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Pathogen Page

Escherichia coli

I. General Information

1. NCBI Taxonomy ID:

2. Disease:

Hemorrhagic colitis

3. Introduction

The microorganisms which inhabit the intestinal tract as normal flora are named enteric bacteria. E. coli belongs to the Family Enterobacteriaceae (from the Greek word enterikos, which pertains to the intestine). The name Escherichia comes from the name, Escherich, who in 1885 first isolated and characterized this bacterium. E. coli is a normal, Gram-negative inhabitant of the intestines of all animals, including humans (Horne et al., 2002). When aerobic culture methods are used, E. coli is the dominant species found in feces. Normally E. coli serves a useful function in the body by suppressing the growth of harmful bacterial species and by synthesizing appreciable amounts of vitamins. A minority of E. coli strains are capable of causing human illness by several different mechanisms. E. coli serotype O157:H7 is a rare variety of E. coli that produces large quantities of one or more related, potent toxins that cause severe damage to the lining of the intestine.

Two main types of E. coli are a direct health threat to humans: enteropathogenic E. coli (EPEC) and enterohemorrhagic E. coli (EHEC). Both are diarrheagenic pathotypes. EPEC colonizes the small intestine, and EHEC colonizes the large intestine. EPEC is spread through the fecal-oral route, from human to human without intermediate animal hosts. It is a major cause of infant morbidity in developed countries, estimated to cause the deaths of several hundred thousand children each year. EHEC is a zoonotic pathogen that can progress to hemolytic uremic syndrome (HUS) that can result in kidney failure as well as neurological complications. These severe complications of HUS can be attributed to the production of Shiga toxin, like those produced by E. coli serotype O157:H7 (Horne et al., 2002). Uropathogenic strains of Escherichia coli (UPEC) are the most common cause of non-hospital-acquired urinary tract infections, responsible for 70-90% of the 7 million cases of acute cystitis and 250,000 cases of pyelonephritis reported annually in the United States. Uncomplicated urinary tract infection (UTI) caused by UPEC represents a prevalent and potentially severe infectious disease (Hagan and Mobley, 2007).

The recognition of EHEC as a pathogenic E. coli resulted from two key epidemiologic observations. The first was the 1983 report by Riley et al. who investigated two outbreaks of a distinctive gastrointestinal illness characterized by severe crampy abdominal pain, watery diarrhea followed by grossly bloody diarrhea, and little or no fever. This illness, designated hemorrhagic colitis (HC), was associated with the ingestion of undercooked hamburgers at a fast-food restaurant chain (Pathport).

4. Microbial Pathogenesis

E. coli O157:H7 can be transmitted by food and water. Infection by E. coli O157:H7 is most commonly caused by the consumption of undercooked, contaminated ground beef or beef products, also caused by contaminated drinking or recreational water, raw milk, and person to person contact. The infection mechanisms by which E. coli O157:H7 causes haemorrhagic colitis and HUS are not fully understood. E. coli O157:H7 is believed to adhere closely to mucosal cells of the large bowel, disrupting the brush border. This adherence is completed through the utilization of a Type IV fimbriae bundle-forming pilus between the E. coli and the intestinal epithelial cells.The adherence can progress to a more intimate attatchment resulting in the formation of A/E lesions (Horne et al., 2002). This process alone may be sufficient to produce non-bloody diarrhoea. Shiga toxins have both local and systemic effects on the intestine and are probably critical to the development of bloody diarrhoea. Shiga toxin (Stx) binds to globotriaoxylceramide receptors (Gb3) on cells in the vascular system and in the kidneys. Interaction with the Gb3 receptor leads to internalization of the toxin, which results in the inhibition of protein synthesis (Horne et al., 2002). Histopathological changes associated with infection include haemorrhage and oedema in the lamina propria with areas of superficial focal necrosis. Beef products still account for most of the E. coli O157:H7 cases; however, other food like salad vegetables, fruits, alfalfa and radish sprouts, unpasteurized apple cider, mayonnaise, yogurt, and salami have also been implicated in recent major outbreaks (Pathport).

5. Host Ranges and Animal Models

Direct links between E. coli O157:H7 in cattle and human infections have been confirmed by bacterial isolation and by the presence of serum antibodies against O157 and Shiga-toxin (Stx) antigens in dairy farm families and their cattle. Cattle are believed to be a major conduit for the passage of E. coli O157:H7 into the food supply, but other animals also shed this microorganism in their feces (Pathport). For this reason, neonatal calves are often used as an animal model in testing EHEC vaccines, as well as gnotobiotic piglets. However, since EPEC is host specific and dpes not induce diarrhea in animals, the pathology of the infection is imitated in animal hosts through the use of specially-adapted veterinary pathogens, such as REPEC (rabbit enteropathogenic E. coli) and RDEC (rabbit diarrheal E. coli). Both of these strains elicit the A/E lesions needed to study the vaccine (Horne et al., 2002).

6. Host Protective Immunity

Possible future treatments for E. coli O157:H7 infection include orally administered shiga toxin-binding resins and toxin-neutralising antibodies. Natural infection with E. coli O157:H7 does not confer immunity, and no human vaccine is currently available (Pathport). Major advances in the production of the vaccine can be made once a better understanding of mucosal immunology is complete. DNA-based vaccination is also a possibility to develope protective immunity against EHEC and EPEC. Construction of these vaccines expressing multiple virulence genes of the pathogen could be effective in producing long-term immune response (Horne et al., 2002).

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