Cardiac diseases of cattle (Proceedings)

Congenital, infectious, neoplastic, nutritional and toxic causes of cardiac disease are occasionally encountered in primary and referral bovine practice. The presentation accompanying these proceedings will review the most commonly encountered conditions with an emphasis on dairy cattle in the Northern United States. In addition the results of a small retrospective study on cases of idiopathic hemorrhagic pericarditis will be presented describing the diagnosis, management and outcome for adult cattle with this condition, based upon clinical cases seen at the University of Wisconsin's Veterinary Medical Teaching Hospital in recent years.

Pericardial disease

Septic pericarditis remains the best documented and most commonly reported pericardial disease in cattle. Within the literature it is most commonly attributed to foreign body penetration through the diaphragm, originating from the reticulum, although the potential does exist for extension of septic intra-thoracic disease independent of reticuloperitonitis. Clinical experience would suggest the latter is far less common, although occasional cases of septic pleural or pulmonary disease will extend to involve the pericardial sac. Aseptic pericardial effusions are most commonly associated with cardiac neoplasia (typically lymphosarcoma) or the recently documented condition of idiopathic hemorrhagic pericardial effusion1,2. Rare cases of cardiac neoplasia other than lymphosarcoma such as mesothelioma and chemidectoma are documented and these can lead to clinically significant accumulations of pericardial fluid and resultant tamponade3.

Idiopathic hemorrhagic pericardial effusion

There have been 2 reports in the literature1,2 of this condition and we have seen a number of cases admitted to our hospital during the last 5 years at the University of Wisconsin. It is an unusual condition but over the last 5 years admissions with this disease have approximately equalled the number of septic pericarditis cases in our hospital. It is most noteworthy from the perspective of outcome and longevity for affected cattle following treatment. As has been previously noted by Firshman et al (2006) pericardial drainage and anti-inflammatory medication can bring about prolonged (>1 year) remission. Our experiences have been similar suggesting that the common presenting signs and examination findings of cardiac tamponade and congestive failure can be reversed for sufficient time frames to allow for reproductive salvage and even a return to productivity in some mature dairy cattle. We have followed some cattle with this condition for several years and a few have gone on to develop a form of epicardial lymphosarcoma, quite distinct from the typical right atrial lymphosarcoma occasionally seen in association with BLV infection. Part of the conference presentation accompanying these proceedings will detail the case presentation, diagnosis, and outcome for cattle affected with this condition.

Endocardial disease

The most common endocardial disease encountered in cattle is septic endocarditis. Most cases are vegetative and valvular in location although concurrent mural endocardial lesions may also be seen. Mural endocarditis in the absence of valvular lesions is extremely rare. The retrospectives that have been published list the right atrioventricular (AV) valve as the most commonly affected, and the left AV valve being the next most likely to be involved4. Microbiological investigation of valvular lesions at post mortem and the blood of affected cattle ante-mortem have demonstrated that Arcanobacterium pyogenes is the most commonly cultured organism3.

Congenital heart disease

The largest retrospective study of congenital cardiac disease in calves published to date has documented that septal defects are most frequently encountered with ventricular septal defects (VSD) (198 out of 704) outnumbering atrial septal defects (ASD) (148 out of 704)5. As ultrasound has become a more commonly employed diagnostic tool for the evaluation of neonates with murmurs, or other clinical signs consistent with a potential cardiac defect (cyanosis, persistent tachycardia, stunted growth), it has become evident that a small number of individuals with small, solitary defects may survive and live functional, productive lives. Small VSDs without concurrent evidence of shunting, cardiac chamber dilation or notable growth retardation would be the best examples of this in the author's experience. Inevitably, ethical questions regarding the reproductive use of animals that have been diagnosed with a congenital defect swiftly follow the diagnosis if owners are debating whether or not the animal is to be culled. Categoric evidence linking common congenital heart defects in cattle with specific patterns of genetic inheritance is lacking although it is appropriate to broach the possibility of a hereditary component with owners.

Myocardial disease

Within the US, primary myocardial conditions are rare. Geographic areas that are selenium deficient have been historically notorious for sporadic cases of nutritional myodegeneration (white muscle disease), in which myocardial lesions can contribute to sudden death. The majority of cattle that are affected with white muscle disease have clinical and biochemical evidence of skeletal muscle injury that lead to a suspicion of the disease ahead of cardiac signs. However, in endemic areas one should be aware of the potential for the condition to cause sudden death, or a brief period of respiratory distress alongside clinical evidence of cardiac disease prior to death, in young cattle. The potential for involvement of the myocardium and epicardium following Histpohilus somni infection will be familiar to veterinarians working with feedlot cattle, but seems to be very unusual in dairy cattle. Most frequently the myocardial lesions will be noted during post mortem examination of a feedlot animal in which the predominating clinical and pathologic findings related to the respiratory tract.

