Age affected: Weaners, growers / finishers.
Causes: Vitamin E or selenium deficiency, high fat diets.
Effects: Inappetence, weakness, sudden death.
Mulberry heart disease results from a deficiency of Vitamin E (alpha-tocopherol) in the ration, exacerbated by low methionine and cystine levels and high fat levels in the diet. Oxidised fat, copper and the wet storage of cereals, particularly propionic acid-stored barley may all reduce the Vitamin E levels. Selenium levels appear to be normal in many cases of this condition, but tissue Vitamin E levels are low even when dietary levels are apparently adequate. Alpha tocopherol acts both as an antioxidant and as a stabiliser of membrane lipids. A specific loss of membrane bound arachidonic and linolenic acids occurs in Vitamin E deficiency and this is associated with low dietary levels of these acids. The major clinical signs of this complex deficiency appear to result from the effects on energy metabolism. The cells most severely affected in the pig are hepatocytes (liver cells) and muscle cells in the heart and skeletal muscle. The syndrome develops as a result of congestive heart failure, coupled with hydropericardium. Heredity may play a part as Landrace pigs have been said to be susceptible.
Mulberry heart is not transmissible, but occurs in successive batches of pigs of the same origin kept under similar conditions and on the same rations.
Pigs of any age may be affected, but the condition occurs commonly in 20-50 kg animals. Affected pigs are anorexic and depressed with muscle weakness and lowered body temperature. They may become cyanotic before death which occurs within 24 hours of the onset of the clinical signs. Recovery has been recorded, but mortality is usually 100%. Sudden death is common. Deaths may occur after handling and affected animals within a group may show some signs of circulatory embarrassment such as lethargy, cyanosis and dejection. Muscle tremor may occur, especially at the shoulders. There may be stiffness, a limp or recumbency.
Clinical signs which include inappetence and depression, muscle weakness, lowered body temperature and cyanosis before death may suggest mulberry heart disease when seen in pigs weighing between 20 and 50 kg.
The post-mortem findings may be used to confirm a diagnosis. The heart lesions are characteristic. The carcase is usually in good condition with fluid and shreds of fibrin in all body cavities. The liver is enlarged and mottled. The pericardial cavity is full of gelatinous fluid and fibrin and the surface of the heart is streaked with haemorrhages running from the base to apex. Similar haemorrhages occur in the endocardium (inside of the heart). They lie immediately below the membrane and appear microscopically as areas of free red cells with no obvious myonecrosis (dead muscle fibres). Microangiopathy (damaged small blood vessels)) may be present and in most cases degeneration of the muscle may also be present. Oedema Disease, Actinobacillus pleuropenumoniae and Streptococcus suis Type II infection may also cause sudden death with fluid or fibrin in body cavities. Death from the porcine stress syndrome usually follows exertion. The histopathology and liver Vitamin E analysis usually confirm.
The use of high levels of Vitamin E (2-3 times the recommended levels) prevents the development of the condition and implies a Vitamin E deficiency. Injection with alpha-tocopherol or alpha-tocopherol-selenium preparations is of value in affected groups of animals. Vitamin E is also available as a component of the fat soluble vitamin mixtures. Control depends upon ensuring that adequate levels of dietary vitamin E are present in the final ration (10,000 -20,000 IU (3.0-6.0 g/tonne). The suggestion that Vitamin E should be included at five times the fat percentage of the ration measured in mg/kg feed is usually adequate but actively oxidising fats may need up to 20 times the fat percentage. Vitamin E may be restored to normal within a few hours by injection but may take 2 weeks by feed supplementation.