Transport tetany occurs after the stress of prolonged transport, typically in cows and ewes in late pregnancy, although it is also seen in lambs transported to feedlots and in cattle and sheep transported to slaughter. Crowded, hot, poorly ventilated transport vehicles (railroad cars or trailers) with minimal or no access to feed or water appear to predispose animals to the condition; however, prolonged travel by foot is also a risk factor. The disease is characterized by recumbency, GI stasis, and coma, and is generally fatal.
Although cows in late gestation are most commonly affected, the disease is also seen in cows that have recently calved, as well as in bulls, steers, and dry cows. Risk factors include heavy feeding before shipment, deprivation of feed and water for >24 hr during transit, and unrestricted access to water and exercise immediately after arrival. Exposure to hot environmental conditions is also associated with an increased incidence. Although the specific cause of tetany is unknown, the condition may be a form of acute hypocalcemia precipitated by late pregnancy and early lactation, or by fasting before or during transit. Physical stress is undoubtedly related. Hypomagnesemia may be a precipitating factor in cattle and a contributing factor in sheep.
Clinical signs in cattle may occur while in transit or as long as 48 hr after arrival. Early clinical signs include restlessness and excitement, trismus, and grinding of teeth. A staggering gait may be seen, and later, if recumbent, cattle often demonstrate paddling of the hindlegs. Rumen hypomotility and GI stasis are seen, and animals become completely anorectic. Tachycardia and rapid, labored respiration may develop. Abortion may be a complication. Cattle that do not recover gradually become more obtunded to the point of coma and die within 3–4 days. Moderate hypocalcemia and hypophosphatemia may be seen in cattle. Some sheep are hypocalcemic and hypomagnesemic, but others show no measurable biochemical abnormalities. No specific lesions are found at necropsy other than lesions associated with prolonged recumbency, most commonly ischemic muscle necrosis. In lambs, early signs include restlessness, staggering, and partial hindlimb paralysis followed by lateral recumbency. Death can occur rapidly or after 2–3 days of recumbency. In lambs, mild hypocalcemia may be noted. Recovery rates are fair even with treatment. The relationship of clinical signs with transport or forced, prolonged exercise is diagnostic.
Some animals respond to treatment with combinations of parenteral calcium, magnesium, and glucose. IV injections of calcium borogluconate (25% solution at 400–800 mL/cow or 100 mL/ewe) or calcium borogluconate with magnesium sulfate (5% solution, same volumes) can be administered slowly. A dose of 50 mL/day can be given SC to affected lambs in feedlots. Repeated injections may be warranted, but failure to respond is common (50%) and most likely due to concurrent muscle necrosis. Additional treatment considerations include IV administration of large volumes of polyionic fluids such as lactated Ringer’s solution. Animals should be offered good quality feeds (eg, alfalfa hay), fresh water, and soft bedding with good footing underneath. Sedation may be necessary if animals are hyperexcitable or convulsing.
If prolonged transport times of cows or ewes in advanced pregnancy is unavoidable, animals should be fed a restricted diet several days before shipment, then provided adequate feed, water, and rest periods during transport. Administration of ataractic agents (unless transport is to slaughter) such as promazine hydrochloride before loading is recommended, especially for nervous animals. Upon unloading at the destination, animals should be allowed limited access to water for the first 24 hr and minimal exercise for 2–3 days.