Hemorrhagic Vasculopathy of Turkeys
(Hypertensive Angiopathy, Sudden Death Syndrome of Turkeys, Aortic Rupture, Perirenal Hemorrhage Syndrome, Dissecting Aneurysm)
Death from acute internal hemorrhage is a common condition in commercial male turkeys and usually presents as perirenal hemorrhage syndrome (PHS) or aortic rupture, two distinct conditions. PHS is a noninfectious cardiovascular disorder usually affecting rapidly growing male turkeys 8–19 weeks of age, characterized by sudden death, perirenal hemorrhage, and hypertrophic cardiomyopathy. Mortality is usually 0.5%–2% but can be higher; birds often die without premonitory signs. Sudden, unexpected death in otherwise healthy, rapidly growing male turkeys can also be caused by rupture of the abdominal aorta.
Healthy, rapidly growing flocks are more likely to be affected. The pathogenesis of PHS is unknown but is apparently unrelated to pulmonary function or hypertension. Inadequate or inappropriate cardiac response to exercise, resulting in systemic hypotension, vasodilation, and ventricular arrhythmia, are factors that likely contribute to the death of the turkey. Acute congestive heart failure secondary to cardiac hypertrophy is often associated with PHS. Renal hemorrhage likely results from severe passive congestion and dissection of blood through the fragile renal parenchyma; acute blood loss is not always the primary cause of death because the extent of perirenal hemorrhage is variable and often mild. A physical rupture in the renal artery or adjacent vessels is usually not identified.
A genetic predisposition for aortic rupture is strongly suspected because the disease occurs more often in particular breeds of commercial turkeys. The condition has also been described in chickens, ostriches, and waterfowl but is considered a classic disease of turkeys. Death from aortic rupture results from massive, acute hemorrhage into the coelomic cavity. Losses in affected flocks usually are 1%–2% but can reach 10%.
Both perirenal hemorrhage syndrome and aortic rupture are similar, noninfectious cardiovascular disorders usually affecting rapidly growing male turkeys 8–19 weeks of age and are characterized by sudden death and acute internal blood loss. Mortality is usually 1%–2% but can be higher, sometimes spiking over several days. Birds are usually in excellent body condition and often die without premonitory signs. PHS is apparently unrelated to pulmonary function or hypertension. Inadequate or inappropriate cardiac response to exercise, resulting in systemic hypotension, vasodilation, and ventricular arrhythmia occurring in PHS are factors that likely contribute to the death of the turkey. Aortic rupture has also been described in chickens, ostriches, and waterfowl but is considered a classic disease of turkeys. Aortic rupture likely has a genetic predisposition because the condition occurs more often in particular breeds of commercial turkeys and is associated with hypertension.
Perirenal hemorrhage syndrome is often associated with acute congestive heart failure secondary to cardiac enlargement/hypertrophy. Microscopic changes of perirenal hemorrhage syndrome are consistent with the gross findings and include pulmonary congestion and edema with renal perivenous and parenchymal hemorrhage. Intimal vacuolation and medial hyperplasia of arteries and arterioles have been described in multiple organs, particularly kidney, spleen, and lung, of PHS turkeys; however, similar lesions can be observed to a lesser extent in tissues of healthy turkeys. Microscopic changes of aortic rupture, often a laceration near the branch of the cranial mesenteric artery, include intimal thickening or large, sclerotic plaques accompanied by fragmentation of elastic fibers and degenerative changes of smooth muscle cells at the site of the gross lesion in cases of aortic rupture. The aortic tunica intima and media are thrown into deep folds and separated from the tunica adventitia. Accumulation of lipid in the thickened intima and in the fibrous plaques can be identified by special stains. Fibers of the tunica media may show degeneration and infiltration with heterophils and macrophages.
These two forms of vascular rupture and hemorrhage can occur simultaneously in the same flock. Diagnosis of perirenal hemorrhage syndrome and aortic rupture are based on history, typical gross lesions, and absence of infectious agents. PHS can occasionally include extensive abdominal hemorrhage that resembles signs of aortic rupture. However, PHS is usually accompanied by cardiac enlargement/hypertrophy, and a distinct aortic rent can usually be detected in turkeys with aortic rupture.
Although there is no specific treatment for perirenal hemorrhage syndrome, factors that decrease growth rate and activity also tend to decrease PHS. Reserpine (0.5 ppm feed) decreases PHS, but aspirin (0.005%) or increased calcium has no effect. Reserpine is no longer listed in the Feed Additive Compendium as approved for use in feed for turkeys, so it cannot be used in commercial flocks. Increased room temperature and step up/step down lighting programs have also reduced PHS. Activities that increase cardiovascular stress (eg, moving birds, tilling litter, noise) should be minimized, especially between 7 and 15 weeks of age. Lower ambient temperatures (55°F [13°C]), intermittent lighting, and leaving toes unclipped increase mortality from PHS.
Copper deficiency, hypertension, hormonal influences, diet, zinc deficiency, pharmaceuticals, and parasites are precipitating factors for aortic rupture, but as with PHS, there is no specific recommended treatment. To reduce incidence of aortic rupture, rations can be supplemented with copper at 125–250 ppm from at least 4 weeks of age until market, but this is not a dependable preventive measure. Limiting feed intake or protein during the growth period to slow the growth rate might help to reduce the occurrence of aortic rupture. As with PHS, activities that increase cardiovascular stress should be minimized.
Perirenal hemorrhage syndrome and aortic rupture are two forms of a fatal cardiovascular syndrome seen in rapidly growing male turkeys.
Diagnosis is based on history and finding characteristic gross lesions in the absence of infectious agents.
There is no effective treatment, but ensuring adequate dietary copper, minimizing stress, and limiting feed intake during the rapid growth phase from 7–15 weeks of age may reduce the incidence.