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Biomedical subjects

G N Rowland

Publications and source records attributed to G N Rowland.

74 records · Page 5Linked to original sources

Sodium sesquicarbonate toxicity in broiler chickens.

A case of feed misformulation resulted in the addition of sodium sesquicarbonate (SSC) into broiler chicken feed. SSC is a buffering agent used in the manufacture of high urea ruminant feeds that were also produced in this feed mill. Within 2 days of receipt of the tainted broiler feed on the farm, chickens were exhibiting polydypsia and wet droppings and had increased levels of mortality. The postmortem lesions were dehydration, fluid-filled intestines, swollen, pale kidneys, and visceral urate deposits. Histopathology of the kidneys revealed dilated tubules with a giant cell response, loss of tubular epithelium, and a few needlelike crystals. The mortality within 4 days of exposure in three severely affected houses reached 17%. An analysis of the feed revealed sodium levels ranging from 2.59% to 4.88%, with chloride levels of 0.24%-0.40%. Ten percent of the ration was thought to be SSC that contains 36% sodium. To determine if the presence of the SSC caused the problems observed, a controlled study was undertaken. One hundred fifty 3-wk-old broilers were evenly distributed into three floor pens. One group was fed a normal grower ration, a second group was fed a ration containing 5% SSC, and a third group received a ration with 10% SSC. Mortality, packed cell volumes (PCV), total serum proteins, and histopathology of the kidneys were determined. The 10% SSC group had a 6% mortality. Dehydration was evident by elevated PCV within 1 day of ingestion of either ration containing SSC. Microscopic lesions in the kidney were more severe in chickens ingesting SSC when compared with control groups.

Animal Feed↗

Intravascular cartilaginous emboli in the spinal cord of turkeys.

A flock of 15-wk-old tom turkeys experienced an acute onset of paresis and ataxia in 75% of the birds after handling. Cartilaginous emboli were found in the spinal cord vasculature from one of five turkeys at this initial presentation. Most of the flock recovered within 6 days, but 3% remained paretic. Myelomalacia was present in three turkeys that failed to recover. Two of these turkeys had cartilaginous and osseous emboli within the medullary spaces of the vertebral bodies, internal vertebral venous sinuses, and spinal cord. The third turkey had vascular and spinal cord necrosis consistent with thrombosis and resultant ischemia. These changes suggest that turkeys may be susceptible to a syndrome analogous to fibrocartilaginous embolism of the spinal cord in mammals. The articular cartilage of the vertebral body endplate may be the source of the emboli. The turkeys with emboli had articular cartilage defects consisting of matrix eosinophilia, chondrocyte loss, multicellular cluster formation, cartilage detachment, and cartilage clefts. Cartilaginous emboli in the spinal cord should be considered as a potential cause for acute paresis and ataxia, especially in flocks with preexisting abnormalities of the vertebral articular cartilage surfaces.

Animals↗