washing. lab glasswares
2. 2% benzalkonium chloride: foreceps, thermometer
3. 2% glutaraldehyde: Instruments-catheters, laryngoscope, endotracheal tubes
4. 6% hydrogen peroxide: removal of blood clots from tubes,catheters, dressing wounds
5. Benzalkonium chloride: hand wash, foreceps, catheters , instruments
6. Phenol: disinfecting toilets
7. Povidone iodine: surgical scrub, painting skin, dressing, hand wash
8. Ethyl alcohol: antiseptic at injection site, furniture disinfection
Relative efficacy of classes of antiseptics and disinfectants.
Classs of antiseptics/disinfectants
Type of activity Alcohol Iodine, Chlorine Chlorhexid Quaternary Glutarl

Iodophors ine ammonium dehyde
compounds
Bactericidal ++ +++ ++ +++ ++ +++
Lipid enveloped ++ ++ +++ +++ + +++

Virucidal
Nonenveloped - + +++ + - ++
virucidal
Sporicidal - + + - - ++
Effec in soap ++ +++ ++ + - ++
Effecive in hard +* ++ ++ + - ++
water
Effecive organic - - - +++ - ++

material

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*- not to be diluted in water
*****

134
134
CLINICAL PHARMACOLOGY OF MISCELLANEOUS CLASS OF
ANTIBACTERIALS
V.C.MEERA
The following is a brief description of various miscellaneous class of

antibacterials
Polymyxins : Two members- .Colistin (Polymyxin E)(Available as sulphates for oral and
topical use) and Polymyxin B. The spectrum is gram negative bactericidal. They are
commonly used topically due to their systemic toxicity(nephrotoxic, neurotoxic,
neuromuscular blocking effects) . They are synergestic t with sulfonamide and
trimethoprim against variety of enterobacteriaceae.colistin is synergestic with rifampin
(In vivo) against multidrug resistant P.aeruginosa and is employed in coliform mastitis.
Vancomycin-: The spectrum is gram positive aerobic cocci and bacilli bactericidal. It is
used against staphylococcal bone and soft tissue.infections in in dog.Dogs-3 mg/kg PO,
2 to3 times daily & 10-20 mg/kg IV , 3 to 4 times daily. Ototoxicity and nephrotoxicity,
and thrombophlebitis are the adverse effects. Its administration along with
aminoglcosides should be avoided as it may potentiate the toxicity of aminoglycosides.
Spectinimycin: is an aminicyclitol antibiotic, bacteristatic against many gram nagative

bacteria, mycoplasmas.. It is used in dog cat, horse pigs for the treatment of enteric &
respiratory infections.. Dogs & cats- 5-10 mg/kg IM, 2 times daily.; Cattle- 8-12 mg/kg
IM, 3 times daily; Calves- 20-30 mg/kg IM, once times daily.; Horses- 20 mg/kg IM, 3
times daily.; Pigs-10 mg/kg PO, 2 times daily.No significant adverse effects have been
obseveved (by parenteral route). On high doses may produce neuromuscular blockade.
Concurrent use along with tetracyclines or chloramphenicol may produce antagonistic
effect.
Rifampicin: is a semisynthetic bactericidal for both intracellular & extracellular

organisms. High activity against gram positive bacteia & mycobacteria also against some
gram negative organisms like Brucella, shows activity against yeast & fungal
microorganisms when combined with amphoterecin B.It is used for treating Rhodococcus
equi and other bacterial infections in Foals- 5 mg/kg PO, 2 times daily (in combination
with erythromycin 25 mg/kg, PO, 3 times daily.; Dogs & Cats - 5 mg/kg PO, 1- 2 times
daily.; For CNS fungal infections; Dogs & Cats-10-20 mg/kg PO, 3 times daily in
combination with amphotericin B & flucytocine. Hepatotoxicity in animals with pre-

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exsiting liver diseases. In horse ( IV ) CNS depression, sweating, heamolysis anorexia. In
few cases partial immunosuppression of lymphocytes. GIT disturbances – nausea,
vomition, anorexia, abdominal cramps, diarrhea & hypersensitivity reactions are the
avderse ffects. As a potent inducer of hepatic microsomal enzymes it may enhances
elimination half life of several drugS viz. digitalis, coticosteroides etc.Synegestic effect
with amphotericin B against some fungi.
Furazolidone is bacteriostatic , broad spectrum activity ( both gram positive & negative
organisms).Also active against giardia toxoplasmas. Coccidia & histomonas. It is used
for enteric infectios: Dogs – 2.2 mg/kg PO, 3 times daily for 7 days.; Cats- 4 mg/kg PO,
2 times daily for 7-10 days.; Horses- 4 mg/kg PO, 3times daily; GIT disturbances –
inappetence, nausea, vomition, anorexia, abdominal cramps, diarrhea. And CNS effects-
tremors, ataxia, convulsions, visual impirement. May be seen
Fusidic acid (Sodium fusidate) : is bacteriostatic effective only on gram-positive

bacteria such as Staph. and Corynebacterium. It is used topically for minor local skin
infections, wounds. It should not be used with quinolones, with which they are
antagonistic
Methanamine (Hexamine) : a urinary antiseptic have antibacterial activity is due to

release of formaldehyde in water. It is bacteriostatic agent but becomes cidal in acidic
urine. Active against both gram positive & negative organisms.Methamine mandalate -
Dogs – 10-20 mg/kg PO, 1-2 times daily.GI disturbances (nausea, vomiting & diarrhea),
gastritis, painful & frequent micturation, albinuria, hamaturia, cystitis, CNS symptoms
produced occasionally.Use of urinary alkanizing drugs e.g. Na bicarbonate, carbonic
anhydrase inhibitors may antagonise its action.Sulphonamides combine chemically with
hexamine in urine leads to antagonism.Concurrent use of urinary acidifires such as
ascorbic acid, methionine enhances its action.
Tiamulin: Is a semi-synthetic derivative of pleuromutilin. It is typically available for oral

use as the tiamulin base or the hydrogen fumarate salt. Tiamuli nHCl as injectable.. It
is bacteriostatic against gram positive pathogens including Mycoplasma spp.,
Spirochaetes (e.g. Treponema) and obligate anaerobes. It is useed for enteric pneumonia
complex-Pigs-15 mg/kg IM, once daily for 3 days & 8.8 mg/kg PO, 3-5days
In chickens and turkeys-reductions in water intake. Rarely, redness of the skin, primarily
over the ham, may occur in which case it is recommended that medication is discontinued
and the affected animals moved to clean pens. In oral overdose tiamulin may cause
transient salivation, vomiting and CNS depressions (calming effect), in which case the
drug should be removed and affected animals should be treated symptomatically and

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supportively if necessary. Tiamulin should not be administered to animals having access
to feeds containing polyether ionophore antibiotics (monensin, lasalocid, narasin,
salinomycin, and maduramycin) as adverse reactions may occur. Concomitant use with
other drugs that bind to the 50S ribosomal sub-unit (e.g. lincomycin, erythromycin, and
tylosin) may lead to decreased efficacy as a result of competition at the active site.
Virginiamycin:is bactericidal against a wide range of organisms including staphylococci,

streptococci and enterococci. It is commonly used as feed additive Overdose may result
in gastric disturbances, dyspnea, emesis, tremor and ataxia.
Novobiocin: Spectrum mainly gram positive; Most gram negative resistant; but some
Haemophilus sp., Neisseria sp., and Proteus sp. may be susceptible.Dogs: 10 mg/kg q8h
PO; Cattle:For treatment of mastitis in dry cows:Infuse contents of one syringe into each
quarter at the time of drying off; not later than 30 days prior to calving. For treatment of
mastitis in lactating cows-using the penicillin/novobiocinproduct. Fever, GI
disturbances , rashes and blood dyscrasias after systemic use. It acts similarly to
probenecid by blocking the tubular transport of drugs. thus the elimination rates of drugs
excreted in this manner (e.g., penicillins, cephalosporins) could be decreased and half-
lives prolonged.
Mupirocin: gram positive bactericidal spectrum; is used topically for staphylococcal and
streptocococcal skin infections, wounds, burns etc
*****

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HANDLING OF VETEROLEGAL POISONING CASES
M.VIJAY KUMAR
Generally every veterinarian is encountered with two types of cases in

poisoning of farm animals. Accidental and Malicious poisoning. The necropsy of the
animals and the rapid diagnosis is helpful in the treatment of other affected animals in
case of accidental poisoning. In case of malicious poisoning, which may turn up into
medico legal case, the identification of poison is a must to establish the cause of death. In
all poisonous cases, chemical analysis of the biological specimens is essential to know the
cause of death or illness. Therefore, every veterinarian should know the salient points in
collection and despatch of toxicological specimens to a laboratory.
History of the case is of great importance in the diagnosis of poisoning. This

includes the number of animals in the farm, number of affected, method of feeding,
regularity of feeding, recent changes in the rations or attendants, whether pastures have
been sprayed with pesticides or fertilizers, if rodenticides have been used and remnants of
the bait removed and disposed properly, storage of poisonous substances etc. Inspection
of the surroundings for empty pesticides or paint containers that are not really empty,
presence of poisonous plants in the farm environment. Also, the possibility of industrial
effluents coming in contact with grazing/watering sources should be given thought of.
POST MORTEM: Necropsy by routine procedure is to be performed as soon as possible

after the death of animal. Examine the animal externally and note incisions (for sui
poisoning, snake bite etc.,) on the skin or mucous membranes. Examine the oral cavity for
corrosive lesions (acids/alkali) or changes in colour of mucous membrane (nitrate, co,
cyanide poisoning). As most of the toxins gain entry through gut, examination of gut
mucosa, the contents, their smell, colour and pH (acids, alkali, urea) is a valuable guide in
diagnosing toxicoses. Poisoning by salts of heavy metals results in significant post
mortem lesions but poisoning by alkaloids like strychnine produces very feeble lesions.
The natural orifices, sub-cutaneous fat tissue, muscles, bones and teeth (in fluorine
poisoning), body cavities, and internal organs should be examined. The stomach should
be punctured rather than cut open for organoleptic examination to note the character of
smell. Puncture ensures greater accuracy and a longer time smell. Some of the poisons
which emit characteristic smell are: bitter almond -hydrogen cyanide poisoning, garlic

134
odour - phosphorus poisoning, rotten garlic or horse radish smell - selenium, tobacco
odour –nicotine, acetylene odour - zinc phosphide and ammoniacal odour- urea.
Check the pH of the stomach contents by pH paper. Any variation in the normal
pH of the sps. being examined indicates abnormality. (In urea poisoning-alkaline pH is
observed in rumen liquor due to release of ammonia).
The colour of stomach contents also indicates the cause of poisoning. Copper salts
impart a greenish blue colour whereas picric and nitric acid impart yellow colour to the
contents. The contents of the stomach vary from traces to flakes of paints or lead objects,
grains or baits, seeds etc., like wise small and large intestine should be examined. Blood
should be examined for its colour and clotting characters. Cyanide poisoning imparts
cherry red colour, arsenic imparts rose red colour and nitrate poisoning turns blood brown
in colour. In abrus and cyanide poisoning-blood remains fluid after death.Examination of
other visceral organs should be done in relation to their size, colour etc. eg: - spleen size
is decreased and colour is changed to dark brown or black in copper poisoning and spleen
size is increased in T-2 mycotoxicoses.Lymph nodes are swollen, haemorrhagic,
oedematous and dark upon exposure to radiation. Bone marrow becomes pale and
gelatinous with yellowish tint.The description of morphological changes should be noted
clearly and absence of changes should be notified. The most important lesions found
should be underlined.
In case of small animals (poultry, small dogs, lab animals) the cadavers are sent as
it is, in case of large animals the stomach contents are collected from the vicinity of patho
anatomic changes in the gastric mucosa. If there are no changes a representative sample
is collected, but in medium sized animals the stomach tied at oesophageal and duodenal
end, intestine tied at both ends and bladder with tied ends is sent separately.
Collection of samples: A successful toxicological investigation requires appropriate

specimens, history and clinical signs, necropsy lesions and circumstantial evidences. All
the specimens are to be taken in separate containers (polythene jars/covers), securely tied,
properly labelled with particulars of date, case No., organs collected, species, name of
preservative used etc. A sample of the preservative used, brief history of the case along
with treatment given particulars should be sent. It is always preferable to send the
specimens through a special messenger. In medico legal cases, the specimens should be
sealed in the presence of a witness. The quantity for the kind of sample to be sent is as
follows.
Wholeblood:10-20ml; Serum:10-20ml;Milk:50-100ml;Urine:50-100 ml;Water: 200 ml;

Faeces : 50 g ; Feed : 0.5 - 1kg.

