Localized cutaneous calcinosis associated with leptospirosis in a 4-month-old beagle puppy.

A 4-month-old male beagle dog was presented for a 15-day history of firm cutaneous nodules. Histopathological examination of skin biopsies revealed calcinosis cutis. However, re-evaluation 40 d later confirmed spontaneous resolution of the lesions without specific treatment. Two weeks before development of the skin lesions, this dog had been hospitalized and treated for acute renal and hepatic disease attributed to leptospirosis, with both PCR and serology positive for Leptospira australis. Calcinosis cutis secondary to a systemic disease (leptospirosis, blastomycosis) has been rarely reported. In this case, the suspected pathogenesis included organic stress (cortisol hypersecretion) and abnormal calcium/phosphorus metabolism during acute renal failure. To our knowledge, this is the third published case of cutis calcinosis associated with leptospirosis in dogs. Key clinical message: Previous leptospirosis should be considered in a dog with calcinosis cutis. The cutaneous lesions appeared after acute leptospirosis and regressed spontaneously.

Calcinose cutanée localisée associée à une leptospirose chez un chiot Beagle de 4 mois. Un Beagle mâle de 4 mois a été présenté en consultation à la suite de l'apparition de nodules cutanés fermes 15 jours auparavant. L'examen histopathologique de biopsies cutanées a révélé une calcinose cutanée. Le contrôle à 40 jours a confirmé une résolution spontanée des lésions sans traitement spécifique. Deux semaines avant le développement des lésions cutanées, ce chien avait été hospitalisé et traité pour une maladie rénale et hépatique, attribuée à une leptospirose. Les examens PCR et sérologique étaient positifs pour Leptospira australis. La calcinose cutanée secondaire à une maladie systémique (leptospirose, blastomycose) est rarement rapportée et le mécanisme étiopathogénique suspecté comprenait un stress organique (hypersécrétion de cortisol) et un déséquilibre du métabolisme phosphocalcique lors de l'épisode d'insuffisance rénale aiguë. À notre connaissance, il s'agit du troisième cas publié de calcinose cutanée associée à la leptospirose chez le chien.Message clinique clé:Une potentielle leptospirose antérieure doit être mentionnée chez un chien atteint de calcinose cutanée. Les lésions cutanées semblent apparaître de manière décalée et régresser spontanément.(Traduit par Claude Muller).

Systemic calcinosis in a Quarter Horse gelding homozygous for a myosin heavy chain 1 mutation.

CASE DESCRIPTION: A 9-year-old Quarter Horse gelding was presented for lethargy, decreased appetite, polyuria and polydipsia (PU/PD), and severe muscle wasting suggestive of immune-mediated myositis. CLINICAL FINDINGS: The horse displayed lethargy, fever, tachyarrhythmia, inappetence, PU/PD, and severe epaxial and gluteal muscle wasting. Clinicopathologic findings were consistent with previously reported cases of systemic calcinosis in horses, including increased muscle enzyme activity, hyperphosphatemia, increased calcium-phosphorus product, hypoproteinemia, and an inflammatory leukogram. A diagnosis of systemic calcinosis was established by histopathologic evaluation of biopsy specimens from skeletal muscle, lung, and kidney. TREATMENT AND OUTCOME: Symptomatic treatment was complemented by IV treatment with sodium thiosulfate to reverse calcium-phosphate precipitation in soft tissue and PO aluminum hydroxide to decrease intestinal phosphorus absorption and serum phosphorus concentration. CLINICAL RELEVANCE: This is the first report in the veterinary literature of an antemortem diagnosis of systemic calcinosis in the horse that was successfully treated and had favorable long-term outcome.

Chronic Vitamin D Intoxication in Captive Iberian Lynx (Lynx pardinus).

