1. Amebiasis
Tuberculosis
Typhoid
Enterocolitis (Diarrheal diseases)
Infectious Enterocolitis
Lecture 15

2. 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

3. 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.

4. 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

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 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

7. • 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.

8. Morphology
• Amebiasis is seen most frequently in the
cecum and ascending colon,
although the sigmoid colon, rectum, and
appendix can also be involved.

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

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

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

13. • Parasites may penetrate splanchnic vessels
and embolize to the liver to produce
abscesses in about 40% of patients with
amebic dysentery.

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

15. Extra-ntestinalAmebiasis

16. Pyogenic- Liver Abscess

18. Liver abscess

19. 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.

21. • 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.

22. 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

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

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

25. 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.

26. Mycobacterium Tuberculosis
• Pathogenic Mechanism:
• Invasion, mural inflammatory foci with
necrosis and scarring.
• Source: Contaminated milk, swallowing of
coughed-up organisms

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

28. 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

29. 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

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

31. Source
• Milk, beef, eggs, poultry.

32. Morphology
Enlarged Peyer’s patches in the terminal ileum
Mesenteric lymph nodes are also enlarged.

33. • 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.

34. • 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.