134
Mode of preservation : 1. Ice for about 72 hrs. 2. Alcohol (95% ethyl alcohol) 1 ml/g
of tissue is the ideal preservative for toxicological specimens. Formaline should never be
used as it hardens the tissue without giving scope for scraping and interferes in the
analysis. Blood and serum should be refrigerated and never frozen. A sample of the
preservative used should be sent. It is always better to have a duplicate sample stored
properly in a refrigerator for future reference Sample for analysis should include a
suspected source material; often gut contents, so that ingestion of suspected material can
be proved. Secondly, a sample of tissue (depending on tissue affinity of the suspected
poison) must be included, to prove that absorption of the poison has occurred. It is
always advisable to include a sample of liver to confirm absorption of orally ingested
poison. In survival cases the following materials may be sent for analysis:Stomach wash,
ruminal contents, vomitus, blood, urine, saliva, dung, water and feed, suspected forage/
poisonous plant/s is the ideal samples for laboratory analysis. Most xenobiotics are
ingested. Therefore, one of the unique advantages of analyzing gastrointestinal contents
is that qualitative tests can be easily carried out in order to determine the animal has oral
access or not. Guidelines for submitting specimen for toxicological examination is listed
in Table 1.
Table 1: Toxicological specimens for laboratory examination

Sl.No. Suspected Specimen required Remarks
poison
1. HCN/Cyanide Forage / ingesta, whole Rush samples frozen in air
blood tight bottle to laboratory
Liver GIT/ Stomach contents in 1%
mercuric chloride is ideal
2. Organochlorine Cerebrum, fat, liver, Use only glass containers,

pesticides/ kidney, ingesta
Avoid aluminum foil for
Chlorinated wrapping specimens
hydrocarbons
3. Organophosphates Feed, ingesta, liver, urine -
&Carbamates
4. Znic phosphide Liver, kidney, gastric -

contents
5. Nitrate/nitrite Forage, ingesta, body Ingesta in chloroform or
fluids, Serum . Ocular fluid formalin filled air tight
water samples container
6. Oxalates Fresh forage, kidneys Fix in formalin

134
7. Ammonia/Urea Whole blood or serum, Frozen / 1-2 drops of
urine Rumen contents saturated solution of
mercuric chloride
8. Heavy metals(Lead, Kidney, whole blood, liver Heparinized, do not use
Mercury) and urine EDTA
9. Mycotoxins Forages, feed sample, liver, Use airtight containers or
kidney, brain plastic bags. Cloth bags for
dry feeds
Note: Always send a sample of preservative if used in separate container with proper
label *****

134
GENERAL LINE OF TREATMENT OF POISONINGS
M.VIJAY KUMAR
In majority of cases of poisonings, treatment with an antidote is not possible,

instead prompt medical intervention to improve the condition of the animal can ensure its
survival. These practices focus on promoting the removal of the poison or neutralizing it,
whilst maintaining the vital functions of the animal.
Decontamination of the skin: Some substance (hydrocarbons, acids, alkalis,
agrochemicals, etc.) may, as a result of an accident or a spillage, contaminate the feathers
or fur of animals. In general it is important that in such circumstances the following are
undertaken:
• Epidermal structures (wings, nails, claws, feathers, fur) should be cleaned with the
greatest care, paying particular attention to areas such as the ears, between toes, etc.
• Avoid licking and ingestion of the poison, and to limit cutaneous absorption.Use
soapy water (preferably a soap with a low pH), rinsing repeatedly with copious tap
water
• Dry carefully and thoroughly (e.g. with a hair dryer)The following must never be
used: organic solvents (alcohol, white spirit, etc.) or oily substances which may
actually increase percutaneous absorption of the toxin.
• Do not rub the area vigorously; cleaning and drying must be gentle but thorough
Gastric emptying: Emetics:Use emetics if ingestion has taken place within the
preceding 2-3 hours. Never induce vomiting in following circumstances: If caustics or
hydrocarbons have been ingested; If the condition of the animal does not allow such
treatment, specifically if the patient is presenting with convulsions (unless controlled),
coma or severe respiratory difficulties; this avoids any secondary complications due to
aspiration.; in pregnancy and ingestion of slow releasing drug formulations.
Apomorphine: a central depressive effect and the possibility of cardio-toxicity
(arrhythmias) -Dogs: 0.05-0.1 mg/kg s.c or im; contraindicated in cats or pigs; Xylazine:
acts within 10-20 minutes; 0.25-0.5 ml of a 2% sol.,s.c.Ipecachuana (10% syrup) for
dogs and cats: Acts in 20-30 minutes; orally, 10-20 ml for a dog, 2-5 ml for a cat
administered in a phased manner. Alternatives: Sodium chloride (salt), p.o, 1-3 teaspoons
in warm water; Hydrogen peroxide, by mouth, 1 ml/kg; Copper sulphate is not
recommended as it is an irritant and facilitates the absorption of poisons. Preferred in
pigs (4% solution, max: 60ml,p.o)
Gastric lavage in dogs is indicated: if ingestion has taken place in the preceding 2-4
hours and on anaesthetized animals with endotracheal intubation. Use 10 ml/kg of an
isotonic solution of sodium chloride (occasionally sodium bicarbonate); repeat the

134
procedure until the washout fluids is clear. Emergency gastrotomy with manual emptying
may be necessary in some cases of plant poisoning or indigestible materials (such as
plastic, polyurethane foam).
Purgatives: Never use irritant purgatives and oil-based purgatives as they facilitate
absorption. Sodium sulphate, magnesium sulphate are preferred; PO, as enema, using
solutions of various strengths (make up to 20%):Small animals : 2-25 g, Large animals:
100-200 g (max: 300 – 400g); Liquid paraffin (mineral oil), by mouth:Dogs: 5-15ml,
Cats: 2-6ml
Diuretics: Increase glomerular filtration by instituting a forced diuresis or osmotic
diuresis: 5% glucose solution, by slow IV infusion: Large animals: 2-5 ml/kg per
24h, Small animals: 5-20 ml/kg per 24hr; 10% glucose solution, by slow IV infusion:
Large animals: 0.5-1 ml/kg per 24 h, Small animals: 1-2 ml/kg per 24 hr; 10%
mannitol solution, by IV infusion:Large animals: 1-2 ml/kg per 24 h, Small animals: 2
ml/kg per 24 hr; :Frusemide (im or iv), Large animals: 0.5-1 mg/kg, Small animals: 2.5-5
mg/kg
Reduce tubular reabsorption by modifying urinary pH.: Forced acid diuresis to eliminate
weak bases can be done by:Ammonium chloride, PO: Large animals: 20-40 g, Small
animals: 2-5 g; Arginine chloride, im, or iv-Large animals: 7-10 g, Small animals: 0.1-0.2
g/kg; Ascorbic acid, iv, all species: 40 mg/kg
Forced alkaline diuresis to eliminate weak acids: Sodium bicarbonate, 1.4%w/v, iv
infusion, Large animals: 2-4 ml/kg per 24 hr; Small animals: by regular monitoring of the
acid – base balance (number of ml to perfuse = base deficit (in mmol) x 0.6 x body wt in
(kg)ringer’s lactate, IV: all species: 5-10 ml/kg per hr; Use a diuretic such as
acetazolamide
Dialysis: In cats and dogs peritoneal dialysis with an appropriate dialysate 20-25 ml/kg
is suggested. Repeat the procedure several Times as necessary. Very effective in case of
renal failure/renotoxicity. Commercial preparations meant for human use can be
employed
Neutralization of poisons with in the gastrointestinal tract
Adsorbents Activated vegetable charcoal (fine medicinal charcoal).-the most effective
and most highly polyvalent adsorbents. They can be administered preferably as a
suspension in water, several minutes to 24 hours after ingestion, if possible before any
emetic. Large animals: 250-500 g, Small animals: 5-50 g; Other adsorbents: Magnesium
oxide (magnesia), Kaolin, Universal antidote (vegetable charcoal 10g+ magnesia 5g +
kaolin 5g + tannin 5g with water added up to 200 ml)

134
General chemical antidotes: Substances which form a complex or insoluble precipitate
with poisons and neutralize them in the gastrointestinal tract. The effects are often
limited and debatable. This category includes: Water-containing albumens (proteins
which are capable of forming insoluble complexes with heavy metals and which
neutralize acids and bases); Tannins (these precipitate heavy metals aluminum, lead,
silver and some alkaloids) ; Less useful against copper, mercury and nicotine), Lugol’s
iodine can partially precipitate heavy metals like Pb, Hg, Ag and Strychnine. and Ferric
hydrate .
Milk is commonly believed to act as the best general antidote; in fact, milk promotes the
absorption of liposoluble poisons. A cardinal rule, therefore, is “never administer milk”.
Additional treatment measures: vary according to the symptoms observed, important
agents used to support vital functions (respiration and circulation) are: Doxapram: A
respiratory stimulant, Dog/Cat: 2 mg/kg, iv, repeat as required ; Caffeine and
theophylline: Cardiovascular and respiratory stimulants, with diuretic action. Dosage:
100-250 mg iv, im, hypodermally or as required and Nikethamide:. Dog: 22-44 mg/kg,
im, iv.
Rational Use of Charcoal : Charcoal is ineffective against cyanide. It can adsorb
vitamins/minerals and continued use may prove to be harmful. Make slurry of the
activated charcoal using lukewarm water. 2-8 g/kg should be given in a concentration of
1g/5-10ml water by a stomach tube using either a funnel or a large syringe. Administer a
cathartic (sodium sulphate or magnesium sulphate) 30 minutes after the administration of
charcoal. In pet animals this technique can be modified if the charcoal is used in
conjunction with an emetic or gastric lavage (Normal saline: 10 ml/kg) with endotracheal
intubation.
*****

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CLINICAL MANAGEMENT OF POISONINGS OF
B.KALA KUMAR
In veterinary field toxicities are often found as a result of ingestion of poisonous

substances while grazing or through water. Suspicion of poisoning is also aroused when
illness occurs in a number of previously healthy animals, all affected at a same time,
sharing the same signs, necropsy findings, to the same degree of severity. Poisoning in
most occasions is accidental in farm animals, but may occasionally be deliberate .
SOURCE OF POISONINGS
1. Insecticides:Insecticides are the major source of poisonings in livestock.. Most of the

insecticides are basically ‘neurotoxic’, hence they may share some of the clinical signs,
Insecticides can be classified in to following categories: 1. Organochlorines: Eg: Aldrin,
Endosulfan, Lindane, Dicofol etc 2. Oraganophosphates. Eg: Acephate, Malathion,
Parathion, Methyl parathion, Dimethoate, Phosphamidon,, Chlorpyriphos,
Chlorfenvinphos, Monocrotophos etc 3. Carbamates. Eg: Carbaryl, Metacil, Dimetan,
Pyramat etc. 4. Pyrethroids (Synthetic): Deltamethrin, Cypermethrin,Permethrin,
Allerthrin etc. 5. Miscellaneous: Chloro-nicotinic acid (nicotine), Arsenic
compounds,Captan
Organochlorines: By virtue of their high lipid solubility these agents can enter the
neuronal membrane with ease and therefore interfere with normal functioning of the nerve
membrane sodium channel. The clinical signs of toxicity can be broadly categorized in to:
Behavioural signs - Anxiety, aggressiveness, abnormal posturing, maniac symptoms like

jumping over inanimate objects, wall climbing etc. Neurological signs – Hypersensitive
to external stimuli, spasm and twitching of fre-and hind quarter muscles, fascicualtions of
facial and eye lid muscles and variations in body temperature (subnormal temperature to
hyperthermia, up to 116°F). Autonomic effects: Marked salivation (normally thick/ sticky
saliva), Mydriasis, frequent urination, defecation and lacrimation.
Organophosphates: Clinical essentially appears as a result of irreversible inhibition of

