Communicable Disease Nursing

EABFQ

Communicable Diseases
Communicable Diseases are Primary Cause of Mortality Gap between Rich and Poor Countries  Non-communicable diseases account for 59% of all deaths worldwide estimated to rise from 28m in 1990 to 50m in 2020


Communicable Diseases
      

About 60% of deaths caused by communicable diseases can be attributed to: HIV/AIDS Malaria Tuberculosis Measles Diarrheal disease Acute respiratory infection

Communicable Disease
is an illness due to an infectious agent or its toxic products which is easily transmitted or communicated directly or indirectly from one person or animal to another ** Both infectious and contagious diseases are communicable** **All contagious diseases are communicable **All but not all communicable diseases are contagious**


Philippines top 10 leading causes of morbidity & mortality in the year 2007:
          

Diarrhea Bronchitis Pneumonia Influenza Hypertension Tuberculosis Malaria Heart diseases Cancer Accidents Chronic obstructive pulmonary disease and other respiratory diseases Diabetes and Kidney diseases.

Host and Microbial Interaction

INTRODUCTION Although most microorganisms live in harmony with the human body, somecalled pathogenscan infect the body and cause disease. Infectious diseases range from mild illnesses, such as a cold, to fatal illnesses, such as AIDS. We occasionally come into contact with people or animals that are infected and thus expose ourselves to the pathogens of their diseases. In fact, our environment is such that everyday we live with some risk of exposure to diseases.

Communicable Disease = any disease that spreads from one host to another, either directly or indirectly Contagious Disease = disease that easily spreads directly from one person to another Infectious Disease = disease not transmitted by ordinary contact but require a direct inoculation through a break in a previously intact mucous membrane. On the other hand, all contagious diseases are infectious.

Examples of communicable diseases include herpes, malaria, mumps, HIV/AIDS, influenza, chicken pox, ringworm, and whooping cough. Cancer, on the other hand, is not a communicable disease.

Carrier is an individual who harbors the organism and is capable of transmitting it to a susceptible host without showing manifestations of the disease. Contact - is any person or animal who is in close association with an infected person, animal, or freshly soiled material

Classification of Infectious Diseases:



Based on Occurrence of Disease: 1. Sporadic Disease = disease that occurs only occasionally & irregularly with no specific pattern i.e. botulism, tetanus 2. Endemic Disease = constantly present in a population, country or community i.e. Pulmonary Tuberculosis; malaria

3. Epidemic Disease = patient acquire the disease in a relatively short period of time ; greater than normal number of cases in an area within a short period of time i.e, i.e, cholera; typhoid 4. Pandemic Disease = epidemic disease that occurs worldwide i.e. HIV infection; SARS

Based on Severity or Duration of Disease 1. Acute Disease = develops rapidly (rapid onset) but lasts only a short time i.e. measles, mumps, influenza

2. Chronic Disease = develops more slowly (insidious onset) disease likely to be continual or recurrent for long periods i.e. TB, Leprosy 3. Subacute Disease = intermediate between acute and chronic i.e. bacterial endocarditis 4. Latent Disease = causative agent remains inactive for a time but then becomes active to produce symptoms of the disease i.e. chickenpox shingles (zoster); amoebiasis

Based on Extent of Affected Hosts Body 1. Local Infection = microbes invade a relatively small area of the body 2. Generalized (Systemic) Infection = spread throughout the body by blood or lymph i.e. measles 3. Focal Infection = local infection that spread but are confined to specific areas of the body

Based on State of Host Resistance: Resistance:

1. Primary Infection = acute infection that causes the initial illness 2. Secondary Infection = one caused by an opportunistic pathogen after primary infection has weakened the bodys defenses 3. Subclinical (Inapparent Infection) = does not cause any noticeable illness

Period of Decline s/sx subside pathogen replication is brought under control vulnerable to secondary infection Period of Convalescence


Replication of pathogenic organisms is stopped

regains strength and the body returns to its pre diseased state = recovery has occurred

Nurse Alert!!!!


Note that in the case of acquired immunity against a pathogen the progress of disease may end during the prodromal period as a consequence of the rapid immune system response to the infection. For example, acquired immunity might be as a consequence of vaccination or previous natural exposure to the pathogen.

MICROBES against HUMAN

Definitions:  Symptoms subjective evidence of disease that is experienced or perceived subjective changes in body function noted by patient but not apparent to an observer  Signs objective evidence of a disease the physician can observe and measure  Syndrome a specific group of signs and symptoms that accompany a particular disease

Incidence the number of people in a population who develop a disease during a particular time period Prevalence = the number of people in a population who develop a disease, regardless of when it appeared = refers to both old and new cases

Stages of Diseases

Stages of Disease


Incubation Period
- time interval between the initial infection and the 1st appearance of any s/sx - patient is not yet aware of the disease Prodromal Period - early, mild appearance of symptoms of the disease Period of Illness  Time of greatest symptomatic experience ( pt. is sick) - overt s/sx of disease WBC may increase or decrease can result to death if immune response or medical intervention fails

INFECTION - condition caused by the entry and multiplication of pathogenic microorganisms within the host body

CONDITIONS THAT AFFECT INFECTION DEVELOPMENT

 

  

Pathogenicity ability to cause disease Infective dose (sufficient number of microorganisms needed to initiate infection) Virulence ( disease severity) and Invasiveness of microorganisms ( ability to enter and move through tissue) Organisms specificity ( host preference) Resistance of the host Immunity of the host **Cycle of infection must be completed**

Chain of Infection

Chain of Infection
The chain begins with the existence of a specific pathogenic microorganism

The second link is the reservoir, an environment where the pathogen can survive.

Chain of Infection

The third link is the means of escape from the reservoir. ( Mode of Exit )

The fourth link is the mode of transmission from the reservoir to the host.

Chain of Infection
The fifth link is the means of entry into the host ( Mode of entry)

And the last link is the host's susceptibility to the pathogenic microorganism

Infection control: 1st line of defense

 

Hand hygiene, first line of defense and the hygiene, most important practice in preventing infection. Handwashing single most important way of preventing transfer of microorganisms

IMMUNITY
- is the condition of being secure against any particular disease, particularly the power which a living organism possesses to resist and overcome infection - is the resistance that an individual has against disease

IMMUNE SYSTEM PROTECTION AGAINST INFECTIVE OR ALLERGIC DISEASES BY A SYSTEM OF ANTIBODIES, IMMUNOGLOBULINS AND RELATED RESISTANCE FACTORS. FACTORS. ANTIBODY - a specific immune substance produced by the lymphocytes of the blood of tissue juices of man or animal in response to the introduction into the body of an antigen

1.
1.

ANTIGEN TRIGGERING AGENT OF THE IMMUNE SYSTEM; FOREIGN SUBSTANCE INTRODUCED INTO THE BODY causing the body to produce antibodies TYPES OF ANTIGENS: ANTIGENS: INACTIVATED ( KILLED ORGANISM) ORGANISM)
2. 3.

Not long lasting Multiple doses needed Booster dose needed

2. ATTENUATED ( LIVE WEAKENED ORGANISM) ORGANISM) 1. single dose needed 2. long lasting immunity ** all vaccines lose their potency after a certain time.

TYPES OF IMMUNITY


NATURAL =innate; within the HOST; Immune System ACQUIRED = outside the HOST Natural = active or passive Artificial = active or passive

Types of Immunity A. NATURAL : 1. Natural active through exposure or diseases; had the disease & recovered 2. Natural Passive maternal antibodies; acquired through placental transfer

B. ARTIFICIAL ( Laboratory ) 1. Artificial active introduction of antigen Ex. Vaccines ; toxoids ( No exposure yet; preventive measure) = gives long immunity months to years 2. Artificial passive- introduction of passiveantibodies Ex. Antitoxins; immunoglobulin ( gammaglobulin), antiserum, convalescent serum Ex. TAT ( tetanus antitoxin) ( w/ exposure to the causative agent) = gives short immunity 3-4 weeks

Immunity

NATURAL - INHERENT BODY TISSUES

ACQUIRED

Outside the host

1. NATURAL ( HUMAN)

2. ARTIFICIAL ( LABORATORY)

A. ACTIVE -HAD THE DISEASE & -RECOVERED

B. PASSIVE - MATERNAL ANTIBODIES

A. ACTIVE - VACCINES - TOXOIDS

B. PASSIVE - ANTITOXINS - IGS

Infection control and prevention

  

Immunization Active Passive

IMMUNIZATION
- is the induction or introduction of specific protective antibodies in a susceptible person or animal, or the production of cellular immunity in such a person or animal. - A PROCESS BY WHICH RESISTANCE TO AN INFECTIOUS DISEASE IS INDUCED OR AUGMENTED.

Active Immunization
1. 2. 3. 4. 5. 6. 7. 8. 9.

BCG DPT OPV/IPV Measles MMR TB Hepatitis B Varicella Hemophilus influenzae B (Hib)

Active immunization not routinely given

1. 2. 3. 4. 5. 6. 7.

Cholera vaccine Rabies Typhoid Influenza A & B Meningococcal Pneumococcal vaccine HPV vaccine

Passive immunization
1. 2. 3. 4. 5. 6. 7.

Diphtheria antitoxin Hepatitis B immunoglobulin (HBIG) Measles immunoglobulin Varicella immunoglobulin (VZIG) Rabies Human immunoglobulin (RIG) Tetanus human immunoglobulin (TIG) Tetanus Toxin ( ATS)

NURSE ALERT !!!

ALL VACCINE LOSE THEIR POTENCY AFTER A CERTAIN TIME. EXPIRY DATE SHOULD BE NOTED ON THE LABEL

What damages vaccine ??

Heat and sunlight damages vaccine Esp. LIVE VACCINE

Freezing damages the KILLED vaccine And TOXOID

Use water only in cleaning the refrigerator Or freezer. ( antiseptics, disinfectants and detergents Or alcohol lessen potency of vaccine )

Cold Chain System

KEEP VACCINES IN CORRECT COLD TEMPERATURE (0-8 c)

Immunization
  

EPI : PPD 996 GOAL : universal child immunization ( Proc. No. 6) Common Goal to Prevent childhood diseases covered by the EPI ( expanded program immunization)
1. 2. 3. 4. 5. 6.

Tb Measles Diphtheria, Pertusiss Polio , Tetanus Hepatitis

IMMUNOGLOBULINS ( IGS)


IgG
MOST PREVALENT ANTIBODY 80%, PRODUCED LATER IN THE IMMUNE RESPONSE, ONLY Ig THAT CAN CROSS PLACENTA

 

IgA
FOUND IN COLOSTRUM, TEARS, SALIVA, SWEAT

IgM
PRINCIPAL ANTIBODY OF BLOOD, QUICKLY PRODUCED IN RESPONSE TO AN ANTIGEN, RESPONDS TO ARTIFICIAL IMMUNIZATION

 

IgE
RESPONDS TO ALLERGIC REACTION

IgD
UNKNOWN, ANTIGEN RECEPTOR, FOUND IN THE SURFACE OF B CELLS

Expanded Program of Immunization

BCG At birth ID Once None, mild fever, local rxn

DPT MMR OPV Measles Hep B

6 weeks 15 wks 6 weeks 9 mos At birth

IM

3 x (4weeks int) Local rxn, acute encephalopathy

oral SQ IM

3 x (4wks int) Once 3 x ( 2,4,6 )

None Fever Mild local rxn

SpecialSpecial-use Vaccine
Meningoccocal Rabies Typhoid Japanese encep Pneumococcal Epidemic areas Exposures travellers travellers immunocompro SQ ID/IM IM SC IM/SQ None Local rxn Local rxn Anaphylactic Local rxn

Contraindications when giving immunizations:

 

Severe febrile illness Live virus vaccine are generally not administered with altered immune system Allergic reaction

Permanent C.I.
  

