PROF. DR. HJ. WAN OMAR ABDULLAH Medical Parasitology Unit,

Faculty of Medicine and Health Sciences,

Universiti Putra Malaysia

I. Introduction to Medical Parasitology & Entomology and Luminal Protozoa

I. Zoological Normenclature:

Entamoeba histolytica

(Genus), (Species)

Causative agent of the disease

-- amebiasis

II. Epidemiology – distribution; endemic;

III. Morphology

IV. Life cycle – Environment, Human, Animals

Developmental stages in environment & human

body . Infective forms to man

V. Symptomatology

VII. Pathology

VIII. Diagnosis

IX. Treatment

X. Prevention and Control

Module: Medical Parasitology & Entomology

PARASITOLOGY- science that deals with organisms that seek shelter

and nourishment on or within other living organisms.

Helmintology – helminths/worms - Metazoa

ENTOMOLOGY – science that deals with

arthropods of medical importance

Protozoology – PROTOZOA – unicellularSTAGES IN LIFE CYCLE OF PROTOZOA

Infective stage – Cysts, Oocysts, Sporozoites, Spores- dormant stages and

Resistant;

Vegetative stage – Trophozoites – take nourishment

from the hosts; invasive causing pathology; most are motile.

PROTOZOA

• According to degree of pathogenicity, protozoa can be categorized into – (I) pathogenic; (2) Non-pathogenic (commensals); (3) whose pathogenicity are debatable.

• 4 types according types of organs for locomotion– Amoebae - pseudopodia; Flagellates - flagella; Ciliates - cilia and Sporozoa – absence of locomototion.

LUMINAL PROTOZOA

- COLONIZE THE LUMINAL ORGANS- intestinal tract and the urogenital tract

- TWO STAGES – i) Trophozoite (vegetatative/invasive); ii) Cyst (infective)

• Entamoeba histolytica – AMOEBIASIS, AMEBIC DYSENTRY; AMOEBIC LIVER ABSCESS

Life cycle: inhabit the large intestine; the cyst is the infective stage. On ingestion – excyst into amoebulae – trophozoites which is the vegitative stage – invade the mucosa to absorb nourishment from tissues dissolved by its cytolytic enzymes and also ingest RBCs.

• Pathology and Symptomatology: primary lesion is ULCER - invasion of the wall of large intestine – ulcer is flask shaped. Complications – amoebic granuloma (amoeboma); appendicitis, stricture, intestinal perforation

• Secondary lesions occur as a result of METASTASIS of trophozoites to extraintestinal organs – liver is most frequently affected – Hepatic amoebiasis; pulmonary amebiasis; cerebral ameobiasis; cutaneous amebiasis; spleenic abscess.

• Symptoms: : Diarrhea; dysentery – stool containing blood, mucous and shreds of necrotic mucosa, acute abdominal pain, tenderness and fever. Chronic ameobiasis – recurrent attacks of dysentery. Abdominal tenderness, HEPATOMEGALY; weight loss and emaciation.

• Ulcer of large intestine Amoebic ulceration Amebic liver abscess

GIARDIA LAMBLIA (INTESTINALIS)

• Disease – giardiasis

• Life cycle: trophozoites in duodenum and proximal jejunum;

and biliary duct.. Attach to intestinal mucosa – Not invasive.

• PATHOLOGY AND SYMPTOMATOLOGY

• Principal lesion – atrophy and shortening of the villi- Factors are still unknown. Possibily the mucosal abnormalities are due to mechanical, toxicity effect – impaired absorption of carotene, folate and vitamin B 12. Production of disaccharidases and other mucosal enzymes are greatly reduced; uptake of bile salts by Giardia inhibits the digestion of fats by pancreatic lipase – Collectively these lead to Malabsorption syndrome. greasy stool clinically refer as STEATORRHEA

• Main symptom is diarrhoea; others are abdominal distension, flatulence, bulky stool and weight loss.

ISOSPORA BELLI - IsosporiasisMan is definitive host- sexual and asexual multiplication takes place in intestinal mucosa. Oocyst are discharged in the stool- infectious to man. An opportunistic infection in patients with AIDS thru ingestion of sporulated oocysts. serious disease characterize by malabsorption syndrome, wt. loss, and even fatal outcome. Int. biopsies – shortened villi, hypertrophied crypts, lamina propria infiltrated with eosinophils, polymorphs and round cells. Atropy (blunting; shortening) of the villi as in in severe giardiasis

CRYPTOSPORIDIUM PARVUMCryptosporidiasis is often the cause of profuse watery diarrhoea in AIDS patients. Produce disease in immunocompetent hosts as well- outbreaks of diarrhoea in veterinary workers dealing with calves; common cause of diarrhoea among travelers and day care centers. Sexual and asexual multiplication in the enterocytes. Oocysts are excreted in patients stool. Clinical symptoms: Diarrhoea, nausea, vomitting, abdominal cramps and fever. Severe fluid loss (dehydration) from diarrhoea and vomitting can lead to a fatal outcome in children.

CYCLOSPORA CAYETANENSIS

Diarrhoeal diseases among travelers and children in slump areas. Most cases are reported in immunodeficient patients. Bowel biopsies revealed intracellular organisms in jejunal enterocytes. Infective form is the oocyst but detail of the life cycle not yet known.

MICROSPORIDIA sp.

