Stealth warfare The interactions of EPEC and EHEC with host cells

Emma Allen-Vercoe and Rebekah DeVinney

Although the Gram-negative bacterium Escherichia coli is normally considered to be a harmless commensal of the gastrointestinal flora, there are some exceptions to this rule. In the past few decades it has become increasingly evident that there are serotypes of E. coli that may cause disease in susceptible hosts. Disease states range from the invasive infections of the urinary tract caused by uropathogenic E. coli (UPEC) to the more typical diarrheal disease caused by several groups of E. coli serotypes, including enteropathogenic E. coli (EPEC) and enterohemorrhagic E. coli (EHEC). There is an increasing realization that bacteria-host interactions with pathogenic E. coli are far more complex and intricate than originally imagined. Studying the ways that bacteria such as EHEC and EPEC are able to subvert host cell functions to their own ends can be thought of as a "window" through which we are able to view the inner workings of the eukaryotic cell. In this chapter we examine some of the mechanisms by which EHEC and EPEC are able to coerce their host; we also examine the sequelae of these interactions.

EPEC usually refers to E. coli serotypes O55:[H6], O86:H34, O111:[H2], O114:H2, O119:[H6], O127:H6, O142:H6, and O142:H34, where square brackets indicate the occurrence of nonmotile strains (Nataro and Kaper, 1998). Infection with EPEC typically causes a chronic watery diarrhea, accompanied by a low-grade fever and nausea. These symptoms can lead to rapid dehydration of the patient, and, because of this, EPEC is a leading cause of infant mortality, particularly in developing countries where rehydration therapy may be difficult. In the Western world, isolated incidences of EPEC infection are often associated with daycares and nurseries (Nataro and Kaper, 1998), where young children closely associate with one another and facilitate the spread of infection.

EHEC usually refers to serotype O157:H7 and less commonly to serotype O111:H-. An EHEC infection is often heralded by the onset of watery diarrhea, which progresses rapidly to severe bloody diarrhea (hemorrhagic colitis) in many patients, regardless of age (Nataro and Kaper, 1998). In the very young and very old, as well as in immunocompromised patients, the disease can be complicated by the onset of hemolytic-uremic syndrome (HUS), which is characterized by hemolytic anemia, thrombocytopenia, and renal failure. HUS is caused by the secretion by EHEC of shiga-like toxin (SLT), a potent cytotoxin with a predilection for human kidney cells. A description of the mechanisms of action of SLT and the many effects on the host cell is beyond the scope of this chapter but is reviewed by O'Loughlin and Robins-Browne, 2001. The onset of HUS, even with rapid treatment, can prove fatal to a patient. Outbreaks of EHEC infection are becoming increasingly high £ profile in North America and Europe. The low infectious dose required to g cause infection may allow the organism to spread rapidly. A recent outbreak g of EHEC O157:H7 in Walkerton, Ontario infected close to 2000 people and led to seven deaths (Kondro, 2000).

Neither EPEC nor EHEC are generally regarded as invasive pathogens; however, some limited evidence has suggested that EPEC in particular may, ^ in fact, be able to invade host cells under the right conditions (Czerucka et al., o 2000). Additionally, both EPEC and EHEC use a highly specialized mecha-

  • nism that allows the bacteria to adhere tightly to the epithelial cell surface and g subvert normal host cell functions by direct interaction. In this chapter, the
  • mechanisms and consequences of both EPEC and EHEC infections of the
  • host are discussed, and the subtle differences between EPEC and EHEC inter

" action with host cells, which are beginning to emerge as research progresses, are highlighted.

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