Enzootic Calcinosis - The Merck Veterinary Manual

Enzootic Calcinosis
(Enteque seco, Enteque ossificans, Espichamento, Espichacao, Manchester wasting disease, Naalehu disease, Weidektankheit)

Etiology and Pathogenesis

Clinical Findings

Lesions

Diagnosis

Control

Enzootic calcinosis is a disease complex of ruminants and horses caused by plant poisoning or mineral imbalances and characterized by extensive calcification of soft tissues. The prevalence of the disease in cattle varies widely (10-50%) in areas of Argentina, Brazil, Papua-New Guinea, Jamaica, Hawaii, and Bavaria. It is said to cause up to 60% mortality and affect 17% of the sheep in southern Brazil and Mattewara (India), respectively. Incidence elsewhere (Australia, Israel, South Africa, and southern USA) is less well documented, and in many areas enzootic calcinosis is rare or nonexistent.

Etiology and Pathogenesis:

Known causes fall into 2 categories: plant poisonings and mineral imbalances in the soil, the first probably being the more important. Cestrum diurnum (wild jasmine, day-blooming jessamine, king-of-the-day), Trisetum flavescens (golden oats or yellow oat grass), Nierembergia veitchii , Solanum esuriale , S torvum , and S malacoxylon (glaucophyllum) contain 1,25-dihydroxycholecalciferol (calcitriol) glycoside or a substance that mimics its calcinogenic action. Studies indicate that S malacoxylon has the required enzyme systems for the synthesis of calcitriol from vitamin D₃. No concrete evidence incriminating other plants is available.

The imbalance of minerals in certain soils in Hawaii, India, Austria, and possibly elsewhere has been thought to be the main etiologic factor; dietary mineral imbalance may contribute to the calcification chiefly associated with plant poisoning. Excessive phosphate or calcium, absolute or conditioned magnesium deficiency, and deficiency of potassium and nitrogen have all been incriminated or suspected.

Osteodystrophy of bulls after prolonged intake of excessive calcium is a similar condition; calcification of the cardiovascular system associated with aging and such cachectic diseases as tuberculosis is not identical. Excessive vitamin D₃ and normal or excessive calcium intake induces aortic calcification and atherosclerosis in ruminants.

Normally, the conversion of 25-hydroxycholecalciferol (calcifediol) to calcitriol in the kidney is controlled by a feedback mechanism. The calcitriol-like factor in the leaves of plants bypasses this mechanism, and more calcium is absorbed than can be accommodated physiologically. Hypercalcemia promotes calcitonin production, calcinosis, and osteoporosis.

Changes in plasma calcium, phosphorus, and magnesium are different in different species. Horses develop hyperphosphatemia; plasma calcium remains normal but rises with excess doses of calcitriol. Frequently, both serum calcium and inorganic phosphorus are increased in cattle. Hypomagnesemia also may be present.

Clinical Findings:

The disease is progressive and chronic, extending over weeks or months. The earliest signs are stiffened and painful gait, which is most pronounced when the animal rises after prolonged rest. Forelimbs are particularly affected, and some animals even walk or graze on their knees. When standing, the forelimbs bow forward because the joints cannot be extended completely. The animal shifts weight to the forepart of the hooves or, alternatively, to each forelimb to ease stress on the carpus, which is thickened and painful. The distal joints become abnormally straight. When affected animals are forced to walk, their gait is awkward, stiff, and slow, and their steps are short. After walking only short distances, breathing becomes shallow and diaphragmatic, the nostrils are flared, and the head and neck are extended. Varying degrees of heart murmur are detectable, usually as a double or blurred second sound; these are exaggerated after exercise. Pulse rate is increased after slight exercise. Jugular pulse is prominent in some cases.

As the disease progresses, the animal loses weight and becomes weak and listless. The coat becomes shaggy, dull, and faded, particularly in cattle. There is wasting of muscles, a prominent skeleton, tucked up abdomen, kyphosis, and raised tailhead. Ovarian function is impaired. Appetite is usually unimpaired but sometimes becomes depraved. Calcification of vessels is palpable on rectal examination.

Osteodystrophy is seen in calcinosis due to T flavescens and C diurnum toxicities in Bavarian cattle and Florida horses, respectively. Severely affected horses stand with forelimbs somewhat abducted and luxated caudally at the shoulder joints. The flexor tendons, particularly the suspensory ligaments, are painful. Fetlock joints are overextended to varying degrees.

Lesions:

Degeneration and calcification of soft tissues are seen, with emaciation and varying amounts of excess fluid in the thoracic and abdominal cavities and pericardial sac. The cardiovascular system is the first to be involved, followed by lung, kidney, and tendons. The heart and aorta show the most marked effects. The left side of the heart is more affected than the right. In extreme cases, calcified foci are seen on valves and chordae tendinae. White, elevated plaques of irregular size and shape are seen on the luminal surface; in advanced cases, these are seen throughout the length of the aorta and its main branches. Mineral deposits are found on the pleura, on the surface and edges of the diaphragmatic and apical lobes of lungs, in the renal artery and pelvis of the kidney, and on the ligaments and tendons (particularly of the forelimbs). Capsular thickening and irregular erosions of articular surface of cartilage and joints are seen, especially of the carpus and hock.

The basic histologic evidence is necrosis and calcification of connective tissue, followed by cellular proliferation in the affected area.

Diagnosis:

This is usually based on the history, signs, and lesions but may be difficult at early stages. Radiography and electrocardiography may be helpful.

Control:

Removal of the causal factor(s) is essential, but when the disease is associated with the mineral content of the soil, control may be difficult. Change of pasture, forage, and environment may effect clinical improvement and even diminish the soft-tissue mineral deposits. Experimentally, daily administration of 15 g of aluminum hydroxide, PO, prevented the development of calcinosis in sheep fed T flavescens .