15.

HEPATITIS A

➢ is a viral liver disease that can cause mild to severe illness.

➢ Most people who are infected recover completely with no permanent liver damage.

CAUSATIVE AGENT: Hepatitis A Virus (HAV)

➢ a nonenveloped RNA virus that is classified as a picornavirus.

➢ First isolated in 1979

➢ can be stable in the environment for months

➢ Stable at low pH levels and moderate temperatures

➢ Inactivated by high temperature (185°F [85°C] or higher), formalin, and chlorine.

INCUBATION PERIOD: approx. 28 days (average 15-50 days)

MODE OF TRANSMISSION:

1. fecal-oral transmission- Replicates in the liver. After 10-12 days, virus is present in blood and is excreted via the biliary system into
the feces. Peak titers occur during the 2 weeks before onset of illness. Although virus is present in serum, its concentration is several
orders of magnitude less than in feces. Virus excretion begins to decline at the onset of clinical illness, and has decreased significantly
by 7-10 days after onset of symptoms. Most infected persons no longer excrete virus in the feces by the third week of illness. Children
may excrete virus longer than adults.

CLINICAL MANIFESTATION

⚫ Abrupt onset of fever

⚫ Malaise, anorexia, nausea, abdominal discomfort, dark urine and jaundice

⚫ Fulminant hepatitis is the most severe rare complication, with mortality estimates up to 80%

DIAGNOSTIC TEST

Serologic testing- (+) IgM anti-HAV

HEPATITIS B

➢ Serum hepatitis

➢ With severe complication such as massive liver damage

CAUSATIVE AGENT: Hepatitis B virus (HBV)

➢ Very limited tissue tropism

➢ Includes liver, pancreas, gall bladder

➢ HbsAg appears in blood for 30-60 days after exposure

INCUBATION PERIOD: 50-189 days or 2-5 mos (average 90 days)

MODE OF TRANSMISSION

⚫ Person to person contact

CLINICAL MANIFESTATION

⚫ PRODROMAL PERIOD- acute attack of symptoms

-fever, chills, malaise, abdominal pain

- anorexia, nausea, vomiting

- jaundice, dark urine, pale gray to dark colored stool

⚫ FULMINANT HEPATITIS-full-blown

- with severe symptoms

- ascites, bleeding tendencies

- fatal

DIAGNOSTIC PROCEDURE

1. SEROLOGIC TEST

- HAV and HBV (compliment fixation test)

- IgM and IgG levels

- SGOT & SGPT levels (determinants of normal liver function)

- ALT & AST levels

2. BILE EXAMINATION IN BLOOD & URINE

- Radio-immunoassay hemaglutinin test

- Blood count

- HBsAg

PREVENTIVE MEASURE

⚫ Hepa B vaccine recommended pre-exposure

⚫ Hepatitis immune globin (HBIg) within 72 hours to those exposed directly by ingestion, prick or inoculation

⚫ Practice safe sex

⚫ Proper screening of blood donors

⚫ Strict universal and standard precautions

⚫ Handwashing before and after every procedure

⚫ Get adequate rest, sleep, exercise & eat nutritious food

HEPATITIS C

⚫ Blood-borne infectious disease

⚫ Known as “non-A, non-B hepatitis”

⚫ Often asymptomatic, but can cause scarring of liver (fibrosis) and cirrhosis (adequate scarring)

⚫ Clients with chronic Hepa C are considered infectious

⚫ No vaccine available

CAUSATIVE AGENT: Hepatitis C virus (HCV)

➢ Also with high rate of chronic diseases such as chronic hepatitis B, cirrhosis, hepatocarcinoma

DIAGNOSTIC EXAM

➢ Serologic test for specific antibody or more months after onset of acute hepatitis

MODE OF TRANSMISSION

⚫ Body piercing

⚫ Mother to baby transmission

⚫ Blood transfusion

⚫ Sharing needles and other equipments

⚫ Tattoing

⚫ Sexual contact
CLINICAL MANIFESTATIONS

⚫ Same with Hepa B

⚫ Changes in sense of smell and taste

⚫ Dark colored urine and gray-colored stols

⚫ Skin rashes, erythematous patches, urticaria on mouth and face

⚫ Liver tendencies, hepatomegaly, splenomegaly, cervical adenopathy (swelling of lymph nodes)

HEPATITIS D

➢ rare

➢ Found only in patients with acute or chronic hepatitis B

CAUSATIVE AGENT: Hepatitis D virus

➢ Small circullar RNA virus

➢ Replication defective-cannot propagate in absence of another virus---> occurs only with Hepa B infection in humans

➢ Requires the presence of Hepa B antigen (HBsAg)

MODE OF TRANSMISSION

➢ Risk factors similar with HBV infection

➢ Transmitted by blood and blood products

➢ Can be acquired by:

