Hyperparathyroid disorders in the dog: primary, secondary and cancer-associated (pseudo)

Hyperparathyroid disorders were diagnosed in four dogs: one had primary hyperparathyroidism, characterized by parathyroid adenoma and hyper-calcaemia; one had renal secondary hyperparathyroidism, characterized by parathyroid gland hyperplasia, hypocalcaemia and renal failure; and two had cancer-associated hyperparathyroidism (pseudohyperpara-thyroidism), characterized by the presence of neoplasia, parathyroid gland atrophy, hypercalcaemia and absence of skeletal metastases. Significant clinicopathologic findings included serum concentrations of calcium, phosphorus and immunoreactive parathyroid hormone (PTH), presence or absence of parathyroid and bone lesions, and the presence of non-parathyroid neoplasia.     

Cystic bone lesions in related Old English Sheepdogs

At 6 months of age, an Old English Sheepdog with swollen and painful distal radial/ulnar metaphyses was found to have multiple cystic lesions in left and right radius and ulna. Cystic bone lesions were also detected radio-graphically in two clinically normal littermates and in the sire and dam of the litter. Radiographic changes of nutritional secondary hyperparathyroidism were found in the three affected pups and in two other individuals from the litter of eight.
The cystic lesions in one pup were drained surgically and the cyst wall curetted, while the other two pups were not treated. The lesions in all three pups gradually resolved and had almost completely disappeared by 10 months of age.     

Babesiosis in a litter of pups

Babesia canis infection was diagnosed in a litter of seven 3-week-old Mastiff pups kept in a north Florida kennel. The pups were evaluated because of poor weight gain; the smallest pup also was markedly lethargic. Six of the pups were anemic and thrombocytopenic. A positive linear correlation between PCV and absolute reticulocyte count suggested that the variation in PCV may have been related more to the ability of a pup to increase erythrocyte production than to a difference in magnitude of erythrocyte destruction. All pups recovered from clinical signs and hematologic abnormalities attributable to babesiosis within 2.5 weeks after treatment with diminazene aceturate. Transient neurologic signs observed in 1 pup 3 days after treatment were believed to represent an adverse drug reaction. The dam of the litter had a serum titer of 1:640 for B canis, but appeared healthy, as did approximately 30 other adult dog in the kennel. The strain of B canis infecting dogs in the kennel caused severe illness and death in some pups, but clinically inapparent disease in adult dogs.     

Neosporosis in Beagle dogs: clinical signs, diagnosis, treatment, isolation and genetic characterization of Neospora caninum

Clinical neosporosis was diagnosed in a litter of five pups born to a Beagle bitch from Virginia, USA. Four of the pups developed limb weakness starting at 4 weeks of age. The dogs were suspected to have neosporosis based on clinical signs and empirically treated with Clindamycin (75 mg, oral, twice daily, total 150 mg) starting at 9 weeks of age and the dosage was doubled at 13 weeks of age. Antibodies to Neospora caninum were detected in sera of the dam and pups when first tested serologically at the age of 4 months. The owner donated the pup with the worst clinical signs and the dam for research; both dogs were euthanized. Viable N. caninum was isolated in gamma interferon gene knock out (KO) mice and in cell culture from the pup killed at 137 days of age. Tissue cysts, but no tachyzoites, were found in histological sections of brain and muscles. The isolate was also identified as N. caninum by PCR and sequence analysis and designated NC-9. N. caninum was neither isolated by bioassay in KO mice nor found in histological sections of tissues of the bitch. Clinical signs in the remaining three pups improved considerably after a 6-month treatment with Clindamycin; N. caninum antibody titers were still persistent in these pups at 23 months of age. Results indicate that medication with Clindamycin can improve clinical condition but not eliminate N. caninum infection.     

Shetland Sheepdog leukodystrophy

Three litters of Shetland Sheepdog pups born to the same bitch and 2 different sires were studied because of uncontrollable seizures or progressive neurologic dysfunction. Four pups from the 1st litter, 1 from the 2nd litter, and 4 from the 3rd litter had severe diffuse spongy degeneration of the white matter of the brain and spinal cord. An inherited basis for this syndrome was suspected. The purpose of this study was to evaluate the pups with currently available screening tests for the metabolic, biochemical, infectious, and toxicologic causes of leukodystrophy seen in humans and animals. Computed tomography scans revealed diffuse hypomyelination in the affected pup. Complete postmortem examination, including histopathology and electron microscopy, delineated a leukodystrophy resembling human Canavan's disease, but amino acid and organic acid metabolism abnormalities were not detected. No etiology for Shetland Sheepdog leukodystrophy has been found, but this condition represents another familial disease in the purebred dog population.     