To document the biochemical and pathologic features of vitamin D intoxication in lynx and to characterize mineral metabolism in healthy lynx, blood samples were obtained from 40 captive lynx that had been receiving excessive (approximately 30 times the recommended dose) vitamin D3 in the diet, and from 29 healthy free ranging lynx. Tissue samples (kidney, stomach, lung, heart and aorta) were collected from 13 captive lynx that died as a result of renal disease and from 3 controls. Vitamin D intoxication resulted in renal failure in most lynx (n = 28), and widespread extraskeletal calcification was most severe in the kidneys and less prominent in cardiovascular tissues. Blood minerals and calciotropic hormones in healthy lynx were similar to values reported in domestic cats except for calcitriol which was higher in healthy lynx. Changes in mineral metabolism after vitamin D intoxication included hypercalcemia (12.0 ± 0.3 mg/dL), hyperphosphatemia (6.3 ± 0.4 mg/dL), increased plasma calcidiol (381.5 ± 28.2 ng/mL) and decreased plasma parathyroid hormone (1.2 ± 0.7 pg/mL). Hypercalcemia and, particularly, hyperphosphatemia were of lower magnitude that what has been previously reported in the course of vitamin D intoxication in other species. However, extraskeletal calcifications were severe. The data suggest that lynx are sensitive to excessive vitamin D and extreme care should be taken when supplementing this vitamin in captive lynx diets.

Hypervitaminosis D and Metastatic Calcification in a Colony of Inbred Strain 13 Guinea Pigs, Cavia porcellus.

A commercial diet fed to a colony of inbred strain 13 guinea pigs for approximately 6 weeks was subsequently recalled for excessive levels of vitamin D. Twenty-one of 62 animals exhibited clinical signs, including anorexia, lethargy, and poor body condition. Nine affected and 4 clinically normal animals were euthanized for further evaluation, including serum chemistry, urinalysis, and gross and/or histopathology. Macroscopic findings included white discoloration in multiple organs in 8 animals, and microscopic evaluation confirmed multiorgan mineralization in tissues from 7 animals. Serum 25-hydroxyvitamin D levels were elevated in 10 animals. Serum inorganic phosphorus and alkaline phosphatase levels were increased in all exposed animals; however, total calcium and ionized calcium levels were not significantly higher in exposed animals than in control strain 13 guinea pigs from a different institution. The data support a diagnosis of hypervitaminosis D with metastatic calcification. Following the diet recall, the remaining guinea pigs increased their food intake and regained body condition. Diagnostic testing of 8 animals euthanized approximately 3 months after returning to a normal diet demonstrated that serum parathyroid hormone remained significantly lower, and ionized calcium and ionized magnesium were significantly higher, in recovered animals compared to controls and exposed animals. These results indicate that diagnostic tests other than serum calcium are necessary for a diagnosis of hypervitaminosis D in guinea pigs.

Tumoral calcinosis form of hydroxyapatite deposition disease in related red-bellied short-necked turtles, Emydura subglobosa.

Ten of 12 red-bellied short-necked turtles from a single clutch presented at 9 months of age with multiple white to tan nodules on their feet. Histologically, the nodules were composed of large periarticular deposits of mineralized crystalline material that extended into the joint spaces of interphalangeal joints and was surrounded by granulomatous inflammation and fibrosis. Crystallographic analysis determined the material to be apatite (calcium phosphate hydroxide) consistent with the tumoral calcinosis form of hydroxyapatite deposition disease (HADD). HADD has previously been described in aquatic turtles and rarely lizards and must be differentiated from gout in reptiles. A cause for the tumoral calcinosis lesions in these turtles could not be determined; however, based on previous reports in this species, a species-specific predilection, in conjunction with unknown environmental factors, is suspected. The use of the terms HADD, pseudogout (calcium pyrophosphate crystal deposition disease), and calcinosis circumscripta has been inconsistent, creating confusion in the literature.

Influence of diet on calcium metabolism, tissue calcification and urinary sludge in rabbits (Oryctolagus cuniculus).

