Communicable Diseases

COMMUNICABLE DISEASES
NEUROLOGICAL SYSTEM
TETANUS ALSO KNOWN AS LOCK JAW
Description: An acute infection associated with painful muscular spasm
Etiology:
Caused by Clostridium tetani which are found on soils and human feces
Mode of transmission:
Contamination of wound
Incubation period:
5 – 10 days
Pathophysiology:
The organism enters the wound and under low oxidation reduction potential the or
ganism reproduces and secretes tetanolysin which causes RBC and WBC lysis. Tetan
ospamin which attaches to and destroy inhibitory neurons which leads to painful
muscle spasm.
Signs and symptoms
Fever, lock jaw, the most important sign is trismus and risus sardonicus. While
laryngospasm is the most life threatening condition.
Diagnostic procedure
None. History of wound and possible contamination are usually enough to arouse s
uspicion and take necessary management.
Management
Wash wound, apply wound antiseptic.
Assess for history of immunization
Give tetanus toxoid for negative history of immunization
Administer Antitoxin after negative skin test
Penicillin is the drug of choice
Prepare for intubation.
NGT feeding may become necessary. Avoid over stimulation to prevent painful musc
le contraction.
Diazepam is the drug of choice for muscle spasm
MENINGITIS
Description:
An acute inflammation of the meninges
Etiology:
Caused by Nesseria meningitides this is usually a normal inhabitant of the nasop
harynx.
Droplet infection
Incubation period:
2 – 10 days
Pathophysiology:
The organism enters the bloodstream after invading the respiratory tissues. Reac
hes the spinal cord and of course the meninges. It stimulates chemotaxis that le
ads to leukocyte infiltration of the meninges. As a result inflammation follows.
This builds up pressure, pus and compresses sensitive nervous tissues, that may
decrease the level of consciousness and in more severe cases pus could impede b
lood flow and brain infarct my ensue.
Signs and symptoms

The most significant finding indicating meningeal irritation: brudzinski and ker
nigs sign. Other sign observable are headache, opisthotonus, fever and petechiae
Lumbar puncture (CSF analysis)
Management
Institute droplet precaution
Rifampicin or Ciprofloxacin for prophylaxis
Ampicillin is the drug of choice
Ceftriaxone for systemic and CNS infection given in combination with Ampicillin
to combat resistant organism.
Mass prophylaxis is not needed provided that all children in day care centers wh
o have been exposed are exempted hence they need prophylaxis, this also includes
all other children who are close to the infected patient such as when they shar
e eating utensils.
Nurses and Doctors are not at risk of having the disease except when close conta
ct occurred like in mouth to mouth resuscitation.
ENCEPHALITIS
Description:
Inflammation of the tissues of the Brain
Etiology:
Mosquito borne – Japanese enceph, West Nile enceph etc
Viral borne – Complication of chicken pox or measles
Amebic – Acanthamoeba hystolytica
Mosquito borne – bite of the infected mosquito
Viral – may be droplet or airborne
Amebic – accidental entry in the naso - pharynx due to swimming in infested waters
.
Incubation period:
Mosquito borne – varied
Viral – 5 – 15 days
Amebic – 3 – 7 days
Pathophysiology:
The infectious organism regardless of the type penetrate the brain and causes in
flammation of the brain tissues itself. The inflammatory response compresses the
brain structure which explains the rapid deterioration of the LOC. Encephalitis
is more severe than meningitis.
Signs and symptoms
Marked decrease in LOC. Brudzinski and kernigs may also be present if meningeal
irritation result. The most significant though is the appearance of decorticate
and decerebate rigidity.
Lumbar Tap (CSF analysis) EEG
Management
Primarily supportive. The body can neutralize the organism thru the presence of
antibody.
Amebic encephalitis may benefit from metronidazole.
Anti inflammatory may be given
Mannitol could decrease ICP
POLIOMYELITIS
Description:
An acute paralytic infection that destroys the affected nerves.
Etiology:
Caused by polio virus 1 (Brunhilde), 2 (Lansing), 3 (Leon)
Fecal – oral route. Particularly rampant among those in the squatters area who hav
e no access to sanitary toilet facilities
Incubation period:
7 – 14 days
Pathophysiology:
The virus enters the oral cavity and reproduces in the intestines which later pe
netrate the intestinal wall causing viremia and reaching the motor nerves and th
e spinal cord. The virus reproduces inside the nerve and as they are released, t
he infected cell die, hence paralysis results.
Signs and symptoms
Pokers sign, Haynes sign, tonsillitis, abdominal pain and flaccid paralysis
Stool exam, pandys test, EMG
Management
Prevention OPV
No anti viral therapy. Toilet hygiene must be reinforced
Watch out for respiratory paralysis
Assist in rehabilitation (physical therapy and comfort measures
RABIES
Description:
Another acute viral infection which have a zoonotic origin
Etiology:
Primarily carried by mammals specially land and aerial mammals. In the Philippin
es Dogs and Cats are among the most important reservoir. The causative organism
is Rhabdo Virus
Bite of infected animal. Scratch wound from cats can also cause infection since
cats usually lick their paws.
Incubation period:
10 days for man 14 days for animals
Pathophysiology:
The virus replicates at site of infection which later proceeds to infect the nea
rby axons and then reaches the nerve itself. From that point onwards the virus t
ravels along the nerve pathway to reach the brain. In the brain the virus incite
s inflammatory reaction that gives rise to the appearance of encephalitis like s
ymptoms later the organism descends from the brain and exit to affect other nerv
es in the body. The affectation of trigeminal nerve causes throat spasms which g
ives rise to its classic finding “hydrophobia”
Signs and symptoms
Hydrophobia, aerophobia, laryngeal, Pharyngeal spasm excessive salivation.
Fluorescent antibody Staining, Negri bodies found in brain biopsy of the infecte
d animal
Management
Human Diploid Cell Vaccine, Rabies Immunoglobulin, Rabies Anti serum. tetanus an
ti serum is also given if with negative or inadequate immunization history
Wash wound with soap and water, may apply wound antiseptic
Once sign and symptoms are present passive immunization is already useless. Supp
ortive therapy comes next.
Protect from glare and sunlight, protect from water and air current. Cover IV bo
ttle and tubing with carbon paper or any other else that can effectively hide th
e iv fluids. Secure consent and restrain the patient. Observed contact and drop
let precaution.
LEPROSY
Description:
A chronic infection that usually affects the peripheral nerves and leads to pare
sthesias
Etiology:
A possible zoonotic infection which is rarely cultured in laboratory but seen to
be growing freely among armadillo. Causative organism is Mycobacterium leprae
Droplet infection is the most important transmission. Skin contact may cause inf
ection only if there is an open lesion with prolonged contact.
Incubation period:
6 months to 8 years
Pathophysiology:
The organism enters the body via droplet infection. It is ingested by macrophage
s but can’t be killed, as this circulating macrophage
reaches the skin the bacteria penetrate the nerves. Later due to immune recognit
ion WBC attacks the infected cell which results to the destruction of the affect
ed cell hence the appearance of paresthesias and consumption of the involved ext
remity becomes apparent due to immune response it self.
Signs and symptoms
Painless wound, paresthesias, ulcer that does not heal, leonine appearance, made
rosis. Nerve involvement with acid fast bacilli is the pathognomic sign of lepro
sy
Scraped incision method.
Management
Institute concurrent disinfection specially of nasal discharge.
Prevention is achieved by BCG immunization
Rifampin, Dapsone and lampreme are effective treatment against this infection
CIRCULATORY SYSTEM
DENGUE HEMORRHAGIC SHOCK SYNDROME
Description:
An acute arthropod borne infection which causes massive bleeding.
Etiology:
Causative organism is Dengue virus 1, 2, 3 and 4 the primary vector is Aedes egy
pti other wise known as tiger mosquito because of the black stripes present at t
he dorsal legs of the insect. The mosquito prefers to thrive on clean stagnant w
ater.
Bite of the infected vector mosquito
Incubation period:
6 – 7 days
Pathophysiology:
The virus is carried by the infected mosquito and transferred through bites in t
he victim. Once the proboscis pierced the capillaries it also leaves the viral o
rganism. The virus mixes in the bloodstream survive and reproduce causing viremi
a which explains the appearance of generalized flushing. The virus will then suc
cessfully enters the bone marrow and arrest the maturation of megakaryocyte. Sin
ce the precursor of platelets can not take full course it will result to massive
drop in the patient’s platelet count which significantly raises the risk for hemo
rrhage.
Signs and symptoms
Petechiae, bleeding, epitaxis, Herman’s sign and fever
Tourniquet test, platelet count.
Management
Watch out for bleeding. Minimize injections and other parenteral procedures if p
ossible. Apply pressure for 10 minutes on injection site.
Avoid aspirin use acetaminophen provide TSB as an adjunct to anti pyretics.
Monitor platelet closely. Prepare for platelet concentrate or fresh whole blood
as the need may call for it.
Hydrate with PNSS
Preventive measure focuses on 4 o clock habit
Use DEET as an effective mosquito repellant
Use mosquito nets
MALARIA
Description:
Another type of mosquito borne infection most common in the tropics
Etiology:
The causative organisms are Plasmodium Vivax, Falciparum, Ovale, and Malariae. T
he primary vectors are anopheles mosquitoes.
Bite of the infected mosquito
Incubation period:
For Falciparum 12 days, for Vivax and Ovale 14 days and for Malariae 30 days
Pathophysiology:
From the bite of the infected mosquito the organism enters the body via bloodstr
eam and immediately proceed to the liver in the form of sporozoites. Inside the
hepatocytes reproduction continues until the host burst releasing the parasite i
n the form trophozoites that enters the RBC, inside it the organism divides and
form schizont. This will later produce merozoites that enters RBC the process ca
uses drop in the number of circulating RBC leading to anemia and cachexia.
Signs and symptoms
A cycle of hot stage (high fever) followed by diaphoretic stage (sweating) and t
hen cold stage (chilling). The cycle repeats leading to malarial cachexia
Malarial smear or peripheral blood smear
Management
Chloroquine is the drug of choice. Primaquine must be given to prevent relapse.
Prevent by using mosquito repellant and mosquito net
Chloroquine is the drug of choice for prophylaxis.
FILIRIASIS
Description:
A chronic lymphatic disorder that is related to elephantiasis
Etiology:
Causative organism is Wuchereria bancrofti primary vector Culex spp.
Bite of the infected mosquito
Incubation period:
6 – 12 months
Pathophysiology:
The organism enters the body after the vectors’ bite, it then matures and migrate
on the lymphatic vessels but it usually affects those in the lower extremity. Th
e protozoal parasite crowds and destroy the filtering ability of the lymph nodes
which then leads to the accumulation of lymph or body fluids causing edema and
at worst cases gross deformity hence it could lead to elephantiasis.
Signs and symptoms

