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Transcript of L15 amebiasis
- 1.AmebiasisTuberculosisTyphoidEnterocolitis (Diarrheal diseases)Infectious EnterocolitisLecture 15
2. Amebiasis(Amebic Dysentery)Causal agent: Entamoeba histolytica is well recognizedas a pathogenic amoeba.Geographic Distribution: Worldwide, with higherincidence of amebiasis in developing countries.In industrialized countries, risk groups include malehomosexuals, travelers and recent immigrants, andinstitutionalized populations.History: Loosh was first described in 1875 3. Epidemiology Prevalence of amebic infection varies with level of sanitationand generally higher in tropics and subtropics than intempearate climates. *Worldwide prevalence is about 10% to 50% *Cyst passers are important source of infection The true estimated prevalence of E. histolytica is close to 1%worldwide. Entamoeba histolytica is the second leading cause ofmortality due to parasitic disease in humans. (The first beingmalaria). Amebiasis is the cause of an estimated 50,000-100,000 deaths each year. 4. Transmission 1-driect contact of person to person( fecal-oral) 2- Veneral transmission among homosexualmales( oral-anal 3- Food or drink contaminated with feces containingthe E.his. cyst 4- Use of human feces (night soil) for soil fertilizer 5- contamination of foodstuffs by flies, and possiblycockroaches 5. Pathogenesis Effective factores: 1- strain virulence: 2- susceptibility of the host; nutrition status, immune-sys. 3- breakdown of immunologic barrier (tissue invasion) 6. Clinical symptomsAsymptomatic infection Symptomatic infectionIntestinal Amebiasis Extraintestinal AmebiasisDysenteric Non-Dysenteric colitis Hepatic Pulmonary The extra fociLiver abscces Acut nonsupprativeIntestinal Amebiasis symptoms: Diarrhea or dysentery, abdominal pain, cramping , anorexia,weight loss, chronic fatigue 7. E. histolytica cysts, which have a chitin wall andfour nuclei, are resistant to gastric acid, acharacteristic that allows them to pass throughthe stomach without harm. 8. Morphology Amebiasis is seen most frequently in thececum and ascending colon,although the sigmoid colon, rectum, andappendix can also be involved. 9. Dysentery develops when the amebae attachto the colonic epithelium, induce apoptosis,invade crypts, and burrow laterally into thelamina propria. 10. This recruits neutrophils, causes tissuedamage, and creates a flask-shapedulcer with a narrow neck and broad base. 11. Histologic diagnosis can be difficult, sinceamebae are similar to macrophages in sizeand general appearance. 12. Parasites may penetrate splanchnic vesselsand embolize to the liver to produceabscesses in about 40% of patients withamebic dysentery. 13. Amebic liver abscesses, which can exceed 10cm in diameter, have a scant inflammatoryreaction at their margins and a shaggy fibrinlining. 14. Extra-ntestinalAmebiasis 15. Pyogenic- Liver Abscess 16. Liver abscess 17. This is an amebic abscess of liver. Abscesses may arise in liver when there is seeding ofinfection from the bowel, because the infectious agents are carried to the liver from theportal venous circulation. 18. The abscesses persist after the acuteintestinal illness has passed and may, rarely,reach the lung and the heart by directextension from the liver. 19. AMEBIC COLITIS Simulate ulcerative colitis or Crohns disease Gross: ulceration covered by exudate, with normalintervening mucosa Site: cecum and ascending colon L/M: nonspecific Flask shaped ulcer, Trophozoites of E. histolytica Erythrocytosis by trophozoites usually present Can be detected by Heidenhains iron hematoxylinstain and PAS 20. Amebae may also spread via thebloodstream into the kidneys and brain. 21. Clinical features Abdominal pain, bloody diarrhea, or weightloss. Occasionally, acute necrotizing colitisand megacolon occur, and both areassociated with significant mortality. 22. Treatment The parasites lack mitochondria or Krebscycle enzymes and are thus obligatefermenters of glucose. Therefore,metronidazole, which inhibits the enzymepyruvate oxidoreductase that is required forfermentation, is the most effectivetreatment. 23. Mycobacterium Tuberculosis Pathogenic Mechanism: Invasion, mural inflammatory foci withnecrosis and scarring. Source: Contaminated milk, swallowing ofcoughed-up organisms 24. Clinical features Chronic abdominal pain, complications ofmalabsorption, stricture, perforation, fistulas,hehmorrhage. 25. Morphology Ingested Mycobacterium tuberculosis inciteschronic inflammation and granulomaformation in mucosal lymphoid tissue--particularly Peyers patches in the terminalileum and regional lymph nodes 26. TUBERCULOSIS Site: ileocecal area Gross: ulceration with diffuse fibrosisextending through wall stenosis andobstruction Tuberculous peritonitis L/M: ulceration, granuloma and desmoplasia Vasculitis, non-specific, diffuse, chronicinflammation with fibrosis AFB for definite diagnosis 27. TYPHOID FEVER Typhoid fever, also referred to as entericfever, is caused by Salmonella typhi andSalmonella paratyphi. 28. Source Milk, beef, eggs, poultry. 29. MorphologyEnlarged Peyers patches in the terminal ileumMesenteric lymph nodes are also enlarged. 30. Neutrophils accumulate within thesuperficial lamina propria, and macrophagescontaining bacteria, red blood cells, andnuclear debris mix with lymphocytes andplasma cells in the lamina propria. 31. Mucosal shedding creates oval ulcers,oriented along the axis of the ileum, thatmay perforate. The draining lymphnodes also harbor organisms and areenlarged due to phagocyte accumulation.