Rabbits absorb more calcium (Ca) from their diet than they require, and excrete surplus via urine, which therefore contains a typical 'sludge'. This makes rabbits susceptible to Ca-containing uroliths. But given the Ca content of diets of free-ranging specimens, and the limited reports of urinary sludge and Ca contents in free-ranging lagomorphs, we can suspect that rabbits are naturally adapted to high urinary Ca loads. We fed four groups of New Zealand hybrid rabbits [n = 28, age at start 5-6 weeks) pelleted diets consisting of lucerne hay only (L, Ca 2.32% dry matter (DM)], lucerne:oats 1:1 (LG, Ca 1.36%), grass hay only (G, Ca 1.04%), or grass:oats 1:1 (GG, 0.83%) for 25 weeks, with water available ad libitum. Diets were not supplemented with Ca, phosphorus, or vitamin D. Rabbits on diets LG and GG had lower food and water intakes, lower faeces and urine output, grew faster and had higher body mass at slaughter (mainly attributable to adipose tissue). Apparent Ca digestibility decreased in the order L-LG-G/GG. Rabbits on L had larger and heavier kidneys, more urinary sediment at sonography, and a higher urinary Ca content than the other groups. No animal showed signs of urolithiasis/calcinosis at X-ray, sonography, or gross pathology. Kidney/aorta histology only sporadically indicated Ca deposits, with no systematic difference between groups. Under the conditions of the experiment, dietary Ca loads in legume hay do not appear problematic for rabbits, and other factors, such as water supply and level of activity may be important contributors to urolithiasis development in veterinary patients. However, due to the lower Ca content of grass hay, the significantly lower degree of urinary sludge formation, and the significantly higher water intake related with grass hay feeding, grass hay-dominated diets are to be recommended for rabbits in which urolithiasis prevention is an issue.

Acute selenium toxicosis in polo ponies.

Just prior to an international polo event, 21 horses from one team exhibited clinical signs of central nervous system disturbance, hyperexcitability, sweating, ataxia, tachycardia, dyspnea, pyrexia, and rapid death. The suspected cause of this peracute onset of illness and death included intentional contamination of feed or iatrogenic administration of performance-enhancing drugs resulting in a severe adverse reaction. Six horses were submitted to the Bronson Animal Disease Diagnostic Laboratory for necropsy and toxicological examination. The clinical signs and sudden death, the similarity to earlier work by the lead author of selenium toxicosis in calves, as well as published reports, prompted investigators to focus on selenium testing. Sixty-four hours following receipt, the laboratory detected toxic selenium concentrations in the tissues of these animals. Following further investigation of the case by regulatory officials, it was determined that all affected horses had received an intravenous injection of a compounded "vitamin/mineral" supplement just prior to the onset of signs. The compounded supplement contained toxic levels of selenium. The present report illustrates the in-depth laboratory investigation of the cause of acute death in 6 polo ponies due to selenium toxicosis. In addition to solving this high profile case, the toxic levels of selenium found in livers (6.13 ± 0.31 mg/kg wet weight), kidneys (6.25 ± 0.3 mg/kg wet weight), and sera (1.50 ± 0.11 µg/ml) of these affected animals may provide important diagnostic criteria for future interpretations of selenium concentrations in tissues of horses.

Suspected systemic calcinosis and calciphylaxis in 5 horses.

Five horses were presented with signs of myopathy along with systemic malaise, hyperfibrinogenemia, hyperphosphatemia, and an elevated calcium phosphorus product (Ca*P). Postmortem findings were consistent with systemic calcinosis, a syndrome of calcium deposition in the tissue of organs including lungs, kidneys, muscle, and heart that has not been previously described in horses.

Nutritional metabolic bone disease in juvenile veiled chameleons (Chamaeleo calyptratus) and its prevention.