Allergy Encephalopathy without known cause Convulsion within 7 days after Pertussis vaccine

Temporary C.I
   

Pregnancy Immunocompromised Very severe disease Previously received blood product/transfusion

EPIDEMIOLOGY AND DISEASE TRANSMISSION

Reservoirs of Infection:
= any site where the pathogen can multiply or merely survive until it is transferred to the host


Human Reservoir
= principal living reservoir of human disease 1. Direct Transmission = usually associated with signs and symptoms 2. Carriers = harbor the pathogen without associated signs and symptoms

Types of Carriers:
Incubatory Carrier - capable of transmitting pathogens during the incubation period Convalescent Carrier - transmit disease during convalescence or recovery period Active Carrier - completely recovered from disease but continue to harbor the pathogen indefinitely Passive Carrier - carry the pathogen without ever having the disease

Recognition of Susceptible Host

Susceptible Host
     

Recognition of high risk patients Immunocompromised DM Surgery Burns Elderly

Nosocomial Versus Community Acquired Infection

Preventing the Spread of Communicable Disease

Community vs. Nosocomial

Community Acquired Infection

- infection present or incubating at the time of consultation

Nosocomial Infection or hospital acquired

- infection that develop during the course of hospital stay
& was not evident at time of admission

Percentage of Nosocomial Infections

    

17% 34% 13% 14% 22%

Surgical UTI LRI Bacteremia Other (incldng skin Infxn)

Factors for Nosocomial Infection Microorganism/Hospital Environment  Most common cause Staph aureus, Staph Enterococci E. coli, Pseudomonas, Enterobacter, Klebsiella Clostridium Difficile Fungi ( C. Albicans) Other ( Gram (-) bacteria) ( 70% are drug resistant bacteria Compromised Host  One whose resistance to infection is impaired by broken skin, mucous membranes and a suppressed immune system

INFECTION CONTROL MEASURES

General Control Measures

Prevention of Airborne Contamination
     

Cover mouth and nose ( coughing or sneezing) Limit number of persons in a room Removal of dirt and dust Open room to fresh air and sunlight Roll linens together Remove bacteria from the air (air filters)

Handling of Food and Eating Utensils

          

Use high quality foods Proper refrigeration and storage of food Proper washing, preparing, and cooking of food Proper disposal of uneaten food Proper hand washing Proper disposal of oral and nasal secretion Cover hair and wear clean clothes and apron Provide periodic health exam for kitchen workers Keep cutting boards clean Prohibit anyone with respiratory or GIT disease from handling food Rinse and wash utensils with a temperature above 80C

Handling of Fomites
    

Use disposable equipments Sterilize or disinfect equipment Use individual equipment for each patient Use single use thermometers Empty bedpans and urinals properly and wash with hot water, store in dry ,clean area or storage Place used linens and personal care equipments, and soiled laundry in a bag

Medical Asepsis  CLEAN TECHNIQUE: Involves procedures and practices that reduce the number and transfer of pathogens  Will exclude pathogens ONLY Attained by:  Frequent and thorough hand washing  Personal grooming  Proper cleaning of supplies and equipment  Disinfection  Proper disposal of needles, contaminated materials and infectious waste  Sterilization

Surgical Asepsis  STERILE TECHNIQUE : Practices used to render and keep objects and areas sterile  Exclude ALL microorganism Attained by:  Use strict aseptic precautions for invasive procedures  Scrub hands and fingernails before entering O.R.  Use sterile gloves, masks, gowns and shoe covers  Use sterile solutions and dressings  Use sterile drapes and create an sterile field  Heat sterilized surgical instruments

1. Universal Precaution ( Standard Precaution )

Defined by center for disease control (CDC) 1996  Primary strategy for reducing the risk of & controlling Nosocomial infections  Used for care of all hospitalized patients, regardless of diagnosis and are presumed infectious  Protect healthcare workers from contamination and infection ( i.e. HIV, HBV) Hand Washing  Routine: Plain (non microbial) soap  Outbreak Control: Antimicrobial/Antiseptic Agent  Wash After: 1.touching blood and other body fluids 2. touch contaminated items 3. removal of gloves 4. between patient contact, task, procedure


Infection Control Signage

Universal Precaution Materials

Gloves  Must be worn when touching blood, body fluids, secretions, excretions and contaminated items, mucous membranes and non- intact skin non Change gloves between tasks or procedures  Remove gloves after use and before going to another patient Masks, Eye Protection, Face Shields, Gowns  Wear in procedures that can generate splashes or sprays of blood, body fluids, secretions or excretions or cause soiling of clothing Environmental Control  Routine care, cleaning and disinfection of environmental surfaces

Patient Care Equipment  Prevent contaminating yourself or transfer microbes to others  Properly clean, disinfect or sterilize  Dispose single use items Linens  Handled, transported and processed to prevent contamination and transfer of microorganisms Occupational Health and Blood borne Pathogens  Never recap used needles  Puncture resistant containers

Revised C.D.C. Isolation Precaution

( centers for disease control)


2. Transmission-Based Precautions TransmissionThe second tier of precaution  Precaution are instituted for patients who are known to be or suspected of being infected with highly transmissible infection.


THREE TYPES OF TRANSMISSIONTRANSMISSIONBASED PRECAUTIONS: PRECAUTIONS:

1. Airborne precautions  2.Droplet precautions  3.Contact precautions


Infection Control Signage

Infection Control Signage

Infection Control Signage

Personal Protective Equipment ( PPE)

( Barrier Technique)  mask  gloves  gown  shoe cover  goggles

Transmission based precautions for Hospitalized patient :

Category Precaution Single Room Masks Gowns Gloves

Airborne

Yes, with (-) (air pressure ventilation Yes

Yes

No

No

Droplet

Yes, mask for persons close to patient yes

No

No

Contact

Yes

yes

yes

Isolation
- is a protective procedure that limits the spread of infectious diseases among hospitalized clients, hospital personnel, and visitors. It is the separation from other persons of an individual suffering from a communicable disease. - other terms are: protective aseptic are: technique or barrier technique.

Quarantine - is the limitation of

freedom of movement of persons or animals which have been exposed to communicable disease / s for a period of time equivalent to the longest incubation period of that disease. Surveillance -

Seven categories recommended in isolation

1.

Strict isolation
  

Use mask , gown and gloves (MUST) Private room For highly contagious or virulent infections

2. 3. 4. 5. 6. 7.

Contact isolation Respiratory isolation TB isolation Enteric isolation Drainage/secretion precaution Universal precaution when handling blood and body fluids

Type : STRICT Purpose: Prevent Transmission of highly contagious or virulent infections spread by air and contact Specification:
Private Room necessary Hand Washing X Gown X Masks X Gloves X Articles Discard or bag and label and send for decontamination and reprocessing. Diseases requiring Isolation Diphtheria (pharyngeal) , Lassa fever, Smallpox , Varicella.

Type :

Contact

Purpose: Prevent Transmission of highly transmissible

infections that do not require strict isolation.

Specification:

Private Room necessary Hand Washing X Gown wear if soiling is likely Masks wear in close contact with client Gloves wear if touching infective material. Articles Discard or bag and label and send for decontamination and reprocessing.

Diseases requiring Isolation Acute Resp. infection in infant and young children, Herpes simplex, Impetigo, multiple resistant bacterial infection.

Type : Respiratory Purpose: Prevent Transmission of infectious diseases

primarily over short distances by air droplets.

Specification:

Private Room necessary Hand Washing X Gown not necessarily Masks wear in close contact with client Gloves not necessarily Articles Discard or bag and label and send for decontamination and reprocessing.

Disease requiring Isolation Measles, Meningitis, Pneumonia,

Hemophilus Influenza in children , Mumps.

Type :

Tuberculosis

Purpose: For client with PTB who

has positive sputum or chest x-ray that indicates active xdisease

Private Room necessary Hand Washing X Gown Wear if soiling is likely Masks wear if client is coughing and does not consistently cover mouth Gloves not necessarily Articles Rarely involved in transmission of TB. Should still be thoroughly cleansed and disinfected.

Specification:

Disease requiring Isolation Tuberculosis

Type : Enteric Purpose: Purpose:

Precautions

To prevent infections that are transmitted by direct or indirect contact with feces.

Specification: Private Room Indicated if clients hygiene is poor and there is risk of contamination with infective materials. Hand Washing X Gown wear if soiling is likely Masks not necessary Gloves wear if touching infective material Articles Discard or bag and label and send for decontamination and reprocessing.

Disease requiring Isolation Hepatitis, viral (type A),

Gastroenteritis caused by highly infectious organism cholera, Diarrhea, acute with infectious etiology.

Type : DrainageDrainage-

secretion precautions
material or

Purpose: To prevent infections that are transmitted by direct or

drainage from infected site.

Specification:

indirect contact with purulent

Private Room not necessary Hand Washing X Gown wear if soiling is likely Masks not necessary Gloves wear if touching infective material Articles Discard or bag and label and send for decontamination and reprocessing.

Disease requiring Isolation Abscess, Burn infection,

conjunctivitis, decubitus- ulcer skin or wound decubitusinfection.

Type : BloodBlood-

body fluid precaution

Purpose: To prevent infections that are transmitted by direct or indirect contact with blood or body fluid. Specification: Private Room Only if clients hygiene is poor
Hand Washing X Gown Wear if soiling with blood or body fluid is likely Masks not necessary Gloves wear if touching blood or body fluid. Articles Discard or bag and label and send for decontamination and reprocessing.

Disease requiring Isolation AIDS, Hepatitis, viral (Type B)

Malaria, Syphilis, primary and secondary.

Reverse Isolation
 

Protective or neutropenic isolation Used for patients with severe burns, leukemia, burns, leukemia, transplant, transplant, immuno deficient persons, persons, receiving radiation treatment, leukopenic patients Those that enter the room must wear masks and sterile gowns to prevent from introducing microorganisms to the room

AFB ISOLATION
- VISITORS - report to nurses station before entering the room - MASKS worn in patients room - GOWNS prevent clothing contamination - GLOVES for body fluids and non intact skin - HANDWASHING - after touching patient or potentially contaminated articles and after removing gloves - articles discarded, cleaned or sent for decontamination and reprocessing - room remains closed - patients wear masks during transport

Additional Pointers
Regarding Disposal Precaution Secretion: Secretion: Patient should be instructed to expectorate into tissue held close to mouth. Suction catheters and gloves should be disposed of in impervious, sealed bags. Excretion: Excretion: Strict attention should be paid to careful hand washing; disease can be spread by oral- fecal oralroute. Blood: Blood: needles and syringes should be disposable. Used needles should not be recapped. They should recapped. be placed in a puncture-resistant container that is punctureprominently labeled Isolation Specimens should be labeled Blood Precaution.

Environmental Control


Routine care, cleaning and disinfection of environmental surfaces PRECAUTIONS FOR INVASIVE PROCEDURES: PROCEDURES:


wear gloves during all invasive procedure + goggles + mask

Work Practice Precaution



Prevent injuries caused by needles, scalpels and other sharps instrument or devices when cleaning used instrument, when disposing of used needles  Do not recap used needles, bend , break nor remove
 

them from disposable syringes or manipulate them. Place sharps in puncture resistant containers If gloves tears or a needle-stick or other injury occurs, needleREMOVE the gloves, wash hands, and wash sites of the needle stick thoroughly then put new gloves


Report injuries and mucous membrane exposure to appropriate infection control officer.

Waste management


is the collection, transport, processing, recycling or disposal of waste materials. Involves:

    

1. sharps 2.Solid infectious cotton swab, dressing 3. Anatomic Infectious placenta / organ 4.Solid non-infectious used IV / bottle IV non5.General waste scrap paper / food material

Philippines set-up set

black plastic bags are for non-biodegradable and nonnoninfectious

wastes such as cans, bottles, tetrabrick containers, styropor, straw, plastic, boxes,  wrappers, newspapers.


Green plastic bags are biodegradable wastes such as fruits and vegetables' peelings, leftover food flowers, leaves, and twigs.

Philippines set-up set

Yellow plastic bags are for infectious waste

such as disposable materials used for collection of blood and body fluids like diapers, sanitary pads, incontinent  pads; materials (like tissue paper) with blood secretions and other exudates; dressings, bandages, used cotton balls, gauze; IV tubings, used syringes; Foleys catheter/ tubings; gloves and drains.


Means of controlling the spread of CD

1. 2. 3.

Elimination of the source of infection Interruption of transmission Protection of susceptible host.

INFECTIOUS DISEASE

INFECTIOUS DISEASES
CLASSIFIED AS:
      

Blood/ vector borne Enteric diseases Eruptive fever Respiratory diseases CNS infection Diarrheal Diseases EMERGING DISEASES

INFECTIOUS DISEASES
CLASSIFIED AS :
1.

Blood/ vector borne

a. DHF b. Malaria c. Leptospirosis d. Filiariasis

2.

Enteric diseases
a. Typhoid fever b. Viral Hepatitis c. Schistosomiasis

3.

Eruptive fever
a. Measles (Rubeola) b. Varicella c. German Measles ( Rubella) d. Small pox

4.

