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State the common bacterial infections of the intestines.
Secretory diarrhoea
• Vibrio cholerae, enterotoxigenic and enterohaemorrhagic E.coli
• Generally non-invasive
• Secretory diarrhoea with no faecal leucocytes
Inflammatory diarrhoea
• Enteroinvasive E.coli, Shigella, Campylobacter, non-typhoidal Salmonella
species
• Readily invade intestinal epithelium
• Provoke intense polymorph reaction
2. Describe the pathological features of tuberculous enteritis. (C2)
primary infection of small intestines
Secondary infection of small intestines
Ilio-caecal tuberculosis
Primary infection
• Inconspicuous intestinal lesion
Gross enlargement of mesenteric lymph nodes
(characteristic of bovine TB in UK, now eliminated through introduction of tubercle-
free herds of cattle and pasteurization of milk)
Describe the pathological features of tuberculous enteritis. (C2)
primary infection of small intestines
Secondary infection of small intestines
Ilio-caecal tuberculosis
Secondary infection
Occur as complication of extensive pulmonary tuberculosis - swallowing infected
sputum
• Ulcer in ileum - typical alimentary lesion
• Ulcers enlarge and follow paths of lymphatic around the circumference of
intestines → encircle the bowel (transverse mucosal ulcers)
• Heals by fibrosis → results in stricture formation in subsequent cicatrisation
• Inflammatory exudate on serosal surface may organize → form fibrous adhesions
Describe the pathological features of tuberculous enteritis. (C2)
primary infection of small intestines
Secondary infection of small intestines
Ilio-caecal tuberculosis
Ilio- caecal tuberculosis
Distinct form of infection
• Ulcerative, granulomatous and fibrotic process occur around ilio-caecal valve
• Variable extension into ileum and caecum
• Thickening and stenosis present picture frequently indistinguishable from
Crohn's disease
• Active intra-intestinal TB can be treated with chemotherapy
• Surgery required for treatment of complications:
• Intestinal obstruction by strictures and adhesions
• Perforation of ulcers and malabsorption due to widespread mucosal
involvement and blockage of lymphatic drainage
Complications of Tuberculous Enteritis
Intestinal obstruction due to kinking by adhesions
Perforation, with "walled-off" or generalized peritonitis
Malabsorption syndrome due to extensive involvement of small bowel and mesenteric
lymphatics, and enteroenteric fistulae
Pathological features of Amoebiasis in large
intestines
Disease of large intestine
• Causative agent: protozoan Entamoeba histolytica common in subtropical regions; affects 10% world's population
• Mode of spread: faeco-oral transmission of amoebic cysts
• Cysts pass unharmed through stomach; cyst wall dissolved on r
active amoebae released
• Cysts secrete cytolytic enzymes - enables passage through intestine
Histologically:
• Lead to deep, flask shaped ulcers,
extending into the submucosa
• Architectural distortion of adjacent
mucosa - mimicking ulcerative colitis
Common sites affected
• Caecum and ascending colon - most involved
• Sigmoid colon, rectum and appendix - may be involved
Complications of amoebic enteritis
Complications:
1. Blood spread may result in liver abscesses - potentially fatal complication
2. Rarely abscesses reach lung and heart by direct extension
3. Spread to kidneys and brain via blood spread
Clinical presentation of amoebic enteritis
1. Asymptomatic - present with mild diarrhoea, dysenteric and invasive infection
2. Occasionally present as acute necrotizing colitis and megacolon
• Both associated with significant mortality