Nutritional metabolic bone disease (NMBD) is one of the most frequently observed pathological conditions in herpetoculture. To develop guidelines for NMBD prevention in growing veiled chameleons (Chamaeleo calyptratus), 56 hatchlings were divided into 6 groups [group UV, with UVB exposure; group No: no supplements; group CaAUV: with calcium (Ca), vitamin A, UVB; group CaA: with Ca, vitamin A; group CaADUV: with Ca, vitamin A, cholecalciferol, UVB; and group CaAD, with Ca, vitamin A, cholecalciferol] and reared for 6 mo on locust-based diets. The nutrient composition of the locusts' diet and the locust-based diet for the chameleons was determined. The diagnosis included the detailed description of clinical findings, histopathology, measurements of serum Ca, 25-hydroxycholecalciferol (25-OHD(3)), liver 25-OHD(3), vitamin A, bone mineral density, and bone mineral concentration. Chameleons that received no dietary supplementation of Ca, vitamin A, and cholecalciferol developed NMBD. When Ca and vitamin A were supplemented, the chameleons did not develop NMBD, independently of additional UVB and dietary cholecalciferol. The best prevention for NMBD was achieved by chameleons that received locusts gut-loaded with 12% Ca and dusted with 250,000 IU/kg (75 mg/kg) vitamin A and 25,000 IU/kg (0.625 mg/kg) cholecalciferol plus provision of long (10 h/d), low irradiation exposure (3-120 µW/cm(2)) to UVB. Chameleons that were fed diets low in vitamin A, cholecalciferol, and Ca were diagnosed with fibrous osteodystrophy. We noticed an interaction of vitamin A and cholecalciferol supplementation in the storage of vitamin A in the liver and formation of colon calcifications. From these findings, recommendations for the rearing of juvenile chameleons were derived.

An unusual case of generalized soft-tissue mineralization in a suckling foal.

An atypical case of severe soft-tissue mineralization in a 3-week-old foal from a herd of Andalusian horses is described. The herd clinical history and the laboratory findings were compatible with a diagnosis of secondary hyperparathyroidism due to a mineral imbalance in the diet (low calcium and high phosphorus intake). Mares showed a marked increase in serum parathyroid hormone (PTH) approximately 10 times normal levels. Serum PTH was marginally elevated in foals. Clinical signs (unthriftiness, painful joints, lameness in one or more limbs, and stiff gait) were more pronounced in foals than in mares. Two foals died and necropsy of one of them revealed extensive soft-tissue mineralization of arterial walls and pulmonary parenchyma. Clinical signs in mares and foals resolved by 4 weeks after diet adjustment.

Severe calcification of mucocutaneous and gastrointestinal tissues induced by high dose administration of vitamin D in a puppy.

A three-month-old male Bull Terrier was referred to the Animal Medical Centre, Nihon University with chief complaints of subacute emesis and lethargy. Severe leukocytosis, high CRP, hypercalcemia and hypochloremia were detected. Moreover, severe calcification of gingival mucosa and abdominal skin, and abnormalities of the skeletal system were discerned. Abdominal X-ray and endoscopic examination revealed ulcer and hemorrhage on the mucosal membrane of the stomach. This might have been due to injections of high dose vitamin D at 3 and 2 weeks ago by another practioner, according to the detailed history of medication. After two months, a gastrointestinal and skin disorder disappeared, although calcification of the stomach membranes remained and abnormality of the skeletal system had worsened. Therefore, vitamin D should be carefully administrated to a puppy.

Tumoral calcinosis in a dog with chronic renal failure.

A 2-year-old male German shepherd dog in poor bodily condition was evaluated for thoracic limb lameness due to a large, firm mass medial to the left cranial scapula. Radiography revealed several large cauliflower-like mineralized masses in the craniomedial left scapula musculature, pectoral region and bilaterally in the biceps tendon sheaths. Urinalysis, haematology and serum biochemistry showed that the dog was severely anaemic, hyperphosphataemic and in chronic renal failure. The dog was euthanased and a full post mortem performed. A diagnosis of chronic renal failure with secondary hyperparathyroidism was confirmed. The mineralised masses were grossly and histopathologically consistent with a diagnosis of tumoral calcinosis. Tumoral calcinosis associated with chronic renal failure that does not involve the foot pads is rarely seen.

Metastatic calcinosis circumscripta treated with an oral charcoal absorbent in a dog.

