Chapter 192 Escherichia coli
Escherichia coli are important causes of enteric infections as well as urinary tract infections (Chapter 532), sepsis and meningitis in the newborn (Chapter 103), and bacteremia and sepsis in immunocompromised patients (Chapter 171) and in patients with intravascular devices (Chapter 172).
Because E. coli are normal fecal flora, pathogenicity is defined by demonstration of virulence characteristics and association of those traits with illness (Table 192-1). The mechanism by which E. coli produces diarrhea typically involves adherence of organisms to a glycoprotein or glycolipid receptor, followed by production of some noxious substance that injures or disturbs the function of intestinal cells. The genes for virulence properties and for antibiotic resistance are often carried on transferable plasmids, pathogenicity islands, or bacteriophages. In the developing world, the various diarrheagenic E. coli cause frequent infections in the first few years of life. They occur with increased frequency during the warm months in temperate climates and during rainy season months in tropical climates. Most diarrheagenic E. coli strains (except STEC) require a large inoculum of organisms to induce disease. Infection is most likely when food-handling or sewage-disposal practices are suboptimal. The diarrheagenic E. coli are also important in North America and Europe, although their epidemiology is less well defined in these areas than in the developing world. Recent data in North America suggest that the various diarrheagenic E. coli could be the etiology of as much as 30% of infectious diarrhea in children <5 yr of age.
Enterotoxigenic Escherichia Coli
ETEC account for a sizeable fraction of dehydrating infantile diarrhea in the developing world (10-30%) and of traveler’s diarrhea (20-60% of cases). ETEC are also responsible for 3-39% of overall diarrhea episodes in children in the developing world. The typical signs and symptoms include explosive watery, nonmucoid, nonbloody diarrhea, abdominal pain, nausea, vomiting, and little or no fever. The illness is usually self-limited and resolves in 3-5 days, but occasionally lasts >1 wk.
ETEC cause few or no structural alterations in the gut mucosa. Diarrhea is caused by colonization of the small intestine and subsequent elaboration of enterotoxins. ETEC strains secrete a heat-labile enterotoxin (LT) and/or a heat-stable enterotoxin (ST). LT, a large molecule consisting of five receptor-binding subunits and one enzymatically active subunit, is structurally, functionally, and immunologically related to cholera toxin produced by Vibrio cholerae. LT stimulates adenylate cyclase, resulting in increased cyclic adenosine monophosphate (cAMP). ST is a small molecule not related to LT or cholera toxin. ST stimulates guanylate cyclase, resulting in increased cyclic guanosine monophosphate (cGMP). The genes carrying these toxins are encoded on plasmids.
Colonization of the intestine requires fimbrial colonization factor antigens (CFs or CFAs), which promote adhesion to the intestinal epithelium. CFs are antigenic fimbriae that are currently targets for vaccine development. There are at least 25 CF types; these antigens are composed of coli surface (CS) antigens and can be expressed alone or in combination. Prevalent colonization factors include CFA/I, CS1-CS7, CS14, and CS17. However, CFs have not been detected on all ETEC strains. A large proportion of strains produce a type IV pilus called longus, which functions as a colonization factor and is found among several other gram-negative bacterial pathogens. ETEC strains also have the common pilus, produced by commensal and pathogenic E. coli strains. Among the nonfimbrial adhesions, TibA is a potent bacterial adhesin that mediates bacterial attachment and invasion of cells.
For many years, the O serogroup was used to distinguish pathogenic from commensal E. coli. Because the pathogenic E. coli are now defined and classified by using probes or primers for specific virulence genes, determining the O serogroup has become less important. Of the >180 E. coli serogroups, only a relatively small number typically are ETEC. The most common O groups are O6, O8, O128 and O153, and these serogroups only account for half of the ETEC strains based on some large retrospective studies.
Enteroinvasive Escherichia Coli
Clinically, EIEC infections present either with watery diarrhea or a dysentery syndrome with blood, mucus, and leukocytes in the stools, as well as fever, systemic toxicity, crampy abdominal pain, tenesmus, and urgency. The illness resembles bacillary dysentery, because EIEC share virulence genes with Shigella spp. EIEC are mostly described in outbreaks; however, endemic disease occurs in developing countries where these bacteria can be isolated. In some areas of the developing world as many as 5% of sporadic diarrhea episodes and 20% of bloody diarrhea cases are caused by EIEC strains.
EIEC cause colonic lesions with ulcerations, hemorrhage, mucosal and submucosal edema, and infiltration by polymorphonuclear leukocytes. EIEC strains behave like Shigella in their capacity to invade gut epithelium and produce a dysentery-like illness. The invasive process involves initial entry into cells, intracellular multiplication, intracellular and intercellular spread, and host-cell death. All bacterial genes necessary for entry into the host cell are clustered within a 30-kb region of a large virulence plasmid; these genes are closely related to those found on the invasion plasmid of Shigella spp. This region carries genes encoding the entry-mediating proteins, which code for proteins forming a type III secretion apparatus required for secreting the invasins (IpaA-D and IpgD). IpaB and IpaC have been identified as the primary effector proteins of epithelial cell invasion. The type III secretion apparatus is a system triggered by contact with host cells; bacteria use it to transport proteins into the host cell plasma membrane and inject toxins into the cytoplasm.
EIEC encompass a small number of serogroups (O28ac, O29, O112ac, O124, O136, O143, O144, O152, O159, O164, O167, and some untypable strains). These serogroups have lipopolysaccharide (LPS) antigens related to Shigella LPS, and, like shigellae, are nonmotile (they lack H or flagellar antigens) and are usually not lactose fermenting.
Enteropathogenic Escherichia Coli
EPEC are a major cause of acute and persistent diarrhea in children <2 yr of age in developing countries (20-30% of infant diarrhea). In developed countries, EPEC are responsible for occasional outbreaks in daycare centers and pediatric wards. Profuse watery, nonbloody diarrhea with mucus, vomiting, and low-grade fever are common symptoms. Persistent diarrhea (>14 days) can lead to malnutrition, a potentially serious outcome of EPEC infection in infants in the developing world. Studies have shown that breast-feeding is protective against diarrhea due to EPEC.
EPEC colonization causes blunting of villi, inflammatory changes, and sloughing of superficial mucosal cells; these lesions can be found from the duodenum through the colon. EPEC induce a characteristic attaching and effacing (A/E) histopathologic lesion, which is defined by the intimate attachment of bacteria to the epithelial surface and effacement of host cell microvilli. Factors responsible for the A/E lesion formation are encoded by the locus of enterocyte effacement (LEE), which is a pathogenicity island that contains the genes for a type III secretion system, the translocated intimin receptor (Tir) and intimin, and multiple effector proteins such as the E. coli–secreted proteins (EspA-B-D). Some strains adhere to the host’s intestinal epithelium in a pattern known as localized adherence
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