AChE, causing accumulation of acetylcholine in the neuro-muscular junction leading to
‘spastic paralyses. The cause of death is due to respiratory collapse. Muscaranic signs

134
(miosis, watery, drooling saliva, urination, colic and /or defecation, lacrimation are the
common signs followed by nicotinic effects (muscle fasciculations, tremors) and C.N.S
effects( ataxia, convulsions and later depression of respiratory and circulatory centers).
Hypotension, bradycardia and dyspnoea are observed in poisoned animals.
Carbamates: The inhibition of AChE enzyme by carbamates is ‘reversible’, therefore, on

most occasions animals recovers on own unless ingested large quantity of pesticide.
Synthetic pyrethroids: Although these compound process low insect: mammalian

toxicity ratio, treatment of poisoned animals may be a difficult task probably because of
multiple mechanisms involved in toxicity and variations among pyrethroid class (type-I &
type-II). Hypersalivation, lacrimation, mucoid nasal discharge, excitement, in-
coordination, extension of limbs are observed in deltamethrin toxicity in buffalo calves.
Few pyrethroids also cause contact dermatitis.
2. Rodenticides:.
Anticoagulant rodenticides: These include warfarin (less used now a days) and second
generation anticoagulant rodenticides viz: Bromadiolone , brodifucoum. The main source
of poisoning is the ingestion of residues of the rodenticides or baits intended for killing
rodents.. The poor coagulation mechanism cause massive internal haemorrhages over
aperiod of time. Normally after period of about 2-5 days clinical signs appears and these
include anorexia, pulmonary coughing (epitaxis, dyspnoea),hypothermia, haematuria,
stiffness of hind quarters and sudden death. Internal haemorrhage, blood in the
GIT(gastroenteritis), haemopericardium and menigeal/cerebral bleeding and
haemorrhages in joints are the pathological lesions one can observe during necropsy. The
affected animals should be shifted to quiet and warm place and the line of treatment
include Vitamin-K1 in physiological saline (Vitamin-K3 not recommended) and cardio-
vascular support.
Zinc phosphide/ Aluminium phosphide: It is one of the cheapest and quite effective
rodenticide. Monogastric species are more sensitive rather than ruminants. Clinical signs
include anorexia, lethargy, abdominal pain, bloat (in ruminants), deep respiration, ataxia,
prostration and dyspnoea, gasping, convulsions and death. Post-mortum lesions include
pulmonary congestion, edema, sub-pleural haemorrhages, congestion of liver and
kidneys. Acetylene odour may be detected in stomach. No specific treatment is possible,
however symptomatic and supportive care maybe given. Gastric lavage with 5% Sodium
bicarbonate, Calcium boro-gluconate injection, anticonvulsants and measures to prevent
shock can be undertaken as a life saving measure.

134
3. Herbicides & Fungicides:Dinitro-compounds: Dinitrophenol, DNP; dinitro-orthro
cresol, DNOC); are some of the commonly used as herbicides. Accidental ingestion of
foliage sprayed with these compounds may lead to toxicity in ruminants. These
compounds induce methaemoglobinemia (intravascular haemolysis),hyperthermia, dark
coloured blood and gastroenteritis. Rapid onset of rigor mortis, yellowish-green coloured
tissues/urine may be recorded during post mortem examination.
Zeneb & Thiram: Zeneb (Zinc-ethylene dithiocarbonate) and Thiram (Tetra-methyl

thiuron sulfide) are the two most commonly used fungicides in agricultural practice.
Although acute poisonings is less likely to observe in field, chronic toxicities may get
unnoticed. Zeneb can induce thyroid hyperplasia, hypothyroidism, degenerative changes
in myocardial, skeletal tissues and depletion of testicular germ cells. Thiram exposure
may cause conjunctivitis, rhinitis, bronchitis, abortion (ewes) and teratogenic effects.
4. Hydrocyanic acid (HCN) /Cyanide:The most prevalent form of HCN poisoning in

livestock is caused by various cyanogeneetc plants capable of producing hydrocyanic
acid. Such plants contain cyanogenetic glucocides (dhurrin in sorghum, amygdalin in
bitter almond etc.) which hydrolyzed in to HCN in ruminants. Wilted, drought affected,
injured (chopping, rinsing etc.) plants are more dangerous than fresh plants because of
their preformed HCN. Any plants possessing 20mg HCN per 100gm (wet wt.) may serve
as potential source of HCN poisoning. Other source of cyanide poisonings are: industrial
grade Na/K and calcium cyanide (also fertilizer) and effluents from vicinity of
electroplating/metal coating industries workshop.
Hyperoxygention of blood would lead to cherry red/ bright red colour of venous blood .
Intoxicated animals shows salivation (frothy), bradypnoea, mydriasis, ataxia,tremors,
epileptiform scizure, cardiac arrhythmia and clonic-tonic convulsions. Invariably loss of
conscious, coma and death with several jerky and convulsive movements if poisoned
animals are not attended with in a with in 1 hour after the appearance of clinical initial
signs. Odour of the breath is ammonical/ bitter almond due to benzaldehyde production
(often bloating, regurgitation is observed). Opening of rumen during post-mortem
examination impart similar odour. Animals suspected for HCN poisoning must be
differentiated from nitrite and other sr milar agents before initiating antidote therapy . In
addition to antidotes, per oral administration of Cobalt chloride(10 mg/kg)and glucose is
also indicated.
5. Nitrate/Nitrite:Drought is one of the root causes of nitrite toxicity in cattle/buffaloes.

Nitrates are reduced to nitrite in ruminates. Otherwise, pigs are most sensitive species for
nitrate toxicity. Contamination of drinking water with sewage, several plants species
(Amarantus sps,Palak etc.), plants grown in highly acidic soil, water logging and rich

134
nitrated fields / effluents zone, deep well water or pond water originated from leaching
of top soil (after -nitrate fertilizer application) are some of the common source of nitrite
poisonings. Water soaked/entry of moisture may also render paddy hays/ corn in to nitrite
rich within 18-22 hours. Frequent application of fields with non-toxic weed killer 2,4-D
and nitratic fertilizer favour accumulation of nitrtes in plants. Any forage that contains
over 1.5% nitrate (expressed as pot. nitrite) is considered relatively unsafe for livestock
and should be fed with extreme caution. Nitrite ions induce meth-haemoglobenaemia as
well as marked vasodilatation. Clinical signs include cyanosis, staggering gait, muscular
tremors, rapid pulse, dyspnoea and dilated pupil. Opisthotonus, polyurea, chocolate
brown colour of the blood and cyanotic mucous membranes are the characteristic features
of nitrite toxicity. Untreated animals die with out a struggle. Reducing agents like
Methylene blue or Ascorbic acid are the antidotes (see table 2 for details). Mineral oil or
mucilaginous substances and diluted vinegar (4-5 lt. in cold water, per os) must be
administered to counter GI irritation and further reduction of nitrates in the rumen
respectively. Cardiovascular support (vasoconstrictor); and stimulants to counter
prostration.
6. Poisonous plants: Toxicities/ death due to ingestion of poisonous plants are also often
being the etiology of poisoning in the farm animals. Commonly with plant poisonings
there are perplexing epidemiological features. For example, animal already grazing in the
dangerous field are often unaffected while recently introduced may be poisoned. Drought,
starved, ailing from pica, hungry, ravenous animals, curiously excited animals (often do
not eat), and young animals less discriminate plants with different texture (attraction).
Poisonous plants often show geographical limitations in their distribution, particularly
industrial enterprises may create ‘poison hazard’ in local areas (Ipomea carnea,
Amaranthus spinosus) and certain agricultural practices / soil type may also pose
toxicities (eg. Nitrite, Selenium). Severe drought followed by rain/moisture/humid
atmosphere favour accumulation nitrite in many plants. Similarly re-emergence of fresh
leaves following harvesting also contains dangerous levels of HCN.
Essentially the source of plant poisoning can be classified into: a. naturally occurring b.
Commercial crops/byproducts and c. Conventional and non-conventional fodders.
Immature sorghum, maize, flax (linseed); Manihot esculenta (tapioca) newly emerging
bamboo shoots and rubber leaves are the common source of HCN poisonings. Accidental
ingestion of castor bean, rotten beat roots, adult nicotine leaves,Mimosa invisa (used to
increase nitrogen fixation in soil) may become fatal.. Plants or foliage belonging to
Brassicaceae sps.(Cruciferae) family i.e kale, rape,turnip, cabbage,reddish plants and
mustard seeds or meal may elicit severe toxicities in animals when fed /ingested large
quantity due to the presence of glucosinolates in such plants..Digestive

134
disturbance(enteritis),goiter polioencephalomalacia (rape blindness), pulmonary
emphysema are the sequelae. Bloat, photosensitization is also observed. Affected animals
are to be treated symptomatically.
Feeding of urea treated straws in excess/or fed to un-acclimatized animals may lead to
urea poisoning, long term feeding of subabul may lead to hypothyrodism and feeding of
fungus infested straws (sorghum, paddy or leguminous fodders) may pose threat of
mycotoxicosis when fed relatively for a long period. Ficus tsjhela (Karnataka-Kerala
boarder, Western Ghats); Acccia leucopholea (HCN), Amaranthus spinosus (nitrite);
Jatropa curcus (purging nut); Crotalaria juncia (hepatotoxic pyrrolizidine alkaloids:
monocrotaline);Flax(linseed, HCN); Ipomea carnea (LSD alkaloid like effects, also
source of nitrite and cause photosensitization). Strychnous nux-vomica (coastal
Karnataka); Abrus precatorius (Gulaganji); marking nut, Calitropis gigantica (yakka),
croton oil and Yellow oleander are also some of the plant source of accidental poisonings
and/or recorded in case of malicious poisoning in animals.
Antidotes and supportive treatments for common poisonings in large animals
Poison/toxicity Antidote/ treatment Dosage and method of treatment
Hydrocyanic acid Sodium nitrite followed Administer 1% sodium nitrite @ 15-

(HCN) /Cyanide by Sodium thiosulfate 25mg/kg,i.v followed by 25% sodium
thiosulphate @ 1.25gm , slow i.v
Na nitrite + Na thiosulfateCattle:
3gm + 15gm in 20ml water, s.c;
Sheep/goats: 2gm+5gm in 15ml
water,s.c. Cobalt chloride @10.2
mg/kg, per os; Approx. 4 lt. vinegar in
10-20lt. cold water; A large dose of
vitamin B12 and anticonvulsants, if
necessary. Give cobalt chloride
10mg/kg per-orally. Fluid therapy with
dextrose-saline is ideal
Nitrate/nitrite Methylene blue 1% Methylene blue @ 8.8mg/kg, i.v

and repeat 30 min later and if
Or necessary administer at 6-8hr. interval
Broad spectrum antibiotics intra-
Ascorbic acid
ruminally; Administer 8-10L cold
water and give osmotic purgatives
Treat for hypotension/shock,
(vasoconstrictors like 1:1000, 0.5 ml