Recurrent low grade fever, lymphangitis, nocturnal asthma and in worst cases ele
phantiasis
Microscopic examination of peripheral blood.
Management
Use of mosquito repellant and nets
Hetrazan is effective against Filiriasis adverse reaction though are seen in a n
umber of patients, if such may be present may use Ivermectin
RESPIRATORY SYSTEM
DIPHTHERIA
Description:
An acute infection of the upper respiratory system whose complication may includ
e the lower respiratory tract.
Etiology:
The organism, Corynebacterium diphtheriae is ubiquitous.
Droplet infection is the means of spread
Incubation period:
1 – 7 days
Pathophysiology:
The organism infects the oral cavity which later due to its ability of releasing
toxins causes the death of the involved tissues. This gives rise to the appeara
nce of psudomembarne which may be dislodge and block the airway. As toxins are s
ecreted the heart, kidney and the nerves absorb it, this toxins halt protein syn
thesis of the infected cell which later on causes its death.
Signs and symptoms
Pathognomonic Sign is pseudo membrane. Tonsillitis may also be present. Fever an
d malaise. If complication arises paralysis, endocarditis and kidney failure may
be seen.
Throat swab
Management
Gather specimen for culture
Prepare for epinephrine and possible intubation
Be ready for antitoxin therapy after checking for allergy
Administer penicillin or erythromycin
PERTUSIS
Description:
A widespread organism that threaten any one who have no immunity against it.
Etiology:
Causative organism is Bordetella pertussis
Droplet infection
Incubation period:
7 – 21 days
Pathophysiology:
The organism enters the upper respiratory tract attaches to the respiratory epit
helium and causes an increased production of cyclic amino phosphate that essenti
ally leads to hyperactivity of the mucous secreting cells. Thick tenacious secre
tions blocks the airway. The organism also halts the mucociliary escalator leavi
ng coughing reflex the last effective protective mechanism of expelling sputum.
Due to its relative tenaciousness the body experiences difficulty in coughing ou
t phlegm thus we observe patient to manifest violent cough.
Signs and symptoms
Pathognomonic of this infection is violent cough w/out intervening inhalation fo
llowed by an inspiratory whoop.
Vomiting may be present, Increased in ICP and IOP are also seen. Hernia is also
a high risk incident.
Throat swab
Management
Penicillin, Erythromycin ; Mucolytic may be ordered.
Nebulization may also be indicated; Provide small feedings
Apply abdominal binder ; Avoid dust and drafts
TUBERCULOSIS
Description:
A chronic lung infection that leads to consumption of alveolar tissues
Etiology:
Causative organism is acid fast bacillus mycobacterium tuberculosis.
Droplet infection as well as airborne
Incubation period:
2 – 4 weeks
Pathophysiology:
The bacilli is inhaled and taken in the alveoli where macrophage will ingest but
fail to kill the organism. As these macrophages migrate to nearby lymph nodes i
t will die and leave the capsulated bacteria undigested. Once the body’s immune sy
stem dropped, the bacteria will be activated and stimulate immune response which
likewise damage the alveolar tissues leading to casseation necrosis and could e
ventually consume the entire lungs if the process is repeated frequently
Signs and symptoms
Afternoon fever, night sweats, cough for 2 weeks, anorexia weight loss.
Sputum microscopy, CXR, Mantoux test
Management
Institute DOTS
Check for sensitivity to any of the drug mentioned
Provide B6 if receiving Izoniazid
Watch out for visual problem if receiving Ethambutol
Ethambutol is contraindicated for children who can’t verbalize visual problems yet
.
PNEUMONIA
Description:
an acute usually bacterial in nature
Etiology:
most common causative organism is strptococcus pneumoniae ubiquitous, orgainsm a
nd may be transferred among population that has poor ventilation and impaired re
spiratory cilliary function. certain disease like measles may promote the develo
pment of pneumonia
Droplet infection
Incubation period:
24 to 72 hrs usually 48 hrs
Pathophysiology:
the organism enters the respiratory tract and if the cilliary mechanism fails to
prevent its further entry the organism then infects the lower respiratory cente
rs where it stimulate an inflammatory reaction. this response leads to migration
of WBC in particular with neutrophil hence leukocyte infiltration is seen in ch
est x-rays as consolidation. the build up puss increases the alveolar presure ca
using in atelectasis once collapsed alveoli cant participate in gas exchange any
more leading to impaired DOB.
Signs and symptoms
Rusty colored sputum is the pathognomonic sign this is caused by WBC infiltrates
, RBC and sputum. DOB, increased RR, coughing and in late cases lethargy, cyanos
is and death.
sputum exam
Management
Co Trimoxazole and gentamycin are the drug of choice. although Co-tri is used mo
re widely than gentamycin because of its oral preparation which are allowed to b
e administered by midwives for patient in far flung areas.
instruct the mothers to continue the administration of antibiotic for 5 straight
days
TSB if in case fever may arise
Promote proper room ventilation
avoid crowding as much as possible
Use Pneumococcal vaccine as indicated
COLDS (CORYZA)
Description:
The causative agent comes from adenovirus and rhino virus.
Droplet infection, direct contact.
Incubation period:
1 – 3 days
Pathophysiology:
As the virus enters the respiratory tract, it attaches itself to the mucous memb
rane and causes local irritation and inflammation. In response, the mucous membr
ane releases mucous to flush out the virus. Since there is an increased in the p
roduction of the mucous it usually flows back and causes rhino rhea and because
of the naso-lacrymal duct, increased mucous production impedes the drainage of t
ears thus watery eyes is present.
Complications:
Children – otitis media and bronchopneumonia
Adult – sinusitis
Signs and symptoms
• General malaise
• Fever, chills
• Sneezing, dry and scratchy throat
• Teary eyes, headache
• Continues water discharge from nares
Management
a. Provide adequate rest and sleep
b. Increase fluid intake
c. Provide adequate and nutritious diet
d. Encourage vitamins specially vitamin C
INFLUENZA (LA GRIPPE OF FLU)
Description:
A highly contagious disease characterized by sudden onset of aches and pains.
Etiology:
Influenza virus A, B, C
Droplet infection, contact with nasopharyngeal secretions
Incubation period:
24 – 48 hrs.
Pathophysiology:
Upon entry in the upper respiratory tract, it is deposited in the same site and
penetrates the mucosal cells. Causing lysis and destruction of the ciliated epit
helium the virus releases neuramidase that decreases the viscosity of the mucosa
. Facilitating the spread of the infected exudates to the lower respiratory trac
t, this causes intestinal inflammation, and necrosis of the alveolar and bronchi
olar epithelium. Thus, the alveoli are filled with exudates containing WBC, RBC
and hyaline cartilage. This places the patient to increased possibility of acqui
ring bacterial pneumonia usually caused by S. Aureus.
Signs and symptoms
Respiratory – most common
• fever
• anorexia
• chills
• muscle pain and aches
• coryza
• sore throat
• bitter taste
• orbital pain
Intestinal
• vomiting
• severe abdominal pain
• fever
• obstinate constipation
• severe diarrhea
Nervous
• headache
Management
a. provide adequate rest and ventilation
b. tepid sponge bath to reduce the temperature
c. monitor the vital signs
d. provide adequate nutrition
e. assist the patient in conserving strength when she is very weak
f. drug of choice:
• antibiotics
• sulfonamides
INTEGUMENTARY SYSTEM
LEPROSY
(HANSEN’S DISEASE, HANSENOSIS, LEPRAE, LEONTHIASIS)
Description:
A chronic infectious disease characterized by the appearance of modules in the s
kin or mucous membranes or by changes in the nerves leading to anesthesia, paral
ysis or other changes
Etiology:
Mycobacterium leprae (acid fast bacillus), sporadic/endemic cases, occurs in tro
pical and semitropical countries throughout the world. It can be contracted in c
hildhood (manifested at age 15 and diagnosed by the age of 20 years).
Prognosis:
> the longer the time of active disease, severe lesions, the more rapidly they h
ave advanced without ability to produce the lepromin reaction – the poorer the pro
gnosis
> case under 21 years old – high relapse rate
Prolonged intimate skin to skin contact, nasal secretions
Incubation period:
Prolonged, undetermined and varies from one to many years
Pathophysiology:
The bacterium, which is an acid-fast bacillus, attacks the skin tissues and peri
pheral nerve, which causes skin lesions, anesthesia, infection and deformities
Signs and symptoms
Assessment:
1. Tuberculoid type – shows high resistance to Hansen’s bacilli. Clinical manif
estations are mainly in the skin and nerves and usually are used or non-infectio
us.
2. Lepromatous type – minimal resistance to the multiplication, existence of
the bacillus, constant presence of large numbers in the lesions and form globi (
characteristic manifestations in the skin and mucus membranes) and peripheral ne
rves.
3. Open or infectious cases
4. Indeterminate type – clinical manifestations are located chiefly in skin a
nd nerves; lesions are flat macules.
5. Borderline
Clinical Manifestations:
1. Early stage
• loss of sensation
• paralysis of extremities
• absence of sweating (anhydrosis)
• nasal obstruction
• loss of hair (eyebrows)
• eye redness
• change in the skin color
• ulcers that does not heal
• muscle weakness
2. Late symptoms
• contractures
• leonine appearance (due to nodular and thickened skin of the forehead and face)
• madarosis (falling of eyebrows)
• gynecomastia
• sinking of bridge of nose
3. Cardinal signs
• presence of Hansen’s bacilli
• presence of localized areas of anesthesia
• peripheral nerve enlargement
a. Lepromin reaction – a positive test develops a nodule at the site of inocu
lation (first and third week)
b. Wassermann reaction
Management
Planning and implementation
a. Prevention
• separate infants from lepromatous parents at birth
• segregate and treat open cases of leprosy
• require public health supervision and control of cases of Hansen’s disease
b. Medical management
1. Multiple drug therapy
• paucibacillary treatment – six months or until negative (-) results occur
• rifampicin – once a month
• dapsone - once a day
2. Multibacillary treatment – for 2 consecutive years or until negative (-) f
or leprosy test
• rifampicin once a month
• lamprene once a day
• dapsone once a day
c. full, wholesome generous diet
d. alcohol or TSB may be used for high fever
e. patient should have a daily cleansing bath and change of clothing
f. good oral hygiene
g. normal elimination should be maintained
h. meticulous skin care for ulcers
MEASLES
(RUBEOLA, MORBILLI, 7 – DAY MEASLES)
Description: An extremely contagious exanthematous disease of acute onset whi

