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MULTI-EDUCATIONAL REVIEW GROUP EXPERTS, INC.

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COMMUNICABLE DISEASE NURSING

A. BASIC CONCEPTS:

COMMUNICABLE DISEASES – an illness due to an infection agent or its toxic products which is transmitted directly
or indirectly to a well person or animal or thru an agency of an intermediate of an animal host, vector of the inanimate
environment.

DIFFERENCE BETWEEN CONTAGIOUS AND INFECTION DISEASE

- CONTAGIOUS DISEASE – easily spread directly from persons to person; all contagious diseases are infectious
- INFECTIOUS DISEASES – applied to diseases not transmitted by ordinary contact, but require a direct
inoculation of a break in the previously intact skin or mucus membrane

I. FACTORS RESPONSIBLE FOR THE TRASMISSION OF INFECTION

1. CAUSATIVE OR ETIOLOGIC AGENT - mode of action of infectious agent

2. RESERVOIRS OF INFECTION- living bodies that harbor, sustain and maintain the growth and maintain the growth
and multiplication of infectious agent

TWO TYPES OF RESERVOIRS:

A.HUMAN RESERVOIR - main reservoirs of infection;
 Infected persons from whom the infectious agent if transmitted to other person.
 FRANK OR TYPICAL – persons who are obviously ill and manifest typical signs and symptoms
 SUBCLINICAL – infected persons where the disease is so mild that signs and symptoms are
inapparent; referred to as missed or abortive, ambulatory / walking cases.
 CARRIERS – infected persons who do not manifest any recognizable signs and symptoms (strictly
speaking no disease but the most dangerous)
 CONTACT – close association
 SUSPECT – medical history reveals that he has the disease
B. ANIMAL RESERVOIR

3. MODE OF TRANSMISSIONS:
A. BY CONTACT TRANSMISSION
 direct contact ( person to person )
 indirect contact ( usually thru an inanimate object )
 droplet contact ( from coughing, sneezing or talking )
B. BY VEHICLE ROUTE ( thru contaminated items )
 food – salmonellosis ( poisoning )
 water – shigellosis
 drugs – bacteremia resulting from infusion of a contaminated product
 blood – hepatitis B
C. AIRBORNE TRANSMISSION
 droplet nuclei – residue of evaporated droplets that remain suspended in the air
 dust particle containing the infectious agent
 organism shed into skin thru environment
D. VECTOR BORNE TRANSMISSION -via contaminated or infected arthropods such as flies, ticks and
others.
E. VERTICAL TRANSMISSION – from the mother to the neonate (AIDS,HEPA B and C, malaria,syphilis)

4. MODE OF ENTRY/PORTAL OF EXIT

 RESPIRATORY TRACT – most common
 GI TRACT – easiest way thru indirect contamination
 GENITOURNARY
 DIRECT INFECTION OF SKIN / MUCUS MEMBRANE
 PERCUTANEOUS INFECTION – infections, bites and stings

5. SUSCEPTIBLE HOST – humans or animals that don’t have resistance to infection.

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FACTORS AFFECTING ENTRANCE OF INFECTION TO THE BODY:

1. Age, sex, genetic constitution
2. Nutritional status, fitness, environmental factors
3. Absent or abnormal immumoglobulins
 IMMUNOGLOBULIN (lg) – related proteins that act as antibodies
4. General physical, mental and emotional health
5. Status of hematopoitic system, efficacy of reticuloendothelial system
 EFFICACY OF RETICULOENDOTHELIAL SYSTEM (RES) – concerned with defense against microbial
infections
6. Presence of underlying disease (DM, leukemia)
7. Patients treated with radiation, chemotherapy, corticosteroids or other immunosuppressive agents

II. PATTERNS OF OCCURRENCE AND DISTRIBUTION

1. SPORADIC – intermittent occurrence of a few isolated and unrelated cases in a given locality
- disease occasionally present here and there.
 High immune and low susceptibility ( e.g rabies )
2. ENDEMIC – continuous occurrence thru out a period of time of the usual number of cases in a given locality
 Low immune and low susceptibility ( e.g. malaria, schistosomiasis )
3. EPIDEMIC – occurrence of an unusually large number of cases in a relatively short period of time
 Low immune and high susceptibility (e.g AIDS )
4. PANDEMIC – simultaneous occurrence of epidemics of the same disease in several countries
- Worldwide epidemic
 Low immune and high susceptibility ( e.g. AIDS )

* HERD IMMUNITY – state of immunity of the community

III. PRINCIPLES PHILOSOPHY OF IMMUNIZATION

IMMUNIZATION - the prevention of communicable diseases thru the utilization of specific immunizing agents, by
the use of which the body protects itself against infections and diseases
RESISTANCE / IMMUNITY – the boy’s ability to withstand infection, but it does not absolutely mean that one who
possesses it is free from disease

TYPES OF IMMUNITY
1. NATURAL IMMUNITY – inborn protection.
a. RACIAL – inherent to a certain race (e.g blocks against yellow fever)
b. HEREDITARY – thru genes
c. CONGENITAL – resistance of the body in the uterus thru placenta (e.g. measles)
d. INDIVIDUAL – to distinct person (e.g body built)

2. ACQUIRED IMMUNITY - after birth.

a. ACTIVE – antibodies are manufactured by the tissues of the body
b. PASSIVE – antibodies are already formed and introduced into the body

* TYPES OF ACTIVE IMMUNITY

a. NATURAL ACTIVE ACQUIRED – initiated by the production of the antibodies following a clinical attack
infection.
b. ARTIFICIAL ACTIVE ACQUIRED – acquired by the production of the antibodies which is artificial
(e.g vaccination)

*TYPES OF PASSIVE IMMUNITY

a. NATURAL PASSIVE ACQUIRED – antibodies produced by a natural process (e.g breastfeeding,
colostrums, maternal antibodies )
b. ARTIFICIAL PASSIVE ACQUIRED – man develops antibodies (e.g. serum, Ig)

IV. STAGES OF ILLNESS

1. INCUBATION PERIOD – the time interval between the first exposure to the appearance of the first signs and
symptoms
2. PRODROMAL PERIOD – the premonitory sign, indicates the impeding attack.
3. PERIOD OF ILLNESS – manifesting typical signs and symptoms
4. PERIOD OF CONVALESCENCE – on the road recovery

 RESPONSIBILITY TO THE COMMUNICABLE DISEASE PATIENTS

1. Give nursing care
2. Prevent others from contracting the disease
3. Prevent oneself from contracting disease
4. Prevent cross infection
5. Disseminate information to others
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V. GENERAL CARE OF PATIENTS WITH COMMUNICABLE DISEASE

1. PREVENT THE SPREAD OF THE COMMUNICABLE DISEASE

a. Health education
b. Immunization
c. Environmental sanitation
d. Supervision in the preparation of food

2. CONTROL MEASURES
a. ISOLATION - the separation of persons suffering from communicable disease or carriers of the infecting
organism from other persons and placing them under such condition that direct transmission to susceptible
person is prevented based on the: period of communicability ( time wherein the body is still discharging the
microorganism)

 ENTERIC ISOLATION
 Purpose: To prevent the spread of the disease that can be transmitted thru direct contact with
infected feces.
 RESPIRATORY ISOLATION
 Purpose: To prevents omission of organism by means of droplets that are coughed, sneezed and
breath into the environment
 STRICT ISOLATION
 WOUND AND SKIN PRECATIONS
 Purpose: To prevent cross infection of personnel and patients from infection transmissible by direct
contact with wounds and other conditions resulting to skin secretion and heavily contaminated
particles.
 REVERSE ISOLATION
 Purpose: To protect the patients from acquiring other disease because of lowered resistance

b. QUARANTINE – limitation of movement based on longest incubation period; client has NO signs of infection.
c. DISINFECTION – destruction of the pathogen
 concurrent – done in the presence of an infection.
 terminal – done after the patient is discharge from the hospital.
o Medical asepsis
o Gowning – protects the inner part
o Mask - filter the microorganism
o Medical Handwashing – simplest and the most effective
o Placarding – placing reminder in patient room

DISEASES OF AND ACQUIRED THRU THE RESPIRATORY TRACT

A. DISEASE CAUSED BY BACTERIA

1. PULMONARY TUBERCULOSIS ( PHTISIS, CONSUMPTION ) wasting away of the body,

KOCH’S DISEASE – Robert Koch identified the microorganism.
CAUSATIVE AGENT: Mycobacterium tuberculosis
MODE OF TRANSMISSION: droplet infection
INCUBATION PEROID: 2-10 weeks
CLINICAL MANIFESTATIONS:

I. PRIMARY INFECTION – vague symptom

- first infection with tubercle bacilli
- most cases; (+) tuberculin test / PPD
INFECTION WITHOUT SIGNS AND SYMPTOMS
 change in behavior ( restlessness and irritability )
 easy fatigability
 crepitation and rales
II. POST PRIMARY TUBERCULOSIS
 visibly ill due to fever
 distressing cough
 distressing breath sounds
III. CHRONIC PTB
a. Generalized signs and symptoms:
1. general malaise, anorexia , easy fatigability, apathy, irritability, indigestion
2. tachycardia, dyspnea, cyanosis
3. fever – late in the afternoon
4. night sweats – acute exudates involvement ( advanced cases )
5. loses weight
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6. malaise
7. hemoptysis
DIAGNOSTIC TEST:
1. Sputum acid – fast bacilli staining
- best diagnostic test.

