Guide to Microbial & Parasitic Horse Diseases

A Concise Guide to the Microbial and Parasitic Diseases of Horses
G.R. Carter1, P.A. Payne2 and E. Davis3 (Eds.)

Professor Emeritus of the Department of Medical Sciences and Pathobiology, Virginia-Maryland Regional
1
College of Veterinary Medicine, Virginia Tech, Blacksburg, Virginia, USA. 2Department of Diagnostic Medicine /
Pathobiology, College of Veterinary Medicine, Kansas State University, Manhattan, KS, USA. 3Department of
Clinical Sciences, College of Veterinary Medicine, Kansas State University, Manhattan, KS, USA.
 Preface
G.R. Carter, P.A. Payne and E. Davis (Last updated: 30-Nov-2007)
List of Microbial and Protozoal Diseases by Organ System

 Respiratory System
 Digestive System
 Nervous System
 Reproductive System
 Skin, Subcutaneous Tissue and Mammary Gland
 Musculoskeletal System
 Urinary System
 Hemolymphatic System
 Miscellaneous Diseases
Microbial Diseases
G.R. Carter and E. Davis (Last updated: 30-Nov-2007)
 Microbial Diseases A to D
 Microbial Diseases E to F
 Microbial Diseases G to L
 Microbial Diseases M to R
 Microbial Diseases S to Z
 Immunization Summary
Parasitic Diseases
P.A. Payne and G.R. Carter (Last updated: 27-Mar-2008)
 Protozoan Diseases
 Helminths In English, en español
 Cestodes, Hydatidosis, Trematodes and other Trematodes
 Diagnosis, Treatment and Management of Helminth and Cestode Infections
 Arthropods
 Fly and Mosquito Control
 Ticks, Mange, Pediculosis (Lice), Chiggers / Harvest Mites (Trombiculidiasis) and Straw Itch Mites (Forage Mites)
Selection, Collection, and Submission of Specimens for Diagnosis

Sources for Additional Information

List of Microbial and Protozoal Diseases by Organ System
G.R. Carter1, P.A. Payne2 and E. Davis3
1
College of Veterinary Medicine, Virginia Tech, Blacksburg, Virginia, USA. 2Department of Diagnostic Medicine-
Pathobiology, College of Veterinary Medicine, Kansas State University, KS, USA. 3Department of Clinical
Sciences, College of Veterinary Medicine, Kansas State University, Manhattan, KS, USA.
Microbial Diseases: A through D

G.R. Carter1 and E. Davis2
1
College of Veterinary Medicine, Virginia Tech, Blacksburg, Virginia, USA. 2Department of Clinical Sciences,
College of Veterinary Medicine, Kansas State University, Manhattan, KS, USA.
List of Microbial and Protozoal Diseases by Organ System | Microbial Diseases : A through D | E through F | G
through L | M through R | S through Z | Immunization Summary | Parasitic Diseases | Selection, Collection, and
Submission of Specimens | Table of Contents
Table of Content
 Actinobacillus equuli Infection

 African Horse Sickness
 Anthrax
 Aspergillosis
 Blastomycosis
 Borna disease
 Botulism
 Candidiasis
 Clostridial Enterotoxemia of Horses
o Clostridiosis
o Clostridia-associated Enterocolitis of Horses
 Coccidioidomycosis
 Colibacillosis
 Colitis X
 Contagious Equine Metritis
 Corynebacterium Pseudotuberculosis Infection
o Ulcerative Lymphangitis
o External and Internal abscesses
 Cryptococcosis
 Dermatophilosis (Rain scald)
 Dermatophytosis (Ringworm)
Actinobacillus equuli Infection

(Sleepy foal disease)
This is frequently an acute disease of very young foals characterized by diarrhea and bacteremia with possible
serious complications.
Cause
The Gram-negative coccobacillus, Actinobacillus equuli, a commensal in the intestine of solipeds.
Occurrence
The infection occurs worldwide in foals 12 - 72 hours postpartum and also in older horses. The agent may persist
on premises resulting in repeated infections.
Transmission
The foal may acquire the organism in utero, during parturition or after. Infection may be oral or via the umbilicus.
Migrating strongyles may carry the organism and infect young foals.
Clinical Features
Signs begin with fever, depression, a reluctance to nurse and diarrhea. Death may follow in 24 hours. Those
living several days may develop a bacteremia followed by a purulent nephritis, meningitis, pneumonia, peritonitis
or septic arthritis. Lesions may be minimal in peracute cases.
Older horses may have purulent arthritis and infected aneurysms leading to various infections. Abortion has also
been attributed A. equuli.
Diagnosis
There are a number of enteric diseases of foals that can be confused with Actinobacillus equuli infection (see
Foal Diarrhea and Septicemia).
A definitive diagnosis requires the isolation and identification of the pathogen.
 For culture and histopathology: In the live animal, feces, unclotted blood for culture (10 - 20 ml), joint fluid,
and transtracheal aspirates if pneumonia is suspected. If a necropsy is performed, portions of affected
tissues and vital organs, both fresh and fixed, should be submitted. Bone marrow cultures of ribs or long
bones may be more useful if the foal has been dead for several hours.
 The causal bacterium can be isolated and identified without difficulty. The gross and microscopic pathologic
changes may offer supportive evidence in a diagnosis.
Treatment
 This is usually administered empirically before the results of the antibiotic susceptibility test are received.
Broad spectrum and other antibiotics are used; the combination of amikacin sulfate and sodium ampicillin
has been effective in foals. Gentamycin / penicillin have been useful in adults.
 Comprehensive supportive care with fluid therapy as indicated.
Prevention
 Prophylactic administration of broad-spectrum antibiotics is indicated in situations such as failure of

adequate transfer of colostrum.
 Sanitary practices at parturition including disinfection of the umbilical stump. Foaling areas should be
disinfected.
African Horse Sickness

African horse sickness is an arthropod-borne, viral disease which is manifested in a severe highly fatal form as
well as chronic and mild forms.
Cause
Each of nine immunologically distinct serotypes of an orbivirus (Reoviridae) can cause the disease. The
distribution of serotypes varies with regions. There is a group specific complement fixation antigen.
Occurrence
This disease, which is endemic to the African continent, has spread in recent years to a number of Middle
Eastern countries, Portugal, Spain, Pakistan, and India. Large numbers of Equidae have had to be destroyed to
control outbreaks. The disease has been largely controlled outside of Africa.
Horses, mules, donkeys, zebras and dogs are naturally susceptible. Elephants, dogs and zebras are thought to
be reservoirs of the virus.
Transmission
The virus serotypes are transmitted by biting arthropods, particularly members of the Culicoides (biting midges;
no-see-ums).
Pathogenesis
The primary sites of replication are thought to be lymph nodes, lungs and spleen. Following viremia, endothelial
cells are infected with viral replication resulting in vascular damage and an increase in vascular permeability with
hemorrhage and edema.
Clinical & Pathologic Features
The disease occurs in severe, chronic and mild forms. In the severe pulmonary form there is acute onset of
paroxysmal coughing, choking, and frothy fluid from the nostrils, labored breathing, high temperature and edema
of the respiratory tract. The course is rapid and may be as short as five days.
The more chronic form is characterized by hydropericardium, hemorrhage and edema of the subcutis of the head
and neck regions. Swelling may also involve eyelids, brisket, and ventral aspects of thorax and abdomen. Some
horses may exhibit signs of both pulmonary and cardiac disease, whereas others may only experience a mild
transient infection with fever and loss of appetite for several days followed by recovery.
Mortality usually ranges from 20 to 95%.
Lesions observed at necropsy vary according to the form of the disease and may include edema of the lungs,
hydrothorax, and gelatinous exudates in the subcutaneous, interlobular, and intramuscular sites and lymph
nodes.
Diagnosis
Some diseases that could be confused with African horse fever (AHF) are: surra, anthrax, equine infectious
anemia, equine viral arteritis, purpura hemorrhagica, chemical and plant poisonings.
A presumptive diagnosis may be made in endemic areas on the basis of history, clinical signs and pathologic
changes. Laboratory confirmation is essential.
 Clinical specimens: freshly collected and refrigerated whole blood taken at or before the febrile period and
spleen at necropsy; serum.
 The virus is isolated in one day old mice inoculated intracerebrally, in embryonated eggs or in various cell
cultures. The brains of infected mice are used as a source of antigen for serological tests.
 The virus and serotype are identified by virus neutralization tests or immunofluorescence.
 ELISA, complement fixation and agar gel immunodiffusion procedures are used. for detection of antibodies
and antigen.
 A RT (reverse transcriptase) PCR procedure has been used to detect viral nucleic acid.
Treatment
None.
Prevention
 Strict import regulations are enforced to prevent introduction of AHS virus into countries free of the disease.
The US requires a two-month quarantine of Equidae from Africa.
 In outbreaks affected animals are slaughtered; those not affected are vaccinated with the polyvalent vaccine.
 Modified live polyvalent virus vaccines of mouse or cell culture origin are generally effective. The polyvalent
vaccine may be followed by a homologous type vaccine when the virus has been typed.
 Prevent exposure of animals to potential vectors and control of the latter with insecticide sprays.
Anthrax
Anthrax is a subacute to acute, toxemic bacterial disease of warm-blooded animals and humans. The disease in
Equidae is infrequent except in endemic regions.
Cause
The cause is Bacillus anthracis, a large, gram-positive, spore-forming bacillus. Virulence of strains depends on
possession of a polypeptide capsule and the capacity to produce toxin. The protein exotoxin consists of
protective antigen (PA), a lethal factor (LF) and an edema factor (EF).
The highly resistant spores are killed by steam under pressure and in the autoclave at 121°C for 15 minutes and
boiling for 40 minutes.
Spores can survive for decades in the soil; flooding may disseminate them. Contaminated feed, oil-cake,
tankage, bone meal, hides, other animal products and anthrax carcasses are other possible sources of spores.
Occurrence
The disease occurs worldwide mainly in areas where the highly resistant spores are prevalent (endemic areas).
Anthrax usually appears periodically in these locales. In horses it is most often sporadic, but multiple cases can
appear in endemic regions. The disease in ruminants is acute and in the horse most often subacute but also
terminating in death.
Mechanical transmission by biting flies has been reported.
Pathogenesis
Spores enter most often by ingestion; infrequently by inhalation or wounds. When ingested, spores carried by
macrophages lodge in the pharyngeal or intestinal mucosa where they germinate. The tripartite exotoxin
produces massive local hemorrhagic edema and vegetative cells invade the lymphatics, and when these are
overwhelmed, bacteremia and septicemia usually follow with death within hours.
The incubation period is 2 - 3 days and the course 1 - 4 days. Horses may be found dead. Signs include high
temperature, depression, dyspnea, edema of the neck, ventral chest and abdomen, and severe colic and
dysentery. Unclotted blood is frequently discharged from body openings.
The principal pathologic features are hemorrhagic edema and general vascular damage. Most cases terminate
fatally. Rigor mortis may be incomplete.
Diagnosis
It should be kept in mind that anthrax may occur in endemic regions when vaccination has been neglected.
Consider acute infectious diseases such as salmonellosis, and leptospirosis; acute poisonings such as arsenic,
bracken fern, sweet clover, and lead; colic, purpura hemorrhagica; and sudden death from lightning or sunstroke.
To prevent sporulation, the carcass should not be opened.
 Clinical specimens: At lease two swabs and two smears of peripheral blood from, for instance, an ear vein.
 With experience, a diagnosis of anthrax can be made on the basis of finding typical large, capsulated rods in
smears stained by Giemsa, Wright's, or Loeffler's methylene blue. However, it is advisable when possible to
isolate and identify B. anthracis. It should be remembered that clostridia (large gram-positive rods) invade
carcasses shortly after death.
 The anthrax agent, viable or dead, can be identified by florescent antibody staining and by a polymerase
chain reaction (PCR) procedure. A rapid (same day) PCR based test for identifying B. anthracis is employed
in Public Health laboratories.
 Western blot and ELISA are used to detect antibody.
Treatment
 Early treatment with penicillin, tetracyclines, amoxicillin, ciprofloxacin, erythromycin, chloramphenicol,

enrofloxacin, streptomycin and sulfonamides.
 Vaccination of well animals; long acting tetracyclines for in contact animals. Only those animals treated in
the early stage of infection survive.
Prevention
 Annual vaccination with Sterne's spore vaccine in endemic areas; two doses, one month apart, are given
horses, with an annual booster.
 Anthrax is a reportable disease in many countries requiring the application of strict regulatory measures.
 As mentioned above carcasses should not be opened as spores form in the presence of air. Carcasses
should be incinerated at the site of death, taken to a rendering plant (with great care to prevent
contamination) or buried deeply and covered with quick lime.
Public Health Significance

Humans are highly susceptible to anthrax. Great care must be taken in handling infected Equidae to avoid
infection of people and animals.
Aspergillosis
Aspergillosis is a noncontagious fungal disease of a number of animal species which occurs in several different
forms.
Aspergillus fumigatus is the main species involved. Other potentially pathogenic species are A. flavus and A.
nidulans.
These fungi occur widely in nature, and the usual mode of infection is by inhalation of airborne spores (conidia)
with the production of granulomatous lesions in the respiratory tract from which there may be dissemination to
other tissues and organs.
Infections may also, but less frequently, begin in the alimentary tract. In the horse acute enteritis is a possible
predisposing factor in diffuse pulmonary aspergillosis.
Disseminated aspergillosis is more common in immunosuppressed animals and in those under prolonged
antibiotic treatment.
The principal forms of aspergillosis in the horse are as follows:
 Guttural pouch mycosis: Discussed later under this name.

 Equine abortion (as a result of Aspergillus infection): See Infectious Equine Abortion, under Reproductive
System.
 Pulmonary aspergillosis and intestinal aspergillosis of horses are rare. If they become systemic they are
almost always fatal and diagnosis is most often made following necropsy.
 Corneal ulceration. This is frequently caused by Aspergillus spp. Diagnosis includes detection of septate
hyphae in corneal scrapings.
Diagnosis
This is discussed under guttural pouch mycosis and infectious equine abortion.
 Diagnosis is usually based on the isolation and identification of the Aspergillus species and the finding of
typical septate hyphae in clinical material and tissue sections. Because this fungus is widespread in nature,
mere isolation may not indicate significance.
Blastomycosis
(North American blastomycosis)
Blastomycosis is usually a severe fungal disease, principally of dogs and humans, and rarely the horse.
The nature of the disease is similar in susceptible species. The canine disease has received the greatest
veterinary attention and is the basis for the following discussion.
Cause
Blastomyces dermatitidis, a soil-borne, dimorphic fungus. The mycelial phase occurs in soil that is moist, acidic
and rich in decaying vegetation; the yeast form occurs in vivo.
Occurrence
The disease in horses is rare and sporadic.
It is probably worldwide in distribution, although the number of cases reported outside of North America is
relatively small. The endemic area in the United States includes the Middle Western, southeastern, and
Appalachian states.
Pathogenesis
Infection is by inhalation of spores (conidia) and infrequently by a skin wound; however, most cutaneous lesions
are derived from primary pulmonary infection.
The infection may be confined to the lungs and regional lymph nodes or metastasize to produce the disseminated
disease with involvement of the skin, bone, eye and other tissues and organs.
Although there are usually a number nodules (granulomas) in the lungs and thoracic lymph nodes, in some cases
metastases may come from very limited pulmonary involvement.
Occasionally the infection is confined to lesions involving the skin. Such infections may persist for months.
The incubation period is variable and may be as long as several months. The course likewise is variable.
Clinical signs depend on the stage and extent of the disease. Fever, coughing, dyspnea, anorexia, nasal
discharge, and progressive loss of condition are characteristic. The CNS is rarely involved. Subcutaneous
purulent, ulcerative granulomas may be seen in the disseminated disease.
Radiographs disclose swollen bronchial lymph nodes and nodular pulmonary lesions.
As the disease spreads, signs reflecting involvement of various organs are observed. The disseminated disease
is almost always fatal.
Diagnosis
The disease is rare in the horse and is unlikely to be diagnosed clinically unless advanced. Cryptococcosis,
nocardiosis, coccidioidomycosis, histoplasmosis, tuberculosis, chronic granulomatous infections of the skin and
pneumonia due to other agents should be considered.
Definitive diagnosis requires identification of the causal fungus.
 Chest radiographs may suggest blastomycosis.

 Diagnostic specimens are obtained by transtracheal aspiration or bronchoalveolar lavage, transthoracic
biopsy and from granulomatous nodules or abscesses involving the lungs and skin. An ocular tap is used if
the eye is thought to be involved.
 Examination of materials in wet mounts (KOH) for the characteristic thick-walled, single-budding yeasts.
Gram-stained smears disclose the characteristic fungal forms.
 The finding of the typical organisms in biopsies or affected lung is highly diagnostic.
 Culture at room(25°C) and incubator temperature(37°C) on appropriate media. Mycelial growth occurs at the
former temperature and the yeast form at the latter.
 Serological tests are of little value.
Treatment
Because of the rarity of equine blastomycosis there is little information on treatment. The treatments given below,
which are long term, have been used in dogs and humans.
 In very severe cases amphotericin B is included. Fluconazole has been effective in systemic candidiasis in
horses. Treatment must be continued for at least two months. The disease may recur in a substantial
number of cases in months or years. Horses inconsistently absorb itraconazole.
 In cases confined to the skin and subcutis, long term treatment is initiated and lesions are removed
surgically.
In spite of treatment, the prognosis is grave for animals with disseminated blastomycosis.
Prevention
There are no practicable preventive measures.
Blastomycosis is not considered contagious, but one should avoid contact with infectious material. There are rare
reports of humans acquiring the disease while performing human and animal necropsies.
Borna Disease
Borna disease is a neurologic, viral infection of horses, sheep and a wide range of other animals.
Cause
A single-stranded RNA virus, the only species in the family Bornaviridae.
Occurrence
The disease, which has a low morbidity, occurs in Germany, Switzerland and neighboring countries. Serological
surveys in recent years have shown a wide distribution of antibodies to the virus in animals and humans in
Central Europe, East Africa, North America and Japan. The clinical disease has not been seen in animals in the
USA. In addition to horses and sheep, infection has been found in donkeys, mules, cattle, rabbits, llamas,
alpacas, ostriches and cats. Young horses are most susceptible. Other animal species have been infected
experimentally. Rabbits and guinea pigs are particularly susceptible. Infections in some animal species are
subclinical.
There are reports of a feline Borna disease virus (BDV) causing a spontaneous, non-suppurative
encephalomyelitis in cats called "staggering disease."
Transmission
The virus is present in the saliva and nasal secretions with spread by direct and indirect contact.
Pathogenesis
The agent enters peripheral nerves and passes to the central nervous system where it has been shown
experimentally to target the limbic/hypothalamic region.
The virus has been isolated from blood mononuclear cells.
The incubation period is estimated to be ≈four weeks.
Clinical signs include fever, dysphagia, salivation, hyperesthesia, tonic spasms, lassitude, somnolence and
paralysis. Roughly 90% of affected animals die about three weeks after the onset of signs. It resembles clinically
West Nile encephalomyelitis of horses and the well-known equine encephalitides. Although both sheep and
horses can be infected by aerosol, the natural means of transmission is still in doubt. There is some evidence
that humans can contract the infection.
Diagnosis
The equine encephalidides, West Nile virus infection, botulism, rabies, tetanus, Japanese B encephalitis, hepatic
encephalopathy and some plant poisonings could be confused with Borna disease.
Definitive diagnosis requires isolation and identification of the virus.
 Clinical specimens: brain, fresh and fixed. Serum.

 The virus can be propagated on the chorioallantoic membrane, in monkey kidney cells and lamb kidney
cells.
 Virus is detected in tissues by immunohistochemical and PCR procedures. Finding eosinophilic intranuclear
inclusions (Joest-Degen bodies) is supportive.
 An indirect immuofluorescence assay and ELISA are used to detect antibody.

As yet there is no evidence that humans can acquire Borna disease virus from animals. Serological surveys have
found that antibodies to BDV in humans are widespread in North America, East Africa, Japan and Central
Europe. The possible link between BDV infection and human psychiatric disorders is being actively investigated.
Botulism
Botulism is a noncontagious, neurotoxic, bacterial disease of a wide range of animals and humans.
Cause
Botulism is caused by Clostridium botulinum, a large, gram-positive, spore-forming, anaerobic rod. Its highly
resistant spores occur widely in soil.
The vegetative cells produce neurotoxins in decomposing food, animals (carrion), and plant materials; rarely in
the alimentary tract and wounds. Types A, B, C, D, E, F, and G of C. botulinum have been identified on the basis
of antigenic differences in neurotoxins.
Types B, C, and D toxins have been encountered in equine botulism; type B botulism occurs mainly in foals two
weeks to 8 months of age. Common sources of toxin in equine botulism are moldy hay, grain, and haylage, and
dead rodents and birds in hay.
The toxins are inactivated by heating at 100°C for 20 minutes; spores are killed in the autoclave at 121°C for 15
minutes.
Occurrence
Botulism occurs worldwide as spores are ubiquitous. It is generally uncommon except in endemic areas where
spores are common. With good husbandry practices botulism is rare. Occurrence is usually sporadic, but
outbreaks do occur in endemic regions.
Forms of Botulism
In classic botulism toxin is produced in spoiled or decaying organic material as mentioned above. There is also
botulism resulting from the action of toxin produced in tissues. It is called toxicoinfectious botulism. Examples are
wound botulism, human infant botulism (gastrointestinal), and shaker foal syndrome (see below). In
toxicoinfectious botulism the toxin may be produced in gastric lesions (e.g., ulcers), liver necrosis, septic wounds,
and navel and pulmonary abscesses.
Shaker foal syndrome is caused by intoxication attributable to toxin produced by C. botulinum type B in the sites
and lesions just mentioned above. This disease of foals occurs sporadically from two weeks to eight months of
age,
Pathogenesis
In classic botulism the offending food is ingested and the toxin then absorbed from the gut and carried by the
blood to peripheral nerve synapses where it blocks the release of acetylcholine at motor end-plates leading to
muscular paralysis with death resulting from respiratory and cardiac failure.
Clinical Features
Depending upon the amount of toxin consumed, signs are noted 3 - 7 days after ingestion.
Clinical signs depend upon the amount of toxin absorbed. Generally there are progressive motor paralysis,
weakness, difficulty in chewing and swallowing, impaired vision, and finally death due to cardiac or respiratory
failure. Peracute cases may die without showing clinical signs. Ordinarily death ensues within 1 - 5 days.
Severe muscular weakness, motor paralysis, prostration, and the inability to rise are the principal clinical signs of
shaker foal syndrome. Foals may die without displaying signs. The course is usually less than 72 hours.
Diagnosis
Rabies, equine encephalomyelitis, equine protozoal myeloencephalitis, ragwort poisoning, forage poisoning and
other diseases affecting the nervous system should be considered.
Botulism has been called a "catch-all" clinical diagnosis. A definitive laboratory diagnosis is rather complicated
and not always practicable.
 Clinical specimens: Food including forage and carrion (e.g., dead animals in hay) suspected of harboring
botulinus toxin (handle with care). Serum or plasma: preferably 20 ml. Tied-off stomach and a portion of
small intestine if gastrointestinal botulism (rare) is suspected. Liver or a large portion thereof. In shaker foal
syndrome attempts are made to recover toxin and organisms (culture) from the lesions and sites referred to
above (shaker foal syndrome).
 The specimens, except serum, are processed (suspended in physiological saline) in order to obtain toxin.
The filtrate obtained or serum is used in animal tests, most frequently in mice, to demonstrate toxicity.
 Suspected food is sometimes fed to laboratory animals.
 If toxin is demonstrated in the serum, liver extract, food, etc., by animal inoculation, a strongly presumptive
diagnosis of botulism can be made. An ELISA has been used to detect the type of toxin in samples. A
definitive diagnosis depends on the identification of the type of C. botulinum involved.
 The culture of C. botulinum alone from food is not sufficient for a diagnosis, as the organism is ubiquitous.
An animal may die of botulism and not have a demonstrable amount of toxin in its serum by the mouse test.
 PCR tests have been developed to detect toxin in food and feces.
Treatment
 Botulinum antitoxin of the appropriate type, or a polyvalent product, has been used in treatment with variable
success; however, once signs have developed and toxin is fixed to receptors, the efficacy of antitoxins is
questionable.
Prevention
 Avoid feeding spoiled feed; prevent exposure to decomposing animals in hay and other feed, and on
pastures.
 In endemic areas foals of unimmunized mares can be vaccinated at a week to 10 days of age; weanlings
and yearlings are given the series of toxoid with an annual booster.
 To prevent toxicoinfectious botulism (e.g., shaker foal syndrome), mares in endemic areas are given type B
toxoid at the 8th, 9th, and 10th month of pregnancy, and with subsequent pregnancies vaccinate 4 - 6 weeks
before foaling.

