High-mountain Disease: Introduction
(Brisket disease, Pulmonary hypertensive heart disease) |  |
| High-mountain disease or brisket disease is noninfectious, congestive heart failure (CHF) of cattle. It is primarily caused by pulmonary hypertension associated with high altitudes. The disease affects cattle in mountainous ranges of the world and is seen most commonly at elevations above 2,000 m (~6,500 ft) in the western USA, western Canada, and South America. Rarely, similar lesions have been described in severely stressed and parasitized sheep and deer. Etiologically similar
hypoxia-related heart failure has also been described in chickens in the Andes mountains and humans living at extreme elevations. The incidence in cattle on high mountain pastures averages ~2% with variations from 0.5-5%. Though closely associated with altitude, other genetic, physiologic, environmental, and toxic factors play important roles in disease development and progression. Newly introduced cattle tend to be more susceptible than native cattle. Clinical signs and lesions
generally take about 2 mo to become obvious. In those areas in North America where cattle spend summer and fall grazing at high altitudes and return to lower elevations later in the fall, the disease is usually manifest in late summer. In areas where cattle live year round at high altitudes, the disease incidence is greatest in winter or early spring. This may be due to the stress of winter weather and late pregnancy. It affects all sexes, ages, and breeds, but not necessarily
equally. It is more common, for instance, in steers <1 yr old. |
| Etiology: |
| Although many factors may contribute to the incidence of high-mountain disease, the pathogenesis seems directly related to the chronic hypoxia, hypocapnia, and respiratory alkalosis of a high-altitude environment. These changes collectively result in pulmonary vasoconstriction, pulmonary hypertension, and ultimately CHF. There is marked interindividual and interspecies variability in hypoxia-induced increases in pulmonary vascular resistance. Strong responses are seen in
cattle, horses, and pigs, while humans, dogs, guinea pigs, and llamas are weak responders. These findings and the high incidence of disease in cattle indicate that they are uniquely susceptible. |
| The role of genetics in high-mountain disease is supported by high familial incidence with marked variation in susceptibility between animals and between species. While the cause or genes involved have not been identified, it may be related to altered chemoreceptor activity and myocardial metabolism. Previous damage, such as that caused by bronchopneumonia, interstitial pneumonia, emphysema, pulmonary fibrosis, anemia, or a ruptured diaphragm, all increase dyspnea, pulmonary
vascular resistance, and pulmonary hypertension. |
| Although various range plants, both browse and nonbrowse-types, have been associated with increased incidence of high-mountain disease, only
locoweed has been experimentally shown to induce the disease. When consumed by cattle at high elevation, locoweeds (certain
Oxytropis
and
Astragalus
spp
that contain swainsonine), markedly increase the prevalence and severity of CHF. The condition develops relatively more quickly (eg, within 1-2 wk) and the incidence may be as high as 100%. Swainsonine, the locoweed toxin, is excreted in milk, and nursing calves may also develop CHF. Locoweed-poisoned cows often abort and many develop severe hydrops amnii. Poisoned animals have the signs and lesions of both high-mountain disease and locoweed poisoning. Locoweed
poisoning probably directly contributes to increased pulmonary vascular resistance and hypertension; immunohistochemistry and electron microscopy studies have shown that poisoning causes severe swelling and cytoplasmic vacuolation of pulmonary intravascular macrophages and endothelial cells. The myocardium also is compromised by locoweed as there is extensive vacuolation of the myocardial interstitial cells. The toxin also inhibits enzymes that have key roles in glycoprotein
synthesis, packaging, and excretion. This results in altered glycosylation of key endocrine and paracrine hormones and their receptors. All of these changes probably contribute to the inappropriate pulmonary vascular resistance that appears to be the initiating factor in the pathogenesis of high-mountain disease. |
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| Clinical Findings: |
| The clinical changes of CHF of high-mountain disease usually develop slowly over several weeks. Periods of severe cold or other environmental stress appear to precipitate the onset of signs. Affected animals initially appear depressed and reluctant to move. As the syndrome progresses, subacute edema develops in the brisket region and extends cranially to the intermandibular space and caudally to the ventral abdominal wall. Marked distention and pulsation of the jugular vein are
usually prominent, and profuse, fluid diarrhea may develop. Respiration is labored, and animals may appear cyanotic. As the disease progresses, affected cattle become more reluctant to move and may become recumbent. With forced exertion, severely affected animals may collapse and die. |
Lesions:
| Generalized edema is especially severe in the ventral subcutis, skeletal musculature, perirenal tissues, mesentery, and wall of the GI tract. Ascites, hydrothorax, and hydropericardium are consistent findings. The liver lesions, due to chronic passive congestion, vary from an early “nutmeg” appearance to severe lobular and vascular fibrosis. The lungs may have varying degrees of atelectasis, interstitial emphysema, edema, and pneumonia. The heart has marked right
ventricular hypertrophy and dilatation; the cardiac apex is displaced to the left, making the enlarged heart appear round. Pulmonary arterial thrombosis is frequent. Microscopically, there is hypertrophy of the media of small arteries and arterioles in the lungs. This disease must be differentiated from other diseases that cause CHF in cattle, eg, traumatic pericarditis, chronic pneumonia, congenital anomalies, and primary myocardial lesions. |
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| Treatment and Control: |
| Affected animals should be moved with minimal restraint, stress, and excitement to a lower altitude. General supportive therapy, including diuretics, may be beneficial. At high altitudes, use of oxygen may be considered for valuable animals. Because the disease may recur, affected animals should not be returned to high altitudes and, because an inherited susceptibility is likely, they should not be retained for breeding. Although it has been suggested that measurement of
pulmonary arterial pressure of new sires may allow selection of resistant animals, this has not been proven. Extensive studies in humans exposed to high altitudes have shown that baseline Doppler studies of pulmonary pressures and circulation have little predictive value of tolerance to altitudes. |
| Because locoweed poisoning has been directly linked to the development of CHF in cattle, care should be taken to minimize the exposure of susceptible animals by ensuring that animals have a good selection of forage. Poisoned animals should be moved to pastures free of locoweed before severe and irreversible damage occurs. |
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