134
adrenaline, slow iv); Blood
transfusion, if possible
Heavy metals British anti- BAL: 3mg/kg as 5% mixture of 10%

Lewisite(BAL) benzyl benzoate in mineral oil. Give
(Arsenic,antimony, deep i.m injection every 4hr. on first
mercury) two days, every 6hr. on third day and
then b.i.d for next 10 days. In cattle
Arsenic/Mercurial
and horse sodium thiosulfate can also
insecticides)
be used @ 8-10gram in the form of 10-
20%solution (i.v) or 20-30gram per-
orally in 300ml water.
Arsenic poisoning
d-penicillamine Fluid therapy and other supportive
treatment as required. Administer @
30-40mg ,i..v + 60-80mg/kg; P.O,
b.i.d or t.i.d for 3-4 days
Urea No antidote Administer 20-30lt. water and drench

4-6lt. 5 % acetic acid ;
Reduce the rumen pH Anticonvulsants, if required
Strychnine Phenobarbital sodium Phenobarbitone sodium,30mg/kg,i.v
(Strychnous- nux Chloral hydrate Chloral hydrate @ 5g/45 kg, i.v

vomica)
Drench tannic acid and then purgative
Rest the animal in cool, noise free & in

dark room after a dose of purgative
Lead Calcium disodium EDTA Make 6.6% solution and administer @

73 mg/kg,i.v (repeat or two treatment
daily for 3 days if required).
Combined thrapy with thiamine HCl
@2-4mg/kg/day, s.c is more effective,
Anticonvulsants, if required
Warfarine Vitamin- K1 Vitamin-K1: 300-500mg, S.C,every 4-

6hr.Blood transfusion transfusion @
Bromodiolone 20ml/kg or plasma @ 9ml/kg body wt;
Sedatives/tranquilizer
Pyrethroids No specific antidote, but Diazepam: 0.5-2 mg/kg, i.vAtropine

SO4 as required

134
(Deltamethrin, Diazepam HCl + Activated charcoal (1-2kg), P.O Fluid
Atropine SO4 therapy
Cypermethrin etc.)
Carbamate insecticides Atropine sulphate 0.25mg-0.5mg/kg,give ¼ intravenously

and remaining ¾ by intra-muscular or
sub-cutaneous route
Organophosphates Atropine sulphate + Atropinization: 0.25mg-0.5mg/kg,give

¼ i.v,remaining ¾ by i.m or s.c for
2-PAM every 3-6 hours. Observe for papillary
dilatation and recovery symptoms and
Or
continue treatment as required.
DAM(diacetyl
2-PAM: 20%solution @ 25-
-monoxime)
50mg/kg,i.v or intra-muscualrly,
Activated charcoal,P.O
Fluid therapy and supportive care
Organochorines Pentobarbitone sodium 30mg/kg,i.v and supportive care

( D.D.T;, B.H.C & Or Chloral hydrate
endosulphan etc.,) 5g/45 kg ,i.v and supportive care
Dinitro-herbicides In ruminants only: Treat Methylene blue: 2-4%,8-10mg/kg,i.v

(Dinitro-orthocresol- for Methaemoglobinemia every 8hr. Or Ascorbic
DNOC & with methylene blue acid: 5-10mg/kg,i.v; every8hr. for first
Dinitrophenol-DNP) 24-48hr.Note: Do not give antipyretics
Or to control hyperthermia. Administer
saline purgatives. Fluid therapy with
Ascorbic acid
DNS
*****

134
134
CARE AND MANAGEMENT OF CRITICAL PATIENTS IN
CLINICS
VIVEK.R.KASARALIKAR
Critically ill patient is special challenge to the clinician because the underline
problem is not evident for about 24 to 48 hours after initial presentation. Expeditious
therapy in right time can be life saving, whereas delayed adequate therapy may be
ineffective therapeutic failure. Most common clinical conditions in ambulatory patients
are trauma with internal/ external hemorrhage, poisoning and post surgical complication.
In fact, specialized care of emergent patient begins with initial phone call from the owner
and instructions to be given regarding first aid and transport procedures. Level of
consciousness, breathing pattern and external hemorrhage should be enquired on priority.
The important first aid measures are:
• Immobility and transport on firm flat surface

• Mouth to nose resuscitation in critical patient which is unconscious and not breathing
(Ten to twelve times per minute)
• Pulsating arterial bleeding is controlled by digital pressure and pressure bandage
• Penetrating foreign objects should be left in place till specialized help is available
• Head elevated by 200 in altered mental status after head or spinal injury
Evaluation and initial treatment: Three important assessment criterion in emergency

patients are A, B and C by evaluating certain parameters .
A – Airway: Airway patency should be evaluated on priority. Noisy breathing without

need of stethoscope suggests Large airway problem e.g. trachea and bronchus, whereas,
inspiratory dyspnoea implies extra-thoracic airway compromise. Loud expiratory sounds
reflect towards pathology of intra-thoracic airway including bronchioles and lung
parenchyma.
B – Breathing: Sequence of respiratory compromise is increased in respiratory rate

initially, followed by change in respiratory pattern. Laboured open mouth breathing with
development of cyanosis suggests significant compromised pulmonary function.
In both the above conditions, immediate Oxygen administration is the priority. Intra-nasal
catheter is the best choice for compromised breathing patients, whereas slash tracheotomy

134
with endotracheal intubation is preferred in unconscious and apneic patients (Nasal
Oxygen flow rate should be kept at 50 – 100 ml/kg/min).
C– Circulation: Hemodynamic and cellular changes that occur as a result of abnormality

in circulation is referred as shock or peripheral circulatory failure.; is clinically classified
in to four main categories.
 Hypovolemic: occurs due to atleast 15-25 % t deficit in circulatory blood volume

 Cardiogenic shock: occurs due to failure of heart to pump requisite quantity of
blood in to circulation
 Distributive shock: due to impaired distribution of circulatory blood volume as a
result of peripheral vasodialatation
 Septic shock: This is endotoxin mediated shock
Therapeutic management of critically ill patient:
3. Cardio-pulmonary Resuscitation (CPR):Hallmarks of Cardio-pulmonary arrest are

a) stage of apnea with cyanosis of visible mucous membranes b) absence of palpable
pulse c) absence of heart sounds and d) dilatation of pupils
Guidelines for Cardio-pulmonary resuscitation
d) Positioning of animal:Lateral recumbency on small animal examination table is

optimal position in small sized dogs (< 7 kgs), whereas dorsal recumbency is
preferred for large sized dogs.
e) Resuscitation:Chest compression coupled with mouth to nose ventilation should be

performed in patients in apneic stage.Compression rate should be 60 to 120 per
minute and the compression – ventilation ratio should be 15:2. It means for every 15
compressions 2 cycles of ventilation should be performed.
4. Management of shock: Assessment of shock is governed by these parameters

• Pale to cyanotic mucous membranes
• Tachycardia with weak pulse
• Significant fall in Systolic blood pressure (Below 60 mm of Hg)
• Central Venous Pressure (CVP) less than 5 mm of H2O
• Elevated level of Blood lactate (> 80 mg/dl)
• Significant increase in Capillary Refill Time (CRT)
Therapeutic management: Emphasis should be given to
 Fluid therapy:The main aim of fluid therapy is to restore circulation and improve the
tissue perfusion. Choice between crystalloid and colloidal solutions should be
determined. Crystalloid supplements fluid along with electrolytes, whereas colloidal

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solutions expand the plasma volume.Commonly used colloidal solutions are: Dextran
70, Hexastarch,Gelatin polymers, Frozen plasma, Packed cell component. Commonly
used crystalloids are: Normal Saline, Lactated Ringer’s solution, Dextrose Normal
Saline, 7.5 % Normal saline and Hypertonic dextrose solution
 Corticosteroids:Stabilization of cell membrane, blocking of arachidonic acid
metabolism and gluconeogenesis are few important roles of corticosteroids in the treatment
of shock
 Cyclo-oxygenase inhibitors:These decrease the prostaglandin synthesis and other
vaso-active amines.Eg; Flunixin Meglumin( 0.25 mg/kg); Ketoprofen(0.5- 2.2 mg/kg)
 Antibiotic therapy in septic shock: Broad spectrum antibiotic therapy has additional
advantage in endotoxin related shock. Anti-bacterials with synergistic action are also
preferred in septic shock. III to IV generation ceophalosporin like cefoperazone,
ceftrioxone and cefixim are frequently used in small animal practice.
 Control of hemorrhage and blood transfusion: Antifibrinolytic drugs are preferred
to counteract extensive hemorrhage. PAMBA (Para amino methyl benzoic acid), EACA
(Epsilon amino caproic acid) and Botropase have fast styptic activity
 Alpha Adrenergic agonist: These drugs help in improving cardiac output and thereby
improve tissue perfusion. Dopamine used @ 5 – 10 µg/kg/min as constant infusion has
positive ionotropic effect and increase the systolic pressure.
*****

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MANAGEMENT OF MYCOTOXINS AND ZOOTOXINS OF
M.VIJAY KUMAR
Mycotoxins are the toxic metabolites released by moulds under certain

conditions conducive for their growth. Acute or chronic toxicoses can result from
exposure to feed or bedding contaminated with toxins that may be produced during
growth of various saprophytic or phytopathogenic fungi or molds on cereals, hay, straw,
pastures, or any other fodder. The principles that characterize mycotoxic diseases: the
cause may not be immediately identified; they are not transmissible from one animal to
another; treatment with drugs or antibiotics has little effect on the course of the disease;
outbreaks are usually seasonal because particular climatic sequences may favor fungal
growth and toxin production and study indicates specific association with a particular
feed.
There are various types of mycotoxins and are classified as follows. Based on the
causative organism: Aflatoxins - Aspergillus flavus, A. parasiticus.;Rubratoxins -
Penicillium rubrum, P.purpurogenum.; T-2 toxins - Fusarium sp. F.gramaenareum and
F. roseum.; Ergotoxins – Claviceps purpurea and C. paspali.Among these most common
are aflatoxins. Aspergillus moulds grow rapidly when the moisture is <15%and the
temperature is 24-25ºC.They commonly affect GNC, CSC, coconut cake, sunflower cake,
wheat, sorghum, millets, soybean, peas and almonds.
Susceptibility:Ducks, rabbits, dogs, pigs, calves, chicken, cows, quail and sheep are
susceptible in the order of preference. Broilers are more susceptible than layers. Calves
are more susceptible than adult dairy cattle. Maximum allowable conc. in dairy cattle is
20 ppb (0.02 ppm)Depending on fluorescence aflatoxins are classified into B1, B2, and G1,
G2. B1 is most toxic and need to be converted into its active metabolites.Toxicity is
through ingestion of aflatoxin-contaminated feed. Aflatoxins are not accumulated to any
appreciable extent by animal tissues with the exception of milk.
Signs:Acute - sudden death or anorexia, depression, dyspnoea, coughing, nasal discharge,
anaemia, epistaxis, bloody faeces, possible convulsions and death. Subacute - jaundice,
hypoprothrombinemia, haematomas and haemorrhagic enteritis. Chronic - decreased feed
efficiency, decreased productivity and weight gain, rough hair coat, anaemia, enlarged
abdomen, mild jaundice, depression and anorexia. Abortions may occur.