Enterocytozoan bieneusi – most common microsporidium causing entritis in AIDS patients, an opportunistic pathogen but can also cause disease in immunocompetent patients. A characteristic feature of microsporidium is the spore with coiled organelle- polar filament, which is extruded from the spore to inject infectious material, the sporoplasm into the host cell to initiate infection. Within an infected cell, a complex process of multiplication takes place, resulting in the production of new spores- 1 to 4 microns in size– require electron microscopy to examine. Excreted via feces and urine.

• BALANTIDIUM COLI• Largest protozoa and only pathogenic ciliate of man. Causing balantidiasis, balantidial

dysentery.

• Lives in the lumen, mucosa and submucosa of the large intestine. Cyst is the the infective form. Trophozoites invade and multiply in the intestinal wall but do not metastasis therefore no extraintestinal complication. Form nests and necrotic ulcers of the large intestine (bigger than the ulcer of E.h). In acute infection, bowel movement is 6 to 15 times of liquid stools per day, with mucus, blood and pus.

• Chronic disease- intermittent diarrhoea alternating with constipation, tender colon, anemia and cachexia. Most infections are asymptomatic.

• .

BLASTOCYSTIS HOMINIS

Lack cell wall, strictly anaerobic and have a variety of

morphologic forms. Sometimes B. h is found in large numbers

in fecal specimen of patients with diarrhoea especially in AIDS

patients. No morphologic or physiologic evidence of pathology

can be attributed to this organism; Bh has been associated

with Irritable Bowel Syndrome (IBS)

DIENTAMOEBA FAGILIS

Amoeboflagellate of the intestinal tract that is found only as

trophozoite (No cyst). Has two nuclei; resembles trichomonads

antigenically and ultrastructurally. Sometimes may ingest

RBCs and produces a moderate, persistent diarrhoea and other

gastrointestinal symptoms.

DIAGNOSIS OF INTESTINAL INFECTIONS WITH PROTOZOA

Clinical dx is based on history of travel to or residence from an endemic area with GIT signs.Parasitological diagnosis- microscopy identification of parasite in feces;Concentration technique – formalin ether; increase the chance of detection especially in very light infectionsigmoidoscope useful in obtaining materials from the intestine microscopy.Intestinal biopsy - Demonstrating intracelluar stages in mucosa and sub mucosa.For Giardiasis (1) Duodenal aspiration – examine the contents; (2) Enterotest (string test) for Giardia- weighted gelatin tied to string- “fish” for giardiaLab. Culture – grow the parasite in media – increase chance of detection.Serological tests – detection of specific antibodies to parasite antigens; detection of parasite antigens e.g ELISA.Hepatic amoebiasis – exploratory puncture and examine for E.h trop.in liver abscess.

CONTROL AND PREVENTION OF INTESTINAL INFECTIONS WITH PROTOZOA

• In general, the prevention of intestinal protozoal infectionsis largely a problem of sanitation and hygiene.

• Infections can be reduced or even eliminated in a community by:

• (1) sanitary disposal of fecal wastes;

• (2) the protection of susceptible individuals,

• (3) treatment of infected individuals;

• (4) wash hands and vegetables;

• (5) Screened toilets and latrines from flies, cockroaches – mechanical vectors

• Cryptosporidium – for vet., med. and lab personnel, contact with infected material must be avoided by use of gloves, gowns and hand-washings. Instruments and equipments should be autoclaved. Disinfect with common bleach (chlorox)

TREATMENT OF INTESTINAL INFECTIONS WITH PROTOZOA

• Amoebiasis

• Carriers should be treated with luminal amoebicide to reduce risk of transmission and protect patient from invasive amoebiasis – Diloxanide;

• Invasive amoebiasis – systemic amoebicide – Metronidazole plus tetracycline in severe cases of amoebic dysentery to lessen the risk of superinfection, int. perforation and peritonitis. Or Chloroquine in combination with metronidazole.

• Giardiasis – Tinidazole in a single dose; Albendazole- also a broad spectrum anthelminthic is currently the drug of choice.

• Cryptosporidium – Spiramycine, 1 gm t.i.d for 2 weeks.

TRICHOMONAS VAGINALIS

Flagelate of the lumen of the urogenital tract- vagina, urethra, epididymis and

prostate. Only trophozoite stage known to exist i. e absence of cyst stage.

Epidemiology: incidence is about 10 – 20 % in women. Higher among women

with poor feminine hygiene. One seventh of female patients complaint of

symptoms; but detection rate in their husbands are low.

Mode of transmission: sexual contact, direct contact with infected female,

contaminated toilet articles eg towels, toilet seats and infection acquired in babies

while passing the birth canal at birth.

Pathology and Symptoms:

Bacterial flora, physiological status of the vagina eg pH are some of the

determining factors.

Causing persistent vaginitis, complain of itching and burning sensation; vaginal

wall is injected, tender, hyperemia, petechial haemorrhage and some areas become

granular – strawberry vagina. The surface is covered with frothy, seropurulent,

creamy or yellowish discharge – leucorrhoea. In males, there may be urethritis

and protato vesiculitis.

Diagnosis: 1. Clinically, symptoms of burning sensation, frothing discharge,

punctate lesions of the vagina; 2. Parasitological-microscopic examination of

motile trichomonads in fresh vaginal discharge and prostate secretion;

3. Laboratory culture- allowing the trichomonads to multiply in numbers and

increase chance of detection.

Treatment:

1.Metronidazole (Flagyl) (note: carcinogenic and mutagenic)

2. Insufflation (powder) or suppositories (pills)

i) silver picrate; ii) furazolidone, iii) iodochlorhydroxyquin

3. Vinegar douches: 1 ounce vineger in a quart of water- trichomonads does poorly at pH below 5.