Infections of the GI and Diarrheal Illness
Clinical Syndromes
1. Gastritis - inflammation of the stomach - pain in the upper abdomen, sometimes bleeding
2. Gastroenteritis - inflammation of stomach & intestines - primarily diarrhea, sometimes
nausea, vomiting, crampy abdominal pain
3. Colitis - intestinal syndrome that primarily involves the colon or large intestines.
4. Enterocolitis - inflammation of mucosa of both large & small intestine = dysentery - diarrhea
often contains blood & mucus.
5. Hepatitis - liver damage causes a clinical syndrome called hepatitis. Patients with hepatitis
become jaundiced because bilirubin builds up in their bodies.
Pathogens
Cause disease by 3 mechanisms:
a. action of toxins
b. adherence to & effacement of microvilli  inflammation
c. invasion of intestinal epithelial cells
A. Toxins cause disease – microbes are not present in the body
Toxin types
Action on intestine/intestinal cells
Enterotoxin
results in net secretion w/out intestinal damage
Cytoskeleton-altering toxin
alters cell shape, may injure cells but is not lethal
Cytotoxin
causes cell damage and ultimately cell death
Neural toxin
alters smooth muscle activity in intestines
1. Bacterial Food Poisoning - Intoxications NOT infections –
a. Clostridium botulinum - botulism - canned foods, spores survive 5 hrs boiling & germinate
under anaerobic conditions in can  neural toxin  gut – binds to epithelial cell and is
transported across  bloodstream  presynaptic regions (disease of CNS, symptoms begin 1248h)
b. Staphylococcus aureus - most common – 2 different heat [100ºC for 30 min] & enz stable
enterotoxins stimulate vegus nerve (so also a neural toxin) of stomach lining  emetic response
(vomiting),w or w/o diarrhea 30 min to 8 hrs after ingestion. These toxins also function as
superantigens and stimulate T cells to over secrete IL2. 1ug of toxin is enough to induce
symptoms, can be achieved when # of Staph in food reaches 1,000/gram. Resolves within 24h.
c. Bacillus cereus
2 distinct presentations caused by two different toxins – only one is atrue intoxication
 emetic – cereulide (an enterotoxin) targets vagus nerve nausea & vomiting 1-5 hrs after
ingestion of toxin - lasts ~1-6 hrs. can be difficult to distinguish from S. aureus food poisoning.
B. True infections – microbes enter and then colonize the GI - 3 mechanisms for damage
1. Pathogens colonize epithelial surfaces of small intestine & then release toxins
Vibrio cholera - cholera
Source Pathology
1. Ingestion of large numbers (> 108)
2. Flagella & mucinase allow Vibrio to reach epithelial cells
3. Attachment by way of fimbriae to receptors on brush border & crypt cells of small intestine
4. Damage due to production of toxin called cxt that is an ADP ribosyl transferase. Toxin binds
to receptors for the glycolipid GM1 ganglioside by the B subunit & A enters epithelial cells 
disrupts adenylate cyclase (cxt - enterotoxin, cytotoxin, neural toxin)
5. Secretion of large quantities of Cl- into intestine, causing H2O & and Na+ to follow 
hypersecretion of fluids & electrolytes
Incubation –
Symptoms -
Txt -
Also
enterotoxigenic E. coli strains (ETEC) - traveler’s diarrhea – 2 enterotoxins – LT-1 similar to
cholera toxin. ST – activates guanylate cyclase activity  increase in cGMP  increased fluid
secretion.
B. cereus – ingested diarrheal toxin produced in the small intestine (cytotoxin targets villi 
villus necrosis)  diarrhea 8-16.5 hrs after ingestion
2. Pathogens attach to and enter epithelial cells, multiply intracellularly & destroy (efface)
microvilli of epithelial cells (may release toxins), and induce diarrhea.
Shigella spp. (dysenteriae, boydii, flexneri, sonnei) – shigellosis - 14,581 U.S. / 212 MI
Source Pathology
1. Ingestion - only 10 organisms required - most effective of bacterial pathogens of GI
2. Adhere specifically to epithelial cells of colon by way of outer membrane proteins (OMP)
3. Induce parasite-directed endocytosis by M cells of GALT (Gut Associated Lymphoid Tissue)
that transport Shigella across intestinal epithelium
4. Phagocytized by macrophages but escape from phagolysosome into cytoplasm
5. Trigger macs to produce IL-1, also triggers apoptosis
6. IL-1 induces inflammation & stimulates edema & extravasation of neutrophils (PMNs) across
epithelial barrier.
7. movement of PMNs across destroys the epithelial barrier & Shigella can now move across in
massive number.
8. Further induce prod of cytokines & intense inflammation w/ destruction of epithelium
S. dystenteriae also secretes a cytotoxin
Incubation –
Symptoms -
Txt –
Complications -
Also
Enterohemorrhagic E. coli (EHEC) including E. coli O157:H7 4,323 U.S ./ 158 MI
Human diarrhoeal viruses (rotavirus, Norwalk virus) - gastroenteritis
Virus replicates in intestinal epithelial cells, damages transport mechanisms in the gut, leads to
loss of water, salt, glucose  diarrhea
Infected cells are destroyed but no inflammation, no blood. Shed at rate of 1,000 million virus
particles/g feces.
Campylobacter  enteritis + diarrhea
Entamoeba histolytica  amoebic dysentery
3. Pathogen attaches to, enters, & multiplies in deep tissues that are normally sterile submucosal or subepithelial tissues – sometimes will spread systemically.
Salmonella enteritidis, S. typhimurium  salmonellosis 44,468 U.S. / 911 MI
Salmonella typhi, paratyphi – invasive species  typhoid fever
Source Pathology
1. Ingestion of large numbers (105-109)
2. Attach specifically to fibronectin of epithelial cells of small intestine
3. Transported by M cells of GALT
4. Invade gut wall  ulcerations & hemorrhage. Also spread to intestinal lymphatics & are
phagocytized by macs but escape from phagolysosome into cytoplasm
5. Produces toxin that increase cAMP & fluid secretion  loose, watery diarrhea & nausea
(enterotoxin and cytoskeletal altering toxin)
6. Causes influx of PMN (nontyphoid) that confines infection to GI
7. OR influx of macrophages (typhoid) and systemic spread
S typhi organisms spread through the reticuloendothelial system, mainly to the liver, spleen,
and bone marrow. Within 14 days, the bacteria appear in the bloodstream, facilitating
secondary metastatic foci (eg, spleen, heart). In some patients, gallbladder infection leads to
long-term carriage of S typhi or S paratyphi in bile and secretion to the stool
Salmonellosis
Incubation –
Symptoms –
Txt Complications –
Also
Hepatitis A virus - 1,849 cases U.S. / 70 MI
Reoviruses
Enteroviruses (includes poliovirus)