Diagnosis of Cardiovascular Disease by Presenting Sign

Heart disease is not common in goats and the world litera­ture on caprine cardiovascular disease is sparse. One Indian study on the prevalence of gross cardiac abnormali­ties in slaughtered goats found approximately 3.5% of 2720 hearts examined to be abnormal (Chattopadhyay and Sharma 1972).

Sudden Death

Attribution of sudden death to cardiac disease must be approached cautiously in goats. The presence of gross or microscopic lesions in the heart at necropsy does not always mean that heart disease contributed to the clinical picture. Some changes may be artifactual, related to autoly­sis, blanching of the heart muscle during rigor mortis, or uneven staining of histologic sections (Newsholme and Coetzer 1984). In addition, a number of abnormalities may be noted in the heart, pericardium, or great vessels that represent subclinical conditions unrelated to the cause of death. These are discussed below in the section on subclin- ical cardiovascular conditions.

Peripheral evidence of cardiac dysfunction may be a bet­ter indicator of heart involvement than abnormalities of the heart itself. These include passive congestion, lung edema, and fluid accumulation in the thorax, pericardium, or abdomen. Histologic evaluation in all cases of the heart should be performed to identify definitive changes when present. The following cardiac causes of sudden death must be considered.

Nutritional Muscular Dystrophy

Nutritional muscular dystrophy or white muscle disease can affect the heart muscle and skeletal muscle, and may be responsible for sudden death caused by cardiac failure, particularly in young kids.

Cardiotoxic Plants

A number of plants may cause heart failure and sudden death in goats. In North America, potentially cardiotoxic plants include the ornamental plants oleander (Nerium oleander), foxglove (Digitalis purpurea), lily of the valley (Convallaria majalis), and yew (Taxus spp.). Other weeds and shrubs include Indian hemp (Apocynum cannabi- num), false hellebore (Veratrum spp.), and milkweed (Asclepias spp.) (Fowler 1986). Yew and false hellebore contain toxic alkaloids, while the other plants contain cardiac glycosides. In all cases, such poisonings would be sporadic and require careful documentation of exposure. Rumen contents should be examined for identifiable plant parts. The outcomes of these cases often depend on the level of exposure. If non-lethal doses are consumed, clinical signs may persist for several days, because the half-life of most cardiac glycosides is between 24 and 36 hours.

Successful management of yew toxicity in goats has been reported. Two goats died within 24 hours of ingesting the ornamental shrub and three remaining goats showed signs of bradycardia, hypothermia, depression, and weakness. Rumenotomies were performed on these goats to remove ingested plants, and mineral oil, electrolytes, and activated charcoal were added to the rumen. All three survived (Casteel and Cook 1985).

In South Africa, gousiekte, or “quick disease,” occurs commonly enough to produce serious economic loss in livestock, including goats. It is caused by six different plants in the family Rubiaceae: Pachystigma pygmaeum, Pachystigma thamnus, Pachystigma latifolium, Pavetta schumanniana, Pachystigma harborii, and Fadogia hom- blei. It is a cumulative poisoning and usually requires sev­eral weeks of ingestion of these plants before clinical disease occurs. Goats are more susceptible than sheep (Hurter et al. 1972). The toxic principle in these plants has been isolated. It is a water-soluble, heat-stable, cationic polyamine that has been termed pavetamine (Fourie et al.

Other South African plants that can result in sudden death include Cotyledon orbiculata and Dichapetalum cymosum. The succulent plant C. orbiculata contains bufadeniolides, which are cardiac glycosides. When large amounts of the plant are consumed by goats over a short period of time, sudden death from heart failure can occur (Tustin et al. 1984). This may be preceded by signs of weakness, prostration, tachycardia, and pupillary constriction.

The toxic principle in D. cymosum, a plant known as gif- blaar, is monofluoroacetic acid. Death occurs within a few hours of ingestion. Peritoneal, pericardial, and thoracic effusions may be observed at necropsy, and histologic examination of the heart may demonstrate multiple small foci of myocardial necrosis, with lymphocytic infiltration. However, these are not consistent findings (Newsholme and Coetzer 1984). A related species, D. barteri, has been identified as a cause of sudden death in goats eating branches of the tree in Nigeria (Adaudi 1975; Nwude et al. 1977).

Sudden death in South African goats has also been reported three days after ingestion of avocado leaves (Persea americana), presumably because of heart failure (Grant et al.

In the Sudan, a commonly grazed annual shrub, Cassia occidentalis, has been demonstrated to produce a toxic myodegeneration of cardiac muscle in goats (Suliman and Shommein 1986). C. occidentalis is also found in the south­western United States and is known as coffee weed, senna, or coffee senna. It has been associated with death in graz­ing cattle because of skeletal and cardiac myodegeneration, so goats must be considered at risk.