RESULTS OF SPUTUM MICROSCOPY

O - negative for bacilli
+ - 1 – 4 bacilli
++ - 5 – 10 bacilli
+++ - 10 – 20 bacilli
++++ - more than 20 bacilli
2. Chest x-ray
3. Mantoux test – most common tuberculin testing
- intradermal injury of purified protein derivative (PPD), results read after 48-72 hours ;
- induration of 10 mm or more is POSITIVE.
4. Stemeedle – multiple – puncture of six needles
- using PPD
(+) - induration of 4 or more points to be read after 3 – 7 days

TREATMENT ( NEW COURSE )

DRUGS:
R– rifampicin 450 mg
I – isoniazid 300 mg
P – pyrazinamide 500 mg
E – ethambutol 400 mg
S – streptomycin 1g

Category Cases Intensive Phase Maintenance

Phase
I - sputum positive new RIPE ( 2 months) RI (4 months)
patient
- PTB with extensive lung
damage (-AFB)
- Extrapulmonary TB
II - TB relapses and failures RIPES ( 2 months) RIE ( 5 months)
RIPE ( 1 month)
III - TB with sputum negative RIP (2 months) RI (2 months)
but + x-ray
- Extrapulmonary TB (not
serious)

NURSING CARE
1. CBR
2. ADEQUATE NUTRITION
3. AMBULATORY CHEMOTHERAPY
4. NPO – HEMOPTYSIS
5. OXYGEN INHALATION
6. BLOOD TRANSFUSION
7. COAGULANTS - Vit. K AND HEMOSTAN

2. BACTERIAL MENINGITIS (SPOTTED FEVER CEREBROSPINAL FEVER, EPIDEMIC, CEREBROSPINAL FEVER,

MENIGOCOCCAL MENINGITIS )
CAUSATIVE AGENT: Neisseria meningitidis ( other strains: Haemophilus influenza – common in young children,
Streptococcus pneumonia – common in adults, Straphylococcus aureus )
PERIOD COMMUNICABILITY
- until meningococci are no longer present in the mouth and nasal discharges.
INCUBATION PERIOD : 3 – 6 days
MODE OF TRANSMISSION : respiratory droplets
CLINICAL MANIFESTATION:
1. NUCHAL RIGIDITY - pathognomonic sign; meningal irritation
2. NECK, SHOULDER AND BACK STIFFNESS
- due to spasm of extensor muscles
3. OPISTHOTONUS – postural abnormality characterized by hyperextension of the back and neck muscles and
retraction of the head and arching forward of the trunk
4. POSITIVE NEUROLOGIC EXAM
+ KERNIG’S SIGN - if thigh is flexed on the abdomen, patient cannot extended his legs
+ BRUDZINSKI’S SIGN – when the neck is flexed on the chest flexion of knees and hips is produced
- when passive flexion of one side of the lower extremity is made, similar movement will be seen on the
opposite extremity
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DIAGNOSTIC EXAM :
1. LUMBAR PUNCTURE – to decrease ICP and introduced meds
- to obtain specimen
2. POSITIVE NEUROLOGIC EXAM
NURSING CARE:
1. Isolate the patient – quiet and darkened room
2. Prevent stress provoking factors
3. Prevent injury during episodes of convulsions
4. Maintain fluid and electrolyte balance
5. Provide balanced diet, low fat
6. Maintain personal hygiene and cleanliness

3. DIPHTHERIA – characterized by formation of pseudomembranre commonly in the faucial area and tonsils by the
exotoxin produced by Corynebacterium diphtheriae (KLEBS-LOEFFLER BACILLUS)
- common in children 6 months to 5 years ( rare below 6 mos. due to immunity passed from the mother )
MODE OF TRANSMISSION:
1. Direct contact of mouth secretions
2. Indirect thru toys an clothing that are contaminated
INCUBATION PERIOD: 2 to 6 days
PATHOGNOMONIC SIGN : Pseudomembrane
PERIOD OF COMMUNICABILITY
1. 1 to 2 days in treated patients
2. 2 to 4 weeks in treated patients
THREE TYPES ( with signs and symptoms )
1. NASAL – pseudomembrane in nose, excoriation of upper lips with serosanguinous secretions
2. PHARYNGREAL – sore throat, bull’s neck appearance ( swelling of neck ), difficulty in swallowing loss of weight
and anorexia
3. LARYNGEAL – hoarseness may be cough, laryngeal obstruction and respiratory arrest
- pseudomembrane may be coughed out by the 6 th to 10th day which could cause death secondary to airway
obstruction

TREATMENT:
1. SERUM THERAPY ( DIPHTHERIA ANTITOXIN )***
GOAL : neutralization of the toxin
- skin testing is done to determine allergy
2. ANTIBIOTICS – destruction of microorganism
e.g penicillin or erythromycin
3. ISOLATION OF THE PATIENT – until 2 to 3 cultures from both nose and throat with 24 hours interval have (- )
results
4. TRACHEOSTOMY – laryngeal obstruction
NURSING INTERVENTION:
1. CBR – prevent complications
2. ORAL HYGIENE
3. MAINTAIN FLUIDS AN D ELECTROLYTES
4. ADEQUATE NUTRITION
5. ICE COLAR – relieve pain
PREVENTION AND CONTROL:
1. ACTIVE IMMUNIZATION – DPT VACCINE
2. COVERING OF MOUNTH WHEN COUGHHING/SNEEZING
3. PROPER DISPOSAL SECRETIONS
COMPLICATIONS:
1. TOXIC MYOCARDITIS – action of the toxin in he heart muscle (usually during the 10 th to 14th day )
2. NEURITIS – absorption of toxin in the nerve
DIAGNOSTIC TEST:
1. SCHICK’S TEST – determine susceptibility or immunity
- ID injection of diluted Diphtheria toxin and read 48 to 72 hours after
- reveals local circumscribed area of redness usually 4 to 3 cm in diameter
2. NOSE AND THROAT SWAB
3. MALONEY’S TEST – determine hypersensitivity to Diphtheria toxoid
- ID injection of 0.1 cc of fluid toxoid
- Reveals erythema ( abnormal flushing ) within 24 hours of injection

4. PERTUSSIS ( WHOOPING COUGH )

- characterized by repeated attacks or spasmodic coughing which consist of a series of explosive expiration,
typically ending in a long drawn force inspiration which produces the characterized crowing sound the “whoop” &
usually followed by vomiting.
- Caused by Bordetella pertussis (Whooping Cough Syndrome – caused by B. parapertussis, B .bronchiseptics,
Adenoviruses )
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MODE OF TRANSMISSION:
- direct contact from droplet spread from infected child during incubation period and catarrhal stage
PERIOD OF COMMUNICABILIY: days after exposure to 3 weeks after of typical paroxysms
INCUBATION PERIOD : 7 to 14 days ( dis. is only about 6 weeks )
CLINICAL MANIFESTATION :
A. CATARRHAL STAGE ( last about 1 to 2 weeks )
- nasopharyngeal secretions
- wheezing and cough
- low grade fever
- stage of hypercommunicability
B. PAROXYSMAL STAGE
- beginning at the end of 2nd week and last for 4 to 6 weeks
- spasmodic cough – whoop which is provoked by eating, crying and exertion
- subconjunctival hemorrhage – rupture of capillaries
- abdominal hernia
- convulsions – due to anoxia and intracerebral hemorrhage
- during the attack, the child is cyanotic, eye bulging or popping out, tongue protrudes, lacrimation, choking spells
and may be with epistaxis
C. CONVALESCENT STAGE
- end of 4th week or 6th week
- attack begins to diminish unless there is 2ndary respiratory tract infection
DIAGNOSTIC TEST :
COUGH PLATE – culture from nasopharyngeal secretions

