To determine if sheep scrapie agent(s) in the United States would induce a disease in cattle resembling bovine spongiform encephalopathy, 18 newborn calves were inoculated intracerebrally with a pooled suspension of brain from 9 sheep with scrapie. Half of the calves were euthanatized 1 year after inoculation. All calves kept longer than 1 year became severely lethargic and demonstrated clinical signs of motor neuron dysfunction that were manifest as progressive stiffness, posterior paresis, general weakness, and permanent recumbency. The incubation period was 14-18 months, and the clinical course was 1-5 months. The brain from each calf was examined for lesions and for protease-resistant prion protein. Lesions were subtle, but a disease-specific isoform of the prion protein was present in the brain of all calves. Neither signs nor lesions were characteristic of those for bovine spongiform encephalopathy.

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...

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Abstract.A commercially acquired anti-human macrophage antibody (anti-CD68; EBM 1 1) was used in an immunocytochemical technique to detect macrophages in formalin-fixed, paraffin-embedded tissues from cattle, pigs, humans, rats, turkeys, dogs, and cats. In healthy cattle, the antibody labeled alveolar macrophages, pulmonary intravascular cells (presumably intravascular macrophages), and macrophage-like cells in other tissues. In bovine lungs infected with Pasteurellu haemolyticu, EBM 1 1 antibody labeled 95% of alveolar macrophages and macrophages within alveolar septa but only 0-2% of streaming or "oat" leukocytes. Alveolar macrophages were also stained by EBM 1 1 in pigs but not in rats, turkeys, dogs, and cats. The antibody also stained macrophage aggregates in the mesenteric lymph nodes and intestinal lamina propria of Mycobucterium purutuberculosisinfected cattle. This study shows that the anti-CD68 (EBM I 1) antibody is a useful marker of macrophages in normal bovine tissues or tissues from areas of acute or chronic inflammation that have been routinely processed. The study also adds strength to the growing evidence suggesting that streaming leukocytes seen in pneumonic pasteurellosis are neutrophils.