Pretreatment clinical and laboratory findings in dogs with primary hyperparathyroidism: 210 cases (1987-2004)

OBJECTIVE: To evaluate pretreatment clinical and laboratory findings in dogs with naturally occurring primary hyperparathyroidism. DESIGN: Retrospective study. ANIMALS: 210 dogs with primary hyperparathyroidism and 200 randomly selected, age-matched control dogs that did not have primary hyperparathyroidism. PROCEDURE: Medical records for dogs with primary hyperparathyroidism were reviewed for signalment; clinical features; and results of clinicopathologic testing, serum parathyroid hormone assays, and diagnostic imaging. RESULTS: Mean age of the dogs with primary hyperparathyroidism was 11.2 years (range, 6 to 17 years). The most common clinical signs were attributable to urolithiasis or urinary tract infection (ie, straining to urinate, increased frequency of urination, and hematuria). Most dogs (149 [71%]) did not have any observable abnormalities on physical examination. All dogs had hypercalcemia, and most (136 [65%]) had hypophosphatemia. Overall, 200 of the 210 (95%) dogs had BUN and serum creatinine concentrations within or less than the reference range, and serum parathyroid hormone concentration was within reference limits in 135 of 185 (73%) dogs in which it was measured. Urolithiasis was identified in 65 (31 %) dogs, and urinary tract infection was diagnosed in 61 (29%). Mean serum total calcium concentration for the control dogs-was significantly lower than mean concentration for the dogs with primary hyperparathyroidism, but mean BUN and serum creatinine concentrations for the control dogs were both significantly higher than concentrations for the dogs with primary hyperparathyroidism. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that urolithiasis and urinary tract infection may be associated with hypercalcemia in dogs-with primary hyperparathyroidism, but that development of renal insufficiency is uncommon.     

Neospora caninurn Infection in English Springer Spaniel Littermates

Progressive paraparesis developed in four male English Springer Spaniel pups from a litter of five during the first 10 weeks of life. Two of the pups, which had the earliest onset of neurologic signs, were euthanatized without further workup. However, a detailed investigation was completed on the remaining two littermates at 12 weeks of age. Both pups had progressive paraparesis for 3 to 4 weeks before presentation, with one dog developing subsequent asymmetric pelvic limb extensor rigidity. Based on results from neurologic examination, cerebrospinal fluid (CSF) analysis, electrophysiology, and muscle/nerve biopsy, a presumptive diagnosis of protozoal polyradiculitis and polymyositis was made. Necropsy of the most severely affected pup confirmed the clinical diagnosis of inflammatory nerve root and muscle disease but no organisms were found. To increase the potential yield of organisms, the second pup was placed on immunosuppressive doses of corticosteroids and euthanatized 2 weeks later. Numerous organisms were found in lesions in muscle and the central nervous system. Organisms grew in tissue culture and were isolated from the peritoneal fluid of gerbils inoculated with infected tissue. Organisms were not isolated from inoculated mice, guinea pigs, rabbits, and hamsters. No parasites were seen in feces or tissues of three cats fed infected dog tissues. Serologic testing demonstrated a strong positive titer to Neospora caninum in both pups, and electron microscopy showed the characteristic morphology of this parasite.     

Neuroaxonal dystrophy in a litter of papillon pups

A litter of five 14-week-old papillon puppies was referred for investigation of pelvic limb ataxia. Clinical examination revealed signs of ataxia, hypermetria and depressed postural reflexes affecting all four limbs. The severity of these signs varied between members of the litter. The condition became progressively worse and by 19 weeks of age all but the least severely affected pup (the single male of the litter) had deteriorated to the point that euthanasia was indicated on humane grounds. Pathological examination revealed widespread changes in both white and grey matter of the neuraxis caudal to the fore-brain, particularly involving the dorsolateral white matter of the spinal cord, which were characterised by axonal swellings typical of neuroaxonal dystrophy.     

Treatment of primary hyperparathyroidism in a Miniature Horse using chemical ablation of abnormal parathyroid tissue localized by 3‐phase computed tomography

A 15‐year‐old Miniature Horse mare with persistently increased plasma calcium (total and ionized) and serum parathyroid hormone concentrations was presented for suspected primary hyperparathyroidism. Ultrasonography of the thyroid region identified an enlarged heterogeneous mass axial to the right thyroid lobe suggestive of an enlarged parathyroid gland, which was further confirmed using sestamibi nuclear scintigraphy and 3‐phase computed tomography. Percutaneous ultrasound‐guided ethanol ablation of the mass, a method not previously described in the horse, was performed under general anesthesia resulting in rapid normalization of plasma ionized calcium and serum parathyroid hormone concentrations. Ablation of abnormal parathyroid gland tissue may be a suitable alternative to surgical resection in certain cases of primary hyperparathyroidism in the horse.     

