Communicable

Disease Nursing
Florence V.Quintana RN
Host and Microbial Interaction
INTRODUCTION

Although most microorganisms

live in harmony with the human
body, some—called
pathogens—can 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, 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 Host’s
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:

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 body’s defenses
3. Subclinical (Inapparent Infection)
= does not cause any noticeable illness
 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
 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
 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 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.

 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
 ANTIGEN
TRIGGERING AGENT OF THE IMMUNE
SYSTEM; FOREIGN SUBSTANCE
INTRODUCED INTO THE BODY causing
the body to produce antibodies
TYPES OF ANTIGENS:
1. INACTIVATED ( KILLED ORGANISM)
1. Not long lasting
2. Multiple doses needed
3. Booster dose needed
2. ATTENUATED ( LIVE WEAKENED
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 antibodies 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 ACQUIRED
- INHERENT BODY TISSUES Outside the
host

1. NATURAL 2.
ARTIFICIAL
( HUMAN)
( LABORATORY)

A. ACTIVE B. PASSIVE A. ACTIVE B.

PASSIVE
-HAD THE DISEASE & - MATERNAL - VACCINES -
ANTITOXINS
 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. BCG
2. DPT
3. OPV/IPV
4. Measles
5. MMR
6. TB
7. Hepatitis B
8. Varicella
9. Hemophilus influenzae B (Hib)
 Active immunization not
routinely given
1. Cholera vaccine
2. Rabies
3. Typhoid
4. Influenza A & B
5. Meningococcal
6. Pneumococcal vaccine
7. HPV vaccine
 Passive immunization
1. Diphtheria antitoxin
2. Hepatitis B immunoglobulin (HBIG)
3. Measles immunoglobulin
4. Varicella immunoglobulin (VZIG)
5. Rabies Human immunoglobulin (RIG)
6. Tetanus human immunoglobulin (TIG)
7. 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. Tb
2. Measles
3. Diphtheria, Pertussis
4. Polio ,
5. Tetanus
6. Hepatitis
 IMMUNOGLOBULINS
( IG’S)
 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 6 weeks IM 3 x (4weeks int) Local rxn, acute

encephalopathy
MMR 15 wks

OPV 6 weeks oral 3 x (4wks int) None

Measles 9 mos SQ Once Fever

Hep B At birth IM 3 x ( 2,4,6 ) Mild local rxn

 Special-use Vaccine
Meningoccocal Epidemic areas SQ None

Rabies Exposures ID/IM Local rxn

Typhoid travellers IM Local rxn

Japanese encep travellers SC Anaphylactic

Pneumococcal immunocompro IM/SQ 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
 Susceptible Host

 Recognition of high risk patients

 Immunocompromised
 DM
 Surgery
 Burns
 Elderly
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% Surgical

34% UTI


 13% LRI
 14% Bacteremia
 22% 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
80°C
 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
 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
 The 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 TRANSMISSION-

BASED 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 Single Masks Gowns Gloves
Precautio Room
n

Airborne Yes, with Yes No No

(-) air
pressure
ventilation

Droplet Yes Yes, mask No No

for persons
close to
patient

Contact Yes 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
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
1. Contact isolation
2. Respiratory isolation
3. TB isolation
4. Enteric isolation
5. Drainage/secretion precaution
6. 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 disease

Specification: 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.

Disease requiring Isolation – Tuberculosis

Type : Enteric Precautions

Purpose:To prevent infections that are transmitted

by direct or indirect contact with feces.

Specification: Private Room – Indicated if client’s 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 : Drainage- secretion precautions
Purpose: To prevent infections that are transmitted by direct or
indirect contact with purulent material or drainage
from infected site.

Specification: 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 infection.
Type : Blood- 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 client’s 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, transplant, immuno deficient
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: 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: Strict attention should be paid to careful

hand washing; disease can be spread by oral- fecal
route.

Blood: needles and syringes should be disposable.

