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 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.
The imbalance of minerals in certain soils, as well as higher altitude (up to 1,500 m above sea level), have been thought to be the main etiologic factors; higher altitude is considered to favor the growth of plants like golden oats at the expense of other plants less suited for this location.
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. In cattle and small ruminants, high serum inorganic phosphorus with elevated or normal serum calcium concentrations have been reported in animals with enzootic calcinosis.
The disease is progressive and chronic, extending over weeks or months. The earliest signs are stiffness and shifting limb lameness, 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. 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. Tachycardia is a common finding, and heart murmurs may be audible on auscultation. Jugular venous pulse is prominent in some cases.
As the disease progresses, the animal loses weight and becomes weak, listless, reluctant to stand, or even recumbent. 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. Appetite is usually unimpaired but sometimes becomes depraved. Calcification of vessels is sometimes 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.
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. Calcification of the biscupid valves results in valve insufficiency and systolic heart murmurs. 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.
This is usually based on the history, signs, and lesions but may be difficult at early stages. Radiography and electrocardiography may be helpful.
Treatment and Control
No practical treatment reversing soft tissue calcification is currently available. 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. Careful pasture management to limit the density of calcinogenic plants can effectively reduce the disease prevalence. Feeding oat grass hay cut after blooming rather than having animals graze on oat grass pasture may reduce the problem, because calcinogenicity of the plant decreases with maturity and with drying. Experimentally, daily administration of 15 g of aluminum hydroxide, PO, prevented the development of calcinosis in sheep fed T flavescens.
Last full review/revision March 2012 by Walter Gruenberg, DrMedVet, MS, PhD, DECAR, DECBHM