TREATMENT:
1. CONTROL COUGH – sedatives or narcotic-derived expectorants
2. ANTIBIOTICS – erythromycin or penicillin.
NURSING CARE :
1. CBR
2. Increase fluid intake – not during attacks
3. Abdominal binders – to prevent abdominal hernia
4. No large nipples – to prevent aspiration
5. No feeding during attacks
6. Isolation during communicability stage
7. Avoid excitement
8. Do not bring to outdoors
PREVENTION:
1. DPT vaccine – may give cross immunity
2. Avoid prolonged skin to skin contact

B. VIRAL INFECTIONS
MEASLES ( RUBEOLA ,7 DAY MEASLES, MORBILLI, & RED MEASLES )
- Contagious exanthematous disease of acute onset
- Caused by measles virus ( paramyxovirus – filterable virus )
MODE OF TRANSMISSION :
- droplet infection OR AIRBORNE.
- indirect thru contaminated articles with respiratory secretions
INCUBATION PERIOD: 10 to 22 days
PERIOD OF COMMUNICABILITY : 5h day of incubation period until the day of the rash

THREE STAGES
A. PRE-ERUPTIVE STAGE (highly communicable)
- fever
- catarrhal symptoms – inflammation of the mucous membrane
- respiratory symptoms – common cough and colds
- enanthem sign – eruption in the mucous membrane
o KOPLIK’S SPOTS – pathognomonic sign, small whitish pinpoint spots in inner cheeks due to
epithelial necrosis
- STIMSON’S LINE – puffiness of eyelids with reddish line on conjunctiva
B. ERUPTIVE STAGE - following appearance of KOPLIK SPOTS all signs during the first stage will disappear
- exanthem – eruption on the skin; maculopapular rashes (red in color )
o starts from hairline behind the ears, face , neck, upper and lower extremities (concentrates on the
face and trunk) on the day
- anorexia and irritability
- pruritus
- lethargy
C. POST-ERUPTIVE STAGE – fine desquamation of skin and rashes in the name manner as they appear (observe
for branny desquamation)
DIAGNOSTIC TEST:
1. NOSE AND THROAT SWABBING
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2. URINALYSIS
3. BLOOD CHEMISTRY – increased lymphocytes
4. COMPLEMENT-FIXATION or HEMAGGLUTINATION TEST (confirmatory test )
TREATMENT: NO THERAPY FOR UNCOMPLICATED MEASLES (SELF-LIMITING)
PREVENTION: IMMUNIZATION WITH MEASLES VACCINE
NURSING INTERVENTIONS:
1. SYMPTOMATIC AND SUPPORTIVE
a. Eye-care – wash face and avoid direct sunlight
b. Oral hygiene
c. Skin-care – no strong soaps and alcohol
d. Anti-pyretics for fever
e. Hypoallergenic diet
f. Vitamin A as ordered – to protect the epithelial lining of the resp. tract, GIT and eyes.
2. VASELINE – applied to edges of eyelids to prevent them from sticking together.
3. PENICILIN FOR SECONDARY INFECTIONS

GERMAN MEASLES ( 3 DAY MEASLES , RUBELLA )

- caused by rubella virus and characterized exanthem and fever with minimal complications but has teratogenic
effect on offspring during pregnancy
MODE OF TRANSMISSION : airborne droplet nuclei or close contact
INCUBATION PERIOD: 10 to 21 days
PERION OF COMMUNICABILITY: entire course of illness
CLINICAL MANIFESTATIONS:
1. FEVER AND MALAISE
2. LYMPHADENOPATHY –enlargement of lymph nodes
a. postauricular lymph nodes
b. post cervical lypmh nodes
c. suboccipital hymph nodes
3. PINKISH MACULOPAPULAR RASH - begins on the first day, starting on the face rapidly to trunk and limbs and
fades on the third day leaving no pigmentation nor desquamation
4. FORSCHEIMER’S SPOT – small red lesions on soft palate and mucous membrane
5. SPLEENOMEGALY
6. TESTICULAR PAIN ON YOUNG ADULTS
CONGENITAL DEFECTS TO FETUS:
- bilateral congenital cataract
- congenital heart disease
- microcephaly with MR
DIAGNOSTIC TEST:
- HEMAGGLUTINATION-INHIBITION TEST (HI)
- antibody test most useful technique for diagnosis
- COMPLEMENT – FIXATION TEST (CF)
- ELISA ( Enzyme Linked Immunosorbent Assay ) – determine amount of substance using antibody reaction
TREATMENT/ NURSING CARE : PURELY SYMPTOMATIC (SELF-LIMITING)
PREVENTION:
- LIVE ATTENUATED : RUBELLA VACCINES – from 1 week to puberty (MMR – 15 th month of age)
- GAMMA GLOBULIN – may be given to a pregnant client exposed to rubella.

CHICKEN POX ( VARICELLA )

- Highly contagious disease caused by herpes virus characterized by vascular eruptions on the skin and mucous
membrane.
MODE OF TRANSMISSION: direct thru droplet infection or airborn; indirect thru linen and fomites.
INCUBATION PERIOD : 10 to 21 days
CLINICAL MANIFESTATIONS:
1. Mild fever and malaise
2. Rash – start from the truck and spread to other parts, progression completed in 6 to 8 hours
a. macule – lesion that is flat
b. papule – an elevated lesion
c. vesicle – filled with clear fluid
d. crust – a scab lesions caused by secretions of a vesicle drying on the skin
e. pustule – vesicle affected and filled with pus
3. PRURITUS – accompanying annoying symptom
DIAGNOSTIC TEST:
1. DETERMINATION OF VARRICELLA-ZOSTER ANTIBODY by:
a. COMPLEMENT –FIXATION TEST
b. FLOURESCENT AND MEMBRANE ANTIGEN
TREATMENT : SYMPTOMATIC (SELF-LIMITING)
NURSING INTERVENTIONS:
1. Isolation until crust have fallen off
2. Calamine lotion over rashes
3. Antipyretics – for fever.
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4. Handwashing and cutting of fingernails

HERPES ZOSTER ( SHINGLES , ZOSTER, ACUTE POSTERIOR GANGLIONITIS )

- an acute viral infection of the nerve structure caused by variety of Varicella-Zoster virus (Chicken Pox )

MODE OF TRANSMISSION: direct thru droplet infection / indirect thru infected articles
PERIOD OF COMMUNICABILITY: until the last crust falls off
INCUBATION PERIOD : 1 to 2 weeks

CLINICAL MANIFESTATIONS:
1. vesicular rashes that appear in clusters, painful, and unilateral.
2. Vesicles formation – last for 1 to 2 weeks
3. Fever and regional lymphadenopathy
4. GASSERIAN GANGLIONITIS ( IRIDOCYCLITIS & CORNEAL ANESTHESIA)
5. RAMSAY HUNT SYNDROME – paralysis of the auditory canal secondary to infection of seventh cranial nerve
DIAGNOSTIC EXAM
1. Viral culture of the vesicles
2. Smear of the vesicular fluid
TREATMENT : ACYCLOVIR (drug of choice)
NURSING ACTIONS:
1. Compress of NSS or Potassium permanganate on lesions
2. Symptomatic treatment with antipyretics & analgesics
3. Proper disposal of secretion - reduce possibility of recurrence

MUMPS ( EPIDEMIC PAROTITIS )

- acute viral infection of the salivary glands particularly the parotids caused by paramyxovirus group.
MODE TRANSMISSION: person to person, thru droplet infection
PERIOD OF COMMUNICABILITY: 7 days before and 9 days after parotid glands swell
 Confers lifelong immunity, transplacental immunity is 6 months.
CLINICAL MANIFESTATION:
1. Slight malaise with low grade fever
2. Headache
3. Pain below the ear when moving the jaws
4. Parotid glands (70%) are swollen , painful, enlarge and tender
5. Pain on chewing and swallowing – earliest symptom
6. Constitutional manifestation may last about days while glands remain swollen for 5 to 19 days
NURSING INTERVENTIONS:
1. Isolation precaution
2. Support to comfort and corticosteroids to relieve pain in orchitis
3. Bed rest
4. Cold application
5. Soft bland diet
INCUBATION PERIOD: 14 to 28 days
DIAGNOSTIC TEST:
1. Blood exam – high leukocyte count
2. Viral culture – from mouth swabs, saliva
3. Viral serology – COMPLEMENT –F IXATION
TREATMENT : SYMPTOMATIC (SELF-LIMITING)

 ORCHITIS – may occur even without swelling of the parotids

- may produce sterility, a dreaded complication on males

NURSING CARE OF PATIENS WITH DISEASE OF AND ACQUIRED THROUGH THE G.I.T.

