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
organism reproduces and secretes tetanolysin which causes RBC and WBC lysis.
Tetanospamin 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.

None. History of wound and possible contamination are usually enough to arouse
Diagnostic procedure suspicion 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
muscle 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

nasopharynx.

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Mode of transmission: Droplet infection

Incubation period: 2 – 10 days

Pathophysiology: The organism enters the bloodstream after invading the respiratory tissues.
Reaches the spinal cord and of course the meninges. It stimulates chemotaxis
that leads 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 blood flow and brain infarct my ensue.

Signs and symptoms The most significant finding indicating meningeal irritation: brudzinski and
kernigs sign. Other sign observable are headache, opisthotonus, fever and
petechiae

Diagnostic procedure 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 who
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 share
eating utensils.
Nurses and Doctors are not at risk of having the disease except when close
contact 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

Mode of transmission: Mosquito borne – bite of the infected mosquito

Viral – may be droplet or airborne

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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
inflammation 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.

Diagnostic procedure 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)

Mode of transmission: Fecal – oral route. Particularly rampant among those in the squatters area who
have 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
penetrate the intestinal wall causing viremia and reaching the motor nerves and
the spinal cord. The virus reproduces inside the nerve and as they are released,
 the infected cell die, hence paralysis results.

Signs and symptoms Pokers sign, Haynes sign, tonsillitis, abdominal pain and flaccid paralysis

Diagnostic procedure 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 Philippines
Dogs and Cats are among the most important reservoir. The causative organism is
Rhabdo Virus

Mode of transmission: 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
nearby axons and then reaches the nerve itself. From that point onwards the
virus travels along the nerve pathway to reach the brain. In the brain the virus
incites inflammatory reaction that gives rise to the appearance of encephalitis
like symptoms later the organism descends from the brain and exit to affect
other nerves in the body. The affectation of trigeminal nerve causes throat
spasms which gives rise to its classic finding “hydrophobia”

Signs and symptoms Hydrophobia, aerophobia, laryngeal, Pharyngeal spasm excessive salivation.

Diagnostic procedure Fluorescent antibody Staining, Negri bodies found in brain biopsy of the infected
animal

Management Human Diploid Cell Vaccine, Rabies Immunoglobulin, Rabies Anti serum. tetanus
anti serum is also given if with negative or inadequate immunization history

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Wash wound with soap and water, may apply wound antiseptic
Once sign and symptoms are present passive immunization is already useless.
Supportive therapy comes next.
Protect from glare and sunlight, protect from water and air current. Cover IV
bottle and tubing with carbon paper or any other else that can effectively hide
the iv fluids. Secure consent and restrain the patient. Observed contact and
droplet precaution.

LEPROSY

Description: A chronic infection that usually affects the peripheral nerves and leads to
paresthesias

Etiology: A possible zoonotic infection which is rarely cultured in laboratory but seen to
be growing freely among armadillo. Causative organism is Mycobacterium leprae

Mode of transmission: Droplet infection is the most important transmission. Skin contact may cause
infection 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
macrophages but can’t be killed, as this circulating macrophage
reaches the skin the bacteria penetrate the nerves. Later due to immune
recognition WBC attacks the infected cell which results to the destruction of
the affected cell hence the appearance of paresthesias and consumption of the
involved extremity becomes apparent due to immune response it self.

Signs and symptoms Painless wound, paresthesias, ulcer that does not heal, leonine appearance,
maderosis. Nerve involvement with acid fast bacilli is the pathognomic sign of
leprosy

Diagnostic procedure 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
egypti other wise known as tiger mosquito because of the black stripes present
at the dorsal legs of the insect. The mosquito prefers to thrive on clean stagnant
water.

Mode of transmission: 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
the victim. Once the proboscis pierced the capillaries it also leaves the viral
organism. The virus mixes in the bloodstream survive and reproduce causing
viremia which explains the appearance of generalized flushing. The virus will then
successfully enters the bone marrow and arrest the maturation of
megakaryocyte. Since 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 hemorrhage.

Signs and symptoms Petechiae, bleeding, epitaxis, Herman’s sign and fever

Diagnostic procedure Tourniquet test, platelet count.

Management Watch out for bleeding. Minimize injections and other parenteral procedures if
possible. 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

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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.
The primary vectors are anopheles mosquitoes.