1. CO-INFECTION- acquired Hepa D virus infection at the same time with HBV infection

2. SUPER INFECTION- infected with Hepa D virus at any time during acute HBV infection

DIAGNOSTIC EXAM

⚫ Detection of intrahepatic delta or IgM

CLINICAL MANIFESTATION

⚫ Doesn’t always cause symptoms

⚫ Same with Hepa B

⚫ Changes in sense of taste and smell

⚫ Joint pain

⚫ Abdominal pain

⚫ Vomiting

⚫ Loss of appetite

⚫ Dark urine

⚫ fatigue

⚫ Red beefy tongue (Chronic Hepatitis B)

⚫ If the infection lasts for six months or longer, the condition is known as chronic Hepatitis D

HEPATITIS E

➢ Same with Hepa A as to mode of transmission and clinical manifestation

➢ Never becomes a chronic illness, but on rare occasions the acute illness damages and destroys so many liver cells causing
fulminant liver failure

➢ FULMINANT LIVER FAILURE- liver no longer function and may cause death

CAUSATIVE AGENT: Hepatitis E virus (HEV)

➢ Single-stranded RNA virus

➢ Inconsistently shed in stools, thus detection is difficult

MODE OF TRANSMISSION

➢ Fecal-oral route and water-borne

➢ Common cause of hepatitis transmitted via intestinal tracts

➢ Spread by drinking contaminated water

➢ Pregnant women have higher risk of dying from fulminant liver failure

➢ Patients who recovered from acute Hepa E infection do not carry HEV- cannot pass the infection to others

CLINICAL MANIFESTATION

➢ Flu-like illness with chills and high fever

➢ Diarrhea, fatigue and abdominal pain

➢ Nausea, vomiting and anorexia

➢ Jaundice and dark colored urine

➢ Pruritus urticaria- skin lesions/infection

➢ Abdominal tenderness, ascites

16. HERPES SIMPLEX

➢ Viral disease characterized by appearance of sores and blisters on skin

➢ Usually occurs around the mouth, nose or genitals and buttocks

➢ “Virus of love”

➢ Related to the viruses that cause infectious mononucleosis, chicken pox and shingles

CAUSATIVE AGENT: Herpes Simplex virus (HSV)

TYPES OF HSV

1. TYPE I HSV- “Oral herpes”

- causes sores around the mouth, lips, nose, chin or cheeks sometimes called as “Fever blisters or cold sores”

-can cause sold sores during infancy or childhood

-can cause genital herpes but most cases are caused by herpes type 2

-patients may barely notice the symptoms or need medical attention for relief of pain

INCUBATION PERIOD: 2-20 days after contact with infected person and usually lasts for 7-10 days

MODE OF TRANSMISSION

⚫ Kissing

⚫ Sharing utensils, towels, clothes or beddings

2. TYPE II HSV- causes genital sores- affecting buttocks, penis, vagina or cervix

- with minor rash or itching, painful sores

- fever, muscular pain and burning sensation during urination may also occur

INCUBATION PERIOD: 2-20 days

MODE OF TRANSMISSION

➢ Sexual contact

➢ Affects about 20% sexually active individual

➢ Can also be spread by skin-to-skin contact

CLINICAL MANIFESTATION

⚫ MILD TO MODERATE

1. ORAL HERPES- in buccal mucosa and tongue

2. LABIAL HERPES- “cold sores” or “fever blisters” on the lips

3. OCULAR HERPES- herpetic keratitis may lead to blindness

4. CUTANEOUS HERPES- affect skin on any part of the body

5. ERYTHEMA MULTIFORME- allergic reaction as a complication of HSV infection

⚫ SEVERE TO FATAL

1. CONGENITAL HERPES- neonatal herpetic infection

- usually acquired from maternal infection at a time of delivery

2. ECZEMA VARICELLIFORME ERUPTION- also called as “Kaposi varicelliform eruption”

- occurs commonly in persons with severe skin disorders (Seborrhic dermatitis)

- common to HIV patients

3. ENCEPHALITIS- most common non-epidemic forms of herpes infection

DIAGNOSTIC PROCEDURES

1. PCR blood test

2. Cell culture

3. Serologic examinations- HSV Antigen

PREVENTIVE MEASURE

➢ Practice universal and standard precaution

➢ Personal hygiene and thorough hand washing

➢ Safe sex

17. HERPES ZOSTER- (“Shingles/Acute Posterior Ganglionitis”)

➢ Highly communicable before appearance of first rash until 5-6 days after the last crust disappears

CAUSATIVE AGENT: Varicella Zoster Virus (VZ virus)

➢ Can cause herpes zoster and varicella/chocken pox

➢ Occurs in partially immune individual due to previous varicella infection

INCUBATION PERIOD: unknown, but clinically believed to be 3-17 days

MODE OF TRANSMISSION

➢ Direct contact through droplet infection and airborne spread

➢ Indirect contact through material or articles freshly soiled by secretions and discharges from infected person

➢ VZ virus lies dormant in certain nerve fibers after the initial exposure- becomes active as a result of aging, stress, immune
suppression, certain medications