DISEASE CAUSED BY BACTERIA

TYPHOID FEVER ( ENTERIC FEVER, TYPHUS ABDOMINALIS )

- general infection caused by Salmonella typhi involving primarily the lymphoid tissue ( PEYER’S PATCHES ) of the
small intestine.

MODE OF TRANSMISSION: ingestion of contaminated food and water

PERIOD OF COMMUNICABILITY: as long as bacteria is excreted
INCUBATION PERIOD: 10 days 20 days
STAGES:
A. PRODROMAL STAGE: fever , abdominal pain, constipation / diarrhea
B. FASTIGIAL STAGE – 3 CARDINAL SYMPTOMS
1. Intermittent ladder like fever
2. ROSE SPOTS (pathognomonic) - macules that disappears after applying pressure on abdomen and chest.
3. Splenomegaly
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DIAGNOSTIC TEST:
1. WIDAL TEST – blood serum agglutination test; best done during 8 th day (2nd stage)
3 ANTIGENS USED
- (+) antigen O – active typhoid stage
- (+) antigen H – previously infected or vaccinated individual
- (+) antigen VI – common in carries
2. TYPHIDOT EXAM – may be done on the 2nd week of illness.
3. BLOOD CULTURE – best done on the 1st week or 1st stage; will confirm typhoid fever.
4. URINE CULTURE - done during the 1st 2 weeks.
5. STOOL CULTURE - best done during the 3rd stage.
TREATMENT:
1. CHLORAMPHENICOL – drug of choice.
PREVENTION:
1. Immunization with CDT ( cholera, dysentery , typhoid )
2. Proper disposal of feces
3. Hand washing
4. Proper preparation, storage and cooking foods
NURSING INTERVENTIONS:
1. Supportive care – fluid and electrolytes
2. Monitor intake and output
3. Increase fluid intake
4. High caloric, low residue and non-irritating foods
5. Watch for complications:
a. Perforation of the intestines
S/Sx: sudden sharp abdominal pain rigidity and shock
b. Typhoid Psychosis Stage – organism goes to the brain
S/Sx: Coma vigil look – blank stare dilated pupils
CARPHOLOGIA – involuntary picking of lines
SULTUS TENDINUM- involuntary twitching of the tendons of the wrist

CHOLERA (EL TOR)

- characterized by vomiting and massive watery diarrhea with rapid dehydration and shock.
- can occur in epidemics and caused by :
 Vibrio coma - OGAWA, INABA, HIROJIMA
 Vibrio cholerae – CLASSIC, EL TOR
 Spirillum cholerae, Spirillum cholerae asiatica
MODE OF TRANSMISSION: fecal-oral thru contaminated food and water
PERIOD OF COMMUNICABILITY: not known but presumed till (+) stool culture
CLINICAL MANIFESTATIONS:
A. MILD CASES – undetectable
B. SEVERE CASES – starts with colicky pain in abdomen and mild diarrhea (ENTERALGIA)
1. Stool is yellow at first
2. Marked mental depression
3. Headache
4. Continuous vomiting – dehydration
5. Thirst is terrible
6. Violent cramps of lower extremity
7. Patient may collapse
8. Temperature of 104 deg F
9. RICE WATERY STOOL & WASHER WOMANS HANDS (pathognomonic signs )
PREVENTION:
1. Immunization with CDT
2. Control of lies breeding places
3. Water sterilization
4. Proper disposal waste
INCUBATION PERIOD: 1 to 3 days and vary from few hours to 5 days
DIAGNOSTIC EXAM: Culture of stool and vomitus
NURSING ACTIONS:
1. Isolation
2. Personal hygiene
3. Intake and output monitoring
4. Proper disposal of feces
5. Precaution of five F’s ( food, flies. Feces, fingers, & fomites )
TREATMENT:
1. FLUID REPLACEMENT - IV
2. oral rehydration – ORESOL
3. antibiotics – PENICILLIN OR TETRACYCLINES
4. correction of electrolyte imbalance like hypokalemia and metabolic acidosis.
 10

BACILLARY DYSENTERY ( SHIGELLOSIS, BLOODY FLUX ) - acute bacterial disease of the intestinal tract that
includes a group of enteric infection caused by stairs of bacillus dysentery.
4 MAJOR SEROLOGIC GROUPS:
1. Shigella dysenteria – most infections
2. Shigella flexner – common in the Phil.
3. Shigella boydei
4. Shigella sonnei
MODE OF TRANSMISSION: ingestion of contaminated food and water
INCUBATION PERIOD: 3 to 4 days (vary from 7 hours to 7 days)
PERIOD OF COMMUNICABILITY: 1 to 2weeks
CLINICAL MANIFESTATION:
1. Fever – initial symptom
2. Vomiting and headache
3. Colicky or cramping abdominal pain and tenderness with anorexia, malaise and weakness
4. Bowel movements – numerous accompanied with abdominal cramps and tenesmus
NURSING INTERVENTION:
1. Maintain fluid and electrolyte balance
2. Assess weight loss, skin turgor, mucous membrane urinary volume
3. Weigh daily
4. Offer liquids
5. Restrict food till nausea and vomiting subsides
6. Supervision on food storage, cooking and preparation
7. Medical handwashing

TREATMENT:
 Fluid replacement
 Cotrimoxazole
 Correction of electrolyte imbalance and metabolic acidosis.
PREVENTION:
1. Fly control program
2. Surveillance of water sanitation
3. Handwashing after defecation
4. Detection and treatment of carries

B. DISEASES CAUSED BY VIRUSES

POLIOMYELITIS ( INFANTILE PARALYSIS, ACUTE ANTERIOR POLIOMYELITIS )

- affects mostly the anterior horn cells of the spinal cord and medulla, cerebellum and mid-brain
CAUSATIVE AGENT: caused by polio virus (LEGIO DEBILITANTS)
Serologic Types (No cross-immunity)
1. Type I – BRUNHILDE, most frequent cause of paralysis, both occurring in epidemic
2. Type II – LANSING, next most frequent
3. Type III – LEON , least common
PERIOD COMMUNICABILITY: most contagious a few days before and after onset of symptoms when the virus is found
in oropharynx for about a week and in feces for 3 months
3 TYPES OF PARALYSIS:
1. SPINAL PARALITIC POLIOMYELITIS: involvement of the anterior horn cells
2. BULBAR PARALYTIC POLIOMYELITS: involvement of cranial nerves
 9th cranial nerve ( gloss swallowing reflex)
 10th cranial nerve ( vagus ) – cardiac and respiratory reflex
3. BULBOSPINAL PARALYTIC POLIOMYELITIS: involvement of brain and spinal cord
CLINICAL MANIFESTATION ( 3 STAGES ): host reacts to any stage and recover
1. INTESTINAL/INVASSIVE PHASE
a. signs, and symptoms of URTI: fever, malaise, headache and sore throat
b. signs and symptoms of GIT disturbance : anorexia, vomiting and abdominal pain
 If patient does not progress to stage 2, polio is an abortive type
2. VIREMIC PHASE (virus in the blood )
a. fever , headache , vomiting an irritability
3. NEURAL PHASE – CNS involvement
a. (+) POKER SPINE – meningeal irritation
b. Any motion that produce anterior flexion of spine cause stiffening of the neck and spine
HYPERSENSITIVITY – touch very irritating
PARALYSIS and FLACCID PARALYSIS
 (+) HAYNE’S SIGN - head falls back when in supine and shoulders elevated
- inability to raise legs to full 90 degrees
 (+) KERNIG’S AND BRUDZINKI’S SIGNS
DIAGNOSTIC EXAM:
1. PANDY’S TEST – isolation of the virus
2. LUMBAR PUNCTURE – CSF exam shows elevated protein level.
3. MUSCLE TESTING – to determine extent of muscle paralysis
 11
TREATMENT : NO SPECIFIC TREATMENT
NURSING INTERVENTIONS:
1. Bed rest – provide firm non sagging bed
2. Analgesics – relieve head and back pains & muscle spasms
3. Hot moist pack – relieve muscle spasms
PREVENTION:
1. POLIO VACCINE IMMUNIZATION
a. SALK – solution of killed viruses
b. SABIN – attenuated viruses
- given oral for 3 doses (2gtts )

