Amebiasis Tuberculosis

Typhoid

Enterocolitis (Diarrheal diseases)Infectious Enterocolitis

Lecture 15

Amebiasis(Amebic Dysentery)

Causal agent: Entamoeba histolytica is well recognized as a pathogenic amoeba.

Geographic Distribution: Worldwide, with higher incidence of amebiasis in developing countries. In industrialized countries, risk groups include male homosexuals, travelers and recent immigrants, and institutionalized populations.

History: Loosh was first described in 1875

Epidemiology• Prevalence of amebic infection varies with level of sanitation

and generally higher in tropics and subtropics than in tempearate 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 of mortality due to parasitic disease in humans. (The first being malaria). 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 homosexual

males( oral-anal• 3- Food or drink contaminated with feces containing

the E.his. cyst• 4- Use of human feces (night soil) for soil fertilizer• 5- contamination of foodstuffs by flies, and possibly

cockroaches

Pathogenesis• Effective factores:• 1- strain virulence:

• 2- susceptibility of the host; nutrition status, immune-sys. • 3- breakdown of immunologic barrier (tissue invasion)

Clinical symptoms Asymptomatic infection Symptomatic infection Intestinal Amebiasis Extraintestinal Amebiasis

Dysenteric Non-Dysenteric colitis Hepatic Pulmonary The extra foci

Liver abscces Acut nonsupprative

Intestinal Amebiasis symptoms: Diarrhea or dysentery, abdominal pain, cramping , anorexia, weight loss, chronic fatigue

• E. histolytica cysts, which have a chitin wall and four nuclei, are resistant to gastric acid, a characteristic that allows them to pass through the stomach without harm.

Morphology• Amebiasis is seen most frequently in the

cecum and ascending colon, although the sigmoid colon, rectum, and appendix can also be involved.

• Dysentery develops when the amebae attach to the colonic epithelium, induce apoptosis, invade crypts, and burrow laterally into the lamina propria.

• This recruits neutrophils, causes tissue damage, and creates a flask-shaped ulcer with a narrow neck and broad base.

• Histologic diagnosis can be difficult, since amebae are similar to macrophages in size and general appearance.

• Parasites may penetrate splanchnic vessels

and embolize to the liver to produce abscesses in about 40% of patients with amebic dysentery.

• Amebic liver abscesses, which can exceed 10 cm in diameter, have a scant inflammatory reaction at their margins and a shaggy fibrin lining.

Extra-ntestinalAmebiasis

Pyogenic- Liver Abscess

Liver abscess

This is an amebic abscess of liver. Abscesses may arise in liver when there is seeding of infection from the bowel, because the infectious agents are carried to the liver from the portal venous circulation.

• The abscesses persist after the acute intestinal illness has passed and may, rarely, reach the lung and the heart by direct extension from the liver.

AMEBIC COLITIS

• Simulate ulcerative colitis or Crohn’s disease• Gross: ulceration covered by exudate, with normal

intervening 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 hematoxylin

stain and PAS

• Amebae may also spread via the bloodstream into the kidneys and brain.

Clinical features

• Abdominal pain, bloody diarrhea, or weight loss. Occasionally, acute necrotizing colitis and megacolon occur, and both are associated with significant mortality.

Treatment

• The parasites lack mitochondria or Krebs cycle enzymes and are thus obligate fermenters of glucose. Therefore, metronidazole, which inhibits the enzyme pyruvate oxidoreductase that is required for fermentation, is the most effective treatment.

Mycobacterium Tuberculosis

• Pathogenic Mechanism:• Invasion, mural inflammatory foci with

necrosis and scarring.• Source: Contaminated milk, swallowing of

coughed-up organisms

Clinical features

• Chronic abdominal pain, complications of malabsorption, stricture, perforation, fistulas, hehmorrhage.

Morphology

• Ingested Mycobacterium tuberculosis incites chronic inflammation and granuloma formation in mucosal lymphoid tissue --particularly Peyer’s patches in the terminal ileum– and regional lymph nodes

TUBERCULOSIS

• Site: ileocecal area• Gross: ulceration with diffuse fibrosis

extending through wall→ stenosis and obstruction

• Tuberculous peritonitis• L/M: ulceration, granuloma and desmoplasia• Vasculitis, non-specific, diffuse, chronic

inflammation with fibrosis• AFB for definite diagnosis

TYPHOID FEVER

• Typhoid fever, also referred to as enteric fever, is caused by Salmonella typhi and Salmonella paratyphi.

Source

• Milk, beef, eggs, poultry.

Morphology

Enlarged Peyer’s patches in the terminal ileum

Mesenteric lymph nodes are also enlarged.

• Neutrophils accumulate within the superficial lamina propria, and macrophages containing bacteria, red blood cells, and nuclear debris mix with lymphocytes and plasma cells in the lamina propria.

• Mucosal shedding creates oval ulcers, oriented along the axis of the ileum, that

may perforate. The draining lymph nodes also harbor organisms and are enlarged due to phagocyte accumulation.