Enzootic calcinosis is a plant intoxication recognized in ruminants and horses that is associated with the consumption of large quantities of plants containing either calcitriol or a calcitriol-like factor. Affected animals show diffuse soft tissue calcification that affects, among other things, the cardiovascular and respiratory tracts. No specific treatment is available.
Enzootic calcinosis (also known as enteque seco, enteque ossificans, espichamento, espichacao, Manchester wasting disease, Naalehu disease, or Weidekrankheit) is a disease complex of ruminants and horses that is 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.
Enzootic calcinosis typically occurs in animals kept in extensive grazing systems. In sheep, morbidity rates between 1 and 90% and mortality rates between 1 and 25% have been reported (1).
Etiology and Pathogenesis of Enzootic Calcinosis
Known causes of enzootic calcinosis fall into two categories: plant poisonings and mineral imbalances in the soil. Plant poisonings are probably more important.
Cestrum diurnum (wild jasmine, day-blooming jessamine, or king of the day), Trisetum flavescens (golden oats or yellow oat grass), Nierembergia veitchii (trailing cup plant), Solanum esuriale, Solanum torvum, and Solanum malacoxylon contain 1,25-dihydroxycholecalciferol (calcitriol) glycoside or a substance that mimics calcitriol's calcinogenic action.
The imbalance of minerals in certain soils, as well as at higher altitude (up to 1,500 m above sea level), has been thought to be the main etiological factor of enzootic calcinosis. 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 in bulls after prolonged intake of excessive calcium is a condition similar to enzootic calcinosis. Calcification of the cardiovascular system associated with aging and cachectic diseases such as tuberculosis is not identical. Excessive vitamin D3 and normal or excessive calcium intake induce aortic calcification and atherosclerosis in ruminants. Hypercalcemia promotes calcitonin production, calcinosis, and osteoporosis.
The effect of hypervitaminosis D3 on plasma calcium, phosphorus, and magnesium varies by species. Horses develop hyperphosphatemia; plasma calcium concentration remains normal but rises with excess doses of calcitriol. In cattle and small ruminants, high serum concentrations of inorganic phosphorus with increased or normal serum calcium concentrations have been reported in animals with enzootic calcinosis.
Clinical Findings of Enzootic Calcinosis
Enzootic calcinosis is progressive and chronic, extending for weeks or months. The earliest clinical signs are stiffness and shifting limb lameness, 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 animals with enzootic calcinosis are forced to walk, they show a stiff and slow gait, with short steps. After walking only short distances, breathing becomes shallow and labored, the nostrils are flared, and the head and neck are extended. Tachycardia is a common finding; when endocardial structures are affected by calcification, heart murmurs might be audible on auscultation, and some animals display a prominent jugular venous pulse.
As enzootic calcinosis 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. Other signs include muscle wasting, a prominent skeleton, tucked-up abdomen, kyphosis, and raised tailhead. Appetite is usually unimpaired but sometimes becomes depraved. Calcification of blood vessels is sometimes palpable on rectal examination.
Osteodystrophy occurs with calcinosis due to T flavescens and C diurnum toxicoses 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 of Enzootic Calcinosis
Degeneration and calcification of soft tissues occur in cases of enzootic calcinosis, 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 lungs, kidneys, and tendons. The heart and aorta show the most pronounced abnormalities.
Calcification of the cardiac valves results in valve insufficiency or stenosis and systolic heart murmurs. White, elevated, mineralized plaques of irregular size and shape occur on the luminal surface; in advanced cases, these mineralized plaques are evident 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 the articular surfaces of cartilage and joints, especially the carpus and hock, also occur.
The basic histological changes in enzootic calcinosis are necrosis and calcification of connective tissue, followed by cellular proliferation in the affected area.
Diagnosis of Enzootic Calcinosis
History and clinical signs
Evidence of soft tissue calcification on radiography, ultrasonography, or necropsy
Diagnosis of enzootic calcinosis is usually based on the patient's history, combined with clinical signs such as emaciation, lameness, and listlessness, as well as cardiac and respiratory abnormalities. At early stages, diagnosis can be difficult.
Abnormal serum calcium, phosphorus, and magnesium concentrations and increased activity of alkaline phosphatase, in combination with the presence of plants with calcinogenic action in the feed or on pasture, are additional clues.
Necropsy reveals varying degrees of tissue mineralization in enzootic calcinosis cases. This mineralization is often apparent when the tissue is cut, and it is particularly common in the cardiovascular and respiratory tracts.
Imaging techniques such as radiography and ultrasonography can be used to visualize soft tissue calcification.
Treatment and Control of Enzootic Calcinosis
No specific treatment
Prevention of prolonged access to plants containing calcitriol
No practical treatment to reverse soft tissue calcification is currently available. Removal of the causative factors of enzootic calcinosis is essential; however, when the disease is associated with the mineral content of the soil, control can be difficult.
Change of pasture, forage, and environment can bring about clinical improvement in animals with enzootic calcinosis. Careful pasture management to limit the density of calcinogenic plants can effectively decrease the disease prevalence.
Feeding oat grass hay that is cut after blooming, rather than allowing animals to graze on oat grass pasture, might decrease the problem, because calcinogenicity of the plant decreases with maturity and with drying.
Key Points
Enzootic calcinosis is a plant intoxication that affects primarily ruminants and horses.
Ingestion of plants containing calcitriol or a calcitriol-like factor results in diffuse soft tissue mineralization.
No specific treatment is available; prevention is by grazing management.
For More Information
Machado M, Castro MB, Gimeno EJ, Barros SS, Riet-Correa F. Enzootic calcinosis in ruminants: a review. Toxicon. 2020;187:1-9.
Also see pet owner content regarding disorders associated with calcium, phosphorus, and vitamin D in horses.
References
Machado M, Castro MB, Gimeno EJ, Barros SS, Riet-Correa F. Enzootic calcinosis in ruminants: a review. Toxicon. 2020;187:1-9. doi:10.1016/j.toxicon.2020.08.009