CLINICAL MANIFESTATION

➢ Affects the ganglion of the posterior nerve roots or the extra-medullary cranial nerve ganglion

➢ Commonly occurs in thoracic segment of trunK and branches of 5 th and 7th cranial nerves

➢ Trigeminal nerve- 5th cranial nerve

- comprises 3 distinct parts: Opthalmic, maxillary and mandibular

- these nerves provide sensation to the skin of the face and also controls the muscles of mastication

- conditions affecting the trigeminal nerve include: trigeminal neuralgia, cluster headache, trigeminal zoster

➢ Facial expression- 7th cranial nerve

- may manifest as facial palsy

COMMON MANIFESTATION

⚫ VESICULAR LESION- appearance same with chickenpox but unilateral and never crosses the midline of the body

- may last for 1-2 weeks

- with burning or stabbing pain, usually worst at night and intensified by movement

- fever, malaise, anorexia, headache, swollen regional lymph nodes

⚫ GASSERIAN GANGLIONITIS- corneal anesthesia due to affected opthalmic nerve

⚫ RAMSY-HUNT SYNDROME- paralysis of facial nerve and vesicle in external auditory canal

DIAGNOSTIC EXAM

➢ Characteristic skin rash may be diagnostic

➢ TISSUE CULTURE TECHNIQUE- isolating the virus from fluid taken from newly developing vesicles

➢ Smear microscopy of vesicles and fluids

PREVENTION AND CONTROL

➢ Immunization against chicken pox

➢ Avoid exposure to infected patients from either Varicella or Herpes zoster

➢ Increase immune response

18. HOOKWORM DISEASE (Ancylostomiasis/Miner’s disease/ Egyptian Chlorosis)

➢ An intestinal parasite in humans

➢ Occurs mostly in tropical and subtropical countries

➢ Usually causes diarrhea and cramps

CAUSATIVE AGENT: Ancylostoma duodenale- most prevalent in Asia and Europe

Necator americanus- common in central and South America and West Africa

Larval hookworms enter the body by burrowing

through the skin, usually that of the sole of the
foot. The first sign of the disease may appear on
the skin as small eruptions that develop into
pus-filled blisters; this condition is sometimes
called “ground itch.” The hookworms then enter
blood vessels and are carried by the blood into the
lungs. After they leave the lungs, they propel
themselves up the trachea, are swallowed and washed
through the stomach, and end up in the intestines.
Here, if left alone, they will establish a
parasitic relationship, using their host's body as
a source of nourishment.

By the time they reach the intestines, about 6 weeks after they entered the body as larvae, the worms
are full-grown adults. Each worm now attaches itself by hooked teeth to the intestinal wall, where
it sucks its host's blood by contraction and expansion of its gullet. If large numbers of worms are
present, they can cause considerable loss of blood and severe anemia. The symptoms include pallor and
loss of energy; the appetite may increase. The thousands of eggs laid every day by each female worm
pass out of the body in the stool, in which they can easily be seen. If the stool is not properly disposed
of, the larvae that hatch from the eggs may infect other persons.

Ancylostoma duodenale Necator americanus

COMMON NAME Old world hookworm New world hookworm

BODY CURVATURE “C” shaped “S” shaped

DENTAL PATTERN 2 pairs of teeth Semi lunar cutting plate

BURSA Dorsal ray, tridigitate or tripartite Dorsal ray bidigitate or bifid

SPICULE Plain, bristle-like Barbed, fused

HABITAT Small intestine Small intestine

DIAGNOSTIC STAGE Ova Ova

INFECTIVE STAGE L3 (filariform) L3 (filariform)

MOT Skin penetration, transmammary Purely percutaneous

A. Ancylostoma duodenale

➢ Adult A. duodenale worms are grayish white or pinkish with the head slightly bent in relation to the rest of the body.

➢ This bend forms a definitive hook shape at the anterior end for which hookworms are named.

➢ Males measure approximately one centimeter by 0.5 millimeter, the females are often longer and stouter.

➢ Males can be distinguished from females based on the presence of a prominent posterior copulatory bursa

B. Necator americanus

➢ smaller than A. duodenale with males usually 5 to 9 mm long and females about 1 cm long.

INCUBATION PERIOD: 40-100 days/2-8 weeks

➢ Hookworm can appear in stools about 4-6 weeks after larvae penetrate the skin

MODE OF TRANSMISSION

⚫ DIRECT CONTACT- through skin of the foot “ground itch”

⚫ ORAL-FECAL ROUTE- through ingestion of contaminated drinking water or food

CLINICAL MANIFESTATION

⚫ Type of severity of symptoms depend on the number of worms present in the intestine

⚫ Abdominal pain or cramps, diarrhea and anorexia

⚫ IRON DEFICIENCY ANEMIA- due to gradual loss of blood as the worms feed on host’s blood and consume 50 mL daily

⚫ 1 hookworm= 50 mL/day

⚫ Small lesions in intestinal mucosa- since small bits of tissues engulfed by the worms