Canine primary hyperparathyroidism and its association with urolithiasis

Primary hyperparathyroidism results from autonomous secretion of parathyroid hormone by a single or multiple parathyroid glands. Clinical signs result from various combinations of hypercalcemia, hypercalcemic nephropathy, urolithiasis, or mobilization of calcium and phosphorus from bone. Following parathyroidectomy, the prognosis for dogs with primary hyperparathyroidism is good if the disorder is diagnosed before renal disease is advanced.     

Juvenile-Onset Distal Myopathy in Rottweiler Dogs

Two juvenile Rottweiler siblings were presented with the complaint of decreased activity and various postural abnormalities, including plantigrade and palmigrade stance and splayed forepaw digits. The neurologic examinations were otherwise normal. Electromyography revealed rare fibrillation potentials and positive sharp waves. Motor nerve conduction velocities were normal, whereas compound muscle action potentials from the interosseous muscles were decreased. These findings were consistent with a primary myopathy. A 3rd pup from a different litter and a 4th pup from a litter with 3 of 8 affected dogs had similar clinical presentations. Histopathologic changes in fresh-frozen muscle biopsy samples were similar in all pups and consisted of myofiber atrophy with mild myonecrosis, endomysial fibrosis, and replacement of muscle with fatty tissue. These changes were more severe in distal muscles than in proximal muscles. Plasma carnitine concentrations (total and free) were decreased in all pups. Muscle carnitine concentrations (total and free) were decreased in 3 of 4 pups and the least affected pup had a borderline low free muscle carnitine concentration. Abnormalities involving major metabolic pathways were not found on quantification of organic and amino acids. Dystrophin immunocytochemistry was normal in 2 dogs tested. Distal myopathies in humans are classified under the dystrophic group of muscle disorders. These 4 cases represent a form of muscular dystrophy apparently not previously reported in dogs.     

Diagnosis and treatment of primary hyperparathyroidism in a bobcat (Lynx rufus)

An 18-yr-old male bobcat (Lynx rufus) presented with chronic moderate weight loss and acute onset of anorexia and lethargy. Hypercalcemia and azotemia were present on the serum chemistry panel. Abdominal ultrasound revealed hyperechoic renal cortices, but no evidence of neoplasia. Ionized calcium and 25-hydroxyvitamin D were mildly elevated, intact parathyroid hormone was severely elevated, and parathormone-related protein was undetected, suggesting primary hyperparathyroidism with possible renal dysfunction. Azotemia lessened in severity following diuresis, but hypercalcemia persisted; thus primary hyperparathyroidism was considered the most probable differential diagnosis. A second ultrasound including the cervical region revealed a solitary intraparenchymal left thyroid nodule. The nodule was surgically excised; histopathology confirmed a parathyroid adenoma. Although primary hyperparathyroidism was suspected, diagnosis was not achieved from serum chemistry values alone. This case emphasizes the importance of diagnostic imaging and histopathology in the investigation of persistently abnormal laboratory values.     

Primary hyperparathyroidism in a dog: biochemical, bone histomorphometric, and pathologic findings

An adult Keeshond had clinical signs associated with hypercalcemia, including inappetence, polyuria, polydipsia, and vomiting. Blood biochemical findings and urinary clearance studies were consistent with a diagnosis of primary hyperparathyroidism. Histomorphometric analysis of trabecular bone in an iliac crest biopsy indicated increased bone remodeling activity. Surgical exploration of the neck revealed an oval mass, which was removed by blunt dissection. Histologic diagnosis was parathyroid gland adenoma. The dog died because of renal failure on the eighth postoperative day. This report defines primary hyperparathyroidism in the dog, thus facilitating diagnosis for the veterinary clinician.     

Congenital peripheral vestibular disease attributed to lymphocytic labyrinthitis in two related litters of Doberman pinscher pups

Five Doberman Pinscher pups from a litter of 10 (litter A) and 3 of 9 pups from a subsequent mating of the same bitch (litter B) had clinical signs consistent with unilateral or bilateral peripheral vestibular disease. Results of CBC, serum biochemical analysis, urinalysis, ophthalmologic examination, deep otoscopic examination, and CSF analysis were normal in all affected pups. Bacteriologic culture results from CSF were negative and affected pups did not have canine distemper antibody titers in CSF. The most severely affected littermates were euthanatized and necropsied at the owner's request. Gross lesions were not found at necropsy, but marked lymphocytic labyrinthitis was discovered microscopically in decalcified sections of the labyrinthine system. The case history and histologic findings were suggestive of an infectious, most likely viral, cause, but organisms were not isolated from specimens of CNS tissue. The involvement of the same bitch in the 2 litters suggests heritable factors. One mildly affected pup apparently recovered or compensated for its vestibular dysfunction.     

