Download GIT Infections and Ulcers

GIT Inflammations
Small & Large Bowel: Enterocolitis
Diarrhea: Increase in stool mass / frequency / fluidity**
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
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
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
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
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
Early fastigium: Peyers patches are raised, convoluted and shaggy
12
Fastigium: Mucosa is bile stained. Peyers patches are hemorrhagic
Can result in perforation / massive internal hemorrhages
13
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
Third Week of fever
Widal test 50% positive
: 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%
Days
Organisms multiply
in gut
1
50%
6
Septicemia
70-90%
14
Ulceration and necrosis
in gut
Body defenses
19
Recovery
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