Amoebae Medical Parasitology PDF

AMOEBAE MEDICAL PARASITOLOGY CLASSIFICATION The clinically relevant protozoa are divided into four groups: Amebas Flagellates Ciliates Sporozoa ENTAMOEBA HISTOLYTICA 'amoebic dysentery' and 'amoebic liver abscess’. E. histolytica is worldwide in prevalence, being much more common in...

AMOEBAE MEDICAL PARASITOLOGY CLASSIFICATION The clinically relevant protozoa are divided into four groups: Amebas Flagellates Ciliates Sporozoa ENTAMOEBA HISTOLYTICA 'amoebic dysentery' and 'amoebic liver abscess’. E. histolytica is worldwide in prevalence, being much more common in the tropics than elsewhere It has been reported that about 10% of world population and 50% of the inhabitants of developing countries may be infected with the parasite It is the third leading parasitic cause of mortality, after malaria and schistosomiasis MORPHOLOGY Entamoeba histolytica occurs in 3 forms: Trophozoite Precyst Cyst. TROPHOZOITE Trophozoite is the vegetative or growing stage of the parasite It is the only form present in tissues. It is irregular in shape and varies in size from 12–60 μm; average being 20 μm. It is large and actively motile in freshly-passed dysenteric stool, while smaller in convalescents and carrriers. Cytoplasm: Outer ectoplasm is clear, transparent, and refractile. Inner endoplasm is fi nely granular, having a ground glass appearance. TROPHOZOITE Pseudopodia are fi nger-like projections formed by sudden jerky movements of ectoplasm in one direction, followed by the streaming in of the whole endoplasm. Typical amoeboid motility is a crawling or gliding movement and not a free swimming one. Nucleus is spherical 4–6 μm in size and contains central karoyosome TROPHOZOITE The trophozoites from acute dysenteric stools often contain phagocytosed erythrocytes. This feature is diagnostic as phagocytosed RBCs are not found in any other intestinal amoebae. The trophozoites divide by binary fission in every 8 hours Trophozoites survive upto 5 hours at 37°C and are killed by drying, heat, and chemical sterilization. Therefore, the infection is not transmitted by trophozoites. Even if live trophozoites from freshy-passed stools are ingested, they are rapidly destroyed in stomach and cannot initiate infection. PRECYSTIC STAGE Trophozoites undergo encystment in the intestinal lumen. Encystment does not occur in the tissues nor in feces outside the body. Before encystment, the trophozoite extrudes its food vacuoles and becomes round or oval It contains a large glycogen vacuole and two chromatid bars. It then secretes a highly retractile cyst wall around it and becomes cyst. A. Trophozoite; B. Precystic stage; C. Uninucleate cyst; D. Binucleate cyst; E. Mature cyst CYSTIC STAGE The cyst is spherical in shape about 10–20 μm in size. The early cyst contains a single nucleus and two chromatid bars The mature cyst contains 4 nuclei “quadrinucleate” With iron hemotoxylin stain, nuclear chromatin and chromatoid bodies appear deep blue or black With iodine stain, the nuclear chromatin and karyosome bright yellow, and the chromatoid bodies appear as clear space, being unstained. LIFE CYCLE E. histolytica passes its life cycle only in 1 host-man Infective form: Mature quadrinucleate cyst Mode of transmission: Man acquires infection by swallowing food and water contaminated with cysts The cysts pass through the stomach undamaged and enter the small intestine Excystation: When the cyst reaches lower part of the ileum, the cyst wall is damaged by trypsin, leading to excystation LIFE CYCLE Metacyst stage: The cytoplasm gets detached from the cyst wall and amoeboid movements appear which quadrinucleate amoeba is liberated. Metacystic trophozoites: The nuclei undergo division to form 8 nuclei, each of which gets surrounded by its own cytoplasm to become 8 small metacystic trophozoites The optimal habitat for the metacystic trophozoite is the submucosal tissue of caecum and colon Some develop into precystic forms and cysts, which are passed in feces to repeat the cycle PATHOGENESIS E. histolytica causes intestinal and extraintestinal amoebiasis. Incubation period is highly variable. On an average, it ranges from 4 days to 4 months. Amoebiasis can present in different forms and degree of severity, depending on the organ affected and the extent of damage caused. INTESTINAL AMOEBIASIS The metacystic trophozoites penetrate the columnar epithelial cells of the colon. Penetration of the amoeba is facilitated by the motility of the trophozoites and the tissue lytic enzyme, histolysin, which damages the mucosal epithelium. Mucosal penetration by the amoeba produces discrete ulcers with