⚫ Infected children:

-protruding abdomen

-lethargic & often mentally and physically underdeveloped

- malnourished, no energy, weak

- pedal edema may be present

⚫ Allergic reactions such as urticaria or hives (acquired in pets)

DIAGNOSTIC PROCEDURE

⚫ Microscopic examination of feces for the presence of ova or egg

⚫ Blood exam reveals eosinophilia

⚫ Physical examination reveals cutaneous larva migrans

PREVENTION

⚫ Avoid walking barefoot

⚫ Good hygiene and proper sanitation

⚫ Proper food handling and preparation

⚫ Health education on proper disposal of excreta (both humans and animals)

19. INFLUENZA (La Grippe)

➢ Acute viral infectious disease

➢ Affecting the respiratory system

CAUSATIVE AGENT: Myxoviruses Type A, A-prime, B and C

➢ RNA containing virus

➢ Communicable until the 5th day of illness (up to 7th day in children)

INCUBATION PERIOD: 24-48 hours

MODE OF TRANSMISSION

⚫ Airborne spread

⚫ Direct contact- through droplet infection

⚫ Influenza virus persists for hours in dried mucus

CLINICAL MANIFESTATION

⚫ Sudden onset

⚫ High fever, chills, malaise, sore throat, coryza (red eye, watery), rhinorrhea, myalgia, and headache

⚫ May manifest severe aches/pain especially at the bacj associated with sweating

⚫ Sometimes with gastrointestinal symptoms and vomiting

⚫ Superimpose bacterial infections such as pneumonia, sinusitis or otitis (ear), may result as a complications

DIAGNOSTIC PROCEEDURE

⚫ WBC count- high WBC

⚫ Viral serology- complement fixation test

- hemoagglutination test

- neutralization test

⚫ The virus may be cultured from oropharyngeal washings or swabs during the first few days of illnesss

PREVENTION

⚫ Immunization

⚫ Health education on personal hygiene and proper protective barrier apparels

⚫ Avoid crowded places

⚫ Wearing masks esp, during illness

⚫ Cover mouth and nose when sneezing or coughing

A. AVIAN INFLUENZA (Bird flu)

⚫ Type of influenza

⚫ First identified in Italy early 1900s & now known to exist worldwide

⚫ Human deaths from bird flu were unknown until 1997 - 6 people died in Hongkong from the particularly virulent H5N1 strain

⚫ Outbreaks from January - August 2004 in Asia and North America

CAUSATIVE AGENT: Avian influenza (AI) virus

⚫ Has many strains- 15 identified subtypes, but all AI virus belong to influenza virus A

⚫ A genus of orthomyxoviridae family

⚫ Negative-stranded and segmented

⚫ H5N1- most virulent strain

⚫ H1N1- most common strain

MODE OF TRANSMISSION

⚫ Spread rapidly among birds through air or manure- wild fowl as resistant carrier

⚫ No evidence of human to human transmission

⚫ Subtypes H5 and H7 are known to be capable of crossing species barrier- dogs and cats a possible infection vectors for H5N1
strain

⚫ Can be transmitted through contaminated feeds, water, equipment and clothing

⚫ No evidence can survive well-cooked meat

CLINICAL MANIFESTATION

⚫ Some signs and symptoms with human influenza

⚫ Fever, sore throat, cough, and pneumonia in severe cases

⚫ Symptoms vary but virulent strains can cause death within a few days

DIAGNOSTIC PROCEDURES

⚫ REVERSE TRANSCRIPTION-POLYMERASE CHAIN REACTION (RT-PCR)

- To amplify and detect genetic material from the influenza A virus or H5 strain (Asian lineage)

- respiratory secretions or swabs as a specimen

PREVENTION

⚫ Vaccination

⚫ Personal protective equipment especially mask

⚫ Avoid direct or close contact with chickens, or other kinds of birds during epidemic season

20. LEPROSY (Hansens’s disease/Hansenosis)

➢ Chronic systemic function

➢ Characterized by progressive cutaneous lesions

CAUSATIVE AGENT: Mycobacterium leprae

Hansen’s bacillus

➢ Acid-fast bacillus that attacks cutaneous tissue and peripheral nerves- producing skin lesions, infection, anesthesia and
deformities

➢ Not highly contagious and has low infectivity

INCUBATION PERIOD: 5 and 1/2 months-8 years

MODE OF TRANSMISSION

⚫ Respiratory droplets

⚫ Inoculation through skin break and mucous membranes

TYPES AND DISTINCTS FORMS

1. LEPROMATOUS LEPROSY (Multibacillary)

- most serious type and most infectious

- (-) lepromin test but skin lesions contain large amounts of Hansen’s bacillus

- causes damage to respiratory tract, eyes, testes, nerves and skin

- LEPROMA- lesions appear as macules, then become nodular or with plagues in character

