■ The natural habitat of E. coli is the intestinal tract of humans and animals. It is therefore considered an indicator organism for fecal contamination of water and foods. E. coli is the most frequent causative pathogen in human bacterial infections. Extraintestinal infections include urinary tract infections, which occur when the tract is obstructed or spontaneously caused by the pathovar UPEC. The most important other coli infections are cholecystitis, appendicitis, peritonitis, postoperative wound infections, and sepsis. Intestinal infections are caused by the pathovars EPEC, ETEC, EIEC, EHEC, and EAggEC. EPEC and EAggEC frequently cause diarrhea in infants. ETEC produce enterotoxins that cause a choleralike clinical picture. EIEC cause a dysenterylike infection of the large intestine. EHEC produce verocytotoxins and cause a hemorrhagic colitis as well as the rare hemolytic-uremic syndrome. E. coli bacteria infections are diagnosed by means of pathogen identification. ■
General characteristics. The natural habitat of E. coli is the intestines of animals and humans. This bacterium is therefore used as an indicator for fecal contamination of drinking water, bathing water, and foods. Guideline regulations: 100 ml of drinking water must not contain any E. coli. Surface water approved for bathing should not contain more than 100 (guideline value) to 2000 (absolute cutoff value) E. coli bacteria per 100 ml.
E. coli is also an important human pathogen. It is the bacterial species most frequently isolated from pathological materials.
Morphology, culture, and antigen structure. The Gram-negative, straight rods are peritrichously flagellated. Lactose is broken down rapidly. The complex antigen structure of these bacteria is based on O, K, and H antigens. Fim-brial antigens have also been described. Specific numbers have been assigned to the antigens, e.g., serovar O18:K1:H7.
Pathogenesis and clinical picture of extraintestinal infections. Extraintestinal infections result from relocation of E. coli bacteria from one's own flora to places on or in the macroorganism where they are not supposed to be but where conditions for their proliferation are favorable.
■ Urinary tract infection. Such an infection manifests either solely in the lower urinary tract (urethritis, cystitis, urethrocystitis) or affects the renal pelvis and kidneys (cystopyelitis, pyelonephritis). In acute urinary tract infections, E. coli is the causative organism in 70-80% of cases and in chronic, persistent infections in 40-50% of cases.
Urinary tract infections result from ascension of the pathogen from the ostium urethrae. Development of such an infection is also furthered by obstructive anomalies, a neurogenic bladder or a vesicoureteral reflux. Urinary tract infections that occur in the absence of any physical anomalies are often caused by the pathovar UPEC (uropathogenic E. coli). UPEC strains can attach specifically to receptors of the renal pelvis mucosa with pyelonephritis-associated pili (PAP, P fimbriae, p. 158) or nonfimbrial adhesins (NFA). They produce the hemolysin HlyA.
■ Sepsis. E. coli causes about 15 % of all cases of nosocomial sepsis (S. aureus 20%). An E. coli sepsis is frequently caused by the pathovar SEPEC, which shows serum resistance (p. 13).
■ Other E. coli infections. Wound infections, infections of the gallbladder and bile ducts, appendicitis, peritonitis, meningitis in premature infants, neo-nates, and very elderly patients.
Pathogenesis and clinical pictures of intestinal infections. E. coli that cause intestinal infections are now classified in five pathovars with differing pathogenicity and clinical pictures:
■ Enteropathogenic E. coli (EPEC). These bacteria cause epidemic or sporadic infant diarrheas, now rare in industrialized countries but still a main contributor to infant mortality in developing countries. EPEC attach themselves to the epithelial cells of the small intestine by means of the EPEC adhesion factor (EAF), then inject toxic molecules into the enterocytes by means of a type III secretion system (see p. 17).
■ Enterotoxic E. coli (ETEC). The pathogenicity of these bacteria is due to the heat-labile enterotoxin LT (inactivation at 60 °C for 30 minutes) and the heat-stable toxins STa and STb (can tolerate temperatures up to 100 °C). Some strains produce all of these toxins, some only one. LT is very similar to cholera toxin. It stimulates the activity of adenylate cyclase (see p. 298). STa stimulates the activity of guanylate cyclase. (cGMP mediates the inhibition of Na+ absorption and stimulates Cl- secretion by enterocytes.) ETEC pathogenicity also derives from specific fimbriae, so-called colonizing factors (CFA) that allow these bacteria to attach themselves to small intestine epithelial cells, thus preventing their rapid removal by intestinal peristalsis. The enterotoxins and CFA are determined by plasmid genes. The clinical picture of an ETEC infection is characterized by massive watery diarrhea. The disease can occur at any age. Once the illness has abated, a local immunity is conferred lasting several months.
■ Enteroinvasive E. coli (EIEC). These bacteria can penetrate into the colon-ic mucosa, where they cause ulcerous, inflammatory lesions. The pathogen-esis and clinical picture of EIEC infections are the same as in bacterial dysentery (p. 288). EIEC strains are often lac-negative.
■ Enterohemorrhagic E. coli (EHEC). These bacteria are the causative pathogens in the hemorrhagic colitis and hemolytic-uremic syndrome (HUS) that occur in about 5 % of EHEC infections, accompanied by acute renal failure, thrombocytopenia, and anemia. EHEC possess specific, plasmid-coded fimbriae for adhesion to enterocytes. They can also produce pro-phage-determined cytotoxins (shigalike toxins or verocytotoxins). Some authors therefore designate them as VTEC (verotoxin-producing E. coli). EHEC strains have been found in the O serogroups O157, O26, O111, O145, and others. The serovar most frequently responsible for HUS is O157:H7.
■ Enteroaggregative E. coli (EAggEC). These bacteria cause watery, and sometimes hemorrhagic, diarrhea in infants and small children. Adhesion to enterocytes with specific attachment fimbriae. Production of a toxin identical to STa in ETEC.
Diagnosis. Extraintestinal infections are diagnosed by identifying the pathogen in relevant materials. Diagnosis of a urinary tract infection with midstream urine requires determination of the bacterial count to ensure that an infection can be distinguished from a contamination. Counts >105/ml tend to indicate an infection, <103/ml a contamination, 104/ml could go either way. Specific gene probes are now being used to make identification of intestinal pathogen E. coli bacteria less difficult.
Therapy. Antibiotic therapy must take into consideration the resistance pattern of the pathogen. Aminopenicillins, ureidopenicillins, cephalosporins, 4-quinolones, or cotrimoxazole are useful agents. Severe diarrhea necessitates oral replacement of fluid and electrolyte losses according to the WHO formula: 3.5 g NaCl, 2.5 g NaHCO3,1.5 g KCl, 20 g glucose per liter of water. When required, intestinal activity is slowed down with loperamide.
Epidemiology and prevention. Transmission of intestinal infections is usually indirect via food, drinking water, or surface water. Fifty percent of travelers' diarrhea cases are caused by E. coli, in most cases ETEC.
The most effective preventive measures against intestinal infections, e.g., when travelling in countries with warm climates, is to eat only thoroughly cooked foods and drink only disinfected water. Studies have demonstrated the efficacy of chemoprophylaxis with anti-infective agents in preventing traveler's diarrhea, whereby the agents used must not reduce the normal aerobic intestinal flora (4-quinolones and cotrimoxazole are suitable). This method is hardly practicable, however, in view of the large numbers of travelers.
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