(NY) Lead (Pb) toxicosis in a four-month-old Hereford calf was confirmed through diagnostics at the AHDC, following a rule out of rabies at the public health laboratory. The calf presented with circling, blindness, and bruxism, and died after drinking a bottle. On necropsy, the veterinarian found metal pieces in the stomach. Two other cows in the herd were acutely blind and down. One of the cows was tachycardic (heart rate 120) and displaying muscle tremors. Upon walking the pasture, the veterinarian found an old lead battery plate, similar to what was seen in the calf's stomach. The calf's liver was submitted to the AHDC and the Pb concentration was 56.82 mg/kg, which is consistent with toxicosis.
Because cattle are curious and indiscriminate eaters, they are prone to acute lead poisoning, which causes encephalopathy. Top differentials include polioencephalomalacia, hepatoencephalopathy, and rabies. When lead is ingested, adult cattle absorb 1-2%, but milk calves absorb up to 50% systemically. Lead binds to erythrocytes and when red blood cells die, it is stored primarily in bone as triphosphate salt. Eventually, 90% percent of lead is distributed to the bone and the remainder is in soft tissues. Lactating cows resorb bone to release calcium and can have fluctuating Pb concentrations in milk depending on stage of lactation. The half-life of lead can vary tremendously in cattle and can be excreted in milk for months to years after exposure. Treatment is chelation therapy via intravenous or subcutaneous calcium disodium ETDA, which removes Pb from bone. Bovine lead toxicosis is reportable in New York.