Eaec

Disease Infant diarrhea

Traveler's diarrhea Gastroenteritis (food poisoning) Fever Usually absent

Toxins LT and ST Primary site Small intestine Invasiveness Not invasive Mucosa Intact mucosa pathology

Incidence Common

Infant diarrhea Traveler's diarrhea Persistent diarrhea in children Present No toxins Small intestine Invasive 'Attaching and effacing' lesions 'Pedestals' Common

Dysentery Hemorrhagic colitis Hemolytic uremic syndrome Absent SLT

Large intestine Not invasive 'Attaching and effacing' lesions

Rare

Dysentery

Present No toxins Large intestine Invasive Necrosis and ulcerations similar to Shigella Very rare

Traveler's diarrhea Persisent diarrhea in chilren

Sometimes? ST ('EAST') Small intestine? Not invasive Intact mucosa

Fairly rare?

developed and less developed countries. ETEC diarrhea is often misdiagnosed as a viral diarrhea since ETEC are not detected in stool samples by routine microbiology unless special instructions are given to the clinical laboratory.

ETEC produce several types of pili or fimbriae, such as type 1 pili and a number of specialized pili called colonization factor antigens (CFA), that act as mucosal adhesins enabling ETEC to colonize the small intestine. These CFA are plasmid-encoded. Recently, ETEC have been reported to possess a long polar pilus termed 'longus'. Like V. cholerae, ETEC adhere to the epithelium in the small intestine but do not usually penetrate the intestinal mucosa.

The pathogenesis of ETEC diarrhea involves the colonization of the small intestine by ETEC followed by the elaboration of diarrheagenic enterotoxins. On the intestinal mucosa, ETEC elaborate a heat-labile enterotoxin (LT) inactivated by heating at 100°C for 30 min and a heat-stable enterotoxin (ST). There are two subtypes of LT: plasmid-encoded LT-1 and chromosome-encoded LT-2. LT-1 shares a high degree of amino acid sequence identity with V. cholerae toxin and, like cholera toxin, is a classical AB toxin composed of one A (active) subunit and five B (binding) subunits. The B subunits bind to a specific ganglioside (Gml) on the epithelial cells of the small intestine but are not internalized. The A subunit is subsequently activated by cleavage of a peptide bond and internalized. The A subunit catalyzes the ADP-ribosylation of membrane-bound adenylate cyclase resulting in increased cAMP and increased secretion of fluids and electrolytes. Thus, ETEC produces a watery noninflammatory diarrhea similar to cholera diarrhea.

ST toxins appear to be a group of small peptides ranging from 18 to 50 amino acids in length. ST-I binds to a glycoprotein receptor, thereby activating a membrane-bound guanylate cyclase. The increase in cGMP increases the secretion of fluids and electrolytes to cause an LT-like watery diarrhea. ST-II appears to cause increased fluid secretion by a different mechanism and has been found so far only in porcine ETEC strains. The small ST peptides are nonimmunogenic.

Enteropathogenic E. coli (EPEC) cause only sporadic cases of diarrhea in developed countries bur are a major cause of diarrhea in the Third World, especially in children less than 1 year of age. There are three stages in the pathogenesis of EPEC. In the first stage, EPEC attach to epithelial cells in the small intestine by a 'nonintimate' association facilitated by bundle-forming pili (BFP). The genes responsible for this adherence are located on a plasmid called EAF (EPEC adherence factor). EPEC form microcolonies on the intestinal mucosa during this stage. During the second stage, a signal transduction event is triggered in the host epithelial cell which activates host cell tyrosine kinases resulting in increased host cell intracellular calcium. In the third stage, a protein produced by EPEC called intimin allows EPEC to associate more closely with the host epithelial cells ('intimate' association). This association causes rearrangement of host cell actin resulting in deformation and destruction of epithelial microvilli ('effacement') and the formation of 'pedestal-like' structures of filamentous actin on which EPEC rests. This process is therefore called 'attaching and effacing' and the genes involved are designated eae. EPEC] do not produce LT or ST and diarrhea is probably a consequence of the damaged intestinal epithelial cells no longer being able to absorb water effectively. It is unclear whether EPEC actually invade the intestinal mucosal barrier.

In developed countries, EPEC diarrhea is limited to occasional outbreaks in nurseries and day-care centers. In less developed countries, however, EPEC diarrhea occurs at a high incidence and a high mortality, especially in children 6-12 months old. EPEC is also a recognized cause of chronic diarrhea of children in less developed countries.

Enterohemorrhagic E. coli (EHEC) possess powerful cytotoxins called Shiga-like toxins (SLT-1 and SLT-II), since they are antigenically and functionally similar to the classical Shiga toxin of Shigella dysen teriae. SLT-I is identical to Shiga toxin whereas SLT-II is 56% homologous. SLT is an AB type toxin consisting of one A subunit and five B subunits. The B subunits bind to a membrane glycolipid while the A subunit is internalized and causes cell death by enzy-matically modifying ribosomal RNA thereby preventing elongation factor 1-dependent binding of amino acyl tRNA.

EHEC can cause attaching and effacing lesions similar to EPEC, but the site of EHEC infection is the colon rather than the small intestine. EHEC SLT causes capillary thrombosis and associated inflammation of the colonic mucosa leading to hemorrhagic colitis. There is an acute inflammatory response and mucosal tissue destruction resulting in bloody diarrhea, the hallmark of hemorrhagic colitis. Symptoms usually resolve in 3-10 days.

E. coli 0157:H7 is the EHEC serotype most often associated with hemorrhagic colitis and may produce larger amounts of SLT than other EHEC serotypes. E. coli 0157:H7 hemorrhagic colitis was first recognized in 1982 and appears most prevalently in the USA in the Pacific Northwest, although cases do occur nationwide. Because of these hemorrhagic colitis outbreaks, hospital laboratories now test specifically for E. coli 0157:H7. Most cases of E. coli 0157:H7 have occurred following the ingestion of undercooked ground beef, although other contaminated sources also have been identified. Approximately 1 % of apparently healthy cattle carry E. coli 0157:H7 in their gastrointestinal tracts and meat becomes contaminated during slaughter and in the process of making ground beef. It is now recommended that ground beef be cooked at a temperature of155°C.

Approximately 13% of patients with hemorrhagic colitis, most commonly children between 1 and 4 years of age, develop a sequelae called hemolytic uremic syndrome (HUS). EHEC toxins can cause direct renal endothelial damage and alter platelet function. The kidney damage may be irreversible and even lead to death. HUS is now the leading cause of acute renal failure in children.

Enteroinvasive E. coli (EIEC) is a newly recognized E. coli virotype (since 1971). EIEC cause an invasive dysenteric form of diarrheal disease, similar to that of S. dysenteriae but less severe. EIEC invade the mucosal epithelium of the colon and multiply, behav ing like an intracellular pathogen. No toxins have been identified. Fortunately, EIEC diarrhea is rare, occurring primarily in developed countries in children less than 5 years of age.

Enteroaggregative E. coli (EAEC) is the newest category of diarrhea-causing E. coli and, as the name implies, was first recognized because of the aggregation of EAEC in vivo on intestinal epithelium and also in vitro on certain tissue culture cells. The pathogenesis of EAEC is not understood, but EAEC appear to possess particular adhesins called GWPQ fimbriae, the name derived from the primary amino acid sequence. EAEC also produce a stable toxin called EAST (enteroaggregative ST). EAEC may be a cause of so-called persistent diarrhea of infants and young children.

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