Great care should be exercised in handling materials suspected of containing botulinus toxin.
Candidiasis
Candidiasis is an endogenous, fungal disease of some animals, including, infrequently horses, which is
characterized by infection of the skin, and mucous membrane of the alimentary and genital tracts.
Cause
The disease is caused by the yeast-like fungus Candida albicans, a commensal in the alimentary tract. There are
reports of other Candida spp., causing arthritis and endometritis in horses.
Occurrence
Candidiasis which is worldwide in occurrence is frequent in humans but uncommon in animals including Equidae.
Young and debilitated animals are most often affected. Prolonged antibiotic treatment and immunodeficiency may
predispose animals to candidiasis. Foals on prolonged antibiotic and corticosteroid therapy have developed
serious oral Candida infections.
Clinical Features
The oral form of the disease with ulcerative pseudomembranous inflammation of the mouth, extending
sometimes to the esophagus and stomach is observed in foals. Genital candidiasis is seen in brood mares and
ascending infections may lead to mycotic placentitis and abortion in late gestation. Moist skin creases are
occasional sites of Candida infection. Systemic infections involving vital organs have been described in horses on
prolonged antibiotic treatment.
Diagnosis
Candidiasis has to be distinguished from a number of other diseases affecting the mucous membranes of the
alimentary and genital tracts. White to gray patches consisting of pseudomembranes on the skin and mucosa are
characteristic.
 Collect material by deeply scraping the surface of affected tissue below the pseudomembrane or other
extraneous material. If Candida abortion is suspected, stomach contents, liver, lung and placenta should be
examined. Smears and wet mounts are examined for the characteristic yeast-like cells and pseudohyphae.
Definitive diagnosis requires the isolation and identification of C. albicans.
 Systemic infections are almost always diagnosed after necropsy by culture and histopathologic examination
of tissues.
Treatment
 Nystatin, clotrimazole, ketoconazole or iodine solutions are used topically.

 Amphotericin B or fluconazole are used to treat systemic candidiasis. Prolonged treatment is required.
Clostridial Enterotoxemia of Horses

Two kinds of clostridial enterotoxemia are recognized in horses, namely, clostridiosis and Clostridia-associated
enterocolitis in horses. We will discuss first, clostridial enterotoxemia in general then each of the equine forms
separately.
General
Clostridial enterotoxemia is an acute, highly fatal intoxication of farm animals including horses.
It is caused by the large, gram-positive, anaerobic, spore-forming rod Clostridium perfringens. Types A, B, C, D,
E, and F of this species have been identified on the basis their capacity to produce different exotoxins. Clostridial
enterotoxemias are worldwide in occurrence and the various types of C. perfringens are sometimes part of the
normal flora of the intestine of animals; type A is the most common.
Spores of the various types are present in soil and the environment. Enterotoxemia results when toxin-producing
strains of C. perfringens grow excessively in the intestine usually as a result of some enteric disturbance, such
as, overeating and abrupt changes in diet. The toxins are produced in the intestine and absorbed, resulting in
enteritis and toxemia.
Each of the C. perfringens types produces two or more toxins. The biological activity of the toxins of each type of
Clostridium perfringens of importance in horses is as follows:
All types produce an α toxin - lecithinase.
 Type A: enterotoxin - cytotoxic

 Type B: β toxin - lethal, necrotizing
 εtoxin - increases intestinal and capillary permeability, lethal
 Type C: β toxin - lethal, necrotizing
 Enterotoxin - cytotoxic
Clostridiosis
This is a clostridial enterotoxemia of horses of all ages caused mainly by C. perfringens type A and less
frequently by type C. Some cases of enterotoxemia in neonatal foals have been attributed to C. perfringens type
B.
There is sudden onset, fever, anorexia, and diarrhea with copious, watery, foul-smelling, dark, sometimes bloody
feces. The course is short, 24 - 48 hours, and many cases terminate fatally.
The type A toxins, lecthinase and enterotoxin, damage the mucosa of the cecum and colon resulting in
hemorrhagic typhilitis and colitis. On necropsy degenerative changes are seen in cardiac musculature.
Diagnosis
This is based upon demonstration of toxin in intestinal content or feces usually by inoculation of mice. If the test
for toxin is positive an ELISA may be used to identify the toxin type. Detail of the procedures are given below
under the discussion of clostridia-associated enterocolitis in horses
Treatment
 C. perfringens type A, B or C antitoxin or antiserum.

 Balanced electrolyte solution administered intravenously
 Oral metronidazole or chloramphenicol are considered effective if given early
Prevention
 Avoid changes in feeding that may lead to alteration of the microbial intestinal flora.
 Oral metronidazole or chloramphenicol is given to neonatal foals and horses at high risk. On farms that have
had problems it is recommend that all neonatal foals receive metronidazole daily for the first 2 weeks of life.
An example would be a farm that has lost a foal and the diagnosis was C. perfringens. All subsequent foals
for that year and the next year would also get metronidazole.
Clostridia-Associated Enterocolitis in Horses

This acute, enteric disease of foals and adult horses is now considered to be an enterotoxemia mainly caused by
toxigenic strains of C. perfringens or C. difficile.
Unlike C. perfringens type A, C. difficile is ordinarily not part of the equine normal intestinal flora but is found in
soil and the environment.
The A and B toxins of C. difficile, or the toxins of C. perfringens type A (lecithinase and enterotoxin) are
considered to be principally involved as well as less frequently types B and C. The A toxin of C. difficile is an
enterotoxin which causes injury to tissue and increased secretion into the intestine; type B toxin is a necrotizing
cytotoxin.
There are reports that Clostridium sordellii and C. cadaveris have also been associated with the syndrome.
It is thought that the disease occurs when there are excessive numbers of causal clostridia in the intestine
probably as a result of overeating or a change in ration. Stress and particularly prolonged administration of
antibiotics have been implicated.
Clinical Features
Lesions are those of a necrotiziing enterocolitis. Among the signs are diarrhea, dysentery, abdominal pain,
dehydration, convulsions, opisthotonus, ataxia, severe toxemia, sepsis and coma. Animals are often found dead.
Diagnosis
(For both clostridiosis and clostridia-associated enterocolitis in horses.)
The acute nature of the disease and history help distinguish the enterotoxemias from other enteric infections with
enteritis, diarrhea and dysentery. A definitive diagnosis requires laboratory confirmation.
 Clinical specimens: At least 20 - 30 ml of ileal content in a tied-off portion of intestine. It is advisable to also
include contents from the large intestine. In the absence of contents at least 25 g of feces should be
submitted. The contents or feces should be fresh, immediately refrigerated or frozen, and dispatched to the
laboratory.
 Extensive intestinal necrosis may be seen at necropsy.
 Intestinal content or fecal filtrate is inoculated into mice to determine if toxin is present. If present, the toxin
type of C. perfringens can be identified by an ELISA procedure. There is also an ELISA procedure for
identification of the toxins of C. difficile. PCR procedures are also available for the aforementioned purposes
in some reference laboratories.
 Smears from scrapings of intestinal mucosa are gram-stained to determine if clostridial organisms are
present. The presence of large, gram-positive rods in considerable numbers is supportive.
 The duodenal mucosa is cultured for C. perfringens and C. difficile. Culture of C. perfringens and/or C.
difficile in large numbers from the ileal contents and duodenum is supportive of a diagnosis of enterotoxemia
but is not definitive.
 A tentative laboratory diagnosis is sometimes based on the demonstration of toxin in the bowel contents by
mouse inoculation along with typical clinical signs, lesions, and history.
 A PCR procedure is available in some laboratories for the identification of C. perfringens types.
 Commercial kits employing ELISA, PCR and particle latex agglutination are available for the identification of
the toxins of C. difficile.
Treatment
 Balanced electrolyte solution administered intravenously

 Oral metronidazole or chloramphenicol is considered effective if given early. Antiserum is sometimes used.
Prevention
 Oral metronidazole or chloramphenicol are given to neonatal foals and horses at high risk
 Vaccines are not available for horses.
Coccidioidomycosis
This is a noncontagious fungal disease of domestic animals, various wild animals and humans. It is usually a
subclinical respiratory infection but has the potential to become systemic.
Cause
The soil- and dust-borne dimorphic fungus, Coccidioides immitis. The mycelial form occurs in soil.
Occurrence
The disease occurs in the arid (desert), acid-soil regions of the United States (mainly Arizona and California) and
some regions of South America where the very light, soil-borne arthrospores are common.
Dogs are affected most significantly; cats rarely develop the clinical disease; reports of the disease in horses are
few.
Pathogenesis
After inhalation of arthrospores(arthroconidia) to lungs, surviving spores may give rise to large spherules in lung
tissue which contain numerous endospores. These mature spherules break releasing large numbers of infectious
endospores. Most often infection results in a benign, subclinical form of the disease with little involvement of the
lungs. The disease may infrequently progress from granulomas in the lung to the disseminated form with
granulomatous lesions developing in various tissues and organs. This complication is usually attributed to an
impaired cellular immune response.
Clinical Features
Manifestations of coccidioidomycosis in the horse, which are rare, include nasal granuloma, abortion, and
systemic disease.
Clinical signs depend upon the stage of the disease. Signs of the disseminated disease may include: fever,
chronic cough, lameness, anorexia, enlarged joints, and diarrhea.
Diagnosis
Coccidioidomycosis is a rare cause of chronic pulmonary disease in the horse. Most diagnoses of
coccidioidomycosis, with the possible exception of cases in the dog, are made by microscopic examination of
material from lesions or by histopathologic examination after necropsy.
Pulmonary nodules can be seen in radiographs.
Note: The arthrospores of coccidioidomycosis are highly infectious for humans. Many laboratory infections have
occurred.
 Clinical specimens: Transthoracic aspirates if pulmonary disease is suspected. Exudate and biopsies taken
from nodules and lesions involving the liver, spleen and lymph nodes in the disseminated disease. Affected
tissues for histopathologocal examination. Paired sera, or sequentially drawn sera.
 Examination of specimens in wet mounts, smears and sections for the characteristic large spherules
containing endospores. Stains and fluorescent antibody may be used.
 Culture with identification is a time consuming process. Unlike some other dimorphic fungi the yeast form
(spherules) is not seen on either Sabouraud (25°C) or blood agar (37°C).
 Complement fixation (CF) test and the agar gel immunodiffusion (AGID) test are useful. The titer rises as the
disease progresses. If the CF and AGID tests are positive, it indicates a recent or active infection. It should
be kept in mind that many animals in areas where the fungus occurs in nature have antibodies.
Treatment
Little information is available on the treatment of the equine disease. The following drugs have been effective in
dogs and humans.
 Ketoconazole or fluconazole is given in some cases for as long as a year.

Although human infections are not ordinarily traced to animals, it is advisable to prevent human exposure to
infected animals. Arthrospores that are particularly infectious could possibly develop on dressings.
Colibacillosis
This is a severe bacterial, enteric infection of foals which begins shortly after birth and frequently progresses to a
septicemia. (See also foal diarrhea and septicemia)
Cause
It is caused by strains of the Gram-negative rod, Escherichia coli, a commensal in the intestine of all domestic
animals.
Some strains have the capacity to invade and become septicemic. Contributing to this may be the dosage of
bacteria and/or an inadequate amount of colostrums (failure of passive transfer FTP).
Transmission
The organism may be acquired from its surroundings orally or via the umbilicus.
Clinical Features
The disease is seen in foals 2 - 4 days old and the course with septicemia is usually 1 - 2 days.
The onset is sudden with pyrexia, depression, reluctance to suckle, respiratory difficulty and colic. Septic shock
from endotoxemia accounts for neutropenia, pyrexia and hypotension. With septicemia there may follow
involvement of lungs, septic arthritis, meningitis, osteomyelitis and commonly death.
It is estimated that E. coli accounts for about one quarter of all foal septicemias making it the most common
pathogen associated with neonatal sepsis.
When E. coli causes diarrhea it begins toward the end of the first week and is not followed by sepicemia.
Diagnosis
Septicemia may be caused by other bacteria (foal diarrhea and septicemia) thus a definitive diagnosis requires
isolation and identification of E. coli.
 Blood is cultured from the live foal or no longer than one hour after death as other bacteria invade the
carcass shortly after death. E. coli grows readily and is easy to identify. Recovery of the organism from
various organs some hours after death is not necessarily significant.
Treatment
Many strains of E. coli are resistant to commonly used antimicrobial drugs. Susceptibility testing may be useful
for later cases.
 Adequate colostrum is important. Test for FTP (failure of passive transfer). Greater than 800mg of IgG per
deciliter (dl) indicates an adequate passive transfer of colostral antibodies. If colostrums is not available 2 - 4
liters of plasma may be administered.
 Ampicillin (or penicillin) combined with amikacin is recommended for septic foals; amikacin is effective for
the E. coli.
 General supportive therapy including fluid replacement for dehydration.
Prevention
 Prophylactic administration of broad-spectrum antibiotics, or amikacin plus penicillin is indicated in some

situations.
 Sanitary practices at parturition including disinfection of the umbilical stump. Foaling areas should be
disinfected
Colitis-X
This is an non-contagious, peracute, fatal disease, mainly of adult horses.
Cause
Although the precise cause is not known it is widely thought that the disease is an enterotoxemia caused by C.
difficile.
Occurrence
The disease is seen occasionally with one or more horses being involved. It is usually associated with stress
such as those resulting from surgery, transport, and lack of food or water.
Clinical Signs
These include rapid breathing, tachycardia, sometimes colic, severe depression, profuse watery diarrhea,
hypovolemic and septic shock and great dehydration. Death occurs in 3 - 48 hours.
Diagnosis
Clinical features resemble those of acute salmonellosis, Potomac horse fever, clostridial enterotoxemias and
endotoxemia. The cardinal characteristics are severity, short course and unknown cause.
Treatment
 Given the rapid onset and short course of the syndrome treatment is not usually effective.
 Large amounts of intravenous fluids are given to cope with dehydration.
 Flunixin meglumine may be is administered for toxemia. The nonsteroidal anti-inflammatory drug
phenylbutazone has also been used.
 Metronidazole, penicillin and other antibiotics are sometimes administered.
Contagious Equine Metritis
Contagious equine metritis (CEM) is a highly contagious, bacterial, venereal disease of horses.
Cause
The cause is the fastidious, gram-negative rod, Taylorella equigenitalis.
Although the stallion may carry the causal agent, it does not show clinical signs. Mares may also be
asymptomatic carriers.
Occurrence
It has been reported from Australia, England, Ireland, a number of European countries and the United States. It is
most prevalent in Europe and rare in North America. A recent occurrence of the disease in the US was traced to
horses imported from Europe.
Transmission
It is mainly spread during mating but also by contact with fomites and via equipment and instruments.
Clinical Features
Infection is followed by the development of an edemic endometritis, cervicitis, and vaginitis with copious,
mucopurulent vaginal discharge. Mares may remain infected for several months.
There may be female infertility, estrus cycle of abnormal length, female infertility (usually temporary), weak
neonatal foals, and possible abortion. The female fetus may become infected leading to a subsequent mare
carrier state.
Diagnosis
The copious mucopurulent vaginal discharge occurring after breeding or during the breeding season is highly
suspicious. Bacteria other than T. equigenitalis can, on occasion, cause a purulent metritis in mares.
All suspected cases should be reported to regulatory authorities.
The disease can only be diagnosed definitively by the isolation and identification of the causal agent.
 For culture: Swabs from the cervix, urethra, and clitoral fossa including the clitoral sinuses of the mare and
the urethral fossa and penile sheath of the stallion should be refrigerated and sent to the laboratory in a
transport medium (preferably Amies) as soon after collection as possible. Regional laboratories may provide
suitable swabs and transport media.
Repeated swabings may be necessary to confirm the carrier state in stallions.
 A polymerase chain reaction procedure has been developed for the demonstration of the causal organisms
in clinical materials that are culturally negative.
 For serology: Clotted blood samples or serum.
Among the serologic tests used are: complement fixation (CF), passive hemagglutination, ELISA, and
agglutination (plate and tube).
Serologic tests may serve as an aid in identifying infected mares, but they are not reliable for detection of
carriers.
 Stallions can be test-mated to susceptible mares and the latter screened by culture for T. equigenitalis.
Treatment
 Carrier stallions are treated by cleansing the penis and sheath with various antiseptics, e.g., chlorhexidine
surgical scrub, followed by nitrofurazone ointment.
 Treatment of mares with antimicrobial drugs is not always effective even though T. equigenitalis is broadly
susceptible to antibiotics. Many mares remain clitoral carriers after treatment.
 Irrigation of the clitoral fossa with chlorhexidine and application of nitrofurazone ointment is sometimes
successful in eliminating the carrier state.
Prevention
 This is a reportable disease in North America. Importation to the US of noncompetitive entertainment horses
for no longer than 90 days is permitted.
 Quarantine or isolation with attempts to eliminate actively infected animals and positive carriers by the
measures described above and surgery (clitoral sinusectomy).
 Antibiotics added to semen inactivate the organism.
Corynebacterium Pseudotuberculosis Infections

The small, gram-positive bacterium, Corynebacterium pseudotuberculosis, causes two significant diseases,
ulcerative lymphangitis in horses and mules, and external (pectoral) and internal abscesses in horses.
The causal agent is a facultative intracellular parasite that produces exotoxins. It may remain viable on fomites
and in soil for months. Two biotypes are recognized one of which causes disease in small ruminants and the
other in horses and mules.
Discussion of the two forms of equine C. pseudotuberculosis infection follows.
Ulcerative Lymphangitis
Ulcerative lymphangitis is a contagious disease of horses and mules, characterized by the development of
nodules along lymphatics in the region of the fetlock.
The disease occurs most commonly in tropical and subtropical countries and is infrequently seen in the United
States except for California.
The main source of the causal bacterium is pus discharged from nodules. As mentioned, causal agent can
survive on fomites and in the environment for months. The organisms gain entrance via wounds and abrasions
usually in the fetlock area. The infection progresses slowly and the inflammation and swelling may cause
considerable pain. The nodules, which may extend upward on the leg, eventually rupture leaving ulcers that
exude greenish-tinged pus. Some infections persist and become chronic.
Diagnosis
The disease is clinically characteristic and where it is frequent, a laboratory diagnosis is not usually sought. A
definitive diagnosis requires isolation and identification C. pseudotuberculosis.
 For culture: Pus is collected on a swab, preferably from an excised developing nodule. Discharging nodules
may have considerable extraneous bacteria.
Treatment
 Penicillin G given IV alone or in combination with rifampin orally until lesions resolve ,then trimethoprim sulfa
or rifampin is administered orally to prevent relapses,
 Some the nodules may be dealt with surgically.
 Heat packs, poultices and hydrotherapy; irrigation, and the application of ointments.
Prevention
 If feasible infected animals should be isolated. Avoid crowding and circumstances that contribute to injuries.
Improvement in sanitation if indicated.
External and Internal Abscesses

(Pigeon breast, pigeon fever)
External (pectoral) abscesses occur in horses in southwestern US during the late summer and fall.
The mode of infection is via skin wounds and abrasions with arthropods such as stable and domestic flies and
Habronema spp. larva considered to be mechanical vectors. Various fomites may also be involved in spread.
Usually multiple abscesses occur in the lower pectoral region and extend along the ventral abdominal wall.
Abscesses may reach a diameter of 20 cm before rupturing.
About 8% of horses with external abscesses develop by hematogenous spread internal abscesses. These occur
most often in the lungs and liver and less commonly in the kidney and spleen. Generalized infection and abortion
have been reported.
Among the clinical signs are fever, anorexia, weight loss, lethargy and abdominal pain.
Diagnosis
External abscesses are sufficiently characteristic and familiar in California and arid western regions of the US to
afford a presumptive clinical diagnosis. Internal abscesses may be suspected when external abscesses are
present. Confirmation of their presence is based on clinical signs, diagnostic imaging. clinicopathologic data and
serology.
 A definitive diagnosis in pectoral abscesses is based on isolation and identification of C. pseudotuberculosis

from material taken from abscesses.
 The serological procedure employed for internal abscesses is the synergistic hemolysis inhibition test which
measures the IgG to the exotoxin. It is performed by California State Laboratory System and is not indicated
for external abscesses
Treatment
 For external abscesses: Surgical drainage; flush with iodine or other antiseptic solution.
 For internal abscesses the antimicrobial treatment is similar to that described above for ulcerative
lymphangitis.
 General supportive therapy.
Prevention
 Strict sanitary practices should be employed to prevent spread of the very resistant causal agent.
 Fly control, and routine deworming to control habronema.
 As yet there is no vaccine or toxoid available.
Cryptococcosis
Cryptococcosis is a subacute to chronic and occasionally fatal, fungal disease, mainly of dogs and cats, and
rarely of Equidae.
Cause
The cause, Cryptococcus neoformans, is a soil-borne fungus, which multiplies in avian feces and particularly in
that of pigeons; however, it is not found in the intestinal tract of live pigeons. It occurs worldwide. This oval
shaped, budding yeast has a wide polysaccharide capsule.
Pathogenesis
The mode of infection is by inhalation of dust-borne yeast cells to the upper and lower respiratory tracts.
The disease begins most commonly as a paranasal infection that often, if not treated, extends to the meninges
and brain (particularly in cats and horses), and lungs. Abortion has been reported in mares.
In the disseminated disease, metastases develop in various tissues and organs, and in the absence of treatment
it ends fatally. Impairment of cell-mediated immunity may increase susceptibility.
Clinical Signs
These will depend on the character and location of the infection. They may include: sneezing, cough, nasal and
ocular discharge, and with CNS involvement, ataxia, circling, blindness, and locomotor dysfunction.
Diagnosis
Paranasal cryptococcosis must be distinguished from other respiratory diseases.
 The disease in horses is almost always characterized by obstructive nasal growth(s) and can be
presumptively diagnosed on the basis of clinical signs and the demonstration of yeast-like cells (different
from those of blastomycosis and coccidioidomycosis) in wet mounts(nigrosin or India ink to display capsules)
and Gram-stained smears of material taken from lesions.
 Clinical specimens: Material is collected aseptically from the nasal passages in the paranasal form. It may
be advisable in certain cases to take biopsies. If there is evidence of involvement of the brain and meninges,
cerebrospinal fluid (CSF) should be collected. At necropsy: Portions of affected tissues, fresh and fixed, are
submitted. Serm.
 All materials collected, including CSF, are examined by stains and wet mounts, then cultured for C.
neoformans. Fixed tissues are examined for the typical lesions containing the yeast-like organisms.Although
C. neoformans is not the only capsulated cryptococcus, the association of a capsulated yeast-like organism
with the morphology of cryptococci from an animal with typical clinical signs or lesions is considered
sufficient for a firm diagnosis.
 A latex agglutination test is available commercially for the detection of C. neoformans antigen, in urine,
serum, and CSF. An indirect florescence assay for antibody is also used although a negative test does not
exclude cryptococcosis.
Treatment
There is little information available on treatment of the equine disease. What follows is based on
recommendations for dogs and cats. Treatment must be for extended periods.
 Amphotericin B and flucytosine (5-fluorocytosine) are used, alone or in combination. Fluconazole has also
been effective. Resistance to these drugs has been reported.