- with gradual thickening of the skin

-granulomatous condition develops

- Ulceration in nasal mucous membrane occurs

-slow involvement of peripheral nerves- gradual destruction of nerves and loss of sensation

- Atrophy of skin and muscles, then eventual melting or absorption of small bones- natural amputation may occur

2. TUBERCULOID LEPROSY

- affects peripheral nerves and surrounding skin, especially on the face, eyes and testes

- with rapid involvement of peripheral nerves causing anesthesia

- (+) lepromin test, but bacillus is rarely isolated from the lesions

- elevated macules with clearing at the center and more clearly defines than the lepromatous form

3. DIMORPHOUS LEPROSY (Borderline)

- has the characteristics of both lepromatous and tuberculoid leprosy

- skin lesions are diffused and poorly defined

CLINICAL MANIFESTATION

1. NEURAL INVOLVEMENT- earliest manifestation of leprosy are the results of nerve damage

- loss of sensation, peripheral anesthesia

- claw hand- due to atrophy of hand muscles

- ocular complications due to paralysis of eyelids

2. SKIN

- lepromatous and tuberculoid leprosy differ in cutaneous manifestations

- LEPROMATOUS (lion face)

- start as erythematous macules and papules

-becomes enlarge and form leproma, especially on earlobes, nose, eyebrows and forehead

- TUBERCULOID

-raised, large erythematous plagues appear on skin with clearly defined borders

- becomes rough, hairless, and hypopigmented

-leaving an anesthetic scar

3. EYES

-specific ocular manifestations found in lepromatous and borderline leprosy only

-photophobia, conjunctivitis, iridocytitis, opacity of cornea, insensitivity and ulcerations- can lead to blindness

4. UPPER RESPIRATORY TRACT

- common in lepromatous leprosy

 - epistaxis (nose bleeding), ulcerations of uvula and tonsils

- nasal ulcerations and septal perforations- may result to nasal collapse

5. VICERAL LEPROSY

- heavy concentrations of lesions in liver, lymphs and reticuloendothelial system

- testicular damage occurs in lepromatous leprosy

DIAGNOSTIC PROCEDURE

⚫ LEPEROMIN TEST- a skin test that is used to determine what type of leprosy a person has

-involves the injection of a standardized extract of the inactivated “leprosy bacillus” under the skin.

⚫ Tissue smear and biopsy

⚫ Identification of signs and symptoms

⚫ BLOOD TEST- RBC and ESR, serum calcium, albumin and cholesterol level

PREVENTION AND CONTROL

⚫ Report all cases and suspects of leprosy

⚫ Health education especially to mode of transmission

⚫ Isolation of patients

⚫ Newborn infants should be separated from leprous mothers

⚫ BCG vaccine can be protective when given during the first 6 months of life

21. LEPTOSPIROSIS (Weil’s disease/Canicola fever/Hemorrhagic jaundice/Mud fever/Swine Herd disease/Rat fever)

➢ Zoonotic infectious disease

➢ Carried by both domestic and wild animals

CAUSATIVE AGENT: Leptospira interrogans

➢ A spirochete of the genus Leptospira

➢ Chiefly saprophytic aquatic organism found in river, lake, lake waters, sewage and in sea

➢ With 150 serotypes divided among 18 serogroups- some species are pathogenic to man and animals

➢ WEIL’S DISEASE- specifically caused by serovar “icrterohemmorhagiae”

SOURCE OF INFECTION

➢ Contaminated food and water

➢ Infected wildlife and domestic animals especially rodents

1. RATS

A. Leptospira icterohemorrhagiae- source of Weil’s disease common among miner, sewer, and abattoir

B. Leptospira batavia- some of infection attacking the rice field workers

2. DOGS

A. Leptospitra canicola- common among veterinarians, breeders and dog owners

3. MICE

A. Leptospira grippotyphosa- affects farmers and flax workers

MODE OF TRANSMISSION

⚫ Through ingestion or contact with skin or mucous membrane of infected urine, semen or carcasses of domestic or wild animals

⚫ Transmitted through mucous membrane by the eyes, nose, mouth, and break in the skin

⚫ Common during ir in floody areas

CLINICAL MANIFESTATIONS

⚫ Severity of symptoms- asymptomatic to fatal

1. SEPTIC STAGE

- abrupt onset of remittent fever lasting 4-7 days

- red eyes, severe headache, muscles and joint pain especially legs

- chills, anorexia, abdominal pain

- respiratory distress a severe frustrations

- fever subsides with lysis

2. IMMUNE OR TOXIC STAGE

- can be with or without jaundice lasting for 4-30 days

- iritis, headache, meningeal manifestations such as disorientation and convulsions

- with CSF findings of septic meningitis

- oliguria, and anuria with progressive renal failure

- congestive heart failure, shock and coma in severe causes

- death may occur on 9th-16 days

3. CONVALESCENCE STAGE

- relapse may occur during 4th-5th weeks

LABORATORY DIAGNOSIS

⚫ Leptospira Antigen-Antibody Test (LAAT)

