The increased summertime prevalence of cattle carriage of enterohemorrhagic Shiga toxin-producing Escherichia coli O157:H7 (STEC O157) is associated with the increased summertime incidence of human infection. The mechanism driving the seasonality of STEC O157 carriage among cattle is unknown. We conducted experimental challenge trials to distinguish whether factors extrinsic or intrinsic to cattle underlie the seasonality of STEC O157 colonization. Holstein steers (n ؍ 20) exposed to ambient environmental conditions were challenged with a standardized pool of STEC O157 strains four times at 6-month intervals. The densities and durations of rectoanal junction mucosa (RAJ) colonization with STEC O157 were compared by season (winter versus summer), dose (10 9 CFU versus 10 7 CFU), and route of challenge (oral versus rectal). Following summer challenges, the RAJ STEC O157 colonization density was significantly lower (P ؍ 0.016) and the duration was shorter (P ؍ 0.052) than for winter challenges, a seasonal pattern opposite to that observed naturally. Colonization was unaffected by the challenge route, indicating that passage through the gastrointestinal microbiome did not significantly affect the infectious dose to the RAJ. A 2-log reduction of the challenge doses in the second-year trials was accompanied by similarly reduced RAJ colonization in both seasons (P < 0.001). These results refute the hypothesis that cattle are predisposed to STEC O157 colonization during the summer months, either due to intrinsic factors or indirectly due to gastrointestinal tract microbiome effects. Instead, the data support the hypothesis that the increased summertime STEC O157 colonization results from increased seasonal oral exposure to this pathogen.
Shiga toxin-producing Escherichia coli serotype O157:H7 (STEC O157) is an important zoonotic pathogen estimated to cause Ͼ70,000 cases of human infection annually in the United States (1, 2). Human disease is characterized by mild to severe, frequently hemorrhagic diarrhea, and the development of a severe sequela, the hemolytic-uremic syndrome, in approximately 5 to 10% of patients (3). Cattle are an important asymptomatic reservoir host of STEC O157, which may be transmitted to humans by ingestion of contaminated meat, produce, or water or by direct contact with cattle carrying the pathogen (4-6). The seasonal variation in STEC O157 fecal shedding by cattle, specifically the higher summertime prevalence, occurs in diverse regions, including Canada, England, Italy, South Korea, the Netherlands, Turkey, and the United States (7-20). Similar summertime peak shedding is also reported in sheep (11,15,21). Contrary patterns have been occasionally reported, including a higher wintertime prevalence (22, 23) or no seasonal variation (24-26); however, these are unusual and sometimes are confounded by other factors such as a change to indoor housing (22).The seasonal summertime shedding of STEC O157 in cattle parallels both seasonal increases in carcass contamination at abattoirs and the in...