ch most often affects children and the chief symptoms of which are referable to
the upper respiratory passages.
Etiology: The causative agent is the paramyxovirus
Mode of transmission: Nasal throat secretions, droplet infection, indirect con
tact with articles
Incubation period: 8 – 20 days
Pathophysiology:
As the virus enters the body it immediately multiplies in the respiratory epithe
lium. It disseminate by way of the lymphatic system causing hyperplasia of the i
nfected lymphoid tissue. As a result there is a primary viremia which infects th
e leukocyte and involves the whole reticuloendothelial system. As the infected c
ells die it necrose and release more viruses to infect other leukocytes leading
to secondary viremia, which also causes edema of upper respiratory tract produci
ng its symptoms and it may predispose to pneumonia.
Complications:
• otitis media
• bronchopnuemonia
• severe bronchitis
Prognosis:
• death rate is highest in the first two years of life (20%)
• after 4 years – uncommon
• over all mortality – less than
Signs and symptoms
Assessment:
a. Stages
1. incubation period (average of 10 days)
2. Pre-eruptive stage or stage of invasion (3-6 days)
• from the appearance of the first signs and symptoms to the earliest evidence of
the eruption.
• fever, severe cold
• frequent sneezing
• profuse nasal discharge
• eyes are red and swollen with mucopurulent discharge (lids stick together)
• Stimson’s sign (puffiness of lower eyelids with definite line of congestion on the
conjunctivae)
• redness of both eardrums
• vomiting, drowsiness
• hard, dry cough
• Koplik’s spot (appears on second day): small bright, red macules or papules with a
tiny or bluish-white specks on the center and can be found on the buccal cavity
• macupapular rashes (seen late in 4th day): appears first on the cheeks or at the
hairline
• true measles rash: slightly elevated sensation to touch, appears first on the fa
ce and spreads downward over neck, chest trunk, limbs and appearing last on the
wrist and back of the hand
3. Eruptive stage
• characterized by a general intensification of all local constitutional symptoms
of the pre-eruptive stage with the appearance of bronchitis and loose bowels
• irritability and restlessness
• red and swollen throat
• enlargement of cervical glands
• fever subsides
4. Desquamation stage
• follows after the rash fades
• follows the order of distribution seen in the formation of eruption
No specific diagnostic exam except only for the presence of leucopenia.
Management
a. prevention
• education of parents regarding the disease
• passive immunization of infants and children (gammaglobulin)
• active immunization (1st year of life)
b. management
• drugs
antibiotics
sulfodiazine
• isolation
• meticulous skin care – warm alcohol rub to prevent pressure sores
• good oral and nasal hygiene
• increase oral fluid intake
• proper care of the eyes – eye screen to avoid direct light; wear dark glasses
• ears should be cleaned after bath if there is discharges – patient should lie the
affected ear down or towards the bed
• give ample of fluids during febrile stage
GERMAN MEASLES (RUBELLA, ROTHEIN, ROSEOLA, 3-DAY MEASLES)
Description:
An acute infectious disease characterized by mild constitutional symptoms, rose
colored macular eruption which may resembles measles and enlargement and tendern
ess
Etiology:
Caused by myxovirus. Occurs mostly in spring and seen mostly in children over 5
years of age
Direct contact
Incubation period:
14 – 21 days
Period of communicability – 7 days before to 5 days after the rash appears
Pathophysiology:
As the virus gains entrance to the nasopharynx, it immediately invades the neare
st lymph gland causing lymphadenopathy. Later on, the virus enters the blood str
eam that stimulates the immune response, which is the cause of rashes found in t
he body of infected individual. If rashes has appeared it means that viremia has
subsided. Since the disease is generally mild and serious complication is very
unlikely, what should be watched out rather are its congenital effects because i
t can cross the placental barrier, which may kill the fetus or cause congenital
rubella syndrome.
Complications:
• otitis media
• encephalitis
• transient albuminuria
• arthritis
• congenital defects for babies who’s mother were exposed in early pregnancy
Prognosis: very favorable
Signs and symptoms
• fever, cough
• loss of appetite
• enlargement of lymph nodes
• sweating
• leucopenia
• vomiting (in some cases)
• headache, mild sore throat
• desquamation follows the rash
• enanthem of uvula with tiny red spots
• rash (cardinal symptom) accompanied with cervical adenitis: begins on the face i
ncluding the area around the mouth; oval, pale, rose-red papules about the size
of a pinhead; covers the body within 24 hours and gone by the end of the 4th day
Management
Planning and implementation
a. Prevention: vaccination
• gamma globulin – given to pregnant women with negative history and who have been e
xposed in the first trimester of pregnancy
• include in MMR given at 15months to the baby
b. management
• isolation – (catarrhal stage – to prevent infection to others)
• bed rest for first few days
• meticulous skin care especially after the rash fades
• good oral and nasal hygiene (use of petroleum jelly if lips become dry)
• no special diet is necessary, increase oral fluid intake
VARICELLA (CHICKEN POX)
Description:
A very contagious acute disease usually occurring in small children, characteriz
ed by the appearance of vesicles frequently preceded by papules, occasionally fo
llowed by postules but ending in crusting
Etiology:
Varicella zoster virus (airborne)
Droplet infection, direct contact
Incubation period:
2 -3 weeks
Pathophysiology:
The virus gain entrance via the upper respiratory tract it crosses the mucous me
mbrane and cause systemic infection followed by appearance of numerous macupapul
ar rash. The rash are fluid filled that contain polymorphonuclear leukocytes.
Period of communicability: highly contagious from 2 days prior to rash to 6 days
after rash erupt.
Full blown case imports permanent immunity.
Complications:
• pneumonia
• nephritis
• encephalitis
• impetigo
• pitting or scarring of the skin
Signs and symptoms
• slight fever: first to appear
• body malaise, muscle pain
• eruption (maculopapular) then progresses to vesicle (3-4 days); begins on trunk
and spreads to extremities and face (even on the scalp, throat and mucus membran
es)
• intense pruritus
• vesicles ended as a granular scab
• irritability
Management
1. Drugs
• penicillin – can be used when the crusts are severe or infected to prevent scarrin
g or secondary invasion
• alkalinizing agent to prevent nephritis and to stop vomiting
• acyclovir, immunosin – antiviral
• hydrocortisone lotion 1% for itching
2. isolation in a room by itself
3. provide a well ventilated, warm room to the patient
4. warm bath should be given daily to relieve itching; use a calamine lotio
n
5. avoid injuring the lesions by using soft absorbent towel and the patient
should be patted dry instead of rubbed dry
6. maintain good oral hygiene, if lesions are found in the mouth or nasal p
assages, antiseptic prep may be used
7. diet should be regular
HERPES ZOSTER (SHINGLES)