⚫ Leptospira Antibody Test (LAT)

⚫ Liver function test- elevated AST, ALT, GGT

⚫ BUN & creatinine

⚫ ELISA

PREVENTION AND CONTROL

⚫ Environmental sanitation

⚫ Proper drainage system and control of rodents

⚫ Effective information dissemination

⚫ Vaccination of domestic animal

⚫ Treatment of infected person/humans and pets

22. MALARIA (Ague)

➢ Acute and chronic parasitic disease

➢ Confined mainly to tropical and subtropical countries

➢ Causes more disability and heavier economic burden than any other parasitic disease

➢ TROPHOZOITE- a growing stage in the life cycle of some sporozoan parasites, when they are absorbing nutrients from the host.

CAUSATIVE AGENT: Protozoa of Genus Plasmodia

➢ Replicates inside the cell and induces RBC cytolysis, causing the release of toxic metabolic byproducts into the bloodstream that
the host experiences as flulike symptoms.

SPECIFIC SPECIES OF PROTOZOA CAUSING MALARIA:

1. Plasmodium falciparum (malignant tertian)

- most serious malarial infection

- Development of high parasitic densities in the blood (RBC)

- common in the Philippines

- infects RBCs of all ages, resulting to high levels of parasitemia (>5% RBCs infected)

- TROPHOZOITE: normal; Maurer’s cleft (under certain staining conditions)

2. Plasmodium vivax (tertian)

- non-life threatening except for the very and the very old

- manifested by chills every 48 hours on the 3 rd day onward, especially if untreated

- - TROPHOZOITE: enlarged; fine Shuffner’s dot (under certain staining conditions)

3. Plasmodium malariae (quartan)

-less frequently seen than the first 2 types

- non-life threatening

- fever and chills every 72 hours usually on the 4 th day after onset

- TROPHOZOITE: normal; Ziemann’s stippling (under certain staining conditions)

4. Plasmodium ovale (ovale tertian)

-rare type of protozoan species

- rarely seen in the Philippines

- TROPHOZOITE: normal; Shuffner’s dot (under certain staining conditions)

5. Plasmodium knowlesi

-a species that infects primates – has led to human malaria, but the exact mode of transmission remains unclear.

*Female Anopheles mosquito- primary vector of malaria

- breeds in clear, flowing, and shaded streams

- assumes a 30 inches position on walls, trees or curtains

- bigger in size than ordinary mosquito

- usually does not bite a person in motion

LIFE CYCLE

The natural history of malaria involves cyclical infection of humans and female Anopheles mosquitoes. In humans, the parasites
grow and multiply first in the liver cells and then in the red cells of the blood. In the blood, successive broods of parasites grow
inside the red cells and destroy them, releasing daughter parasites (“merozoites”) that continue the cycle by invading other red
cells.
The blood stage parasites are those that cause the symptoms of malaria. When certain forms of blood stage parasites
(gametocytes, which occur in male and female forms) are ingested during blood feeding by a female Anopheles mosquito, they
mate in the gut of the mosquito and begin a cycle of growth and multiplication in the mosquito. After 10-18 days, a form of the
parasite called a sporozoite migrates to the mosquito’s salivary glands. When the Anopheles mosquito takes a blood meal on
another human, anticoagulant saliva is injected together with the sporozoites, which migrate to the liver, thereby beginning a
new cycle.
Thus the infected mosquito carries the disease from one human to another (acting as a “vector”), while infected humans transmit
the parasite to the mosquito, In contrast to the human host, the mosquito vector does not suffer from the presence of the
parasites.

INCUBATION PERIOD:
⚫ P. falciparum- 12 days
⚫ P. vivax & ovale- 14 days
⚫ P. malariae- 30 days

MODE OF TRANSMISSION
⚫ Bite of an infected female Anopheles mosquito
⚫ Blood transfusion and placental transmission

CLINICAL MANIFESTATION
⚫ Paroxysms with shaking chills- abrupt/series attacks; lasts for 12 hours and may attack daily
⚫ Profuse sweating, myalgia, orthostatic hypotension (also known as postural hypotension, occurs when a person's blood
pressure falls when suddenly standing up from a lying or sitting position)
⚫ Splenomegaly, hepatomegaly
⚫ In children: continuous fever, convulsion, GI symptoms, splenomegaly
⚫ Cerebral malaria- is the most severe pathology caused by the malaria parasite, Plasmodium falciparum.
- severe headache, vomiting, changes in sensorium

DIAGNOSTIC PROCEDURES:
⚫ Malarial smear
⚫ Rapid diagnostic test (RDT)- blood test for malaria that can be conducted outside the lab and in the field
- give results within 10-15 minutes
- detects malarial parasite Antigen in the blood

PREVENTION AND CONTROL

⚫ Malarial cases should be reported
⚫ Destruction of breeding grounds of mosquitoes
⚫ Use of mosquito nets
⚫ DEFERRRALS
- Most travelers to an area with malaria are deferred from donating blood for 1 year after their return.
- Former residents of areas where malaria is present will be deferred for 3 years.
- People diagnosed with malaria cannot donate blood for 3 years after treatment, during which time they must have
remained free of symptoms of malaria.
⚫ Proper screening of blood donors

23. PNEUMONIA
➢ Acute infectious disease caused by pneumococcus
➢ an infection that inflames the air sacs in one or both lungs.
➢ A variety of organisms, including bacteria, viruses and fungi, can cause pneumonia.