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Postmortem Lesions: Wide spread heamorhages,Icterus,Gastroenteritis,Hepatic
necrosis,Massive centrilobular necrosis,fibrosis of bile duct,Enlarged liver,Hydrothorax,
Ascites,Oedema of Gall bladder wall,Pericellular cirrhosis
Diagnosis: based on History,Clinical signs,PM findings,Detection of Aflatoxin M1 in
milk & urine,liver, kidney,Serum liver enzymes SGOT,SGPT,ALP elevated,Reduced
prothrombin activity,Hyperbilerubinemia,Tlc,HPLC,RIA,ELISA
Differential diagnosis: Warfarin (haemorrhages), coal tar (mottling of liver)

Copper poisoning (haemoglobinuria, hemolysis); Pyrrozolidine alkaloids
(present in plants), CCl4, blue-green algae, crotalaria are hepatotoxic.
Treatment: 1. Avoidance of contaminated feed. 2. Hydrated sodium calcium alumino
silicate (HSCAS) adsorb aflatoxins @5kg /ton 3. Stanozolol (2 mg / kg) I/M decreases
hepatic necrosis 4. Oxytetracycline (10mg / kg) I/M decreases hepatic necrosis.( Never
administer oxytetracycline and stanzolol combination, they are mutually antagonistic) 5.
Activated charcoal 6.7 mg / Kg I/R as 30% W/V slurry in M/15, PH 7 PBS(Along with
charcoal,stanzolol/oxytetracycline(any one) ) 6. GSH Precursors Cysteine,methionine
@2.2mg/kgi/p 7. Multi vitamins Like E,K & Selenium 8. Feeding easily digestible and
low fat diet containing adequate protein
Sample collection : Samples can be taken at various stages:growing crops or during
transport or storage. Whenever possible, samples should be taken after particulate size has
been reduced (Ex: by shelling or grinding) and soon after blending has occurred (as in
harvesting, loading, or grinding).Most effective if small samples are taken at periodic,
predetermined intervals from a moving stream of grain or feed. These individual stream
samples should be combined and mixed thoroughly, after which a subsample of 10 lb (4.5
kg) should be taken.. A suggested method of probe sampling is to sample at 5 locations,
each 1 ft (30 cm) from the periphery of a bin, plus once in the center. This should be done
for each 6 ft (2 m) of bin depth. Thus, taller bins would require more samples, and the
total weight should be >10kg.
Dry samples are preferable for transport and storage. Samples should be dried at 176-
194°F (80-90°C) for > 3 hr to reduce moisture to 12-13%. If mold studies are to be done,
drying at 140°F (60°C) for 6-12 hr should preserve fungal activity.Containers should be
appropriate for the nature of the sample. For dried samples, paper or cloth bags are
recommended. Plastic bags should be avoided unless grain is dried thoroughly. Plastic
bags are useful for high-moisture samples only if refrigeration, freezing, or chemicals are
used to retard mold growth during transport and storage. Once a sample has been cooled
or frozen, warming may induce condensation and allow mold growth.

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Zootoxins :Out of 236 species of snakes in India, only 50 are venomous, However, the
common poisonous snakes of India that man and animal come into contact, are : Cobra,
Krait, Russel’s viper and Sea scaled viper, Apart from these, the other venomous snakes
found in India includes Sea snakes, Pit viper and King cobra.. In animals, many a time
incidence of snakes bite is near leg region and nostrils.
Sensitivity: Horse>Man>Sheep>Cattle>Goat>Dog>Pig>Cat
Venom composition: The venom compositions vary significantly among various class of
poisonous snakes. Therefore, the course of toxicity as well as well as cause of death
will be different, and obviously therapeutic approach will also vary. On most
occasions, the identification of snake is not available or doubtful. The nature of
toxicity of poisonous snakes are: Elapidae: Cobra , King Cobra, Krait- Neurotioxic;
Viparidae: Russel viper- Haemotoxic; Crotalidae: Pit Viper- Neutrotoxic
Haemotoxic. All the bites from venomous snakes do not lead to death due to “dry
bites” which means that no venom was injected. But, some snake venoms (krait) do
not have immediate effect even in a bad bite, it is wise to give veterinary/medical
care.
Cobra:. identified by their “defence display” by spreading their long bones to their
famous hood. ; are most active at dust, having along the wedges of agricultural fields in
search of rats/mice. For this reason they live mostly in cultivated area.. The cobra venom
is rich in enzymes, cardiotoxic, neurotoxic factors. The cobra venom is rich in enzyme
acetylcholinesterase. Therefore, rapid depletion of acetylcholine (ACh) at neuromuscular
junction occurs following envenomation. This leads to “muscular paralysis” (flacid
paralysis). In addition to it, the alpha-neurotoxin is a powerful cholinoceptor blocker
(nicotinic receptors). These factors hinder the function of muscles involved in respiration
and consequently death occurs due to “respiratory paralysis”. It is important to
identify the “big four” dangerous snakes. At first sight cobra looks like a non-venomous
rat snake, but, remember that the rat snake has a pointed head and larger eyes and it can
run faster.
Krait: The common krait has bluish-bluck body with white cross bands and the head is
short and blunt. Kraits venom is 10 times as powerful as that of the cobra and of all the
Asian snakes its venom is the most toxic (neurotoxic). Kraits are noctoural. They are
active at night and rest during the day. They are found throughout India and live mostly in
sandy soil in rat burrows. Their favarite hiding places are piles of wood (on bricks which
provide many pray to shelter in. They are canibalistic- eat snakes, rats, lizards and birds.
Famale lays eggs (10-15) and stays with them until hatch.

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Russel viper: is a fat and bulky snake, but it can move with surprising speed when in
danger. Its regular chain-like pattern and flat arrow shaped head make it easy to
recognise. Its fangs are along and curved.. Venom is rich in proteolytic enzymes,
hemolytic factors.
Pit vipers: are forest snakes and feed on frogs and lizards. Commonly found in coffee
and tea plantations in India. Pit vipes have a small “pits” between nostrils and eyes. They
are heat sensitive and can detect change in temperature when warm blooded animal
comes near. Venom is not powerful and seldom results in death.
First-Aid treatment: The first aim, in case of cobra/krait bite is to retard the absorption
of venom from the site of bite. ;done by applying a torniquet, provided site of bite is
suitable for that. Do not disturb/ or/excite the animal with little care incise the area (1/4)
and bleed. It is always better to avoid KMnO4 solution for wound wash and instead use
5% soap wash in 30 min. after bite. It is not advisible to apply torniquet in case of vipers
bite as this venom is rich in spreading factors (local tissue necrosis).
Hospital treatment: The nature of hospital treatment practically depends on identity of

the poisonous snake. Polyvalent antivenin is the drug of choce in the absence of identity.
It is better to avoid administration of antihistaminic as they are found to increase toxic
potential of certain vipers venom. Popularly, hospital treatment can be remembered as
“AAA”: A = Antivenin.; A = Antibiotic (broad spectrum) andA = Antitetanus / Gas
gnagrene antitoxins.
The antivenin (monovalent/polyvalent) should be administered IV at the rate of

100 ml. (small animals) or 10-50ml. (large animals). Administer antivenom with 1:00
epinephrine (0.5-1 ml. s/c) to avoid shock. Apply 1-2ml. of antivenin over the wound (site
of bite in case of viper bite. Monitor the cardio vascular activity constantly. Narcotic
analeptic is recommended in case of cobra bite to counteract intense pain. Epinephrine
and corticosteroid to overcome hypotension and shock. Employ plasma volume expander
(6% dextran-40) and calcium gluconate to reduce hemolysis. In case of viper bite, even if
the patient survive, amputation may be performed to avoid spread of local tissued
necrosis or gangrene formation.
Note: - Anitivenom should be stored at 40C. Do not administer if they are discoloured or
after the date of expiry.
*****

134
CLINICAL CONSIDERATIONS IN ADVERSE EFFECTS OF
DRUGS
U. SUNILCHANDRA
Adverse drug effects includes all adverse /side effects associated with a drug;
including that observed in overdose/poisoning with drugs or effects that may occur during
therapy. The mportant adverse effects of the drugs, in general are discussed in this
article.
Drug allergy/ hypersensitivity : Most common drug allergens implicated in producing

anaphylactic reactions in domestic animals include penicillins, cephalosporins,
sulfonamides, streptomycin, tranquliisers, vancomycin, vitamins, insulin, tetracyclines,
quinolones, salicylates, phenothiazines, chloramphenicol, heoparin, lidocaine,
erythromycin, angiotensin converting enzyme inhibitors, methyl dopa, vitamin K, iron
injections, exogenously administered repeated injections of
hormones(LH,hCG,PMSG),thiopentone, suxamethonium,non-depolarising
muscle relaxants, ester local anaesthetics and plasma expanders (dextrans, starches and
gelatins). Other agents that can cause anaphylactoid reactions include vaccines, food and
insect stings.
Clinical signs are manifested by the involving various organ systems.Cardiovascular

system:hypotension and cardiovascular collapse. tachycardia, arrhythmias, cardiac arrest.;
Respiratory System :oedema of the glottis, tongue and airway structures may cause stridor
and airway obstruction. Bronchospasm - may be severe.; Gastrointestinal: abdominal
pain, diarrhoea or vomiting.; Haematological.: coagulopathy. ; Cutaneous : flushing,
erythema, urticaria. signs may be seen. Adrenaline (1:1000 epinephrine) is the most useful
drug for treating anaphylaxis as it is effective in bronchospasm and cardiovascular collapse.
The dose of 0.01ml/kg.IV or 0.2 – 0.5ml/kg, IM is repeated in 10-15minutes if clinical
signs are not resolving. Ensure adequate breathing. Intubation and ventilation may be
required.Venous return may be aided by lifting the patient's legs or tilting the patient head
down Antihistamine agents: H1 blockers and corticosteroids are also administered

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Hepatotoxicity : Drug-induced liver damge is manifested by highly variable, ranging
from asymptomatic elevation of liver enzymes to fulminant hepatic failure. The type of
drug induced hepatotoxicity is often accompanied by fatigue, fever, and rash, usually
developing after few weeks of therapy. The clinically important potential hepatotoxic
drugs:
acetaminophen,amoxicillin,chlorpromazine,ciprofloxacin,diclofenac,erythromycin,fluconaz
ole, isoniazid,methyldopa,rifampin, tetracycline,phenobarbitone, phenytoin,
primidone,diazepam (in cats), mebendazole, carprofen, diethylcarbamazine, oxibendazole,
sulfonamides, anabolic steroids, vincristine etc. Treatment is to discontinue the suspected
drug. Specific therapy against is limited to the use of N -acetylcysteine (acetaminophen
toxicity) and L-carnitine( valproate toxicity).
Nephrotoxicity:
The most common drugs with nephrotoxic potentiality are aminoglycosides, NSAIDs,
sulfonamides, tetracyclines, amphotericin B, antiviral agents, methotrexate, the older
cephalosporins, cimetidine, ciprofloxacin, furosemide, penicillins, phenytoin, rifampin,

thiazide diuretics, polymixin etc. Crystalluria, hematuria and obstruction of renal tubules
occurring with sulfonamides are prevented by adequate water intake during the therapy and
alkalinisation of the urine with urinary alkaliser (eg: sodium bicarbonate) supplementation.
The prevention or minimizing the drug induced nephrotoxicity is by administering single
daily dose; reducing the treatment course ; avoiding concurrent administration of other
nephrotoxic drugs or reducing the doses in conditions of renal insufficicency/impairment.
Drug interactions:. may lead to diminished or an enhanced effect of a drug or may lead to
toxicity. Some pharmacodynamic drug interactions include : GC and NSAIDs (increased
gastrointestinal toxicity), furosemide and ACE inhibitors (increased diuretic effect),
sucralfate and gastric acid secretion inhiobitors( decerased efficacy of sucralfate), NSAIDs
and anticoagulants(increased bleeding), opioids and general anaesthetics(enhanced
respiratory depression by opioids) etc.
Some pharmacokinetic drug interactions that may affect negatively the absorption of the
administered former drug include: fluoroquinolones with cations Na+ and Cl -. Al and Mg,,
Orally active penicillins with antacids, tetracyclines with milk, antacid, laxatives, digitalis
with phenolphthalein (laxative), erythromycin with anti-cholinergic drugs, linocomycin with
kaolin, and orally administered antibiotics with large dose of atropine. The examples of
pharmacokinetic drug interactions during metabolism: phenobarbital with
griseofulvin(decreasedefficacy),chloramphenicol(decreasedefficacy),primidone/phenytoin(i