Description: Acute viral infection of the peripheral nervous system due to re
activation of varicella zoster virus. The virus causes an inflammatory reaction
in isolated spinal and cranial sensory ganglia and the posterior gray matter of
the spinal cord. Contagious to anyone who has not had varicella or who immunosup
ressed.
Signs and symptoms • neuralgic pain
• malaise
• burning
• fever
• cluster of skin vesicles along course of peripheral sensory nerves (unilateral a
nd found in trunk, thorax or face); appears 3-4 days
Management 1. drugs
• analgesics
• corticosteroids
• acetic acid compresses or white petrolatum
• anti-viral (acyclovir)
2. isolate client
3. apply drying lotion
4. administer medications as ordered
5. instruct client to preventive measures
SCABIES
Description:
An infection of the skin produced by burrowing action of a parasite mite resulti
ng in irritation and the formation of vesicles or postules.
Etiology:
Itchmite, sarcoptes scabei, occurs in individual living in area of poverty where
cleanliness is lacking.
Direct contact with infected persons, indirect contact through soiled bed linens
, clothing and others.
Incubation period:
-
Pathophysiology:
Both female and male parasites live on the skin. A female parasite burrows into
the superficial skin to deposit eggs. Pruritus occurs and scratching of skin may
produce secondary infection. Scattered follicular. Eruption contains immature m
ites. Inflammation may produce postules and crust. Eggs is hatched in 4 days. La
rvae undergo a series of matts before becoming adult. Life cycle is complete in
1-2 weeks.
Signs and symptoms
• intense itching especially at night
• sites – between fingers or flexor surfaces of wrists and palms, around nipples, um
bilicus, in axillary folds, near groin or gluteal folds, penis, scrotum.
Presence on skin of female mite, ova and feces upon skin scrapping.
Management
a. Take a warm soapy shower bath or bath to remove scaling debris from crus
ts.
b. Apply prescribed scabicide such as:
• lindane lotion (kwell) 1%
• crotamiton (Eurax) cream or lotion
• 6-10% precipitate of sulfur in petrolatum
c. encourage to change clothing frequently
RINGWORM (TRICHOPHYTOSIS)
Description:
A group of diseases caused by a number of vegetable fungi and affecting various
portion of the body in different ways (skin, hair, nails)
Etiology:
TINEA PEDIS (Athlete’s foot) – a superficial fungal infection due to trichophyton Ru
brum, mentagrophytes, or epidermophyton floccosum which may manifest itself as a
n acute, inflammatory, vesicular process or as chronic rash involving the soles
of the feet and the inter-digital web spaces. particularly common in summer, con
tracted swimming area and locker rooms.
TINEA CORPORIS or TINEA CIRCINATA – ringworm of the body.
TINEA CRURIS (Jock itch) – superficial fungal infection of the groin which may ext
end to the inner thigh and buttocks areas and commonly associated with tinea ped
is.
TINEA CAPITIS (ringworm of the scalp) – caused by microsporum canis, trichophyton
tonsurans.
• usually spread through child to child contact, use of towels, combs, brushes and
hats
• kitten and puppies may be the source of the infection
• primarily seen in children before puberty
Signs and symptoms
TINEA PEDIS
• scaly fissures between toes, vesicles on sides of feet
• pruritus
• burning and erythema
• lymphangitis and cellulites may occur
TINEA CORPORIS or TINEA CIRCINATA
• intense itching
• appearance: begins as scaling erythematous lesions advancing to rings of vesicle
s with central clearing and appears on exposed areas of body.
TINEA CRURIS
• dull red brown eruption of the upper thighs and extends to form circular plaques
with elevated scaly or vesicular borders.
• itching
• seen most in joggers, obese individuals and those wearing tight undercoating.
TINEA CAPITIS
• reddened, oval or round areas of alopecia
• presence of kerion: an acute inflammation that produces edema, postules and gran
ulomatous swelling
TINEA PEDIS
• direct examination of scrapings (skin, nails, hair)
• isolation of the organisms in culture
TINEA CAPITIS
• wood’s lamp
• microscopic evaluation
Management
TINEA PEDIS
a. Prevention: instruct client to keep feet dry such as by using talcum pow
der.
b. Management:
• Drugs: topical agent, clotrimazole, miconazole, tolnaftate
• Systemic anti-fungal therapy: griseofulvin, ketoconazole
• Elevate feet for vesicular type o pain infection.
TINEA CORPORIS or TINEA CIRCINATA