Used needles should not be recapped. They should
be placed in a puncture-resistant container that is
prominently labeled “ Isolation “ Specimens should be
labeled “ Blood Precaution”.
Environmental Control

 Routine care, cleaning and

disinfection of environmental surfaces

PRECAUTIONS FOR INVASIVE

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,
REMOVE 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
 5.General waste – scrap paper / food
material
 Philippines set-up
 black plastic bags are for non-
biodegradable and noninfectious
 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
 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. Elimination of the source of
infection
2. Interruption of transmission
3. 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
1. 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

3. Respiratory diseases
a. Pneumonia
b. Diphtheria
c. PTB
d. Mumps
5. CNS Infections  7. Emerging
a. Encephalitis
b. Meningitis
Diseases:
c.Meningococcemia  SARS
d. Rabies
e. Tetanus
Birds FLU
f. Snake bite
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 Fever, 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
** Life span of the mosquito is 4
months
Pathognomonic sign: Herman’s rash
Dengue Fever, H-Fever, Dandy
Fever, Breakbone 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
 Vector- Aedes aegypti

-Day 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
 CRITERIA FOR DIAGNOSIS:
 Fever ,acute, high continous, lasting
for 2-7 days
 Positive
torniquet test
 Spontaneous bleeding

(petechiae,purpura,ecchymoses,pistaxis,
gum bleeding, hematemesis, melena)
 Laboratory: thrombocytopenia </=
100,000mm3, hemoconcentration- an
increase of at least 20% in the
hematocrit or its steady rise
 Assessment:
 Tourniquet test (Rumpel Leedes 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); 10-15 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:
 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
Dengue Fever
DHF
Vector caries virus (AEDES aegypti)
Febrile phase
2-7 days
Bite host ( IP 3-10d)

First 2 days s/sx : Fever , headache, myalgia ,anorexia

Vascular injury Vomiting, sorethroat, rashes
Plasma leakage
(+) petechiae , (+) TT
IMPROVE

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

Circulatory failure
Dengue progress -hypotension death
-narrow pulse pressure
,20mm Hg (shock)
S/sx:
Mild dengue – abrupt onset of fever,
headache, muscle and joint pains,
anorexia, abdominal pain.
Petecchiae, Herman’s 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 pt’s 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
1. Search and destroy breeding
places of dengue causing
mosquitoes such as old tires,
coconut husks, roof 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:
 1. Plasmodium falciparum ( malignant tertian)
 Most fatal ; common in the Philippines
 2. Plasmodium vivax ( Benign tertian)
 Non-life threatening except for the very
young & 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 travel
by anopheles mosquito to human liver

mature to be released into invade RBC as they

a blood stream as merozoites 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)
 Chattering of lips, shakes
 Keep the patient warm
 Hot water bath
 Expose to heat
 Warm drinks
 Last about 10-15min

2. . Hot stage (3-4Hrs)

 Recurring high grade fever , headache , abdominal pain

and vomiting
 TSB , cold compress
 Light clothing,
 MALARIA (Ague)
 Clinical manifestation :
 I. Cold stage ( 10-15mins)
 II. Hot stage (3-4Hrs)

 III. Wet stage

 Profuse sweating

 Keep patient comfortable

 Keep them warm and dry

 Increase fluid intake

Diagnostics:
1. Malarial smear - Peripheral blood
extraction (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 within 10-15 mins.
This is done to detect malarial parasite
antigen in the blood.
Pathonomonic sign: Stepladder fever
Medical Mgmt:
A. IVF’s
B. Anti- Malarial Drugs
Chloroquine ( 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 interval. 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)
 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 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 , sorsogon ,
quezon , masbate , mindoro , romblon , marinduque ,
bohol , samar , leyte , palawan , sulu , tawi-tawi and
basilan.
 Malayi : Palawan , eastern samar , agusan ,sulu

Vector: Culex, Mansonia, Anopheles,

Aedes
 Filariasis ( elephantiasis )

Mosquito bites
Aedes poiculus , culex
faligans and Person infected – bitten by mosquito
anopheles flavirostris Transmitted to another person

Bites a person with lymphatic filariasis Larvae migrate to LN, reach

& infect the mosquito Sexual maturity & cycle is
completed

Microscopic worms pass from mosquito

Through the human skin, travel to LN , grow as adult
Note: a person needs
Many mosquito bite
Adult worm lives for 7 yrs in lymph vessels Over several months- years to get
Mate release into blood stream- microfilaria 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 observed.

