Major outbreaks of illness in the 1990s have focused our attention on Escherichia coli O157:H7 as the major cause of Shigatoxin E. coli–induced human diseases. However, current evidence suggests that we need to expand our understanding and be concerned about other E. coli serotypes, as well.
Escherichia coli is not that harmless gut bacterium that we were taught about in Microbiology 101, at least for those of us who took our microbiology in the 1960s and ’70s. There are four recognized classes of enterovirulent E. coli (EEC group) that cause gastroenteritis in humans: enteropathogenic E. coli (EPEC), enteroinvasive E. coli (EIEC), enterotoxigenic E. coli (ETEC), and enterohemorrhagic E. coli (EHEC). The first three of these cause illness with diarrhea as a hallmark symptom (ETEC is the in famous “travelers’ diarrhea”). EHEC is the cause of bloody diarrhea and worse. E. coli O157:H7 is the most notorious member of the EHEC group.
Similarities between Shiga-toxin produced by Shigella dysenteriae type 1 prompted investigators to select the name for the toxin produced by E. coli O157:H7 as Shiga-like toxins and to call the microorganism Shiga-toxin-producing E. coli (STEC). Coincidentally, the same toxins were named Verotoxin by other investigators because such toxins were capable of killing Vero cells derived from the African green monkey kidney. The dire health/ food safety concern is the association between STEC serotypes and hemolytic uremic syndrome (HUS), which affects about 5% of persons, generally children, who develop bloody diarrhea. The hallmark feature of HUS is renal failure. Of those developing HUS, about 5% may die. Infection can progress (usually in the elderly) to thrombotic thrombocytopenic purpura (HUS with neurologic complications) and can be fatal. Shiga toxins are thought to cross the epithelial cell barrier of the gut and target microvascular endothelial cells of the intestine, kidney, and central nervous sytem. The infective dose may be as few as 10 organisms.
Major food vehicles for E. coli O157:H7 include raw hamburger, raw milk, and ruminant products, but food and clinical microbiologists have become increasingly concerned about cross contamination to other foodstuffs, such as bean sprouts and apple juice. The organism is extremely hardy and survives in harsh environments. Person-to-person contact, such as might occur in day-care centers, is a common mode of transmission. Antimicrobial agents administered to counter infection may stimulate the expression and enhance the release of Shiga toxins.
The movement of E. coli O157:H7 genes among other serotypes is of major domestic and international public health concern. Several investigators have found non-O157 serotypes that have the virulence attributes of O157:H7. Such strains have been identified in the United States and globally have been associated with human disease. However, because very few of the small number of laboratories who are looking for Shiga-toxin are capable of identifying non-O157 serotypes, the estimates of the number of non-O157 serotypes found may be quite conservative. In the U.S., non-O157 serotypes included O111, O26, O145, O103.
It is essential that regulatory agencies, the food industry and other proactive bodies:
• Recognize the enormous potential for the spread of Shiga-like toxin genes to non-O157:H7 strains
• Identify alternative tests for rapid detection of STEC to reduce the risk of exposure and infection.
• Provide increased funding for the development of Shiga-like toxin test methods which can be used clinically or in the field.
• Support the development of cost-effective vaccines.
• Educate physicians, health-care workers, child- and elder-care providers, and foodservice workers about epidemic potential, hygienic precautions, and treatment modalities.
• Amplify university extension and community service programs to educate the consumer and producer.
• Educate the public about potential benefits of irradiation and other nonthermal modes of food processing.
• Establish a research priority that targets a better understanding about gene transfer and its role in pathogen emergence.
More non-O157 serotypes expressing STEC may become a threat to human health. The consequences of exposure to STEC can be devastating and fatal, particularly among young children and the elderly.
Seldom has a single bacterial strain had such a wide-ranging impact on the regulatory community. There is just cause, however, as the disease caused by O157:H7 and its relatives can be so devastating. Numerous and rigorous new rules have been imposed on several industries as a direct result of E. coli O157:H7. It has changed the way consumers and foodservice workers view ground meats, sprouts, certain fresh vegetables, and other commodities. The emergence of new STECs may compound an already vexing problem for regulators and consumers. Steps taken now to prepare for the emergence of new STECs may save lives later.
by STANLEY T. OMAYE