a. Prevention: infected pet is a common source and should be inspected and
treated by a veterinarian.
b. Management
• see treatment for tinea pedis
• wear clean cotton clothing next to skin
• use clean towel daily
• dry all areas and skin folds thoroughly
• use self monitoring for signs of re-infection after a course of therapy.
TINEA CRURIS
a. Prevention: avoid nylon underclothing, tight-fitting underwear and prolo
nged wearing of wet bathing suit.
b. Management:
• Drugs – topical therapy (miconazole cream); griseofulvin (oral)
• avoid excessive washing or scrubbing; wear cotton underwear.
TINEA CAPITIS – same with other fungal infection
GASTROINTESTINAL DISORDERS
TYPHOID FEVER (ENTERIC FEVER)
Description:
A general infection characterized by the hyperplasia of the lymphoid tissues, es
pecially enlargement and ulcerations of the Peyer’s patches and enlargement of the
spleen, by parenchymatous changes in various organs and liberation of an endoto
xin in the blood.
Etiology:
Salmonella typhosa, prevalent in temperate climates, high incidence in fall, and
mostly affected are the males and in youth and infant.
Infected urine and feces and intake of contaminated food and water
Pathophysiology:
The organism enters the body via the GI tract and invades the walls of the GI tr
act leading to bacteremia that localizes in mesenteric lymph nodes, in the masse
s of lymphatic tissue, in the mucus membrane of the intestinal wall (Peyer’s patch
es) and in small, solitary lymph follicles in the ileum and colon thus ulceratio
n of the intestines may result.
Complication:
• perforation of the intestine – from erosion of one of the ulcers
• intestinal hemorrhage – from erosion of blood vessels
• relapse
• thrombophlebitis
• urinary infection
• meningitis
Signs and symptoms
a. Gradual onset
• severe headache, malaise, muscle pains, non-productive cough
• chills and fever, temperature rises slowly
• pulse is full and slow
• skin eruption – irregularly spaced small rose spots on the abdomen, chest and back
; fades 3-4 days
• splenomegally
b. Second week
• fever remains consistently high
• abdominal distention and tenderness, constipation or diarrhea
• delirium in severe infection
• coma-vigil look; pupils dilate and patient appears to stare without seeing
• sultus tendium –twitching of the tendon sets
c. Third week
• gradual decline in fever and symptoms subsides
• white blood cell counts
• blood or bone marrow culture
• positive urine and stool cultures in later stage
• blood serum agglutination – (+) at the end of scond week
Management
a. Prevention: decontamination of water sources, milk pasteurization, indiv
idual vaccination of high risk persons, control carriers.
b. Drugs
• chloramphenicol
• ampicillin
• sulfamethoxazole
• trimethoprim
• furazolidone
c. intravenous infusion – to treat dehydration and diarrhea
d. Nursing care
• give supportive care
• position the patient to prevent aspiration
• use of enteric precautions
• TSB for high fever
• encourage high fluid intake
• monitor for complications
e. intestinal decompression procedure, IV fluids and surgical intervention –
for perforation
f. withhold food, blood transfusions and bowel resection – for intestinal hem
orrhage
LEPTOSPIROSIS (WEIL’S DISEASE, CANICOLA FEVER, HEMMORHAGIC JAUNDICE, ICTEROHEMORRH

