GIT InflammationsSmall & Large Bowel: Enterocolitis

Diarrhea: Increase in stool mass / frequency / fluidity**

GIT InflammationsSmall & 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

GIT InflammationsSmall & 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

GIT InflammationsSmall & 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

GIT InflammationsSmall & 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

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

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

11

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

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% positiveThird Week of fever : Stool and urine culture 80% positive

Widal test 70 - 90% positive

Carrier : Stool and Urine Culture

Incubation Invasion Fastigium Lysis Convalesc

Days 1 6 14 19Organisms multiply Septicemia Ulceration and necrosis Body defenses Recovery

in gut in gut

Blood cultureStool / urine culture

Widal test

80-90%

80%

20% 50% 70-90%

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

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