Chapter17: INTESTINES:Infectious Enterocolitis Flashcards
Enterocolitis can present with a broad range of symptoms including what?
diarrhea, abdominal pain,
urgency, perianal discomfort, incontinence, and hemorrhage( Table 17-7 ).
This global problem is responsible for more than 12,000 deaths per day among children in developing countries and half of all deaths before age 5 worldwide.
Bacterial infections, such as enterotoxigenic
Escherichia coli, are frequently responsible, but the most common pathogensvary with age,
nutrition, and host immune status as well as environmental influences( Table 17-7 ).
For example, epidemics of cholera are common in areas with poor sanitation, as a result of inadequate public health measures, or as a consequence of natural disasters or war.
Pediatric infectious diarrhea, which may result in severe dehydration and metabolic acidosis, is commonly caused by enteric viruses.
TABLE 17-7 – Features of Bacterial Enterocolitides
Infection Type
- Cholera
- Campylobacter spp.
- Shigellosis
- Salmonellosis
- Enteric (typhoid) fever
- Yersinia spp.
- Escherichia coli
- Enterotoxigenic
(ETEC) - Enterohemorrhagic
(EHEC) - Enteroinvasive (EIEC)
- Enteroaggregative
(EAEC)
- Enterotoxigenic
- Pseudomembranous
colitis (C. difficile - Whipple disease
- Mycobacterial infection
TABLE 17-7 – Features of Bacterial Enterocolitides
Geograph
- Cholera: India, Africa
- Campylobacter spp. :Developed countries
- Shigellosis : Developing countries
- Salmonellosis: Worldwide
- Enteric (typhoid) fever: India, Mexico, Phillipines
- Yersinia spp. : Northern and central Europe
- Escherichia coli
- Enterotoxigenic (ETEC)
- Developing countries
- Enterohemorrhagic (EHEC)
- Worldwide
- Enteroinvasive (EIEC)
- Developing countries
- Enteroaggregative (EAEC)
- Worldwide
- Enterotoxigenic (ETEC)
- Pseudomembranous colitis (C. difficile: colitis (C. difficile): Developing countries
- Whipple disease: Rural > urban
- Mycobacterial infection: Worldwide
TABLE 17-7 – Features of Bacterial Enterocolitides
Reservoir
- Cholera: Shellfish
- Campylobacter spp. Chickens, sheep, pigs, cattle
- Shigellosis :Humans
- Salmonellosis: Poultry, farm animals, reptiles
- Enteric (typhoid) fever: Humans
- Yersinia spp. : Pigs
-
Escherichia coli
-
Enterotoxigenic (ETEC)
- Unknown
-
Enterotoxigenic (ETEC)
-
Enterohemorrhagic (EHEC)
- Widespread, includes cattle
-
Enteroinvasive (EIEC)
- Unknown
-
Enteroaggregative (EAEC)
- Unknown
- Pseudomembranous colitis (C. difficile: colitis (C. difficile):Humans, hospitals
- Whipple disease: Unknown
- Mycobacterial infection: Unknown
TABLE 17-7 – Features of Bacterial Enterocolitides
Transmission
- Cholera: Fecal-oral, water
-
Campylobacter spp.: Poultry, milk,
other foods - Shigellosis :Fecal-oral, food, water
- Salmonellosis: Meat, poultry, eggs, milk
-
Enteric (typhoid) fever: Fecal-oral,
water - Yersinia spp. : Pork, milk, water
-
Escherichia coli
-
Enterotoxigenic (ETEC)
- Food or fecaloral
-
Enterohemorrhagic (EHEC)
- Beef, milk, produce
-
Enterotoxigenic (ETEC)
-
Enteroinvasive (EIEC)
- Cheese, other foods, water
-
Enteroaggregative (EAEC)
- Unknown
- Pseudomembranous colitis (C. difficile: colitis (C. difficile):Antibiotics allow emergence
- Whipple disease: Unknown
- Mycobacterial infection: Unknown
TABLE 17-7 – Features of Bacterial Enterocolitides
Epidemiology
- Cholera:Sporadic, endemic, epidemic
- Campylobacter spp.: Sporadic; children, travelers
- Shigellosis :Children
- Salmonellosis: Children, elderly
- Enteric (typhoid) fever: Children. adolescents, travelers
- Yersinia spp. : Clustered cases
-
Escherichia coli
-