Mode of transmission: 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
bloodstream and immediately proceed to the liver in the form of sporozoites.
Inside the hepatocytes reproduction continues until the host burst releasing the
parasite in 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 causes 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
then cold stage (chilling). The cycle repeats leading to malarial cachexia

Diagnostic procedure 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.

Mode of transmission: 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. The 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
elephantiasis

Diagnostic procedure Microscopic examination of peripheral blood.

Management Use of mosquito repellant and nets

Hetrazan is effective against Filiriasis adverse reaction though are seen in a
number 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
include the lower respiratory tract.

Etiology: The organism, Corynebacterium diphtheriae is ubiquitous.

Mode of transmission: 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 appearance
of psudomembarne which may be dislodge and block the airway. As toxins are
secreted the heart, kidney and the nerves absorb it, this toxins halt protein

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synthesis of the infected cell which later on causes its death.

Signs and symptoms Pathognomonic Sign is pseudo membrane. Tonsillitis may also be present. Fever
and malaise. If complication arises paralysis, endocarditis and kidney failure may
be seen.

Diagnostic procedure 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

Mode of transmission: Droplet infection

Incubation period: 7 – 21 days

Pathophysiology: The organism enters the upper respiratory tract attaches to the respiratory
epithelium and causes an increased production of cyclic amino phosphate that
essentially leads to hyperactivity of the mucous secreting cells. Thick tenacious
secretions blocks the airway. The organism also halts the mucociliary escalator
leaving coughing reflex the last effective protective mechanism of expelling
sputum. Due to its relative tenaciousness the body experiences difficulty in
coughing out phlegm thus we observe patient to manifest violent cough.

Signs and symptoms Pathognomonic of this infection is violent cough w/out intervening inhalation
followed by an inspiratory whoop.
Vomiting may be present, Increased in ICP and IOP are also seen. Hernia is also a
high risk incident.

Diagnostic procedure
 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.

Mode of transmission: 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 it
will die and leave the capsulated bacteria undigested. Once the body’s immune
system dropped, the bacteria will be activated and stimulate immune response
which likewise damage the alveolar tissues leading to casseation necrosis and
could eventually consume the entire lungs if the process is repeated frequently

Signs and symptoms Afternoon fever, night sweats, cough for 2 weeks, anorexia weight loss.

Diagnostic procedure 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:
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an acute usually bacterial in nature

Etiology: most common causative organism is strptococcus pneumoniae ubiquitous, orgainsm

and may be transferred among population that has poor ventilation and impaired
respiratory cilliary function. certain disease like measles may promote the
development of pneumonia

Mode of transmission: 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
centers where it stimulate an inflammatory reaction. this response leads to
migration of WBC in particular with neutrophil hence leukocyte infiltration is
seen in chest x-rays as consolidation. the build up puss increases the alveolar
presure causing in atelectasis once collapsed alveoli cant participate in gas
exchange anymore 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, cyanosis and death.

Diagnostic procedure sputum exam

Management Co Trimoxazole and gentamycin are the drug of choice. although Co-tri is used
more widely than gentamycin because of its oral preparation which are allowed to
be 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.
Mode of transmission: Droplet infection, direct contact.

Incubation period: 1 – 3 days

Pathophysiology: As the virus enters the respiratory tract, it attaches itself to the mucous
membrane and causes local irritation and inflammation. In response, the mucous
membrane releases mucous to flush out the virus. Since there is an increased in
the production 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 tears 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
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

Mode of transmission: Droplet infection, contact with nasopharyngeal secretions

Incubation period: 24 – 48 hrs.

Pathophysiology:

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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
epithelium the virus releases neuramidase that decreases the viscosity of the
mucosa. Facilitating the spread of the infected exudates to the lower
respiratory tract, this causes intestinal inflammation, and necrosis of the
alveolar and bronchiolar epithelium. Thus, the alveoli are filled with exudates
containing WBC, RBC and hyaline cartilage. This places the patient to increased
possibility of acquiring 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

skin or mucous membranes or by changes in the nerves leading to anesthesia,
 paralysis or other changes

Etiology: Mycobacterium leprae (acid fast bacillus), sporadic/endemic cases, occurs in

tropical and semitropical countries throughout the world. It can be contracted in
childhood (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
have advanced without ability to produce the lepromin reaction – the poorer the
prognosis
> case under 21 years old – high relapse rate

Mode of transmission: 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
peripheral nerve, which causes skin lesions, anesthesia, infection and deformities