Because humans can contract this disease, human exposure to infected animals should be avoided. However,
humans are not thought to have been acquired the disease from infected animals.
Dermatophilosis
(Rain scald)
This contagious, bacterial disease of domestic and other animals is characterized by dermatitis of the superficial
layers of the skin.
Cause
It is caused by the gram-positive bacterium (actinomycete), Dermatophilus congolensis. This branching organism
segments into motile zoospores which contribute to its spread.
Occurrence
It occurs worldwide and is more prevalent in tropical and subtropical countries. The disease in horses is usually
sporadic but multiple cases are seen under some circumstances. Infected horses are the primary source of this
bacterium. It has not yet been shown to occur in nature.
Transmission
Spread is by direct and indirect contact, and fomites such as tack, brushes and blankets. Warm, moist and wet
conditions, and exposure to rain contribute to its occurrence and spread. Biting arthropods and trauma may
initiate infections. An infected individual may be the source of infection. Stress, poor condition and inadequate
nutrition contribute to susceptibility.
Clinical Features
The organism penetrates the epidermis from which it subsists and multiplies. Crusts and scabs are characteristic
features. In horses the lesions are seen most commonly on the dorsum and legs. Initial lesions may be
circumscribed but later they may coalesce resulting in an extensive encrustation. Additional signs may be
alopecia, matted and dirty hair, cracked skin, skin pustules and ulcers. Some lesions may be painful.
Diagnosis
Scabies, warts, dermatophytosis and pyoderma are among diseases to be considered. The characteristic
encrustations and scabs allow for a presumptive clinical diagnosis. Some clinicians consider laboratory
confirmation unnecessary.
 Clinical Specimens: Exudates, scabs, crusts, and plucked hair are collected. A definitive diagnosis can
usually be made by demonstrating the characteristic structures of D. congolensis in gram- or Giemsa-
stained smears. These structures include cocci and segmentation giving the appearance of "train tracks".
The organism may be more difficult to demonstrate in the chronic disease.
 Isolation, culture, and identification of D. congolensis. Although culture is not usually difficult, it is not
required for diagnosis. There is a good correlation between the results of the examination of smears and of
culture.
Treatment / Prevention
 Affected horse(s) should be isolated. Acute cases are often of short duration and clear up without treatment.
 This gram-positive organism is susceptible to many antibiotics. Single large doses of penicillin or
tetracyclines are preferred for severe cases. Tetracycline IV or oral doxycyline have been effective,
particularly in persistent cases.
 Washing with antibacterial shampoos (betadine scrub) and gently removing scabs may be beneficial and
reduce spread. Mild cases may respond to good, regular grooming.
 Control of ectoparasites.

Humans have contracted dermatophilosis on rare occasions from infected animals resulting in pustules on the
hands and forearms. Immunosuppressed individuals are at particular risk.
Dermatophytosis
(Ringworm)
This is a contagious, fungal disease characterized by infection of the keratin-containing tissues (skin, nails, and
hair) of many animals and humans.
Cause
The dermatophytic fungi affecting horses are, most importantly, Trichophyton equinum and T. mentagrophytes,
and less frequently Microsporum canis, M. gypseum, and T. verrucosum.
These fungi with the exception of M. gypseum are parasites on animals. Microsporum gypseum occurs naturally
in soil.
Occurrence
Dermatomycosis is a common disease of horses occurring worldwide. It is common in young horses under
stress, e.g., young race horses in training and associated with other horses that may be carriers.
Transmission
Spread is by direct and indirect contact. Infected animals and fomites (e.g., brushes, saddles, etc.) are the usual
sources of the dermatophytes.
Pathogenesis
The infections are superficial, starting in the stratum corneum and invading hair follicles and hair, with the
production of hyphae and spores within (endothrix) and/or on (ectothrix) hairs. The lesions spread out from a
central locus resulting in circular and patchy lesions. The circular or roughly circular lesions of ringworm are
variable in size and develop from raised plaques on the skin. The hair becomes thin, broken, and finally there is
bareness that may become scaly and scabby. In the horse lesions are frequently seen on the head and neck,
and in the saddle and girth areas. It is most common in young, stressed horses; e.g.,race horses in training and
associated with other horses.
Figure 1. Circular crusty lesions of ringworm (dermatophytosis).

Figure 2. Circular crusty lesions of ringworm (dermatophytosis).
Diagnosis
A clinical diagnosis is often made based on the characteristic circular, patchy lesions. Eczema, dermatitis,
pyoderma, dermatophilosis, and mange are among the diseases that should be considered.
The following laboratory procedures provide a definitive diagnosis.
 If feasible, examine lesions with a Wood's lamp; M. canis fluoresces (greenish color). Negative fluorescence
does not exclude ringworm.
 Clinical specimens: Plucked hair (especially those that fluoresce) and skin scrapings from the edge of
lesions. These are sent to the laboratory in a paper envelope (to reduce moisture and the growth of
saprophytic fungi).
 Some veterinarians inoculate one of the several commercial media (Dermatophyte Test Media, Fungassay,
etc.) that are available for the selective growth of dermatophytes. If the results are equivocal, the media may
be submitted to a diagnostic laboratory for interpretation.
 The plucked hair and skin scrapings are first examined microscopically in wet mounts for the presence of
spores and other fungal elements.
 Appropriate media are inoculated. Isolation and identification may take several weeks.
Treatment
Treatment will depend to some extent on economic considerations.
 Isolation of infected animals if feasible. It is often a self-limiting disease.

 Topical: clipping, and thorough washing with mild soap; for local lesions, application of clotrimazole or
miconazole, Lugol's iodine, equal parts tincture of iodine and glycerin. Sprays such as an aqueous solution
of lime-sulfur (2 - 4%), 0.5% sodium hypochlorite , or 1% povidone iodine.
 Systemic treatment is rarely indicated. The imidazole drugs referred to above and griseofulvin are
considered effective. The expense of systemic treatment may be prohibitive. It is rare that a horse with a
normal immune system will require systemic antifungal therapy for dermal dermatophytosis.
Prevention
 Infected animals should be separated from those showing no signs of infection although the latter may have
inapparent infections.
 As dermatophyes can survive for long periods, grooming implements and tack, and premises must be
scrupulously cleaned and disinfected to prevent reinfection.

Humans are frequently infected with ringworm fungi of animal origin. Contact with infected animals, their hair
clippings, bedding, cages, etc., should be avoided.
Microbial Diseases: E through F

1
Table of Content
 Epizootic Lymphangitis
 Equine Adenoviral Infections
 Equine Brucellosis
 Equine Coital Exanthema (Genital Horsepox)
 Equine Encephalomyelitis
 Equine Encephalosis
 Equine Granulocytic Ehrlichiosis
 Equine Herpesvirus 1 (Equine Viral Abortion)
 Equine Herpesvirus 2 Infection
 Equine Infectious Anemia (Swamp Fever)
 Equine Influenza
 Equine Rhinopneumonitis (Equine Herpesvirus 4 Infection)
 Equine Rhinovirus Infection
 Equine Viral Abortion (Equine Herpesvirus 1 Infection)
 Equine Viral Arteritis
 Eumycotic Mycetoma (Maduromycosis)
 Foal Diarrhea and Septicemia
Epizootic Lymphangitis
Epizootic lymphangitis is a chronic, contagious, fungal disease of horses characterized by granulomatous lesions
of the skin and lymphatics.
Cause
It is caused by the dimorphic fungus Histoplasma farciminosum. Although the organism occurs in nature, most
cases are considered to derive from infected animals. The yeast form occurs in the animal host and the mycelial
form in nature. The organism closely resembles H. capsulatum.
Occurrence
It occurs in Asia, North Africa, and some Mediterranean countries. Outbreaks occur when numbers of horses
from different sources are collected in one place.
Mode of Infection/Transmission
The organism from lesions, directly or indirectly, gains entrance via wounds and abrasions. Flies may spread the
fungus mechanically.
Clinical Features
The incubation period is several weeks. The disease is characterized by the development of pyogranulomatous
nodules, involving the skin, mucous membranes, superficial lymph vessels and nodes, which ulcerate and
discharge pus. Most lesions develop on the limbs but they may also be present on the sides, back, and neck. A
pulmonary form has been reported and lesions may involve the eye, nasal mucosa and other tissues.
The morbidity is high but the mortality is low. Animals that recover are immune to reinfection.
Diagnosis
Where glanders occurs the mallein test is used for differentiation. In addition material from lesions of glanders is
negative for the characteristic yeast forms in pus from lesions of epizootic lymphangitis. In endemic regions a
presumptive diagnosis is made based on the characteristic lesions. Definitive diagnosis requires isolation and
identification of the fungus.
 Fresh pus is collected from incised nodules to reduce extraneous organisms. A diagnosis is usually based
on the demonstration of the typical yeast-like cells of H. farciminosum in wet mounts of pus. The organisms
are found in macrophages.
 For culture, appropriate media are inoculated and incubated at 37°C and 25°C to obtain the yeast phase and
the mycelial phase, respectively. Growth and identification of these forms are necessary.
 Fluorescent antibody staining of clinical material can provide a rapid diagnosis.
Treatment
 In general, treatment has not been satisfactory. Iodides have been used orally and intravenously along with
surgical excision. Because of cost antifungal drugs such as amphotericin B and the imidazole derivatives
have not been used.
Prevention
The disease is reportable except in some countries where it is endemic.
 Isolation of clinical cases and elimination of those that do not respond to treatment. Quarantine and
slaughter in countries where the disease is reportable.
Equine Adenovirus Infection

Equine adenoviruses are found in the upper respiratory tract of many horses worldwide. They mainly cause
subclinical or mild upper respiratory infections in most horses, but they can cause serious upper respiratory
disease, conjunctivitis, a progressive pneumonia and diarrhea in Arabian foals with combined immunodeficiency.
This deficiency is inherited as an autosomal recessive characteristic resulting in the absence of functional B and
T lymphocytes. Severe infections have also been reported in neonatal foals lacking colostral protection. The
common mode of infection is inhalation and the source of the virus is infected or carrier horses.
Diagnosis
 Clinical specimens: Nasal and ocular swabs, conjunctival scrapings, lung tissue and paired serum samples.
 Adenoviruses can be isolated and identified in cell cultures. Finding characteristic inclusion bodies in
conjunctival scrapings and lung tissue sections is significant; however, one has to keep in mind that equine
cytomegaloviruses produce very similar inclusion bodies.
 Hemagglutination or other serological procedures are used to test paired serum samples for a significant rise
in antibody titer.
Equine Brucellosis
This infection, caused by Brucella abortus or B. suis is now rare in horses. The infection is acquired from infected
cattle or swine by ingestion of contaminated food or water or via penetration of the skin or mucous membrane.
The bacteremic phase of the disease with pyrexia is not usually evident. It is mainly recognized as a suppurative
bursitis involving the ligamental bursae of the poll ("poll evil") and/or withers ("fistulous withers"). There may be
an initiating blow or injury to the bursal area. Ill fitting harness or saddle may contribute to the inflammatory
process. Not all cases of poll evil and fistulous withers are associated with brucellae; other bacteria such as
Streptococcus zooepidemicus may be involved.
If brucellae are the cause horses will be positive to standard brucella agglutination tests and B. abortus or B. suis
can usually be isolated from fluid taken from an unopened bursa.
The most effective treatment is dissection and removal of the affected bursa. Considering that the brucellae
involved are highly infectious for humans (also cattle and swine) great care should be taken to avoid exposure.
Equine Coital Exanthema
(Genital horsepox)
This is usually a benign, venereal, viral disease, which occurs mainly during the breeding season.
Cause
It is caused by equine herpesvirus 3 (Herpesviridae).
Occurrence
This infrequent, worldwide disease is perpetuated by asymptomatic carriers.
Transmission
The virus is transmitted during breeding.
Clinical Features
It usually runs an uneventful short course of less than two weeks and is characterized by the formation of papules
followed soon by pustules then ulcers about two cm in diameter on the mucosa of the vulva, penis, and prepuce.
The ulcers heal with the production of scabs. Affected skin may lose pigmentation.
Although lesions are seen most commonly involving the genital tract, they may also occur in the mouth and
nostrils, on teats of the mare, and the muzzle of nursing foals.
Diagnosis
The lesions are sufficiently characteristic to allow for a reliable clinical diagnosis. Laboratory diagnosis is not
usually sought.
 Clinical specimens: Scrapings from the affected mucosa of the vulva and penis. Paired serum samples.
 The virus can be seen with the electron microscope and cultivated and identified in equine cell cultures.
Histological and cytological examinations for the characteristic inclusion bodies.
 Virus neutralization and complement fixation test can be used to detect rising titers.
Treatment
 Lesions are cleansed. Antibiotics may be used to control secondary bacteria. Six weeks sexual rest is
recommended.
Prevention
 Horses should not be bred if lesions are present. No vaccine is available.
Equine Encephalomyelitis
(Equine encephalitis)
This name refers to the equine encephalomyelitis caused by one of three antigenically distinct alphaviruses
(Togaviridae). The three diseases they cause are Eastern, Western and Venezuelan encephalomyelitis. Equine
encephalitis is also caused by a bornavirus (Bornaviridae), the flaviviruses (Flaviviridae), West Nile virus and
Japanese encephalitis virus.
Cause
The three causal alphaviruses are serologically related to each other and like other viruses in the genus multiply
in mosquitoes as well as in vertebrates. Some flaviviruses may amplify, WNV will amplify in mosquitoes when the
ambient temperatures are > 80 F day and night. This is why the disease is such a problem in late summer
months.
Transmission
The viruses are spread mainly by the bites of mosquitoes but also by ticks, lice, and mites. The natural reservoir
is wild birds and forest rodents, which are referred to as amplification hosts. Each of the three viruses has its own
cycle of particular mosquito species and amplification host. The mosquito is infected for life. The horse is
considered a dead-end host, except for VEE for which amplification may occur.
Occurrence
The occurrence of these three virus infections in horses may vary greatly from year to year, from a few to multiple
cases. In the temperate zones most cases are seen in the mid to late summer and in the tropics most often in the
wet season.
The geographic distribution of the three equine encephalitides is as follows:
 Western equine encephalomyelitis (WEE): Generally occurs west of the Mississippi; mortality rate is 20 -
40%. Also occurs in Canada, Mexico, and South America. Two antigenic variants occur; one, the more
pathogenic, is found in North America, and the other in South America.
 Eastern equine encephalomyelitis (EEE): Generally occurs east of the Mississippi; mortality rate is 90%.
Also occurs in Canada, Mexico, Caribbean islands, South and Central America. Viral subtypes have different
geographic locations.
 Venezuelan equine encephalomyelitis (VEE): Also occurs in Mexico, South and Central America and
southwestern United States; mortality rate is 50 - 80%. Viral subtypes occur.
West Nile virus occurs worldwide. In NA it is typically seen in mid to late summer.
Pathogenesis
The pathogenesis of the three alphaviruses is similar. The virus multiplies at the site of injection by the mosquito.
Then it travels by the lymphatics to regional lymph nodes where it multiplies in neutophils and macrophages and
initiates a viremia with subsequent infection and multiplication in other organs including the CNS. The extent of
the viremia and the damage to the CNS varies among the three viruses.
Clinical Features
The three encephalidides are clinically indistinguishable. They are characterized first by fever, and reluctance to
drink. About two weeks later neurologic signs appear which may include deranged consciousness, head
pressing, walking in circles, weight loss, seizures and finally recumbency and paralysis. As mentioned above
EEE and VEE have the highest mortality. Surviving horses may have visual and other neurological deficits. By
the time neurologic signs appear viremia has ceased.
WNV pyrexia, altered mentation, hyperesthesia, hyperreactivity or dementia. Initial week is generally worst,
subsequently improvement is noted. Complete resolution may take 6 months.
Diagnosis
Seasonal occurrence and a history of previous outbreaks often suggest viral equine encephalomyelitis. Rabies,
Borna disease, botulism, equine protozoal encephalomyelitis, neosporosis, some plant poisonings, moldy corn
poisoning (leukoencephalomalacia), tetanus, listeriosis, and other infections of the central nervous system should
be considered.
A definitive diagnosis is made by finding a substantial increase in specific antibody between paired sera or
isolation and identification of the virus.
 Clinical specimens: Whole brain or head; portions of the brain, fresh and formalized. Serum; paired samples
are preferre.
 Isolation, cultivation, and identification of the viruses using chicken embryos or cell cultures. The three
viruses can be differentiated by virus neutralization and the antigen capture ELISA for IgM for WNV.
 Examination of tissue sections of brain disclose characteristic microscopic changes with EEE, i.e.,
perivascular cuffing with neutrophilia. No gross lesions are seen.
 Complement fixation, hemagglutination inhibition, and virus neutralization tests are used to detect antibody.
Antibodies may develop 2 - 3 days after clinical signs. A rise in the titer between paired sera is significant.
Animals may die before there is an appreciable antibody response.
Treatment
 Supportive. Some horses may survive but have permanent CNS damage with the alphaviruses. The
prognosis for WNV is generally favorable for horses that stay standing. Once recumbent horses are less
likely to survive any of the encephalitidies.
Prevention
Mosquito control. Stabling during outbreaks.
 Inactivated bivalent or trivalent vaccines are currently available. There is no cross protection between
strains. The initial vaccine series should include a series of 3 vaccinations at 3 - 4 week intervals. Foals
should initially be vaccinated at 4 months of age. Depending on the geographic location boosters should be
administered 2 - 4 times annually.*
 Horses that recover from the disease are immune for life.

These viruses infect humans, sometimes seriously. Measures should be taken, including mosquito control, to
protect personnel who might be exposed when the disease occurs or is suspected.
*From, Davis, E. Refresher on equine immunity and vaccines. DVM magazine, Fall, 2007.
Equine Encephalosis
This disease of horses, caused by a species in the orbivirus genus (Reoviridae), was called encephalosis
because infections were usually subclinical and without CNS signs; however, a small number of peracute cases
were noted with neurological signs. It has features similar to African horse sickness also caused by an orbivirus.
Equine encephalosis has only been reported from southern Africa.
Five serotypes of virus have been identified and serologic surveys indicate a high incidence of infection with each
type. Brain edema, fatty liver degeneration, and enteritis are observed at necropsy. The orbivirus can be isolated
from organs and blood.
Equine Granulocytic Erhlichiosis
This is a sporadic, non-contagious, bacterial (rickettsial) disease whose wide host range includes horses and
burros.
Cause
The causal rickettsia is Anaplasma phagocytophilia (formerly Ehrlichia equi) which closely resemble the agent of
human granulocytic ehrlichiosis (HGE), tickborne fever and bovine petechial fever.
Occurrence
The disease occurs frequently in California and has been identified in some other states of the US and in
Canada, Europe and South America. Older horses are most severely affected; the disease is mild in young
horses. Natural infections occur in horses, burros. lamas, dogs, and some rodents.
Transmission
It is thought that the principal vector for horses is the tick Ixodes pacificus.
Clinical Features
The incubation period is 1 - 2 weeks. The disease in horses younger than a year is usually mild; some infections
are clinically inapparent.
Signs in older horses include fever, anorexia, mild anemia, icterus, petechial hemorrhages, edema of the limbs,
and reluctance to move. Neutropenia and thrombocytopenia. Recovery is usually spontaneous in 2 - 3 weeks
Diagnosis
Diseases to be considered include equine infectious anemia, piroplasmosis, purpura hemorrhagica, leptospirosis,
Potomac horse fever, and equine viral arteritis.
 Stained smears of blood and buffy coat are examined for the characteristic morulae (inclusions) of A.
phagocytophilia in neutrophils and monocytes. A PCR procedure can detect the DNA of the agent in buffy
coat. PCR at UC Davis is the routine test at this time.
 Paired sera: An indirect fluorescence assay (IFA) is used to detect a rising antibody titer. An IFA is available
for the diagnosis of the other ehrlichiosis of horses, Potomac Horse Fever.
Treatment
 Tetracyclines daily for at least a week are effective. Recovered horses are immune and no longer carriers.
Prevention
 Isolation of infected animals and strict control of ticks.

