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| Microscopic image of Escherichia coli (ATCC 11775). Gram staining, magnification:1,000. | SEM Image of E. coli strain 0157:H7 - rod prokaryote (hemorrhagic bacterium) | TEM Image of E. coli with fimbriae |
Infections by pathogenic strains of E. coli also occur in many domestic and wild species. Pathogenic symptoms induced by these diarrhoeagenic E. coli can be due to production of toxins or other virulence traits. E. coli strains that induce diarrhoea in their hosts can be divided into five main categories on the basis of distinct epidemiological and clinical features and specific virulence determinants:
Clinically, ETEC induce a watery diarrhoea in infected hosts by action of the two toxins, LT and ST. The LT enterotoxin is very similar to cholera toxin in both structure and mode of action. ST is known to bind to and activate a guanylate cyclase enzyme located on apical membranes of host cells. This leads to secretion of fluid and electrolytes resulting in a watery diarrhoea. Incubation period is approximately 1-2 days and illness can last 3 days to several weeks.
EHEC are mostly represented by a single strain, serotype O157:H7, which causes a diarrheal syndrome with copious bloody discharge and no fever. There is a toxic effect on the kidneys, and diarrhoea caused by this strain can be fatal, particularly in infants, due to acute kidney failure. Infection in humans is often associated with ingestion of inadequately cooked hamburger meat. Incubation period is approximately 3 to 4 days and duration of illness is about 1 week. EIEC are similar to Shigella in their pathogenic mechanism and clinical symptoms. EIEC bacteria penetrate and multiply within epithelial cells of the colon causing widespread cell destruction. The clinical syndrome is identical to Shigella dysentery and includes a dysentery-like diarrhoea with fever. EIEC do not produce LT or ST toxin and, unlike Shigella, do not produce shiga toxin. The incubation period is less than 24 hours. EPEC cause a watery diarrhoea similar to ETEC, but do not produce ST or LT toxins. These strains are a principal cause of infant diarrhoea in developing countries. The illness typically lasts 1 to 3 days.
EAEC adhere to epithelial cells in a characteristic stacked-brick pattern known as the aggregative adherence (AA) pattern. When they adhere to small and large bowel mucosal surfaces they stimulate mucus production, leading to a thick mucus-containing biofilm encrusted with EAEC. They can also secrete toxins, such as heat-stable enterotoxin 1 (EAST1), Pet and Pic, which are associated with damage to the mucosa. EAEC were originally recognized as one of the predominant etiologic agents of persistent diarrhoea in developing countries and they remain an important cause of acute as well as protracted diarrhoea in many parts of the world, including industrialized countries.
Several assays are available for detection of diarrhoeagenic E. coli, including biochemical reactions, serotyping and phenotypic assays based on virulence characteristics. However, molecular detection by PCR has become a commonly-used method to detect and identify these bacteria because the method gives rapid and reliable results in addition to its high sensitivity and specificity.
Certain strains of E. coli behave as pathogens in dogs and cats causing gastro-intestinal and extra-intestinal diseases. Among the five known groups of diarrhoeagenic E. coli, namely enteropathogenic E. coli (EPEC), Enterotoxigenic E. coli (ETEC), Enteroinvasive E. coli (EIEC), shiga-toxin producing E. coli (STEC) and Enteroaggregative E. coli (EAEC), only EPEC and ETEC were clearly associated with enteric disease in young dogs. ETEC isolates from diarrhoeic dogs were found to be positive for the heat-stable enterotoxins STa and STb but negative for heat-labile enterotoxin (LT). Canine ETEC were found to be different from those of other animals and humans by their serotypes, production of alpha-haemolysin and adhesive factors and by the production of uncharacterised types of enterotoxins by some ETEC. Canine EPEC could be distinguished from EPEC of humans or other animals by their serotypes and by the eae-protein intimin which mediates intimate adherence of EPEC to intestinal mucosa cells. STEC were occasionally isolated from faeces of healthy and diarrhoeic dogs but their role in canine diarrhoea is not yet well known. EIEC and EAggEC were not reported to occur in dogs or cats. Very little is known on diarrhoeagenic E. coli in cats and further epidemiological investigations on this subject are needed. Besides its role in gastro-intestinal infections, E. coli can cause infections of the urogenital tract and systemic disease in dogs and cats. Extra-intestinal pathogenic E. coli strains from dogs and cats belong to a limited number of serotypes and clonal groups and are frequently found as a part of the normal gut flora of these animals. Many of these E. coli strains carry P-fimbriae and produce alpha-haemolysin and a necrotizing cytotoxin (CNF1). Some of the frequently isolated types of extra-intestinal pathogenic E. coli from dogs, cats and humans were found to be highly genetically related but showed differences in their P-fimbrial adhesins which determine host specificity. Transmission of extra-intestinal and enteral pathogenic E. coli between dogs and humans was reported.
E. coli infection in cats can also cause an effusive pneumonitis/ pneumonia. In a number of cases, cats had exposure to outdoor areas where sheep and cattle grazed.