Respiratory diseases
a. Pneumonia b. Diphtheria c. PTB d. Mumps

5. CNS Infections
a. Encephalitis b. Meningitis c.Meningococcemia d. Rabies e. Tetanus f. Snake bite

7. Emerging Diseases:  SARS Birds FLU

6.Diarrheal diseases
a. E.coli b. Staphyloccus aureus c. Cholera d. Rotavirus e. Salmonella f. Parasitism

VECTOR BORNE DISEASES

Dengue Fever, H-Fever, Dandy HFever, Breakbone Fever, Phil Hemorrhagic fever
Acute Febrile Disease  Flavivirus, dengue virus 1,2,3,4 Incidence: Rainy season, urban areas IP: 3 to 10 days ( average 4-6 days 4** Life span of the mosquito is 4 months


Dengue Fever, H-Fever, Dandy Fever, HBreakbone Fever, Phil Hemorrhagic fever
THE DISEASE PRESENTS WITH FEVER AND HEMORRHAGIC MANIFESTATIONS AND LABORATORY FINDINGS OF THROMBOCYTOPENIA AND HEMOCONCENTRATION Pathogenesis 1. increased capillary fragility d/t immune complex reactions 2. thrombocytopenia d/t faulty maturation of megakaryocytes 3. decreased blood clotting factors

VectorVector- Aedes aegypti

biting mosquito ( they appear 2 hours after sunrise and 2 hours before sunset. Low flying ( Tiger mosquito white stripes, gray wings ) - Breeds on clear stagnant water

- Day

CRITERIA FOR DIAGNOSIS: DIAGNOSIS:

 Fever

,acute, high continous, lasting for 227 days

 Positive

torniquet test  Spontaneous bleeding (petechiae,purpura,ecchymoses,pistaxis, gum bleeding, hematemesis, melena)  Laboratory: thrombocytopenia </= 100,000mm3, hemoconcentration- an increase hemoconcentrationof at least 20% in the hematocrit or its steady rise

 

Assessment: Tourniquet test (Rumpel Leedes test) test) screening test, done by occluding the arm veins for about 5 minutes to detect capillary fragility.
Keep cuff inflated for 6 10 minutes ( child); 101015 minutes ( adults)  Count the petechiae formation 1 square inch ( 20 petechiae/sq.in)(+)TT


Platelet count ( decreased) confirmatory test

Classification of Dengue Fever according to severity



 

Grade I Dengue fever, saddleback fever plus constitutional signs and symptoms plus positive torniquet test Grade II Stage I plus spontaneous bleeding, epistaxis, GI, cutaneous bleeding Grade III Dengue Shock Syndrome, all of the following signs and symptoms plus evidence of circulatory failure Grade IV Grade III plus profound shock and massive bleeding, undetectable BP and pulse

Laboratory criteria DHF: DHF:  Platelet count Thrombocytopenia <100,000  Hct increased by 20 % or more


1st 2 clinical criteria plus 2 laboratory criteria or rising Hct DHF( dengue hemorrhagic fever) Shock w/ high hematocrit and marked thrombocytopenia DSS ( dengue shock syndrome)

Other :  PT (Prothrombin Time)  APTT (Activated Partial Thromboplastin Time)  Bleeding time  Coagulation time Period of communicability pts. are usually infective to mosquito from a day before the febrile period to the end of it  The mosquito becomes infective from day 8 to 12 after the blood meal & remains infective all throughout life

pathophysiology
DHF
Febrile phase 2-7 days
First 2 days Vascular injury Plasma leakage (+) petechiae , (+) TT

Dengue Fever Vector caries virus (AEDES aegypti) Bite host ( IP 3-10d)
s/sx : Fever , headache, myalgia ,anorexia Vomiting, sorethroat, rashes

IMPROVE

3rd day WBC, PLT Ct , Hct >20% (+) Pleural effussion

Dengue progress

Circulatory failure
-hypotension -narrow pulse pressure ,20mm Hg (shock)

death

S/sx: Mild dengue abrupt onset of fever, headache, muscle and joint pains, anorexia, abdominal pain. Petecchiae, Hermans rash (5th-7th day; purplish macules w/ blanched areas on extremities) Severe dengue DHF/DSS *TRIAD: fever, rashes and muscle pain Bleeding leading to hypovolemic shock

Medical MX
         

There is no effective antiviral therapy for dengue fever. Treatment is entirely SYMPTOMATIC Paracetamol for headache ( never give ASPIRIN) IVF for hydration & replacement of plasma BT for severe bleeding O2 therapy is indicated to all patients in shock Sedatives for anxiety & apprehension No IM injections Nasal packing with epinephrine Gastric lavage Giving cytoprotectors

Nursing Mx
      

Symptomatic tx Mosquito free environment to avoid further transmission of infection Keep patient at rest during bleeding episodes VS must be promptly monitored For nose bleeding, maintain pts position in elevated trunk, apply ice bag to bridge of nose Observe for signs of shock Restore blood volume ( supine with legs elevated)

Dengue hemorrhagic Fever



PREVENTION : DOH 1995 Program

    

C- hemically treated Mosquito Net L arvae eating fish Gold fish E nvironmental Sanitation 4 0 clock habit A antimosquito soap lanzones peeling N atural mosquito repellant Neem tree , eucalyptus
, oregano

PREVENTION
  

 

Cover water drums and water pails at all times to prevent mosquitoes from breeding. Replace water in flower vases once a week. Clean all water containers once a week. Scrub the sides well to remove eggs of mosquitoes sticking to the sides. Clean gutters of leaves and debris so that rain water will not collect as breeding places of mosquitoes. Old tires used as roof support should be punctured or cut to avoid accumulation of water. Collect and dispose all unusable tin cans, jars, bottles and other items that can collect and hold water

Prevention & Control

The 4-S Against DENGUE 41. Search and destroy breeding places of dengue causing mosquitoes such as old tires, coconut husks, roof tires, husks, gutters, gutters, discarded bottles, flower vases & other containers that can hold clean stagnant water

2. Self protection measures such as wearing of long sleeve shirts and long pants and using mosquito repellants are a must during daytime. 3. Seek early consultation when early signs such as fever and rashes set in 4. Say NO to indiscriminate fogging except for dengue outbreak

Malaria

MALARIA (Ague) King of Tropical Disease

 

Acute and chronic parasitic diseases Causative agent : Protozoa of genus Plasmodia 4 species of Protozoa: Protozoa:  1. Plasmodium falciparum ( malignant tertian)  Most fatal ; common in the Philippines  2. Plasmodium vivax ( Benign tertian)  Non-life threatening except for the very Nonyoung & old ; manifest chills q48H on the 3rd day onward if untreated

MALARIA (Ague) King of Tropical Disease

 3.

Plasmodium malariae (Quartan)  Less frequently seen ; non life threatening , fever & chills usually occur q72H usually on the 4th day after the onset  4. Plasmodium ovale  rare

Vector Female Anopheles mosquito

Vector: (night biting)  Female anopheles mosquito or minimus flavirustris = infectious but not contagious = thrives in clear, free flowing shaded streams usually in the mountains = bigger in size than the ordinary mosquito = brown in color, usually does not bite a person in motion = assumes a 36 degree position when it alights on walls, trees, curtains and the like

Incubation Period:  1. 12 days for P. falcifarum  2. 14 days for P. vivax and Ovale  3. 30 days for P. malariae Period of Communicability:  Untreated or insufficiently treated patient may be the source of mosquito infection for more than three years in P. malariae; one to two years in P. vivax; and not more than one year on P. falcifarum

Pathogenesis


Anopheles mosquito >> gets parasites in the blood of infected person >>parasites multiply in mosquito >>parasites invade the salivary gland of mosquito >> mosquito bites the individual & thus, injects the parasites >> parasites invade RBC where they grow & undergo asexual propagation >> RBC ruptures or bursts releasing tiny organisms ( MEROZOITES) >> merozoites invade new batch Of RBC to start another schizonic cycle

Pathology  the most characteristic pathology of malaria is destruction of red blood cells, hypertrophy of the spleen and liver and pigmentation of organs.  The pigmentation is due to the phagocytocis of malarial pigments released into the blood stream upon rupture of red cells

Plasmodium Life Cycle

Malaria


Transmission :

sporozoites, injected by anopheles mosquito

travel to human liver

mature to be released into a blood stream as merozoites

invade RBC as they undergo sexual reproduction to

PATHOPHYSIOLOGY :


produce zygotes

RBC decreases deformability and oxygen transport, increase adhesion and fragility leading to anemia

Clinical Manifestation
uncomplicated  fever, chills, sweating every 24 36 hrs  Complicated  sporulation or segmentation and rupture of erythrocytes occurs in the brain and visceral organs.  Cerebral malaria  changes of sensorium, severe headache and vomiting  seizures


MALARIA (Ague)


Clinical manifestations :

1. Cold stage
 Chilling

sensation of the body ( 10-15 mins) 10 Chattering of lips, shakes  Keep the patient warm  Hot water bath  Expose to heat  Warm drinks  Last about 10-15min 102. . Hot stage (3-4Hrs) (3 Recurring high grade fever , headache , abdominal pain and vomiting  TSB , cold compress  Light clothing,

MALARIA (Ague)


Clinical manifestation :
I. Cold stage ( 10-15mins) 10 II. Hot stage (3-4Hrs) (3 III. Wet stage  Profuse sweating  Keep patient comfortable  Keep them warm and dry  Increase fluid intake


Diagnostics: 1. Malarial smear - Peripheral blood extraction (extract (extract blood at the height of fever or 2 hrs before chilling ( AGUE) 2. Rapid diagnostic test ( RDT) blood test for malaria conducted outside the lab & in the field- result is fieldwithin 10-15 mins. This is done to detect malarial 10parasite antigen in the blood.

Medical Mgmt: A. IVFs B. Anti- Malarial Drugs AntiChloroquine ( less toxic); Premaquine For chloroquine resistant plasmodium quinine Prophylaxis chloroquine or mefloquine, pyrimethamine/sulfadoxine (fansidar) C. Erythrocyte exchange transfusion for rapid production of high levels of parasites in the blood.

Nursing Considerations


   

If entering an endemic area, travellers are advised to take chloroquine from 1-2 weeks at weekly 1interval. Protection is good for 1 year Patient must be closely monitored Soaking of mosquito nets in an insecticide solution Bio pond for fish On stream clearing cut vegetation overhanging stream banks to expose the breeding stream to sunlight Vectors peak biting is at night (9pm-3am) (9pm-

Planting of neem tree ( repellant effect)  Zooprophylaxis ( deviate mosquito bite from man to animals  Wear long sleeves/ pants/Socks  Apply insect repellant on skin  Screening of houses Notes:  Malaria stricken mother can still breastfeed  Chloroquine ca be given to a pregnant woman  If there is drug resistance, give quinine SO4  BT in anemia  Dialysis in renal failure  Decreased fluids in cerebral edema  No meds to destroy sporozoites


Category of provinces
Category A no significant improvement in malaria for the past 10 years. >1000 - Mindoro, isabela, Rizal, Zamboanga, Cagayan, Apayao, kalinga  Category B - <1000/year - Ifugao, abra, mt. province, ilocos, nueva ecija, bulacan, zambales, bataan, laguna  Category C significant reduction -pampanga, la union, batangas, cavite, albay


Filariasis, Elephantiasis Lymphatic Filariasis

   

Extremely debilitating and stigmatizing disease caused by PARASITIC worm Affect men, women and children Causes extensive disability, gross disfigurement. CAUSATIVE AGENT: Wuchereria AGENT: bancrofti ( african eye worm)


Only live in lymphatic system

MOT : person to person by mosquito bite

FILARIASIS

FILARIASIS


Parasitic disease caused by an african eye worm ( microscopic thread like worm)
Wuchereria bancrofti & Brugia malayi  Wuchereria :Camarines norte/sur , albay , norte/ sorsogon , quezon , masbate , mindoro , romblon , marinduque , bohol , samar , leyte , palawan , sulu , tawi-tawi and basilan. tawibasilan.  Malayi : Palawan , eastern samar , agusan ,sulu


Vector: Culex, Mansonia, Anopheles, Aedes

Filariasis ( elephantiasis )
Mosquito bites Aedes poiculus , culex faligans and anopheles flavirostris
Bites a person with lymphatic filariasis & infect the mosquito

Person infected bitten by mosquito Transmitted to another person

Larvae migrate to LN, reach Sexual maturity & cycle is completed

Microscopic worms pass from mosquito Through the human skin, travel to LN , grow as adult

Adult worm lives for 7 yrs in lymph vessels Mate release into blood stream- microfilaria

Note: a person needs Many mosquito bite Over several months- years to get Filariasis

Organs affected : kidney & lymph system

Fluid collects and causes swelling in the arms, breast, legs and for men genitalia  Swelling decrease function of lymph system


Susceptible to bacterial infection

Skin harden and thicken ELEPHANTIASIS  Conjuctival filariasis worm migrate eye cause blindness if untreated known as Onchoceriasis.


Assessment : s/sx
Chills, headache and fever between 3 months and 1 year after the insect bite  Swelling redness and pain in arms ,legs or scrotum  Areas of abscesses may appear as result of drying worm or secondary bacterial infection  Lymphadenitis. Oophoritis, orchitis


Diagnostics :Nocturnal Blood smear

 Demonstration

of microfiliaria in fresh blood obtained between 10:00 to 2:00 am  Patient s history must be taken and pattern of inflammation and signs of lymphatic obstruction must be Blood /vector-borne observed. observed.