A five-year-old West Highland white terrier dog was admitted to the teaching hospital of Nippon Veterinary and Animal Science University due to swelling and pain of the foot pads. Examinations revealed that the dog had renal failure and calcinosis circumscripta on its foot pads. The diagnosis was metastatic calcinosis circumscripta secondary to renal failure. An oral charcoal adsorbent (Kremezin) was used to treat this condition. Following this treatment, a significant decrease in the Ca x P value (the serum calcium level x the serum phosphorus level) was observed, and the dog's condition improved dramatically. This case suggests that charcoal adsorbent (Kremezin) may be useful for treating metastatic calcinosis circumscripta in dogs.

1,25(OH)2 vitamin D concentration in the plasma of Solanum glaucophyllum intoxicated rabbits.

OBJECTIVE: To test Solanum glaucophyllum calcinotic effects in adult New Zealand White rabbits in relation to cumulative dose and active principle concentration in plasma. DESIGN: An intoxication assay with controls. PROCEDURE: Rabbits were orally dosed with aqueous extracts of dry leaves of S glaucophyllum for 5, 7 or 9 days. During the experiment, body weight, calcaemia and phosphataemia were measured; retinal blood vessel calibre was observed by ophthalmoscopic examination of the ocular fundus. 1,25(OH)2 vitamin D plasma concentration was determined at the end of the experimental periods. Soft tissue calcium concentration and the presence of calcinotic lesions were studied after euthanasia. RESULTS: Toxic effects were evident in S glaucophyllum treated groups (loss of body weight, elevation of soft tissue calcium concentration, and presence of calcinotic lesions). Plasma 1,25(OH)2 vitamin D concentrations were negatively correlated with final body weight (r = -0.97; P < or = 0.001), and positively correlated with renal calcium concentration (r = 0.74; P = 0.02). There was also a significant regression of plasma 1,25 (OH)2 vitamin D concentration on the cumulative dose of S glaucophyllum (R2 = 0.87; P < or = 0.001). CONCLUSIONS: The procedure described here offers a sensitive and practical experimental model for the study of the pathogenesis of enteque seco.

Primary hypoparathyroidism in a cat complicated by suspect iatrogenic calcinosis cutis.

An adult male cat presented to the Ontario Veterinary College after having a seizure at the humane society. The cat was diagnosed with primary hypoparathyroidism and was treated with calcium and vitamin D3 supplementation. Calcium supplementation included subcutaneous (SC) administration of diluted calcium gluconate according to protocols described in recent literature. Seven days after SC calcium administration, firm SC masses developed in the intrascapular area where the injections were given and in the dependent axillary area. These areas became raised, formed crusts, necrosed, and left scars. Although not histopathologically confirmed, the author postulates that this was a direct reaction to SC calcium gluconate administration.

[Enzootic calcinosis in 16 cows from 6 dairy farms in Unterengadin]. / Enzootische Kalzinose bei 16 Kühen aus 6 Milchviehbetrieben im Unterengadin.

Enzootic calcinosis was diagnosed in 16 cows, which originated from 6 dairy farms located in the Unterengadin valley in Switzerland between 1,402 and 1,650 metres above sea level. During the winter, the cows were fed haylage, which contained up to 50 per cent golden oat-grass (Trisetum flavescens), and hay and grain. The first symptoms of enzootic calcinosis were noted in March 1998, when some of the cows developed locomotor abnormalities. Additional cases were diagnosed during the following three months. The most important clinical findings were decreased milk production, weight loss, frequent recumbency, difficulty in rising, kneeling while rising and feeding, stilted gait, arched back, shifting weight from one foot to another and reluctance to remain standing after being roused. Of the 16 cows, 5 had elevated concentrations of serum calcium and 10 had decreased concentrations of serum magnesium. All cows had normal or decreased concentrations of serum phosphorus, because the feeding of haylage containing golden oat-grass had been discontinued two months previously. In all of the cows, the most important postmortem findings were severe calcification of the aorta, iliac artery, brachiocephalic trunk and pulmonary artery.

