Invasive
Enteritis
(Local Invasion)
Barriers to GIT infection:
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Stomach acidity (low pH).
Mucus layer and gut motility (peristalsis)→ prevent
adhesion.
The glycocalyx (mucin rich layer) covers the epithelial
cells surface→ entrap invading bacteria.
Shedding of mucosal epithelium lining the GIT.
Bile secretion prevent the growth of non-enteric
bacteria and enveloped viruses.
M cells (microfold) of Peyer’s patches which have a
surveillance function (sampling).
Normal flora of intestinal tract.
Secretory IgA.
Establishment of Infections in the Digestive System:
Changes in the defense mechanisms:
o Changes in stomach acidity:
Shigella species and E.coli O157:H7
(Enterohemorrhagic E. coli) are acid resistance →
need low pathogenic dose.
Increase of gastric pH by surgery or proton-pump
inhibitors: decrease pathogenic dose of acid sensitive
pathogen. e.g. Salmonella species and V. cholerae.
o Alterations of normal flora; broad spectrum
antibiotics.
- Invasion of gut by virulent microbial strains.
- Pseudomembrance colitis; Clostridium difficile.
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o Anatomic alterations:
• Obstructions of secretions flow (gallbladder
stones).
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Surgery may create intestinal “blind loops” where
there is no moving stream of intestinal contents.
- Absence of flushing action of intestinal secretions
will lead to bacterial overgrowth syndrome (fat
malabsorption, diarrhoea, vitamins deficiency).
Infection and type of Site
diarrhea
Etiology
Secretory warty diarrhea:
Copious, no tissue
invasion,
no blood, no pus.
Small intestine
V. cholerae, Enterotoxigenic E.
coli, EPEC, ETEC, B. cereus
(diarrheal syndrome),
C. perfringens.
Bloody watery diarrhea:
copious, tissue invasion,
few pus, blood-tinged,
Ileum, colon
Salmonella, Campylobacter
jejuni, Yersinia.
Hemorrhagic colitis:
Colon
copious, bloody, no pus, no
tissue invasion.
EHEC, EIEC
Dysentery: small volume,
blood, mucus, pus stool.
Tissue invasion.
Shigella, Entamoeba histolytica
(no pus in the stool).
Colon
Dysentery
Causative agents of dysentery:
• Entamoeba histolytica (amoebic dysentery, protozoa).
• Shigella dysenteriae (bacillary dysentery).
Shigella dysentery:
- Gram negative, non motile, non capsulated bacilli.
- Four serotypes:
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S. dysentery .
S. flexneri.
S. boydii.
S. sonnei.
S. dysentery type 1 is the most sever.
- Reservoir: human colon only (no animal carriers).
- Transmission: person to person fecal-oral.
- Pathogenic dose: less than 200 CFU.
- Incubation period: 2-3 days.
Pathogenesis of Shigella dysenteriae:
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Shigella resist stomach acidity and pass the small
intestine to reach the colon → invade M cells →
engulfed by the microphage where they multiply until
they rupture → infect the epithelia and pass from cell
to cell by actin polymerization → cell death and
slough (shallow ulcers→ mucus+ blood in the stool).
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Dying macrophages release IL-1→ neutrophils
attraction (pus in stool) and marked inflammation.
Shigella produce shiga toxin type I which inhibit
protein synthesis → epithelial and endothelial death→
more bleeding ulcers.
 If shiga toxin reach the blood: hemolytic-uremic
syndrome:
about 5–10 days after onset of diarrhea, oliguria,
hematuria, kidney failure, thrombocytopenia and
destruction of red blood cells.
Symptoms:
Fever, lower abdominal pain, tenesmus, small volume
diarrhea bloody with mucus.
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Hemorrhagic Colitis: Enterohemorrhagic E. coli:
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Reservoir: cattle; bovine feces, pork.
Transmission: food (hamburger, beef burger), contaminated
water and milk, person- person fecal-oral.
• Pathogenic dose: 10-100 CFU. Incubation period: 3-5 days.
Pathogenesis:
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EHEC resist stomach acidity, bind to the colon cells and
multiply outside the cells, damage the cells in the same way
as EPEC.
Produce verotoxin (shiga like toxin)→ inhibit protein
synthesis → epithelial and endothelial death →
hemorrhagic colitis (profuse bloody diarrhea, no pus cells
in the stool).
Shiga like exotoxins; Hemolytic-uremic syndrome.
No tissue invasion so no pus cells in the stool.
Symptoms: hemorrhagic diarrhea without fever.
Bloody Watery Diarrhea: Salmonella, C. jejuni,
Yersinia
A- Campylobacter jejuni infection:
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Microbiology: gram negative spiral, microaerophilic
bacilli.
