Escherichia coli O86:K61 has long been associated with outbreaks of infantile diarrhea in humans and with diarrheal disease in many animal species. Studies in the late 1990s identified E. coli O86:K61 as the cause of mortality in a variety of wild birds, and in this study, 34 E. coli O86:K61 isolates were examined. All of the isolates were nonmotile, but most elaborated at least two morphologically distinct surface appendages that were confirmed to be type 1 and curli fimbriae. Thirty-three isolates were positive for the eaeA gene encoding a gamma type of intimin. No phenotypic or genotypic evidence was obtained for elaboration of Shiga-like toxins, but most isolates possessed the gene coding for the cytolethal distending toxin. Five isolates were selected for adherence assays performed with tissue explants and HEp-2 cells, and four of these strains produced attaching and effacing lesions on HEp-2 cells and invaded the cells, as determined by transmission electron microscopy. Two of the five isolates were inoculated orally into 1-day-old specific-pathogen-free chicks, and both of these isolates colonized, invaded, and persisted well in this model. Neither isolate produced attaching and effacing lesions in chicks, although some pathology was evident in the alimentary tract. No deaths were recorded in inoculated chicks. These findings are discussed in light of the possibility that wild birds are potential zoonotic reservoirs of attaching and effacing E. coli.Escherichia coli O86:K61 has long been associated with outbreaks of infantile diarrhea in humans (24). This serotype is classified historically as enteropathogenic E. coli (EPEC) along with serotypes O55, O111, and O127 among others and has been implicated as a major cause of acute and persistent infantile diarrhea in developing parts of the world (39). Smallbowel biopsies of children infected with EPEC revealed discrete colonies of bacteria attached to the mucosa (58). Binding of EPEC to the brush border triggers a cascade of transmembrane and intracellular signals leading to cytoskeletal reorganization and formation of a specific lesion, termed an attaching and effacing (A/E) lesion, which involves intimate bacterial attachment to the host cell and associated effacement of microvilli (43). Jerse et al. (34) first described the eaeA gene of EPEC serotype O127:H6 that encodes intimin, a surfacearrayed protein essential for intimate association with enterocytes. Subsequent analysis showed that this gene is one of a cluster of over 40 genes within the locus of enterocyte effacement (LEE) that encode a type III secretion system essential for A/E lesion formation (45). EPEC possess plasmid-encoded factors, such as the bundle-forming pili (bfp) and the plasmidencoded regulator (per), which also play roles in intimate adherence of EPEC (45). Similar A/E lesions are produced by enterohemorrhagic E. coli (EHEC) (51, 55), Hafnia alvei (2), Citrobacter rodentium (10), and rabbit diarrheagenic E. coli (15). The deduced amino acid sequences of the EaeA protein products of...