DISEASE CAUSED BY PARASITES

AMOEBIASES (AMOEBIC DYSENTERY)

- infection caused by Entamoeba histolytica involving colon but may affect soft tissues or organ

CLINICAL VARIATION
1. ACUTE AMOEBIC DYSENTERY
- stools contained blood and mucus which may give rise to amoebic hepatitis or liver abscess
2. CHRONIC AMOEBIC DYSENTERY
- with recurrent attack of diarrhea or relatively mild dysentery
3. AMOEBIC COLITIS – characterized by episodes of abdominal discomforts
- frequently stimulating appendicitis
4. CARRIERS – with stools containing the organism but remains free from symptoms
CLINICAL MANIFESTATION:
1. Symptomatic for carries
2. Attacks of diarrhea alternating , blood streaked and mucoid
3. Eructations
4. Fever
5. Anoxia, weight loss and weakness
NURSING ACTION:
1. Isolation of patient
2. Health teaching:
- Sterilizations of water
- Cover left-over foods
- Hand washing
3. Increases fluid intake
DIAGNOSTIC EXAM:
1. Stool exam
2. Serologic test – indirect hemagglutination
TREATMENT: Metronidazole, Chloroquine , Diloxanide furoate

COMPLICATIONS
1. Liver abscess - ANCHOVY SAUCE-appearance of the abscess (thick reddish brown fluid similar to a chocolate)
2. Lung abscess
3. Brain abscess

HELMINTH INFECTIONS – worm infection

A. TRICHINOSIS - caused by nematode (Trichinella spirilia) – round worms taken thru ingestion of uncooked pork
products secondary to feeding of uncooked garbage
B. ANCYLOSTOMIASIS (HOOKWORM DISEASE ): thru contaminated soil by human feces containing hook worm ova
caused by :
 Ancylostomna doudenale – common in Asia Necator americanus – common in America
C. ASCARIASIS – caused by Ascaris lumbricoides which is large round worm. Fertilaized eggs contaminates food and
water.
D. ENTEROBIASIS (PINWORM, THREAWORM or SEATWORM ) – caused by Enterobius vernicularis thru and oral
transmission of eggs or indirect transmission from contaminated clothing, beddings or food characterized by
nocturnal anal itchiness
E. TAENIASIS – caused by: Taenia saginata – beef tapeworm / Taenia solium – pork tapeworm
F. TRICHURIASIS ( WHIPWORM ) caused by: Trichuris trichura from soil and food contaminated with feces.
G. PARAGONOMIASIS (PULMONARY DISTOMIASIS) - caused by Paragonimus westennani (lung fluke) from ingestion
of raw or insufficiently cooked crab or crayfish containing larvae.
MODE OF TRANSMISSION:
1. indirect contact – ingestion of contaminated food or water
2. direct contact but unusual ( orogenital, or anal sexual activity )
INCUBATION PERIOD: 3 to 4 weeks ( days for severe infection while several months for sub acute or chronic forms
PERIOD OF COMMUNICABILITY: entire duration of illness
CLINICAL MANIFESTATION:
1. Voracious appetite – greedy in eating
2. Pot belly – protruding abdomen
 12
3. Malnourished with Anemia
DIAGNOSTIC EXAM:
- Stool exam
NURSING CARE:
1. Symptomatic
2. Focused on hygiene of the patient
TREATMENT:
1. Anti-Helminthes – Combantrin or Antiox
PREVENTION:
1. Proper preparation of food
2. Proper disposal of waste
3. Precaution of the five P’s

NURSING CARE OF PATIENTS WITH DISEASE OF AND ACQUIRED THROUGH SKIN

A. DISEASE CAUSED BY TRAUMA AND INOCULATION

TETANUS ( LOCKJAW ) - infectious disease caused by an anaerobic bacteria(cannot leave in the presence of
oxygen) which produces a potent exotoxin
2 FORMS:
1. VEGETATIVE - destroyed by heat, chemical
2. SPORE-BEARING
MODE OF TRANSMISSION – direct and indirect contamination of wound, umbilical stump in newborn
INCUBATION PEROD: 3 days to 3 weeks with average of 10 days
PERIOD OF COMMUNICABILITY: not transmitted persons to person directly
CLINICAL MANIFESTATIONS:
1. LOCKJAW or TRISMUS – painful spasm of the masticatory muscles because Trigeminal nerves are affected
2. RISUS SARDONICUS / SARDONIC SMILE- due to spasm of the facial nerves are affected
3. OPISTHOTONUS – arching of the back
4. MUSCULAR SPASM – general rigidity
 TONIC – continuous contraction of muscles
 CLONIC – alternate contraction an relaxation of muscles
5. BOARDLIKE ABDOMEN
6. PHOTOPHOBIA – eyes partially close
7. LARYNGEAL / PHARYGEAL SPASM
8. IRRITABILITY AND RESTLESSNESS
9. CONVULSIONS
PREVENTION:
1. Consider every break in the skin as potential of entry: wash wounds thoroughly
2. Active immunization – DPT immunization, tetanus toxoid for women
3. Passive immunization – ATS or TIG
TOXINS PRODUCED:
1. TETANOSPASMIN – responsible for muscular spasm
2. TETANOLYSIN – lysis of the RBC
SOURCES OF INFECTION:
1. Animal or human feces
2. Soil and dust containing spores
3. Unsterile instruments
DIAGNOSTIC EXAMS:
1. History of punctured wound
2. Clinical manifestations
3. CSF is normal
4. Blood exam – normal or slightly elevated WBC ct.
TREATMENT ( 3 OBJECTIVES )
1. NEUTRALIZE THE TOXIN
a. Anti- tetanus serum (ATS)
b. Tetanus immune globulin (TIG)
c. Tetanus antitoxin (TAT) or tetanus horse serum antitoxin
d. Skin testing is imperative, if positive, desensitize the person by giving the serum in fractional doses
2. DESTRUCTION OF MICROORGANISMS: penicillin, tetracyclines, erythromycins
3. PREVENTION AND CONTROL OF SPASMS – Diazepam
NURSING CARE:
1. Proved quiet semi dark environment
2. Minimal handling
3. Prepare tongue depressions
4. Maintain an adequate airway
5. Closely guard the patient
6. Support during spasm and convulsions
7. No restraints
8. Adequate fluid and electrolytes
9. High calorie liquid to soft diet
 13
RABIES (LYSSA, HYDROPHOBIA ) - severe viral infection of the CNS that is communicated to human in the saliva of
infected animals or human caused by rabies virus (RHABDOVIRUS) – filterable virus and inactivated by
sunlight
2 TYPES OF RABIES VIRUS:
a. STREET VIRUS - natural virus invading / transmitted in the saliva
b. FIXED VIRUS – do not usually invade the salivary glands with constant incubation period of 4 to 6 days
INCUBATION PERIOD:
a. In dogs and cats - 1 week to 7 ½ month
b. In man - 4 to 8 weeks
MODE OF TRANSMISSION: contamination of a bite/scratch or other break in the skin from saliva
 RABIED ANIMAL
a. DUMB STAGE – quiet, stays n corner with copious salivation
b. FURIOUS STAGE – easily agitated, hydrophobic
CLINICAL MANIFESTATION: Presence of NEGRI BODIES in brain tissues (round or oval bodies found in the cytoplasm
of neurons in animal with rabies)
PERIOD OF COMMUNICABILITY: in dogs and cats, from 3 to 5 days before the onset of symptoms until the entire
course of illness
 RABIED MAN
c. MENTAL DEPRESSIONS STAGE – copious salivation quiet and depress
d. EXCIMENT PHASE – restless, irritable, hydrophobic and aerophobic
3 STAGES:
A. PRODROMAL OR INVASSION STAGE
1. Characterized by fever, anorexia, malaise, sore throat, copious salivation, lacrimation, perspirations, irritability,
hyperexcitability, apprehension, restlessness, drowsiness, mental depressions , insomia and melancholia
2. Pain in the region of the original infection, headache and nausea
3. Sensitivity to light, sound and changes in temperature
4. MYALGIA – general body pain
5. Numbness, tingling burning or cold sensation in are of the bite, dilation of pupils, husky voice, mild difficulty in
swallowing
B. STAGE OF EXCITEMENT – stimulated by noise and touch
1. Characterized by marked excitation, apprehension and even terror
2. Delirium assoc. with nuchal stiffness and depression
3. Maniacal behavior, alternating listlessness and depression
4. Sensitive to light, noise and faint odors, eyes fixed and glossy, cold clammy skin
5. Characteristic symptom manifest – violent, severe painful spasms of the muscles of the mouth, pharynx and
larynx when attempting to swallow food or water and even the sight of it known as Hydrophobia
6. Aerophobia – fear of air
7. Drooling of saliva – in order to avoid painful spasm associated with swallowing
8. Fever of 3 to 4 days with tonic-clonic contraction of muscles
9. Death may during episodes of spasm or due to cardiac / respiratory failure
10. Patient deteriorates rapidly and progresses to terminal stage within 1 to 3 days
C. TERMINAL OR PARALYTICS STAGE:
1. Quiet an unconscious, loss of bowel and bladder control
2. Tachycardia, labored irregular respiration and steadily rising temperature
3. Spasms cease and progressive increasing paralysis sets in
4. Respiratory distress or paralysis, circulatory collapse or heart failure, coma ensues and death to respiratory
paralysis
5. Patient dies within 24 o 72 hours upon manifestation of signs and symptoms of rabies

