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(Aortic rupture, Internal hemorrhage)
Dissecting aneurysm is a fatal disease of
turkeys 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.
Etiology:
The cause is unknown. Probably several
factors contribute to the development of fatal cases in turkeys. 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 ?-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.
Clinical Findings and Lesions:
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.
Diagnosis:
The diagnosis is made by finding large
clots of blood in the celomic cavity (aortic rupture) or within the
pericardial sac (auricular rupture) of rapidly growing male turkeys.
The condition should be differentiated from hypertensive angiopathy
( Perirenal Hemorrhage Syndrome Of Turkeys:
Introduction), 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. Reserpine
(0.0001% in the ration for not more than 5 days, and 0.00002% when
fed continuously) in birds >4 wk old reduced losses, probably by
reducing blood pressure. Some studies have indicated that the
incidence of aortic rupture can be reduced by adding copper at 240
ppm to the diet.
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