Brisket Disease Research Articles

The Use of Pulmonary Arterial Pressure (PAP) for Improved Beef Cattle Management.

Pulmonary arterial pressure (PAP) determines cattle's susceptibility to High Altitude Disease (HAD), also known as Brisket Disease, High Mountain Disease, and right-sided heart failure (RHF). This non-infectious disease causes pulmonary hypertension due to hypoxia. PAP measures the resistance of blood flow through the lungs. It is estimated that 1.5 million head of cattle are raised in high-altitude environments (above 1500 m), and HAD accounts for 3-5% of calf death loss yearly. In addition, there have been increasing concerns about feedlot cattle succumbing to RHF at moderate elevations. This review focuses on the historical background, explanation of PAP measurement and scores, genetic implications, and the relationship between PAP and economically relevant traits. Specifically, traits such as gestation length, birth weight, weaning weight, and yearling weight may impact PAP scores. In addition, environmental effects and other factors impacting PAP score variations are discussed. Information gaps and research needs are addressed to determine where missing information could improve the understanding of PAP while also benefiting beef cattle producers in high-elevation production systems.

Identification of the molecular mechanisms underlying brisket disease in Holstein heifers via microbiota and metabolome analyses

Brisket disease (BD) is common among Holstein heifers in high-altitude environments, and this disease may result in serious economic loss. At present, no effective treatment is available for brisket disease. In this study, liver and cecum samples were collected from five heifers with BD and five healthy heifers (HH) for analyses of the metabolome and microbiota. The mean pulmonary arterial pressure and systolic blood pressure were significantly higher in BD heifers, whereas the average breathing rate, blood oxygen saturation, and glucose level were significantly lower in BD group than in the HH group. Further, 16S rDNA data showed that the abundance of Firmicutes was significantly lower and that of Bacteroidetes was significantly higher in BD group than in the HH group. At the genus level, the BD group heifers harbored fewer Ruminococcaceae and Lachnospiraceae than the HH group. Several metabolites, including beta-d-fructose, d-ribose, 1,4-beta-d-glucan, sucrose, and glucose-6-phosphate were present at low levels in BD heifers. Moreover, the mean pulmonary arterial pressure was negatively correlated with beta-d-fructose (r = − 0.74; P = 0.013), d-ribose (r = − 0.72; P = 0.018), and acetyl-tyrosine-ethyl-ester (r = − 0.71; P = 0.022). We also found that mean pulmonary arterial pressure was negatively correlated with most of the genera, including those in the families of Lachnospiraceae and Ruminococcaceae. In summary, the decreased levels of metabolites and microbial genera might affect BD by limiting the energy supply. This study may help us better understand the role of the microbiota in BD and provide new insights into the management of feeding to decrease the rate of BD in Holstein dairy cows in the Qinghai-Tibetan plateau.

Brisket Disease Is Associated with Lower Volatile Fatty Acid Production and Altered Rumen Microbiome in Holstein Heifers

Simple SummaryDevelopment of the dairy industry in the high-altitude plateau environment through incorporation of Holstein cows is complicated by the risk of brisket disease. While the physiological effects of brisket disease are well-studied, its effects on rumen function and microbial community composition are not. There are clear shifts in volatile fatty acids production and rumen microbial community composition in Holstein heifers suffering from brisket disease. Observed shifts reveal key genera associated with healthy and disease states and suggest that bovine brisket disease is associated with impaired rumen functioning. This work supports further understanding of the roles of key rumen taxa in bovine brisket disease, with particular focus on candidate rumen biomarkers in healthy animals that may be able to reduce economic losses for farmers.Brisket disease is heritable but is also associated with non-genetic risk factors and effects of the disease on the rumen microbiome are unknown. Ten Holstein heifers were exposed to the plateau environment for three months and divided into two groups according to the index of brisket disease, the mean pulmonary arterial pressure (mPAP): brisket disease group (BD, n = 5, mPAP > 63 mmHg) and healthy heifer group (HH, n = 5, mPAP < 41 mmHg). Rumen fluid was collected for analysis of the concentrations of volatile fatty acids (VFAs). Extracted DNA from rumen contents was analyzed using Illumina MiSeq 16S rRNA sequencing technology. The concentration of total VFA and alpha-diversity metrics were significantly lower in BD group (p < 0.05). Ruminococcus and Treponema were significantly decreased in BD heifers (p < 0.05). Correlation analysis indicated that 10 genera were related to the mPAP (p < 0.05). Genera of Anaerofustis, Campylobacter, and Catonella were negatively correlated with total VFA and acetic acid (R < −0.7, p < 0.05), while genera of Blautia, YRC22, Ruminococcus, and Treponema were positively related to total VFA and acetic acid (R > 0.7; p < 0.05). Our findings may be a useful biomarker in future brisket disease work.