CAUSATIVE AGENT: Streptococcus pneumoniae- most common bacterial cause

Staphylococcus aureus
Haemophilus influenzae
Klebsiella pneumoniae (Friedlander’s bacilli)
5 MAIN CAUSES OF PNEUMONIA: bacteria, viruses, mycoplasma, other infectious agents, such as fungi, various chemicals

INCUBATION PERIOD: ranges from 1-3 days with sudden onset of shaking chills, rapidly rising fever and stabbing chest pains
aggravated by coughing and respiration

MODE OF TRANSMISSION: droplet infection, indirect contact

CLASSIFICATION of PNEUMONIA:

1. COMMUNITY-ACQUIRED PNEUMONIA- acquired in the course of one’s daily life- at work, at school, or at gym
2. NOSOCOMIAL PNEUMONIA- develops while the client is in the hospital
3. ASPIRATION PNEUMONIA- occurs when a foreign matter is inhaled (aspirated) into the lungs, most commonly when a gastric
content enters the lungs after vomiting
4. PNEUMONIA CAUSED BY OPPORTUNISTIC ORGANISMS- strikes people with compromised immune system

ANATOMICAL CLASSIFICATION OF PNEUMONIA

1. BRONCHOPNEUMONIA (LOBULAR/CATARRHAL PNEUMONIA)- most common type of pneumonia

- infection usually starts from the bronchus and the bronchioles and spreads to the alveoli of the periphery
- lobules are inflamed and consolidated
- sometimes these lobules are not inflamed but are collapsed due to mucopurulent plugging of the bronchioles
- this pneumonia is caused by pneumococcus Klebsiella pneumoniae, and Haemophilus influenzae
- the onset of this type of pneumonia is slow and the fever is lower
- the period of communicability remains unknown, however, it is believed that the disease remains infectious
2. LOBAR PNEUMONIA (CROUPOUS PNEUMONIA)- a consolidation of the entire lobe
- manifested by chills, chest pain on breathing, and cough with blood-streaked sputum (prune-juice/rusty)
- as the disease progresses, the prune-juice color of the sputum may be replaced by thinner/yellow color
- in unfavorable cases, the heart weakens and death occurs from heart failure, edema of the lungs, or severe general
exhaustion
3. PRIMARY ATYPICAL PNEUMONIA (VIRUS PNEUMONIA)- solidification of the lungs that comes in patches
- cough is often delayed in appearing and greenish to whitish secretions are often raised in coughing on 3 rd-5th days

GENERAL CLASSIFICATIONS OF PNEUMONIA

1. Primary pneumonia- produced as a direct result of inhalation or aspiration of pathogen or noxious substance
2. Secondary pneumonia- develops as a complications to a disease

CLINICAL MANIFESTATION
⚫ Sudden onset of chills with rising fever
⚫ Stabbing chest pain aggravated by respirations and coughing
⚫ Paroxysmal or choking cough
⚫ Sputum is rusty/prune juice in color, considered as pathognomonic to pneumonia
⚫ Pain on the abdomen mistaken as appendicitis
⚫ Herpes may appear on the lips
⚫ Body malaise
⚫ Respiratory grunting with marked tachypnea and flaring of the nares
⚫ Labored respiration
⚫ Pulse is rapid and bounding
⚫ Diaphoresis- sweating, especially to an unusual degree as a symptom of disease or a side effect of a drug
⚫ Convulsion and vomiting in children
PATHOGNOMONIC- represents a marked intensification of a "diagnostic" sign or symptom

DIAGNOSTIC PROCEDURE
1. Physical findings for patient with lobar pneumonia
A. Patient has a malar paleness ans dilated pupils with fever, fast respiration and relatively ion pulse
B. Patient’s sputum is rusty with hacking paroxysmal cough
C. Chest movement on affected side is diminished
2. Chest X-Ray
3. Sputum analysis, sputum smear, and culture
4. Blood/serologic exam

PREVENTION AND CONTROL

⚫ Prevent common cold, influenza, and other Upper respiratory infection
⚫ Immunization with pneumonia vaccine
⚫ Environmental factors, such as exposure to cold, pollution, and physical conditions of fatigue/alcoholism

24. POLIOMYELITIS (Infantile Paralysis/Heine-Medin disease)

➢ Acute infectious disease characterized by changes in Central Nervous System which may result in pathologic reflexes, muscle
spasm and paresis or paralysis
➢ about 0.5 percent of cases there is muscle weakness resulting in an inability to move
➢ Lower motor neurons
➢ Anterior horn involvement named “Anterior poliomyelitis”