Anaplasma phagocytophilia is closely related but not identical, to the HGE agent. There is as yet no evidence
that the rickettsia of the equine disease causes HGE.
Equine Herpesvirus 1 Infection (see Equine Viral Abortion)
Equine Herpesvirus 2 Infection
Equine Herpesvirus 2 (EHV 2)
This virus occurs widely in the respiratory tract of horses. Its pathogenic significance is considered questionable
although it has been suggested as the cause of a "herpetic" keratoconjunctivitis.
Equine Infectious Anemia
(Swamp fever)
Equine infectious anemia (EIA) is a persistent viral disease varying widely in severity from subclinical to life
threatening.
Cause
A lentivirus (Retroviridae), which after initial infection, persists for life. Equids are the only reservoir of the virus.
Occurrence
Worldwide and all ages of Equidae are susceptible. The disease is more prevalent in swampy, low-lying areas
where mosquitoes are common. It is now infrequent in North America.
There remain pockets of infected animals in some states in the USA. Many infections are clinically
inconsequential; however, under some circumstances there are high morbidity and mortality.
Transmission
The virus is present in the blood of infected animals and transmission is mainly by blood-sucking flies,
mosquitoes, and also other biting arthropods, contaminated hypodermic needles and surgical instruments. The
amount of viable virus in vectors declines rapidly after a half hour. Transmission is dose dependent, i.e., a certain
amount of virus is necessary for infection. Infection can also be acquired by ingestion of contaminated food and
water. The fetus may be infected transplacentally, and neonates via the first milk.
Incubation period is usually 1 - 3 weeks, but may be as long as three months.
Clinical Features
Once infected the animal remains so indefinitely. Animals with the acute and chronic forms may have the
following clinical signs: depression, intermittent fever, progressive weakness, loss of condition and weight,
anemia, thrombocytopenia (acute stages) jaundice, edema of the lower chest, abdomen and limbs, and petechial
hemorrhages. The acute disease is particularly severe and the mortality is high; however, the overall mortality
rate is less than 30 percent. Horses with the chronic form may suffer relapses and die, or live for months or
years. Those with the inapparent form show no signs but remain permanently infected.
Diagnosis
Purpura hemorrhagica, ehrlichiosis, influenza, babesiosis, leptospirosis, severe parasitic infections, and various
anemias have features similar to EIA. It is frequently known that EIA occurs in an area.
 Serum is required for the agar gel immunodiffusion test (Coggins test). A positive test indicates clinical or
subclinical infection. All animals that are positive are potential sources of infection. Positive nursing foals
should be retested in six months if they have not nursed from an infected mother for 60 days.
 A competitive ELISA has been approved as an alternative official test. ELISA horse-side commercial kits are
available for the detection of antibody to equine infectious anemia virus. Because of possible false positives
with the ELISA a Coggins test is recommended for confirmation.
Treatment
 None except supportive therapy.
Prevention
 The requirements for testing vary considerably from state to state in the USA, and in other countries.
 All horses that test positive must be reported to federal animal health authorities in the USA. The options for
owners are euthanasia or branding and quarantining. The latter includes keeping the animal at least 200
yards from other equids for life. Negative horses on the premises should be retested periodically
 The spread of infection can be reduced by stringent insect control.
 Visiting mares and new horses should be isolated until a negative test is available.
 It is recommended that all horses have an annual test for the disease. Negative tests are required before
horses can enter exhibitions or competitive events. Immunization is not practiced.
Equine Influenza
Equine influenza is an acute, highly contagious, rapidly spreading viral infection of the respiratory tract of horses
and donkeys.
Cause
One of two antigenically related but not reciprocally immunogenic, serologic varieties of type A influenza virus,
designated A/Equi 1 and A/Equi 2. A/Equi 1 virus has not been recovered since 1980. Subtypes are designated
by their hemagglutinin and neuraminidase antigens; A/Equi 1 is H7N7 and A/Equi 2 is H3N8
The source of the virus is horses with apparent or inapparent infections. There is probably a short-term carrier
state.
Occurrence
It is worldwide in distribution and endemic in many regions. New Zealand is free of the disease. All ages are
susceptible and all animals in a group or stable may be affected.
Transmission
The mode of infection is mainly by droplet inhalation. The virus is present in saliva and nasal secretions.
Outbreaks are frequently associated with horse shows, sales, polo matches, racetracks, and other locations or
events where horses are commingled.
Clinical Features
The incubation period is usually 1 - 3 days but may be up to seven days. The course is 1 - 3 weeks in
uncomplicated infections.
The virus multiplies in, and destroys, epithelial cells of the trachea and bronchi. Severity, which ranges from
inapparent, mild to acute, is largely dependent on immune status. The young, old, and debilitated are most likely
to develop complications such as rhinitis, pneumonia, chronic bronchitis, pleuritis, and heaves. Streptococcus
zooepidemicus is the most common and important secondary invader.
The signs are those of a febrile upper respiratory infection. The dominant sign is a dry hacking cough,
paroxysmal. Serous nasal discharge, weakness and anorexia are frequent. A profuse purulent, persisting nasal
discharge indicates secondary bacterial infection. Pneumonic signs are uncommon except in severe cases.
Diagnosis
There are many causes of respiratory infection, but particularly characteristic of equine influenza are, a rapid
spreading respiratory infection with high fever and dry hacking cough. On the basis of these features and history
a presumptive diagnosis is frequently made.
A definitive diagnosis is based on laboratory identification of the virus or a rise in titer in paired sera.
 Nasal swabs taken as soon as possible after onset of illness. The virus is isolated and identified in chicken
embryos or cell cultures.
 Paired serum samples are preferable. Hemagglutination inhibition, complement fixation, and virus
neutralization tests are used for antibodies. A fourfold rise in titer between paired serum samples indicates
recent infection.
 Antigen can be detected using commercially available ELISA kits for identification of human influenza A.
Treatment
 Ordinarily, treatment is not necessary. Antibiotics are used for secondary bacterial infections if fever persists
for more than 3 - 4 days. Horses should not be worked until at least four weeks after the last clinical signs.
Prevention*
 All horses on breeding and training facilities should be regularly vaccinated for equine influenza.
 Intranasal vaccination: Intranasal vaccination with the modified-live/A2MLV has been found effective with
rapid onset of immunity. Horses 11 months of age or greater should receive an initial series of 2 vaccines, 4
weeks apart. If the disease risk is high vaccination may be initiated at 9 months of age. Biannual vaccines
should be administered after the initial series. This vaccine is not recommended for pregnant mares.
 Inactivated vaccine: Foal vaccination should begin at 9 months of age with an initial series of 3 vaccinations
every 3 - 4 months until about 2 years of age (high risk). Adult horses are given the initial series followed by
vaccination 4 to 6 months.
 To reduce exposure horses newly introduced to a stable should be isolated and kept under observation for
at least three weeks.
*Modified and reproduced with permission from, Davis, E.: Refresher on equine immunity and vaccines. DVM
magazine, Fall, 2007.
Equine Rhinopneumonitis
(Equine herpesvirus-4 infection, equine viral rhinopneumonitis)
In the absence of complications this is usually a mild respiratory disease of young horses.
Cause
Equine herpesvirus 4 (EHV 4) of the family Herpesviridae. A source of the virus is thought to be older horses that
under stressful circumstances shed the virus.
Occurrence
The virus is endemic in horses worldwide. Previously unexposed foals over two months of age, weanlings and
yearlings are most susceptible.
Transmission
Infection is by inhalation of aerosol droplets and transmission is by contact and fomites. Spread can be rapid.
Clinical Features
Incubation period is from 2 - 10 days and. the course is usually about seven days. Infections vary in severity,
depending mainly on immune status, from subclinical to mild, and infrequently acute. Under conditions of stress
and crowding some individuals may develop bronchopneumonia with secondary bacterial infection. Foals
occasionally develop a severe pneumonia that can be fatal.
Signs depend upon severity and may include fever, anorexia, cough, rhinitis, and a profuse nasal discharge,
which may become purulent. Deaths are infrequent.
Diagnosis
Not all infections may be serious enough to warrant laboratory investigation. Foals are most seriously affected.
Definitive diagnosis requires laboratory confirmation.
 Nasal swabs, whole blood: Isolation and identification of the virus in cell cultures.
 Acute and convalescent sera: Demonstration of a significant increase of specific antibody between paired
sera using virus neutralization or other serologic procedures.
Treatment
 None, except in foals that develop complications. Antimicrobial therapy is employed for secondary bacterial
infection.
Prevention
 Recently acquired horses and horses returning from racetracks, shows, etc., should be quarantined for 3 - 4
weeks.
 Inactivated virus vaccines, monovalent (EHV-4) or bivalent (EHV-4 and EHV-1), are recommended. An initial
series of three vaccinations at 3 - 4 months of age are recommended with subsequent boosters.
Equine Rhinovirus Infection

Rhinoviruses comprise a genus in the family Picorniviridae. Three species of rhinoviruses are considered to
occur in horses. These viruses are prevalent in the upper respiratory tract of horses worldwide.
Transmission is mainly by inhalation of aerosols and direct and indirect contact. The virus can remain viable on
the premises for days.
Infections occur most frequently in young horses under stress. After an incubation period of 3 - 7 days there is a
mild upper respiratory infection, which may include rhinitis, pharyngitis and regional lymphadenitis. Infections are
often subclinical. Rhinoviruses can be isolated and identified in cell cultures from nasal swabs.
Diagnosis can be made on the basis of significant titers with the virus neutralization test. These infections are not
significant enough to warrant particular preventive measures.
Equine Viral Abortion
(Equine Herpesvirus 1 Infection)
Equine herpesvirus 1 (EHV 1) can cause mild upper respiratory infection, abortion and/or serious neurologic
disease.
A recently identified mutant form of EHV-1 is responsible for myelitis in horses, particularly those in crowded
stressful conditions such as show or race facilities.
Occurrence
EHV-1 is carried by many horses worldwide and all ages are susceptible. The outcome of the infection depends
mainly on the immune status of the individual.
Transmission
Infection is by inhalation and direct and indirect contact.
The respiratory infection varies in severity. Signs may include transient fever, nasal discharge, inappetance and
depression. Secondary bacterial infection delays recovery.
No apparent infection or a respiratory infection may precede abortion which usually takes place at 8 - 10 months,
and about 2 - 4 weeks after exposure of the pregnant mare. Aborted fetuses may have edematous lungs and
small tan areas of focal necrosis involving the liver, lungs, and spleen. Some foals are born live, but are weak
and usually die.
Other important syndromes attributed to EHV 1 are a highly fatal viremia in foals less than one week of age and
an encephalomyelopathy in horses of all ages and both sexes.
The neurologic disease can be primary or follow abortion or respiratory infection caused by EHV 1. Serious
outbreaks occur independently of abortion or respiratory disease. The virus infects vascular endothelial cells and
particularly those of the brain and spinal chord. There follows an immune-mediated vasculitis with secondary
hemorrhage and infarction throughout the CNS. The neurologic manifeststation has a rapid onset with evidence
of neurologic involvement appearing within 24 hours. Clinical signs include weakness, fever, incoordination,
ataxia, paralysis, and death in severe cases. Mildly affected horses, and even those recumbent, may recover.
Severely affected horses do not recover and are sacrificed.
Diagnosis
Because horses usually recover uneventfully from the respiratory disease, the cause is not usually determined. In
view of the threat this disease poses to pregnant mares, it is advisable to determine the precise cause of all
respiratory diseases affecting horses. The need for definitive diagnosis becomes even more urgent when
abortions and neurologic disease occur.
Abortions due to equine viral arteritis (EVA) virus occur at any time during gestation, and the mare is clinically ill
at the time of abortion. In addition, autolysis of the fetus is common with EVA infection. Other infectious agents
do not usually cause multiple abortions.
 In the respiratory form: The virus can be isolated and identified from nasal swabs using cell cultures.
 In the abortion form: Small, multifocal, yellow-white, or tan areas of necrosis throughout the fetal lung and
liver are strongly suggestive of EHV 1 abortion. Fetal pulmonary edema and hepatic necrosis are
characteristic. The finding of the typical inclusion bodies in fetal tissue is strongly supportive of a diagnosis.
A rapid diagnosis can be made by identification of the virus in fetal cells by immunofluorescence. The virus
can be isolated and identified from fetal tissues using cell cultures.
 In the neurologic form: The virus is difficult to isolate from the CNS. A significant increase in specific
antibody between acute and convalescent sera with neurologic signs is sufficient for a diagnosis. Vasculitis
in the CNS is supportive evidence.
 PCR test, buffy coat and / or nasal swab samples for submission.
Treatment
 There is none. Supportive care, antiinflammatories. Antiviral agents such as acyclovir have been
investigated, but the bioavailability in horses is poor.
Prevention
 Isolation or quarantine of aborting mares and horses with neurologic signs and individuals testing positive to
EHV-1 disease. New mares should be isolated from pregnant mares.
 *Immunity is usually of short duration. Inactivated virus vaccines, monovalent (EHV-1) or bivalent (EHV-1
and EHV-4) are employed with vaccination of mares at three, five, seven and nine months of gestation. A
booster should also be given 4 - 6 weeks before foaling date.
Adult horses should be vaccinated every 4 - 6 months, young horses (high risk, travel, commingling) may be
better protected with booster vaccines every 3 to 4 months.
Foal vaccines should be initiated at 4 - 6 months of age with a series of 3 vaccines. The initial 2 vaccines should
be administered at an interval of 4 weeks with the third vaccine to be administered 8 weeks later.
A modified live vaccine is available for EHV-1 infection
 Horses returning from shows, racetracks, sales, etc., should be isolated for 3 - 4 weeks prior to mixing with
resident horses and particularly pregnant mares.
 Negative horses should be kept in premises that have been thoroughly cleaned and disinfected.
*From, Davis, E., Refresher on Equine Immunity and Vaccines. DVM magazine, Fall, 2007.
Equine Viral Arteritis
(Pinkeye)
This is a highly contagious, systemic, viral disease of equids, which is frequently accompanied by abortion.
Cause
The cause is an arterivirus (Arteriviridae) strains of which may vary in virulence.
Occurrence
The disease occurs in most countries of the world. Although occurring in all breeds of horses the prevalence is
said to be higher in standardbreds and warmbloods. Young horses and particularly stallions are the principal
reservoir of the virus.
Transmission
The modes of transmission are: via the respiratory tract (respiratory secretions), direct contact and fomites,
venereal and in utero (uncommon). Infected stallions may shed virus in their semen for long periods (months to
years) and play a very significant role in transmission naturally (coitus) or artificially. It is estimated that 20 - 30%
of infected stallions become carriers. After recovery from the disease, their fertility is not affected.
Clinical Features
Most infections are mild or subclinical. The more severe disease occurs in outbreaks in susceptible horses that
have been infected at shows, sales, racetracks, and breeding farms.
The acute form is characterized by fever, an acute catarrhal inflammation of the upper respiratory tract, and
abortion. The clinical signs, mainly attributable to infection of the small arteries, are variable. They include
conjunctivitis, myalgia, edema of the limbs, colic, and diarrhea. An urticarial-like eruption of the skin of the
abdomen, thorax and neck may be seen. As indicated signs vary greatly in severity and last 2 - 14 days. Infection
confers long lasting immunity.
Abortions frequently accompany outbreaks. They may be multiple and usually take place between the 5th and
10th month of gestation and within 10 to 30 days after exposure. The aborted fetus is partially autolyzed and
devoid of distinguishing lesions.
A severe pneumonia has been reported in young foals.
Diagnosis
There are a number of causes of equine abortion including equine herpesvirus 1 thus a definitive diagnosis is
important. Other causes of abortion (not usually multiple) are various bacteria and fungi. Among diseases to be
considered are equine infectios anemia, influenza, allysium intoxication, equine rhinopneumonitis and purpura
hemorrhagica.
 Fresh fetus or portions of fetal lung, liver, lymph nodes and spleen; nasal and conjunctival swabs and
semen. These are used for virus isolation and identification in cell cultures. PCR can be used to identify virus
in nasal and conjunctival swabs, semen and whole blood.
 Portions of the above tissues are fixed for histopathologic examination. There are no characteristic gross or
microscopic lesions. The absence of inclusion bodies in fetal tissues helps rule out equine viral abortion
(EHV 1).
 Serum: Virus neutralization is the most commonly used test. Complement fixation and an ELISA have also
been employed. Infected horses show rapid serum conversion. Serologically negative stallions are not
carriers.
Prevention
 The modified live vaccine is effective and widely used. Since immunity is not induced immediately the
vaccine should be administered to stallions not less than 3 weeks before breeding. Similarly, mares should
be vaccinated not less than 3 weeks before breeding. After vaccination mares should be isolated from
horses that may transmit the virus since they will not be immediately protected after immunization. Pregnant
mares, and foals less than 6 weeks of age, should not be vaccinated.*
 It is preferred to use serologically negative stallions although vaccinated mares can be bred to carrier
stallions without developing clinical disease. Caution should be used with mares bred to infected stallions,
because they are a source for shedding virus following breeding. Strict isolation of such mares should be
maintained for 3 weeks after breeding.
 Horses returning from shows, racetracks, sales, etc., should be isolated for 3 - 4 weeks prior to mixing with
resident horses and particularly pregnant mares.
 When the disease occurs appropriate sanitary measures should be taken to prevent spread.
*From, Davis, E.: Refresher on equine immunity and vaccination. DVM magazine, Fall, 2007.
Eumycotic Mycetomas
(Maduromycosis)
Eumycotic mycetomas (mainly subcutaneous mycotic abscesses) consist of pyogranulomatous processes, which
may be fibrotic and cystic, and are produced by several species of fungi.
Grains or granules consisting of dense micro-colonies of fungi are found in the granulomatous lesions and
exudates. The grains may be dark or white depending on the causal fungi.
Most reports of this mycosis have involved dogs but there have also been rare reports of infections in horses,
cattle, and cats. The causal fungi which occur in nature are probably worldwide in occurrence. The lesions occur
in subcutaneous tissues most commonly involving the extremities but they also have also been found in other
locations. Incision of the lesions reveals brown or black fungous microcolonies or white micro-colonies embedded
in a large mass of granulation tissue. The lesions may ulcerate, discharge pus and form fistulas and sinus tracts.
Lesions vary greatly in size.
The following species of dematiaceous (black or brown pigment) fungi, which produce dark-grained micro-
colonies, have been recovered from different animals:
 Curvularia geniculata
 Cochliobolus spicifer
 Helminthosporium spp.
 Madurella mycetomatis
White-grained mycetomas are caused by nonpigmented fungi, e.g., Acremonium spp., Pseudallescheria boydii
and others.
Diagnosis
A diagnosis of eumycotic mycetoma can be made if the characteristic grains or microcolonies are seen in lesions
and exudates. Precise diagnosis is dependent upon the demonstration, isolation, and identification of the causal
fungus.
 For direct examination and culture, use biopsies, pus or exudates from abscesses. The characteristic grains
or microcolonies can be seen grossly. The microcoloies are selected and examined in wet mounts for the
characteristic fungal elements. The fungi grow readily on Sabouraud agar in 2 - 3 weeks at room
temperature. Identification of species may require a reference laboratory.
 Biopsy and portions of lesions, fixed. The finding of grains and the fungal elements in tissue sections is
confirmatory.
Treatment
 Surgical measures are generally the only curative therapy.

 Given the nature of the lesions treatment is not usually successful. Fibrotic and cystic lesions resist drug
penetration. Drugs that would be indicated are amphotericin B and/or ketoconazole.
Foal Diarrhea and Septicemia

Colostrum that contains antibodies, protein, minerals and vitamins is produced by the mare in late pregnancy.
Optimal colostral quality is achieved when a mare is immunized properly with booster vaccines administered at
approximately 9 months of gestation. The proteins within colostrum are instrumental in providing protection to the
newborn foal from various infectious diseases. The window for colostral absorption is in the first 24 hours of life,
after this time gut closure occurs and macromolecules are no longer absorbed. The antibodies present in
colostrum are predominately composed of IgG and IgA. If "passive transfer" fails (FPT), the foal is particularly
vulnerable to an array of infectious agents. In order to ensure that adequate colostral absorption has occurred, a
foal-side ELISA test can be performed at 8 - 12 hours after birth to determine if the foal has an adequate IgG
concentration in circulation.
Management of FPT can be dealt with by administration of several pints of colostrum that are ideally
administered before the foal is 15 - 18 hours of age. After this time gut closure is occurring and optimal
absorption is unlikely to occur. Sources for colostrum maintained as "banks" are common on large breeding
farms. Banked colostrum can be stored frozen (-20°C) for such emergencies, preferably collected within the
previous 12 months. If colostrum is unavailable, frozen hyperimmune equine plasma should be administered by
the intravenous route at a dose of 1 - 2 liters for the average 45 kg foal. The dose will be determined by whether
the foal received any colostrum. In cases of complete FPT, 2 liters of plasma should be administered
intravenously through an indwelling jugular catheter.
Foal Diarrhea
Foal diarrhea is the most common disease afflicting foals. Some of the microorganisms causing foal diarrhea also
have the potential to cause foal septicemia. Most of the bacteria causing foal diarrhea are found widely in the
environment. Infection is by ingestion and is most serious when it affects the newborn.
The diarrhea is most often watery, sometimes bloody and accompanied by depression and fever. The organisms
most often involved are:
Gram-negative:
Escherichia coli (see Colibacillosis). It is estimated that E. coli accounts for about a quarter of all foal septicemias.
Klebsiella spp. – gram-negative, enteric organism
Salmonella spp. (see Salmonellosis)
Gram-positive:
Clostridium difficile (see Clostridia-associated enterocolitis in horses)
Clostridium perfringens type C (see Clostridiosis)
Rhodococcus equi – diarrhea, three weeks to three months
Rotavirus Infection (see Rotavirus infection) - in foals less than three months of age; most serious during the first
two weeks of life.
Some other bacterial species are infrequently involved.
Diagnosis
It should be kept in mind that a diarrhea called foal heat diarrhea, or ninth day diarrhea occurs naturally in most
neonatal foals. It is non-infectious and characterized by soft pasty yellow feces that usually clears-up within a
week.
Definitive diagnosis requires detection or isolation and identification of the causal agent from feces.
Treatment
This is discussed above in reference to FPT and under the various diseases referred to above.
Prevention
This is discussed under the various diseases referred to above.
Foal Septicemia
Some cases of diarrhea may progress to a septicemia. Infection may take place prenatally, perinatally or
postnatally. Frequent modes of infection are via placenta, umbilicus (navel ill), and by ingestion or inhalation.
Initial infection takes place during the first week and septicemia may follow within hours leading to localization in
various tissues, organs and joints, with concomitant endotoxemia and septic shock. Some manifestations of
these infections are omphalitis, septic polyarthritis, pneumonia, pleuritis, and peritonitis. They vary somewhat in
character depending upon the particular causal bacterium. Many cases terminate fatally within a week.
For clinical features see discussion of Colibacillois and Actinobacillus equuli infection.
The following bacteria have been implicated in septicemia of foals:
Escherichia coli (see Colibacillosis). It is estimated that E. coli accounts for about a quarter of all foal septicemias.
Actinobacillus equuli (see Actinobacillus equuli Infection) Klebsiella spp. – gram-negative, enteric organism
Streptococcus zooepidemicus – gram-positive, important pathogen of horses
Staphylococcus spp. – gram-positive, usually endogenous opportunist
Salmonella spp. (see Salmonellosis)
Enterobacter spp. – gram-negative, enteric organism
Pseudomonas aeruginosa – gram-negative, often resistant to antimicrobials
Clostridium difficile (see Clostridia-associated enterocolitis in horses)
Note, only gram-negative organisms gives rise to endotoxemia.
Diagnosis
This is discussed under the particular disease discussions referred to above. The laboratory diagnosis is
essentially the same for the various bacteria and consists of culture of fresh blood, biopsy, joint fluid, etc., and
identification of isolates.
Treatment and Prevention
These are essentially the same for the various causal bacteria and are discussed under Colibacillosis and
Actinobacillus equuli Infection
Microbial Diseases: G through L

1
Table of Content
 Geotrichosis
 Glanders (Farcy)
 Guttural Pouch Mycosis
 Hendra Virus Infection
 Histoplasmosis
 Infectious Abortion: General
 Infectious Mastitis
 Infectious Metritis
 Japanese B Encephalitis
 Leptospirosis
 Listeriosis
 Louping Ill
 Lyme Disease (Borelliosis)
Geotrichosis
This is a rare, sporadic, non-contagious disease of horses, cattle, dogs, fowl, and other species caused by the
fungus Geotrichum candidum. It is characterized by small, granulomatous lesions that most often involve lungs,
kidney, wall of the digestive tract, or lymph nodes. The infection is seldom systemic and usually only one or
several organs or tissues are involved. The disease is ordinarily mild and the lesions unrelated to death, are
found at necropsy or slaughter.
Geotrichum candidum occurs in soil and decaying organic matter.
Diagnosis
Geotrichosis is rarely diagnosed in the living animal.
 In the necropsied animal tissue sections and scrapings from lesions are examined. Direct examination:
Characteristic morphologic elements of the fungi can usually be seen in wet mounts of material from lesions.
Ovoid yeast-like cells are free and found in macrophages and giant cells. Short chains of the yeast-like cells
and pseudohyphae may also be seen.
 Culture: Definitive diagnosis is dependent upon the isolation and identification of G. candidum.
 Histopathology: Septate hyphae, yeast-like cells, and arthroconidia are seen in tissue sections. These forms
resemble some of those seen in candidiasis and histoplasmosis.
Treatment
 Because this infection is rarely diagnosed antemortem, treatment is usually not a consideration. An
imidazole derivative such as ketoconazole would probably be effecive.
Glanders
(Farcy)
Glanders is a highly contagious, bacterial disease of horses, mules and donkeys, which has been eradicated
from most regions of the world.
Cause
Glanders is caused by the gram-negative rod, Burkholderia mallei (formerly, Pseudomonas mallei), an obligate
parasite. It can survive on premises for more than a month
Occurrence
The disease occurs in solipeds in North Africa, regions of Asia, Eastern Europe, and the Middle East and Brazil.
The source of the agent is always infected solipeds. Humans and carnivores are susceptible and if not treated
may die.
Transmission
The modes of infection are by ingestion, mainly of contaminated food and water, by skin wounds and inhalation.
Clinical Features
The incubation period is about two weeks.
The disease is seen in various forms. Generally speaking the acute form occurs in donkeys, the chronic form in
horses and the subacute form in mules. In the chronic form, tubercles develop on the nasal mucosa, in the lungs
or involving the skin. The resulting nodules of the nasal passages and skin eventually ulcerate and discharge
pus. The skin form, with nodules along the lymphatics of limbs is referred to as farcy.
Clinical signs include, fever, mucopurulent nasal discharge, epistaxis, respiratory distress and lameness. The
course of the chronic form, seen mainly in horses, may be months. Some chronic cases recover and are sources
of infection.
The acute form is a septicemia with fever, mucopurulent nasal discharge, cough and respiratory distress which
terminates fatally within a few days.
Figure 1. Chronic glanders in a horse with multiple lesions on the back and foreleg. (Courtesy of Dr. Rinaldo
Mota, Brazil). To view click on figure
Figure 2. Chronic glanders in a horse with nodules and abscesses on the back,pectoral region and foreleg.
(Courtesy of Dr. Rinaldo Mota, Brazil). To view click on figure
Diagnosis
Epizootic lymphangitis, ulcerative lymphangitis, sporotrichosis, nocardiosis and zygomycosis have some clinical
features which resemble glanders.
A definitive diagnosis is based on the isolation and identification of B. mallei from lesions.
 The mallein test (delayed hypersensitivity skin test), which is reliable, is used to screen horses for glanders,
e.g., horses being imported to some countries. The complement fixation test and ELISA are used to detect
specific antibody.
 Swabs are taken from ulcers and incised nodules; pus may also be aspirated by syringe from nodules; skin
biopsies: Isolation and identification of B. mallei.
 If a necropsy is performed, portions of nodules and affected lung should be submitted, fresh for culture, and
fixed, histopathologic examination.
Treatment
 In most countries solipeds with glanders are slaughtered.
Prevention
 Glanders is a reportable disease in many countries and if it is detected, the premises are quarantined and
clinical cases and reactors to the mallein test are slaughtered.