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ncreasedhepatotoxcity),corticosteroids(decreased efficacy);fluoroquinolones with
theophylline (theophylline toxicity-CNS stimulation) etc.
Teratogenicity: Typical manifestations include congenital malformations( birth defects),

intrauterine growth restriction, carcinogenesis and fetal demise. Interference in the
formation process of major body structures(first 12 weeks of conception) cause teratogenic
effect.Classes of teratogens include radiation, maternal infections,chemicals,and drugs
Cytotoxic drugs (antineoplastic drugs),anticoagulants(warfarin),vitamin A analogues
(etretinate, isotretinoin),
anticonvulsants(carbamazepine,phenytoin,sodiumvalproate),Cardiovasculardrugs(Angiotens
in-convertingenzymeinhibitors,AngiotensinIIinhibitors,losartan,spironolactone),
Endocrinological drugs (carbimazole,propylthiouracil,chlopropamide, sulphonylureas),
Antifungaldrugs(griseofulvin,ketoconazole,triazolesfluconazole,itraconazole,terbinafine),car
diovasculardrugs(betablockers,minoxidil),Antiinflammatorydrugs(NSAIDs;3rdtrimester),an
tibiotics(tetracycline,ciprofloxacin, chloramphenicol, nitrofurantion, vancomycin,
aminoglycosides), antihelminthics (mebendazole,albendazole, oxfendazole) and others
( misoprostol ,statins). Before using a drug, consideration must be given to any potentially
harmful effects on the fetus or mother. To minimize the fetal risks, the lowest possible
effective dose should be used. Antineoplastic drugs, radio isotopes and oestrogens are the
potential carcinogens and mutagens.
CNS disturbances:. Antibiotics to avoid, or use with care in patients with seizures include
enrofloxacin, cephalosporins and penicillins (in renal disease), and imipenum.
Metronidazole in higher doses; more common in cats. Ivermectin (related drugs
-milbemycin, moxidectin), loperamide and vincristine are expelled from the CNS by p-
glycoprotein. Collies, Shetland sheepdogs, English sheepdogs, and Australian shepherds are
susceptible to these drugs when administered at normally therapeutic concentrations. The
other common drugs with potentiality of CNS disturbances:
levamisole,tetramisole,loperamide,tinidazole,metoclopramide,promethazine,
prochlorperazine, terbutaline,chlorpromazine, methylxanthines, piperazine, respiratory
stimulants (doxapram,nikethamide)and antihistaminics (sedation,also possible), all of
which may result in transcient CNS stimulation depending on the dose and condition.
Photosensitization: Photosensitivity reactions or photosensitization is a clinical condition

in which skin (areas exposed to light and lacking significant protective hair, wool, or
pigmentation) is hyperreactive to sunlight due to the presence of photodynamic agents.
Tissue injury is thought to result from the production of reactive oxygen intermediates or
from alterations in cell membrane permeability. It is most commonly seen in
cattle,sheep,goats,and
horses.Tetracyclines,fluoroquinolones,sulophonamides,antihistaminics,diuretics(thiazides,lo

134
op),tricyclicantidepressants,phenothiazines and corticosteroids are examples of drugs with
phototoxic potentiality. Photosensitive animals on prolonged exposure to sunlight- scratch
or rub lightly pigmented, exposed areas of skin (ears, eyelids, muzzle), inducing typical
skin lesions : erythema, edema, serum exudation, scab formation, and skin necrosis . In
cattle, and especially in deer, exposure of the tongue while licking may result in glossitis,
ulceration and deep necrosis. Treatment involves palliative measures (steroids, topical
antibiotic)
Gastrointestinal disturbances: manifested by nausea, vomition, diarrhoea, abdominal

pain are most commonly observed after the oral administration of macrolides,
tetracyclines, piperazine, cephalosporins, oxyclozanide, fluoroquinolones, penicillins,
nitrofurans, rafoxanide, NSAIDs, sulphonamides, antineoplastic drugs. Unless severe as in
case of anticancerous drugs, most of them are transcient and are self limiting.
Local pain, tissue injury and irritation :. Bleeding from the injection site and hematoma
formation can occur if blood vessels are injured during particularly intramuscular
injections.. Skin necrosis, neurological damage, and loss of limb can follow. The sciatic
nerve is commonly injured by gluteal IM injections and the radial nerve injury at the
shoulder, commonly manifested by paresis, necrosis etc. Numerous drugs like
quinpyramine salts, suramin, diminazine, b complex injectables, multivitamin
injectables,cephalosporins, tetracyclines, NSAIDS, oil based injectables, the long-acting
injectable medications may result in complications at IM injection sites. The extravasation
of anticancerous drugs outside the vein may result in thrombophlebitiis and tissue necrosis.
*****

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COMMON HOUSEHOLD SUBSTANCES OF TOXIC
POTENTALITY
U. SUNILCHANDRA
Household products being formulated as complex chemical mixtures

with multiple active ingredients designed for specific applications may be hazardous to
pets and children with accidental exposure.The common route of exposure of the
household hazardous compounds may be dermal, oral, ocular or inhalational. Some of
the important indoor substancse with higher toxic potentiality are described especially
with reference to pets.
SOAPS AND DETERGENTS: This class include soaps,shampoos, spray cleaners,
dishwash liquids , powders, laundry products, disinfectants, fabric softeners and
sanitizers. Bath soaps and bar soaps usually have low toxic potential, causing mild
gastroenteritis with vomition, on ingestion. Demulcents and diluents: milk , rinsing with
water for dermal and ocular exposure; Induction of emesis if soap is non
alkaline( noncorrosive), if there is no spontaneous vomition within thirty minutes of
ingestion and, fluid and electrolyte therapy.
Nonionic detergents ( alkyl ethoxylate; sources: shampoos, dishwash detergents,laundry

detergents) generally have low order of 218oxicoses218 and toxicity, being non
corrosive. Anionic (alkyl sodium sulfonate, dioctyl sodium sulfosuccinate, sodium lauryl
sulfate; sources: shampoos, dishwash detergents, laundry detergents) and cationic
( benzalkonium chloride, ,cetirimide; sources: fabric softeners, germicides, disinfectants,
sanitizers) detergents (Quaternary ammonium compounds) are corrosive and highly toxic.
Ethanol and isopropanol, often found in cationic detergents ;enhance gastrointestinal
absorption and damaged skin favours percutaneous absorption.
Toxicity related clinical signs are vomition, diarrhoea, gastrointestinal

discomfort, intravascular hemolysis in impaired liver condition, dermal irritation, corneal
damage ; Oral-corrosive damage, salivation,muscle weakness, respiratory and CNS
depression, seizures, collapse, comapredominantly seen with cationic detergents.
Treatment involves dilution with milk, water, egg white, administering act.charcoal,
saline cathartics, fluids, antibiotic, analgesics and thorough washing the skin with soap
and water and eye lavage with isothermic isotonic saline for 20minutes.
CORROSIVES :. Acidic corrosive (Hydrochloric acid, sulfuric acid, nitric acid,

phosphoric acid, sodium bisulfite) product examples are antirust compounds, toilet bowl

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cleaners, automobile batteries, gun barrel cleaning fluid and swimming pool cleaning
agents. Alkaline (sodium hydroxide, potassium hydroxide, sodium carbonate, potassium
carbonate, ammonium hydroxide, potassium permanganate) product examples are drain
cleaners, washing products, liquid cleansers and toilet bowl products. On dermal and
ocular exposure: serious burns, extremely painful, corneal/conjuctival necrosis,
perforation and opacity. On ingestion: corrosive burns of mucosal membranes ( milky
white/ grey, turning to wrinkled black). Vocalization,depression,,panting, inability to
swallow.haematemesis, abdominal pain, polydypsia, respiratory distress, shock,
secondary pneumonia from aspiration of vapours, gastrointestinal bleeding, perforation
and fistula are the other signs observed depending on the severity. Oral dilution with egg
white , milk or water, skin and eyes thourghly flushed with copious water and sterile
saline respectively; therapy for shock: IV fluids, steroids within 48 hours, which reduce
the fibroblastic activity and inflammation, reduce the stricture from circumferential
alkaline burns. Analgesics and antibiotics prophylactically in animals with perforations.
Attempts to neutralize burns chemically(as exothermic reactions produce elevated local
heat and thermal burns), gastric lavage, induction of emesis are contraindicated. .
Charcoal is ineffective in binding to caustics.
DISINFECTANTS: found in cleanimg products include quaternary ammonium

compounds, phenol, pine oil, bleaches, alcohols; are more toxic than soaps and detergent
compounds
Phenols: highly reactive,corrosive contact poisons; denatures and precipitates cellular

proteins of all contacting cells. nephrotoxic, hepatotoxic and neurotoxic; rapidly absorbed
through ingestion, inhalation or skin. Cats are highly sensitive. Sources of phenolic
compounds: flooring materials, coal tar, creosote, tar paper. It results in intense pain,
areas of coagulative necrosis; treated by glycerol, polyethylene glycol washing, thorough
rinsing with water , dressings soaked in 0.5% soda bica. Also may cause corrosive
burns of mouth, oropharynx, oesophagus. Vomition, salivation,ataxia, panting, weakness,
tremor, coma, seizures, methhaemoglobinaemia, respiratory alkalosis, severe liver and
kidney damage. Demulcents-milk, egg white, gastric lavage and emesis(contraindicated
if severe damage) activated charcoal, saline cathartic, 1% methylene blue, 4mg/kg;IV;
ascorbic acid 20mg/kg,PO; N-acetyl cysteine 140mg/kgIV, 70mg/kg PO. Q,id for 3 days.
Ocular exposure is treated by sterile saline wash.
Bleaches: preparations contain sodium hypochlorite.Calcium hypochlorite and

trichloroisocyanuric acid are present in industrial strength bleaching solutions ,swimming
pool chlorine products and chlorine laundry bleaches. Non chlorine bleach preparations
or colorfast bleaches contain sodium peroxide, sodium perborate or enzymatic detergents.
Generally, the toxicity of bleaches is of lower degree, resulting in irritation of

134
ropharynx, salivation, vomition and abdominal pain. Bleaching of hairs, pulmonary
irritation- coughing , dyspnoea and retching on inhalation may also be seen. Nonchlorine
bleach products, (sodium perborate, sodium peroxide) are alkaline and severe gastric
irritatants causing renal damage and CNS excitation, depending on the amount ingested.
Treatment: Milk and water orally; washing with soap and rinsing with abundant
water/sterile saline on dermal/ocular exposure. Induction of emesis and orogastric
lavage is contraindicated to avoid the risk of causing further oesophageal irritation. Milk
of magnesia (2-3ml/kg) can be administered and other clinical signs are treated
symptomatically.
Deodorants: composed of aluminum chloride and aluminum chlorohydrate; which have

moderate toxicity potential. Ingestion can cause oral irritation, necrosis, gastroenteritis
and nephrosis.; which can be treated by orogastric lavage, antiemetics and
gastroprotectant drugs.
SOLVENTS AND ALCOHOLS: The most commonly encountered solvent (acetone:

sources: nail polish remover, varnishes, glues )and alcohols include
isopropanol(perfumes,cologne, grooming products), methanol (antifreeze products,
automotive wind shield clesnser, consumer products) and alcohol (alcoholic beverages,
cosmetics, mouthwashes ,common baker’s and brewer’s yeast). Activated charcoal is
ineffective in binding to the alcohols, not to be used. Clinical signs noticed are CNS and
respiratory depression acidosis, ataxia, hypothermia, cardiac arrest, coma; which is
treated by emesis induction, (if < 2 hrs); IV fluid Ringers lactate/ saline solution with
NaHCO3(1-3mEq/kg). Ethanol reduce severity of methanol poisoning.
Petroleum distillates: The compounds include cyclohexane, alkanes and alkenes.

