Experimental Infection of Calves with Escherichia coli O104:H4 outbreak strain

Abstract

In 2011, a severe outbreak of hemolytic-uremic syndrome was caused by an unusual, highly virulent enterohemorrhagic E. coli (EHEC) O104:H4 strain, which possessed EHEC virulence traits in the genetic background of human-adapted enteroaggregative E. coli. To determine magnitude of fecal shedding and site of colonization of EHEC O104:H4 in a livestock host, 30 (ten/strain) weaned calves were inoculated with 1010 CFU of EHEC O104:H4, EHEC O157:H7 (positive control) or E. coli strain 123 (negative control) and necropsied (4 or 28 d.p.i.). E. coli O157:H7 was recovered until 28 d.p.i. and O104:H4 until 24 d.p.i. At 4 d.p.i., EHEC O104:H4 was isolated from intestinal content and detected associated with the intestinal mucosa. These results are the first evidence that cattle, the most important EHEC reservoir, can also carry unusual EHEC strains at least transiently, questioning our current understanding of the molecular basis of host adaptation of this important E. coli pathovar.

Vertical and Horizontal Transmission of ESBL Plasmid from Escherichia coli O104:H4

“…pESBL encodes two broad spectrum beta-lactamases, enabling host cells to be resistant against these antibiotics. Even without antibiotic selection, pESBL was shown to be stably maintained in the host cell in both in vitro (test tube) and in vivo (animal infection model) cultivations [ 13 , 14 , 15 , 16 ]. Furthermore, pESBL is suggested to help persistence of the host E. coli in ruminant intestine, thus supporting this environmental reservoir of the pathogen [ 16 ].…”

“…pAA mediates aggregative adherence, a feature of enteroaggregative E. coli , and pESBL confers resistance to beta-lactam antibiotics [ 11 , 12 ]. While pAA is dispensable and can be lost from the host E. coli , pESBL was shown to present utmost stability [ 13 , 14 , 15 , 16 ]. Besides, pESBL was shown to transmit among Enterobacteria such as between E. coli and from E. coli to Klebsiella , by conjugation [ 14 ], which is consistent with the ‘plasmid host range’ of IncI conjugative plasmids.…”

The Role of Escherichia coli Shiga Toxins in STEC Colonization of Cattle

“…The mucosa overlaying lymphoid follicles in the terminal rectum are the prime colonization site for STEC of serotype O157:H7 in cattle [21,156]. However, STEC O157:H7, in particular in the first days after infection, also colonize the mucosa of ileum, cecum, and colon [19,157]. Non-O157 STEC lack a tropism for the terminal rectum [21,157,158].…”

“…However, STEC O157:H7, in particular in the first days after infection, also colonize the mucosa of ileum, cecum, and colon [19,157]. Non-O157 STEC lack a tropism for the terminal rectum [21,157,158]. Similarities in the expression patterns of surface markers including CD77 of IEL from ileum, colon and cecum (C. Menge and E. A. Dean-Nystrom [National Animal Disease Center, Ames, IA], unpublished) strongly imply that IEL all along the gastrointestinal tract of cattle are sensitive to Stxs.…”

Decreased STEC shedding by cattle following passive and active vaccination based on recombinant Escherichia coli Shiga toxoids

“…Calves get infected orally with a plethora of different STEC strains present in their environment early in life, but rarely develop clinical signs of infection. Many STEC strains are able to colonize the bovine intestine [ 2 – 6 ], including non-O157:H7 [ 7 – 9 ]. Cattle may shed these bacteria for several month in quantities that may be considerably high at some sampling points [ 10 – 13 ] making cattle, besides other ruminants, an important reservoir for STEC strains associated with human diseases.…”