Treatment :
Drugs Ivermectin , albendazole and DIETHYLCARBAMAZINE (DEC)- 6mg/KBW (DEC)in divided doses for 12 consecutive days  Eliminate the larvae  Impairing the adult worms ability to reproduce  Kill the adult worm  Surgery excision of subcutaneous nodule  Elephantiasis of the legs elevate and provide elastic bandages


Management Guidelines


Supportive Therapy
Paracetamol  Antihistamine for allergic reaction due to DEC  Vitamin B complex  Elevation of infected limb, elastic stocking


PREVENTIVE MEASURE
Health teachings  Environmental Sanitation


Mgmt: Mgmt: Environmental sanitation

 Personal

Hygiene  Provide mosquito nets  Long sleeves, long pants & socks  Mosquito repellant  Take yearly dose of medicine that kills worms circulating in the blood  Screening of houses

Leptospirosis (Weils disease)

Weils disease, Mud fever, Trench fever, Flood fever, Spirochetal jaundice, Japanese 7 Days fever, Leptospiral jaundice, Hemorrhagic jaundice, Swine Herds disease, Canicola fever  a zoonotic systemic infection caused by Leptospires, that penetrate intact and abraded skin through exposure to water, wet soil contaminated with urine of infected animals. Species:  L. Manilae, L. Canicula, L. Pyrogens  Incubation Period: 6-15 days 6

Spirochete, Leptospira interrogans, gram (-) ( Weils syndrome severe form MOT: MOT:  Contact of skin or open wound from soil water contaminated with urine or feces of infected rats (main host)  INGESTION OF CONTAMINATED FOOD/H2O


S/SX: Anicteric Type (without jaundice)  manifested by fever, conjunctival infection  signs of meningeal irritation Icteric Type (Weil Syndrome)  Hepatic and renal manifestation  Jaundice, hepatomegally  Oliguria, anuria which progress to renal failure Oliguria,  Shock, coma, CHF  Convalescent Period

Diagnosis
 

Clinical history and manifestation Culture

  

Blood: during the 1st week CSF: from the 5th to the 12th day Urine: after the 1st week until convalescent period

  

LAAT (Leptospira Agglutination Test) other laboratory BUN,CREA, liver enzymes

Treatment


Specific
Penicillin 50000 units/kg/day  Tetracycline 20-40mg/kg/day 20

   

NonNon-specific Supportive and symptomatic Administration of fluids & electrolytes Peritoneal dialysis for renal failure

LEPTOSPIROSIS
JAUNDICE IS A BAD PROGNOSTIC SIGN CASE FATALITY RATE : 40%

Blood /vector-borne

Prevention Control & Nursing Considerations:

    

Avoidance of exposure to urine & tissues from infected animals ( flood) Rodent Control Hygienic control in slaughterhouses, farmyard buildings & bathing pools Use of protective clothing & boots Primarily a disease of domesticated & wild animals transmitted via direct or indirect contact. It enters the skin, mucus membrane, conjunctiva, inhalation Disease is usually short lived & mild but severe infection can damage kidneys & liver

HEPATO-ENTERIC HEPATODISEASES

GIT

Typhoid Fever
Salmonella typhosa, gram (-) typhosa, ( Carried only by humans Bacterial infection transmitted by contaminated water, milk, shellfish ( oyster ) & other foods Infection of the GIT affecting the lymphoid tissue ( payers patches) of the small intestine Most severe form of salmonellosis caused by salmonella typhi MOT: MOT: oral fecal route 5 Fs : Fingers, Fomites, Flies, Feces, Food & Fluids Fomites,


Pathophysiology
Oral ingestion Bloodstream Reticuloendothelial system (lymph node, spleen, liver) Bloodstream Gallbladder Peyers patches of SI necrosis and ulceration

Typhoid Fever Ulceration of the Peyer's Patches

Typhoid Fever
Clinical Manifestations: Incubation Period: 1-2 weeks 1401. Prodromal 1st week: Step ladder fever 40-41 deg, headache, abdominal pain, GI manifestations 3 cardinal signs of pyrexial stage: 1.ROSE SPOTS ( irregular rashes found on the chest, abdomen, back 2. Remittent fever ( ladder like) 3. Spleenomegaly

Typhoid Fever Rose Spots

 

2. Fastidial = 2nd week ( Typhoid) a. High fever, typhoid psychosis w/ hallucination, confusion, delirium


Drug of choice: Antibiotics

1. Chloramphenicol  2. Ampicillin  3. Cotrimoxazole


b. Severe abdominal pain c Sordes typhoid state

1st week step ladder fever (BLOOD) 2nd week rose spot and fastidial  typhoid psychosis (URINE & STOOL) 3rd week (complications) intestinal bleeding, perforation, peritonitis, encephalitis, 4th week (lysis) decreasing S/SX 5th week (convalescence)

Dx: Dx: Blood culture (typhi dot) 1st week (typhi dot) Stool and urine culture 2nd week Widal test Mgmt: Chloramphenicol, Mgmt: Chloramphenicol, Amoxicillin, Sulfonamides, Ciprofloxacin, Ceftriaxone ** Observe standard precaution until 3 negative stool culture**

Nursing Interventions
Environmental Sanitation  Food handlers sanitation permit  Supportive therapy  Assessment of complications (occuring on the 2nd to 3rd week of infection ) - typhoid psychosis, typhoid meningitis - typhoid ileitis


Schistosomias/Snail Fever/Bilharziasis/Katayama
   
 

Causative agent : Oriental Blood Fluke Schistosoma japonicum (affects intestinal tract) S. hematobium ( affects urinary tract) S. mansoni ( affects intestinal tract)
IP: IP: 2 months Source: Source: feces of infected persons


Dogs, pigs, cows, carabaos, monkeys, wild rats

serve as HOSTS

Pathogenesis- Snail fever

Larvae ( cercaria)

Ulceration in the mucosa Eggs able to escape in the lumen Of intestine, excreted in the feces Some eggs carried by portal Circulation, filtered in the Liver , formed granulomas Granulomas are resolved & replaced by fibrous tissues Scar formation occur Diseases progresses Liver enlarges due To increasing fibrosis Blood flow interrupted Result to portal hypertension

Penetrate skin Work their way to Liver venous portal circulation In portal vessel , they mature in 1-3 months
Mature worms live in copula in the portal vessels Migrate to some part of the body Female cercaria lays egg in the blood vessels Large intestine or bladder

Schistosomias/Snail Fever/Bilharziasis/Katayama
   


Causative agent : Oriental Blood Fluke Schistosoma japonicum (affects intestinal tract) S. hematobium ( affects urinary tract) S. mansoni ( affects intestinal tract)
IP: 2 months Cycle: Egg - larvae (miracidium) - intermediary host (oncomelania quadrasi/tiny amphibious snail) cercaria ( infective stage)

Egg - larvae (miracidium

intermediary host (oncomelania quadrasi/tiny amphibious snail) snail)

Schistosomias/Snail Fever
MOT: penetration of cercaria to the skin >parasites live in the blood vessels of intestines>cercaria migrates to the liver for maturation> gets out of the liver & goes against blood flow> obstruction of hepatic portal vessels> inc pressure>portal hpn>leads to esophageal & gastric varices, ascites & hepatomegaly

Assessment :
 Swimmers itch

or cercarial dermattitis itching within 24hrs after penetration of the skin by cercaria last 2-3 days  Migratory phase : sensitized individual develop systemic reaction of FEVER, CHILLS , SWEATING , DIARRHEA , COUGH and EOSINOPHILIA  Acute Phase : (+) fever , generalized lympagenopathy, hepatomegaly and splenomegaly ( KATAYAMA FEVER) 2-3 2weeks after initial infection and last for 1-2 1months

Diagnostics:
 Fecalysis

or direct stool exam  Kato katz technique  Liver and rectal biopsy  ELISA ( enzyme link Immunosorbent Assay)  COPT ( circum-oval precipitin test) circumconfirmatory diagnostic test


Prevention : proper disposal of feces ; snail

control

Treatment: Praziquantel for 6 mos PO  Fuadin



Prevention & Nursing Considerations: Considerations:

       

Wear knee rubber boots Avoid washing clothes or bathing in streams Use potable water supply Proper & sanitary disposal of human feces Snail control may be undertaken by chemicals ( Niclosemide) Niclosemide)- Molluscides Annual stool exam in endemic places Educate people about transmission Proper maintenance of Latrine

Viral hepatitis

VIRAL HEPATITIS


A diffuse inflammation of the cells of the liver that produces liver enlargement and jaundice
 Hepatitis

A (HAV) fecal-oral route fecal Hepatitis B ( HBV) contact with body fluids  Hepatitis C (HCV) percutaneous exposure to blood ( non A non B)  Hepatitis D (HDV)- contact with body fluids (HDV) Hepatitis E (HEV) water , fecal-oral route fecal-

VIRAL HEPATITIS
HAV
IP MOT
15-50d 15-

HBV
45-180d 45-

HCV
14-182d 14-

HDV
14-70d 14-

HEV
15-64d 15-

Fecal oral

Parenteral Percutaneous placental During IP Entire clinical course Years if carrier

Blood transfusion As carriercarrierindefinite 1 wk before clinical onset

Same w/ B

Fecal oral

commun Till 1 wk icability after onset of jaundice

Throughout Unknown clinical disease

Virus infect liver-interlobular infiltration Necrosis and hyperplasia of kuffer cells

Failure of the bile to reach intestine in normal amount Obstructed jaundice s/sx: dark urine, pale feces, itchness

Liver cell damage Necrosis and autolytic type destroy parenchyma

VIRAL HEPATITIS


Assessment : s/sx
 Prodromal

/ Preicteric  S symptoms of URTI  W weight loss  A anorexia , chills , fever  R right upper quadrant pain  M malaise  Icteric  J jaundice  A acholic tool  B bile colored urine ( tea colored)

Laboratory :
Liver function test  SGPT/SGOT  Specific : the presence of IgM antibody  Hepatitis A IgM HAV  Hepatitis B HbsAg acute or chronic infected  AntiAnti-HBs resolved or immunity  HbeAg infected risk of transmitting  AntiAnti-HBe lower risk of transmitting  AntiAnti-HBc acute resolved or chronic HBV infection  IgM anti-HBc acute with recent antiHBV infection window phase


Enteric fever

VIRAL HEPATITIS


Analysis
Knowledge deficit related to unfamiliarity with the disease course and treatment  Activity intolerance related to decreased metabolism of nutrient / increased basal metabolic rate caused by viral infection  High risk for Diversional activity deficit secondary to isolation / lack of energy  High risk for altered body nutrition : less than body requirement secondary to anorexia


VIRAL HEPATITIS


Treatment
No specific treatment  Bed rest essential  Diet : high carbohydrate , low fat , low protein  Vitamin supplement ( B complex)


VIRAL HEPATITIS


Nursing Mgt
Isolation of patient ( enteric isolation)  Standard precaution  Patient should be encouraged to rest during acute or symptomatic phase  Improved nutritional status  Utilize appropriate measures to minimize spread of the disease


VIRAL HEPATITIS


Nursing Mgt
  

Observe patient for Melena and check stool for the presence of blood Provide optimum i and oral care Increase in ability to carry out activities
  

Encourage the patient to limit activity when fatigued Assist the client in planning period of rest and activity Encourage gradual resumption of activities and mild exercise during recovery

PREVENTION AND CONTROL  Handwashing every after use of toilet  Travelers should avoid water and ice if unsure of their purity  Educate on the mode of transmission of the disease.

ERUPTIVE FEVER

MEASLES
 

 

Extremely contagious Breastfed babies of mothers have 3 months immunity for measles The most common complication is otitis media The most serious complications are pneumonia and encephalitis

RNA, Paramyxoviridae  Measles virus is rapidly inactivated by heat, UV light, & extreme degrees of acidity & alkalinity  Active immunity (MMR and Measles vaccine)  Passive immunity (Measles immune globulin)  Lifetime Immunity IP: 8-12 days 8MOT: Direct ( droplets, airborne); Indirect ( fomites) *Contagious 1-2 days before rash and 4 days after the 1appearance of rash


Measles, Rubeola, Morbili, 7 Day Fever, Hard Red Measles,

Sources of Infection: Infection:

Patients blood  Secretions from the eyes, nose & throat Diagnostics:  Nose & throat swab  Urinalysis  Blood exams ( CBC, leukopenia, leukocytosis)


Rashes: maculopapaular,
cephalocaudal (hairline and behind the ears to trunk and limbs), confluent, desquamation, pruritus)

Clinical manifestations: manifestations:

1. Pre-eruptive stage: Pre(2-4 days) - malaise, cough, conjunctivitis, , fever, (2kopliks spots ( PATHOGNOMONIC SIGN) SIGN) (1-2 mm blue white spots on red background along (12nd molars), stimsons ( puffiness of eyelid) photophobia 2. Eruptive stage: Rash is usually seen late on the 4th day MaculoMaculo-papular rash 3. Stage of convalescence: convalescence: Rashes fade away, desquamation begins,fever subsides Cx: pneumonia, meningitis,

MEASLES
 Fever

persist means (+) complication  Bronchopneumonia- most common Bronchopneumonia Otitis media, reactivation of previous TB  Bronchitis, laryngitis, exacerbation malnutrition  Encephalitis

MEASLES


Diagnostic procedure
Physical examination  Nose and throat swab  Urinalysis  CBC ( leukopenia & leukocytosis)  Complement fixation or hemogglutinin test


Eruptive fever

 1. 2. 3. 4. 5.