Glanders in humans is a life-threatening disease almost always acquired from solipeds. Great care must be taken
to avoid exposure.
Guttural Pouch Mycosis
This mycosis of horses involves, initially, fungal invasion of the medial (occasionally lateral) compartment of the
guttural pouch.
The guttural pouch is a natural out-pouching of the eustachian tube, located at the base of the skull. The purpose
of this structure is believed to allow for cooling of blood prior to brain perfusion, it is a structure that is unique to
Equidae. Because of the location and the anatomic compartmentalization is remains predominately closed when
the head is elevated. Contamination with fungal organisms may occur with survival of the pathogen maintained
by plaque formation over large blood vessels.
Cause
This disease is most often caused by Aspergillus spp. These fungi are widespread in nature and may be found in
the air passages of horses. Colonization may occur as a result of aneurysmal dilation of vasculature. Fungal
colonization leads to erosion of the underlying mucosa and vascular structures or inflammatory injury to the
adjacent nerves.
Occurrence
Although not common, it is sufficiently frequent to be important in equine veterinary practice worldwide. The
disease occurs most frequently in warm, damp environments. In some individuals impairment of cell-mediated
immunity may be a factor.
Transmission
The disease is not contagious. There are many possible sources of the infecting Aspergillus fungi.
Clinical Features
The affected pouch is thickened, hemorrhagic, partially necrotic and covered by a pseudomembrane. Abnormal
clinical features are best observed with endoscopic evaluation.The two most important clinical signs, in addition
to nasal discharge, are epistaxis (sometimes to the point of exsanguination) due to fungal erosion of the wall of
the internal or external carotid artery or the external maxillary artery, and dysphagia due to neuritis of the
laryngeal and pharyngeal nerves. The large vessels traverse through the medial compartment of the guttural
pouch, rarely lesions occur in the lateral compartment.
Diagnosis
Cryptococcosis, tumors and other infections of the upper respiratory tract should be considered. Diagnosis is
confirmed by observing, with an endoscope, the diphtheritic membrane involving the guttural pouch.
 Parts of the lesion are obtained with the biopsy attachment of the fiberoptic endoscope. Great care must be
taken not to rupture the lesion. Direct examination: Septate hyphae in wet mounts or stained sections
strongly suggest Aspergillus infection.
 Swabs from discharging areas and tissue are cultured for fungi and bacteria. Fungi other than Aspergillus
may be isolated, but the latter are by far the most frequent in guttural pouch mycosis.
Treatment
 Antifungal drugs have generally not been effective. Systemic therapy has not been successful in removing
fungal plaques.
 Surgical: Arterial embolization is performed and the plaque is thus deprived of nutrients.
 Local: Topical application of itraconazole may be effective for small lesions. Care should be taken when
infiltrating substances into the guttural pouch since irritating substances, such as betadine solution may
further damage the structure required for proper swallowing function.
Hendra Virus Infection

(Acute equine respiratory syndrome, equine morbillivirus pneumonia)
This is an infrequent, acute, viral disease of horses and humans acquired from bats in Australia and New Guinea.
Cause
It is caused by the hendra virus of the genus henipavirus in the family Paramyxoviridae. It is closely related to
nipawvirus of the same genus which infects swine and humans.
Occurrence
The disease occurs infrequently and has only been reported in horses and humans in Australia and New Guinea.
Transmission
The reservoir of the virus is fruit bats (Pteropus spp.), which occur in Australia and New Guinea. The infection in
bats is subclinical. The virus is present in secretions and urine and spread is presumed to be by direct or indirect
contact and aerosol. Transmission from horse to horse is thought to be infrequent.
The principal feature of the disease is an interstitial pneumonia of varying severity. Clinical signs are mainly those
of a respiratory infection and they include fever, anorexia, respiratory distress and a characteristic frothy,
sometimes blood tinged, nasal discharge. Widespread edema and neurologic signs may also be evident. The
fatality rate may exceed 60%.
The virus mainly targets the vascular system, which begins in the lungs then spreads by viral infected
macrophages to other organs and in some animals to the brain. The virus attacks the vasculature of various
tissues and organs including the spleen, liver, kidneys, myocardium and brain.
Diagnosis
 Portions from lungs, spleen, liver, lymph nodes and brain: The virus can be isolated in a number of cell lines
and identified by virus neutralization. It can be detected in tissues by PCR.
 Paired sera: Testing acute and convalescent sera by ELISA or virus neutralization for increase in titers.
 Histopathologic examination and staining of tissues with labeled Hendra virus antiserum.
Prevention
 The disease has been controlled by quarantine and slaughter of all infected animals. Given the
omnipresence of the virus reservoir there is little that can be done to prevent infections in horses.

The disease in humans, characterized by non-suppurative encephalitis or interstitial pneumonia, has been
frequently fatal. Special precautions should be taken to prevent exposure to potential sources of the virus.
Histoplasmosis
Histoplasmosis is a noncontagious, fungal disease of some animals including the horse, and humans, which is
characterized by subclinical, chronic, and infrequently, severe systemic infections.
Cause
Histoplasmosis is caused by the soil-borne, dimorphic fungus Histoplasma capsulatum. The mycelial form grows
abundantly in bird feces but is not present in the intestine of live birds. The yeast form is found in tissues.
Occurrence
It is worldwide in distribution, but is more frequent in certain geographic regions, e.g., in the United States,
primarily in the northeast, central, and south-central states. Histoplasmosis is rare in the horse.
It is an infection of the reticuloendothelial system and is characterized by the formation of tubercle-like
granulomas in, most frequently, the lungs and less frequently the intestine. The infection is often inapparent or
subclinical in normal, healthy individuals. The disease may progress at the initial site and spread to other organs
in individuals whose cell-mediated immunity is impaired. It is usually seen in either a predominantly pulmonary or
intestinal form.
Both forms of the disease occur, albeit rarely, in the horse and both, if not treated, may become systemic and
fatal.
Clinical signs will depend upon the form of the disease. In addition to respiratory or enteric signs there are, as the
disease progresses, fever, depression, loss of weight and condition. Untreated disseminated cases terminate
fatally.
Diagnosis
The disease is difficult to diagnose clinically. Radiographs of the thorax are helpful in the pulmonary form. Given
the rarity of the disease it is most likely to be diagnosed after necropsy by the histopathologic examination of
tissue sections; however, laboratory tests make possible an antemortem diagnosis.
 The following are employed in the diagnosis of histoplasmosis but not all are practicable for the horse: Fine-
needle aspiration, and biopsies of lymph nodes and liver; exfoliative cytology using scrapings from ulcer
base (skin or mucous membrane), bone marrow aspirate, or peripheral blood (buffy coat). Smears from the
aforementioned specimens are stained by the Giemsa, Wright, and fungal stains for demonstration of the
intraphagocytic yeast cells.
 At necropsy, fresh and fixed portions of lung, liver, spleen, intestinal wall, skin, or any other tissue containing
granulomas: Demonstration of the typical yeast cells in macrophages in stained smears and sections of vital
organs is presumptive evidence of histoplasmosis.
 Isolation and identification of H. capsulatum from vital organs is required for definitive diagnosis. This is time
consuming in that the two phases must be grown for more than a week on different media and at different
temperatures.
 In humans the complement fixation test is used on paired sera. An immunodiffusion test is considered the
most specific and reliable serological procedure. Increase in titers indicates a progressive infection.
Treatment
Treatment regimens are not available for the horse. The information that follows is based on treatments for dogs
and cats.
 Amphotericin B is used for severe cases. Long-term use of the imidazoles (miconazole and ketoconazole) is
effective.
Prevention
 Infected animals should be isolated although transmission to other animals and humans is not thought to
occur.
Infectious Abortion (General)

The most important infectious diseases causing abortions are equine viral abortion (equine herpesvirus 1
infection) and equine viral arteritis. Abortions occasionally occur with Potomac horse fever and leptospirosis
which are discussed separately.
The principal microbial agents causing, usually sporadic abortions, are the following:
Bacteria:
 Streptococcus zooepidemicus, and other streptococci.

o Klebsiella pneumoniae
 Pseudomonas aeruginosa
 Escherichia coli
 Leptospira grippotyphosa and L. pomona (Leptospirosis)
Fungi: (Infrequent):
 Aspergillus spp.
 Mucor spp.
 Coccidioides immitis (Rare)
 Candida albicans (Rare)
There are rare reports of other fungi causing abortion. In spite of thorough work-ups the cause of more than 50%
of equine abortions go undetermined.
Diagnosis
See Diagnosis under leptospirosis, equine viral abortion and equine viral arteritis.
In bacterial abortion the infection is usually ascending (via cervix). There is an edematous placentitis with a
brown fibronecrotic vaginal exudate.With chronic placentitis the growth of the fetus may be retarded and if
expelled dead fetus may show autolysis. A purulent vulval discharge may be present.
In mycotic abortion the infection is usually ascending. The chorioallantois is thickened and a variable amount of
exudates is present. Abortion is usually late in gestation and there is fetal growth retardation. There also may be
a purulent vulval discharge
The diagnostic procedures carried out are ordinarily based upon the history, suspected disease, and results of
direct examinations of fetal and placental materials. The following specimens are optimum for a comprehensive
laboratory examination:
 10 ml of maternal blood for serologic tests, preferably taken at the time of abortion and two weeks later.
Collect from in-contact animals and those that have aborted.
Placenta, fresh for microbiology and formalized for histopathology.
Uterine discharge on swabs if placenta is not available.
Fresh, whole fetus: Culture organs and fetal stomach.
Fetal lung and liver, fresh and fixed: For culture and histopathology
Infectious Mastitis
Mastitis occurs infrequently and usually in the drying-off period. One or both glands may be affected.
The principal cause is Streptococcus zooepidemicus; Streptpcoccus equi, S. equisimilis, S. viridans, and
Staphylococcus aureus are occasionally involved. As in bovine mastitis the gram-negative bacteria
Pseudomonas aeruginosa, E. coli, and Klebsiella spp. are sometimes implicated.
Signs are: often low fever, abnormal secretion, which may appear normal to sero-flocculent, painful swelling of
the gland and contiguous tissue, walking stiffly and standing with legs apart to relieve discomfort. The mare may
be reluctant to let the foal nurse.
Diagnosis
 Milk samples are taken aseptically into sterile vials as described in Section 4.The milk is cultured and an
antimicrobial susceptibility test is conducted if indicated.
Treatment
 Antimicrobial treatment is determined by the results of the antimicrobial susceptibility test.

 Because the equine teat has two orifices medication is introduced into each orifice separately. Bovine
mastitis preparations containing cephalosporins are useful. The teat should be stripped prior to instillation of
antibiotics. Prompt treatment helps avoid abscessation and lasting damage to the glandular tissue. Both
glands should be treated and in severe cases systemic treatment is recommended. Frequent stripping may
be helpful.
 Hydrotherapy, e.g., use of warm water via a hose, and warm compresses.
 Flunixin meglumine may be indicated to relieve pain.
Infectious Metritis
(This discussion excludes contagious equine metritis which is discussed separately).
Cervical swabs are used to determine if mares have endometritis. Equine cervical swabs and their use is
described in Selection, Collection, and Submission of Specimens for Diagnosis section.
Cervical swabs are preferably taken during estrous when the cervix is open. Smears should be made from swabs
on glass slides for cytological examination. Staining the smears after fixation will indicate whether or not there is
an infectious process. Five or more neutrophils per high-power field suggest infection. The cytological
examination is important because the caudal genital tract has a normal flora.
Swabs are cultured, and if there is an indication of an infection by the cytological examination, antimicrobial tests
are conducted on the principal isolates.
The bacteria most frequently recovered and presumed to have a potential for infection are: Streptococcus
zooepidemicus (most common), Escherichia coli, Pseudomonas aeruginosa, Klebsiella pneumoniae,
staphylococci, and other streptococci. Rhodococus equi and Actinobacillus equuli are occasionally isolated.
Yeasts and fungi are infrequent causes of endometritis and if involved, it is usually after prolonged antibiotic
administration.
Endometritis may be confirmed by the cytologic examination of endometrial biopsies.
Treatment
 After culture and antimicrobial susceptibility tests and following uterine lavage appropriate antibiotics are
instilled. Solutions of amphotericin B or clotrimazol are used for fungal infections.
 Commercially available immunostimulant preparations are frequently used.
Japanese B Encephalitis
Japanese B encephalitis is an arthropod-borne disease of horses, swine, and humans, caused by a flavivirus
(Flavoviridae).
The disease is characterized by encephalitis in horses that is usually milder than that caused by the viruses of
the three well-known alphavirus equine encephalitides.
The disease occurs in Japan and some other Asian countries. The human disease is usually mild but in
outbreaks the case fatality rate ranges from five to 40%.
Mosquitoes (Culex spp.) are the principal vectors.
Pregnant sows may abort and neonatal swine may die. The reservoir of the virus is birds, swine bats and some
other animals.
The laboratory diagnosis is similar to that of the three important equine encephalitides, i.e., serologic tests,
isolation, and identification of the virus.
The disease is sufficiently prevalent in humans to warrant the use of a live attenuated vaccine.
Leptospirosis
Leptospirosis is an infrequent, spirochetal disease of horses which is most commonly associated with abortion
and uveitis.
Cause
The principal cause is the serovar Leptospira pomona. Less commonly implicated in disease are serovars, L.
grippotyphosa, L. hardjo, L. canicola and L. icterohemorrhagiae. Leptospira bratislava is carried by some horses
without causing disease. Leptospira pomona, L. hardjo, and other serovars can occasionally be isolated from
normal horses.
Occurrence
The disease occurs worldwide in horses of all ages.
Transmission
Urine of infected cattle, swine and horses are probably the most common sources of pathogenic leptospires
including L. pomona and L. hardjo. Other serovars are shed by various wild rodents (particularly the rat and
mouse) and dogs. The organism can survive for days in alkaline water, and contaminated ponds and streams
can be sources of infection.
Most infections result from direct or indirect exposure to infectious urine. Infection is via nasal, oral or conjunctival
mucous membranes and abraded skin.
Clinical Features
Equine leptospirosis is usually characterized by a mild or subacute form with fever, depression, and icterus,
resulting occasionally in abortion and recurrent uveitis. The more sever infection, which is uncommon, may be
accompanied by hemoglobinuria, icterus and general weakness. Uveitis (moon blindness) in one or both eyes
with keratitis and conjunctivitis may develop months after infection. The lesions may be severe enough to cause
blindness. It is not clear whether eye lesions result from ocular infection or immune complex-mediation.
Leptospires have been recovered from equine eyes. Renal infection occurs but is infrequent.
Pregnant mares may abort shortly after infection with leptospira or several weeks later. The cause is usually L.
Pomona. Leptospirosis is estimated to account for up to 5% of abortions annually. Abortion results from infection
of the uterus and placenta. The fetus may be dead or foals premature, stillborn or sick.
Diagnosis
A clinical diagnosis is difficult. When abortion occurs, diseases such as equine viral abortion, equine viral arteritis,
and abortion due to other causes should be considered.
Laboratory diagnosis has been based on the microscopic agglutination test employing paired serum samples,
direct culture and detection of leptospires in tissue by immunofluorescence. The serological procedures are
complex and mainly carried out in reference laboratories. Direct culture is slow and impracticable. It is advisable
to contact the diagnostic laboratory to determine what diagnostic procedures are available and what clinical
specimens are required.
 Recently, PCR procedures have been developed for detection of leptospiral DNA in serum, urine and
tissues. They have the advantages of accuracy and rapidity and will probably supplant older diagnostic
procedures.
Treatment
 Treatment should be as early as possible. Tetracyclines, streptomycin, doxycycline, dihydrostreptomycin,

and penicillin have been effective.
 An antimicrobial combined with cortisone has been used to treat uveitis.
Prevention
 Because clinical leptospirosis is infrequent in horses, equine vaccines have not been developed.

It should be kept in mind that animal leptospires can cause serious disease in humans. Care should be taken to
avoid exposure.
Listeriosis
(Circliing disease)
Listeriosis is a non-contagious, bacterial disease of horses characterize most often by a neurologic infection or
abortion.
Cause
The disease is caused by the small, gram-positive, motile rod, Listeria monocytogenes. A number of serotypes
have been identified based on cell wall and flagellar antigens. The organism is found widely in soil and is carried
as a commensal in the intestine of many animals and thus is shed in the feces. It is very temperature resistant
and can grow at 4°C, a characteristic that aids in its isolation.
Occurrence
The disease, which occurs worldwide, is usually sporadic. All ages are susceptible. The abortion form is more
common in the horse than the neurologic and septicemic forms.
Clinical Features
In general, the disease is characterized by a neural form seen most often in ruminants with fully developed
stomachs and a visceral or septicemic form occurring most often in monogastric animals; however, there are
exceptions in the occurrence of these forms. The neural form of the disease (excepting abortion) is most often
seen in horses. Micro-abscesses are found in the brain stem. The visceral form is not usually diagnosed ante
mortem.
Clinical signs of the neurologic form are depression, anorexia, disorientation, difficulty eating and swallowing,
circling, head-pressing, incoordination, falling and being unable to rise.
If the pregnant mare is infected with listeria in early pregnancy abortion may follow. If infection occurs later in
pregnancy the fetus may be stillborn, or live with septicemia or visceral lesions. The latter are responsible for
small necrotic foci in the liver and cardiac muscle. These lesions, which are characteristic of the visceral form,
can be seen with the naked eye.
Diagnosis
Because there are a number of equine diseases with neurologic signs laboratory confirmation should be sought.
Visceral listeriosis is not usually diagnosed ante mortem.
Neurologic signs, e.g., circling, head-pressing, and incoordination suggest listeriosis; however, there are other
diseases with neurologic signs, e.g., rabies, toxemias, brain abscesses and various encephalidides thus
laboratory confirmation should be sought.
 Neural form: Brain stem, fresh and fixed. Isolation and identification. Histopathologic examination:
microabscesses in the brain stem strongly suggest listeriosis.
 Visceral form: Fresh and fixed portions of liver. Isolation and identification. Histopathologic examination.
 Abortion: Fetus and placenta. Isolation and identification. Repeated culturing (cold enrichment) may be
necessary for all forms.
 A definitive diagnosis is made on the basis of the isolation and identification of L. monocytogenes.
Treatment
 Treatment is usually of little value after neurologic signs are seen.

 The drugs of choice are the tetracyclines at a maximum dosage level. Erythromycin, penicillin, and
trimethoprim-sulfonamide are also used at maximum dosage.
Louping Ill
(Ovine encephalomyelitis)
Louping ill is an acute, non-contagious, viral encephalomyelitis that occurs rarely in horses.
It is principally a disease of sheep, less commonly of cattle, other animals, and humans. It occurs widely in the
British Isles, and in several countries in Europe.
The cause is a flavivirus (Flavoviridae) which is transmitted by the sheep tick, Ixodes ricinus. After tick infection
there is a viremia for 1 - 5 days; clinical signs appear when the virus enters the CNS. These include diphasic
fever, locomotor incoordination, trembling, salivation, coma, paralysis and often death. The course is similar in all
susceptible animals. In humans it causes a mild influenza-like infection, with usually, not serious neurological
symptoms.
Diagnosis
 Definitive diagnosis is based on the isolation and identification of the virus. Histopathologic examination of
the brain provides additional evidence of the disease.
Prevention
 Tick control; dips are less effective than topical acaricides.

 An inactivated cell culture vaccine has been effective in cattle, sheep and goats.
Lyme Disease
(Borreliosis)
Lyme disease is a tick transmitted, non-contagious, multi-organ, bacterial infection of horses, some other animals
and humans.
Cause
The large spirochete Borrelia burgdorferi causes Lyme disease in North America and Europe. There is evidence
that strains causing the disease in parts of Europe and in Asia have minor differences as determined by
molecular studies. These differences are thought to account for differences in the virulence of these strains for
humans and animals.
Occurrence
The disease has been reported from Australia, Europe, Japan, and the former U.S.S.R., and from most states in
the USA. Its occurrence in the US is greatest in the North East, the Mid-Atlantic and North Central states, Texas
and the Pacific Northwest.
Most infections in animals are thought to be subclinical. The clinical disease occurs in about 10% of infected
horses.
Transmission
The principal vector in the United States is the deer tick Ixodes dammini (scapularis). Ixodes pacificus is a vector
on the West Coast region of the USA. Other Ixodes spp. are vectors in other geographic regions. Small
mammals, particularly rodents including field mice, white-tailed deer, and dogs are reservoir hosts.
Transmission is at its peak from the late spring until fall when the ticks are most active.
Clinical Features.
After infection the spirochete multiplies and is spread to organs throughout the host. Disease is manifested
mainly in the heart, the brain, the joints or the kidneys.
The first signs seen in horses are fever, back soreness, lameness, shifting limb from limb, stiffness, loss of
appetite and depression. Signs are related to the location and proliferation of the spirochete. The most apparent
signs in the horse derive from a polyarthritis with hot, painful swollen joints. There may be encephalitis, uveitis
and cardiac and/or renal involvement with less obvious clinical signs. Without treatment the infection may
become chronic and persist for weeks to months.
Diagnosis
Diagnosis is often difficult given the varied clinical manifestations of the disease. History, clinical signs, laboratory
data, cardiac assessment, and the response to antimicrobial therapy should be considered.
 Unclotted blood, cerebrospinal fluid, joint fluid and urine. The organism has been difficult to demonstrate by
microscopy in these specimens. The PCR procedure has been used in some laboratories to aid in the
detection of organisms. A fluorescent antibody (monoclonal antibody) procedure is used to detect organisms
in tissue. Culture is time-consuming and impracticable
 Serum: At present the indirect florescence assay, the ELISA, and Western blot for antibodies to B.
burgdorferi are the most useful diagnostic procedures. The Western blot procedure is considered more
specific than the ELISA. A major difficulty is that serologic tests may only indicate exposure to the causal
agent, and although many horses are exposed few develop the clinical disease. Rising titers from paired
serum samples, and high titers along with characteristic signs in endemic areas are strongly suggestive of
Lyme disease.
Treatment
 Early, aggressive treatment is important in preventing chronic, lingering infections. Penicillin and tetracyline
(oxytetracycline) need to be given IV for two weeks; changing to oral administration may contribute to
persistent infection. If only oral is feasible three weeks is recommended.
Prevention
 A vaccine is not yet available for horses.