pinhead center and raised edges. Sometimes, the invasion remains superfi cial and heals spontaneously. More often, the amoeba penetrates to submucosal layer and multiplies rapidly, causing lytic necrosis and thus forming an abscess. INTESTINAL AMOEBIASIS The abscess breaks down to form an ulcer. Amoebic ulcer is the typical lesion seen in intestinal amoebiasis The ulcers are multiple and are confi ned to the colon, being most numerous in the caecum and next in the sigmoidorectal region. Ulcers appear initially on the mucosa as raised nodules with pouting edges. They later break down discharging brownish necrotic material containing large numbers of trophozoites. The typical amoebic ulcer is flask-shaped in cross section, with mouth and neck being narrow and base large and rounded. INTESTINAL AMOEBIASIS The ulcers generally do not extend deeper than submucosal layer, but amoebae spread laterally in the submucosa causing extensive undermining and patchy mucosal loss. Amoebae are seen at the periphery of the lesions and extending into the surrounding healthy tissues. Occassionally, the ulcers may involve the muscular and serous coats of the colon, causing perforation and peritonitis. The deep ulcers form scars which may lead to strictures, partial obstruction, and thickening of the gut wall. This amoebic granuloma or amoeboma may be mistaken for are malignant tumor. CLINICAL FEATURES The incubation period is highly variable from 1–4 months. The clinical course is characterized by prolonged latency, relapses and intermissions. The typical intestinal amoebiasis is amoebic dysentery. The stools are large, foul-smelling, and brownish black, often with bloodstreaked mucus intermingled with feces. The RBCs in stools are clumped and reddish-brown in color. E.histolytica trophozoites can be seen containing ingested erythrocytes. CLINICAL FEATURES The patient is usually afebrile and nontoxic. In fulminant colitis, there is confluent ulceration and necrosis of colon. The patient is febrile and toxic. Intestinal amoebiasis does not always result in dysentery. Quite often, there may be only diarrhea or vague abdominal symptoms popularly called ‘uncomfortable belly’ or ‘growling abdomen.’ Chronic involvement of the caecum causes a condition simulating appendicitis. EXTRAINTESTINAL AMOEBIASIS Hepatic Amoebiasis Pulmonary Amoebiasis Metastatic Amoebiasis Cutaneous Amoebiasis Genitourinary Amoebiasis HEPATIC AMOEBIASIS Several patients of amoebic colitis develop an enlarged tender liver without detectable impairment of liver function or fever. It is probable that liver damage may not be caused directly by the amoebae, but by lysosomal enzymes and cytokines from the inflammatory cells surrounding the trophozoites. In about 5–10% of persons with intestinal amoebiasis, liver abscesses may ensue. The center of the abscess contains thick chocolate brown pus (anchovy sauce pus), which is liquefi ed necrotic liver tissue. HEPATIC AMOEBIASIS Liver abscess may be multiple or more often solitary, usually located in the upper right lobe of the liver. Jaundice develops only when lesions are multiple or when they press on the biliary tract. Untreated abscesses tend to rupture into the adjacent tissues through the diaphragm into the lung or pleural cavity, pericardium, peritoneal cavity, stomach, intestine, or inferior vena cava or externally through abdominal wall and skin. The incidence of liver abscess is less common in women and rare in children under 10 years of age. PULMONARY AMOEBIASIS Hepatobronchial fistula usually results with expectoration of chocolate brown sputum. Amoebic empyema develops less often. The patient presents with severe pleuritic chest pain, dyspnea, and non-productive cough. TREATMENT Luminal amoebicides: Diloxanide furoate, iodoquinol, paromomycin, and tetracycline act in the intestinal lumen but not in tissues. Tissue amoebicides: Emetine, chloroquine, etc. are effective in systemic infection, but less effective in the intestine. Dosage of chloroquine in amoebic liver abscess is 1 g for 2 days followed by 5 g daily for 3 weeks. Both luminal and tissue amoebicides: Metronidazole and related compounds like tinidazole and ornidazole act on both sites and are the drug of choice for treating amoebic colitis and amoebic liver abscess PROPHYLAXIS General prophylaxis is as for all fecal-oral infections. Food and water have to be protected from contamination with human exc reta. Detection and treatment of carriers and their exclusion from food handling occupations will help in limiting the spread of infection. Health education and inclusion of healthy personal habits helps in control.