Age affected: Newborn, piglets pre-weaning.
Causes: Starvation; chilling; infections.
Effects: Empty abdomen, cold, lethargic, coma, convulsions, death.
The prime cause of this condition is an inadequate intake of milk. This may be due to failure of the sow to provide sufficient milk or failure of the piglet to suck. The presentation of the sow’s udder may also be important as may be competition between piglets. The newborn piglet normally possesses carbohydrate reserves in the form of hepatic (liver) glycogen (animal starch) stores (10-14 mg/100g) and blood glucose levels of 80-100 mg/100 ml (24 hours after birth). Gluconeogenesis (the generation of glucose from protein) is not efficient until 7 days of age and glycogen reserves become depleted if the milk supply is inadequate. Feeding normally provide adequate carbohydrate, but, if interrupted, blood glucose levels fall until clinical signs of deficiency appear at a blood-glucose concentration of 50 mg/100 ml. The original glycogen stores may already be depleted by delay in parturition. There is no brown fat so that piglet cannot use fat to generate heat. Low environmental temperatures (below 34˚C for the single neonate or 25-30˚C for the piglet able to huddle) lead to increased utilisation of glycogen reserves in the liver and skeletal muscles and to the more rapid development of clinical signs. Low birth weight increases heat loss.
This condition is not transmissible. Some of the predisposing causes such as mastitis in the sow or infectious disease in the piglet are transmissible.
Piglets aged less than 7 days are affected and, at blood glucose levels of 50 mg/100 ml, may show uncertain gait, and later support themselves by placing their noses on the ground and straddling their hind limbs. More severely pigs rest of their abdomens but eventually fall on their sides and develop convulsions. These consist of ‘galloping’ of the forelegs, champing and frothing of the jaws in ‘air hunger’ and are accompanied by slowing of the heart rate (to 80 beats/min), a decline in rectal temperature, shivering, dullness, and, in the earlier stages, a weak stages. Animals enter a coma and die. Death normally occurs 24-36 hours after the commencement of the signs. These signs may occur alone or together with those of any disease which prevents sucking.
Hypoglycaemia should be suspected when the clinical signs of staggering, failure to rise, convulsions with galloping movements, air hunger, coma and death occur in very young piglets. The presence of agalactia in the sow, presence of a large litter and low environmental temperature all provide supportive evidence. Post-mortem examination provides further evidence. Blood glucose levels of affected pigs are usually less than 50 mg/100 ml and may be as low as 7 mg/100 ml. Confirmation of the importance of hypoglycaemia in the syndrome can be obtained on farm from the response to treatment and in the laboratory from from blood glucose and liver glycogen determinations.
Affected pigs have stomachs which are empty or contain a little curd. Hepatic glycogen is often absent in hypoglycaemic pigs. Other diseases affecting baby pigs such as TGE, Aujeszky’s disease and bacterial meningitis may be present and confirm that the hypoglycaemia is secondary to piglet illness.
Affected animals can be given intraperitoneal injections of 15 ml of 5% glucose solution every 4-6 hours, or oral glucose by stomach tube, and kept at a minimum of 30-35°C (85-95°F). If the sow is unable to feed them, an artificial sow milk replacer should be given by stomach tube initially or they should be fostered onto another sow. Reduction in draughts and the provision of dry bedding and additional heating will also improve their changes of survival Agalactia or mastitis in the sow should be treated promptly and support provided over the period of inadequate milk supply. Piglet disease should be treated promptly or prevented by vaccination to reduce piglet failure. Animals with temporary conditions such as splay leg should be enabled to suck and supported until they can do so.