Enterotoxigenic (ETEC)
- Infants, adolescents, travelers
-
Enterohemorrhagic (EHEC)
- Sporadic and epidemic
-
Enteroinvasive (EIEC)
- Young children
-
Enteroaggregative (EAEC)
- Children, adults, travelers
-
Enterotoxigenic (ETEC)
- Pseudomembranous colitis (C. difficile: colitis (C. difficile):Immunosuppressed, antibiotic-treated
- Whipple disease: Rare
- Mycobacterial infection:Immunosuppressed
TABLE 17-7 – Features of Bacterial Enterocolitides
Affected GI Sites
- Cholera:Small intestine
- Campylobacter spp.: Sporadic;
- Shigellosis :Left colon, ileum
- Salmonellosis: Colon and small intestine
- Enteric (typhoid) fever: Small intestine
- Yersinia spp. :Ileum, appendix, right colon
-
Escherichia coli
-
Enterotoxigenic (ETEC)
- Small intestine
- Enterohemorrhagic (EHEC)
- Colon
-
Enteroinvasive (EIEC)
- Colon
-
Enteroaggregative (EAEC)
- Colon
-
Enterotoxigenic (ETEC)
- Pseudomembranous colitis (C. difficile: colitis (C. difficile):Colon
- Whipple disease: Small intestine
- Mycobacterial infection:Small intestine
TABLE 17-7 – Features of Bacterial Enterocolitides
Symptoms
- Cholera:Severe watery diarrhea
- Campylobacter spp.: Watery or bloody diarrhea
- Shigellosis : Bloody diarrhea
- Salmonellosis: Watery or bloody diarrhea
- Enteric (typhoid) fever: Bloody diarrhea, fever
- Yersinia spp. :Abdominal pain, fever, diarrhea
-
Escherichia coli
-
Enterotoxigenic (ETEC)
- Severe watery diarrhea
-
Enterohemorrhagic (EHEC)
- Bloody
diarrhea
- Bloody
-
Enteroinvasive (EIEC)
- Bloody diarrhea
-
Enteroaggregative (EAEC)
- Nonbloody diarrhea,afebril
-
Enterotoxigenic (ETEC)
- Pseudomembranous colitis (C. difficile: colitis (C. difficile):Watery diarrhea, fever
- Whipple disease: Malabsorption
- Mycobacterial infection:Malabsorption
TABLE 17-7 – Features of Bacterial Enterocolitides
Complications
- Cholera: Dehydration, electrolyte imbalances
- Campylobacter spp.: Arthritis, Guillain-Barré syndrome
- Shigellosis :Reiter syndrome, hemolyticuremic syndrome
- Salmonellosis: Sepsis, abscess
- Enteric (typhoid) fever: Chronic infection, carrier state, encephalopathy, myocarditis
- Yersinia spp. :Autoimmune, e.g., Reiter syndrome
-
Escherichia coliEnterotoxigenic (ETEC)
- Dehydration, electrolyte imbalances
-
Enterohemorrhagic (EHEC)
- Hemolyticuremic syndrome
-
Enteroinvasive (EIEC)
- Unknown
-
Enteroaggregative (EAEC)
- Poorly defined
- Pseudomembranous colitis (C. difficile: colitis (C. difficile):Relapse
- Whipple disease: Arthritis, CNS disease
-
Mycobacterial infection:Pneumonia,
infection at other sites
Describe the Vibrio cholerae.
Vibrio cholerae are comma-shaped, Gram-negative bacteria that cause cholera, a disease that
has been endemic in the Ganges Valley of India and Bangladesh for all of recorded history.
Since 1817, seven great pandemics have spread along trade routes to large parts of Europe, Australia, and the Americas, [56] but, for unknown reasons these pandemics resolved and cholera retreated back to the Ganges Valley.
Cholera also persists within the Gulf of Mexico.
What is the MOT of V. cholerae?
is primarily transmitted by contaminated drinking water.
However, it can also be present in food and causes sporadic cases of seafood-associated disease in North America.
Why is there a marked seasonal variation of Vibrio cholerae?
There is a marked seasonal variation in most climates due to rapid growth of Vibrio bacteria at warm temperatures
What is the only reservoir of V. cholerae?
the only animal reservoirs are shellfish and plankton.
Relatively few V. cholerae serotypes are pathogenic, but other species of Vibrio can also cause disease.