 Tick control, including avoidance of tick infested areas is very important. Use of topical insecticides; those
containing permethrins and/or pyrethrums, and fibronil are effective.
 Thorough daily grooming with removal of ticks. The small deer ticks can persist in the less accessible areas
of the body.

Prevent tick bites, remove ticks and use repellants if indicated. Vaccines are now available to protect humans.
Microbial Diseases: M through R

1
Table of Content
 Malignant Edema (Closridial Myositis)

 Melioidosis
 Paecilomycosis
 Papillomatosis (Warts)
 Phaeohyphomycosis
 Potomac Horse Fever (Equine Monocytic Ehrlichiosis)
 Pythiosis (Oomycosis)
 Rabies
 Respiratory Infection: General
 Rhinosporidiosis
 Rhodococcal Pneumonia of Foals
 Rotavirus Infection
Malignant Edema
(Clostridial myositis)
Malignant edema is an infrequent, acute, bacterial, toxemic disease of horses and other animals that is typically
fatal.
Cause
Clostridium septicum, Cl. perfringens and Cl. novyi are the most common etiologic agents. Other causes are: Cl.
chauvoei, Cl. sordellii, and Cl. fallax. These are large, anaerobic, spore-forming gram-positive rods that occur in
nature and in the intestines of some animals.
Occurrence
The disease is worldwide in distribution and occurs most commonly in cattle and sheep but infrequently in
horses. The organism is shed in the feces of many animals, thus, spores are widely present in the soil. Cases are
sporadic unless a number of animals have been wounded.
Clinical Features
Spores enter via wounds, vaccinations, abrasions, surgical and inoculation procedures including drugs such as
flunixin given intramuscularly. The latter germinate and proliferate in necrotic tissue (anaerobic) producing
exotoxin. Organisms spread rapidly via subcutaneous tissues to involve mainly muscles resulting in a necrotizing
myositis. In less than 48 hours of the initial infection the lesion spreads and enlarges. There is extensive tissue
necrosis, infiltration of bloody gelatinous fluid and painful swelling. The following are characteristic of the lesions
in muscle: red (hemorrhagic), gelatinous, little gas, and pitting on pressure. The skin becomes cold and leathery.
The clinical signs are those of a profound toxemia and include fever, depression tachycardia, rapid breathing and
anorexia. The mortality rate may exceed 90%.
Diagnosis
The lesion is sufficiently characteristic to make a presumptive diagnosis.
 Specimens: In the dead animal, a portion of the muscle and smears prepared from the lesion; in the live
animal, material may be taken from the lesion with a syringe for smears and culture.
 Procedures: Fluorescent antibody (FA) staining of smears is quick and reliable. Because of its accuracy and
rapidity, FA staining has largely replaced culture. The latter is expensive and time consuming. It is very
important that the specimen (muscle) be fresh, for other clostridia often invade the lesions shortly after
death, particularly in warm weather. It should also be kept in mind that C. septicum is a rapid postmortem
invader. Histologic evaluation can often separate primary infection from postmortem invasion, should this be
necessary Identification of C. septicum by FA staining or by culture from fresh lesions constitutes a definitive
diagnosis of malignant edema.
Figure 1. Hot, painful swelling of malignant edema.
Treatment
 To be effective treatment must be early; the course of malignant edema is usually short and frequently fatal.
Penicillin is given systemically along with tissue fenestration and accompanying supportive therapy.
Melioidosis
Melioidosis is a sporadic, usually chronic, bacterial disease of animals and humans characterized by the
presence of suppurative or caseous lesions in various tissues and organs.
Cause
The disease is caused by the gram-negative bacterium, Burkholderia pseudomallei (formerly, Pseudomonas
pseudomallei).
Caused by the gram-negative bacterium, Burkholderia pseudomallei (formerly Pseudomonas pseudomallei) and
characterized by a septicemia in the acute form, and the presence of multiple, suppurative abscesses or nodules
in the lymph nodes and viscera in the less severe but sometimes progressive, chronic form.
Occurrence
It occurs in South East Asia, Australia, Papua, New Guinea, some Caribbean islands, Ivory Coast and some
South American countries. Greater international travel in recent years may have contributed to a wider
occurrence.
The disease occurs in domestic animal species, some wild animals, rodents, laboratory animals, humans, and
also animals in zoos, including primates. The disease is infrequent in Equidae.
Most infections are thought to be subclinical. The organism is a facultative intracellular parasite and may remain
dormant in tissue for months or years.
Transmission
This saprophytic organism lives freely and widely in tropical soil and water and is acquired via wounds, ingestion,
and inhalation.
Clinical Features
Many animals are no doubt exposed but few develop clinical disease. Various stresses and impaired immunity
are considered predisposing factors. A bacteremia leads to infection in any of lungs, liver, spleen, brain, joints
and lymph nodes resulting in development of numerous suppurative and caseous abscesses. Signs depend on
the location of lesions.
Horses are susceptible and the disease is usually fatal after a course of several months. Among the signs
observed are neurologic disturbances, respiratory distress, colic, and diarrhea. In general the course of the
disease is quite variable and frequently is weeks to months in duration.
An acute septicemic form occurs in humans and animals which if untreated cases is fatal.
Diagnosis
A presumptive diagnosis is made at necropsy in endemic regions on the basis of multiple abscesses seen in the
liver, spleen, lungs and lymph nodes. Given the variable clinical character of the disease in the live animal, a
definitive diagnosis is based on laboratory identification of the causal agent.
 Material from fresh abscesses is cultured. The organism grows readily and is easily identified. Organisms in
clinical material have been detected using PCR and DNA probes.
 Serologic procedures including complement fixation and indirect hemagglutination could if available be of
value in non-endemic regions.
Treatment
There is little information on the treatment of melioidosis in the horse. The cost of prolonged treatment would be a
consideration.
 Ceftazidime administered for several weeks has been effective in human melioidosis.
Prevention
 Isolation of infected animals. Slaughter is mandatory in some countries.

 Disinfection of stables and safe disposal of bedding and manure when diarrhea due to melioidosis occurs.
 An effective vaccine is not yet available.

Humans are susceptible to melioidosis so great care should be taken to avoid contact with infectious materials.
Paecilomycosis
This is an infrequent, systemic mycosis, caused by Paecilomyces lilacinus and P. variotii, which usually begins as
a pulmonary infection. The fungi are widely distributed in soil and decaying organic material.
Although generally considered nonpathogenic these fungi have the capacity to produce infections in animals,
including the horse, dog, and cat, that are immunocompromised, debilitated or subject to prolonged
administration of antibiotics.
Lesions consisting of multiple gray-white, granulomatous nodules, that occur in the lungs and other tissues and
organs.
Diagnosis
 A strongly presumptive diagnosis is made on the basis of demonstrating the characteristic elements in wet
mounts and sections from lesions. These elements consist of septate pseudohyphae, oval conidia, and thin-
walled spores.
 Definitive diagnosis is based upon the demonstration of the fungal elements and the isolation and
identification of the fungi.
Treatment
 There is little information on treatment. Ketoconazole and other imidazole antifungal drugs may be effective
although the economics of extended treatment in the horse may be a limiting consideration.
Papillomatosis
(Warts)
Papillomatosis, or warts, is a viral disease of horses and other animals characterized by the formation of benign
tumors (papillomas) involving the skin and oral mucous membrane.
Cause
A papilloma virus of the family Papillomaviridae. The virus is resistant and remains viable for long periods of time
in contaminated mangers, harness, saddles, stables, fences, etc.
Occurence
Papillomatosis is a common disease of worldwide distribution. Warts are usually seen in horses up to three years
of age. Warts in older horses persist longer.
Transmission
Spread is by direct and indirect contact. The disease is self-limiting on individuals and sometimes will clear up
spontaneously. Warts, and tissues and blood from them, are highly infectious.
Clinical Features
Papillomas occur mainly around the nose, eyes and lips, vary in size and usually disappear within 2 - 3 months.
They are also seen distally on limbs, vulva, penis, ear and udder. Congenital papillomas occur on the head, neck,
back, and croup of newborn foals that are infected in utero. The so-called aural plaques, considered to be a flat
form of warts, are found on the inner surface of both ears.
Diagnosis
A laboratory diagnosis is not ordinarily carried out, as the lesions (warts) are clinically characteristic. However, if
the warts are atypical they could be confused with sarcoid.
 Histopathologic examination of tissue biopsies is confirmatory. The causal virus has not been grown in cell
cultures.
Figure 2. Groups of warts (papillomas) often involving muzzle.
Treatment
 Surgical excision is not usually indicated in horses.

 Warts in horses are usually a benign. A self-limiting disease; lesions usually regress spontaneously in time.
The value of topical treatment is questionable.
Prevention
 There is no evidence that autogenous vaccines are of value in prevention or treatment.

 Avoid crowding of young horses and foals and maintain optimum sanitation. Isolate if feasible.
Phaeohyphomycosis
Phaeohyphomycosis is a general term used to describe infections caused by dematiaceous (dark-pigmented)
fungi. These fungi are widespread saprophytes and the disease occurs worldwide.
It is a rare disease of horses and only several dematiaceous species have been implicated, including Alternaria
alternaria, Pseudallescheria boydii, Bipolaaris spicifera and Curvularia geniculata.
The fungi enter via a wound or at the site of trauma and produce a granulomatous nodule or mass involving the
dermis at or near the site of entry. Location is variable and can be nasal, paranasal, chest, head and limbs. The
nodules enlarge, ulcerate and have fistulous tracts. It may spread peripherally and, on occasion, to the
lymphatics and other tissues and organs. The disease is chronic and if not treated it may persist and progress.
Diagnosis
Laboratory examination is necessary to distinguish this disease from others with somewhat similar features.
 Material from granulomatous lesions and biopsies or portions of lesions, fixed: The characteristic
brown/dark-pigmented, branching, hyphal elements can be seen in wet mounts. The same fungal structures
are seen in stained sections. Finding the fungal elements in tissue sections is confirmatory.
 Definitive diagnosis is based on the isolation and identification of the fungus, which may take as long as 6
weeks to grow. The precise identification of the fungus may have to be carried out in a reference laboratory.
Treatment
 Surgical excision of the lesion in some cases. Amphotericin B, locally and systemically. The imidazole drugs
may be effective.
Potomac Horse Fever

(Equine monocytic ehrlichiosis)
Potomac horse fever (PHF) is a non-contagious, rickettsial disease of horses characterized by fever, enterocolitis
and frequently a profuse diarrhea.
Cause
It is caused by the rickettsia Neorickettsia risticii (formerly Ehrlichia risticii) and thus "ehrlichiois" is one name for
the disease. This rickettsia is closely related to N. helminthoeca the cause of Salmon poisoning in dogs.
Occurrence
The disease was first reported in Maryland (USA) in 1979 but is now known to occur widely in North America,
Europe and in some countries of South America and Asia. It is seasonal in North America occurring, often
sporadically, from May to October.
The disease is transmitted via the ingestion of caddisflies parasitized with metaceraria infected with N. risticii. The
trematode species producing the cercaria is not known. The way in which this rickettsia is maintained in nature is
likewise unknown.
Clinical Features
After ingestion the organism proliferates and causes a marked enterocolitis leading to fever, anorexia,
listlessness, and usually, but not always, diarrhea. Some mares abort in mid to late gestation, with placentitis,
retained placenta and fetal infection. Others may develop swelling of the lower limbs and ventral abdominal wall.
Laminitis may be seen as a complication in a large percentage of horses. Upwards to 30% of untreated horses
with the clinical disease die.
Diagnosis
The diseases that most resemble PHF clinically are salmonellosis, clostridiosis, and colitis-X. Because diarrhea is
not always present, other infectious febrile diseases may resemble PHF. Ulcerative gastroenteritis is the most
visible lesion at necropsy.
The disease can only be diagnosed with certainty by laboratory means.
 Acute and convalescent sera are preferred. The indirect immunofluorescence assay (IFA) test and the
ELISA for the detection and titration of antibodies are available in a number of laboratories. Results may be
too late to initiate effective therapy. These procedures (IFA and ELISA) are used almost exclusively for the
diagnosis of PHF. Vaccine titers are lower than those due to natural disease.
 The use of PCR to identify the agent in feces and blood is rapid and reliable.
 Isolation and cultivation of the agent in cell cultures is time-consuming and not practicable for many
laboratories
 Unclotted blood or blood smear for direct examination. Demonstration of the morulae of rickettsia in stained
blood smears (in monocytes and neutrophils) is indicative of PHF. Because of the irregular presence of the
rickettsiae in smears, this procedure is not usually carried out.
 There is no serologic cross reaction between the rickettsia of this disease and Anaplasma phagocytophila
(formerly E. equi) the cause of equine granulocytic ehrlichiosis.
 The organism can be isolated, cultured, and identified in macrophage cultures although this is not a routine
diagnostic procedure.
Treatment
 Tetracyclines given IV for 4 - 5 days are effective if administered early. Early fluid supportive therapy is
beneficial.
Prevention
 Until the mode of transmission is fully known little can be done in the way of preventing infection. Efforts
directed at reducing exposure to biting insects and ticks are not thought to be effective.
 Vaccination is recommended where the risk of disease is high. The efficacy of vaccination remains
questionable, but the severity of disease may be reduced in properly vaccinated individuals. Strain
difference in N. risticii may account for the lack of efficacy of the vaccine in some situations. The initial dose
should be given at 5 to 6 months of age with a second and third dose to follow at 3 - 4 week increments.
Boosters are then recommended at 4 to 6 month intervals depending on the risk of disease. Boosters should
be given in May to June in endemic regions.*
*From: Davis, E. Refresher on equine immunity and vaccination. DVM magazine, Fall, 2007.
Pythiosis
(Oomycosis)
Pythiosis is a chronic, infrequent, skin disease of horses characterized by granulomatous abscesses in
subcutaneous tissues.
Cause
It is caused by the fungus-like microorganism Pythium insidiosum (formerly called Hyphomyces destruens). It is a
plant pathogen that occurs in water and produces motile zoospores that can infect the skin via wounds and
abrasions.
Transmission
The fungus gains entrance via wounds involving the hoof, hock, fetlock, head, neck, and lips. Several cases of
intestinal pythiosis have been described in the horse.
Occurrence
The disease, which was originally called phycomycosis, is seen mainly in tropical and subtropical areas including
Australia, New Guinea, India, Japan, Indonesia, the Caribbean, and South America. A number of cases have
been reported from southern United States.
Clinical Features
In horses the lesions are usually large, roughly circular, granulomatous with ulceration and necrosis of skin and
underlying connective and muscle tissue. Fistulous tracts are common in advanced cases. Yellow-gray necrotic
cores are characteristic. Lesions are seen involving the lower limbs, chest, abdomen, and genitalia.
Diagnosis
The lesions are similar to those seen with entomophthoromycosis, some neoplasms, and cutaneous
habronemiasis.
 Affected tissue or biopsies, fresh and fixed, or smears from clinical material for direct examination. Pythiosis
is suspected if branching, usually non-septate hyphae, are demonstrable in stained sections and smears
from characteristic lesions.
Cultivation and identification are rather involved and may require the assistance of a mycologist.
Characteristic zoospores seen in cultures aid in identification.
 An agar gel immunodiffusion test is available in some reference laboratories.
Treatment
 Surgery, and amphotericin B, locally or systemically. Iodine lavages. If lesions are extensive the prognosis is
guarded.
 Immunotherapy has shown promise.
Rabies
Rabies is a fatal (rare exceptions), viral encephalitis of all warm-blooded mammals manifested mainly in either a
furious or dumb (paralytic) form.
Cause
Four serotypes of rabies rhabdovirus are recognized. Serotype 1 is responsible for classic rabies and is closely
related antigenically to serotype 4. More varieties of the rabies virus, called ecotypes have been identified using
molecular techniques. Particular ecotypes are associated with one or more animal species. Although susceptible
to common disinfectants and ultraviolet light, the virus retains its viability in tissues for several weeks at room or
refrigerator temperatures.
Occurrence
The disease occurs worldwide except for Australia, New Zealand the British Isles, Hawaii, the Scandinavian
countries, Cyprus, and Japan. It is frequently endemic in wild animals including the skunk, fox, raccoon, wolf,
bobcat, and coyote. There are also periodic epidemics among wild animals. Asymptomatic salivary gland
infections occur in vampire bats resulting in prolonged viremia. Insectivorous and fruit-eating bats may also be
infected.
The various animal species vary in their susceptibility from extremely high to low. The horse is considered
moderately susceptible.
The virus is shed in the saliva from infected salivary glands. The disease almost always results from the bites or
scratches of infected or rabid animals. Vampire bats transmit rabies to equids in South America. The virus
ascends a nerve trunk to the cord and brain. Several cases in humans have resulted from aerosol exposure.
Clinical Features
The incubation period is usually 2 - 8 weeks but can be longer than six months. The course is 3 - 10 days.
The following forms of the diseases are seen:
 Prodromal form: Animals show apprehension, anxiety, and changes in temperament and behavior. Severe
pruritis may develop at the site of infection. This stage lasts from 1 to 3 days.
 Furious form: Aimless wandering; bumps into objects; circling, falling and rolling excitement; irritability; biting
and kicking; chewing foreign materials and self; abnormal sounds; ataxia, paralysis, and death.
 aralytic form: This form is most common. Staggery gait, lameness, recumbency; doesn't usually bite;
muscular tremors; perceived difficulty in swallowing with salivation; colic; paralysis of hind quarters; ataxia
and terminal paralysis. This form is seen most often in the horse; however, the signs can be quite variable.
Diagnosis
The different forms of the disease make a clinical diagnosis difficult. History of exposure to potentially infected
wild animals should be considered.
Listeriosis (rare), cryptococcosis, toxoplasmosis, equine encephalomyelitis, equine protozoal encephalomyleitis,
and other infections of the central nervous system should be considered. Poisons such as lead, strychnine, and
various pesticides should also be considered.
If rabies is suspected great care should be taken in handling the animal to prevent human exposure. The horse
should be confined and if it is rabid, it will die within 10 days of showing signs. It may be advisable for humane
reasons to sacrifice the animal but in either case the head should be submitted, preferably by a veterinarian, to a
diagnostic laboratory that performs rabies diagnosis.
Rabies can only be definitively diagnosed by laboratory means.
 Specimens: The entire carcass or head.

 The fluorescent antibody (FA) procedure is widely used and is the preferred method. It is used on animals
that have died or been killed and is recommended for the immediate examination of wild animals that cannot
be readily held for observation. Smears of the hippocampus major are usually employed, but they can also
be from the salivary gland. Mice are inoculated with selected negative specimens. Correlation of 99.9%
between FA and mouse inoculation results is reported. The florescent antibody procedure recognizes
serotypes 1 and 4.
 Demonstration of Negri bodies in the neurons of the hippocampus major using Giemsa and Sellers' stains.
They are more apt to be found in animals that die of rabies. If Negri bodies are not seen, mice are inoculated
intracerebrally with a suspension of brain.
 In the living animal, a biopsy taken from the skin of the face (including tactile hair) and stained with FA
reagents is recommended for a rapid diagnosis. This is not a standard test and should not be used in
unvaccinated animals where there has been human exposure.
 Other procedures employed for identification of rabies virus are immunoperoxidase staining and the
polymerase chain reaction.
Treatment
 There is no treatment.
Prevention
 A variety of live attenuated and inactivated vaccines are available. Only inactivated vaccines are used in the
US, and only this kind of vaccine, in which the virus is cultivated in various cell lines, is recommended for
horses. Two doses of vaccine are given with an interval of 3 - 4 weeks followed by an annual booster. Brood
mares should be vaccinated before breeding and foals at 6 months of age. All should receive annual
boosters.*
 In endemic areas in the USA Ait is recommended that barns and stables should be racoon-proofed.