Lymphosarcoma represents an important differential for cattle over 2 years of age that present with signs of cardiac disease. The right atrium is a documented predilection site for tumors in bovine leukosis virus (BLV) positive cattle4. Tachyarrythmias, tachycardia with sinus rhythm and outward signs of predominantly right sided congestive heart failure (brisket edema, distended jugular veins and/or true jugular pulsation, prominent, turgid milk veins) would be the common physical examination findings. Occasional cases may auscult with muffled heart sounds similar to a pericarditis case due to effusion within the pericardial sac. During echocardiography it is frequently much easier to determine the presence and extent of the cardiac failure than it is to visualize the neoplastic infiltration of the myocardium.

Dilated cardiomyopathy is a rarely encountered primary myocardial disease in Holstein-Freisian cattle6. It is hereditary and the majority of reports of the condition are from Europe6,7 and Japan8. Affected cattle develop clinical signs of congestive heart failure, typically in young adulthood. Recently the gene associated with this condition has been identified and mapped in the Holstein-Freisian breed9. There are reports of the condition in other European breeds that are not commonly encountered in North America.

Cor pulmonale secondary to high altitude and chronic pulmonary hypertension is a geographically distinct cause of congestive heart failure in North America with which the authors are clinically unfamiliar.

Toxic causes of cardiomyopathy are extremely rare in cattle, although documented cases of ionophore toxicity and plant ingestion do exist in the literature10,11. The greater safety margin for ionophores in cattle compared to horses means that it is extremely unlikely that inadvertent mixing errors will lead to toxicity in adult cattle although it would appear that the safety margin may be lower in calves. Plants such as white snakeroot, coffee senna and hairy vetch are theoretically capable of inducing myocardial injury and resultant cardiac dysfunction. However, the increased confinement of dairy cattle means that these causes are highly unlikely to ever be encountered in dairy practice and still rare in beef practice.

Ancillary diagnostics for cardiac disease in cattle

Electro- and echocardiographic evaluation of the bovine heart are typically confined to the referral or university teaching hospital setting but undoubtedly represent the most useful and eloquent diagnostic information available to us. Referral to a facility in which they can be performed should certainly be considered in individually valuable cattle, whether it be for diagnostic, therapeutic or prognostic purposes. In recent years, possibly fuelled by an increased awareness of their diagnostic utility in other species, there have been a small number of publications describing biochemical markers of cardiac disease in cattle, specifically cardiac troponins I (cTnI) and T (cTnT). Publications so far have been retrospective case studies involving cattle with a variety of cardiac disorders including traumatic pericarditis13, as well as individual case reports on a calf with myocarditis due to foot and mouth infection14, endocarditis15 and an idiopathic pericarditis case2. Human assays for cTnI and cTnT have also been used to measure myocardial injury during experimental endoxtemia in calves16. The diagnostic utility of the troponins would be best served at this point by the establishment of normal reference ranges for adult and neonatal cattle using modern immunoassays that were simultaneously validated for the bovine species.

References

1.Firshman A, et al. J Vet Intern Med 2006;20:1499.

2.Jetsy S, et al. JAVMA 2005;226(9):1555.

3.Buczinski S, et al. Vet J 2010;184 258-263.

Peek S and McGuirk S. Rebhun's Diseases of Dairy Cattle, 2nd ed,; 2008;43.

5.Ohwada K and Murakami T. J Jpn Vet Med Assoc 2000;53:205.

Nart P et al Vet Rec 2004;155:355.

Leifsson P and Angerholm J. J Vet Med Series 2004;51:332.

Furoka H et al J Comp Path 2001;125:159.

Owczarek-Lipska M et al Mamm Genome 2009;20:187

Omidi A et al. Can Vet J 2010,51, 1143.

11.Schweitzer D et al. J Am Vet Med Assoc 1984, 184, 1273.

Mellanby R et al Vet Rec 2007;161:454.

Gunes V et al Vet Rec 2008;162:514

Gunes V et al. Vet Rec 2005;156:714.

Buczinski S and Belanger AM. Can Vet J 2010, 51, 195.

Peek S et al. Can J Vet Res 2008;72:356.