Sources: gasoline (petrol), kerosene, motor fuels, solvent paints and vehicles for
pesticides. Because of low surface tension, chance of aspiration is most common. Dermal
exposure may result in dermatitis. Oral exposure results in aspiration pneumonia, cough,
hyperthermia, cyanosis, CNS depression and pulmonary oedema.. Emetics and oily
purgatives are contraindicated, as they increase the risk of aspiration. Gastric lavage and
activated charcoal should be reserved for ingestion of large amount(2ml/kg) or when
other toxicants are present. Oxygen therapy, rest , flushing the skin and eyes with water
and IV fluids to maintain hydration and electrolyte balance is recommended. Other
solvents (eg: acetone, turpentine) or other hydrocarbons should not be used for removing
the petroleum distillates from skin.
BATTERIES : Automotive or dry cell batteries contain sulfuric acid, that can be
irritating on contact with eyes, skin and gastrointestinal tract., which is treated

134
accordingly as with acid exposure.The sources of small disc/button batteries include
batteries used in calculators, cameras, hearing aids, watches , the content being mainly
mercuric oxide. The dry cell batteries , commonly used in toy flash lights, may contain
the alkaline ( NaOH, KOH; alkaline batteries) or acidic compounds (ammonium chloride,
manganese dioxide, heavy metals- Li, Ni, Zn, Ag, Cd) in them. On ingestion, most of the
intact batteries pass through digestive tract within 24 to 36 hours without producing any
major adverse effects, except for mechanical obstruction occasionally. Gastrointestinal
distress may occur resulting from retention and obstruction, which has to be diagnosed by
radiography and has to be corrected by endoscopy and surgery . If battery is chewed and
split apart, it may cause corrosive damage depending on the chemical content in it.
Timely surgical intervention together with the administration of saline cathartics,
enemas and appropriate chelation therapy with specific chelating agents if any (eg:
DMSA or D-Penicillamine as for Pb), can minimize the corrosive damage caused. Lead
is the major source of toxicity among the metals, resulting in acute or chronic toxicity
upon ingestion. The sources of lead are paints, batteries, solder, plumbing supplies,
lubricating material, ceramic containers, Pb pipes, toys, inks, dyes, used oil from vehicles
that burn leaded gasoline. The clinical signs noticed are Acute- CNS excitability signs,
convulsions, behavioural changes, ataxia, tremor, blindness. Chronic-gastrointestinal
disturbance signs, vomition, pica,diarrhoea, abdominal pain. Treatment is by
administering Ca disodium EDTA, 25mg/kg, q.i.d, SC diluted in 10% dextrose ,Oral D-
penicllamine, 110mg/kg/day, 1-2 weeks, Dimercaptosuccinic acid(DMSA),
10mg/kg,t.i.d.
CYANOACRYLATE ADHESIVES ( SUPERGLUE) : Uncured cyanoacrylate

adhesives form an almost instantaneous bond on contact with hair/skin resulting in
annoyance and frustration of the animal. Cured ones are nontoxic upon ingestion
.Dermal exposed areas are soaked with warm soapy water as quickly as possible. and
with acetone for several minutes, if area is away from face or eye. The hairs may be
clipped to reduce the tension on skin. The surfaces should not be pulled apart, with
direct opposing actions.Ocular : Eyelid/eyeball is thoroughly washed with warm water
and Elizabeth collar is applied to prevent self trauma. The animal will be able to open
eyes on its own with no residual tissue damage within 2-3 days and hence forceful
manipulation should not be done.
Methylxanthines: Sources: Coffee, tea, chocolates, cola/soft drinks, asthma,

analgesic,cold medications. Caffeine, 221oxicoses221is and theobromine are the primary
toxic agents. Clinical signs manifested by vomition, diarrhoea, polyuria, weakness,
hyperexcitability, tremors, seizures, coma and death resulting from cardiac
tachyarrhythmias. If ingestion is less than 2 hours, emetics administration followed by,

134
activated charcoal and saline cathartic is indicated. Since methylxanthines undergo
enterohepatic recycling, charcoal should be administered every 3-6 hours until symptoms
disappear. Antiarrythmics (lidocaine, without epinephrine; 1-2mg/kg,IV- loading dose;
40-60mg/kg/min infusion rate, slow IV- as maintenance dose) or beta blocker
(metoprolol; 0.1- 0.3mg/kg,PO,tid) to control arrhythmia;Diazepam or phenobarbitol to
control seizures and fluid therapy to maintain hydration and electrolyte balance is
recommended. Corticosteroids and erythromycin should be avoided as they decrease
urinary excretion of methylxanthines.
Aspirin : Clinical signs of aspirin toxicoses in cats are dose-dependant and may include
CNS depression, anorexia, vomiting, gastric hemorrhage, 222oxicoses222is , toxic
hepatitis, anemia, bone marrow hypoplasia, hyerpnea and hyperpyrexia, hyperthermia,
hyperglycemia, and glycosuria. Treatment is by GI decontamination with emetics,
activated charcoal and cathartics, within 4 hours of ingestion. Acid-base imbalance is
corrected with a slow infusion of sodium bicarbonate, carefully monitored and adjusted
to avoid pulmonary edema being developed. The resulting hyperthermia should be
controlled by external cooling; the use of antipyretic drugs should be avoided.
Paracetamol: Toxicity Signs: Dirty brown colored gums, dyspnoea, haematuria,

jaundice ,facial and paw edema , cyanosis, hypothermia, and vomiting. Less common
signs include coma, generalized weakness, and death. If ingestion is less than 2 hours,
emetics, activated charcoal and saline or osmotic cathartic are indicated.. If severe
cyanosis is present, oxygen therapy should administered, and the animal should be subject
to as little stress as possible.IV Administration of acetylcysteine, 140mg/kg/hr for 7
hours; Ascorbic acid, 30 mg/kg orally to reduce methemoglobinemia to Hb. Supportive
care including fluid therapy for possible metabolic acidosis is also recommended.The
other drugs used for NSAID 222oxicoses include
ranitidine(2mg/kg,tid,IV,PO),omeprazole(0.7mg/kg,sid,PO),metoclopramide(0.2-
0.4mg/kg, tid,PO,IM), sucralfate (0.5-1g, bid,PO)and misoprostol(2-5µg/kg,tid,PO)
Xylitol: is a sweetener used in sugar free products/chewing gums;induces hypoglycaemia

by stimulating insulin secretion , resulting in weakness,m ataxia, seizures and collapse.
Therapy: Inducing emesis administering activated charcoal, 50% dextroseIV and liver
tonics
Amitraz: poisoning occurs commonly from ingestion of a tick collar. Clinical signs
include ataxia, bradycardia, CNS depression, vomition, diarrhoea, and seizures.
Treatment involves decontamination (emesis, activated charcoal, saline cathartic) and
repeated injections of yohimbine (0.1mg/kg.IV) or atepamizole to reverse its adrenergic
agonistic effects and atropine has to be avoided as it may increase the absorption.

134
*****

134
PHARMACOLOGICAL MANAGEMENT OF BEHAVIOURAL
ABNORMALITIES IN ANIMALS
U.SUNIL CHANDRA
The majority of the drugs prescribed for behavioral problems in pets are
unlicensed and not registered for veterinary use and are used in an extra-label fashion.,
with few exceptions . Clients must be made aware of this and informed consent forms
should be obtained before initiating the treatment. The client cooperation over
administration of these drugs is an important consideration as many of the drugs take a
considerable time to produce desirable effects on the animal, requiring relatively long
term administration (weeks to months). Drugs should always be considered as an adjunct
to behaviour modification therapy, not as a replacement/ substitute. Client compliance is
important as behaviour modifying drugs may take up to six to eight weeks to reach
therapeutic blood concentrations. Drug therapy should always be gradually withdrawn..
An overview of the classes of medications used in behavioural abnormalities of dogs and
cats are described in this article.
Benzodiazepines ( BZDs): The agents are oxazepam, clorazepate, lorazepam, temazepam,

clonazepam, diazepam and alprazolam, the last two being most commonly indicated for
treatment of anxiety related behaviour problems like urine spraying and short treatment for
sound phobias (eg: fireworks, thunderstorms). Diazepam produces short-term anxiolytic
effects and at low doses diazepam retains its amnesic effects, while at higher doses
anxiolysis and sedation are achieved. Responses to diazepam are highly individual, so that
dose response must be titrated. Diazepam should be given prior to an anticipated fearful or
phobic event.Adverse effects of ataxia, hyperexcitability and disinhibition. Alprazolam
may also be used in advance or given after a phobic event in order to impair the dog’s
memory of it. It may therefore be used to block the effects of unanticipated phobic events in
order to prevent them from having an emotional impact on the animal in the future. BZDs
are contraindicated in states of hepatic and renal impairment and for long term use in cats.
Monoamine oxidase inhibitors(MAOIs): Selegiline is used for the treatment of

behavioural disorders with an emotional origin, which includes fears and phobias. It
reduces fearfulness, increases exploratory behaviour and has positive effects on cognition
even in healthy animals. It takes 4-8 weeks to begin to become effective, and is a useful
adjunct to behavioural therapy, especially in individuals that are frequently exposed to noise
events, show signs of a generalisation or are inhibited in situations when they are fearful or
anxious

134
Tricyclic antidepressants (TCAs): Clomipramine and amitryptilline are the TCAs
licensed for use in veterinary medicine., commonly used for separation anxiety, anxiety-
related aggression, urination due to submission or excitement, allergy-related pruritus,
urine marking and hypervocalization. The most common side effects are short term
lethargy or sedation, mild and intermittent vomiting which is usually transient and increases
or decreases in appetite. The antihistaminic effect of these agents may be a useful adjunct in
controlling pruritus due to atopy and food allergies. They are contraindicated in animals
with seizures, urinary retention or history of cardiac arrythmias and within two weeks of
administration of a MAOI
Selective Serotonin ReUptake Inhibitors (SSRIs): Fluoxetine, sertraline and fluvoxamine

are used for treating psychogenic alopecia, allergy-related pruritus, anxiety related
conditions, dominance-related aggression, fearful behaviors, obsessive-compulsive
behaviors, and urine marking. Fluoxetine is approved drug in dogs, for inter-dog aggression
and the treatment of obsessive-compulsive disorders in dogs. It reduces the clearance of
diazepam, its active metabolite nordiazepam and alprazolam, so concurrent use should be
avoided.
Azapirones: Buspirone is the only member, advocated for treatment of mild to moderate
anxiety related problems and urine spraying in dogs and cats. Contraindicated in case of
renal, hepatic impairment, epileptics, allergic reactions and caution is needed as treatment
can lead to an increase in aggression as it may decrease the inhibitory effects of fear. It is
ineffective in cases such as sound phobias or separation anxiety in dogs.
Beta blockers: Porpranolol and pindolol are, indicated in treatment of situational anxieties
in dogs and cats, used before the anticipated situation occurs. They are contraindicated in
animals with cardiac disease, hypotension, and bronchospasm.
Hormonal preparations: Progestins should only be given to neutered animals and

avoided in diabetes mellitus, breeding animals and with concurrent corticosteroid use. The
antiandrogen commonly used is delmadinone acetate. Cabergoline has antiprolactin effects
and is recommended for the treatment of pseudopregnancy in bitches and in spayed bitches
with aggressive behaviour attributable to elelvated prolactin levels.
Antihistamines: They are useful in the management of mild anxiety associated with travel,
inappropriate night time activity and anxiety conditions in which pruritus plays a important
role. They are contraindicated in animals with glaucoma,urinary retention and
hyperthyroidism.Diphenhydramine(0.4 - 0.5 mg/kg po bid-dog; 2-4mg/cat bid-tid-cat) and
Cyproheptadine (0.4 - 0.5 mg/kg po bid-dog; 2 - 4mg/cat bid-tid-cat) are the H1receptor
antagonists that are successful in some cases of spraying in cats.