6.

7.

MANAGEMENT Supportive Hydration Proper nutrition Vitamin A Antibiotics if w/ secondary bacterial infection VaccineVaccine- measles vaccine @ 9 mos and MMR @ 15 mos Anti viral drugs ( Isoprenosine)

Observe respiratory Isolation

Nursing Care
       

Isolation of the patient if necessary TSB for fever Skin care is of utmost importance. The pt. should have a daily cleansing bed bath. Oral & nasal hygiene is a very important aspect of nursing care of patients with measles Restrict to quiet environment Dim light if photophobia is present; care of the eyes is necessary Administer antipyretic Use cool mist vaporizer for cough

German Measles, Rubella, Rotheln Disease, 3 Day Measles



    

= contagious viral disease characterized by fever, URTI, arthralgia, DIFFUSED fine red maculopapular rash) CA - RNA, rubella virus ( Togaviridae) Togaviridae) Immunity: Active natural ( permanent or lifetime) Active immunity - rubella vaccine and MMR Passive immunity - gammaglobulin Period of communicability contagious 7 days before & 7 days after appearance of rash & probably during the catarrhal stage

German Measles, Rubella, Rotheln Disease, 3 Day Measles

IP: 14-21 days 14MOT: Direct contact: droplets spread through the nasopharynx Indirect contact: transplacental
** Highly

communicable infant may shed virus for months after birth**

Rashes: Rashes: Maculopapular, Diffuse/not confluent, No desquamation, spreads from the face downwards

Clinical Manifestations: Manifestations: > FORSCHEIMERS SPOTS (petecchial lesion on buccal cavity or soft palate) > oval, rose red papule about the size of pin head > cervical lymphadenopathy, > low grade fever Dx: clinical CX: CX: rare; pneumonia, meningoencephalitis CX to pregnant women: women:  1st tri-congenital anomalies ( microcephaly, heart tridefects, cataracts, deafness  2nd tri-abortion or bleeding tri 3rd tri-pre mature delivery tri-

Nursing Considerations:
 

 

MMR immunization Use of immunoglobulins ( IGs)- ppost exposure IGs)prophylaxis 72 hrs after exxposure Prevention of congenital measles Avoid exposure

Roseola Infantum, Exanthem Subitum, Sixth disease

Human herpes virus 6  3mos-4 yo, peak 6-24 mos 3mos6MOT: probably respiratory secretions


S/sx: Spiking fever w/c subsides 2-3 days, Face and trunk 2rashes appear after fever subsides, Mild pharyngitis and lymph node enlargement Mgmt: symptomatic

  

Most highly contagious childhood disease Affects adults more severely than children Virus may become dormant

Chicken Pox, Varicella

      

Acute & highly contagious disease of viral etiology Childhood disease & adolescents (adults more severe) Not common in infancy Locally called Bulutong Bulutong Human beings are the only source of infection CA = Varicella Zoster virus, Herpes virus IP 10-21 days 10MOT: MOT: droplet spread > nose & throat secretions > Vesicles ( contagious in early stage of eruption > Airborne

Prodromal period: headache , vomiting, fever period:  Papulovesicular rashes appear on trunk spreading to face and extremties ( centrifugal)
 Macules

papules vesicles with clear fluid inside crusting and scar formation

 The

disease is communicable until the last crust disappear ( D1 before D6 after appearance of rashes)

Period of Communicability 5 days before rashes & 5 days after rashes crusting - dry

Rashes: Maculopapulovesicular (covered areas), Centrifugal rash distribution, distribution, starts on face and trunk and spreads to entire body


Leaves a pitted scar pockmark) (pockmark)

CX = secondary bacterial infection, furunculosis, pneumonia, meningoencephalitis ( rare)



Dormant: remain at the dorsal root ganglion and may recur as shingles (VZV)

Curative & Nursing Considerations:



  

 

If it feels itchy, give oral antihistamine or local antihistamine Avoid rupture of lesions Cut nails short Pay attention to nasopharyngeal secretions/ discharges Disinfection of linen ( sunlight or boiling) Prophylactic antibiotics

Tepid water and wet compresses for pruritus Soothing Baths, cool baths

Treatment:
a. oral acyclovir b. Tepid water and wet compresses for pruritus c. Potassium Permanganate (ABO) a. Astringent effect b. Bactericidal effect c. Oxidizing effect (deodorize the rash)

 

Exclusion from school for 1 week after eruption appears An attack gives lifetime immunity. Second attack is rare Immunoglobulins can be given ( 12 mos) Drug of choice: Acyclovir ( Zovirax ) topical cream applied to crusts

Preventive measures


Active immunization with LIVE ATTENUATED VARICELLA VACCINE

Start at 1 yr old ( 1 dose )  booster 4-12y  If >13 yrs = 2 doses  Given SC


Avoid exposure as much as possible to infected person

  

DNA, Pox virus Last case 1977 spreads from man-toman-toman only Active: Vaccinia pox virus

Small Pox, Variola

IP: 1-3 weeks 1S/sx: Rashes: Maculopapulovesiculopustular

 

Centripetal rash distribution contagious until all crusts disappeared

SMALL POX


Complications:
Scarring  Pneumonia  Blepharitis  Corneal ulceration


  

Mortality rate : 30% Diagnostic : clinical evaluation Treatment : analgesic ( pain) antibiotic for secondary infection

SMALL POX


Nursing mgt
Strict respiratory and contact isolation  Supportive  Adequate hydration  Mandatory reporting


PREVENTION
PrePre-exposure vaccination  Strict isolation of identified cases


Respiratory Diseases

Meningococcemia
CA : Neisseria meningitides ( bacteria) gram (()diplococci  May also be caused by H. Influenzae and S. Pneumoniae MOT: Droplets (urti) to blood stream to CNS


IP: 1-2 days ( even faster) 1 High risk: immunocompromised

S/sx: 1. Meningococcemia usually starts as nasopharyngitis, nasopharyngitis, followed by sudden onset of spiking fever, chills, arthralgia. Bacteria is carried by arthralgia. circulation & when it reaches the meninges of the brain, BLEEDING occurs into the medulla which extends to the cortex & petechial, purpuric or ecchymotic hemorrhage is scattered in the entire body surface appear. 2. Fulminant Meningococcemia (Waterhouse Friedrichsen) septic shock; hypotension, tachycardia, enlarging petecchial rash, adrenal insufficiency

Clinical Manifestation


sudden onset of high grade fever, rash and rapid deterioration of clinical condition within 24 hours

Meningococcal Septicemia Waterhouse-friedrichsen Syndrome

Treatment:


antimicrobial  Benzyl Penicillin 250-400000 u/kg/day ( drug of choice) 250 Chloramphenicol 100mg/kg/day Symptomatic and supportive  fever  seizures  hydration  respiratory function Chemoprophylaxis  Rifampicin 300-600mg q 12hrs x 4 doses 300 Ofloxacin 400mg single dose  Ceftriaxone 125-250mg IM single dose ( Ciprobay) 125-

Nursing Intervention 1. To prevent the occurrence of further complications  -maintain strict surgical aseptic technique when doing dressings or lumbar puncture in order to prevent the spread of microorganism  -administer O2 inhalation to prevent respiratory distress and to maintain a clear open airway  -TSB for fever to prevent convulsions  -observe signs and symptoms of increase intracranial pressure  -change positions at least every 2 hours to prevent pressure sore  -protect the eyes from bright lights and noise

2. Maintain normal amount of fluid and electrolyte balance 3. Prevent spread of the disease, prophylaxis for close contacts ( Rifampicin ) 4. Ensure the patients full comfort, prevent stress provoking factors that may retard convalescence and to prevent from injury 5. Prevent the spread of infection, microorganisms and contamination some precautions should be carried out

6. Maintain personal hygiene and cleanliness and avoid microorganisms to harbor in the patients body 7. Maintain proper elimination of waste product of metabolism 8. Nutritional intake

Diphtheria


CA: Corynebacterium diphtheriae, gram (+)

( Klebs Loefflers Bacillus)

  

 

IP: 2-5 days Period of Communicability: 2-4 wks if untreated, 1-2 days Communicability: 21if treated Active (DPT) and Passive Immunization (Diphtheria antitoxin) Source: Discharges of the nose, pharynx, eyes, or lesion of other parts of the body infected More severe in unimmunized and partially immunized

MOT: MOT: Direct/indirect contact = Airborne/droplet, fomites

Toxin producing organism = EXOTOXIN

1. Nasal invades nose by extension from pharynx 2. Tonsillar low fatality rate 3. NasoPharygeal- more severe type NasoPharygeal- sore throat causing dysphagia - Pseudomembrane in uvula, tonsils, soft palate gray exudate - Bullneck inflammation of cervical LN; neck tissues are edematous - increasing hoarseness until aphonia - wheezing on expiration - dyspnea

4. Cutaneous diphtheria affect mucous membrane & any break on the skin

S/sx: sore throat, fever, Bull-neck appearance( Bullappearance( CHARACTERISTIC SIGN) ,Pseudomembrane,Pseudomembrane-( PATHOGNOMONIC SIGN) gray exudate, foul breath, massive swelling of tonsils and uvula, thick speech, cervical lymphadenopathy, swelling of submandibular and anterior neck), obstruction of respiratory tract

Dx: 1.Schick test susceptibility to diphtheria toxin 2. Moloney - sensitivity to diphtheria toxoid 3. Throat swab (K tellurite and Loefflers coagulated blood serum

Treatment
 

 

 

Neutralize the toxins antidiptheria serum Kill the microorganism penicillin, erythromycin, rifampicin, clindamycin Considered cured after 3 negative throat cultures Prevent respiratory obstruction tracheostomy, intubation CBR up to 2 weeks to prevent myocarditis Strict isolation

Nursing intervention
  

Strict isolation of the hospitalized child Administer anti-toxin antiSupportive

  

Maintenance of adequate nutrition



Encouraged drinks rich in vitamin C

Maintenance of adequate fluid and electrolytes Bed rest for at least 2 weeks


Avoid exertion

  

Ice collar must be applied to the neck Nose and throat must be taken care of Administer antibiotics as prescribed


Penicillin effective for respiratory diphtheria

Pre exposure prophylaxis for Diphtheria, Pertussis, Tetanus

DPTDPT- 0.5 ml IM 1 - 1 months old 2 - after 4 weeks 3 - after 4 weeks 1st booster 18 mos 2nd booster 4-6 yo subsequent booster every 10 yrs thereafter  Household contacts (+) primary immunization and (-) culture - booster dose ((+) culture and (-) immunization treated as a case of (Diptheria


Complications


Myocarditis most common ( caused by diphtheria toxin on the heart muscles) Polyneuritis paralysis of the soft palate, paralysis of the ciliary muscle of the eye, pharyns, larynx, or extremities Airway obstruction can lead to death through asphyxiation

Pertussis/ Whooping Cough

Bordetella pertussis, B. parapertussis, B. pertussis, bronchiseptica, gram (-) ( Pertussis toxin, tracheal cytotoxin, Bacillus Bordet Gengou Bacillus  Common in Infants and young children & fatal to toddlers IP: 5-21 days 5MOT: airborne/droplet; direct contact ( nose & throat secretions); indirect contact ( articles)


S/sx: S/sx:
1. 2. 3.