AGIC SPIROCHETOSIS, SWINEHERD’S DISEASE, MUD FEVER)
Description:
Worldwide in its distribution and especially in areas where sanitation is poores
t; common in Japan. Usually those who are affected are the sewer workers, miners
and swimmers in polluted water.
Etiology:
Leptospira icterohaemorrhagiae carried by wild rat
Incubation period:
5 – 6 days
Signs and symptoms
• sudden onset with chills, vomiting and headache by severe fever and pains in the
extremities
• intense itching of the conjunctivae
• severe jaundice with hemorrhage in the skin and mucus membranes
• hematemesis, hematuria and hepatomegaly for severe cases
• convalescence occurs in the third week unless there is a complication
Positive agglutination test
Management
Prevention – eradication of rats and environmental sanitation
Drugs – antiserum or convalescent serum; penicillin
Nursing care – supportive and symptomatic
DYSENTERY
Etiology:
BACILLARY DYSENTERY (shigellosis, bloody flux) – caused by shigella dyseteriae and
shigella paradysenteriae coming from bowel discharges of infected persons and c
arriers.
VIOLENT DYSENTERY (Cholera) – caused by vibrio cholera, vibrio comma (ogawa and in
aba) from infected feces or vomitus.
BACILLARY DYSENTERY – eating of contaminated foods, hand to mouth transfer of cont
aminated material, flies, objects soiled with discharges of infected person, con
taminated water.
VIOLENT DYSENTERY – direct or indirect fecal contamination of water or food suppli
es by soiled hands, utensils or mechanical carriers such as flies.
Incubation period:
BACILLARY DYSENTERY – 1-7 days (average of 4 days)
• period of communicability – during acute phase and until (-) stool exam
VIOLENT DYSENTERY – from a few hours to five days (average 3 days)
• period of communicability – until the infectious organism is absent from the bowel
discharges (7-14 days)
Signs and symptoms
BACILLARY DYSENTERY
• chills
• fever
• nausea and vomiting
• tenesmus
• severe diarrhea accompanied by blood and mucus
• alternating episodes of diarrhea and constipation (chronic)
VIOLENT DYSENTERY
a. Onset
• acute colicky pain in the abdomen
• mild diarrhea (yellowish)
• marked mental depression
• headache, vomiting
• fever, may or may not be present
b. Collapse stage – after 1 or 2 days
• profuse watery stools (grayish white or rice water)
• thirst
• severe/violent cramps in the legs and feet
• thickly furred tongue
• sunken eyeballs
• ash-gray colored skin
c. Reaction stage – after 3 days
• increased consistency of stools
• skin becomes warm and cyanosis disappear
• peripheral circulation improves
• urine formation increases
BACILLARY DYSENTERY
• stool exam
• serologic test
VIOLENT DYSENTERY
• (+) stool exam/vomitus
Management
BACILLARY DYSENTERY
a. Methods of control and prevention
• recognition of disease and reporting
• concurrent disinfection from bowel discharges
• investigation of source of infection (food, water and milk supplies, general san
itation and search for carriers)
• prevention of fly breeding, screening
• sanitary disposal of human excreta
• protection and purification of public water supplies and prevention of subsequen
t contamination
b. Drugs
• kaolin
• bismuth and paregoric (combination of sulfonamide)
• chloramphenicol
c. Nursing care
• isolation by medical aseptic technique
• daily cleansing bath
• increase oral fluids in acute stage
• TSB for fever
• record and the character of stools passed, amount and frequency of vomiting
VIOLENT DYSENTERY
a. Prevention
• immunization
• screen the sickroom from flies
• protect the food supplies for contamination
b. Drugs – tetracycline
c. Replacement of fluids and electrolytes
d. Isolation
e. Patient should be spared all unnecessary efforts during the acute stage
f. Buttocks should be kept clean with warm water and soap and rubbed dry
g. antiseptic mouthwash in case of vomiting
h. fluids is given as soon as they can be tolerated
MUMPS (INFECTIOUS OR EPIDEMIC PAROTITIS)
Description:
An acute contagious disease the characteristic feature of which is the swelling
of one or both of the parotid glands usually occurring in epidemic form.
Etiology:
Filterable virus, member of myxovirus family, infected oral and nasal secretions
is the source of infection
Complication: orchitis or epididy-orchitis
Prognosis: favorable in most cases of mumps, complete recovery ordinarily takes
place even complications take place.
Direct contact with a person who has the disease or by contact with articles whi
ch is contaminated.
Incubation period:
14 – 21 days
• period of communicability: before the glands is swollen to the time present of l
ocalized swelling
Signs and symptoms
• pain in the parotid region
• headache
• earache
• fever
• difficulty to open the mouth wide
• general malaise
• sore throat
• moderate leukocytosis
• complement fixation test
• skin test for susceptibility to mumps
Management
a. Prevention: immunization (MMR given at 15 months)
b. Drugs – aspirin for fever, cortisone
c. isolation
d. absolute bed rest to prevent complications (at least 4 days)
e. daily bath should be given
f. soft bland diet for sore jaw
g. advise male to wear well fitting support to relieve the pull of gravity
on the testes and blood vessels
h. TSB for fever
i. ice pack/collar application
PARASITISM
Description:
-
Etiology:
• PINWORM (Enteropiasis) – oxyuris vermicularis, occurs from fomites, autoinfection,
fecal contamination, affects one in family and invariably infects entire family
.
• GIANT INTESTINAL ROUNDWORMS (Ascariasis) – ascaris lumbricoides, from sputum and o
va in soil.
• THREADWORM –strongyloides stercoralis, from fecal soil contamination
• WHIPWORM (trichuriasis) – from fecal soil contamination
• HOOKWORM (ancylostomiasis) – from larvae in fecal soil contamination
• TAPEWORM (taeniasis)
Types:
• hymenolepis nana – from fecal contamination
• taenia saginata (beef) – from insufficiently cooked meat
• taenia solium (pork) – contaminated meat
• diphyllobothrium latun – poorly cooked infested fish
PINWORM – mouth
GIANT INTESTINAL ROUNDWORMS – mouth
THREADWORM – enter usually through the skin or feet
WHIPWORM – mouth
HOOKWORM – through skin of the feet
TAPEWORM – mouth
Signs and symptoms
PINWORM
• eosinophilia, itching around the anus, convulsions in children.
GIANT INTESTINAL ROUNDWORMS
• chest pain, cough after two months, malnutrition, indigestion, diarrhea, colicky
abdominal pain.
THREADWORM
• intermittent diarrhea
WHIPWORM – nausea and vomiting, diarrhea, anemia, stunted growth; may cause prolap
se of rectum in children and occasionally appendicitis.
HOOKWORM – anemia, diarrhea, stunted growth, bronchial symptoms, obstruction of th
e biliary and pancreatic duct.
PINWORM – adults and ova in stool
GIANT INTESTINAL ROUNDWORMS – adults and ova in stool
THREADWORM – larvae
WHIPWORM – ova in stool
HOOKWORM – ova in stool
TAPEWORM – ova and segments of the worm in the stool
Management
THREADWORM – Prevention: wear shoes and use sanitary toilets
• use of sanitary toilets
• provide hygiene education of the family
• dispose of the infected stools carefully
• meticulous cleansing of skin especially anal region, hands and nails
• drugs – antihelminthic drugs, piperazine citrate, pyrantel pamoate, mebendazole
HEPATITIS
Description:
Widespread inflammation of the liver tissue with liver cell damage due to hepati
c cell degeneration and necrosis; proliferation and enlargement of the Kupffer c
ells and inflammation of the periportal areas thus may cause interruption of bil
e flow.
Etiology:
TYPE A (infectious hepatitis) – occurs in crowded living conditions; with poor per
sonal hygiene or from contaminated food, milk, water or shellfish. Common occurr
ence during fall and winter months usually affecting children and young adults.
TYPE B (serum hepatitis, SH virus, viral hepatitis, transfusion hepatitis, homol
ogous serum jaundice)
TYPE C (non-A, non-B hepatitis)
TYPE A – fecal/oral route