Blood /vector-borne
 Treatment :
 Drugs  Ivermectin , albendazole and
DIETHYLCARBAMAZINE (DEC)-
6mg/KBW in divided doses for 12
consecutive days
 Eliminate the larvae

 Impairing the adult worm’s 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: 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 (Weil’s
 Weil’s disease,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
 Spirochete, Leptospira
interrogans, gram (-)
 Weil’s syndrome
– severe form
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

 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

 Non-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
DISEASES
GIT
 Typhoid Fever
 Salmonella typhosa, gram (-)
 Carried only by humans

Bacterial infection transmitted by contaminated water,

milk, shellfish ( oyster ) & other foods
Infection of the GIT affecting the lymphoid tissue
( payer’s patches) of the small intestine
Most severe form of salmonellosis caused by
salmonella typhi
MOT: oral fecal route
5 F’s : Fingers, Fomites, Flies, Feces, Food & Fluids
 Pathophysiology
Oral ingestion

Bloodstream

Reticuloendothelial system (lymph node,

spleen, liver)

Bloodstream

Gallbladder

Peyer’s patches of SI necrosis and

ulceration
 Typhoid Fever
Ulceration of the Peyer's Patches
 Typhoid Fever
Clinical Manifestations:
Incubation Period: 1-2 weeks
1. 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: Blood culture (typhi dot) 1st week
Stool and urine culture 2nd week
Widal test
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: 2 months
 Source: feces of infected persons
 Dogs, pigs, cows, carabaos, monkeys, wild rats
serve as HOSTS
Pathogenesis- Snail fever Ulceration in the mucosa
Eggs able to escape in the lumen
Larvae ( cercaria) Of intestine, excreted in the feces

Penetrate skin Some eggs carried by portal

Circulation, filtered in the
Work their way to Liver , formed granulomas
Liver venous portal circulation
Granulomas are resolved
In portal vessel , & replaced by fibrous tissues
they mature in 1-3 months Scar formation occur
Diseases progresses
Mature worms live in copula in the portal vessels
Liver enlarges due
Migrate to some part of the body
To increasing fibrosis

Female cercaria lays egg in the blood vessels Blood flow interrupted
Large intestine or bladder Result to portal
hypertension
 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
(miracidi
um

intermediary
host
(oncomelania
quadrasi/tiny
amphibious
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 :
 Swimmer’s 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
weeks after initial infection and last for 1-2
months
 Diagnostics:
 Fecalysis or direct stool exam
 Kato katz technique

 Liver and rectal biopsy

 ELISA ( enzyme link

Immunosorbent Assay)
 COPT ( circum-oval precipitin test)
confirmatory diagnostic test

 Prevention : proper disposal of feces ;

snail control
 Treatment: Praziquantel for 6
mos PO
 Fuadin
 Prevention & Nursing
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)- 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
 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

 Hepatitis E (HEV) – water , fecal-oral route

 VIRAL HEPATITIS
HAV HBV HCV HDV HEV
IP 15-50d 45-180d 14-182d 14-70d 15-64d

MOT Fecal oralParenteral Blood Same w/ B Fecal

Percutaneou transfusio oral
s n
placental
commu Till 1 wk During IP As carrier- Througho Unknown
nicabilit after Entire indefinite ut clinical
y onset of clinical 1 wk disease
jaundice course before
Years if clinical
carrier onset
 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

 Anti-HBs – resolved or immunity

 HbeAg – infected risk of transmitting
 Anti-HBe – lower risk of transmitting
 Anti-HBc – acute resolved or chronic
HBV infection
 IgM anti-HBc – acute with recent HBV
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
 Measles, Rubeola, Morbili,
7 Day Fever, Hard Red



Measles,
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

MOT: Direct ( droplets, airborne); Indirect ( fomites)
*Contagious 1-2 days before rash and 4 days after the
appearance of rash
 Sources of Infection:
 Patient’s 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:
1. Pre-eruptive stage:
(2-4 days) - malaise, cough,
conjunctivitis, , fever, kopliks spots
( PATHOGNOMONIC SIGN) (1-2 mm
blue white spots on red background
along 2nd molars), stimsons ( puffiness
of eyelid) photophobia
2. Eruptive stage:
Rash is usually seen late on the 4th day
Maculo-papular rash
3. Stage of convalescence:
Rashes fade away, desquamation
begins,fever subsides
Cx: pneumonia, meningitis,
 MEASLES

 Fever persist  means (+) complication

 Bronchopneumonia- most common

 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
 MANAGEMENT
1. Supportive
2. Hydration
3. Proper nutrition
4. Vitamin A
5. Antibiotics – if w/
secondary
bacterial infection
6. Vaccine- measles
vaccine @ 9 mos
and MMR @ 15
mos
7. Anti viral drugs
( Isoprenosine)