In all cases of sudden death when plant toxicity is sus­pected, additional animals at risk should be removed from the potential source and given activated charcoal orally at a minimum dose of 2 g/kg bodyweight (bw).

Heartwater

Heartwater (cowdriosis), discussed in detail later in this chapter, occurs principally in Africa as well as on some Caribbean islands and can cause peracute death in goats. Lesions observed after death are similar to those described for gousiekte. Where both diseases occur, they must be dif­ferentiated by examination of brain tissue for the presence of the rickettsial organisms that cause heartwater.

Foot and Mouth Disease

Foot and mouth disease (FMD) is usually a subclinical infection in goats, or it produces mild to moderate signs of lameness in adults. However, very young kids in infected herds may die suddenly of associated viral, lymphohistio- cytic myocarditis, which can produce a gross lesion of either diffuse gray spots or more organized “tiger” stripes, mainly in the left ventricle and interventricular septum (Kitching and Hughes 2002).

Other Cardiotoxic Agents

Iatrogenic cardiotoxicity is possible in goats because of overdosage with at least two commonly used substances, calcium salts and ionophore coccidiostats. However, con­firmation of sudden death in goats because of these sub­stances is lacking. When treating milk fever (hypocalcemia), it is always advisable to administer intravenous calcium slowly and monitor the heart sounds for arrhythmia, increased rate, or heart block. Goats that are below average weight, have concurrent diseases, or have already been treated by the owner are more likely to experience cardiac irregularities or arrest.

Ionophore toxicity is known to occur in small rumi­nants. Ionophore antibiotics are used in livestock produc­tion as coccidiostats for cattle, sheep, goats, and poultry, and the ionophore monensin is also used as a growth pro- motant that improves feed efficiency and weight gain in beef cattle. Monensin has caused sudden death in sheep fed three or more times the recommended dose of 15-22 parts per million (ppm). The affected sheep readily consumed feed containing this amount, contrary to the general assumption that feed refusal occurs when the level is more than twice the recommended dose. Sudden death occurred in 20-40% of affected sheep and microscopic car­diac lesions, ranging from focal necrosis with perivascular lymphocytic cuffing to necrotizing myocarditis, were pre­sent (Bastianello 1988).

Monensin is approved for oral use in confined goats in the United States as a coccidiostat at a dose of 20 g/ton of feed (22 ppm). Goats experimentally given monensin orally at the rate of 55 ppm in feed for three weeks showed ano­rexia, diarrhea, and an increase in serum sorbitol dehydrogenase, indicating some hepatotoxicity (Dalvi and Sawant 1990). There are no published reports of field cases of monensin toxicity in goats, but experimental data indi­cate that the single-dose oral LD₅₀ for monensin in goats is 26.4 mg/kg bw (Beasley 1999).

There is, however, a report of fatal overdose of goats with the ionophore salinomycin. Angora goats in Turkey were fed salinomycin in their ration at a rate of 680 ppm/kg of feed due to a mechanical mixing malfunction during feed preparation. Of 70 exposed goats, 13 died. Among those for which there was an opportunity for clinical examination before death, signs included listlessness, inappetence, incoordination, dehydration, fluid stool, tachycardia, mus­cle weakness, salivation, panting, and prostration, and death occurring within 15-24 hours. At necropsy there was excessive fluid in the abdomen, thorax, and pericardium. The heart showed petechiation in the ventricles and endo­cardium and microscopically there was prominent myocar­dial hemorrhage (Agaoglu et al. 2002). The recommended dose of salinomycin for use in goats as a coccidiostat is 100 ppm of concentrate fed.

Sudden death also has been reported in goats fed exces­sive amounts of vitamin D. At necropsy, calcification of the coronary arteries and aorta was noted (Neumann et al. 1973).

Trauma

It has been suggested that goats, due to their generally low pain threshold, can die of cardiac failure resulting from neurogenic or catecholamine-induced ventricular dys­rhythmias when subjected to painful procedures such as dehorning without appropriate analgesia or anesthesia (Gray and McDonell 1986).

Aortic Rupture

In tropical regions, nematode infections of the aorta with Spirocerca lupi and/or Onchocerca armillata have been reported in goats (Chowdhury and Chakraborty 1973). These infections may be subclinical or identified at nec­ropsy or slaughter by thickening, nodularity, or calcifica­tion of the aorta. However, S. lupi in the goat aorta can lead to slow bleeding with anemia and emaciation, or to aortic rupture and sudden death (Chhabra and Singh 1972).