Phosphorus deficiency in cattle on two farms in canterbury

A New Zealand canine herpesvirus isolate was inoculated into three 2-day-old puppies via the intraperitoneal route, two other puppies from the same litter being retained as in-contact controls. All pups were left suckling the bitch.

One inoculated pup died of misadventure. The remaining inoculated pups, and one in-contact pup, died with clinical signs of herpesvirus infection, the virus being subsequently recovered from a number of tissues. The remaining in-contact pup also developed typical disease, but recovered, virus being detected only in the tonsils. Lesions were detected in the diseased puppies in a wide variety of organs, and were consistent with previously published reports. No evidence of disease was detected in the bitch, but both she and the recovered pup developed neutralizing antibodies to the virus.     

Hypercalcemia and high serum parathyroid hormone-related protein concentration in a horse with multiple myeloma

A 13-year-old gelding was examined because of weight loss, hyperglobulinemia, and hypercalcemia. Possible causes of hypercalcemia that were considered included renal failure, primary hyperparathyroidism, vitamin D toxicosis, and malignancy. There was no history of vitamin D ingestion, and serum creatinine and parathyroid hormone concentrations were normal, making renal failure and primary hyperparathyroidism unlikely. The hypercalcemia was suspected to be a result of malignancy, but thorough testing did not reveal any neoplastic disease. Eight months later, serum parathyroid hormone-related protein (PTHrP) concentration was high, supporting the suggestion that hypercalcemia was a result of malignancy. In addition, radial immunodiffusion confirmed a selective 300-fold increase in serum IgA concentration. The horse was euthanatized, and postmortem examination revealed neoplastic infiltrates in the kidneys, lymph nodes, liver, and bone marrow. Neoplastic cells had morphologic characteristics of plasma cells, and immunohistochemical staining confirmed that neoplastic cells were expressing PTHrP and IgA. The final diagnosis was multiple myeloma with expression of IgA paraprotein.     

Tremor syndrome and hypomyelination in Lurcher pups

Two male Lurcher pups had continual tremor of the head, trunk and limbs when they began to walk. One pup recovered completely by 16 weeks of age while signs in the other remained static and it was destroyed at 8 weeks of age. Routine examination of haematoxylin and eosin stained, paraffin embedded nervous tissue failed to reveal obvious abnormality but hypomyelination of the spinal cord white matter was found on examination of plastic embedded material. The rôles played by genetic factors and in-utero viral and toxic insults in the pathogenesis of hypomyelination and tremor syndromes in dogs are discussed and a plan is offered for evaluating future cases of these conditions.     

Radioimmunoassay for parathyroid hormone in equids

Radioimmunoassay for parathyroid hormone (PTH) in equids was performed on blood samples from healthy equids and equids with hypercalcemia and hypophosphatemia. The assay was validated for equine carboxy-terminal PTH. Manipulation of serum ionized Ca in healthy equids by infusing Na2 EDTA and CaCl2 produced an expected increase and decrease, respectively, in measurable immunoreactive PTH. Intra-assay and interassay coefficients of variation were 2.6% and 11.7%, respectively. The range of PTH valves for healthy mature horse mares and geldings maintained on pasture was less than 0.27 ng/ml to 0.92 ng/ml and for horse colts fed grain was 0.61 to 1.25 ng/ml. Serum PTH values were measured on 2 equine patients with hypercalcemia, 1 pony with primary hyperparathyroidism and 1 horse with pseudohyperparathyroidism. Both patients had increased serum PTH values.     

Hypocalcemia in a dog

A case of hypocalcemia was presented with a concurrent hyperphosphatemia. Normal renal function tests excluded primary renal insufficiency. The diet was thought to contain a normal ratio of calcium and phosphorus and, therefore, nutritional secondary hyperparathyroidism was not considered. The radiographs showed normal bone density and the dog was not lame. Concentrations of immunoreactive parathyroid hormone were measured in an attempt to classify the etiology. The dog was successfully managed with calcium supplementation and vitamin D(3) or oral calcium alone.     

Suspected pseudohypoparathyroidism in a domestic ferret

A 1.5-year-old ferret examined because of seizures was found to have low serum calcium, high serum phosphorus, and extremely high serum parathyroid hormone concentrations. Common causes of these abnormalities, including nutritional secondary hyperparathyroidism, chronic renal secondary hyperparathyroidism, tumor lysis syndrome, and hypomagnesemia, were ruled out, and a tentative diagnosis of pseudohypoparathyroidism was made. Pseudohypoparathyroidism is a hereditary condition in people that, to our knowledge, has not been identified in ferrets previously and is caused by a lack of response to high serum parathyroid hormone concentrations, rather than a deficiency of this hormone. The ferret improved after treatment with dihydrotachysterol (a vitamin D analog) and calcium carbonate. It was still doing well after 3.5 years of continued treatment.