Dissecting aneurysm is a fatal disease of turkeys. It is characterized by sudden death of rapidly growing birds with massive internal hemorrhage resulting from rupture of aneurysms formed in various parts of the vascular system. The frequency with which the posterior aorta is affected has given rise to the term “aortic rupture.” The disease has been reported in North America, Europe, and Israel. Most breeds of turkeys are susceptible, and the largest and most rapidly growing males, 8–24 wk old, are affected most often; females are also affected but at a lower incidence.
The cause is unknown. Probably several factors contribute to the development of fatal cases. For the disease to occur, birds must be fed and managed in such a way that they are growing 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 females; this may be a factor in the development of spontaneous aortic aneurysms in male turkeys.
Affected birds that had shown no premonitory signs are found dead with marked pallor of the head and neck. Occasionally, a caretaker observes an apparently healthy bird die within a few minutes. The incidence is usually <1% but may be as great as 10%. Formerly, when male turkeys were implanted with stilbestrol, the incidence was as high as 20%.
The carcass is markedly anemic with large quantities of clotted blood in the peritoneal cavity and over the kidneys, or in the pericardial sac. The rupture in the ventral wall of the posterior aorta at about the position of the testes, or in the cardiac atrium, can be located readily by carefully washing away the blood clot. The aortic lumen may contain an organized, adherent thrombus at the site of rupture. Ruptures in smaller blood vessels are more difficult to locate. Almost always, an intimal thickening or a large, fibrous plaque is present in the region of the rupture. The tunicas intima and media are thrown into deep folds and separated from the tunica adventitia. Marked accumulation of lipids in the thickened intima and in the fibrous plaques can be identified by stains. Fibers of the tunica media may show degenerative changes and infiltration with heterophils and macrophages.
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. The condition 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.
Treatment, Control, and Prevention
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.
Last full review/revision March 2012 by Mahesh C. Kumar, BVSc, MS, PhD, DACPV