Catarrhal stage (1-2 wks; highly contagious) sneezing, runny nose,tearing (1- wks; lacrimation, mild cough, low grade fever Paroxysmal stage (2-4 wks) - Clusters of cough that ends with a whoop, (2- wks) whoop, vomiting, exhaustion Convalescent stage (2-3 wks) less frequent cough (2- wks)

Dx: Dx: WHO - >21 days cough + close contact w/ pertussis px + (+) culture OR rise in Ab to FHA or pertussis toxin * throat culture w/ Bordet gengou agar

Cx: bronchopneumonia, pneumonia Management:  liquefy thick secretions with Ferrous iodide  CBR  Warm fresh air is better than cold air w/c induces vomiting ( NO AIRCON)  Hydration and nutrition  Vit C to inc body resistance  Oxygen ( 1-2L/min)- to lessen the 1-2L/min)occurrence of paroxysm  Erythromycin or Ampicillin  Isolation = 4 wks after coughing begins & continued for 7 days after the onset of antiobiotic therapy

Pre exposure prophylaxis for Diphtheria, Pertussis, Tetanus

DPTDPT- 0.5 ml IM 1 - 1 months old 2 - after 4 weeks 3 - after 4 weeks 1st booster 18 mos 2nd booster 4-6 yo subsequent booster every 10 yrs thereafter  Household contacts (+) primary immunization and (-) culture - booster dose ((+) culture and (-) immunization treated as a case of (Diphtheria


Pulmonary Tuberculosis( Kochs Disease/Pthisis/Consumption disease)

 

 

CA: CA: Mycobacterium tuberculosis ( bacteria), acid fast bacilli The organism multiplies slowly & is characterized as acid fast aerobic organism which can be killed by heat, sunshine, drying & ultraviolet light. Sputum of persons with TB is the most common source of the organism spread through droplet ( airborne) Potts disease thoracolumbar Milliary TB kidney, liver, lungs

Is a chronic, or subacute or acute respiratory disease commonly affecting the lungs characterized by formation of tubercles in the tissues which tend to undergo caseation, necrosis and calcification. calcification. IP: 2 10 weeks Mode of Transmission: Transmission:  Direct: droplet ( sneezing, coughing)  Indirect: continuous exposure to infected persons within the family Source of Infection:sputum, blood from Infection:sputum, hemoptysis, nasal discharges and saliva
-

Classification :
Minimal slight lesion  Moderately advanced one or both lung may be involved  Far advanced- more extensive advanced

Clinical classification: classification:



1. inactive TB
Symptoms absent  Sputum negative  CXR no evidence of cavity


2. Active
Tuberculin test positive  CXR progressive  (+) of symptoms  Sputum (+)


3. Activity not determined

Clinical manifestation: manifestation:

Afternoon rise of temperature for 1 mo. or more  Night sweating  Body malaise, weight loss  Cough, dry to productive  Dyspnea, horseness of voice  Hemoptysis pathognomonic  Occasional chest pain  (+) sputum for AFB


PD 996 Compulsory Immunization below 8 years ( 0 -7 yrs) Proclamation # 6 WHO Universal Child Immunization

Etiologic Factors that contribute heavily to the high Incidence & high mortality rate of TB:  Poverty / Overcrowded homes  Protein undernutrition  Deficiencies in Vit A,D,C  Children below 5 years old prone to infection due to inadequate levels of immunity

Pathophysiology
Inhalation Local infiltration of neutrophils and macrophage Multiply and survive in macrophage Destroy bacteria present it to T helper cells in LN Sensitized T cells searches bacteria and release lymphokines Attract macrophages w/c attack bacteria caseous necrosis bacteria dormant
Heal w/ fibrosis, calcification and granuloma; Primary TB

If reactivated, Secondary TB

DX


1. Case Finding: Finding:

A. Sputum Microscopy ( cheapest & confirmatory )  Results take about 3 weeks to confirm  Sputum sample shld be taken 1st thing in the morning upon arising 3 specimens:  1st on the spot = HC  2nd- upon arising = Home  3rd on the spot = HC

  

2. Sputum Culture & Sensitivity 3. Chest X-ray cavitary lesion X4. Tuberculin Test
1. PPD Purified Protein Derivative  2. Mantoux Test- (more reliable) = ID injection of Testtuberculin extract into the inner aspect of forearm to detect infection/exposure to CA. Localized reaction- detected in 48 to 72 hours reaction(+) induration of 10 mm or above


Tuberculin test. Erythema and induration at site of intradermal injection of 5 tuberculin units in a child with primary tuberculosis. This is an unusually severe reaction. Mantoux method.

Classification of PTB
0 = No exposure; No infection 1 = (+) exposure but not infected = INH for 1 mo especially below 5yo 2 = (+) with infection but w/o disease (+) skin test; No S/S; CXR(-) -INH 1 yr CXR(( -) sputum exam 3 = infected & w/ the disease = anti TB drug Tx

CATEGORIES OF TB


category I (new PTB) - (+) sputum(+) chest xray category II (PTB relapse not less than 6 mos) category III (active PTB case) - (-) sputum chest xxray, regression of infiltrates Category 1V partially treated; poor compliance to DOTS Category V PTB suspect ( (+) skin test; (+) family member with PTB

  

Management:  short course 6-9 months  long course 9-12 months  DOTS- directly observe treatment short course DOTS-

* 2 wks after medications non communicable 3 successive (-) sputum - non communicable (rifampicin or INH- prophylactic INH-

TREATMENT:


CATEGORY 1 - NEW PTB, (+) SPUTUM GIVE RIPE 2 MONTHS, MAINTENANCE OF RI 4 MONTHS MONTHS, CATEGORY 2 - PREVIOUSLY TREATED WITH RELAPSES GIVE RIPES 1ST 2 MONTHS, REPS 1 MONTH, MAINTENANCE RIE 5 MONTHS CATEGORY 3 - NEW PTB (-) SPUTUM FOR 3X (GIVE RIP 2 MONTHS, MAINTENACE RI 2 MONTHS

* IF RESISTANT TO DRUGS GIVE ADDITIONAL MONTH/S AS PRESCRIBED

Primary Anti TB Drugs

 

1. Rifampicin = SE = orange colored urine, GI upset, Jaundice, Renal failure, thrombocytopenia

Primary Anti TB Drugs

   

2. Isoniazid (INH) = ( Bacteriostatic) inhibits ( Bactericidal ) kills Used prophylactically to patients (+) of PPD SE = Rashes (give anti-histamine); Peripheral antineuritis ( Give Vit B6- Pyridoxine)50 mg; B6Jaundice; Psychosis

3. Pyrazinamide ( PZA)  SE = Hyperuricemia ( inc uric acid)  Mx: Inc fluid intake 4. Ethambutol = 15-20mg/day 15 SE = Optic neuritis ( dec visual acuity)  Give Vit. B6(Pyrdoxine) 5. Streptomycin  SE = Ototoxicity, 8th cranial nerve damage


( Tinnitus, dizziness, N&V)

MDT side effects  r-orange urine  i-neuritis and hepatitis  p-hyperuricemia  e-impairment of vision  s-8th cranial nerve damage

PTBPTB- NURSING MANAGEMENT

1. 2. 3. 4.

5. 6. 7. 8. 9. 10.

MAINTAIN REPIRATORY ISOLATION Administer medicine as ordered Always check sputum for blood or purulent expectoration Encourage questions and conversation so that the patient can air his or her feelings Teach or educate the patient all about PTB Encourage patient to stop smoking Teach how to dispose secretion properly Advised to have plenty of rest and eat balanced diet Be alert of drug reaction Emphasize the importance of follow-up follow-

PULMONARY TUBERCULOSIS ( Kochs Disease/Phthisis/ consumption Disease)

PREVENTION: 1. Submit all babies for BCG immunization 2. Avoid overcrowding 3. Improve nutritional and health status 4. Advise persons who have been exposed to infected persons to receive tuberculin test if necessary CXR and prophylactic isoniazid.

-Acute contagious VIRAL disease. Characteristic feature is swelling of one or both of the parotid glands  RNA, Mumps virus ; paromyxovirus of the Varicella family( found in the saliva)  Mumps vaccine - > 1yo  MMR 15 mos  Lifetime Immunity IP: 14-25 days, usually 18 days 14Incidence: 5-15 y/o, cold weather, common in men. 5Adults less likely to be attacked ( If so, causes sterility) MOT: droplet, fomites, saliva


Mumps ( Epidemic Parotitis); Infectious Parotitis

S/sx: Pain at the angle of the jaw (Unilateral or bilateral) PATHOGNOMONIC SIGN parotitis, Orchitis - sterility if bilateral, Period of communicability: 6 days before swelling communicability: ; until 9 days after swelling subsides ( 7th 9th day) ** highest communicability 48 hrs after onset of swelling Dx: serologic testing, ELISA Mgmt: supportive Supporter for orchitis Analgesics Antipyretic, cold compress, steroids

Diet : soft. Dont give sour foods Promotive:  Proper disposal of nasal & throat secretions  Bed rest Preventive: MMR vaccine ( 15 mos.) = LIFETIME IMMUNITY


Diarrheal Diseases

Cholera / El Tor
Causative agent: Vibrio coma (inaba, ogawa, hikojima), vibrio cholerae, vibrio el tor; gram (-) ( Curved rod or coma shaped organism; motile  Habitat: small intestine  Can survive longer in refrigerated foods IP: few hours to 5 days MOT: oral fecal route ( by contaminated food, water, shellfish)


S/sx: Severe vomiting, abdominal cramps, massive diarrhea of watery voluminous whitish grayish greenish slightly mucoid stools (Rice watery (Rice stool with flecks of mucus & fishy odor), s/sx of hands, severe dehydration ie Washerwomans hands, sunken eyeball & fontannel, thirst, poor skin turgor Period of communicability: 1st day 10th day ( as communicability: long as CA is seen in feces) Dx: stool culture (+) vibrio cholerae Mgmt: IV fluids, Tetracycline, Doxycycline, Erythromycin, Quinolones, Furazolidone and Sulfonamides (children)

Cholera Sigmoidoscopic view of colonic mucosa

Fatal case of infection

Rice Watery Stool in Cholera

Cholera Cot and Bucket

Nursing Mx:


Replacement of lost F & E

Administer D5LR ( more in Na) DLR ( more in K)  Enteric Isolation  All patients should be isolated until rectal swab shows (-) result ( All water & milk should be boiled for 15 minutes  Food must be protected from flies  Prepare food properly  Proper disposal of excreta  Good environmental sanitation


Bacillary Dysentery Shigellosis

Shiga bacillus: dysenteriae (fatal), flexneri (Philippines), boydii, sonnei; gram (-) ( Shiga toxin destroys intestinal mucosa  Humans are the only hosts IP: 1-7 days 1MOT : oral fecal route ( contamination of fingers, toilet seats, glass & table Ware


Pathophysiology


Shigella >>> releases toxins>>headache >>>>vomiting>>.LBM>>>stool ( bloody, mucoid with pus

S/sx: fever,colicky abdominal pain, diarrhea is fever,colicky watery to bloody with pus, tenesmus ( pain on defecation) Dx: stool culture Mgmt: Oresol, Ampicillin, TrimethoprimTrimethoprimSulfamethoxazole, Chloramphenicol, Tetracycline, Ciprofloxacin

Nursing Mx:
    

Replacement of F & E Good environmental sanitation Sanitary disposal of human feces Clean processing, preparation, serving of food Fly control

SALMONELLA INFECTION ( Salmonellosis)



 

 

Source : contaminated food, drinks ;meat and poultry product. MOT : fecal oral-route oralPeriod of communicability : throughout duration of fecal excretion IP : 6-72H ( < 24H) 6S/SX : abrupt onset nausea, vomiting, abdominal cramps, chills, LBM with bloody mucoid stool occassionally

SALMONELLA INFECTION ( Salmonellosis) Salmonellosis)

 

Physical findings: hyperactive peristalsis, abdominal tenderness and signs of dehydration. Diagnosis:
 

Stool culture Stool examination NonNon-specific

 

Treatment


Correction of fluid and electrolytes Dietary Resistant to antibiotics likes : ampicllin, chloramphenicol and cotrimoxazole

Antimicrobial not indicated unless patient is septic



Paralytic shellfish Poisoning Red Tide Poisoning

Pyromidium Bahamense ( Algae), Dinoflagellates Plankton  Ingestion of Saxitoxin in contaminated bi-valve shellfish bi Saxitoxin binds w/ Na channels leading to loss of skeletal muscle excitability  IP 15 min- 12 hrs minS/sx: Circumoral and extremity numbness, nausea and vomiting, headache ( bec of the toxins),dizziness, muscle and respiratory paralysis, rapid pulse, difficulty of speech ( ataxia) Dx: history Mgmt: emesis/gastric lavage + activated charcoal, supportive


Paralytic shellfish Poisoning Red Tide Poisoning

Dx: history Mgmt: 1. Induce vomiting (gastric lavage + activated charcoal) 2. Drink pure coconut milk ( weakens toxins) 3. Give NaHCO3(25 mgs) in glass of water 4. Avoid using vinegar in cooking shellfish affected by red tide ( 15x increase when mixed with acid) 5. Toxin of red tide is not totally destroyed in cooking 6. Avoid eating tahong , halaan, Kabiya, abaniko during red tide 7. No specific medicines

Botulism


  

Fatal form of food poisoning caused by an endotoxin CA = Clostridium Botulinum MOT = Food borne or contaminated wound IP = 12-36 hrs after eating improperly canned 12foods

 1. 2. 3.

4. 5.

S/SX Severe intoxication Visual difficulty, Dysphagia, dry mouth Descending, symmetrical flaccid paralysis ( weak, soft) Vomiting, constipation, Diarrhea Double vision, difficulty focusing eyes

Dx  Culture of stool & stomach contents  Serum positive of Botulinum toxins Nursing & Medical Management: Management:  1. IV & IM trivalent Botulinum antitoxin  2. IV fluids & Electrolytes  3. Intensive care to manage respiratory failure  4. No questionable canned food should be tested

Intestinal Parasitism

INTESTINAL PARASITISM


are parasites that populate the gastro-intestinal gastrotract. MOT : they are often spread by poor hygiene related to feces


contact with animals, or poorly cooked food containing parasites.

