L15 amebiasis
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L15 amebiasis

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L15 amebiasis L15 amebiasis Presentation Transcript

  • AmebiasisTuberculosisTyphoidEnterocolitis (Diarrheal diseases)Infectious EnterocolitisLecture 15
  • 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
  • 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.
  • 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
  • Pathogenesis• Effective factores:• 1- strain virulence:• 2- susceptibility of the host; nutrition status, immune-sys.• 3- breakdown of immunologic barrier (tissue invasion)
  • 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
  • • 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.
  • Morphology• Amebiasis is seen most frequently in thececum and ascending colon,although the sigmoid colon, rectum, andappendix can also be involved.
  • • Dysentery develops when the amebae attachto the colonic epithelium, induce apoptosis,invade crypts, and burrow laterally into thelamina propria.
  • • This recruits neutrophils, causes tissuedamage, and creates a flask-shapedulcer with a narrow neck and broad base.
  • • Histologic diagnosis can be difficult, sinceamebae are similar to macrophages in sizeand general appearance.
  • • Parasites may penetrate splanchnic vesselsand embolize to the liver to produceabscesses in about 40% of patients withamebic dysentery.
  • • Amebic liver abscesses, which can exceed 10cm in diameter, have a scant inflammatoryreaction at their margins and a shaggy fibrinlining.
  • Extra-ntestinalAmebiasis
  • Pyogenic- Liver Abscess
  • Liver abscess
  • 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.
  • • The abscesses persist after the acuteintestinal illness has passed and may, rarely,reach the lung and the heart by directextension from the liver.
  • AMEBIC COLITIS• Simulate ulcerative colitis or Crohn’s 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 Heidenhain’s iron hematoxylinstain and PAS
  • • Amebae may also spread via thebloodstream into the kidneys and brain.
  • Clinical features• Abdominal pain, bloody diarrhea, or weightloss. Occasionally, acute necrotizing colitisand megacolon occur, and both areassociated with significant mortality.
  • 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.
  • Mycobacterium Tuberculosis• Pathogenic Mechanism:• Invasion, mural inflammatory foci withnecrosis and scarring.• Source: Contaminated milk, swallowing ofcoughed-up organisms
  • Clinical features• Chronic abdominal pain, complications ofmalabsorption, stricture, perforation, fistulas,hehmorrhage.
  • Morphology• Ingested Mycobacterium tuberculosis inciteschronic inflammation and granulomaformation in mucosal lymphoid tissue--particularly Peyer’s patches in the terminalileum– and regional lymph nodes
  • 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
  • TYPHOID FEVER• Typhoid fever, also referred to as entericfever, is caused by Salmonella typhi andSalmonella paratyphi.
  • Source• Milk, beef, eggs, poultry.
  • MorphologyEnlarged Peyer’s patches in the terminal ileumMesenteric lymph nodes are also enlarged.
  • • Neutrophils accumulate within thesuperficial lamina propria, and macrophagescontaining bacteria, red blood cells, andnuclear debris mix with lymphocytes andplasma cells in the lamina propria.
  • • 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.