Reservoir: intestinal tracts of animals esp. poultry,
cattle, sheep, pigs.
Transmission: fecal-oral (direct contact), ingestion of
contaminated meat (poultry), contaminate water , or
unpasteurized milk.
Incubation period: 3-5 days.
Pathogenic dose: 500- 9000 CFU.
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Pathogenesis: invasion and sloughing of the intestinal
cells (jejunum, ilium then colon)→ pus and blood in
the stool.
• Symptoms: fever, abdominal pain, diarrhea ranging
from watery to bloody.
Symptoms may resemble acute appendicitis or
ulcerative colitis.
• Complications: 1-2 weeks after diarrhea (Ag cross
reactivity)
 Aseptic arthritis.
 Guillian-Barr syndrome: demyelination →
progressive, fairly symmetric muscle weakness
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B- Salmonella Enteriditis and Salmonella
Typhimurium:
Reservoir:
- Animals: poultry; chicken, reptiles, and cattle.
- Human: short term carriage.
Transmission:
• Ingestion of infected chicken products (under cooked
chicken, eggs).
• Fecal-oral from patients and carriers.
Pathogenic dose: 106 – 108 (less in achlrohydria and in
those who on antibiotics)
Incubation period: 6-48 hours.
Pathogenesis:
Invade the ileocecal epithelia, M cells and the lymphoid
tissue→ multiply and produce vacuoles → cells death
→ watery diarrhea.
Salmonella survive inside the macrophage →production
of TNF & IL-8 → PMN cells infiltration prevent
mesenteric lymph node and RES invasion and damage
the intestinal epithelial cells→ fever, abdominal pain
and bloody diarrhoea.
Salmonella Typhimurium can reach the blood stream in
sickle cell patients.
C- Yersinia enterocolitica & Y. pseudotuberculosis
Microscopy and cultural characteristics:
Gram negative short coccobacilli. Can grow in room
temperature and refrigerator.
-Invade terminal ileum→ necrotic lesions in Peyer’s
patches (ileitis simulate acute appendicitis) .
Engulfed by dendritic cells→ mesenteric
lymphadenopathy.
- Occasionally cause sever typhoid like illness which is
usually fatal.
Laboratory Diagnosis:
Specimens:
- Stool samples, occasionally rectal swabs.
Use Cary-Blair transport media if delay ≥ 30 minutes is
expected.
- Macroscopic, microscopic and culture.
Macroscopic:
- Consistency (formed, unformed (soft) or liquid)
- Color (white, yellow, brown or black)
- Presence of any abnormal components (e.g. mucus or
blood).
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Microscopy:
For the presence of pus cells, RBCs and bacteria in stool.
- Pus cells >50 cells/ HPF + RBCs → shigellosis.
- Pus cells < 20 cells /HPF + RBCs → salmonellosis,
Campylobacter, Yersinia and invasive E. coli.
- Pus cells 2–5 cells / HPF + RBCs → Enterohemorrhagic
E. coli.
- Pus cells 2–5 cells / HPF without RBCs→ cholera,
Enterotoxigenic and Enteropathogenic E. coli, and viral
diarrhoea.
- In amoebic dysentery the pus cells are mostly
degenerated (ghost cells).
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Culture:
Culture media:
• Mildly selective: MacConkey agar.
• Highly selective: XLD (xylose-lysine-deoxycholate).
• Campylobacter agar: for isolation of Campylobacter.
Incubate in 37Co for 48 hours.
Incubate Campylobacter agar at 42oC and
microaerophilic conditions.
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Identification:
o E. Coli → Lactose fermenter→ yellow colonies on
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XLD.
Shigella, and Yersinia → non-lactose fermenters
→pale colonies on XLD.
Salmonella → non-lactose fermenters → pale
colonies with black dots.
Campylobacter jejuni: gram negative spiral shaped
bacilli that is microaerophilic. (10% CO2, 5% O2,
and 85% N2).
Yersinia: motile when grown at 25C, but not at 37C.
Enterobacteriaceae family: gram negative bacilli that
are oxidase negative.
Can be identified by ordinary tests (oxidase, motility,
indole, sugar fermentation…..) or API 20E.
Serological identification and serotyping.
E. coli on XLD (lactose fermenter,
non H2S producer)
Shigella on XLD (non lactose fermenter,
non H2S producer)
Salmonella on XLD (non lactose
fermenter, H2S producer)
API test
Treatment of bloody diarrhea:
- Rehydration, electrolyte replacement and good
nutrition.
- Drugs to control the hyper-motility are
contraindicated→ septicemia and death.
- Antibiotics:
A. 3rd generation cephalosporins (ceftriaxone or
cefotaxime) given for very young infants, very old
patients and immunocompromised.
B. Quinolones as ciprofloxacin for adult patients.