TYPE B – blood and body fluids (saliva, semen, vaginal secretions), often from con
taminated needles among IV drug abusers, intimate/sexual contact.
TYPE C – by parenteral route, through blood and blood products, needles and syring
es
Incubation period:
TYPE A – 15-45 days
• period of communicability – 3 weeks prior and one week after developing jaundice
TYPE B – 50-180 days
TYPE C – 7-50 days
Pathophysiology:
-
Signs and symptoms
a. Pre-icteric stage
• anorexia
• fatigue
• constipation or diarrhea
• weight loss
• right upper quadrant discomfort
• hepatomegaly
• spleenomegaly
• lymphadenopathy
b. Icteric stage
• fatigue
• weight loss
• light colored stools
• dark urine
• jaundice
• pruritus
• continued hepatomegaly with tenderness
c. Post-icteric stage
• fatigue but increased sense of well being
• hepatomegaly: gradually decreasing
a. All 3 types
• SGPT, SGOT, alkaline phospatase, bilirubin, ER – all increased in pre-icteric
• leukocytes, lymphocytes, neutrophils – all decreased
• prolonged PT
b. HEPA A: Hepa A (HAV) in stool before onset
• Anti-HAV (IgG) – appears soon after onset of jaundice, peaks in 1-2 months and per
sist indefinitely
• Anti-HA (IgM) – positive in acute infection lasts 4-6 weeks
c. HEPA B
• HbsAG (surface antigen) – positive, develops 4-12 weeks after infection
• Anti-HbsAg – negative in 80% cases
• Anti-HBC associated with infectivity, develops 2-16 weeks after infection
• ABeAG – associated with ineffectively and disappears before jaundice
• Anti-Hbe – present in carriers, represents low ineffectivity
Management
a. Prevention
I. Type A
• good hand washing
• good personal hygiene
• control and screening of food handlers
• passive immunization – ISG, to exposed individuals and prophylaxis for travelers t
o developing countries
II. Type B
• screen blood donors HB3Ag
• use disposable needles and syringes
• registration of all carriers
• passive immunization – ISG
• active immunization – hepatavax B vaccine and formalin treated hepatitis B vaccine
given in 3 doses
b. Nursing management
• promote adequate nutrition – small frequent meals of high CHO, moderate to high CH
ON, high vitamin, high caloric diet, avoid very hot or cold foods.
• ensure rest and relaxation
• monitor/relive pruritus – cool, moist compresses, emollient lotion
• administer corticosteroid as ordered
• isolation procedures as required
• ) provide client teaching and discharge planning with regards to:
importance of avoiding alcohol
importance of not donating blood
recognition/reporting of signs of inadequate convalescence
avoidance of persons with known infections
• Drugs – liver protector (essentiale, jectofer, interferon drug
FOOD POISONING
Description:
A gastroenteritis often produced by the presence of a disease organism or its to
xins.
Etiology:
SALMONELLA GASTROENTERITIS – salmonella typhimurium, salmonella paratyphi A, B, an
d C; salmonella newport
STAPHYLOCOCCUS GASTROENTERITIS – coagulase – positive, gram positive: grows rapidly
on food containing carbohydrates
Recovery: within 24 – 36 hours
BOTILISM – clostridium botulinum
Incubation period:
SALMONELLA GASTROENTERITIS – 6 to 48 hours after the ingestion of contaminated foo
d
STAPHYLOCOCCUS GASTROENTERITIS – 2 to 6 hours after ingestion
BOTILISM – 24 hours after the ingestion
Signs and symptoms
SALMONELLA GASTROENTERITIS
• headache
• diarrhea (stools are usually fluid and contain mucus; bloody if in severe infect
ion)
STAPHYLOCOCCUS GASTROENTERITIS
• sudden abdominal pain
• excessive perspiration
• vomiting
• diarrhea
• pallor weakness
BOTILISM
• peripheral nervous system
vomiting
ataxia
constipation
ocular paralysis
aphonia
other neufromascular signs
• paralysis of the respiratory system which may lead to death
SALMONELLA GASTROENTERITIS – history of illness after ingestion of certain foods
Management
SALMONELLA GASTROENTERITIS/STAPHYLOCOCCUS GASTROENTERITIS
• replacement of fluids and salts
• sedatives and anticholinergic to reduce hypermobility of the intestine
• good oral hygiene
• application of heat to abdomen to relieve cramps
BOTILISM
• prevention
regulation of commercial processing of canned foods
education of housewives concerning proper processing of home canned foods
canned foods should be boiled first to destroy the toxins
polyvalent antitoxins (botulinum antitoxin)
• patient with botulinum should be placed on quiet room and avoidance of unnecessa
ry activity
• symptomatic
• intubation for feeding
• tracheostomy – in respiratory failure
• oxygen by IPPB
SEXUALLY TRANSMITTED DISEASE
GONORRHEA (STRAIN, CLAP, JACK, MORNING DROP, G.C. GLEET)
Description:
An infectious disease, which causes inflammation of the mucous membranes of the
genitourinary tract.
Complications:
MALE – bilateral epididymitis, sterility
FEMALE – pelvic inflammatory disease, sterility
NEWBORN – opthalmia neonatorum – mother to child
Etiology:
Neisseria gonorrhea
Sexual contact
Incubation period:
2 – 5 days
Signs and symptoms
MALE
• burning sensation in the urethra upon urination
• passage of purulent (yellowish) discharge
• pelvic pain
• fever
• painful urination
FEMALE
• burning sensation upon urination
• presence or absence of vaginal discharge
• pelvic pain
• abdominal distention
• urinary frequency
• culture and sensitivity
• female: pap smear or cervical smear; male: urethral smear
• blood exam – VDRL
Management
• educate men and women to recognize signs of gonorrhea and to seek immediate trea
tment
• monitor urinary and bowel elimination
• important to treat sexual partner, as client may become re-infected
• make arrangements for follow-up culture 2 weeks after therapy is initiated
• Drugs – penicillin: drug of choice
tetracyclines
ceftriaxone sodium (rocephin)
amoxicillin (augmentin)
SYPHILIS (LEUS, POX, BAD BLOOD DISEASE)
Description:
A contagious disease that leads to many structural and cutaneous lesions
Complications:
a. still birth
b. child born with syphilis
• placenta is bigger than the baby
• persistent vesicular eruptions and nasal discharges
• old man feature
• mucus patches on mouth and anus
c. child born with late syphilis (signs and symptoms after 2 years)
• hutchinson’s teeth
• deafness
• saddle nose
• high palate
Etiology:
Treponema pallidum
Sexual contact
Incubation period:
3 – 6 weeks
Signs and symptoms
a. Primary syphilis
• chancre on genitalia, mouth or anus
• serous drainage from chancre
• enlarge lymph nodes
• maybe painful or painless
• highly infectious
b. Secondary syphilis
• skin rash on palms and soles of feet
• reddish copper – colored lesions on palms of hands and soles of feet
• condylomas: lesions/sores that fused together
• erosions of oral mucus membranes
• alopecia
• enlarged lymph nodes
• fever, headache, sore throat and general malaise
c. Tertiary syphilis
• gumma – the characteristic lesions
• cardiovascular changes
• ataxia
• stroke, blindness
a. positive test for syphilis
• venereal disease research laboratory (VDRL)
• rapid plasma reagin circle card test (CRPR-CT)
• automate reagin test (ART)
• fluorescent treponemal antibody absorption test (FTA-ABS)
• wessermann test
• khan precipitation test
• kline, hinton and mazzin tests
b. darkfield examination
c. culture and sensitivity
Management
• strict personal hygiene is an absolute requirement
• assist in case finding
• instruct client to avoid sexual contact until clearance is given by physician
• encourage monogamous relationship
• explain need to complete course of antibiotic therapy
• Drugs – penicillin, tetracyclins/kithramycin
ACQUIRED IMMUNE DEFICIENCY SYNDROME (AIDS)
Description:
An acquired immune deficiency characterized by a defect in natural
immunity
Etiology:
Retrovirus, human immunodeficiency virus (HIV-1 and HIV-2) previously referred t
o as human T-lymphotropic virus type III (HTLV-III)
Blood transfusion, sexual contact, contaminated needles, perinatal transmission
Incubation period:
6 months to 9 years
Pathophysiology:
Signs and symptoms