DIAGNOSTIC EXAM:
1. History of exposure – bites
2. Development of characteristic symptoms
3. Microscopic exams – presence of NEGRI BODIES in brain tissue and saliva
4. FLOURESCENT RABIES ANTIBODY (FRA) TECHIQUE – highly preferred diagnostic exam wherein the fluorescent
rabies antibody is allowed to react with its specific antigens in culture or smear and the result is in precipitate
form - positive
TREATMENT: SYMPTOMATIC (RABIES IS PREVENTABLE BUT NOT CURABLE )
NURSING CARE : symptomatic and supportive
1. Treatment of wound with soap and water or zephiran betadine
2. Isolate patient – provide restful, quiet and semi dark environment
3. Cover IVF with paper bag – no sight of water
4. Provide comfort
PREVENTION AND CONTROL:
A. ACTIVE IMMUNIZATION
1. DUCK EMBRYO VACCINE (DEV) OR PURIFIED DUCK EMBRYO CONCENTRATED VACCINE - prepared
from cell culture, virus is killed and leaving only vital protein, injected intramuscularly at deltoid or
subcutaneously for 14 days
2. HUMAN DIPLOID CELL VACCINE (HDCV) - more effective than DEV and used in USA where human
exposed to rabies survive
3. ANTI-RABIES VACCINE (ARV) – simple type (used by DOH), needs skin testing given 2 cc subcutaneous
daily for 14 day in the abdominal wall.
 14
B. PASSIVE IMMUNIZATION – not indicated before exposure.
1. RABUMAN – 20 IU single dose/kg of body weight – IM for human
2. HYPER RAB – 20 IU single dose
3. IMOGRAM – same with above but only half the dose, used to infiltrate into the wound (antiserum globulin
prepared from the horse)

MALARIA ( MARSH FEVER, , PERIODIC FEVER, KING OF TROPICAL DISEASE )

- an acute or chromic disease caused by protozoa plasmodia transmitted to man by the bite of infected female anopheles
mosquito ( Anopheles minimus flavirostris ) which is a night biting and breeds in flowing clear and shaded stream
FOUR SPECIES
1. Plasmodium vivax – causes vivax or benign tertian malaria ( 2 days interval of fever )
2. Plasmodium falciparum – most frequently encountered in the Phil., causes malignant tertian malaria or known as
PERNICIOUS MALARIA and is the most serious type
3. Plasmodium ovale – less frequent
MODE OF TRANSMISSION:
1. Person to person thru bites of an infected mosquito
2. Parenterally – blood transfusion or contaminated syringes and needles
3. Mingling of infected maternal blood with that of the infant during delivery
4. Transplacental ( congenital malaria ) – very rare
INCUBATION PERIOD (varies depending on greater or lesser resistance of individual )
1. P. vivax – 17 days or up to several years
2. P. falciparum – 10 to 12 days after mosquito injects sporozoites
3. P. malariae – 10 to 14 days or up to several years
4. P. ovale – 11 to 26 days
PERIOD OF COMMUNICABILITY
1. P. vivax – 3 to 5 days
2. P. falciparum – 7 to 14 days maximum of 1 year
3. P. malariae – 7 to 14 days, maximun of 30 years
4. P. ovale – 3 to 5 days
CLINICAL MANIFESTATION
A. PRODROMAL PHASE
 P. falciparum – headache, anorexia, nausea, fatigue, vague abdominal pains, muscle aches, anemia,
nosebleeding, highly colored urine, orthostatic hypotension, hepatomegaly an spleenomegaly
 P. vivax – headache, photophobia, muscle aches, anorexia, nausea and vomiting
 P. ovale and P. malariae – not significant

COMPLICATIONS:
1. BLACK WATER FEVER- a serious complication of P. falciparum in which there is massive destruction of RBC
leading to blood pigment in the urine ( mahogany colored )
DIAGNOSTIC EXAM:
1. BLOOD SMEAR OF MALARIA PARASITE (BSMP ) – confirms presence of specie and density
- blood taken at the height of the fever, if negative, repeated after 12 hour of the attack
2. SPLEENIC BIOPSY
3. HISTORY OF TRAVEL TO ENDEMIC AREAS
4. QUARANTINE BUFFY COAT
TREATMENT GOALS:
1. Destroy promptly all asexual forms of the parasite in order to care chemical attack
2. Destroy gametocytes so that mosquito is prevented
SPECIFIC THERAPY:
1. 4 AMINOQUINOLINES (Choloroquine, Aminodiaquine and Quimine ) – used to treat all forms
2. PRIMAQUINE – can achieve 2nd goal of treatment
3. PYRIMETHAMINE-SULFADOXINE (FANSIDAR) – safest during pregnancy.

NURSING INTERVENTIONS:
1. Isolation
2. Supportive care
PREVENTION:
1. Eliminate breeding places of mosquitoes
2. Advise travelers of high risk areas
3. Screening of windows

DENGUE FEVER (H. FEVER or HEMORRHAGIC FEVER, ACUTE INFECTIONS THROMBOCYTOPENIC PURPURA
BREAK BONE or DANDY FEVER, DENGUE SHOCK SYNDROME )
- acute tropical disease characterized by severe pain in the eye and in the joints and bones an accompanied by an initial
erythema caused by dengue virus and transmitted by mosquito Aedes aegypti
BREAK BONE/DANDY FEVER – patient experiences pain in the joint and bones and walks on tip toes
MODE OF TRANSMISSION: bite of an infected Aedes aegypti mosquito which is day biting with limited flying movement
INCUBATION PERIOD: 4 to 6 days
HEMORRHAGIC FEVER – is a result of:
 Increase capillary fragility – strong immune complex reaction that produce toxic substance like histamine,
bradykinin, which damage capillary wall
 15
 Thrombocytopenia – due to faulty maturation of megakaryocytes which results in diminished production of
platelets
 Decreased blood coagulation factor – due to acute excessive consumption of platelets due to generalized
intravascular clotting
CLINICAL MANIFESTATION:
1. Sudden onset of hyperpyrexia and headache, patient is flushed and acutely ill
2. Anorexia, nausea and vomiting severe abdominal pain and tenderness
3. Hepatomegaly – 50 to 60 % of cases
CLASSIFICATION OF DENGUE FEVER ACCORDING TO SEVERITY
1. GRADE I – fever, abdominal pain, headache, muscle and joint pains – prognosis good
2. GRADE II - Grade I symptoms plus spontaneous bleeding – prognosis is good
3. GRADE III – Grade II symptoms plus circulatory failure, cold clammy skin, weak pulse and hypotension –
prognosis is guarded
4. GRADE IV – Grade III symptoms plus shock due to blood loss, death – prognosis is critical
DIAGNOSTIC EXAM:
1. POSITIVE TOURNIQUET TEST ( RUMPEL LEED TEST ) – increase capillary fragility.
2. HEMATOLOGIC EXAM – decrease Platelet determination count (150,000 to 400,000/cu.mm )
3. HEMAGGLUTINATION-INHIBITION TEST – most frequently used
TREATMENT : SYMPTOMATIC (SELF-LIMITING)
NURSING CARE:
1. Epistaxis – ice compress on bridge of nose, let patient bite something
2. Gum bleeding – ice chips, bristle toothbrush
3. GI bleeding – observe signs of bleeding, place o NPO. Avoid highly seasoned food
4. DO NOT GIVE ASPIRIN – causes platelet degeneration and may cause further bleeding.