For example, V. parahaemolyticus is the most common cause of seafood-associated gastroenteritis
in North America
What is the pathogenesis of V.cholerae?
Despite the severe diarrhea, Vibrio organisms are non-invasive and remain within the intestinal
lumen.
A preformed enterotoxin, cholera toxin, encoded by a virulence phage and released by
the Vibrio organism, causes disease, but flagellar proteins, which are involved in motility and
attachment,arenecessary for efficient bacterial colonization.
Hemagglutinin, a metalloproteinase, is important for bacterial detachment and shedding in the stool.
What is the mechanism that induces diarrhea in Cholerae toxin?
The mechanism by which cholera toxin induces diarrhea is well understood ( Fig. 17-27 ).
Cholera toxin is composed of five B subunits and a single A subunit.
The B subunit binds GM1 ganglioside on the surface of intestinal epithelial cells, and is carried by endocytosis to the endoplasmic reticulum, a process called retrograde transport. [58]
Here, the A subunit is reduced by protein disulfide isomerase, and a fragment of the A subunit is unfolded and released.
This peptide fragment is then transported into the cytosol using host cell machinery that moves misfolded proteins from the endoplasmic reticulum to the cytosol.
Such unfolded proteins are normally disposed of via the proteasome, but the A subunit refolds to avoid degradation.
The refolded A subunit peptide then interacts with cytosolic ADP ribosylation factors (ARFs) to ribosylate and activate the stimulatory G protein Gsα.
This stimulates adenylate cyclase and the resulting increases in intracellular cAMP open the cystic fibrosis transmembrane conductance regulator, CFTR, which releases chloride ions into the lumen.
This causes secretion of bicarbonate, sodium, and water, leading to massive diarrhea.
Chloride and sodium absorption are also inhibited by cAMP. Remarkably, mucosal biopsies show only
minimal alterations.

FIGURE 17-27 Mechanisms of cholera toxin transport and signaling. After retrograde toxin
transport to the endoplasmic reticulum (ER), the A subunit is released by the action of
protein disulfide isomerase (PDI) and is then able to access the epithelial cell cytoplasm. In
concert with an ADP-ribosylation factor (ARF), the A subunit then ADP-ribosylates Gsα, which
locks it in the active, GTP-bound state. This leads to adenylate cyclase (AC) activation, and
the cAMP produced opens CFTR to drive chloride secretion and diarrhea
What are the clinical features of V.cholerae?
Most exposed individuals are asymptomatic or develop only mild diarrhea.
In those with severe disease there is an abrupt onset of watery diarrhea and vomiting following an incubation period of 1 to 5 days.
The voluminous stools resemble rice water and are sometimes described as having a fishy odor.
The rate of diarrhea may reach 1 liter per hour, leading to dehydration, hypotension, muscular cramping, anuria, shock, loss of consciousness, and death.
Most deaths occur within the first 24 hours after presentation.
Although the mortality for severe cholera is
about 50% without treatment, timely fluid replacement can save more than 99% of patients. Oral
What is the treatment for V.cholerae?
Oral rehydration is often sufficient. [59]
Because of an improved understanding of the host and
Vibrio proteins involved, new therapies are being developed including CFTR inhibitors that
block chloride secretion and prevent diarrhea. [60] Prophylactic vaccination is a long-term goal.
What is the most common bacterial enteric pathogen in developed countries and important cause of traveler’s diarrhea?
Campylobacter jejuni
Campylobacter jejuni is mostly associatd with ingestion of what?
Most infections are associated
with ingestion of improperly cooked chicken, but outbreaks can also be caused by unpasteurized milk or contaminated water.
What is the pathogenesis of Campylobacter infection?
remains poorly defined, but four major virulence
properties contribute:
- motility,
- adherence,
- toxin production, and
- invasion.
What is the function of Flagella in the pathogenesis of Campylobacter jejuni?
Flagella allow Campylobacter to be motile.
This facilitates adherance and colonization, which are necessary for mucosal invasion.
What causes the epithelial damage in the pathogenesis of C. jejuni?
Cytotoxins that cause epithelial damage and a cholera toxin–like enterotoxin are also released by some C. jejuni isolates.
What is the reason for the dysentery in Campylobacter jejuni?
Dysentery is generally associated with
invasion and only occurs with a small minority of Campylobacter strains.