134
Alpha adrenoceptor stimulants: Phenylpropanolamine (1.1-4.4 mg/kg,po,bid )used in the
treatment of sphincter mechanism incompetence in bitches and used to manage house
soiling in these cases. Increased aggression is the possible side effect.
Alpha adrenoceptor antagonists: Nicergoline (250-500 µg /kg,po,sid) is advocated for

sleep disorders, diminished vigour and fatigue. It should not be administered within 24
hours of using alpha 2 agonists such as xylazine or medetomidine.
Xanthine derivatives: Propentofylline is licensed for canine age related behavioural

changes such as dullness, lethargy and cognitive decline,which respond better if
combination therapy with selegiline is used.
Neuroleptics (Antipsychotic agents): Low potency phenothiazine tranqillisers

(acepromazine, chlorpromazine, and thioridazine hydrochloride) commonly used for
sedation and restraint purpose, have side effects of sedation, anticholinergic effects, and α-
adrenergic blockade. High-potency agents (haloperidol, fluphenazine, trifluoperazine
hydrochloride, prochlorperazine, thiothixene, risperidone) result in less sedation and fewer
autonomic side effects but commonly result in extrapyramidal effects.Acepromazine is used
as a short-term tranquilliser during phobic events related with fireworks and thunderstorms
and travel associated behaviour problems. It is believed that immobilising an animal
whileleaving it aware of, and emotionally responsive, to a phobic event may intensify the
experience and lead to worsening of phobia in the future. High doses which may be
required in order to sedate a dog; may result in hypovolaemia, hyperexcitability and
extrapyramidal side effects.
Dosage , route and frequency of administration of drugs used in behavioural

abnormalities of dogs and cats
BZDs: DOGS:Diazepam(0.55 -2..2 mg/kg po sid-bid); Alprazolam (0.01-

0.1mg/kg,PO,bid),Oxazepam (0.2 – 1.0 mg/kg po sid-bid), Clonazepam (0.1 - 0.5 mg/kg po
sid-bid),Clorazepate(0.01-0.1 mg/kg po,bid). CATS: Diazepam(0.2 - 0.4 mg/kg po sid-bid);
Alprazolam (0.125 - 0.25 mg/cat po bid),Oxazepam (0.2 - 0.5 mg/kg po sid-bid),
Clonazepam (0.016 mg/kg sid-qid),Clorazepate(0.125-0.25 mg/kg po bid .
TCAs: DOGS: Amitriptyline (1-2mg/kg,po,bid),Clomipramine (1-3mg/kg,pobid),

Nortriptyline( 0.5 - 1.0 mg/kg posid-bid), Doxepin (3-5mg/kg.po,bid); CATS: Amitriptyline
(0.5 - 1.0 mg/kg po sid),Clomipramine (0.25 - 0.5 mg/kg po sid), Nortriptyline (0.5 - 1.0
mg/kg posid-bid), Doxepin (0.5-2.0mg/kg/po,bid).

134
SSRIs: DOGS: Fluoxetine(0.5-1mg/kg,po,sid),Fluvoxamine (1-
2mg/kg,po,sid),Sertraline(1-2mg/kg,po,bid), Paroxetine (1mg/kg, po, sid) ; CATS:
Fluoxetine(0.5-1mg/kg,po,sid),Fluvoxamine (1-2mg/kg,po,sid),Sertraline(1mg/kg,po,bid.
MAOIs: Selegiline-0.5-1mg/kg, po,sid-dogs,cats; Azapirones: Buspirone-0.5-

1mg/kg,po,bid,(< 5mg/cat
Beta blockers: Propranolol-0.5-3mg/kg,po,bid-dogs; 0.2-1mg/kg,po,bid-cats; Pindolol

-0.125-0.25mg/kg,po, bid (dog); Dopamine2 receptor agonists: Cabergoline-5
mg/kg,po,sid-dog
Antiepileptics: Phenobarbitone -1-8mg/kg,po,bid (dog) 1-2.5mg/kg,bid (cat);

Carbamazepine-4-8 mg/kg,po,bid (dog); Total 25mg, po,bid (cat)
Xanthines: Propentofylline- 2.5-5 mg/kg,po, bid (dog); otal dose-12.5mg, po, sid (cat)
Progestins: Megestrol Acetate - 2.5 - 5 mg po sid (dog); 2.5 - 5 mg po sid (cats);

Medroxyprogesterone Acetate10 mg/kg(female) ;20 (male) SC – max : 3 injections per
year (dog); 10(females); 20 (males) mg/kg, sc – max. 3 injections per year (cat)
po=oral, IV=intravenous, SC=subcutaneous, bid= twice a day, tid=three times a day,

sid= once daily
*****

134
134
DIAGNOSTIC TESTS FOR DETECTION OF COMMON
TOXICANTS IN SAMPLES
M.VIJAY KUMAR
Detection of Heavy metals: Place 10g of tissue (finely minced) in a beaker or test
tube.Add 10 ml of 10% HCl.Introduce a copper wire into the test tube Boil for 10-15 min.
(Do not inhale fumes) Remove the copper wire and place it on a filter paper Observe the
colour of the copper wire. Inference: Black coloration - Arsenic or Bismuth; Shining
silver deposit – Mercury; Dull white deposit – Silver; Dark colour with purple to blue;
violet green - Antimony.
Depending on the colour of copper wire the confirmatory test is conducted.If the deposit
is black it can be confirmed whether it is due to arsenic or bismuth by placing the copper
strip in 1-2 ml. of 10 % potassium cyanide. If the deposit is due to arsenic, it will dissolve,
but if it is due to bismuth or antimony, it will persist.In mercury, colour of the deposit
ranges grayish (50 mg) to shiny silver (100 mg).
Detection of lead : Mince the liver/kidney piece or collect a small amount of scraping
from stomach wall.Add a few drops of conc. nitric acid and heat gently till dry, (never
over heat the sample as it turns black making reading difficult). Add a few drops of water
and two drops of 10% pot. iodide solution.Development of yellow colour indicates
presence of lead.
Detection of Cyanide: a) in biological material: Take 50 g of finely ground tissue or

stomach contents in a 100 ml flask and acidify thecontents with tartaric acid. Take a filter
paper previously moistened with 10 % of guaiacol in alcohol and 0.1% of aqueous copper
sulfate solution.Plug the mouth of flask and warm gently. Allow it to stand for 30
minutes. Observe the colour of paper. If cyanide is present, a blue colour develops.
b) in the plant sample: Preparation of sodium picrate paper-Dissolve sodium

bicarbonate 5 g and picric acid 0.5 g in 100 ml of distilled water. Cut filter paper into
strips of 2. x 6. size. Dip the strips in the reagent and dry in cool place.
Take the given sample in a test tube and add a few drops of water and chlorofom. Plug the
test tube with cotton, hanging the dried picrate paper inside the test tube. The paper
should not touch the fluid in the tube. Heat the tube gently till fumes evolve. Observe the
colour of paper.If the colour of paper changes from yellow to brown it indicates that the
plant sampleis positive for cyanide.(The leaves and stomach contents are to be frozen
immediately after collection inpolythene bag as CN is likely to evaporate).

134
Detection of fluorides: To a small quantity (1-3 ml) of urine or stomach contents add 3
ml of sodium hydroxide solution in a glass or porcelain dish. Add a little quantity of
powdered glass and mix thoroughly. Apply moderate heat till dry. Add 10 ml of
concentrated sulfuric acid and cover the dish with a small plate from the under surface of
which is suspended a drop of 5% sodium chloride solution. Place a small piece of ice on
top of the plate to prevent evaporation of the drop. Heat gently for 3-5 min., carefully
remove the drop and examine under low power of microscope. If the given specimen
contains fluorides, silicon fluoride is formed which appears as small light pink hexagonal
crystals along the rim of the drop, whereas the crystals of sodium chloride are large and
square.
Detection of Nitrite: a) Draw blood (10 ml) without anticoagulant from an affected
animal and also from a known normal animal in 20 ml capacity test tubes.Place them in
boiling water bath for 45 minutes. Cool them.Observe the colour of the blood and the
surface.Blood sample containing nitrite is Salmon pink in colour, does not pull away
fromthe side and the surface is level or concave. Normal blood sample is chocolate
brown,pulls away from the side of tube and the surface is convex.
b)In a plant sample: Dissolve 0.5 g of diphenylamine in 20 ml of distilled water and

make up the volume to 100 ml with sulfuric acid. Store it in amber colored bottle. This is
a full strength solution and can be made into half strength by diluting with equal parts of
80% sulfuric acid. To test a plant, place a drop of the reagent on the cut surface of plant.
Observe the colour.A green to blue colour indicates the presence of nitrate.(A green to
blue colour with a half strength solution indicates positive (++) for nitrate, which could be
toxic to animal).
*****

134

Advances in Veterinary Antimicrobial Therapy and Forensic Toxicology

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RATIONAL MEANS OF ANTIMICROBIAL SELECTION IN

Absorption: The absorption and disposition of antimicrobial agents in the body

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Bacteriostatic (systemic) + bacteriocidal (systemic) Antagonistic

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Vaccine is preparation of processed, innocuous specific antigen sometimes

The antigens are of great help in:

• Inducing immunity in host.

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Vaccine failure in animals and birds:

Failures in vaccination are a common phenomenon which is being encountered by

Animal and Birds

1. Death of live vaccine

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1. Inappropriate route of administration

Animal or birds which are immunosuppressed:

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Death of live vaccine:

Death in storage of vaccine:

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Cold chain failure for the live vaccines:

Vaccine Production defect:

Inappropriate route of administration:

Inappropriate route of administration is of much greater significance in the failure of an

Administration of passively protected animal/bird:

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Vaccine given too late to animal/bird already infected:

Wrong strain or organism used and Non-protective antigens used

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Bacterial and Fungal Diseases

• Hemorrhagic Septicemia : Fixed smears of blood/throat swelling in ailing

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• RP/PPR/BVD: Anticoagulant blood at height of temperature/ Pre-scapular lymph

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2. Subconjunctival (bulbar conjunctiva): This technique requires only topical

3.Retrobulbar medications:are used infrequently for therapeutics. In cattle, the

4. Intravitreal-used infrequently: Antibiotics,antifungal drugs have been effectively used

5. Systemic-P.O., I.V. or I.M: Systemic administration is required for treatment of

Ocular dosage forms : Topical ophthalmic drugs are formulated as ointments,

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Antibacterial ocular drug therapy

Chloramphenicol: Broad spectrum, bacteriostatic. Soluble in both water and fat so it

Aminoglycosides: a.. Neomycin: Usually found in combination with other antibiotics.

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Polypeptides:a.Bacitracin: Bactericidal, active against gram positive microorganisms.

Cephalosporins: a.Cefazolin: Broad spectrum, first generation cephalosporin.Topical

Fluoroquinolones: Eg: Ciprofloxacin ,Levofloxacin, Ofloxacin etc. Broad spectrum,

Antiviral ocular drug therapy

Idoxuridine: Frequency of administration is 1 drop every 4hrs until corneal re-

Vidarabine: 3%Ointment-it is poorly lipid soluble,so corneal penetration is minimal

Trifluridine: 1%Solution-Current drug of choice for feline herpetic keratitis. Antiviral

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