Signs and symptoms Assessment:

1. Tuberculoid type – shows high resistance to Hansen’s bacilli. Clinical
manifestations are mainly in the skin and nerves and usually are used or
non-infectious.
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 nerves.
3. Open or infectious cases
4. Indeterminate type – clinical manifestations are located chiefly in skin
and 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)

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• 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

Diagnostic procedure a. Lepromin reaction – a positive test develops a nodule at the site of
inoculation (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
(-) for 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)
 An extremely contagious exanthematous disease of acute onset which most often
Description: 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 contact with articles

Incubation period: 8 – 20 days

Pathophysiology: As the virus enters the body it immediately multiplies in the respiratory
epithelium. It disseminate by way of the lymphatic system causing hyperplasia of
the infected lymphoid tissue. As a result there is a primary viremia which infects
the leukocyte and involves the whole reticuloendothelial system. As the infected
cells die it necrose and release more viruses to infect other leukocytes leading to
secondary viremia, which also causes edema of upper respiratory tract producing
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,

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appears first on the face 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

Diagnostic procedure 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
tenderness

Etiology: Caused by myxovirus. Occurs mostly in spring and seen mostly in children over 5
years of age

Mode of transmission: 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
nearest lymph gland causing lymphadenopathy. Later on, the virus enters the
blood stream that stimulates the immune response, which is the cause of rashes
found in the 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 it 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 including 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

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• gamma globulin – given to pregnant women with negative

history and who have been exposed 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, characterized
by the appearance of vesicles frequently preceded by papules, occasionally
followed by postules but ending in crusting

Etiology: Varicella zoster virus (airborne)

Mode of transmission: Droplet infection, direct contact

Incubation period: 2 -3 weeks

Pathophysiology: The virus gain entrance via the upper respiratory tract it crosses the mucous
membrane and cause systemic infection followed by appearance of numerous
macupapular 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 membranes)
• 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 scarring 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
lotion
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
passages, antiseptic prep may be used
diet should be regular

HERPES ZOSTER (SHINGLES)

Description: Acute viral infection of the peripheral nervous system due to reactivation 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 immunosupressed.

Signs and symptoms • neuralgic pain

• malaise
• burning
• fever
cluster of skin vesicles along course of peripheral sensory nerves (unilateral and
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

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instruct client to preventive measures

SCABIES

Description: An infection of the skin produced by burrowing action of a parasite mite

resulting 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.

Mode of transmission: 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
mites. Inflammation may produce postules and crust. Eggs is hatched in 4 days.
Larvae 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,
umbilicus, in axillary folds, near groin or gluteal folds, penis, scrotum.

Diagnostic procedure 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
crusts.
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 Rubrum, mentagrophytes, or epidermophyton floccosum which may
manifest itself as an acute, inflammatory, vesicular process or as chronic rash
involving the soles of the feet and the inter-digital web spaces. particularly
common in summer, contracted 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
extend to the inner thigh and buttocks areas and commonly associated with tinea
pedis.

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 vesicles 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
granulomatous swelling

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Diagnostic procedure 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
powder.
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
prolonged 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,

especially enlargement and ulcerations of the Peyer’s patches and enlargement of
the spleen, by parenchymatous changes in various organs and liberation of an
endotoxin 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.

Mode of transmission: 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
tract leading to bacteremia that localizes in mesenteric lymph nodes, in the
masses of lymphatic tissue, in the mucus membrane of the intestinal wall (Peyer’s
patches) and in small, solitary lymph follicles in the ileum and colon thus
ulceration 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

Diagnostic procedure • 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,

individual vaccination of high risk persons, control carriers.
b. Drugs
• chloramphenicol

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• 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
withhold food, blood transfusions and bowel resection – for intestinal
hemorrhage

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

ICTEROHEMORRHAGIC SPIROCHETOSIS, SWINEHERD’S DISEASE, MUD FEVER)

Description: Worldwide in its distribution and especially in areas where sanitation is poorest;
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

Diagnostic procedure 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 carriers.

VIOLENT DYSENTERY (Cholera) – caused by vibrio cholera, vibrio comma (ogawa

and inaba) from infected feces or vomitus.

