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

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

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

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

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)

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

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

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

Early fastigium: Peyers patches are raised, convoluted and shaggy

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

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

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.

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 70 - 90% positive Carrier : Stool and Urine Culture

Incubation Invasion Fastigium Lysis Convalesc 80-90% Blood culture Stool / urine culture Widal test 80% 20% 50% 70-90% Days 1 6 14 19 Organisms multiply Septicemia Ulceration and necrosis Body defenses Recovery in gut in gut

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

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

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

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

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

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

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

Flask shaped ulcers More of necrosis Less of inflammation