Investigation of congestive heart failure in beef cattle in a feedyard at a moderate altitude in western Nebraska.

Right-sided congestive heart failure (brisket disease) commonly occurs in cattle raised at elevations >2,500-3,500 m. We investigated clinical cases resembling brisket disease at a western Nebraska feedyard at a moderate altitude (1,369 m). Over a 15-mo period (2009-2010), we examined 17 cases (16 steers and 1 heifer), all purebred Angus. All animals had clinical right-sided heart failure: brisket and ventral abdominal edema, and severe chronic passive congestion of the liver. Gross examination confirmed right ventricular hypertrophy (left ventricle plus septum: right ventricle weight ratio mean: 1.33 vs. 2.8-4.0 reference interval). Microscopically, all 17 cases had interstitial fibrosis (mean score: 2.4 ± 0.8) and 6 had replacement fibrosis of the right ventricle, whereas 14 had interstitial fibrosis (mean score: 1.2 ± 0.2) and 0 had replacement fibrosis of the left ventricle. Lesions of arteriosclerosis were seen in 9 of 16 cases in 51 of 571 (8.9%) right ventricular coronary arteries, and in 10 of 16 cases in 52 of 366 (14.2%) left ventricular coronary arteries. The probability of coronary arteriosclerosis was greater in papillary ventricular muscle (OR = 11.3; p < 0.0001), left ventricle (OR = 4.8; p < 0.0001), and larger arteries (OR = 1.01; p < 0.0001). Pulmonary arteries and arterioles had lesions compatible with hypoxia-induced pulmonary hypertension. We hypothesize that moderate hypobaric conditions significantly contributed to disease in cattle genetically predisposed to hypoxia-induced pulmonary hypertension. Adiposity, coronary arteriosclerosis, and left ventricular fibrosis may have contributed to the condition; however, the cattle died prior to development of advanced obesity.

Hypoxia-induced pulmonary hypertension and chronic lung disease: caveolin-1 dysfunction an important underlying feature.

Caveolin-1 (cav-1) has been shown to play a significant role in the pathogenesis of pulmonary hypertension (PH). In the monocrotaline model of PH, the loss of endothelial cav-1 as well as reciprocal activation of proliferative and anti-apoptotic pathways initiate the disease process and facilitate its progression. In order to examine the role of cav-1 in hypoxia-induced PH, we exposed rats and neonatal calves to hypobaric hypoxia and obtained hemodynamic data and assessed the expression of cav-1 and related proteins eNOS, HSP90, PTEN, gp130, PY-STAT3, β-catenin, and Glut1 in the lung tissue. Chronic hypoxic exposure in rats (48 h–4 weeks) and calves (two weeks) did not alter the expression of cav-1, HSP90, or eNOS. PTEN expression was significantly decreased accompanied by PY-STAT3 activation and increased expression of gp130, Glut1, and β-catenin in hypoxic animals. We also examined cav-1 expression in the lung sections from steers with chronic hypoxic disease (Brisket disease) and from patients with chronic lung disease who underwent lung biopsy for medical reasons. There was no cav-1 loss in Brisket disease. In chronic lung disease cases, endothelial cav-1 expression was present, albeit with less intense staining in some cases. In conclusion, hypoxia did not alter the cav-1 expression in experimental models. The presence of cav-1, however, did not suppress hypoxia-induced activation of PY-STAT3 and β catenin, increased gp130 and Glut1 expression, or prevent the PTEN loss, indicating cav-1 dysfunction in hypoxia-induced PH.