Observe respiratory
 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)
 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

MOT: Direct contact: droplets spread
through the nasopharynx
Indirect contact: transplacental

**Highly communicable infant may shed

virus for months after birth**
Rashes:
Maculopapular,
Diffuse/not
confluent, No
desquamation,
spreads from the
face downwards
Clinical Manifestations:
> FORSCHEIMER’S 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: rare; pneumonia, meningoencephalitis
CX to pregnant women:
 1st tri-congenital anomalies ( microcephaly,
heart defects, cataracts, deafness
 2nd tri-abortion or bleeding
 3rd tri-pre mature delivery
Nursing Considerations:
 MMR immunization
 Use of immunoglobulins ( IG’s)- ppost
exposure 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

MOT: probably respiratory secretions

S/sx: Spiking fever w/c subsides 2-3 days,

Face and trunk rashes 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”
 Human beings are the only source of infection
 CA = Varicella Zoster virus, Herpes virus
 IP – 10-21 days
 MOT: droplet spread
> nose & throat secretions
> Vesicles ( contagious in early stage of
eruption
> Airborne
 Prodromal period: headache , vomiting, fever
 Papulovesicular rashes appear on trunk 
spreading to face and extremties
( centrifugal)

 Macules papules vesicles with clear

fluid inside crusting and scar formation

 Thedisease 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:
Maculopapulovesicu
lar (covered areas),
Centrifugal rash
distribution, starts
on face and trunk
and spreads to
entire body

 Leaves a pitted scar

(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
 Small Pox, Variola
 DNA, Pox virus
 Last case 1977
 spreads from man-to-
man only
 Active: Vaccinia pox virus

IP: 1-3 weeks

S/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
 Pre-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)

 High risk: immunocompromised
S/sx:
1. Meningococcemia – usually starts as nasopharyngitis, followed
by sudden onset of spiking fever, chills, arthralgia. Bacteria is
carried by 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)
 Chloramphenicol 100mg/kg/day

 Symptomatic and supportive

 fever
 seizures
 hydration
 respiratory function
 Chemoprophylaxis
 Rifampicin 300-600mg q 12hrs x 4 doses
 Ofloxacin 400mg single dose
 Ceftriaxone 125-250mg IM single dose
( Ciprobay)
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 Loeffler’s Bacillus)
 IP: 2-5 days
 Period of Communicability: 2-4 wks if untreated, 1-2 days
if 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: 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
- 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”( CHARA
CTERISTIC SIGN)
,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
Loeffler’s
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
 Supportive
 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
 DPT- 0.5 ml IM
1 - 1 ½ 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.
bronchiseptica, gram (-)
 Pertussis toxin, tracheal cytotoxin,

“ Bordet Gengou Bacillus”

 Common in Infants and young children & fatal
to toddlers
IP: 5-21 days
MOT: airborne/droplet; direct contact ( nose &
throat secretions); indirect contact ( articles)
S/sx:
1. Catarrhal stage (1-2 wks; highly contagious) – sneezing,
runny nose,tearing lacrimation, mild cough, low grade fever
2. Paroxysmal stage (2-4 wks) - Clusters of cough that ends
with a whoop, vomiting, exhaustion
3. Convalescent stage (2-3 wks) – less frequent cough

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
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
 DPT- 0.5 ml IM
1 - 1 ½ 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( Koch’s
Disease/Pthisis/Consumption
disease)
 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)
 Pott’s 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.
IP: 2 – 10 weeks
Mode of Transmission:
 Direct: droplet ( sneezing, coughing)

 Indirect: continuous exposure to

infected persons within the family
Source of Infection:sputum, blood from
hemoptysis, nasal discharges and saliva
 Classification :
 Minimal – slight lesion
 Moderately advanced – one or both
lung may be involved
 Far advanced- more extensive
 Clinical 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:
 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

If reactivated,and
Secondary
granuloma;TB Primary TB
 DX
 1. Case 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
 4. Tuberculin Test
 1. PPD – Purified Protein Derivative
 2. Mantoux Test- (more reliable) = ID

injection of tuberculin extract into the

inner aspect of forearm to detect
infection/exposure to CA.
Localized reaction- detected in 48 to
72 hours
(+) 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
( -) 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

x-ray, 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

* 2 wks after medications – non communicable

3 successive (-) sputum - non communicable
rifampicin or INH- prophylactic
 TREATMENT:

 CATEGORY 1 - NEW PTB, (+) SPUTUM

GIVE RIPE 2 MONTHS, MAINTENANCE OF RI 4
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 neuritis ( Give Vit B6-
Pyridoxine)50 mg; Jaundice; Psychosis
3. Pyrazinamide ( PZA)
 SE = Hyperuricemia ( inc uric acid)

 Mx: Inc fluid intake

4. Ethambutol = 15-20mg/day
 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
 PTB- NURSING
MANAGEMENT
1. MAINTAIN REPIRATORY ISOLATION
2. Administer medicine as ordered
3. Always check sputum for blood or purulent
expectoration
4. Encourage questions and conversation so that the
patient can air his or her feelings
5. Teach or educate the patient all about PTB
6. Encourage patient to stop smoking
7. Teach how to dispose secretion properly
8. Advised to have plenty of rest and eat balanced
diet
9. Be alert of drug reaction
10. Emphasize the importance of follow-up
 PULMONARY TUBERCULOSIS
( Koch’s 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.
 Mumps ( Epidemic Parotitis);
Infectious Parotitis
 -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

Incidence: 5-15 y/o, cold weather, common in men.
Adults less likely to be attacked ( If so, causes sterility)
MOT: droplet, fomites, saliva
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 ; 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. Don’t 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 stool with flecks of mucus & fishy
odor), s/sx of severe dehydration ie
Washerwoman’s hands, sunken eyeball &
fontannel, thirst, poor skin turgor
Period of communicability: 1st day – 10th day ( as
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

MOT : 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
watery to bloody with pus, tenesmus
( pain on defecation)
Dx: stool culture
Mgmt: Oresol, Ampicillin, Trimethoprim-
Sulfamethoxazole, 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
 Period of communicability : throughout
duration of fecal excretion
 IP : 6-72H ( < 24H)
 S/SX : abrupt onset nausea, vomiting,
abdominal cramps, chills, LBM with bloody
mucoid stool occassionally
 SALMONELLA INFECTION
( Salmonellosis)
 Physical findings: hyperactive peristalsis,
abdominal tenderness and signs of
dehydration.
 Diagnosis:
 Stool culture
 Stool examination
 Treatment
 Non-specific
 Correction of fluid and electrolytes
 Dietary
 Antimicrobial not indicated unless patient is septic
 Resistant to antibiotics likes : ampicllin, chloramphenicol
and cotrimoxazole
 Paralytic shellfish Poisoning
Red Tide Poisoning
 Pyromidium Bahamense ( Algae), Dinoflagellates
Plankton
 Ingestion of Saxitoxin in contaminated bi-valve
shellfish
 Saxitoxin binds w/ Na channels leading to loss of
skeletal muscle excitability
 IP 15 min- 12 hrs

S/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 ½ 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 foods
 S/SX
1. Severe intoxication
2. Visual difficulty, Dysphagia, dry mouth
3. Descending, symmetrical flaccid
paralysis ( weak, soft)
4. Vomiting, constipation, Diarrhea
5. Double vision, difficulty focusing eyes
Dx
 Culture of stool & stomach contents

 Serum positive of Botulinum toxins

Nursing & Medical 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 tract.
 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: transmitted through contaminated
fingers into the mouth; ingestion of food
and drinks contaminated by embryonated
eggs
Affects 4-12 years old

