Overview of Dissecting Aneurysm in Turkeys

The cause is unknown. Likely, several factors contribute to the development of fatal cases. For the disease to occur, turkeys must be fed and managed in such a way that they grow rapidly, and they must have a genetic susceptibility. A prolonged lipemia generally develops during the period of rapid growth, and the period of greatest mortality typically corresponds to a sharp rise in blood pressure, with dissecting aneurysms developing at the site of arteriosclerotic plaques. The lipemia may result from a high dietary intake of fat or from the effects of hormonal factors, such as high dietary concentrations of estrogens. Although β-aminopropionitrile, the toxic agent in Lathyrus odoratus, is capable of producing the disease, there is no evidence that this or other nitriles are responsible for dissecting aneurysms in turkeys under natural conditions. The enzyme lysyloxidase, isolated from turkey aortas and active on tropelaston and collagen cross-linking, was found to be much lower in males than in females; this may be a factor in the development of spontaneous aortic aneurysms in male turkeys.

Affected turkeys that had shown no premonitory signs are found dead with marked pallor of the head and neck. Occasionally, a caretaker observes an apparently healthy turkey die within a few minutes. The incidence is usually <1% but may be as high as 10%. In the past, when male turkeys were implanted with stilbestrol, the incidence was as high as 20%.

The diagnosis is made by finding large clots of blood in the coelomic cavity (aortic rupture) or within the pericardial sac (auricular rupture) of rapidly growing male turkeys. Dissecting aneurysm should be differentiated from hypertensive angiopathy (see Perirenal Hemorrhage Syndrome of Turkeys), which is also seen in rapidly growing turkeys. In hypertensive angiopathy, the major lesions include pulmonary edema and supcapsular perirenal hemorrhage.

There is no known treatment. Coagulants and vitamin K are useless, because there is no defect in the clotting mechanism. Losses sometimes may be reduced during the critical period between 16 and 23 wk of age by limiting feed intake or slowing growth rate by reducing the energy level of the diet. High-fat diets should not be fed during this period. Some studies have indicated that the incidence of aortic rupture can be reduced by adding copper at 125–250 ppm to the diet from at least 4 wk of age until market.