PULMONARY ARTERIAL DISEASE ASSOCIATED WITH RIGHT-SIDED CARDIAC HYPERTROPHY AND CONGESTIVE HEART FAILURE IN ZOO MAMMALS HOUSED AT 2,100 M ABOVE SEA LEVEL.

Subacute and chronic mountain sickness of humans and the related brisket disease of cattle are characterized by right-sided congestive heart failure in individuals living at high altitudes as a result of sustained hypoxic pulmonary hypertension. Adaptations to high altitude and disease resistance vary among species, breeds, and individuals. The authors conducted a retrospective survey of right-sided cardiac hypertrophy associated with pulmonary arterial hypertrophy or arteriosclerosis in zoo mammals housed at Africam Safari (Puebla, México), which is located at 2,100 m above sea level. Seventeen animals with detailed pathology records matched the study criterion. Included were 10 maras (Dolichotis patagonum), 2 cotton-top tamarins (Saguinus oedipus oedipus), 2 capybaras (Hydrochaeris hydrochaeris), and 1 case each of Bennet's wallaby (Macropus rufogriseus), nilgai antelope (Boselaphus tragocamelus), and scimitar-horned oryx (Oryx dammah). All had right-sided cardiac hypertrophy and a variety of arterial lesions restricted to the pulmonary circulation and causing arterial thickening with narrowing of the arterial lumen. Arterial lesions most often consisted of medial hypertrophy or hyperplasia of small and medium-sized pulmonary arteries. All maras also had single or multiple elevated plaques in the pulmonary arterial trunk consisting of fibrosis, accompanied by chondroid metaplasia in some cases. Both antelopes were juvenile and died with right-sided congestive heart failure associated with severe pulmonary arterial lesions. To the authors' knowledge, this is the first description of cardiac and pulmonary arterial disease in zoo mammals housed at high altitudes.

Myosin heavy chain 15 is associated with bovine pulmonary arterial pressure.

Bovine pulmonary hypertension, brisket disease, causes significant morbidity and mortality at elevations above 2,000 m. Mean pulmonary arterial pressure (mPAP) is moderately heritable, with inheritance estimated to lie within a few major genes. Invasive mPAP measurement is currently the only tool available to identify cattle at risk of hypoxia-induced pulmonary hypertension. A genetic test could allow selection of cattle suitable for high altitude without the need for invasive testing. In this study we evaluated three candidate genes (myosin heavy chain 15 [MYH15], NADH dehydrogenase flavoprotein 2, and FK binding protein 1A) for association with mPAP in 166 yearling Angus bulls grazing at 2,182 m. The T allele (rs29016420) of MYH15 was linked to lower mPAP in a dominant manner (CC 47.2 ± 1.6 mmHg [mean ± standard error of the mean]; CT/TT 42.8 ± 0.7 mmHg; P = 0.02). The proportions of cattle with MYH15 CC, CT, and TT genotypes were 55%, 41%, and 4%, respectively. Given the high frequency of the deleterious allele, it is likely that the relative contribution of MYH15 polymorphisms to pulmonary hypertension is small, supporting previous predictions that the disease is polygenic. We evaluated allelic frequency of MYH15 in the Himalayan yak (Bos grunniens), a closely related species adapted to high altitude, and found 100% prevalence of T allele homozygosity. In summary, we identified a polymorphism in MYH15 significantly associated with mPAP. This finding may aid selection of cattle suitable for high altitude and contribute to understanding human hypoxia-induced pulmonary hypertension.

Right ventricular hypertrophy with heart failure in Holstein heifers at elevation of 1,600 meters

