There are five different pathogenic E. coli groups which cause gastroenteritis:
· Enteropathogenic E. coli (EPEC): Formerly common culprits of diarrhoeal illness, especially in infants and children.
· Enterotoxigenic E. coli (ETEC): This strain is responsible for most cases of traveller’s diarrhoea, and is endemic in India. The condition varies in severity from mild watery diarrhoea to fatal cholera-like illness.
· Enteroinvasive E. coli (EIEC): These “atypical” strains cause shigella-like dysentery.
· Enterohaemorrhagic E. coli (EHEC)*: These strains are responsible for illnesses ranging from mild gastroenteritis to fatal haemorrhagic colitis and haemolytic uraemic syndrome.
· Enteroaggregative E. coli (EAggEC): These strains are so named because they exhibit a “stacked brick” appearance when attached to the surface of cultural epithelial cells.
· They can cause persistent diarrhoeal illness. A sixth group has recently been identified (Enteroadherent E. coli or EAEC) which may be responsible for some cases of traveller’s diarrhoea.
· Enterohaemorrhagic: contaminated food, especially inadequately cooked beef, raw milk, contaminated water, person-to-person contact.
· Enterotoxigenic: contaminated food and water; faecal transmission by contaminated hands.
· Enteroinvasive: contaminated food.
· Enteropathogenic: contaminated infant foods; transmission by fomites and contaminated hands.
· Enteroaggregative: unknown.
· All serotypes of E. coli can produce Shiga toxins and some may also cause diarrhoea, haemorrhagic colitis, and haemolytic uraemic syndrome (HUS). Serotype O157 appears to be more prevalent in developed countries, while the non-O157 serotypes are more common in other countries.
· E. coli serotype O111.H2
· E. coli serotype O157.H7
· E. coliserotype O111.non-motile
· E. coliserotype O26.H11
· E. coliserotype O103.H2
E. coli serotype O157.H7 may infect all age groups, andhas been reported to occur in both developed and developing countries, although it is apparently more prevalent in developed countries. Children aged less than 5 years have the highest disease rates, followed by persons aged greater than 60 years. The infection is more common in summer.
Infection with the E. coli O111.H2 serotype can cause haemolytic-uraemic syndrome.
· Enteropathogenic strains: 9 to 12 hours in adult volunteers; incubation in infants not known
· Enteroinvasive strains: 10 to 18 hours
· Enterotoxigenic strains: 10 to 72 hours
· Enteroaggregative strains: 20 to 48 hours
· Enterohaemorrhagic strains: 3 to 4 days
· Enteroadherent strains: unknown.
· E. coli O157.H7 infection can be asymptomatic. It can also cause non-bloody or bloody diarrhoea, abdominal cramping, nausea, vomiting, and occasionally fever.
· Average interval between exposure and symptoms is 3 days (range: 1 to 8 days).
· Enterohaemorrhagic: Ranges from mild diarrhoea to severe blood-stained stools.
· Enterotoxigenic: Profuse watery diarrhoea without blood or mucus. Vomiting, abdominal cramping, prostration, acidosis, and dehydration can occur. Illness usually lasts less than 5 days, and is the chief cause of “traveller’s diar- rhoea”.
· Enteroinvasive: Severe abdominal cramps, malaise, watery stools, tenesmus, and fever. Endemic in underdeveloped countries; less common in industrialised countries.
· Enteropathogenic: Watery diarrhoea with mucus. Fever and dehydration can occur. Can be fatal if severe and prolonged.
· Common in infant nurseries and community outbreaks.
· Enteroaggregative: Produces infant diarrhoea which may persist for quite some time.
· Diffuse-adherence: Causes paediatric diarrhoea, principally in preschool-aged children, in developing countries.
· Headache is a commonly reported symptom following consumption of food contaminated with E. coli.
· Complications: Haemolytic-uraemic syndrome (HUS), thrombocytopenic purpura, and death.
a.In HUS (especially in children), apart from renal complications, there could also be pancreatitis, colonic necrosis, glucose intolerance, coma, stroke, seizures, myocardial dysfunction, pericardial effusions, adult respiratory distress syndrome (ARDS), and pleural effusions. Diagnosis can be aided by faecal leukocyte counts (usually less than 10 per high-powered field), barium enema which may demonstrate “thumb- printing”, suggestive of oedema and submucosal haem- orrhage, particularly of the ascending and transverse colon. Colonic mucosa often appears oedematous and hyperaemic when viewed with endoscopy, and some- times superficial ulceration or pseudomembranes are seen. Approximately 5% of patients who develop HUS have significant sequelae, including end-stage kidney disease. In one prospective study, children who went on to develop HUS had higher plasma concentrations of various markers indicating activation of the clotting cascade (prothrombin fragments 1 and 2, tissue plas- minogen activator (t-PA) antigen, t-PA-plasminogen activated inhibitor type 1 complex, and D-dimer).
b. Thrombocytopenic purpura occurs more often in adults and the elderly. It has all the features of HUS, but the renal injury is usually less severe, while the neurological manifestations are more prominent. Thrombocytopeniais thought to result from trapping of platelets in affected organs, and removal by the liver and spleen.
· Stool culture: Differentiation between invasive and toxi-genic strains may be difficult.
· The sorbitol fermentation reaction constitutes an effective screening procedure for patients with haemolytic syndrome and haemorrhagic colitis. Most EHEC strains do not ferment sorbitol, unlike other E. coli organisms.
■■ Traveller’s diarrhoea can be prevented or treated with cotrimoxazole or doxycycline.
■■ Haemorrhagic colitis and haemolytic uraemic syndrome are serious conditions which require urgent hospitalisation and aggressive treatment.
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