PREVENTION:
1. Avoid densely populated areas
2. Destroy mosquito breeding places

LEPTOSPIROSIS (WEIL’S DISEASE, MUDFEVER,SWINEHERD’S DISEASE,CANICOLAFEVER)

- infection carried by animal both domesticated and wild whose excreta is contaminated or food which is ingested or
inoculated thru skin or mucus membrane
CAUSATIVE AGENT: Leptospira pyrogenes L. macilae (commonly found ) L. canicola

PERIOD COMMUNICABILITY: none but leptospira are found in the patients urine between 10 to 20 days after onset
INCUBATION PERIOD: 6 to 15 days
3 STAGES OF CLINICAL MANIFESTATION (ranges from asymptomatic to fatal )
1. SEPTICEMIC STAGE – fever lasting 4 to 7 days which is abrupt and remittent with chills, headache, anorexia,
nausea and vomiting
2. IMMUNE or TOXIC STAGE – with or without jaundice lasting for 4 to 30 days, if severe , death may occur on the
9th to 16th day
 ANICTERIC TYPE – presence of leptospira – leptospires in the urine
 ICTERIC TYPE – known as WEIL’S SYNDROME (hepatorenal failure)
3. CONVALSCENCE – replaces may occur during the 4th to 5th week
 Renal and Hepatic failure– causes of death
DIAGNOSTIC EXAM:
1. CULTURES
a. BLOOD – during the first week
b. CSF – 5th to 12th day
c. URINE – after the 1st week to convalescence
2. AGGLUTINATION TEST
A. LEPTOSPIRA AGGLUTINATION TEST (LAT )
B. LEPTOSPIRA ANTIGEN-ANTIBODY TEST (LAAT)
C. MICROCAPSULE AGGLUTINATION TEST (MCAT)
TREATMENT:
1. PENICILIN G – drug of choice.
2. TETRACYCLINES
NURSING CARE : isolation and monitor I and O religiously.
PREVENTION : environmental sanitation

SCHISTOSOMIASIS ( BLOOD FLUKE, SNAIL FEVER, BILHARZIASIS )

CAUSATIVE AGENT: caused by 3 species of blood fluke

A. Schistosomiasis haematobimm– common in the Near East; Iran, Iraq and Portugal ad causes BILHARZIASIS or
URINARY SCHISTOSOMIASIS
B. Schistosorna mansoni– found in south part of Africa, South America and causes HEPATO-INTESTINAL
SCHISTOSOMIASIS
C. Schistosoma japonicum– endemic in the Philippines and causes KATAYAMA DISEASE or HEPATO-INTESTAL
SCHISTOSOMIASIS
 Oncomelania Quadrasi – snail vector
 16
MODE OF TRANSMISSION – direct penetration of cercaria to the skin ( 3 to 5 minutes )
INCUBATION PERIOD – at least 2 months
LIFE CYCLE OF SCHISTOSOMA JAPONNICUM
Adult male and female in copulation in portal vessels – eggs into the intestimal lumen – eggs pass out with
female hatch upon contact with water and liberate the miracidia ( 1 st stage larvae released into water with urine
and feces ) – penetrate snail host – sporocyst ( 2 nd stage larvae ) develops within the snail ( 4 to 8 weeks ) –
cercaria ( final stage larva ) escape into water ( 1 to 3 days ) – penetrate skin of host ( 3 to 5 minutes ) –
schistosoma carried in circulation – adult in 29 days and start laying eggs
CLINICAL MANIFESTATION:
1. INCUBATION PERIOD - dermatitis on cercarial area; minute lesions with fleeting needle pain (SWIMMER’S
ITCH ) cough , hepatomegaly with portal cirrhosis
2. PERIOD OF EGG DEPOSITION AND EXTRUSION – toxic diarrhea with fresh blood and mucoid stool, patient
becomes ill and bedridden
3. PERIOD OF TISSUE REPAIR AND PROLIFETATION – jaundice, ascites, urine insufficiently , bleeding and
terminal hematuria
DIAGNOSTIC EXAM
a. DIRECT FECAL SMEAR (KATO-KATZ)
b. CIRCUMOVAL PRECIPITIN TEST / CERCARIAL ENVELOPE REACTIONS
 recommended in view of difficulty in demonstrating eggs in feces

TREATMENT : R.A # 4359 – created National Schistosomiasis Control Commission on June 19, 1956
1. TARTAR EMITIC (ANTIMONY POTASSIUM TARTRATE ) – toxic and initiating salt administered by slow IV
injection.
2. STIBOPHEN (FUADIN)
3. PRAZIQUANTEL – drug of choice (TID PO WITH MEALS FOR ONE DAY ONLY)
4. NIRIDAZOLE
NURSING CARE : symptomatic
PREVENTION:
1. Proper disposal of human feces
2. Molluscides spraying
3. Creating foot bridges
4. Wearing of protective clothing / boots
5. agro-engineering measures – irrigation system

LEPROSY – ( HANSEN’S DISEASE, LEPRA, HANSENOSIS, LEONTIASIS )

- chronic mildly communicable disease with insidious outset affecting the skin, mucus membranes and
nervous tissue and eventually producing deformities and caused by Mycobacterium leprae (Hansen’s
bacillus )
MODE OF TRANSMISSION: prolonged skin to skin contact, fomites and droplet infection
INCUBATION PERIOD : 1 to 5 years or more (variable )
PERIOD OF COMMUNICABILITY : as long as there are open lesions

CLASSIFICATION OF LEPROSY
1. TUBERCULOID (TT) – a single anesthetic macules or plaques, borders well defined, peripheral nerve
involvement common
2. BORDERLINE TUBERCULOID (BT) – lesions similar to TT but more numerous, borders of lesions less distinct,
satellite lesions present around larger lesions, peripheral nerve involvement common
3. BORDERLINE (BB) – more lesions than BT, borders more vague, satellite lesions often seen, peripheral
involvement
4. BORDERLINE LEPROMATOUS (BL) – lesions are numerous and similar to BB, some nerve damage
5. LEPROMATOUS (LL) – multiple non-anesthetic, macular or popular, symmetrically distributed lesions, no neural
lesions until late, complications of madarosis, leonine face
6. INDETERMINATE (I) – vaguely defined hypopigmented or erythematous macule ( like chronic dermatitis )
OTHER SIGNS : madarosis – falling of eyebrow
Anhidrosis – absence of sweat
Atrophy of the skin
DIAGNOSTIC EXAM:
1. Mean- from mucocutaneous lesions
2. Lepromin Skin Test – has cross sensitivity to tuberculosis infection and BCG vaccination
 chemical is prepared from lumps/lesions
2. Mitsuda Reaction – more useful for the determination of the type of disease and prognosis
TREATMENT : R.A # 4073 – liberates the treatment of leprosy from segregation in sanitaria to home treatment

National Leprosy Program – puts all legible case leprosy cases of leprosy under the multiple drug therapy
A. Paucibacillary Regimen – few bacilli at any site
Duration : 6 months
Drugs: rifampicin 500 mg. Daily for 6 to 8 months ( not prolonged due to its toxic effect ) dapsone 10
mg / kg / day
Type: indeterminate tuberculoid and tuberculoid
B. Multibacillary Regimen
Duration : 24 months
 17
Drugs : rifampicin 600 mg. Daily dapsone 10 mg / kg / day
Lamprene 1 mg/ kg / day ( not recommended for patients below 18 years of age )
Type : borderline lepromatous,
NURSING INTERVENTION:
1. Isolation
2. Maintain balance nutrition, sleep and rest
3. Help the family to understand and accept to remove social stigma
4. Good personal hygience
5. Handling of infants and young ones should be avoided