A syndrome of progressive right-sided heart failure occurred among yearling Holsteins at a heifer-raising facility and 2 dairies on the Colorado Front Range between 2007 and 2011. Most cases were seen at the heifer-raising facility, where the disease ranked second only to pneumonia as a major cause of death in animals aged <1.5 years. The disease resulted in the death or premature sale of 55 animals over the 5-year period. Affected heifers were 4-15 months old when they developed dyspnea, tachycardia, distention and pulsation of jugular veins, lethargy, and weight loss. Clinical progression in most was rapid (2 days to 2 weeks). Ten cattle with typical clinical signs were examined postmortem between 2008 and 2010. Seven developed clinical signs after transportation 57-238 days earlier from Wisconsin (elevation: < 275 m); the remaining 3 animals were born and raised at an altitude of 1,600 m. At necropsy, the 10 cattle had marked hypertrophy of right ventricular myocardium, dilated right atria, right ventricles, and pulmonary trunks, as well as hepatomegaly, ascites, and serous atrophy of fat. The principal histological change in lungs was hypertrophied tunicae adventitia and media of muscular arteries. Hepatic changes were typical of chronic passive congestion. Ultrastructural changes in heart were consistent with uncomplicated hypertrophy of cardiocytes with no evidence of primary cardiomyopathy. The syndrome most likely represents brisket disease due to pulmonary hypertension at the modest elevation of 1,600 m.

Genotype by environment interaction for growth due to altitude in United States Angus cattle1

The objectives of this study were to determine if sires perform consistently across altitude and to quantify the genetic relationship between growth and survival at differing altitudes. Data from the American Angus Association included weaning weight (WW) adjusted to 205 (n = 77,771) and yearling weight adjusted to 365 (n = 39,450) d of age from 77,771 purebred Angus cattle born in Colorado between 1972 and 2007. Postweaning gain (PWG) was calculated by subtracting adjusted WW from adjusted yearling weight. Altitude was assigned to each record based upon the zip code of each herd in the database. Records for WW and PWG were each split into 2 traits measured at low and high altitude, with the records from medium altitude removed from the data due to inconsistencies between growth performance and apparent culling rate. A binary trait, survival (SV), was defined to account for censored records at yearling for each altitude. It was assumed that, at high altitude, individuals missing a yearling weight either died or required relocation to a lower altitude predominantly due to brisket disease, a condition common at high altitude. Model 1 considered each WW and PWG measured at 2 altitudes as separate traits. Model 2 treated PWG and SV measured as separate traits due to altitude. Models included the effects of weaning contemporary group, age of dam, animal additive genetic effects, and residual. Maternal genetic and maternal permanent environmental effects were included for WW. Heritability estimates for WW in Model 1 were 0.28 and 0.26 and for PWG were 0.26 and 0.19 with greater values in low altitude. Genetic correlations between growth traits measured at different altitude were moderate in magnitude: 0.74 for WW and 0.76 for PWG and indicate possibility of reranking of sires across altitude. Maternal genetic correlation between WW at varying altitude of 0.75 also indicates these may be different traits. In Model 2, heritabilities were 0.14 and 0.27 for PWG and 0.36 and 0.47 for SV. Genetic correlation between PWG measured at low and high altitude was 0.68. Favorable genetic correlations were estimated between SV and PWG within and between altitudes, suggesting that calves with genetics for increased growth from weaning to yearling also have increased genetic potential for SV. Genetic evaluations of PWG in different altitudes should consider preselection of the data, by using a censoring trait, like survivability to yearling.

High-altitude pulmonary hypertension in cattle (brisket disease): Candidate genes and gene expression profiling of peripheral blood mononuclear cells.

