Escherichia coli EnterotoxigenicDevelopingUnknownFoodorfecal-oralInfants,adolescents,SmallintestineSeverewateryDehydration,electrolyte(ETEC)countriestravelers diarrheaimbalancesEnteropathogenicWorldwideHumansFecal-oralInfantsSmallintestineWaterydiarrheaDehydration,electrolyte(EPEC) imbalancesEnterohemorrhagicWorldwideWidespread,includesBeef,milk,produceSporadicandepidemicColonBloodydiarrheaHemolytic-uremicsyndrome(EHEC) cattleEnteroinvasiveDevelopingUnknownCheese,otherYoungchildrenColonBloodydiarrheaUnknown(EIEC)countries foods,waterEnteroaggregativeWorldwideUnknownUnknownChildren,adults,ColonNonbloodydiarrhea,Poorlydefined(EAEC)
PseudomembranousWorldwideHumans,hospitalsAntibioticsallowImmunosuppressed,ColonWaterydiarrhea,Relapse,toxicmegacoloncolitis(C. difficile)
WhipplediseaseRural> urbanUnknownUnknownRareSmallintestineMalabsorptionArthritis,CNSdisease
MycobacterialinfectionWorldwideUnknownUnknownImmunosuppressed,SmallintestineMalabsorptionPneumonia,infectionatotherendemic
CNS, Centralnervoussystem;GI, gastrointestinal.
been endemic in the Ganges Valley of India and Bangladesh for all of recorded history. V. cholerae is transmitted primarily by contaminated drinking water. However, it can also be present in food and causes rare cases of seafood-associated disease. There is a marked seasonal variation in most locales due to rapid growth of Vibrio bacteria at warm temperatures. The only animal reservoirs are shellfish and plankton.
Vibrio organisms are noninvasive but cause disease by producing a toxin that interferes with the absorptive function of enterocytes. Flagellar proteins, which are involved in motility and attachment, are necessary for efficient bacterial colonization, and a secreted metalloproteinase that also has hemagglutinin activity is important for bacterial detachment and shedding in the stool. However, it is the preformed enterotoxin, cholera toxin, which causes disease. The toxin, which is composed of five B subunits that direct endocytosis and a single active A subunit, is delivered to the endoplasmic reticulum by retrograde transport. A fragment of the A subunit is transported from the endoplasmic reticulum lumen into the cytosol, where it interacts with cytosolic ADP ribosylation factors to ribosylate and activate the G protein Gsα. This stimulates adenylate cyclase, and the resulting increases in intracellular cyclic adenosine monophosphate (cAMP) open the cystic fibrosis transmembrane conductance regulator (CFTR), which releases chloride ions into the lumen. This creates an osmotic gradient that draws water into the lumen, leading to massive secretory diarrhea. Remarkably, mucosal biopsy specimens show only minimal morphologic alterations.
Most exposed individuals are asymptomatic or suffer only mild diarrhea. Those with severe disease have an abrupt onset of watery diarrhea and vomiting after an incubation period of 1 to 5 days. The volume of diarrhea may reach 1 L per hour, leading to dehydration, hypotension, electrolyte imbalances, muscular cramping, anuria, shock, loss of consciousness, and death. Most deaths occur within the first 24 hours of presentation. Although the mortality rate for severe cholera is 50% to 70% without treatment, fluid replacement can save more than 99% of patients.