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Twelve ruminally cannulated cattle, adapted to forage or grain diet with or without monensin, were used to investigate the effects of diet and monensin on concentration and duration of ruminal persistence and fecal shedding of E. coli O157:H7. Cattle were ruminally inoculated with a strain of E. coli O157:H7 (10 10 CFU/ animal) made resistant to nalidixic acid (Nal r ). Ruminal and fecal samples were collected for 11 weeks, and then cattle were euthanized and necropsied and digesta from different gut locations were collected. Samples were cultured for detection and enumeration of Nal r E. coli O157:H7. Cattle fed forage diets were culture positive for E. coli O157:H7 in the feces for longer duration (P < 0.05) than cattle fed a grain diet. In forage-fed cattle, the duration they remained culture positive for E. coli O157:H7 was shorter (P < 0.05) when the diet included monensin. Generally, ruminal persistence of Nal r E. coli O157:H7 was not affected by diet or monensin. At necropsy, E. coli O157:H7 was detected in cecal and colonic digesta but not from the rumen. Our study showed that cattle fed a forage diet were culture positive longer and with higher numbers than cattle on a grain diet. Monensin supplementation decreased the duration of shedding with forage diet, and the cecum and colon were culture positive for E. coli O157:H7 more often than the rumen of cattle.Enterohemorrhagic strains of Escherichia coli, especially serotype O157:H7, have been linked in humans with hemorrhagic colitis, hemolytic-uremic syndrome, and thrombocytopenic purpura from eating contaminated foods, such as beef and dairy products, vegetables, cider, etc., contaminated drinking water, or contact with colonized animals or animal environments (2, 3, 17, 18). Significant correlations between bovine fecal and hide prevalence with beef carcass contamination indicate a role for controlling E. coli O157 in live cattle (12). Simulation modeling has shown that reducing the prevalence of E. coli O157 in cattle would substantially reduce contamination of beef (23). Diet and feeding practices are considered to be important factors affecting fecal E. coli O157:H7 (6,7,19,31,32).Data on grain versus forage effects on fecal E. coli O157:H7 are limited and are somewhat conflicting. It is reported that grain feeding, as opposed to hay feeding, favored growth of acid-resistant generic E. coli because of lower ruminal and possibly cecal pH (9). However, Hovde et al. (21) , 1999) studied the effect of grain-to-hay shift on the prevalence of E. coli O157:H7 in cattle and reported that 52% of the cattle maintained on grain continued to shed E. coli O157:H7 but only 18% of the cattle that were switched to hay were culture positive for E. coli O157:H7.Ionophores, particularly monensin, are used extensively in the cattle industry to improve weight gain in cattle on pasture and feed efficiency in feedlot cattle fed grain-based diets (13,28). In other countries, monensin is approved for use in dairy cows for increased milk production, improved feed effici...

A full-length cDNA infectious clone, pKS15-01-Clone, was constructed from an emerging Senecavirus A (SVA; strain KS15-01). To explore the potential use as a viral backbone for expressing marker genes, the enhanced green fluorescent protein (EGFP)-tagged reporter virus (vKS15-01-EGFP) was generated using reverse genetics. Compared to the parental virus, the pKS15-01-Clone derived virus (vKS15-01-Clone) replicated efficiently in vitro and in vivo, and induced similar levels of neutralizing antibody and cytokine responses in infected animals. In contrast, the vKS15-01-EGFP virus showed impaired growth ability and induced lower level of immune response in infected animals. Lesions on the dorsal snout and coronary bands were observed in all pigs infected by parental virus KS15-01, but not in pigs infected with vKS15-01-Clone or vKS15-01-EGFP viruses. These results demonstrated that the infectious clone and EGFP reporter virus could be used as important tools in further elucidating the SVA pathogenesis and development of control measures.

Originally isolated from swine, the proposed influenza D virus has since been shown to be common in cattle. Inoculation of IDV to naïve calves resulted in mild respiratory disease histologically characterized by tracheitis. As several studies have associated the presence of IDV with acute bovine respiratory disease (BRD), we sought to investigate the efficacy of an inactivated IDV vaccine. Vaccinated calves seroconverted with hemagglutination inhibition titers 137-169 following two doses. Non-vaccinated calves challenged with a homologous virus exhibited signs of mild respiratory disease from days four to ten post challenge which was significantly different than negative controls at days five and nine post challenge. Peak viral shedding of approximately 5 TCID/mL was measured in nasal and tracheal swabs and bronchoalveolar lavage fluids four to six days post challenge. Viral titers were significantly (P<0.05) decreased 1.4 TCID/mL, 3.6 TCID/mL and 5.0 TCID/mL, respectively, in the aforementioned samples collected from vaccinated animals compared to non-vaccinated controls at peak shedding. Viral antigen was detected in the respiratory epithelium of the nasal turbinates and trachea by immunohistochemistry from all unvaccinated calves but in significantly fewer vaccinates. Inflammation characterized by neutrophils was observed in the nasal turbinate and trachea but not appreciably in lungs. Together these results support an etiologic role for IDV in BRD and demonstrate that partial protection is afforded by an inactivated vaccine.