High-altitude pulmonary hypertension (HAPH) is a consequence of chronic alveolar hypoxia, leading to hypoxic vasoconstriction and remodeling of the pulmonary circulation. Brisket disease in cattle is a naturally occurring animal model of hypoxic pulmonary hypertension. Genetically susceptible cattle develop severe pulmonary hypertension and right heart failure at altitudes >7,000 ft. No information currently exists regarding the identity of the pathways and gene(s) responsible for HAPH or influencing severity. We hypothesized that initial insights into the pathogenesis of the disease could be discovered by a strategy of (1) sequencing of functional candidates revealed by single nucleotide polymorphism (SNP) analysis and (2) gene expression profiling of affected cattle compared with altitude-matched normal controls, with gene set enrichment analysis (GSEA) and Ingenuity pathway analysis (IPA). We isolated blood from a single herd of Black Angus cattle of both genders, aged 12-18 months, by jugular vein puncture. Mean pulmonary arterial pressures were 85.6±13 mmHg STD in the 10 affected and 35.3±1.2 mmHg STD in the 10 resistant cattle, P<0.001. From peripheral blood mononuclear cells, DNA was hybridized to an Affymetrix 10K Gene Chip SNP, and RNA was used to probe an Affymetrix Bovine genome array. SNP loci were remapped using the Btau 4.0 bovine genome assembly. mRNA data was analyzed by the Partek software package to identify sets of genes with an expression that was statistically different between the two groups. GSEA and IPA were conducted on the refined expression data to identify key cellular pathways and to generate networks and conduct functional analyses of the pathways and networks. Ten SNPs were identified by allelelic association and four candidate genes were sequenced in the cohort. Neither endothelial nitric oxide synthetase, NADH dehydrogenase, TG-interacting factor-2 nor BMPR2 were different among affected and resistant cattle. A 60-gene mRNA signature was identified that differentiated affected from unaffected cattle. Forty-six genes were overexpressed in the affected and 14 genes were downregulated in the affected cattle by at least 20%. GSEA and Ingenuity analysis identified respiratory diseases, inflammatory diseases and pathways as the top diseases and disorders (P<5.14×10-14), cell development and cell signaling as the top cellular functions (P<1.20×10-08), and IL6, TREM, PPAR, NFkB cell signaling (P<8.69×10-09) as the top canonical pathways associated with this gene signature. This study provides insights into differences in RNA expression in HAPH at a molecular level, and eliminates four functional gene candidates. Further studies are needed to validate and refine these preliminary findings and to determine the role of transcribed genes in the development of HAPH.

Effect of Altitude on the Heart and the Lungs

This review focuses on the effects of altitude exposure from 1 to several days or weeks as occurs in tourists, trekkers, and mountaineers who visit high altitude and normally reside near sea level. We briefly review the acute physiological adjustments and early acclimatization that occur in the cardiovascular system and the lungs of healthy individuals. These ensure life-sustaining oxygen delivery to the tissues despite a reduction in the partial pressure of inspired oxygen between 20% and 60% at 2500 and 8000 m, respectively. One of the acute adjustments, hypoxic pulmonary vasoconstriction (HPV), may be disadvantageous in those with a vigorous response and lead to 2 potentially lethal illnesses, high-altitude pulmonary edema (HAPE) and subacute mountain sickness (SAMS), which we present in more detail. Finally, on the basis of knowledge about the acute physiological adjustments and acclimatization and, when available, a review of the literature, we discuss the high-altitude tolerance of patients with coronary artery disease, congestive heart failure, arrhythmias, systemic hypertension, and pulmonary hypertension. ### Circulation The major effects of acute hypoxia on the heart and lung are shown in Figure 1. Hypoxia directly affects the vascular tone of the pulmonary and systemic resistance vessels and increases ventilation and sympathetic activity via stimulation of the peripheral chemoreceptors.1 Interactions occur between the direct effects of hypoxia on blood vessels and the chemoreceptor-mediated responses in the systemic and pulmonary circulation. Figure 1. Effects of hypoxia on systemic and pulmonary circulation. Unraveling the underlying mechanisms of the hypoxic vasodilatation of systemic arterioles is an active area of research. Several mechanisms appear to regulate local oxygen delivery according to the needs of the tissues2,3; for instance, the release of ATP from red blood cells and the generation of NO by various ways appear to regulate local oxygen delivery according to the needs …

Comparative physiology of hypoxic pulmonary hypertension: historical clues from brisket disease

Some of the most valuable contributions to science have come about serendipitously, and, in 1913, when George Glover and Issac Newsom were commissioned by Colorado cattle ranchers to study high mountain disease, there was no way to anticipate the tremendous impact they would have on the study of high-altitude cardiopulmonary physiology. It was through the study of this agricultural malady that the correlation between chronic hypoxia, pulmonary hypertension, medial hypertrophy of the small pulmonary arteries, and right ventricular (RV) hypertrophy was recognized. The amount of vascular smooth muscle comprising the medial layer of pulmonary arteries varies significantly across species and can be used to predict the magnitude of pulmonary hypertension and RV hypertrophy elicited in response to chronic hypoxia. Within species, age and gender both significantly influence the severity of chronic hypoxic pulmonary hypertension and RV hypertrophy. However, despite all that we now know about hypoxic pulmonary hypertension, the specific mechanism(s) that differentiate the hypo- from the hyperresponder have yet to be elucidated. Adventitial fibroblast differentiation, circulating vascular progenitor cells, the presence or absence of specific vascular smooth muscle phenotypes, the upregulation or downregulation of vasoactive mediators, splice variants of oxygen-sensitive transcription factors, upregulation of growth factors, Ca(2+) sensitization, and/or the Rho/Rho-kinases signaling cascade could all potentially play a role in determining the extent of the vascular response to hypoxia within a species. Understanding the mechanisms that determine why some people, as well as some animals, exhibit a marked susceptibility to hypoxia is an important endeavor with far-reaching implications.