CAUSATIVE AGENT: Legio debilitans

Filterable virus
Poliovirus

3 STRAINS OF THE VIRUS (affects man alone)

1. Brunhilde
2. Lansing
3. Leon

INCUBATION PERIOD: 7-21 days for paralytic cases with a repeated range if 3-35 days

PERIOD OF COMMUNICABILITY
1. Patient is capable of transmitting the disease during the first 3 days-3 months of illness
2. Disease is most contagious during the first few days of active disease, possibly 3-4 days before

MODE OF TRANSMISSION:
1. Direct contact with infected oropharyngeal secretions and feces
2. Person-to-person transmission through healthy carriers
3. Indirectly, through contaminated articles and flies, contaminated water, food and utensils

PREDISPOSING CAUSES OF POLIOMYELITIS

1. AGE- about 60% of patients are under 10 years of age
2. SEX- males are more prone to the disease than females with a ratio of 3:2. Death is proportionately higher than males.
3. HEREDITY- poliomyelitis is hereditary
4. ENVIRONMENT AND HYGIENIC CONDITION- excessive work, strain, marked over exertion are also factors causing the
disease
TYPES:

1. ABORTIVE TYPE- accounts for about 4-8% of all cases

 A. does not invade the CNS
B. headache and sore throat
C. slight-moderate fever
D. occasional vomiting
E. low lumbar pain
F. the patient is usually recovers within 72 hours

2. NON-PARALYTIC
A. all the above signs
B. spasms of the muscles of the hamstring
C. changes in deep and superficial reflexes
D. pain the neck, back, arms, legs, and abdomen
E. inability to place the head in between the knees
F. positive Pandy’s test (or Pandy's reaction) is done on the CSF (cerebrospinal fluid) to detect the elevated levels of proteins
(mainly globulins).
G. transient paresis may occur
H. usually lasts for about a week, with meningeal irritation persisting for about 2 weeks

3. PARALYTIC
A. signs and symptoms listed above are present
B. positive (+) Hoyne’s sign or Amoss- knees and hips are flexed, the neck is extended and the back is arched.
C. paralysis occurs
D. less tendon reflexes
E. (+) Kernig sign- A sign indicating the presence of meningitis (inflammation of the meninges covering the brain and spinal cord).
It is done by having the person lie flat on the back, flex the thigh so that it is at a right angle to the trunk, and completely extend the
leg at the knee joint. If the leg cannot be completely extended due to pain, this is Kernig sign;
(+) Brudzinski test/sign- sign is one of the physically demonstrable symptoms of meningitis. Severe neck stiffness causes a
patient's hips and knees to flex when the neck is flexed.
F. weakness of the muscle
G. hypersensitive to touch
H. There is usually urine retention, constipation, and abdominal distension

CLASSIFICATION OF PARALYTIC POLIOMYELITIS:

1. SPINAL PARALYTIC- the most common f orm of paralytic poliomyelitis, results from viral invasion of the motor neurons of the
anterior horn cells, or the ventral (front) grey matter section in the spinal column, which are responsible for movement of the
muscles, including those of the trunk, limbs, and the intercostal muscles
- It is characterized by assymetry, scattered flaccid paralysis on one or both lower extremities
- there is autonomic involvement manifested by excessive sweating
- there is respiratory difficulty

2. BULBAR PARALYTIC- usually develops rapidly and is a more serious type

- motor neuron in the brainstem is attacked and affects the medulla. It weakens the muscles supplied by the cranial nerves especially
The 9th (glossopharyngeal)- which partially controls swallowing and functions in the throat, tongue movement, and taste and the
10th (vagus)- which sends signals to the heart, intestines, and lungs
- facial, pharyngeal, and ocular muscles are paralyzed
- respiratory failure and cardiac irregularities
 - hypothalamic dysfunction as manifested by impaired temperature regulation
- encephalitc manifestations are observed in about 30% of patients such as facial weakness, dyspnea, difficulty in chewing, inability
to swallow or expel saliva, regurgitation of food through the nasal passages

3. BULBOSPINAL- also called as respiratory poliomyelitis

- there is involvement of the neurons both in the brainstem and the spinal cord
- The critical nerves affected are the phrenic nerve (which drives the diaphragm to inflate the lungs) and those that drive the
muscles needed for swallowing.

DIAGNOSTIC PROCEDURE
1. Isolation of the virus from throat washings o r swabs early in the disease
2. Stool culture throughout the disease
3. Culture from the cerebrospinal fluid (CSF)

PREVENTION AND CONTROL

1. Immunization- Oral Polio Vaccine (OPV)
2. Proper disposal of gastrointestinal secretions
3. Isolation
4. Implementation of standard precaution
5. Sanitation of the premises and proper food handling should be strictly observed to avoid contamination by flies