Bacteria entering the bloodstream via translocation from the gastrointestinal tract spread hematogenously and can trigger bacterial chondronecrosis with osteomyelitis (BCO) by infecting osteochondrotic microfractures in the epiphyseal-physeal cartilage of the proximal femora and tibiae. In experiment 1, broilers were fed control feed or the same feed containing BacPack 2X, which includes the prebiotic IMW50 (a mannan oligosaccharide beta-glucan yeast cell wall product) plus the probiotic Calsporin (Bacillus subtilis C-3102). Broilers reared on wire flooring consistently developed higher incidences of BCO than hatchmates reared on wood shavings litter (≥24 vs. ≤4%, respectively; P=0.001). Adding BacPack 2X to the feed on d 1 through 56 delayed the age of onset and reduced the cumulative incidence of BCO on wire flooring when compared with broilers fed the control feed (24.0 vs. 40.7%, respectively; P=0.003). In experiment 2, broilers reared on wire flooring received tap water on d 1 through 62 (control group) or therapeutic levels of the potent fluoroquinolone antimicrobial enrofloxacin in the water on d 35 through 54 (enrofloxacin group). During enrofloxacin administration, half as many birds developed BCO in the enrofloxacin group when compared with the control group (8.1 vs. 19.5%, respectively, on d 35 through 54; P=0.001), whereas both groups had similar BCO incidences subsequent to withdrawing enrofloxacin on d 55 through 62 (14.8 vs. 18.2% for the enrofloxacin vs. control groups; P=0.386). Cumulative lameness incidences for d 1 through 62 were higher for the control group than for the enrofloxacin group (39.0 vs. 25.8%, respectively; P=0.003). These results demonstrate that wire flooring imposes a rigorous challenge that leads to high incidences of BCO that can be difficult to suppress, even with therapeutic doses of enrofloxacin. Prophylactically adding BacPack 2X to the feed reduced the incidence of BCO lameness by a proportion similar to that achieved with enrofloxacin, indicating that probiotics potentially can provide effective alternatives to antibiotics for reducing BCO lameness attributable to bacterial translocation and hematogenous distribution.

A sudden outbreak of mortality in one house of 600 48-week-old male breeder turkeys on a five-house turkey breeder farm was suspected to be feed-related. The turkeys gasped and became recumbent; 21.7% of affected turkeys died. No significant gross lesions were found at necropsy. Histological lesions, limited to skeletal muscle, consisted of degeneration and necrosis and were judged compatible with ionophore toxicosis. Feed samples from the affected house were analyzed by three techniques and shown to contain 13.4 to 18.4 g of salinomycin per ton of feed. An error at the feed mill was blamed for allowing contamination of the turkey feed with broiler starter feed containing salinomycin.

Feed artificially contaminated with various levels of nalidixic-acid-resistant Salmonella montevideo was fed to newly hatched chicks for 7 days. Cloacal and cecal swabs were obtained from the chicks at 7, 14, and 21 days of age to monitor Salmonella colonization relative to the feed contamination level. In one of three trials, less than one Salmonella montevideo per gram of feed was sufficient to establish colonization in 1-to-7-day-old chicks.

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Two floor pen studies were conducted to determine whether compensatory growth occurs following withdrawal of the anticoccidial drug salinomycin from the feed of broilers reared to 46 days of age. There were no significant differences in weight gain or feed conversion between medicated and unmedicated birds whether overall performance or performance during the 1-wk withdrawal period was measured. Feed intake of birds given salinomycin, however, was significantly lower than that of unmedicated birds, and feed intake following withdrawal was greater than that of birds still receiving the drug.