With regard to human exposure it is important to remember that the virus can be in the saliva of infected animals
from 1 to 13 days before clinical signs occur. Inactivated human or animal cell culture vaccines, rabies immune
globulin, and antirabies serum (equine) are widely used for prophylaxis in humans.
*From, Davis, E. Refresher on equine immunity and vaccination. DVM magazine, Fall, 2007.
Respiratory Infections: General
A number of viruses have the capacity to infect the equine respiratory tract, both upper and lower; however, only
a small number are responsible for significant clinical disease. They are equine herpesvirus 1, 4 infection (equine
rhinopneumonitis virus), equine influenza viruses, and equine arteritis virus.
Among the viruses that have been recovered from the equine respiratory tract and whose respiratory disease
significance may be minor or questionable, are equine rhinoviruses and equine herpesvirus 1.
Adenoviral infections in immunocompetent foals are usually mild, but adenoviruses can cause serious upper
respiratory tract infections in Arabian foals with combined immunodeficiency.
The following bacteria and fungi have been implicated in respiratory infections:
 Streptococcus equi: The most common bacterium causing upper respiratory disease in horses.
 Streptococcus zooepidemicus, Bordetella bronchiseptica, Klebsiella pneumoniae, Actinobacillus equuli,
Pasteurella multocida, P. caballi: These bacteria are sometimes associated with respiratory infections in
horses, both as secondary invaders of viral infections, and also occasionally as primary pathogens.
 Equine mycoplasmas: The significance in respiratory disease is not yet known. Mycoplasma felis has been
isolated from pleuritis in a horse.
 Aspergillus spp., (rare): Most often associated with gutteral pouch mycosis.
 Also rare are other fungi including Histoplasma capsulatum and Blastomyces dermatitidis.
Diagnosis
 If any of the four major viral diseases referred to above are suspected, consult the separate discussions for
information on diagnosis.
 Nasal swabs and tracheobronchial aspirates should be submitted for virus, bacterial and fungal isolation.
 Paired sera should be collected for serologic tests.
 PCR for particular pathogens are available through some reference laboratories.
Treatment
 General treatment will depend on the severity of the infection. Specific antimicrobial treatment if indicated.
Prevention
 Prompt isolation of affected animal(s) to prevent possible spread. Further measures will depend upon the
diagnosis.
 See specific diseases for additional information.
Rhinosporidiosis
Rhinosporidiosis is a chronic pyogranulomatous disease of horses, mules, cattle, dogs, and humans caused by
the fungus Rhinosporidium seeberi and characterized by the formation of polyps on the nasal and ocular mucosa
and occasionally on the skin. They may be sufficiently large and numerous to interfere with respiration.
They may be sufficiently large and numerous to interfere with respiration. The fungus, which has not been
cultivated on artificial media, is thought to occur in water as a free-living organism. Spores from the large
sporangia are presumed to gain entry to the nasal mucosa and occasionally the skin, via wounds.
The disease occurs infrequently in the southern United States; most cases are seen in tropical and subtropical
countries.
Diagnosis
Finding the typical nasal and ocular polyps suggest rhinosporidiosis; however, other fungi occasionally cause
granulomatous polyps in these locations.
Definitive diagnosis depends upon the demonstration of the characteristic large sporangia in sections of the
polyps or in nasal discharge.
 Specimens: Nasal discharge and surgically removed polyps, fresh and fixed.
 Nasal discharge and material from surgically removed polyps are examined in wet mounts for the presence
of the characteristic fungal elements. Stained sections of polyps are examined for the sporangia and spores.
Nasal discharge and ground polyps are cultured on bacterial and fungal media. No growth will be obtained
with R. seeberi.
Treatment
 Surgical removal of polyps is usually curative. When there is recurrence, ketoconazole has been effective
although information on treatment in horses is not available.
Rhodococcal Pneumonia of Foals

Rhodococcal pneumonia of foals is characterized by fever, coughing, anorexia, and a bronchopneumonia with
multiple abscesses in the lungs and bronchial lymph nodes.
Causes
The cause is Rhodococcus equi (formerly Corynebaterium equi), a small pleomorphic, heavily capsulated gram-
positive rod which occurs in soil, manure, and litter. More than 25 capsular serological types have been identified
from different animals and geographic regions. It is a facultative intracellular parasite that can survive and
multiply within macrophages.
The organism is carried as a commensal in the alimentary tract of some horses and can sometimes be isolated
from the equine cervix. The numbers of organisms in the intestine and consequently shed in feces may increase
enormously on endemic premises.
Occurence
It occurs worldwide. When it appears it may infect a number of foals and persist as a problem in some stables
presumably because of constant exposure to organisms in manure and soil.
The severe disease is seen mainly in foals 1 - 3 months of age. In foals older than three months, a subacute form
of the disease with a longer course is seen.
Various infections unrelated to pneumonia have been reported, including septicemia in neonatal foals, abortion,
uterine infections, emterocolitis (diarrhea) and subcutaneous abscesses. Extrapulmonary infections occur
occasionally in older horses.
Mode of Infection
Infection is mainly by the inhalation of dust particles laden with R. equi. Dry, dusty lots where organisms are
present or have been shed are frequently associated with infection. The organism is acquired shortly after birth,
within the first week of life. Pulmonary migration of helminth larvae may predispose to infection.
Clinical Features
The age of susceptibility is 1 - 6 months. Younger foals are affected most severely. The course of the severe
disease is 1 - 3 weeks.
After the initial granulomatous response suppurative abscesses of varying size develop in lungs and dependent
lymph nodes. Some foals also have abscesses involving mesenteric lymph nodes and intestine. Other
complications including osteomyelitis, nephritis, pericarditis, and liver abscesses have been reported. Signs
include fever, dyspnea, cough, anorexia, mucopurulent nasal discharge, poor growth, and eventually emaciation.
Figure 3. Extensive abscessation in lungs of foal with rhodococcal pneumonia.
Diagnosis
Of particular significance is a history of previous cases. Radiography will indicate advanced abscessation and
mediastinal lymphadenopathy. Auscultation of lungs may be helpful.
 Transtracheal wash samples are cultured and if positive for R. equi a definitive diagnosis can be made.
 R. equi can be readily cultured from the pus of pulmonary abscesses. Definitive diagnosis depends upon
isolation and identification of R. equi.
Treatment
 Treatment is usually successful if begun early. The combination of azithromycin or clarithromycin and
rifampin given orally for 2 - 3 weeks or longer has been effective. Other effective combinations are
trimethoprim with sulfamethoxazole, and ampicillin wih gentamycin. The latter should be monitored as it can
be nephrotoxic.
 Supportive therapy with fluids to cope with dehydration. A half to 1 liter of mare's serum may be helpful.
Prevention
 Vaccines are not available. Autogenous vaccines have not been effective.
 Passive immunization is employed for prophylaxis; hyperimmune plasma is administered intravenously to
protect foals from 1 - 8 weeks of age when they are considered most susceptible. It should be administered
in the first 1 - 2 days of life and repeated at approximately 28 days of age.
 Mares should not be allowed to foal on premises or quarters known to be contaminated, and foals should not
be kept in such an environment. Dusty, potentially contaminated areas should be scrupulously avoided.
 Routine parasite control program.

Although the likelihood of humans acquiring R. equi infection is probably minimal, a number of human infections
have been reported in immunocompromized patients.
Rotavirus Infection
Rotavirus has been incriminated as a cause of enteritis and diarrhea in foals less than three months of age. It is
most serious during the first two weeks of life and is characterized by depression, a greenish watery diarrhea,
dehydration, and reluctance to nurse. It is usually mild and of short duration unless complicated by bacterial
infection. A chronic form occurs in 10 - 40% of infected foals up to eight months of age causing intermittent
diarrhea.
Diagnosis
Because other agents frequently cause enteric infection with diarrhea laboratory examination is advised.
 The virus can most readily be demonstrated in feces within 24 - 48 hours of the onset of diarrhea.
 The characteristic virus can be seen by the examination of feces with the electron microscope.
 An ELISA has also been used to detect virus in feces. An equally sensitive latex agglutination test is also
available.
 The virus is difficult to isolate and cultivate.
Treatment
 Fluids for the dehydration; antibiotics for complicating bacteria; and general supportive measures.
Prevention
 Foals are usually protected by an adequate amount of colostrum. Affected foals should be kept in isolation.
 If foal rotavirus infection is a continuing problem, a killed virus vaccine is available for pregnant mares. A
three dose series is given during the last trimester of pregnancy (the series needs to be repeated annually in
at risk mares / farms).
Microbial Diseases: S through Z

1
Table of Content
 Salmonellosis
 Sarcoid
 Sporotrichosis
 Strangles
 Tetanus
 Tuberculosis
 Tularemia
 Tyzzer's Disease
 Urinary Tract Infections
 Vesicular Stomatitis
 West Nile Virus Infection*
 Zygomycosis (Basidiobolomycosi, Conidiobolomycosis)
Salmonellosis
Salmonellosis is a contagious, enteric, bacterial disease of many animals and humans characterized by
infections ranging from subclinical to septicemic.
Cause
Salmonellosis is caused by over 2000 serotypes of the gram-negative rod of the genus Salmonella. There are
several classification systems for members of the genus. We will use the traditional species names of which each
represents a particular serotype. New serotypes are given species names based on where they were isolated.
Some Salmonella species show a host predilection. The following species have been implicated frequently in
equine salmonellosis:
 Salmonella typhimurium (probably the most common and most pathogenic)

 S. enteritidis
 S. agona
 S. newport
 S. heidelberg
 S. anatum
Other species have been and will be involved. It is important to remember that there are no host-adapted
Salmonella spp., in horses.
All salmonellae are facultative intracellular parasites. There are frequently a number of subclinical carriers in a
stable that shed salmonellae intermittently. These carriers constitute the reservoir of the disease and the carrier
rate varies considerably from one stable to another.
Transmission
Infection is acquired by ingestion of mainly food and water contaminated with feces from infected or carrier
equids.
Occurrence
The disease is worldwide in distribution and some horses in stables, farms and clinics are carriers. In horses,
various stresses, e.g., long distance transport, deworming, strenuous training, surgery, overcrowding, and
parturition, can trigger serious individual cases and outbreaks. Foals are particularly prone to the septicemic
form. Acute and chronic enterocolitis are seen most commonly in older animals.
Salmonellosis is frequently a problem in transported horses and in hospitalized animals in equine clinics.
Pathogenesis
This is very complex and the following is a considerable simplification. First there is attachment of salmonellae
primarily to M cells within the epithelium. This is followed by penetration through and between mucosal cells into
the lamina propria. Release of endotoxin and enterotoxin contributes to fever, leukopenia, inflammation,
hemorrhage, necrosis, shock, and disseminated intravascular coagulation and diarrhea. The infection may be
limited to the intestine and adjacent mesenteric lymph nodes by phagocytic cells. Salmonellae have the capacity
to survive within macrophages and thus sustain the infection. Varying degrees of necrotic colitis is produced.
Bacteremia occurs infrequently in this enterocolitis stage of the disease.
Various stresses contribute to bacteremia which it may give rise to sepsis. If the latter is not fatal there is
dissemination to various organs including lungs, joints and the gravid uterus. Pneumonia, abortion, meningitis,
polyarthritis, osteomyelitis are some of the sequellae. In adults, laminitis is a major potential complication that
may occur in association with salmonellosis.
Clinical Features
Release of prostaglandins by enterotoxins activates adenyl cyclase resulting in enhanced intestinal fluid and
electrolyte secretion. Endotoxin producing septic shock is thought responsible for the severity of the disease and
death sometimes in less than 24 hours.
Clinical signs depend on the severity of the infection from mild, to acute enterocolitis and most severe,
septicemia.
Acute salmonellosis is characterized by fever, depression, anorexia, severe enteritis, watery diarrhea, and rapid
dehydration. Signs are similar but less severe in the less acute disease. Survivors are sometimes carriers and
thus shedders. In carriers the organism may persist in the mucosa of the colon and cecum and in mesenteric
lymph nodes.
Neonatal foals are subject to septicemic salmonellosis and those that survive may infrequently have with
neurological complications and/or polyarthritis.
Diagnosis
Salmonellosis is such a serious disease of horses that if suspected a laboratory diagnosis should be sought. All
of the diseases, in which chronic and acute gastroenteritis are seen, should be considered. Potomac horse fever,
clostridial enterotoxemia, and several idiopathic enteric diseases should be taken into account.
 Feces taken from the rectum are satisfactory for culture. Feces collected on a swab are sufficient in an
animal showing clinical signs; however, to detect carriers, 10 - 50 g of feces should be cultured. Five
negative fecal cultures on successive days will usually indicate the animal is not infected.
The culture of rectal biopsies rather than feces is sometimes performed to increase test sensitivity. A PCR
procedure has been developed for the examination of feces.
 From necropsied animals (sick or dead) portions of intestine, liver, spleen, lung, tonsil, and mesenteric
lymph nodes are cultured.
 Formalized portions of the above-mentioned tissues are appropriate for histopathology.
 It is not usually difficult to recover salmonellae from animals that have died as a result of salmonellosis.
Salmonellae recovered from lymph nodes and vital organs are especially significant. The finding of the
characteristic lesions of salmonellosis is supportive.
 Carrier animals shed salmonellae intermittently and, as mentioned above, three to five negative cultures on
successive days will usually indicate there is no intestinal infection.
Treatment
 Antimicrobial drugs may be used after susceptibility tests are conducted, although their value is
questionable. Strains that are resistant to more than one drug are common. It may not be possible to
eliminate the carrier state.
 If used, antibiotics are administered to adult horses during the acute stage of disease when the leukopenia is
severe. In young foals, antibiotics are administered through the course of disease to prevent dissemination
to multiple organs.
 Fluid and electrolyte replacement. Non-steroidal anti-inflammatory drugs (NASAID) such as flunixin
meglumine are used to cope with pain and the systemic effects of endotoxemia.
Prevention
 Efforts should be directed toward minimizing exposure, particularly to infected and carrier animals.
Salmonellae can survive for long periods in soil and manure.
 Autogenous bacterins have been used with variable success.

Salmonellosis is a zoonosis and special efforts should be made to avoid exposure to potential sources of
salmonellae.
Sarcoid
This is the most common neoplasm of horses, mules, and donkeys, worldwide.
Cause
It is assumed but has not been proved that the cause is a virus. There is some evidence that bovine
papillomavirus types 1 and 2 may be involved in the cause of sarcoid. This is mainly based on the demonstration
of viral DNA sequences in sarcoid tissue, and the fact that experimental infection with these viruses in horses
results in sarcoid-like lesions.
Transmission
There is evidence that sarcoids are transmissible by direct contact, arthropods and fomites.
Clinical Features
Most sarcoids occur on the extremities, ventral abdomen and head of equids less than four years of age. In
general they are described as flat or raised, pedunculated or verrucous, hairless and firm and adherent to the
underlying connective tissue. They vary greatly in appearance and as many as six different appearing types have
been described. Location varies somewhat with geographic regions. In the US they are seen most frequently on
the head, cervical region and head. Many animals will have multiple lesions. They vary in size from !-20cm. and
may persist for years. They do not metastasize and rarely disappear spontaneously.
Diagnosis
 Diagnosis is usually based on the characteristic appearance.

 Definitive diagnosis requires histologic examination of a biopsy.
Figure 1a. One of several types of sarcoid.
Figure 1b. Fibroblastic sarcoid.
Treatment
 Excision and cryosurgery are preferred treatments; two freeze-thaw cycles are used. Recurrence is 30 -
50% after surgical removal.
 Immunotherapy using BCG vaccine or an extract of Mycobacterium bovis (commercial preparations are
available); regression may take several months; the control rate is about 50%.
 Radiation therapy has a somewhat higher control rate than immunotherapy but is expensive and not widely
available.
Sporotrichosis
Sporotrichosis is an infrequent chronic fungal disease of Equidae characterized by the formation of suppurative
nodules mainly involving limbs.
Cause
The dimorphic fungus, Sporothrix schenckii which is present in soil and decaying wood and vegetation. The
mycelial phase occurs in nature and the yeast phase in affected animals.
Occurrence
The disease is occurs worldwide in many animals and humans.
Mode of Infection
The portal of entry of conidia is most commonly via cutaneous wounds of limbs. The latter have various causes
including slivers, barbs and thorns. Disseminated disease due to the inhalation of the organism or spread from
initial lesions is rare.
Clinical Features
The nodules (≈1 - 3 cm) which frequently suppurate involve mainly the skin, subcutis, superficial lymphatics and
lymph nodes.
In horses, the infection often begins in the lower part of the leg and spreads upward via the lymphatics resulting
in a chain of small, often suppurating, nodules. Ulcerating nodules exude a blood-tinged pus.
In the rare disseminated form there is hematogenous spread to vital organs, bones and CNS with a frequently
fatal outcome.
Figure 2a. Nodules of sporotrichosis.

Figure 2b. Characteristic suppurating nodules of sporotrichosis.
Diagnosis
The disease in the horse and mule resembles in appearance ulcerative lymphangitis (Corynebacterium
pseudotuberculosis) and epizootic lymphangitis (Histoplasma farciminosum). Nocardiosis, cutaneous glanders
and mycetomas caused by various fungi are other diseases that should be considered. Laboratory confirmation
should be sought.
Humans can readily be infected if infectious material enters the skin via cuts or abrasions.
 For direct examination: The cigar-shaped bodies that occur in lesions are very difficult to demonstrate in
stained smears and wet mounts. Fluorescent antibody staining has increased the success of direct
examination.
 For culture: The two phases of this dimorphic fungus can be readily cultured and identified; It takes from 1 -
3 weeks to grow.
Treatment
 Potassium and sodium iodide are used orally and intravenously; they are almost always effective.
 Oral organic iodide (EDDI) should be administered for a minimum of 1 month. Amphotericin B, flucytosine
(5-fluorocytosine), and natamycin (pimaricin) have been effective. Ketoconazole, fluconazole, and
itraconazole are effective. Treatment should be continued for a month after the infection appears to be
cured.

As mentioned above humans can be readily infected if infectious materials enter wounds and the latter may not
be evident. Veterinarians have been infected from horses. Great care must be taken while handling infected
equids to avoid exposure. Associated personnel should be apprised of the risk.
Strangles
Strangles is an acute contagious, bacterial disease mainly of young equids characterized by rhinitis, pharyngitis
and abscesses in dependent lymph nodes.
Cause
It is caused by the gram-positive bacterium, Streptococcus equi also referred to as Streptococcus equi
subspecies equi.
Occurrence
This is a relatively common disease with worldwide distribution. Young horses are most commonly affected but
all ages may be. Susceptibility is dependent on the animal's immune status.
Transmission
Infection is mainly by inhalation and spread may also be by contact and fomites.
The disease is usually acquired from carrier horses. This most often happens when horses from different
locations are brought together, e.g., at shows, sales, polo-fields, and racetracks.
Clinical Signs
The incubation period is 3 - 14 days and the course 2 - 4 weeks with recovery.
Clinical signs include fever, anorexia, difficult swallowing, extension of head and neck and coughing. There is a
rhinitis and pharyngitis with later swelling and eventual abscessation of lymph nodes, particularly the
intermandibular and parapharyngeal that drain the upper respiratory and buccal mucosa. The swelling may lead
to suffocation ("strangles") with the need for emergency tracheotomy. There is profuse purulent nasal discharge.
The abscessed lymph nodes rupture in I - 2 weeks discharging large amounts of pus.
A mild catarrhal form of strangles characterized by fever, nasal discharge and cough is seen in older horses with
some immunity to S. equi.
Figure 3. Strangles: Submandibular swelling due to abscessation.
Among the infrequent sequelae are variably disseminated abscesses and purpura hemorrhagica (Type III
hypersensitivity). Infrequently abscesses of the parapharyngeal lymph nodes rupture leading to infection of the
guttural pouch and sinuses. Horses thus infected may become carriers.
In rare instances the disease may be generalized and terminate fatally. Bastard strangles is an infrequent chronic
form with disseminated abscesses mainly in lymph nodes of the abdomen.
Diagnosis
A diagnosis is usually made on the basis of the characteristic clinical signs; however, laboratory confirmation is
recommended
 Horses suffering from S. equi infection are at risk for developing complications. In severely affected
individuals, upper airway endoscopy, thoracic ultrasonography and thoracic / skull radiographs may be
indicated. Upper airway endoscopy is indicated for those individuals with severe nasal discharge. This
evaluation will aid in identification of exudate and potential for chondroids allowing for facilitated lavage when
necessary.
 Fresh pus for culture is taken on a swab from, preferably, an excised mature abscess. The isolation and
identification of S. equi provides a definitive diagnosis. Older discharging abscesses may yield S. equisimilis,
which is a secondary invader.
 A procedure is available to test for anti-M protein antibodies (IgG); it is referred to as the SeM protein test.
This is particularly useful for those individuals at risk or showing signs of purpura hemorrhagica (PH). The
serum titer will not rise immediately, so in acute cases the values may initially be low (<1:1600), with more
severe disease or (in preparation) as a result* of vaccination high titers (> 1:1600) are obtained. In the
absence of vaccination high titers indicate that PH may be present. Vaccination is contraindicated in
individuals with high titers.
 PCR testing is available for nasal discharge or guttural pouch lavage samples.
Treatment
 Nursing care, complete rest, fluid therapy if indicated.

 Treatment with antimicrobial drugs is controversial. High doses of penicillin, sulfonamides, or trimethoprim-
sulfadiazine for 7 - 10 days are recommended for severe cases and nursing foals. Persisting fever with
pyemia is an infrequent complication for which the outlook is poor. If treatment is early the development of
abscesses can be prevented or reduced.
 Surgical drainage may be indicated. Tracheostomy may be necessary.
Prevention
 Isolation and monitoring of horses to be added to a stable for 3 - 4 weeks.

 *Vaccination is only recommended for high-risk individuals, e.g. introduction to a farm with endemic
strangles. Vaccination appears to reduce disease severity.
 Intranasal vaccine: Horses not previously vaccinated against Strep. equi subsp. equi should receive an initial
series of 2 vaccines approximately 4 weeks apart. Annual boosters are recommended in high risk
individuals.
 M-protein (subunit) vaccine: Adults should be vaccinated with an initial series of 3 vaccines at 4 week
intervals with booster vaccination at 10 - 12 month intervals.
 Foals considered at high-risk should be vaccinated with an intranasal vaccine beginning at 6 months of age
with an initial series of 3 vaccines administered at monthly intervals.
 Booster vaccines should be administered annually.
*Modified and reproduced with permission from Davis, E. Refresher on equine immunology and vaccines, DVM
magazine, Fall, 2007.
Tetanus
Tetanus is an acute, noncontagious, neurotoxic disease of farm and other animals characterized by painful tonic
and clonic spasms of skeletal muscles.
Cause
Clostridium tetani, a large, gram-positive, spore-forming, anaerobic rod. Its highly resistant spores are present in
the soil and feces of animals. The organism is not more prevalent in horse manure, but horses sustain more
wounds that allow for the growth of C. tetani.
Tetanospasmin or neurotoxin of C. tetani is one of the most powerful exotoxins known. It is a heat labile protein
produced by proliferating cells and released during autolysis. This neurotoxin is responsible for the characteristic
tonic and clonic spasms of skeletal muscles. Animal species vary in their susceptibility to the toxin and equids
and humans are the most susceptible. One milligram of pure toxin contains ~100 million mouse lethal doses.
Toxin is elaborated at the site of infection and passes along the axis cylinders of the motor neurons of the
medulla and spinal cord. It binds almost irreversibly to the gangliosides of nerve cells and thus antitoxin may not
be effective. All isolates of C. tetani produce only one antigenic type of neurotoxin. The toxin acts at the inhibitory
synapse where it blocks the normal function of the inhibitory transmitter. This results in excitation of the central
nervous system as evidenced by hyperesthesia and the greater intensity of reflexes.
Occurrence
The disease is worldwide in distribution. Tetanus is seen in veterinary practice most commonly in horses and
sheep. It is rare in dogs and cats. All ages are susceptible. Castration wounds, umbilical infection (tetanus
neonatorum) and parturition (puerperal tetanus) are among the circumstances that can contribute to tetanus in
animals.
Mode of Infection
The spores of C. tetani enter a variety of wounds and if necrosis is present they may germinate, grow and
produce neurotoxin.
Spores may germinate in dirty and neglected wounds with some necrosis (lowered oxidation reduction
potential=anaerobiosis) and when cells autolyse toxin is released at the site of infection.
Clinical Features
The incubation period is usually one to several weeks with an average about two weeks.
The first sign of tetanus to appear in horses is the inability to retract the nictitating membranes. This is followed
by convulsive contractions of the muscles of the fore and hind limbs then other voluntary muscles. Characteristic
of the disease in horses are erect ears, dilated anterior nares and stiff tail. Because of spasms of head muscles
there is difficulty in prehension and mastication. There is general stiffness, marked hyperesthesia with more
intense reflexes. The "sawhorse" stance is particularly characteristic of tetanus in foals. In fatal cases, muscles
throughout the body become involved. When death ensues, it results from spastic paralysis of muscles facilitating
respiration. In nonfatal tetanus, the spasms lessen and fewer muscles are involved. The fatality rate is ~80%
Figure 4. Saw-horse stance of foal with tetanus.
Diagnosis
Some features of tetanus are wounds (not always found, particularly in horses), gradual onset of stiffness,
hyperesthesia, followed by tetanic spasms of all voluntary muscles. The fatality rate in horses without treatment is
close to 100%. In contrast to tetanus, acute strychnine poisoning runs a course of one to several hours.
This disease is so characteristic clinically that a laboratory diagnosis is not required.
 If it is desired to attempt isolation and identification of C. tetani, material (pus, necrotic tissue) from the
wound should be taken so as to minimize exposure to air (oxygen), preferably in an anaerobic transport
system.
 Gram-stained smears from a wound may reveal the characteristic drumstick (terminal spore) bacteria;
however, their absence does not exclude tetanus.
Treatment
 Expose, clean, and disinfect wound.