Dx: 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:
 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)
 CA: Taenia Saginata (cattle), Taenia
Solium (pigs)
MOT: fecal oral route
(ingestion of uncooked, infected meat )
IP: 2-3 mos - years
Dx: 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
Isolation is not needed contaminated fomites
-shared toys, toilet
seat and bath
 Nursing Intervention
 Promote hygiene
 Environmental Sanitation
 Proper waste and sewage disposal
 Antihelmintic medications repeated
after 2 weeks (entire family)
 Hookworm (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, abd’l cramps, diarrhea,
abd’l distention, anemia, perforation
to peritonitis to septicemia
** Isolation is not necessary **
Dx: microscopic exam (stool exam)
Mgmt: Pyrantel Pamoate and
Mebendazole
 don’t 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
 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 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 stools 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 sources (Oral fecal
route)
oral and anal sexual practices
 Extraintestinal amoebiasis- genitalia,
spleen, liver, anal, 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
 MOT : 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: kernig’s,
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: Filterable Virus ( Legio Debilitans)
 3 Strains:
 Legio Brumhilde
 Legio Lansing
 Legio Leon ( rare)
MOT: The virus is transmitted from person to person
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.Pandy’s 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
 Period of Communicability: first three
days after 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
 Types of 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; (+)
pandy’s test; more severe than abortive type (
 3. Paralytic polio – s/sx listed above are
present; flaccid asymmetrical ascending
paralysis (Landry’s sign),
(+) Hoyne’s sign (head drop),
Poker’s 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:
 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, anaerobic ( survives w/o air)
non-motile, vegetative( ability to grow)
 Produces potent exotoxin
 Tetanus spores are introduced into the
wound contaminated with soil
 IP: 4-21 days
 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 Stage III

Incubation Period > 11 days 8-10 days <7days

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
Active-DPT and tetanus toxoid
Passive-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:
anti-toxin
 Tetanus Anti-Toxin (TAT)

Adult,children,infant 40,000 IU ½ IM,1/2 IV

Neonatal Tetanus 20000 IU, 1/2IM, ½ IV
 TIG

Neonates 1000 IU, IV drip or IM

Adult, infant, children 3000 IU, IV drip or IM
 Pre exposure prophylaxis
 DPT- 0.5 ml IM
1 - 1 ½ 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
1. (+) immunization as a child w/
boosters but last shot > 10 yrs –
give TT + TIG/TAT
2. (-) immunization - TT + TIG/TAT

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

 CA:Genus Lyssavirus,
Family Rhabdoviridae
( RNA virus)

 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%
 100% fatal
 Pathophysiology
Bite/wound

Local wound replication

CNS encephalitis

ANS

Salivary glands, adrenal medulla, kidney,

lungs, skeletal muscles, skin, heart
 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
 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
Category I prophylaxis
Observe the dog for 14 days
Licking of intact skin

Category II 1.Active vaccine

Abrasion, laceration, punctured wound 2.Observe dog for 14 days
on the lower extremities

Category III
Abrasion, laceration on upper 1.Active
extremities, head and neck 2.Passive
Dog is killed, lost, died
 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
Pre-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
 SNAKEBITE

Neurotoxic Slow swelling Ptosis, Cobra

then necrosis respiratory
paralysis,
cardiac
problems

Myotoxic None Myalgia on Sea snake

moving
paresis

Vasculotoxic Rapid swelling Bleeding Vipers

abnormalities
 Management

 Lie the victim flat

 ice compress and constrictive
materials are contraindicated
 Transport the patient to the nearest
hospital
 Antivenim administration in patient’s
with signs of envenomation
 It is never too late to give anti-venim
 Antivenim is given thru intravenous
infusion, which is the safest and most
effective route. 2-5 ampules plus D5W
to run over 1-2 hours every 2 hours
 Antimicrobial therapy
 sulbactam/Ampicillin or co-amoxiclav
 Substitute
 Prostigmine IVinfusion, 50-
100ug/kg/dose q 8hrs
 Atropine
Skin Transmission
Diseases
 Leprosy/Hansen’s disease
 Chronic communicable disease of the skin
& the peripheral nerves
 Causative Agent: Mycobacterium Leprae,
acid fast bacilli
 MOT: may be due to prolonged
skin-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 non-infectious a week after starting treatment.
 Paucibacillary- Rifampicin and Dapsone
 Multibacillary-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
p. palpebrarum-eyelids and eyelashes
p. pubis-pubic hair
p. corporis-body

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 at 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 with diarrhea up to 4 days.
 IP: 2-7 days ( max 10d)
 Mortality 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
 Epidemiologic Criteria:
 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).
 SARS
 Treatment
 Antibiotics are ineffective as SARS is a viral disease.
 supportive with antipyretics, supplemental oxygen
and ventilatory support as needed.
 Preventive measures ( HEALTH TEACHING)
 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
 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
 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
 S/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 hours.
 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
 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
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

 Open lesions

 Mechanical escape ( include bite of

insects)
 Blood
 Mode of Transmission:

 1. by contact 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
 Fomites
 Inanimate 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:
 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

 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