Evaluation in rabbits of the fetal effects of maternal ingestion of Solanum malacoxylon.

A study was performed to determine the possible toxic effects on the young of does that had been fed during the gestational period on a ration containing Solanum malacoxylon (Sm), a calcinogenic plant that contains a vitamin D3-glycoside conjugate. Experimental animals received a ration containing 0.03% or 0.04% of Sm leaves on days 6 to 30 of gestation. The levels of calcium, phosphorus and alkaline phosphatase in their sera, as well as their feed intake and body weight, were evaluated weekly. The does were euthanized 3 days after parturition and paraffin sections stained with haematoxylin and eosin were prepared from their heart, lungs, kidneys and aorta for histopathological examination. The young from does in the Sm 0.03% group were euthanized 3 days after birth and biochemical and histopathological determinations were performed, as described for the does. The does in both experimental groups showed decreased feed consumption and those in the Sm 0.04% group showed lower body weights throughout their gestation. Animals treated with Sm 0.04% presented a high incidence of abortion and stillbirth. There were biochemical and histopathological alterations in both experimental groups, which were more prominent in the does in the Sm 0.04% group. Litters from does treated with Sm 0.03% showed mineralization of soft tissue and an increase in phosphorus and calcium levels. These findings indicate that the vitamin D3-glycoside passes through the placental barrier to the fetus.

Vitamin D toxicosis in cats: natural outbreak and experimental study.

A pathological study on 5 of 21 cats affected naturally with systemic calcinosis was performed. The animals ranged in age from 1 to 9 years. Hematology and serum chemistry analyses showed the elevated values of phosphorus, blood urea nitrogen and serum creatinine. X-ray examination disclosed the increased density of systemic bones. Histologically, marked calcification was present at the vascular walls of almost all the organs including the lungs, trachea, kidneys, heart, aorta, alimentary tracts, choroid plexus and bones. In the lungs, kidneys and stomach, the calcified lesions were associated with deposition of oxalate crystals. Serum chemistry showed more elevated values of 25-hydroxycholecalciferol (vitamin D) of the affected cats than the normal level. Retrospective examination revealed that these cats had been fed the commercial pet foods containing a large amount of vitamin D (6,370 IU/100 g diet) from their young age, and its value was about ten times as much as that of the control food (680 IU/100 g diet). Pathological changes found in the cats from the experimental vitamin D3 toxicosis were similar to those in the natural cases. In addition, tissue levels of calcium, phosphorous and zinc in the lungs and kidneys were markedly elevated in both natural and vitamin D-intoxicated cases. These findings suggest that long-term feeding of the pet food containing excessive vitamin D was responsible for the outbreak of the systemic calcinosis in the cats.

Vitamin D3 intoxication in naked mole-rats (Heterocephalus glaber) leads to hypercalcaemia and increased calcium deposition in teeth with evidence of abnormal skin calcification.

Naked mole-rats have no access to obvious sources of vitamin D and therefore have an impoverished vitamin D status. In an investigation into the effects of vitamin D supplementation, inadvertently supraphysiological doses of 130,000 times the normal dose of vitamin D were administered. Within 5 days animals appeared lethargic, with reduced food intake. All but one of the seven animals were killed and blood was collected. Plasma vitamin D metabolites 25(OH)D and 1,25(OH)2D and calcium were determined. Both vitamin D metabolite concentrations exceeded the upper limits of sensitivity of the assays (> 100 ng/ml 25(OH)D and > 210 pg/ml 1,25(OH)2D). Active calcium uptake in the intestine was evident along with concomitant increases in calcium concentration in plasma, bone, and teeth. The remaining animal survived, but showed scab-like formations in the skin around the lower jaw and along the nipple line. X-ray analyses revealed calcium deposition in these cornified regions, although there was no evidence of metastatic calcification in other tissues. Deposition of excess calcium in skin that is regularly sloughed off and in teeth that are continuously worn down and replaced may reduce the vitamin D-induced hypercalcaemia and thus alleviate the effects of vitamin D intoxication.