HIGHLIGHTED TOPIC: Pulmonary Circulation and Hypoxia

In 1946, Ulf von Euler and Goran Liljestrand published revolutionary findings on the impact of hypoxia as a stimulant for vasoconstriction in the pulmonary circulation. More than 50 years later, exploring the mechanistic basis for this relationship is still a vital area of research. Among the many

Syndromes of subacute mountain sickness.

Two clinical syndromes, acute and chronic mountain sickness, have traditionally been associated with high altitude. Recently, two separate entities of subacute nature have been described in infants and adults. In this paper, we review the published literature on these conditions. Subacute infantile mountain sickness is a condition seen predominantly in Han Chinese infants living in Tibet, although it has been described in other high altitude communities as well. It came into prominence only after the large-scale migration of Chinese population from the low altitude of mainland China to the high altitudes of the Qinghai-Tibetan plateau. The condition is characterized by features of severe hypoxic pulmonary hypertension and heart failure. Pulmonary histology is consistent with muscularization of the pulmonary arterioles, but no intimal proliferation or plexiform lesions are seen. The second syndrome, adult subacute mountain sickness, has been described almost exclusively in Indian soldiers living at extreme altitude for prolonged periods of time. In this condition also, hypoxic pulmonary hypertension appears to be the dominant factor responsible for severe congestive heart failure. Both these conditions have several similarities with brisket disease in cattle; hypoxic pulmonary vasoconstriction plays an important role in the pathogenesis, and removal from high altitude results in complete resolution. Thus, it appears that both these syndromes are human counterparts of brisket disease in cattle.

Deficiências e desequilíbrios minerais em bovinos e ovinos &lt;FONT FACE=Symbol&gt;¾&lt;/FONT&gt; revisão dos estudos realizados no Brasil de 1987 a 1998

É apresentada uma revisão dos estudos realizados no Brasil sobre distúrbios no metabolismo mineral em bovinos, sobretudo deficiências minerais, no período de 1987-1998. Esta revisão foi feita em continuação de duas revisões prévias sobre o assunto, que abrangeram os períodos de 1943-1976 e 1976-1987. Nessas revisões são omitidos os estudos realizados apenas através de dosagens químicas de amostras de pastagem e de solo, sendo referidos aqueles baseados em análises de amostras de fígado ou outros tecidos ou fluidos dos animais e/ou experimentação, complementados ou não por análises químicas de pastagem e de solo. Em relação aos macroelementos, destacam-se os estudos sobre a deficiência de fósforo, já estabelecida anteriormente como a deficiência mineral mais importante no Brasil. Valores baixos de ferro em amostras de fígado foram constatados em bovinos afetados pela hematúria enzoótica, o que é compreensível, já que os animais apresentam marcada anemia devido a perda contínua de sangue. Destacaram-se, por outro lado, os valores elevados de ferro em diversas regiões; em algumas delas foi demonstrado que os níveis desse elemento estavam associados a valores baixos de cobre. As deficiências de cobre e cobalto foram as mais frequentes entre as de microelementos. Diversas ocorrências de intoxicação por cobre em ovinos foram comunicadas. A deficiência subclínica de zinco tem sido verificada com bastante frequência. A deficiência subclínica de manganês foi raramente constatada; ao contrário, houve verificações de valores elevados deste elemento. Em relação ao selênio, os dados continuam escassos, insuficientes para se saber qual a importância da deficiência desse elemento em bovinos e ovinos no Brasil; a miopatia nutricional em bezerros foi diagnosticada uma única vez. Entre os estudos realizados neste último período devem ser mencionados, especialmente, aqueles que abordam duas doenças cuja etiologia ainda não foi estabelecida, vulgarmente conhecidas como "ronca" e "doença do peito inchado", ambas de evolução crônica, afetando bovinos adultos. Na enfermidade conhecida como "ronca", os valores hepáticos de cobre são muito baixos e os de ferrro extremamente altos; deve-se considerar a hipótese de que os níveis hepáticos de ferro estão muito elevados em decorrência da sua não-utilização em função da deficiência de cobre. Na "doença do peito inchado", os valores hepáticos de manganês e de cobalto são baixos e os de ferro são muito elevados; é possível que as alterações nos níveis hepáticos de ferro sejam apenas o reflexo do acúmulo de sangue no fígado, uma vez que essa enfermidade é caracterizada por insuficiência cardíaca crônica que cursa com acentuada congestão hepática. Ainda deve ser destacada, no Rio Grande do Sul, a ocorrência de "morte súbita" em bovinos, cujos valores hepáticos para cobre foram muito baixos; nenhuma planta tóxica pode ser responsabilizada por essas ocorrências. Nesta mesma área, a hipomielinogênese congênita em bovinos foi diagnosticada. A ocorrência das deficiências minerais diagnosticadas durante o período correspondente a esta revisão foram lançadas em um mapa, com as respectivas referências bibliográficas.