Two main types of intestinal parasites:



A. Helminths


Tapeworms, pinworms, and roundworms are among the most common helminths

B. Protozoa.

Cause of intestinal Parasitism



high risk for getting intestinal parasites:

Living in or visiting an area known to have parasites  Poor sanitation (for both food and water)  Poor hygiene  Age -- children are more likely to get infected  Exposure to child and institutional care centers


INTESTINAL PARASITISM
 

Some asymptomatic S/SX:

         

Diarrhea Nausea or vomiting Gas or bloating Dysentery (loose stools containing blood and mucus) Rash or itching around the rectum or vulva Stomach pain or tenderness Feeling tired Weight loss Passing a worm in your stool Anemia

Fecal testing (stool exam) can identify both helminths and protozoa.. The "Scotch tape" test identifies pinworm by touching tape to the anus. Then the tape is examine under a microscope for eggs

Ascariasis (Roundworm)
CA: Ascaris Lumbricoides IP: weeks to months MOT: MOT: transmitted through contaminated fingers into the mouth; ingestion of food and drinks contaminated by embryonated eggs Affects 4-12 years old 4Dx: stool for ova Mgmt: Mebendazole,/ Albendazole/ Pyrantel Pamoate

MOT: ingestion of food contaminated by ascaris eggs larvae in large intestine penetrate wall lung where larvae grow and coughed up intestine larvae mature and passed out in feces

Ascariasis ( roundworm infection)



Nursing Intervention: Intervention:

 

    

Isolation is not needed Preventive measures in each home and in the community should be enforced Wash hands before handling food Wash all fruits and vegetable thoroughly Availability of toilet facilities must be ensured Importance of personal hygiene should be explained Proper waste disposal.

Ascariasis ( roundworm infection)



Prevention:
Improved sanitation and hygienic practices  Improved nutrition  Deworming may be advised


Complications


Migration of the worm to different parts of the body Ex. Ears, mouth,nose Loefflers Pneumonia

Tapeworm (Flatworms) (Flatworms)

CA: Taenia Saginata (cattle), Taenia Solium (pigs) MOT: fecal oral route (ingestion of uncooked, infected meat ) IP: 2-3 mos - years 2Dx: Stool Exam Mgmt: Praziquantel, Niclosamide ISOLATION OF HOSPITALIZED PATIENTS. STANDARS PRECAUTIONS RECOMMENDED


Pinworm
Enterobius Vermicularis MOT: fecal oral route S/sx: Itchiness at the anal area d/t eggs of the agent Dx: tape test at night time (agents release their eggs during night time) Mgmt: Pyrantel Pamoate, Mebendazole


Enterobius vermicularis (PIN WORM)

The pinworm lives in the lower part of the small intestine and the upper part of the colon Human the only natural host IP : 1-2 months or longer MOT : indirectly by contaminated fomites -shared toys, toilet seat and bath

Isolation is not needed

Nursing Intervention
   

Promote hygiene Environmental Sanitation Proper waste and sewage disposal Antihelmintic medications repeated after 2 weeks (entire family)

Hookworm (Roundworm) (Roundworm)

CA: Necator Americanus, Ancylostoma Duodenale  IP - few weeks to months to years S/sx: Ground itch or dew itch at site of entry of filariform larvae involving the feet/legs, abdl cramps, diarrhea, abdl distention, anemia, perforation to peritonitis to septicemia ** Isolation is not necessary **


Dx: Dx: microscopic exam (stool exam) Mgmt: Pyrantel Pamoate and Mebendazole  dont give drug without (+) stool exam  members of the family must be examined and treated also Nsg. Intervention: 1. Proper disposal of excreta 2. Avoid walking or playing barefooted 3. Periodic deworming of school age group

Amoebiasis ( Amoebic Dysentery)



Protozoal infection of human beings initially involving the colon, but may spread to soft tissues, most commonly to the liver or lungs. CA: Entamoeba Hystolitica, protozoa Hystolitica,
    

Prevalent in unsanitary areas Common in warm climate Acquired by swallowing Cyst survives a few days after outside of the body Cyst passes to the large intestine & hatch into TROPHOZOITES. It passes into the mesenteric veins, to the portal vein, to the liver thereby forming AMOEBIC LIVER ABSCESS.

Entomoeba histolytica has two developmental stages: 1. Trophozoites/vegetative form Trophozoites/vegetative



Trophozoites are facultative parasites that may invade the tissues or may be found in the parasites tissues and liquid colonic contents. 2. Cyst a. Cyst is passed out with formed or semi-formed semistools and are resistant to environmental conditions.

b. This is considered as the infective stage in the life cycle of E. histolytica Pathology When the cyst is swallowed, it passes through the stomach unharmed and shows no activity while in an acidic environment. When it reaches the alkaline medium of the intestine, the metacyst begins to move within the cyst wall, which rapidly weakens and tears. The quadrinucleate amoeba emerges and divides into amebulas that are swept down into the cecum. This is the first opportunity of the organism to colonize, and its success depends on one or more metacystic trophozoites making contact with the mucosa.

Mature cyst in the large intestines leaves the host in great numbers (the host remains asymptomatic). The cyst can remain viable and infective in moist and cool environment for at least 12 days, and in water for 30 days. The cysts are resistant to levels of chlorine normally used for water purification. They are rapidly killed by desiccation, and temperatures below 5 and above 40 degrees.

MOT: Ingestion of cysts from fecally contaminated MOT: sources (Oral fecal route) oral and anal sexual practices  Extraintestinal amoebiasis- genitalia, spleen, liver, amoebiasisanal, lungs and meninges

lifecycle

s/sx: Blood streaked, watery mucoid diarrhea, abdominal cramps Dx: microscopic stool exam - trophozoites  Pd of Communicability: the microorganism is communicable for the entire duration of the illness Mgmt:  Tetracycline 250 mg every 6 hours  Ampicillin, Quinolones, sulfadiazine  Metronidazole (Flagyl) 800 mg TID x 5 days  Strptomycin SO4, Chloramphenicol  F&E balance

Nsg. Mx
 

Observe isolation & enteric precaution Provide health education & instruct patient to:
Boil water for drinking or use purified water  Avoid washing food from open drum or pail  Cover leftover food  Wash hands after defecation or before eating  Avoid ground vegetables ( lettuce, carrots, etc)


Prevention:
   

 

Health education Sanitary disposal of feces Protect, chlorinate & purify drinking water Observe scrupulous cleanliness in food preparation & food handling Detection & tx of carriers Fly control ( they can serve as vectors)

CNS Infections

MENINGITIS ( Cerebrospinal fever)



 

Is the inflammation of the meninges of the brain and spinal cord as a result of viral or bacterial infection. IP : varies from 1-10 days 1MOT : respiratory droplet
direct invasion through otitis media may result after skull fructure

Caused by bacterial pathogen, N. menigitidis, H. Influenza, Strep. Pneumoniae, Mycobacterium Tuberculosis

Clinical manifestations
    

headache irritability fever neck stiffness pathologic reflexes: kernigs, Babinski, Brudzinski

Diagnostics:
Lumbar puncture  Gram staining  Smear and blood culture  Urine culture


Supportive/Symptomatic:
   

a. Antipyretic b. treat signs of increased ICP c. Control of seizures d. adequate nutrition

Poliomyelitis/Infantile Paralysis/ Heine Medin Disease

- acute infectious disease characterized by changes in the CNS which may result in pathologic reflexes, muscle spasm and paralysis - it is a disease of the lower neurons, and there is anterior horn involvement CA: CA: Filterable Virus ( Legio Debilitans) Debilitans)  3 Strains:
  

Legio Brumhilde Legio Lansing Legio Leon ( rare)

MOT: The virus is transmitted from person to person MOT: by: 1. indirectly through contaminated articles and flies, contaminated water, food & utensils 2. Intimate contact w/ infected person 3. Direct contact thru nasopharyngeal secretions Dx: 1.Pandys Dx: 1.Pandys test culture of CSF (increased CHON)  2. Stool culture throughout the disease  3. Isolation of the virus from throat washings or swab early in the disease

 

IP: 7-21 days 7Period of Communicability: first three days after Communicability: onset of S/SX until three months of illness The disease is most contagious during the first few days of active disease, and possibly from 3-4 days before that 3-

Types of Polio: Polio:

1. Abortive or inapparent type does not invade the CNS ( fever, malaise, sore throat, headache, N&V) pt. usually recovers within 72 hours 2. Non-paralytic all the above signs; marked w/ meningeal irritation; pain in the neck, back, arms legs & abdomen; inability to place the head in between the knees; (+) pandys test; more severe than abortive type (

3. Paralytic polio s/sx listed above are present; flaccid asymmetrical ascending paralysis (Landrys sign), (+) Hoynes sign (head drop), Pokers sign (opisthotonus), (+) Kernig and Brudzinski sign 4. Bulbar ( Brain stem) develops rapidly & is the more serious type; motor neuron in the brainstem is attacked & affects the medulla. It weakens the muscles supplied by the cranial nerves especially the 9th ( glossopharyngeal) & 10th ( vagus); facial, pharyngeal & ocular muscles are paralyzed; respiratory failure & cardiac irregularities

Predisposing causes
   

Age about 60% of patients are under 10 yrs of age Sex males are more prone to the disease than females with a ratio of 3:2 Heredity poliomyelitis is not hereditary Environment & hygienic condition. The rich are more often spared than the poor. Excessive work, strain, marked overexertion are also factors causing the disease.

Pathology


The organism enters the body through the alimentary tract, multiplies in the oropharynx & lower intestinal tract. Then the organisms are spread to the regional lymph nodes & the blood There seems to be subsequent congestion, edema & necrosis in the area

Complications
    

Respiratory failure Circulatory collapse Electrolyte imbalance Bacterial infection Urinary problems r/t retention or paralysis of the urinary bladder

MGMT:  Analgesics for pain. Morphine is contraindicated because of the danger of additional respiratory suppression.  CBR  Moist heat application may reduce spasm & pain  Paralytic polio requires rehabilitation using physical therapy , braces, corrective shoes & in some cases, orthopedic surgery Prevention:  Active OPV (Sabin) and IPV (Salk)

Nursing Management: Management:

       

Carry out enteric isolation Observe the patient carefully for paralysis & other neurologic damage Perform neurologic assessment 1x a day Check BP regularly especially in bulbar polio Maintain good personal hygiene, particularly oral care & skin care Provide emotional support both to patient & family Dispose excreta & vomitus properly Apply hot packs to affected limb to relieve pain & muscle shortening

Tetanus/Lockjaw/Trismus
CA:  Clostridium tetani (gram (+), spore forming, forming, anaerobic ( survives w/o air) non-motile, nonvegetative( vegetative( ability to grow)  Produces potent exotoxin  Tetanus spores are introduced into the wound contaminated with soil  IP: 4-21 days 4 Tetanus neonatorum - umbilical cord

Pathophysiology
Clostridium tetani in puncture wound Release of Neurotoxin (Tetanospasmin) Hemolysin ( tetanolysin attack PNS and CNS GABA and Glycine inhibited Tetanic spasm

Clinical manifestations


     

Difficulty of opening the mouth (trismus or lockjaw) Risus sardonicus ( sneering grin) ngiting aso Dysphagia Generalized muscle rigidity Opisthotonus ( severe arching of the back) Localized or generalized muscle spasm Respiratory paralysis to death

S/Sx: Neonatal tetanus - Poor sucking, irritability, excessive crying, grimaces, intense rigidity, and opisthotonus

Criteria

Stage I

Stage II 8-10 days

Stage III <7days

Incubation Period > 11 days

Trismus

mild

moderate

Severe

Muscle rigidity

mild

Pronounced

Severe, boardlike

Spasm

absent

Mild, short

Frequent, prolonged

Dyspnea, cyanosis

absent

absent

Present

Dx: history, leukocytosis, serum antitoxin levels Mgmt: Anticonvulsant, muscle relaxants, antibiotics, wound cleansing and debridement ActiveActive-DPT and tetanus toxoid PassivePassive-TIG and TAT, placental immunity

Tetanus
Treatment: 1. Specific : -within 72 hours after punctured wound received ATS,TAT or TIG espicially if no previous immunization - Pen G to control infection - muscle relaxant to decrease muscle rigidity. 2. Non-specific - oxygen inhalation

Treatment:
antianti-toxin  Tetanus Anti-Toxin (TAT) AntiAdult,children,infant Neonatal Tetanus  TIG Neonates Adult, infant, children 40,000 IU IM,1/2 IV 20000 IU, 1/2IM, IV 1000 IU, IV drip or IM 3000 IU, IV drip or IM

Pre exposure prophylaxis

DPTDPT- 0.5 ml IM 1 - 1 months old 2 - after 4 weeks 3 - after 4 weeks 1st booster 18 mos 2nd booster 4-6 yo subsequent booster every 10 yrs thereafter  TT 0.5 ml IM TT1 6 months within preg TT2 one month after TT1 TT3 to TT5 every succeeding preg or every year


Antimicrobial Therapy Penicillin !-3 mil units q 4hours !Pedia 500000 2mil units q 4 hrs Neonatal 200000 units IVP q 12hrs or q8hrs

3 types of patients w/ skin wounds post exposure prophylaxis

(+) immunization as a child w/ boosters but last shot > 10 yrs give TT + TIG/TAT 2. (-) immunization - TT + TIG/TAT (1.