Neoplasia

There is one reported case of a 3-year-old pregnant female goat that died suddenly when being chased around its pen to be medicated for undiagnosed chronic respiratory dis­ease of about one month's duration. On necropsy the goat had ovine pulmonary adenomatosis (jaagsiekte), with tumor in both lungs that had also metastasized to the kid­neys and heart. Death was attributed to heart failure secondary to tumor infiltration of the myocardium of the left ventricle (Al-Dubaib 2005). Jaagsiekte is uncommon in goats and is discussed further in Chapter 9.

Abnormal Heart Sounds

Documentation of abnormal heart sounds in goats is limited.

Murmurs

In cases of VSD, grade IV or V out of VI holosystolic mur­murs over both the right and left heart base with palpable thrills on both sides have been reported (Scarratt et al. 1984). An audible S4 sound was heard to precede S1 in one case of VSD (Parry et al. 1982). Systolic murmurs can be heard during the prodromal phase of gousiekte (Pretorius and Terblanche 1967).

Reports of abnormal heart sounds associated with valvu­lar abnormalities are rare. A single case of endocarditis has been reported in a Pygmy goat that presented clinically with a continuous rasping cardiac murmur, increased heart rate, dyspnea, inappetence, fever, and depression. It was determined after death to have traumatic peri- and endocarditis because of heart penetration with a sewing needle (Waldman and Woicke 1984). Two additional cases of vegetative endocarditis in goats have been identified only as incidental postmortem findings (Geisel 1973; Krishna et al. 1976). In a 3-year-old male Pygmy goat with Ebstein's anomaly of the tricuspid valve, a grade III/V pla­teau pansystolic murmur was auscultated over the tricus­pid valve area, and a grade II/V plateau pansystolic murmur was auscultated over the left heart base (Gardner et al. 1992).

Systolic murmurs of variable character have been reported in cases of enzootic calcinosis in goats in Austria (Gufler et al. 1999) and Switzerland (Braun et al. 2000) in association with the consumption of golden oat grass (Trisetumflavescens). Enzootic calcinosis is known to occur in ruminants and horses in various countries around the world where animals consume plants with high concentra­tions of 1,25 dihdroxycholecalciferol (calcitrol) glycoside or substances that mimic its action. Chronic consumption of such plants leads to excessive absorption of calcium and results in calcification of soft tissues, primarily the cardio­vascular system, but also lungs, kidneys, and tendons.

Affected goats show loss of appetite, emaciation, dysp­nea, and abnormalities of carriage and gait, including increased recumbency, difficulty rising, kneeling after ris­ing, stilted gait, arched back, shifting weight from leg to leg, and intermittently carrying a limb off the ground. These locomotor signs are associated with calcification of the flexor tendons and blood vessels of the limbs. Calcification of cardiac structures, including the heart valves and the great vessels, also occurs in enzootic calci­nosis. As a result, physical examination and ancillary diag­nostic testing may reveal tachycardia, a variety of murmurs, possible arrhythmias, pericardial effusions, pleural effu­sions, ascites, and abnormalities in the ECG and echocar­diogram, including evidence of pericarditis, thickening of the aortic orifice, and calcification of the heart valves. Calcification of the aorta is especially remarkable and may be noted in plain radiographs. There is no treatment for enzootic calcinosis, but the condition can be controlled by eliminating or reducing access to the offending plants in the ration. The calcinogenicity of yellow oat grass is reduced if it is made into hay when mature rather than grazed as fresh young grass.

Muffled Sounds

The principal cause of muffled heart sounds in the goat is hydropericardium, resulting from the appropriately named disease heartwater, or cowdriosis. In addition, some of the African poisonous plants cited above may produce pericar­dial effusions. Lymphosarcoma and traumatic reticuloperi- carditis, the two most common causes of pericardial effusion in cattle, are rare in goats (Sharma and Ranka 1978; Waldman and Woicke 1984; Craig et al. 1986; Reddi and Surendran 1988). In one reported case of thymoma, the heart was heard over an increased area of the left thorax, and the palpable cardiac impulse was displaced dorsally by the thoracic mass (Rostkowski et al. 1985).

Friction Rubs

Infectious pericarditis, the most likely cause of friction rubs synchronous with the heartbeat, is infrequently reported in goats (Chattopadhyay and Sharma 1972; Hein and Cargill 1981). When it does occur, it is most often asso­ciated with general mycoplasmal infections. The pericardi­tis is often an extension of the pleuropneumonia commonly associated with mycoplasmal infections, notably Mycoplasma mycoides subspecies mycoides and Mycoplasma Ovipneumoniae (Masiga and Rurangirwa 1979; East et al. 1983; Rodriguez et al. 1995; Williamson et al. 2007). Friction rubs may be heard in association with either the heartbeat or respiration or both. Exudative peri­carditis can also occur in caprine tuberculosis (Savey 1984).