Genetic models with reduced penetrance related to the Y chromosome.

Classical statistical genetics models of a quantitative trait depending on an autosomal gene indicate that father-to-daughter and mother-to-son correlations should be the same. If phenotypes are not sex-dependent, father-to-son and mother-to-daughter correlations also share this common value. On the other hand, if the gene is sex-linked, then the father-to-son correlation is zero. Such models do not explain genetic variation in pulmonary artery pressure (PAP) of cattle--important because cattle with high PAP are known to develop brisket disease, pulmonary heart disease, and congestive heart failure when taken to high altitudes. Data on 966 calves at a ranch in Colorado showed positive correlation (0.2) between sire PAP and male calf PAP but slightly negative correlation (-0.01) between sire PAP and female calf PAP; the dam-to-male calf and dam-to-female calf correlations are both about 0.1. The model presented here postulates an autosomal gene with reduced penetrance (i.e., the trait may remain at a normal level even when the genotype suggests abnormality) and that, in males, the rate of penetrance is related to an abnormality in the Y chromosome and is therefore passed on from father to son. Then under plausible selective breeding assumptions, the pairwise correlation between fathers and daughters can become zero or negative. Explicit formulas are computed for the model covariances, and numerical computations indicate that plausible parameter values can be chosen for the model.

Pulmonary circulation at high altitude.

Hypoxia constricts the pulmonary vessels. An increase in pulmonary vascular resistance is seen in normal subjects during hypoxic breathing at sea level, in acclimatized lowlanders and in high-altitude natives. Hypoxic pulmonary hypertension in all these circumstances is most generally moderate, except in high-altitude natives at exercise. Pulmonary hypertension may become severe during high-altitude pulmonary edema, during infantile or adult forms of subacute mountain sickness, and during chronic mountain sickness. Subacute and chronic mountain sickness may be associated with a right heart failure that would be the human counterpart of brisket disease described in cattle. Subjects susceptible to high-altitude pulmonary edema present with a slight increase in pulmonary vascular resistance at rest and at exercise, and often with an enhanced pulmonary vascular reactivity to hypoxia. However, compared to unselected controls, the overlap is great, so that noninvasive echo-Doppler studies of the pulmonary circulation at sea level are of little predictive value of tolerance to altitudes on an individual basis.