3. (+) tetanus TIG/TAT + TT + Abx + wound cleansing + supportive therapy

Control of spasms  diazepam  chlorpromazine

Preventive Measures  Treatment of wounds  Tetanus toxoid (0,1,6,1,1)

Rabies


Lyssavirus, Family Rhabdoviridae ( RNA virus)

CA: CA: Genus

Bite/wound setting

  

acute viral encephalomyelitis incubation period is 4 days up to 19 years risk of developing rabies, face bite 60%, upper extremities 15-40%, lower extremities 10% 15100% fatal

Pathophysiology
Bite/wound Local wound replication CNS ANS Salivary glands, adrenal medulla, kidney, lungs, skeletal muscles, skin, heart encephalitis

Rabies Virus The rabies virus is usually transmitted to humans by a bite from an infected dog, but the bite of any animal (wild or domestic) is suspect in an area where rabies is present. Symptoms of the disease appear after an incubation period of ten days to one year and include fever, breathing difficulties, and muscle spasms in the throat that make drinking painful. Death almost invariably occurs within three days to three weeks of the onset of symptoms. For this reason, the emphasis of treatment is on prevention. In the United States, veterinarians recommend regular vaccination of domestic dogs.

Clinical Manifestation
  

pain or numbness at the site of bite fear of water fear of air

4 STAGES

1. prodrome - fever, headache, paresthesia, 2. encephalitic excessive motor activity, hypersensitivity to bright light, loud noise, hypersalivation, dilated pupils 3. brainstem dysfunction dysphagia, hydrophobia, apnea 4. death

Dx: history virus isolation from saliva and CSF serial serum Ab sample Staining of brain tissue (dog) - Negri bodies

Postexposure prophylaxis
Category I Licking of intact skin Observe the dog for 14 days

Category II Abrasion, laceration, punctured wound on the lower extremities

vaccine 2.Observe dog for 14 days

1.Active

Category III Abrasion, laceration on upper extremities, head and neck Dog is killed, lost, died

1.Active 2.Passive

Category of bites
 

I intact skin (lick or scratch) II mucosal, non bleeding wounds, abrasions III bleeding bites and above neck, stray dogs, laceration, multiple bites

Mgmt: - wound cleansing - tetanus prophylaxis - Observe and quarantine dog for maniacal s/sx - Active- antirabies vaccine (human diploid cell vaccine) - 7-10 days to induce an active immune response, with immunity x 2 years - Passive human rabies immunoglobulin

Management  No treatment for clinical rabies  Prophylaxis

Active vaccine (PDEV,PCEC,PVRV)  Intradermal (0,3,7,30,90)  Intramuscular (0,3,7,14,28)  (0,7,21)

Post exposure prophylaxis



Antirabies vaccine 1 ml IM day 0, 3, 7, 14, 28 OR 0.1 ml ID day 0 (8 sites), 7 (4 sites), 28, 91 (1 site) OR 0.1 ml ID day 0, 3, 7 (2 sites), 30, 90 (1 site)

Rabies immunoglobulin (HRIG/equine antiserum) 20/40 units/kg IM single shot wound 40%, deltoid 60%

Passive Vaccine  a. ERIG wt in kg x .2 = cc to be injected im (ANST)  b. HRIG wt in Kg x .1333

PrePre-exposure Prophylaxis  Intradermal/Intramuscular (0,7,21)

Infection control  Patient is isolated to prevent exposure of hospital personnel, watchers and visitors  PPE Preventive Measures  Education  Post-exposure and Pre-exposure Prophylaxis PostPre-

SNAKEBITE

Neurotoxic

Slow swelling then necrosis

Ptosis, respiratory paralysis, cardiac problems

Cobra

Myotoxic

None

Myalgia on moving paresis Bleeding abnormalities

Sea snake

Vasculotoxic

Rapid swelling

Vipers

Management
    

Lie the victim flat ice compress and constrictive materials are contraindicated Transport the patient to the nearest hospital Antivenim administration in patients with signs of envenomation It is never too late to give anti-venim anti-

    

Antivenim is given thru intravenous infusion, which is the safest and most effective route. 2-5 ampules plus D5W to run 2over 1-2 hours every 2 hours 1Antimicrobial therapy sulbactam/Ampicillin or co-amoxiclav coSubstitute Prostigmine IVinfusion, 50-100ug/kg/dose 50q 8hrs Atropine

Skin Transmission Diseases

Leprosy/Hansens disease
  

Chronic communicable disease of the skin & the peripheral nerves Causative Agent: Mycobacterium Leprae, acid fast bacilli MOT: may be due to prolonged skinskin-skin contact or droplets IP - years to decades Active immunization (BCG)

Types of Leprosy:


  

1. Lepromatous or Nodular or Gravis ( most severe) Early s/sx: many lesions or patches 2. Tuberculoid high resistant, less severe 3. Mixed type or Borderline or Dimorphous 4. Indeterminate

TYPES: PAUCIBACILLARY 1. Early/Indeterminate hypopigmented / hyperpigmented anesthetic macules/plaques 2. Tuberculoid solitary hypopigmened hypoesthetic macule, neuritic pain, contractures of hand and foot, ulcers, eye involvement ie keratitis MULTIBACILLARY 1. Lepromatous inability to close eyelids unblinking eyes ( lagophthalmos) multiple lesions, Loss of lateral portion of eyebrows (madarosis), corugated skin (leonine facies), septal collapse (saddlenose) clawing of fingers & toes, loss of digits, enlargement of male breasts ( gynecomastia) 2. Borderline between lepromatous and tuberculoid

Mgt:
 

     

Domiciliary home treatment ( RA 4073) Multi Drug Therapy ( MDT) use of 2 or more drugs for the tx of leprosy. Proven effective cure for leprosy & renders patients nonnon-infectious a week after starting treatment. PaucibacillaryPaucibacillary- Rifampicin and Dapsone MultibacillaryMultibacillary-Rifam,Dapsone,Clofazimine Diaminodiphenylsulfone DDS( Dapsone) Rifampicin Clofazimine (lamprene) Treatment is from 9 mos to 18 mos(2 years )

Pediculosis Blood sucking lice/Pediculus humanus

p. capitis-scalp capitisp. palpebrarum-eyelids and eyelashes palpebrarump. pubis-pubic hair pubisp. corporis-body corporis-

MOT: skin contact, sharing of grooming implements s/sx: nits in hair/clothing, irritating maculopapular or urticarial rash Mgmt: disinfect implements, Lindane (Kwell) topical Permethrin (Nix) topical CX: impetigo to AGN, RHD

Scabies
  

Sarcoptes scabiei Pruritus (excreta of mites) Mites come-out from burrows to mate comeat night

MOT: skin contact s/sx: itching worse at night and after hot shower; rash; burrows (dark wavy lines that end in a bleb w/ female mite) in between fingers, volar wrists, elbow, penis; papules and vesicles in navel, axillae, belt line, buttocks, upper thighs and scrotum

Dx: biopsies/scrapings of lesions Mgmt: Permethrin (Nix) cream, crotamiton cream, Sulfur soap, antihistamines and calamine for pruritus, wash linens with hot water, single dose of Ivermectin, treat close contacts

Emerging Diseases

Severe Acute Respiratory Syndrome (SARS)



is a respiratory disease in humans which is caused by the SARS Coronavirus .



SARS appears to have started in Guangdong Province, China in November 2002. Pandemic

MOT : direct Mucous membrane/ droplet / exposure to fomites.

  

Virus is stable in urine/feces for 1-2 days ; for patient 1with diarrhea up to 4 days. IP: 2-7 days ( max 10d) 2Mortality rate 5% only

Heat at 56 c rapidly kills the virus

Severe Acute Respiratory Syndrome (SARS)



Clinical criteria :
 

1. Asymptomatic or mild respiratory illness , fever >38c ( >100.4 F ) 2.One or more clinical finding of respiratory illness


cough / shortness of breath / DOB /hypoxia Contact (sexual or casual) with someone with a diagnosis of SARS within the last 10 days OR Travel to any of the regions identified by the WHO as areas with recent local transmission of SARS (affected regions as of 10 May 2003 were parts of China, Hong Kong, Singapore and the province of Ontario, Canada).

Epidemiologic Criteria:
 

SARS


Treatment
 

Antibiotics are ineffective as SARS is a viral disease. supportive with antipyretics, supplemental oxygen and ventilatory support as needed. Consult doctor promptly early treatment is the KEY Build up good body immunity Maintain good personal hygiene Wear mask if develop runny nose, cough Wear protective mask in public areas Wash hand properly and keep them clean Droplet & contact PRECAUTION

Preventive measures ( HEALTH TEACHING)

      

BIRDS FLU
  

is an AVIAN FLU , a type of influenza known to exist worldwide. Etiologic agent : avian influenza H5N1 strain MOT : spread in air and manure.
Transmitted through contaminated feeds, water, equipment, and clothing  No evidence that virus can survive in well cooked meat  Spread rapidly among birds not infect human easily  No confirmed human-human transmission human

Bird Flu


Human cases of influenza A (H5N1) infection have been reported in :

 Cambodia  China  Indonesia  Thailand  Vietnam.

BIRDS FLU
 

Incubation period : 3-5 days 3S/sx :

 

Symptoms in animal vary - can cause death within few days In human same as in human influenza


Fever/ sorethroat/ cough/ severe cases Pneumonia.

The highly pathogenic form spreads more rapidly through flocks of poultry. This form may cause disease that affects multiple internal organs and has a mortality rate that can reach 90-100% often within 48 90hours.

BIRDSFLU


Prevention & treatment

Avian influenza in human can be detected with : STANDARD INFLUENZA TEST  Antiviral drugs clinically effective in both preventing and treating the disease.



oseltamavir and zanamavir

Vaccines take at least 4 months to produce and must be prepared for each sub-type sub-

Nursing Intervention : Health Teaching



Wash hands with soap and warm water for at least 20 seconds before and after handling raw poultry and eggs. Clean cutting boards and other utensils with soap and hot water to keep raw poultry from contaminating other foods. Use a food thermometer to make sure you cook poultry to a temperature of at least 165 degrees Fahrenheit Consumers may wish to cook poultry to a higher temperature for personal preference. Cook eggs until whites and yolks are firm.

FYI


There are only three known A subtypes of influenza viruses (H1N1, H1N2, and H3N2) currently circulating among humans. Influenza A viruses are constantly changing, and they might adapt over time to infect and spread among humans.

END

Thank You!

Communicable Disease
is an illness due to an infectious agent or its toxic products which is easily transmitted or communicated directly or indirectly from one person or animal to another ** Both infectious and contagious diseases are communicable** **All contagious diseases are communicable **All but not all communicable diseases are contagious**


The Infectious Process



Causative Agent:


Type of bacterium , virus, fungus, parasite, rickettsia, chlamydia etc.

Reservoir the environment in which the agent is found

Human man is the reservoir of diseases that is more dangerous to humans than to other species  Animal responsible for infestations with trophozoites, worms etc  Nonanimal street dust, garden soil, lint from bleeding


Mode of escape from reservoir:

Respiratory Tract  Gastrointestinal Tract  Genito-urinary tract Genito Open lesions  Mechanical escape ( include bite of insects)  Blood


Mode of Transmission: Transmission: 1. by contact transmission: transmission:

Direct contact immediate direct transfer of microorganism from person to person)  Touching, biting, kissing, sexual intercourse


Droplet contact occurs within 3 ft from source  ( from coughing, sneezing or talking to an infective person)





2. Indirect transmission
by vehicle route ( through contaminated items)


Serves as an intermediate means to transport & introduce an infectious agent into susceptible host through susceptible port of entry
 Inanimate

Fomites
objects ( handkerchief, toys, soiled clothes, eating utensils ,surgical instruments, or dressing, IV needle, water, food, milk, serum, plasma

By vector route


Is an animal or flying or crawling insect which serves as an intermediate means of transporting an infectious agent.  Ex. Mosquitoes, snails , flies, ticks and others

3. Airborne Transmission: Transmission:

Droplet neclei ( residue of evaporated droplets that remain suspended in air)  Dust particles in the air containing the infectious agent  Organisms shed into the environment from skin, hair, wounds or perineal area


Mode of Entry of Organisms into the Human Body:

Respiratory tract  Gastrointestinal tract  Genito-urinary tract Genito Direct infections of mucous membranes / skin


Host Factors :
 

   

Age, sex, genetics Nutritional status, fitness, environmental factors General physical, mental & emotional health Absent or abnormal immunoglobulins Status of hematopoietic system Presence of underlying disease ( DM, lymphoma, leukemia Pt. treated w/ certain antimicrobials, corticosteroids, irradiation, immunosuppresive agents