 Muscle relaxants and sedatives. Stomach tube feeding. Dark, quiet environment.
 Penicillin and an adequate dose of tetanus antitoxin; intrathecal administration of antitoxin is used by some
clinicians.
 With comprehensive treatment the fatality rate can be reduced.
Prevention
 To prevent tetanus in a wounded animal that has not been vaccinated or if the vaccine status is not known,
clean and disinfect the wound. Administer antitoxin and toxoid at different locations; a large dose of penicillin
may also be given. Toxoid is given again in 30 days. The potential for serum hepatitis exists following
administration of tetanus antitoxin, so the antitoxin should only be administered to high risk individuals.
 For prevention administer 3 doses of toxoid 3 - 6 weeks apart with a booster dose given annually.
 Foals at 6 months of age are given 3 doses of toxoid at 4 - 6 week intervals with an annual booster.
Tuberculosis
Tuberculosis is rare in horses. Most cases are caused by Mycobacterium avium. In a cutaneous form granulomas
that may ulcerate are found on the upper limbs and abdomen.
In the generalized form tubercular granulomas are found in various organs and tissues including lung, liver,
kidney, lymph nodes, colon and myocardium.
There are reports of infection of cervical vertebrae by M. bovis.
Nodular granulomas involving the skin of legs have been attributed to several species of atypical mycobacteria.
Diagnosis
Tuberculosis in horses is most often diagnosed at necropsy.
 A highly presumptive diagnosis is usually based on the demonstration of typical acid-fast organisms in acid-
fast stained smears from lesions. Smears of biopsies and exudates can likewise be stained for acid-fast
organisms.
 Radiography may be helpful in diagnosis.
 Although culture may be carried out in a local diagnostic laboratory, definitive identification of mycobacteria
may require the aid of a reference laboratory.
 The tuberculin test has not been reliable.
Treatment
 This is not considered advisable or feasible when the disease is generalized

 Surgical resection for granulomas of the skin.
Tularemia
Tularemia is primarily a bacterial disease of wild animals that is occasionally transmitted by various means to
domestic animals including rarely the horse.
Cause
The cause is the small, gram-negative, facultative intracellular bacterium, Francisella tularensis which consists of
two biotypes: the more virulent type A, referred to as tularensis, and the milder type palaeartica. The biotypes
differ in host specificity, biochemical activity, and geographical distribution.
Occurrence
The disease occurs in horses of all ages but is rare.
Biotype A tularensis occurs mainly in the northern hemisphere and is predominant in North America; biotype B,
palaeartica, is found in Eurasia.
Transmission
Wild animals are the reservoir of infection, especially rabbits and hares, but also beaver, muskrat, squirrel,
woodchuck, opossum, skunk, deer, elk, bison, and fox. Domestic fowl can act as a reservoir of infection.
F. tularensis is most frequently transmitted by ticks but also by a large range of biting arthropods including flies,
mites, mosquitoes and lice. Infection also takes place via aerosol and ingestion of contaminated food and water.
Clinical Features
The incubation period is usually less than 10 days. What begins as a localized infection proceeds by infection of
macrophages and their spread to lymph nodes, liver, and spleen with formation of granulomatous, necrotic foci.
Severity of the disease is variable depending upon the location and extent of lesions.
Among the clinical signs are fever, weakness, stiff gait, edema of limbs, anorexia, dyspnea and diarrhea, followed
by prostration and frequently death if untreated.
Diagnosis
A history of exposure to ticks that may have been feeding on a sick or dead wild animal could be suggestive.
Although tularemia is rare in the horse it should be considered when a sporadic, severe, febrile infectious disease
occurs.
If tularemia is suspected, great care should be taken in performing a necropsy. All work with material from
suspected tularemia cases must be carried out in a biologic safety cabinet or alternatively sent to a laboratory
equipped to handle this highly infectious, dangerous organism.
 For serology: Serum samples are taken in the advanced disease and paired samples if obtainable. An
agglutination test is usually positive late in the disease. A 4-fold increase in titer of paired sera is significant.
An indirect fluorescence assay is also available to detect antibodies.
 Portions of liver, spleen, and lymph nodes with the characteristic necrotic foci provide material for smears
and culture. This gram-negative organism, which somewhat resembles a Brucella species, requires a
medium containing cystine for growth. The most rapid means of identifying F. tularensis is by the specific
fluorescent antibody staining of smears from biopsies and lesions. A slide agglutination test using known
specific antisera is also available in some diagnostic laboratories to identify colonies of F. tularensis.
Treatment
 Streptomycin is the drug of choice; tetracyclines including doxycycline are also effective; prolonged
treatment is necessary.
Prevention
 Little can be done other than attempt to reduce of tick exposure.

Francisella tularensis causes a serious disease in humans. As mentioned above great care should be taken to
avoid exposure to this highly infectious agent. Some laboratories decline to attempt culture.
Tyzzer’s Disease
Tyzzer's disease is a severe, usually fatal, bacterial infection of many animals including foals.
Cause
The cause is the large, spore-forming, motile, gram-positive, anaerobic rod, Clostridium piliformis which is part of
the normal intestinal flora of many rodents.
The organism has not been cultivated in artificial media, but can be grown in cell cultures and in the yolk sac of
chicken embryos.
Occurrence
The disease is probably worldwide in occurrence. It has been found in laboratory mice, rats, hamsters, gerbils,
rabbits, nonhuman primates, horses, dogs, cats, and other animals. Although known for many years, it has only
been reported in dogs, cats, and foals in recent years. The age range of susceptibility for foals is usually 1 - 5
weeks. Although usually sporadic there may be a cluster of cases on some farms. Adult horses may be carriers.
Mode of Infection
This by ingestion or arising from the affected individual’s own flora (endogenous). The disease is thought to
possibly result from various stresses.
Clinical Signs
Foals may be found dead or in a coma without showing premonitory signs. The disease is characterized by
enteritis (not in all cases), ileocolitis and focal, necrotic hepatitis.
Some foals may show depression and icterus and die within 24 hours. The course is about 48 hours. Clinical
signs are only apparent for a short period; they include fever, icterus, and occasionally diarrhea. Recovery is rare.
Diagnosis
Acute salmonellosis, Actinobacillus equuli infection, and Rhodococcus equi septicemia (rare), and other acute
microbial infections should be considered. There are no diagnostic procedures for definitive diagnosis in the live
foal.
 For pathology and smears: Portions of the liver, fresh and fixed. The disease is usually diagnosed by finding
the typical liver lesions (multifocal necrosis) and demonstrating the characteristic organisms in hepatocytes
in stained smears. Liver sections stained by the silver impregnation method are also useful for the
demonstration of the organism at the margin of lesions. As mentioned earlier the organism cannot be
cultured in artificial media.
Treatment
 Treatment cannot ordinarily be instituted in time. If suspected large doses of penicillin or ampicillin may be
given intravenously; however, if the individual has the disease it usually dies.
Prevention
 Improvement of sanitation if indicated; reduction of stresses.

 Clostridium piliformis produces spores that require a temperature of 80°C for 30 minutes for inactivation.
Strict sanitary measures should be implemented to prevent spread to other foals.
Urinary Tract Infections

Urinary tract infection refers broadly to infection of the kidney, bladder, or urethra; more than one may be
affected. Cystitis, which is relatively infrequent, is by far the most common urinary tract infection in the horse.
Pyelonephritis occurs occasionally in postpartum mares.
Some characteristics of equine cystitis are as follows:
 Cystitis is more common in the mare.

 It may be secondary to urolithiasis.
 It is usually an ascending infection.
 In older mares cystitis may result from uterine or vaginal infections.
The bacteria most often involved are: Escherichia coli, Proteus mirabilis, Klebsiella spp., Enterobacter spp.,
Pseudomonas aeruginosa, Staphylococcus spp., Streptococcus spp., Corynebacterium renale.
There are frequent efforts to urinate that may be painful. The horse may continue to stand as though urinating,
and strain to do so. Small amounts of urine are passed, and blood and pus may be present.
Diagnosis
Urine for culture should be collected by catheterization. See Section 4 for the handling of urine for submission to
the diagnostic laboratory.
Treatment
 Treatment is indicated if the bacteriological examination indicates a bacteriuria.

 The drug to be used for treatment will depend on the antimicrobial susceptibility test. Among the drugs used
are: trimethoprim-sulfadiazine, enrofloxacin, gentamicin, penicillin, ampicillin, amikacin, cephalosporins (3rd
generation preferred), and tetracyclines.
 The efficacy of treatment is determined by a follow-up bacteriological examination.
Vesicular Stomatitis
Vesicular stomatitis is a contagious viral disease of cattle, horses, pigs, and goats, characterized mainly by the
formation of vesicles, followed by erosions, of the mucous membrane of the mouth.
Cause
The cause is a rhabdovirus (Rhabdoviridae). The two important serotypes are designated New Jersey (most
virulent and common) and Indiana. The latter type has three subtypes that occur in South America where there
are endemic regions. The virus can remain viable in the environment for several days.
Occurrence
The disease occurs periodically in North (mainly southwestern USA), Central and South America. Recent
outbreaks occurred in horses in Arizona, Colorado, New Mexico and Utah.
Horses, cattle, goats, swine and humans are susceptible, as are bighorn sheep, deer and antelope.
Transmission
The disease is spread rapidly by direct contact, biting insects, and fomites.
Clinical Features
The incubation period is usually 2 - 8 days.
Vesicles containing clear fluid are found involving the mucous membrane of the tongue particularly, the mouth
and the coronary band. Lesions have been found less frequently on the nasopharynx, turbinates, larynx, prepuce
and mammary gland. The vesicles swell, break and leave painful ulcers or erosions. Horses drool and are
reluctant to eat and drink, and may display lameness. Most horses recover fully within a month.
Figure 5. Drooling characteristic of vesicular stomatitis.
Diagnosis
When horses sustain a vesicular disease with the characteristics of VS, one can almost be certain that it is VS in
that the horse is not susceptible to foot-and-mouth disease, nor is it susceptible to swine vesicular disease and
vesicular exanthema except that some viral strains of the latter rare disease can produce vesicles in horses.
In many countries, including the USA, vesicular stomatitis is a notifiable disease. Specimens will be collected by
state, provincial, or federal animal health officials.
 Epithelial tissue covering the vesicles in the mouth should be collected and placed in buffered glycerol or
frozen for shipment. If available, vesicular fluid should be collected aseptically in a sterile vial and frozen.
Virus isolations are attempted. Tissue suspensions and vesicular fluid are tested for antigen using the
ELISA, complement fixation (CF) or virus neutralization (VN) procedures. If virus or antigen is not detected
material is passaged in mice, embryonated eggs or cell cultures, then retested.
 Paired serum samples (acute and convalescent), can be used for, ELISA, CF, or VN tests to determine if
there is a rise in vesicular stomatitis antibodies.
Treatment
 None, except the use of mild antiseptics and astringents on the mucosa of the mouth and provision of soft
feed.
Prevention
 In many countries when a suspected vesicular disease occurs, it should be reported immediately to officials
in charge of animal health.
 Affected animals are isolated and quarantine may be applied.
 After outbreaks premises are thoroughly cleaned and disinfected.
 Vaccines are employed in some countries in South America.

Humans can acquire the virus from infected horses. The infection in humans is influenza-like with stomatitis
characterized by blisters in the mouth, fever, headache and general malaise.
West Nile Virus Infection*
The West Nile virus has a reservoir in birds and is transmitted by mosquitoes to horses in which it may produce a
serious encephalitis.
Cause
West Nile virus is a flavivirus which belongs in the Japanese encephalitis serogroup of the family Flaviviridae.
Occurrence
West Nile virus infection (WNVI) occurs in countries of Asia, Africa, Europe and North America. The virus was
introduced to the USA in 1999 and by 2004 it had spread throughout the continental USA. There were > 4000
human cases in 2002, with 274 deaths, mainly in people over 60 years of age. Less than 1% of those infected
were symptomatic. The number of cases will probably decrease as the infection becomes endemic.
During the same period that human cases occurred there were many reports of the disease affecting horses in
the USA More than 15,000 cases were reported in 2002 and somewhat less in 2003. Older horses are more
susceptible. It is estimated that 10 - 30% of the horses infected develop clinical disease.
In 1997 in Israel a neuroparalytic disease of young geese was attributed to WNV. Geese appear to be the only
natural host among domestic avian species.
Transmission
This is mainly by mosquitoes. It is estimated that at least 58 mosquito species can carry the virus. Culex pipiens
is considered the most important for maintaining the virus. Upwards of 300 bird species harbor the virus, many
without evidence of clinical disease. House sparrows are thought to be the most important in dissemination. They
are readily infected and have high levels of virus. Although some birds such as crows, blue jays and magpies
may die of infection, house sparrows don’t.
The incubation period in horses is 7 - 14 days. Signs may appear suddenly or gradually; they may include
incoordination, dragging hooves, buckling at knees, difficulty eating and drinking, stumbling, muscle weakness,
dullness, somnolence, paralysis, inability to rise. Some horses may have a mild infection with low fever, muscle
trembling and evidence of a less severe disease.
Many horses that recover from the disease have residual abnormalities such as irregularities of gait, behavioral
changes and neurological deficits six months after diagnosis. If horses don’t recover sufficiently they may have to
be euthanized. The mortality rate in unvaccinated horses developing clinical disease is ~33%. Horses surviving
infection are considered immune for life.
The lesions in horses are very similar to those of eastern equine encephalitis (EEE). There is perivascular
lymphocyte cuffs, gliosis and neuronal degeneration. What is distinctive with West Nile infection is a poliomyelitis
affecting the gray matter of the spinal cord. The brainstem and midbrain are also affected but not usually the
cerebral cortex. In EEE the whole brain is affected with the cerebrum most affected.
Diagnosis
 Serum IgM with the capture ELISA is the preferred confirmatory diagnostic test.
 Clinical specimens: Whole blood collected during the febrile stage and brain tissue from horses that have
died. Acute and convalescent sera.
 A presumptive diagnosis is often based on clinical signs and the microscopic brain lesions referred to above.
It can also be made on the basis of clinical signs and results of a single serum sample, if those results are
positive and the horse has not been vaccinated.
 A definitive diagnosis can also be obtained by demonstrating a significant increase in specific antibody
between acute and convalescent sera.
 The virus can be propagated on the chorioallantoic membrane, where it produces plaques, and in various
cell cultures.
Treatment
 Steroids to reduce inflammation; general supportive care. An equine product containing specific viral
antibody is being used in early treatment of non-vaccinated horses.
Prevention
 Vaccination is recommended. One inactivated vaccine is given in two doses 3 - 6 weeks apart. A
recombinant vaccine using a canary poxvirus vector is also available. Two doses are given with annual
boosters. A one dose, DNA vaccine (first of its kind licensed in the USA), claims to prevent viremia in WNV
infection. Some practitioners vaccinate every four months with the inactivated product where mosquitoes are
present year-round. Inactivated vaccine is considered safe for brood mares.
 A chimera vaccine (live, weakened yellow fever virus with genes from WNV) has been approved in the USA.
An initial series of two doses is given with an annual booster,
 Strict mosquito control greatly reduces the chances of exposure. Keep horses indoors from dusk to dawn
when insects are most active; keep lights off during the evening and keep stable areas clear of birds and
poultry.

As stated above this virus can infect humans, sometimes seriously. Measures should be taken, including
mosquito control, to protect personnel who might be exposed when the equine disease occurs or is suspected.
*Adapted from, A Concise Review of Veterinary Virology, Carter, G.R., Wise, D.J. and Flores, E.F. 2005,
International Veterinary Information Service (Available from www.ivis.org).
Zygomycosis
(Basidiobolomycosis, Conidiobolomycosis)
This rare mycosis, which mainly affects the nasal mucosa and subcutaneous tissue, is primarily a disease of
horses although some other animals are occasionally affected.
The fungi involved, which occur in soil and decaying organic matter, belong to the genera Basidiobolus and
Conidiobolus. Two of the principal species of these genera are mentioned below but other species can be
involved.
Conidiobolus coronatus, which infects mainly the horse, produces ulcerative granulomatous lesions involving the
mucous membrane of the nasal passages and mouth. Nasal discharge and mechanical blockage may result.
Lesions caused by B. ranarum may be large and involve the skin of the head, neck, and chest. There may be
ulceration, yellow necrotic centers, fistulous tracts, with extension to regional lymph nodes.
Diagnosis
The nature and location of the lesions help distinguish zygomycosis from phaeohyphomycosis and cutaneous
habronemiasis.
 Material (exudates, discharges) from lesions is examined for large, branching, occasionally septate hyphae.
The same fungal elements are seen in stained sections of lesions.
 Exudates, discharges and fresh material from lesions are cultured. Because these fungi are widespread in
nature and are often contaminants in specimens and on media, the finding of the fungal elements in tissue
sections is especially significant. Some fungal cultures may have to be submitted to a reference laboratory
for identification.
Treatment
 Surgical excision with amphotericin B given locally and systemically.

 Immunotherapy, by which particulate fungal material is injected intradermally, is thought to be beneficial.
Microbial Diseases: Immunization Summary

1
For further detail see the disease discussions in Section 2.

In the use of all vaccines it is important to follow carefully the recommendations of the manufacturer.
Recommended for All Horses
 Equine Influenza
 Inactivated vaccine
 Foals: Begin at 9 months with a series of 3 vaccinations.
 Until 2 years of age (high risk): Every 3 - 4 months.
 Yearlings: Every 3 months.
 Non-performance horses: Every 6 months.
 Performance: Every 3 - 4 months.
 Mares: Every 6 months and booster 4 weeks before foaling.
 Intranasal vaccine
 Horses 11 months or older: Initial series of 2 doses, 4 weeks apart. Biannual vaccination.
 Eastern and Western Equine Encephalitis

 Foals: 4 months, if dam properly vaccinated.
 Yearlings: 12 months, then annually.
 Adults: Begin with 3 vaccinations at 3 - 4 week intervals then annual boosters or more depending on
geographic region. Annually.
 Mares: Annually with booster 4 weeks before foaling.
 Equine Viral Abortion / Rhinopneumonitis (EHV - 1 and 4)
 Foals: 4 - 6 months with series of 3 vaccinations.
 Adults: Every 4 - 6 months; annual booster.
 Young horses (high risk): Booster vaccination every 4 - 5 months.
 Mares: 3, 5, 7 and 9 months of gestation to protect against abortion.
 Tetanus
 Tetanus toxoid
 Foals / Weanlings: 3 months and 4 months.
 Mares: Annually and 3 - 5 weeks before foaling.
 Other horses: Annually.
Recommended for Horses in High Risk and Endemic Regions
 Anthrax
 Sterne spore vaccine
 Foals: 2 vaccinations 3 weeks apart. Beginning at 6 months.
 Broodmares: Annually but not during pregnancy.
 Other horses: Annually.
 Botulism
 Inactivated type B vaccine
 Brood mares: Series of 3 vaccinations at 8th, 9th and 10th of gestation; subsequent pregnancies vaccinate at
4 - 6 weeks before foaling.
 Foals: After passively derived antibodies decline – 6 months.
 Equine Viral Arteritis

 Modified live vaccine
 Stallions and mares: Vaccinated not less than 3 weeks before breeding.
 Pregnant mares and foals less than 6 weeks of age: should not be vaccinated. All at risk should be vaccinated.
 Potomac Horse Fever

 Inactivated product. Value questionable.
 All horses: Initial dose given at 5 to 6 months with a second and third dose at 3 - 4 week intervals.
 Boosters given at 4 - 6 month in the spring depending on risk of disease.
 Rabies
 Foals: If adequate passive transfer vaccinate at 6 months.
 Brood mares: Should be vaccinated before breeding.
 All horses: Initial series of 2 vaccinations administered at 3 - 4 week intervals.
 Strangles
 M-protein subunit vaccine
 Foals: At 6 months with a series of 3 vaccinations at monthly intervals.
 Adult horses: Initial series of 3 vaccinations at 4 week intervals with annual boosters.
 Mares: Intranasal vaccine.
 Initial series of 2 doses about 4 weeks apart with annual boosters.
 Venezuelan Equine Encephalitis

 Same regimen as Eastern and Western equine encephalitis above.
 West Nile Virus Infection

 All horses including brood mares: Two doses 3 - 6 weeks apart. Vaccinate as frequent as every 4 months
where mosquitoes are present year-round.
 A live recombinant vaccine
 Two doses are given with annual boosters.
 DNA vaccine
 One dose.
 Chimera vaccine
 An initial series of two doses is given with an annual booster.
 Vaccination is recommended. One inactivated vaccine is given in two doses 3 - 6 weeks apart. A recombinant
vaccine using a canary poxvirus vector is also available. Two doses are given with annual boosters. A one
dose, DNA vaccine (first of its kind licensed in the USA), claims to prevent viremia in WNV infection. Some
practitioners vaccinate every four months with the inactivated product where mosquitoes are present year-
round. Inactivated vaccine is considered safe for brood mares.
A chimera vaccine (live, weakened yellow fever virus with genes from WNV) has been approved in the USA. An
initial series of two doses is given with an annual booster.

Guide to Microbial & Parasitic Horse Diseases

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A Concise Guide to the Microbial and Parasitic Diseases of Horses

G.R. Carter1, P.A. Payne2 and E. Davis3 (Eds.)

List of Microbial and Protozoal Diseases by Organ System

Selection, Collection, and Submission of Specimens for Diagnosis

Sources for Additional Information

Microbial Diseases: A through D

 Actinobacillus equuli Infection

Actinobacillus equuli Infection

 Prophylactic administration of broad-spectrum antibiotics is indicated in situations such as failure of

African Horse Sickness

 Early treatment with penicillin, tetracyclines, amoxicillin, ciprofloxacin, erythromycin, chloramphenicol,

Public Health Significance

 Guttural pouch mycosis: Discussed later under this name.

 Chest radiographs may suggest blastomycosis.

 Clinical specimens: brain, fresh and fixed. Serum.

Public Health Significance

Public Health Significance

 Nystatin, clotrimazole, ketoconazole or iodine solutions are used topically.

Clostridial Enterotoxemia of Horses

 Type A: enterotoxin - cytotoxic

 C. perfringens type A, B or C antitoxin or antiserum.

Clostridia-Associated Enterocolitis in Horses

 Balanced electrolyte solution administered intravenously

 Ketoconazole or fluconazole is given in some cases for as long as a year.

Public Health Significance

 Prophylactic administration of broad-spectrum antibiotics, or amikacin plus penicillin is indicated in some

Corynebacterium Pseudotuberculosis Infections

External and Internal Abscesses

 A definitive diagnosis in pectoral abscesses is based on isolation and identification of C. pseudotuberculosis

Public Health Significance

Public Health Significance

Figure 1. Circular crusty lesions of ringworm (dermatophytosis).

 Isolation of infected animals if feasible. It is often a self-limiting disease.

Public Health Significance

Microbial Diseases: E through F

Equine Adenovirus Infection

 Horses should not be bred if lesions are present. No vaccine is available.

Public Health Significance

 Isolation of infected animals and strict control of ticks.

Public Health Significance

 None except supportive therapy.

Equine Rhinovirus Infection

 Surgical measures are generally the only curative therapy.

Foal Diarrhea and Septicemia

Microbial Diseases: G through L

 In most countries solipeds with glanders are slaughtered.

Public Health Significance

Hendra Virus Infection

Public Health Significance

Infectious Abortion (General)

 Streptococcus zooepidemicus, and other streptococci.

 Antimicrobial treatment is determined by the results of the antimicrobial susceptibility test.

 Treatment should be as early as possible. Tetracyclines, streptomycin, doxycycline, dihydrostreptomycin,

Public Health Significance

 Treatment is usually of little value after neurologic signs are seen.

 Tick control; dips are less effective than topical acaricides.

 A vaccine is not yet available for horses.

Public Health Significance

Microbial Diseases: M through R

 Malignant Edema (Closridial Myositis)

 Isolation of infected animals. Slaughter is mandatory in some countries.

Public Health Significance

 Surgical excision is not usually indicated in horses.