Cardiovascular response to exogenous serotonin in healthy calves

Abstract Objective To characterize the cardiovascular response to IV administration of serotonin (5-hydroxytryptamme [5- HT]) in calves. Animals 5 healthy unsedated Friesian calves. Procedure 41 5-HT administrations were performed: 11 slow infusions (duration, 5 minutes) and 30 bolus infusions (duration, 5 seconds). Cardiovascular function values were recorded before, during, and after the infusions. Results Slow infusion of 5-HT first resulted in a brief period of severe bradycardia, then in sustained tachycardia with a concomitant increase in cardiac output. Systemic blood pressure response to 5-HT was triphasic, with initial hypotension concomitant with bradycardia, then a pressor phase associated with an increase in systemic vascular resistance, and finally, a long-lasting hypotensive phase associated with decreased systemic vascular resistance. Pulmonary hypertension was associated with increased pulmonary vascular resistance, reflecting intense pulmonary vasoconstriction. Bolus infusion at increasing dosages resulted in dose-dependent bradycardia and systemic hypotension, followed by dose-dependent systemic hypertension. Unlike with slow infusion, neither the second tachycardic nor the third systemic hypotensive phases were evident. Conclusions 5-HT induces dose-dependent cardiovascular responses, including a reflex response followed by pulmonary and systemic vasoconstriction, in healthy calves. Clinical Relevance Determining the type of serotonergic receptors responsible for these responses may help to determine whether 5-HT is involved in the mechanisms underlying brisket disease in cattle. (Am J Vet Res 1996; 57:731–738)

Pulmonary circulation in hypoxia.

Hypoxia constricts the pulmonary vessels. An increase in pulmonary vascular resistance is seen in normal subjects during hypoxic breathing at sea level, in acclimatized lowlanders and in high altitude natives. Hypoxic pulmonary hypertension in all these circumstances is most generally moderate, except in high altitude natives at exercise. However, in the absence of high altitude pulmonary edema (HAPE) or chronic mountain sickness, a right heart failure that would be the human counterpart of brisket disease described in cattle, apparently never occurs. In adult patients with HAPE, reported mean pulmonary artery pressures (Ppa) measured during a right heart catheterization range from 22 to 63 mmHg with an average of 39 mmHg. Recent echo-Doppler estimates of systolic Ppa in patients with a HAPE are at an average of 53 mmHg, only moderately higher than in healthy subjects exposed to comparable normobaric or hypobaric hypoxia. Subjects with a previous HAPE often present with an enhanced pulmonary vascular reactivity to hypoxia compared to controls when tested at sea level, but the overlap is great. Non invasive echo-Doppler pulmonary hemodynamic studies at sea level have not been reported to reliably discriminate subjects susceptible to HAPE.

Annual costs associated with disease incidence and prevention in Colorado cow-calf herds participating in rounds 2 and 3 of the National Animal Health Monitoring System from 1986 to 1988

Summary Thirty-nine and 47 randomly selected Colorado cow-calf operations were monitored for health events and their associated costs during rounds 2 and 3, respectively, of the National Animal Health Monitoring System (NAHMS). Data were collected from each operation for a one-year period by NAHMS veterinarians through monthly interviews, and the costs associated with the incidence and prevention of disease conditions were determined and expressed on a per cow basis. The beef producers involved in this study spent an average of $32.75 per cow in round 2 and $40.97 per cow in round 3 on an annual basis for the treatment of disease conditions. These costs were not different between the 2 rounds because of the wide ranges in the individual herd costs for disease incidence in each round. In both years of the study, the largest contributor to the total mean annual cost of disease incidence was the cost of death of diseased animals, and this cost accounted for approximately two-hirds of the total mean annual cost in each round. The total mean annual costs of disease prevention in these herds were $11.24 and $11.19 per cow in rounds 2 and 3, respectively. There were wide ranges in both rounds in the amounts of money spent per cow by individual herds for disease prevention. The largest individual cost of disease prevention in each year was the cost of vaccines/drugs, whereas the smallest individual cost in each round was the cost of veterinary services. Nearly all the preventive veterinary services cost in each study year was attributed to pregnancy examination, brucellosis vaccination, breeding soundness examination of bulls, pulmonary arterial pressure testing, and campylobacteriosis vaccination. The costs of disease incidence and prevention were summed to determine the most costly individual disease conditions in the study herds. Death of unknown cause was the most expensive disease condition in both study years. Diarrhea of unknown cause, nonpregnancy, dystocia, pneumonia, hypothermia-exposure, general disease of parasitism, and brisket disease were other disease conditions that ranked among the ten most costly disease conditions in both rounds of the study. It was concluded that reducing the costs associated with disease has the potential for increasing profits in cow-calf operations.