1. Small & Large Bowel: Enterocolitis
GIT Inflammations
Small & Large Bowel: Enterocolitis
Diarrhea: Increase in stool mass / frequency / fluidity**

2. Small & Large Bowel: Enterocolitis
GIT Inflammations
Small & Large Bowel: Enterocolitis
Diarrhea: Increase in stool mass / frequency / fluidity
Causes –
Secretory (increased fluid output > 500 ml fluid stool / day)
- Infections (viral, enterotoxin, neoplasms)
Osmotic (Osmotic force from intestinal solutes) (Reduces on fasting)
Exudative (mucosal destruction)
- Infections (Bacterial, amoebic)
- Idiopathic inflammatory bowel disease
Malabsorption
Deranged motility
Dysentery: Diarrhea accompanied by pain, urgency, blood

3. Small & Large Bowel: Enterocolitis
GIT Inflammations
Small & Large Bowel: Enterocolitis
Common GI viruses : Rotavirus (Group A), Calcivirus, Adenovirus,
Astrovirus
Enteropathogenic Bacteria: Escherichia coli, Salmonella, Shigella,
Campylobacter, Yersinia, Vibrio cholerae,
Clostridium difficile / perfringens, TB
Parasites: Nematodes (round worms), cestodes (Tape worms),
Entamoeba histolytica, Giardia

4. Small & Large Bowel: Enterocolitis
GIT Inflammations
Small & Large Bowel: Enterocolitis
Bacterial Enterocolitis: (Food poisoning) Caused by
Ingestion of preformed toxin (staphylococcus aureus, vibrio,
clostridium perfringens / botulinum). Symptoms develop
within few hours and subsides in a day or two
Infection by toxigenic organisms: incubation period hours / days
followed by diarrhea or dysentery (travelers diarrhea)
Infection by enteroinvasive organisms: Dysentery after incubation
of few days

5. Small & Large Bowel: Enterocolitis
GIT Inflammations
Small & Large Bowel: Enterocolitis
What makes a bacterium enteropathogenic?
Capable of adhesion to bowel mucosa (plasmid encoded proteins)
and replicate
Capable of producing enterotoxins which result in
- Excessive fluid and electrolyte excretion (eg. Cholera toxin)
- Direct tissue damage (cytotoxins) (Shigella toxin)
- Bind to antigen receptors on T cells in the mucosa and induce
production of cytokines which in turn stimulate motility and
fluid secretion.
Capable of tissue invasion (E coli, Salmonella, Yersinia)

6. GIT Inflammations – Typhoid fever
Etiologic agent: Salmonella typhi, paratyphi A and B
Flagellated gram negative bacillus with O and H antigens
Bacteria excreted in stool, urine, vomitus
Transmitted through the fecal – oral route
Capable of causing local and systemic effects
Potentially life threatening
Chronic asymptomatic carrier state also can exist

7. Systemic manifestations (fever) and Abscesses in many tissues
Infected food / water Colonize in lower bowel
Invade bowel through M cells Initial proliferation of bacteria
( incubation)
(Primary bacteremia)
Travel to RE system, gall bladder and proliferate Secondary bacteremia
(first week of fever)
Systemic manifestations (fever) and Abscesses in many tissues
Resolution of fever

9. MONONUCLEAR CELLS AND MACROPHAGES
Pathology of bowel
Incubation period – mild edema, congestion, hyperplasia of lymphoid tissue
Invasive phase – Dilated small bowel, mucosal hyperemia, serosal exudate widespread Peyer’s patch hyperplasia with invasion by macophages (typhoid or Mallory cells)
Stage of febrile illness (Fastigium) – Mounting immune mechanisms, release of toxins, ulceration of the intestinal lymphoid tissues, (widespread necrotizing typhoid nodules in various organs)
MONONUCLEAR CELLS AND MACROPHAGES

12. Early fastigium: Peyers patches are raised, convoluted and shaggy

13. Fastigium: Mucosa is bile stained. Peyers patches are hemorrhagic
Can result in perforation / massive internal hemorrhages

14. Typhoid – Clinical features:
General symptoms like fever, malaise, chills, anorexia, headache, diarrhea
Bradycardia; Leucopenia
Complications: meningitis, endocarditis, osteomyelitis, disseminated abscesses, splenic rupture, intestinal perforation
In silent carriers (1-5%) , bacteria colonize in gall bladder and are excreted in the stool and urine

15. Mary Mallon (Typhoid Mary) (1869-1938)
Mallon was what's known as a healthy carrier-a person who is contagious but has no symptoms. She had probably come down with a mild, undetected case of typhoid fever in 1900 and had retained active germs ever since.

16. Lab Diagnosis of Typhoid fever
First Week of fever : Blood culture 80-90% positive
Second Week of fever : Stool and urine culture 80% positive
Widal test 50% positive
Third Week of fever : Stool and urine culture 80% positive
Widal test % positive
Carrier : Stool and Urine Culture

17. Incubation Invasion Fastigium Lysis Convalesc
80-90%
Blood culture
Stool / urine culture
Widal test
80%
20% % %
Days
Organisms multiply Septicemia Ulceration and necrosis Body defenses Recovery
in gut in gut

18. Tuberculosis of GIT Major health problem in the developing world
Incidence increasing in association with AIDS
Earlier, there was high association between pulmonary and GI TB
Now GI tuberculosis may exist even with normal lung findings
GIT infection may occur by
Infected unpasteurized milk
Swallowing of infected sputum in patients with active lung lesions
Hematogenous spread from lung lesion
Direct spread from neighbouring areas

19. Tuberculosis of GIT GIT infection may be PRIMARY (not common nowadays)
Infected unpasteurized milk (M bovis).
Pathology will be mainly in mesenteric lymph nodes.
Small transient Gohn focus in gut
- Enlarged caseous lymphnodes (tabes mesenterica)
- Healing with fibrosis and calcification
- Tuberculous peritonitis

20. Tuberculosis of GIT GIT infection may be SECONDARY
Swallowing of infected sputum in patients with active lung lesions
Hematogenous spread from lung lesion
Direct spread from neighbouring areas

21. GIT Tuberculosis
Presents as
Nonhealing ulcers on tongue / oropharynx
Esophageal stricture, fistula
Gastric ulcer, wall thickening
Small bowel ulcers, stricture, perforation, fistula, obstruction
Large bowel ulcers, obstruction, diarrhoea
Anal canal ulcer, fistula, abscess

22. Tuberculosis of GIT - Secondary
- Bowel lesions are more prominent than lymphnode lesions
- Begin in Peyer patches / lymphoid follicles (ulcers), spread through lymphatics and form large transverse ulcers

23. Ulcerative (60%) (ulcers are transverse)
Ileocecal region – 90%
Three forms
Ulcerative (60%) (ulcers are transverse)
Hypertrophic (hyperplastic) (10%) (may mimic carcinoma)
Ulceroproliferative (30%)
Ulcers are typically circumferential (typhoid is longitudinal)
Microscopy Complications

24. Amoebiasis
(Entamoeba histolytica)
Protozoan parasite
Transmission – Fecal oral
Trophozoites attach to colonic epithelium and induce apoptosis, invade colonic crypts and enter lamina propria
Create typical flask shaped ulcers due to proteolytic enzymes and other proteins
Diagnosis by stool examination

25. Flask shaped ulcers
More of necrosis
Less of inflammation