Arrhythmias

Arrhythmias are infrequently documented. They have been reported in association with the cardiac form of tuber­culosis, in cardiotoxicity resulting from cardiac glycoside­containing plants, and in a case of enzootic calcinosis. Atrial fibrillation has been reported with congestive heart failure and pneumonia (Gay and Richards 1983). Gallop rhythms, tachycardia, splitting of the first heart sound, and arrhythmias occur during the prodromal phase of gous- iekte (Pretorius and Terblanche 1967).

Congestive Heart Failure

The clinical signs of congestive heart failure are similar to those seen in other species. They include increased jugular pulse, jugular distension, moist cough, tachycardia, sub­mandibular edema, ascites, exercise intolerance, chronic weight loss, and possibly diarrhea. Not all signs are seen in all cases. Findings in dead goats that are consistent with heart failure include hydrothorax, hydropericardium, hydroperitoneum, pulmonary edema, heart enlargement, and ventricular dilation.

Congestive heart failure in the goat has been attributed to cor pulmonale secondary to pneumonia (Gay and Richards 1983), mediastinal thymoma (Rostkowski et al. 1985), and VSD (Parry et al. 1982). Krimpsiekte and gousiekte, usually recognized as sudden death, may show evidence of congestive heart failure at necropsy. Waterpens, another poisonous plant disease of goats and sheep in South Africa caused by Galenia africana, produces a marked abdominal ascites and death (van der Lugt et al. 1988). The intoxication results in both hepatic and cardiac lesions. Experimental challenge studies with plant extracts indicate that G. africana is primarily hepatotoxic, with myocardial involvement occurring only in the termi­nal stages of the intoxication (van der Lugt et al. 1992). Nutritional muscular dystrophy (white muscle disease) may lead to congestive heart failure when heart muscle damage is not severe enough to produce sudden death.

The differential diagnosis for goats with signs suggesting congestive heart failure should include gastrointestinal helminthiasis and liver fluke disease. These parasitisms can produce edema, ascites, and exercise intolerance sec­ondary to hypoproteinemia and anemia.

Marked jugular distension commonly occurs in goats whose neck chains or collars have been fastened too tightly. This should be differentiated from heart disease.

Reports on therapy for congestive heart failure in goats are limited (Gay and Richards 1983). The principles of therapy and the drugs commonly reported in the dog can be used reasonably as a first approximation in goats. These include reduction of preload with furosemide or other diuretics; reduction of afterload with captopril, hydralazine, or other vasodilators; improvement of con­tractility with digoxin or dobutamine; and restoration of rate and rhythm with lidocaine, quinidine, procainamide, or other appropriate antiarrhythmic drugs (Kittleson 1985; Wilcke 1985).

Subclinical Cardiovascular Conditions

Lesions involving the heart and vasculature are sometimes observed at necropsy in goats when no signs of heart dis­ease have been recognized during the clinical examination. This occurs when other clinical signs overshadow cardio­vascular disease, when cardiovascular disease is subclini- cal, or when lesions observed are non-pathogenic.

Pericardial effusions or pericarditis may be seen in myco­plasmosis, false blackleg (malignant edema), and entero­toxemia due to Clostridium perfringens type D. A non-pathogenic, lymphoreticular hyperplasia of the epi­cardium and pericardium has also been seen histologically from slaughter surveys (Chattopadhyay and Sharma 1972). Hydropericardium has been reported at necropsy in goats poisoned by consumption of the seed pods of the tree Albizia versicolor in Malawi. The predominant clinical pic­ture was one of neurologic disease (Soldan et al. 1996).

Incidental and subclinical myocardial lesions may include gray-white foci of necrosis in the ventricles, pre­sumed to be caused by earlier plant or bacterial toxic insults, metaplastic cartilage development with or without calcification, focal lymphocytic infiltration of the myocar­dial interstitium, granulomatous myocarditis, and parasitic myocarditis. Causes of parasitic myocarditis include sar­cosporidiosis, hydatid cysts, and metacestodes of other tae- niid cestodes, including Cysticercus and Coenurus (Bhalla and Nagi 1962; Chattopadhyay and Sharma 1972; Hein and Cargill 1981).

Aortic abnormalities occur in goats, though in general they contribute little to clinical disease. These include aneurysm, aortitis media, melanosis, intimal fat deposits and intimal fibrosis, cartilaginous and osseous metaplasia, and calcification (Prasad et al. 1972; Geisel 1973). Migratory tracts, nodules, corrugations, aneurysms, and thickening of the aortic wall may be seen in association with oncho­cerciasis (Kaul and Prasad, 1989). Focal aortic necrosis and calcification in goats are frequent lesions in caprine paratu­berculosis (Majeed and Goudswaard 1971). Calcification of the aorta as well as other great vessels is seen in goats with enzootic calcinosis due to consumption of yellow oat grass (T. flavescens), as described above under murmurs.