Mode of transmission: BACILLARY DYSENTERY – eating of contaminated foods, hand to mouth

transfer of contaminated material, flies, objects soiled with discharges of
infected person, contaminated water.
VIOLENT DYSENTERY – direct or indirect fecal contamination of water or food
supplies 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

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• 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

Diagnostic procedure 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 sanitation and search for carriers)
• prevention of fly breeding, screening
• sanitary disposal of human excreta
• protection and purification of public water supplies and
prevention of subsequent 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
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.

Mode of transmission: Direct contact with a person who has the disease or by contact with articles
which is contaminated.

Incubation period: 14 – 21 days

• period of communicability: before the glands is swollen to the time
present of localized swelling

Signs and symptoms • pain in the parotid region

• headache
• earache
• fever
• difficulty to open the mouth wide
• general malaise
• sore throat

Diagnostic procedure • 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
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g.advise male to wear well fitting support to relieve the pull of

gravity on the testes and blood vessels
h.TSB for fever
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 ova 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

Mode of transmission: 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
prolapse of rectum in children and occasionally appendicitis.
HOOKWORM – anemia, diarrhea, stunted growth, bronchial symptoms,
 obstruction of the biliary and pancreatic duct.

Diagnostic procedure 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 hepatic
cell degeneration and necrosis; proliferation and enlargement of the Kupffer
cells and inflammation of the periportal areas thus may cause interruption of bile
flow.

Etiology: TYPE A (infectious hepatitis) – occurs in crowded living conditions; with poor
personal hygiene or from contaminated food, milk, water or shellfish. Common
occurrence during fall and winter months usually affecting children and young
adults.

TYPE B (serum hepatitis, SH virus, viral hepatitis, transfusion hepatitis,

homologous serum jaundice)

TYPE C (non-A, non-B hepatitis)

Mode of transmission: TYPE A – fecal/oral route

TYPE B – blood and body fluids (saliva, semen, vaginal secretions), often from
contaminated needles among IV drug abusers, intimate/sexual contact.
TYPE C – by parenteral route, through blood and blood products, needles and
syringes

Incubation period: TYPE A – 15-45 days

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• 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
• nausea and vomiting
• 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

Diagnostic procedure 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 persist 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 to 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 CHON, 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

toxins.

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Etiology: SALMONELLA GASTROENTERITIS – salmonella typhimurium, salmonella

paratyphi A, B, and 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 food
STAPHYLOCOCCUS GASTROENTERITIS – 2 to 6 hours after ingestion
BOTILISM – 24 hours after the ingestion

Signs and symptoms SALMONELLA GASTROENTERITIS

• headache
• nausea and vomiting
• diarrhea (stools are usually fluid and contain mucus; bloody if in severe
infection)
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

Diagnostic procedure 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
unnecessary 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

Mode of transmission: 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
• nausea and vomiting
urinary frequency

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Diagnostic procedure • 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 treatment
• 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

Mode of transmission: 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

Diagnostic procedure 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
to as human T-lymphotropic virus type III (HTLV-III)

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Mode of transmission: 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

Diagnostic procedure • 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
organism

Etiology:
Chlamydia trachomatis

Mode of transmission: 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

Diagnostic procedure 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
other means such as handling of infected fomites. It is caused by a protozoan
parasites.

Etiology: Trichomonas vaginalis

Mode of transmission: Sexual intercourse, contact with wet towels and wash clothes infected by the
organism

Incubation period: 4 – 20 days, usually 7 days

Signs and symptoms • vaginal discharge

• burning and pruritus of vagina

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• redness of the introitus

usually asymptomatic in men

Diagnostic procedure 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 medical science is being
used not to prolong life but to cause immediate death by infection of various biological
organisms. The following gives an insight of these dangerous biological terrorism leading to
pandemics.

SMALL POX

For about two decades the WHO has declared that the world is already “small
Description: pox free”. Although eliminated in the world over, the specimen is still kept in two
laboratory facility in the United States.

Etiology: Variola virus (DNA virus)

Mode of transmission: 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 after 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
found in soil worldwide. The organism needs to take about 8,000 to 50,000 to put
a person at risk of contracting the disease.

Etiology: Bacillus anthracis

Mode of transmission: • 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
• nausea and vomiting
• abdominal pain
• hematochexia
• ascites
massive diarrhea

Management a.standard precaution is already sufficient to control the spread of

the infection
b.ciprofloxacin/doxycycline is prescribed for mass
exposure/casualty with infecting organism
important pharmacologic interventions are penicillin, erythromycin,
chlorampenicol and gentamycin

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