NURSING CARE OF PATIENTS WITH DISEASE OF AND ACQUIRED THROUGH THE GUT

GONORRHEA ( GC, CLAP, DRIP, STRAIN)

CAUSATIVE AGENT: Neisseriae gonnorheae
MODE OF TRANSMISSION : sexual contact , direct contact with contaminated vaginal secretion during delivery
CLINICAL MANIFESTATIONS:
A. males – burning sensation thick yellowish
B. female – MOSTLY ASYMPTOMATIC; burning sensation upon urination, discharges may or may not be person
COMPLICATIONS:
Pelvic Inflammatory Disease (PID)
- signs and symptoms of PID: fever, pelvic pain, nausea and vomiting abdominal pain
Ophthalmia neonatorum ( newborn )
- signs and symptoms: profuse purulent conjunctival exudates, corneal lacrimation loss of sight
DIAGNOSTIC EXAM : Culture of penile or cervical secretions.
TREATMENT: CEFTRIAXONE + DOXYCYCLINE 9drug of choice)
NURSING CARE : symptomatic and supportive, isolation of patient until recovery from illness
PREVENTION: ABSTINENCE / Faithful partner / CONDOM/ Crede’s prophylaxis

SYPHILIS ( LUES, FRENCH POX , BAD BLOOD )

CAUSIVE AGENT : Treponema pallidum
STAGES OF SYPHILIS
A. PRIMARY STAGE - formation of lesions (chancre)
CHANCRE – elevated red and smooth surface with indurated edges and PAINLESS.
MALE – prepuce or glans penis / FEMALE – labia majors and minora
* symptoms disappear without treatment

B. SECONDARY STAGE – appearance of CONDYLOMATA LATA – lesions with ulcerations and spread all
over the body; also known as SYPHILIS DERMATOSIS.
 falling of public hair and eyebrows
 lesions will disappear without treatment and will proceed to LATENT SYPHILIS (no signs)

C. THIRD STAGE - delayed for years

- GUMMAS ( lesions ) begin to appear
- necrotic tissue destruction

D. FORTH STAGE – PARASYPHILIC STAGE

- Nervous System involvement (neurosyphilis)
S/S : optic atrophy – blindness
: deafness
: paralysis
: insanity

DIAGNOSTIC EXAM:
1. DARKFIELD EXAM - identifies T. pallidum from chancre fluid specimen
2. VDRL TITER
3. WASSERMANN TEST – detection of antibody formed by syphilic patient
4. SEROLOGIC TEST FOR SYPHILIS (STS ) – FTA-ABS

TREATMENT : BENZATHINE PENICILLIN

MODE OF TRANSMISSION : sexual contact / blood transfusion / vertical transmission

NURSING CARE : SYMPTOMATIC

PREVENTION : ABSTINENCE / AVOID SEXUAL CONTACT / USE OF LATEX CONDOM.
MANIFESTATIONS OF CONGENITAL SYPHILIS
- saddle nose, Hutchinson’s teeth (saw-like teeth with mouth and gum deformity ), deafness, intestinal keratitis
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ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS)
- is a chronic viral infection that involves the immune system and later causes different OPPORTUNISTIC infections in
the body;
- causes severe depletion of CD4 T cells in the blood;
- WORLDWIDE phenomenon!!! (pandemic)
- In 2000, 30-40 million people in the world are with HIV / AIDS.
- Discovered lasts 1981;
- FIRST Screening of BLOOD for HIV started last 1985;

- High-Risk Groups for HIV Transmission:

o Homosexual or bisexual men
o Intravenous (IV) drug users
o Transfusion and blood products recipients (before 1985)
o Heterosexual contacts of HIV-positive individuals
o Newborn babies of mothers who are HIV positive

- Causative Agent: Human Immunodeficiency Virus (HIV-1 and HIV-2)

 is a RETROVIRUS;
 the virus contains reverse transcriptase;

- IP: 1 - 3 months to detect the presence of antibodies in the blood;

 2 months – 20 years is the conversion from HIV to AIDS;

- Mode of Transmission:
o Repeated sexual contact – most common;
o Habitual needle accident
o IV drug users thru sharing of needles
o Transplacental or Perinatal transmission
o Blood transfusion – not so common today due to strict blood screening.
o Direct or indirect contact with mucus membranes
o Breast milk (?)

- Clinical Manifestations:
o Most of the time ASYMPTOMATIC;

o When it becomes symptomatic:

 Begins as a MONONUCLEOSIS-like manifestations (fever, anorexia, lymphadenopathy,
weight loss, etc)
 Unexplained weight loss (WASTING SYNDROME!!!)
 Dry and heavy persistent coughing (PCP)
 Oral candidiasis or Oral thrush;
 Diarrhea of >7 days duration;
 Jaundice

o Skin lesions (Kaposi’s sarcoma) – this is an unusual type of cancer;

 seen only among homosexual.

o Opportunistic Infections:
 Pneumocystic carinii pneumonia – most common in the world;
 PTB – most common in the Philippines; Pinoy tayo eh!!!
 Kaposi’s sarcoma – probably secondary to HPV infection;
 Cytomegalovirus retinitis – can cause BLINDNESS!!!
 Toxoplasma encephalitis
 Herpes simplex
 Herpes zoster
 Mycobacterium avium intracellulare (MAI)
 Candidiasis
 Scabies

- *HIV Infection – a client with (+) HIV test confirmed by Western blot.

- *AIDS – a client with HIV (+) plus signs of immunodeficiency and opportunistic infection. CD4 T cells less
than 200/ mm3.

- Diagnostic Examination:
o Enzyme-linked Immunosorbent Assay (ELISA) – for SCREENING!!!
o Western Blot – for CONFIRMATION po ito!!!
o Polymerase Chain Reaction (PCR) – to identify nucleic acid sequence;
o P24 – serologic test to identify circulating antigen;
o CBC with WBC count
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o Chest X-ray
o Urinalysis and fecalysis
o Blood/ urine/ sputum culture for bacteria and fungal infections
o Sputum GS and AFB
o Liver function test
o Renal function test – BUN / Crea

- Medical Management:
- Anti-Retroviral Therapy – to prolong life and prevent the development of opportunistic infections by
INHIBITING VIRAL REPLICATION and keep CD4 T cells more than 200.
- Combination of several anti-retroviral agents is given to fight resistance and to broaden to anti-viral coverage.
- 3 different types of Anti retroviral agents:
 Protease inhibitors:
o Amprenavir
o Ritonavir
o Indinavir
o Saquinavir
 Nucleoside reverse transcriptase inhibitors (NRTI)
o Zidovudine(AZT),
o Didanosine
o Zalcitabine
o Lamivudin
 Non-nucleoside reverse transcriptase (NNRTI)
o Efavirenze
o Nevirapine
o Delavirdine

o Other potential therapies:

 Immunomodulary agents – designed to boost the weakened immune system.
 Anti infective and anti neoplastic agents – to combat opportunistic infection and associated
cancers. (Some are used prophylactically to help prevent opportunistic infections)
 HIV VACCINE .

- Nursing Interventions:
o Abstinence!!! It is the safest way to prevent AIDS. Monogamous relationship or faitfulness.
o practice SAFE SEX (ex. Use of Latex condoms!!!)
o Patient and public awareness is very important.
o Observe and practice STANDARD precaution to all patients. As in to ALL PATIENTS!!!
o In a client with AIDS, reverse isolation should be practiced.

CHLAMYDIASIS
 also known as non-gonococcal urethritis;
 “the most common type of STI;”
 Causes inclusion conjunctivitis and lympho-granuloma-venereum (LGV);

 CAUSATIVE AGENT: Chlamydia trachomatis

 IP: 2 – 3 weeks;
 Mode of Transmission:
o Sexual contact
o Indirect contact with vaginal and urethral secretions;

 Clinical Manifestations:
In MALES:
- urethral discharge;
- burning and itching on urethral orifice;
- burning sensation on urination;
In FEMALES:
- slight vaginal discharge
- dyspareunia
- vaginal itching
- abdominal pelvic pain

 Diagnostic Exams:
 Urinalysis
 Gram stain and Culture of penile and cervical discharges.

 Treatment:
 DOXYCYCLINE – drug of choice.
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AIM HIGH NURSES! GOD BLESS

This is just an outline for Communicable Disease Nursing. Supplemental reading is highly suggested. 