• anorexia
• fatigue
• dyspnea
• night sweats
• fever
• diarrhea
• enlarged lymph nodes
• HIV encephalopathy: memory loss, lack of coordination, partial paralysis, mental
deterioration
• HIV wasting syndrome, emaciation
• positive test for HIV antibody
• positive test for presence of HIV itself
• opportunistic infection: pneumocystic carinii, cystomegalovirus, kaposi’s sarcoma
• ELISA test (enzyme-linked immunosorbent assay) – a screening test
• western blot – a confirmatory test
Management
• provide frequent rest periods
• provide skin care
• provide high-calorie, high protein diet to prevent weight loss
• provide good oral hygiene
• provide oxygen and maintain pulmonary function
• provide measures to reduce pain
• protect the client from secondary infection; carefully assess for early signs
• encourage verbalization of feelings
• teach client the importance of:
informing sexual contacts of diagnosis
not sharing needle with other individuals
continuing medical supervision
CHLAMYDIAL INFECTION
Description:
A sexually transmitted disease that is highly contagious caused by chlamydial or
ganism
Etiology:
Chlamydia trachomatis
2 -3 weeks for males
Incubation period:
Sexual intercourse
Pathophysiology:
-
Signs and symptoms
• pruritus in vagina
• burning sensation in vagina
• painful intercourse
• pruritus of urethral meatus in men
• burning sensation during urination
Culture of aspirated material from vaginal, anal or penile discharges
Management
• doxycycline or azithromycin (recommended for pregnant woman)
• universal precaution should be practiced
TRICHOMONIASIS
Description:
Another type of sexually transmitted disease that may also be transmitted by oth
er means such as handling of infected fomites. It is caused by a protozoan paras
ites.
Etiology:
Trichomonas vaginalis
Sexual intercourse, contact with wet towels and wash clothes infected by the org
anism
Incubation period:
4 – 20 days, usually 7 days
Signs and symptoms
• vaginal discharge
• burning and pruritus of vagina
• redness of the introitus
• usually asymptomatic in men
culture of obtained specimen
Management
• metronidazole
• sitz bath may relieve symptom
• acid douches
• tetracyclines may be given on male who are also infected
BIOTERRORISM AND PANDEMICS
In the recent course of international conflicts, which has lead to war, has used
weapon that are quite different from the conventional ones used before. The med
ical science is being used not to prolong life but to cause immediate death by i
nfection of various biological organisms. The following gives an insight of thes
e dangerous biological terrorism leading to pandemics.
SMALL POX
Description:
For about two decades the WHO has declared that the world is already “small pox fr
ee”. Although eliminated in the world over, the specimen is still kept in two labo
ratory facility in the United States.
Etiology:
Variola virus (DNA virus)
Direct contact or by droplet from person to person
Incubation period:
12 days
Signs and symptoms
• high fever
• malaise
• headache
• back ache
• maculopapular rash in the face, mouth and pharynx (the patients are contagious a
fter the appearance of the rash)
Management
• generally supportive care
• before rendering care transmission precaution should be specifically indicated
• autoclaving of soiled linens is needed
• isolation is necessary until no longer contagious
ANTHRAX
Description:
Also known as whoolsorters disease, the capsulated form of this organism is foun
d in soil worldwide. The organism needs to take about 8,000 to 50,000 to put a p
erson at risk of contracting the disease.
Etiology:
Bacillus anthracis
• inhalation of spores
• ingestion of spores
• entrance through skin lesions
Incubation period:
For inhalation anthrax 60 days, for cutaneous anthrax 1-6 days
Signs and symptoms
a. Inhalation anthrax
• cough
• headache
• fever
• vomiting
• chills
• weakness
• dyspnea
• syncope
b. Cutaneous anthrax
• abdominal pain
• hematochexia
• ascites
• massive diarrhea
Management
a. standard precaution is already sufficient to control the spread of the i
nfection
b. ciprofloxacin/doxycycline is prescribed for mass exposure/casualty with
infecting organism
c. important pharmacologic interventions are penicillin, erythromycin, chlo
rampenicol and gentamycin

Communicable Diseases

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Communicable Diseases

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COMMUNICABLE DISEASES

Signs and symptoms

DENGUE HEMORRHAGIC SHOCK SYNDROME

Signs and symptoms

INFLUENZA (LA GRIPPE OF FLU)

Description: An extremely contagious exanthematous disease of acute onset whi

GERMAN MEASLES (RUBELLA, ROTHEIN, ROSEOLA, 3-DAY MEASLES)

VARICELLA (CHICKEN POX)

HERPES ZOSTER (SHINGLES)

TINEA CORPORIS or TINEA CIRCINATA

TYPHOID FEVER (ENTERIC FEVER)

LEPTOSPIROSIS (WEIL’S DISEASE, CANICOLA FEVER, HEMMORHAGIC JAUNDICE, ICTEROHEMORRH

MUMPS (INFECTIOUS OR EPIDEMIC PAROTITIS)

GONORRHEA (STRAIN, CLAP, JACK, MORNING DROP, G.C. GLEET)

SYPHILIS (LEUS, POX, BAD BLOOD DISEASE)

ACQUIRED IMMUNE DEFICIENCY SYNDROME (AIDS)

Signs and symptoms

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