Th. S. G. A. M. van den Ingh

Improvement in Liver Pathology after 4 Months of D‐Penicillamine in 5 Doberman Pinschers with Subclinical Hepatitis

Five female Doberman Pinschers with increased hepatic copper concentrations and persistent (3-4 years) subclinical hepatitis were treated with D-penicillamine for 4 months. Before and after treatment, the dogs underwent clinical, hematologic (red blood cell, white blood cell, and differential and thrombocyte counts), and clinical chemistry (creatinine, alkaline phosphatase, alanine aminotransferase, and total bile acid concentrations) examinations, and liver biopsies were examined histologically and their copper content measured quantitatively. No adverse effects were observed during treatment, and CBC and serum chemistry test results did not change. The mean liver copper concentration was 1,036 mg/kg dry matter before treatment and decreased to 407 mg/kg after treatment (P = .03). The copper concentrations had decreased (by between 134 and 1,135 mg/kg dry matter) in all of the dogs. The histopathologic appearance had improved or returned to normal in all 5 dogs. We conclude that D-penicillamine effectively reduced copper retention in these dogs and improved the histopathologic appearance of the lesions. However, because D-penicillamine has both copper-chelating and anti-inflammatory properties, it is not possible to draw conclusions on the etiology of this disease.

Polyglandular deficiency syndrome in a boxer dog: Thyroid hormone and glucocorticoid deficiency

Primary hypothyroidism and partial primary adrenocortical deficiency (isolated glucocorticoid deficiency) were diagnosed in an 8-year-old spayed female boxer dog, presented because of progressive symmetrical truncal alopecia, lethargy, and intolerance to cold. The diagnosis was based upon the combination of low, non-TSH-responsive concentrations of plasma thyroxine and low urinary excretion of corticoids together with high plasma concentrations of ACTH. Normal suppressibility of ACTH concentrations by a low dose of dexamethasone indicated an intact feedback system. Plasma growth hormone levels were elevated, most probably because somatostatin release was depressed by the glucocorticoid deficiency. The dog improved during oral replacement therapy with thyroxine until death ensued after 9 months as a result of intercurrent disease. Autopsy revealed thyroid atrophy and lymphocytic adrenalitis with complete destruction of the zona fasciculata and zona reticularis of the adrenal cortex. The combination of primary hypothyroidism and primary adrenocortical deficiency in this dog is identical to the entity known as type II polyglandular autoimmunity or Schmidts syndrome in humans. The adrenocortical insufficiency remained confined to glucocorticoid deficiency during the observation period; on no occasion did electrolyte concentrations in the plasma reach values suggestive of mineralocorticoid deficiency.

Primary and metastatic carcinomas in the digits of cats

Summary In the period 1993–1998, digital carcinomas in 64 cats were examined. In all animals primary complaints were painful digit(s). Eight cats had a primary squamous cell carcinoma which involved one digit or two adjacent digits of one leg. Fifty‐six cats had metastases of a pulmonary carcinoma in the digits, and in general multiple digits of different legs were involved. In many of these cats metastases also occurred in other organs, including the skin and muscles. No primary sweat gland carcinomas of the digits were seen. Primary squamous cell carcinomas of the digits were characterized by cornification and the absence of PAS‐positive cells, PAS‐positive secretory material. Immunohistochemically, these neoplasms stained negative with the monoclonal antibody CAM 5.2 directed against Keratin 8 (K 8). The metastases of pulmonary carcinomas to the digits showed one or more of the following histological features: goblet cells, ciliated epithelial cells, PAS‐positive cells or lakes, and/or a PAS‐positive lining of luminal membranes and no cornification. Immunohistochemically, they showed positive staining for CAM 5.2 (K8). Thoracic radiographs from three cats with a primary squamous cell carcinoma showed no abnormalities, whereas all cases of metastases from a pulmonary carcinoma to the digits available for follow‐up showed evidence of a primary pulmonary carcinoma on radiography and/or postmortem examination (25 out of 56). The conclusion of this study was that most carcinomas in the digits of cats were metastases of a primary pulmonary carcinoma (87.5%). Primary squamous cell carcinomas occurred infrequently. The prognosis of metastases of a pulmonary carcinoma in the digits is poor with an averagae, survival time of 4.9 weeks, in contrast to 29.5 weeks in cats with a squamous cell carcinoma. These data stress the importance of taking thoracic radiographs of cats with digital tumours before surgical intervention.In the period 1993-1998, digital carcinomas in 64 cats were examined. In all animals primary complaints were painful digit(s). Eight cats had a primary squamous cell carcinoma which involved one digit or two adjacent digits of one leg. Fifty-six cats had metastases of a pulmonary carcinoma in the digits, and in general multiple digits of different legs were involved. In many of these cats metastases also occurred in other organs, including the skin and muscles. No primary sweat gland carcinomas of the digits were seen. Primary squamous cell carcinomas of the digits were characterized by cornification and the absence of PAS-positive cells, PAS-positive secretory material. Immunohistochemically, these neoplasms stained negative with the monoclonal antibody CAM 5.2 directed against Keratin 8 (K 8). The metastases of pulmonary carcinomas to the digits showed one or more of the following histological features: goblet cells, ciliated epithelial cells, PAS-positive cells or lakes, and/or a PAS-positive lining of luminal membranes and no cornification. Immunohistochemically, they showed positive staining for CAM 5.2 (K8). Thoracic radiographs from three cats with a primary squamous cell carcinoma showed no abnormalities, whereas all cases of metastases from a pulmonary carcinoma to the digits available for follow-up showed evidence of a primary pulmonary carcinoma on radiography and/or postmortem examination (25 out of 56). The conclusion of this study was that most carcinomas in the digits of cats were metastases of a primary pulmonary carcinoma (87.5%). Primary squamous cell carcinomas occurred infrequently. The prognosis of metastases of a pulmonary carcinoma in the digits is poor with an average survival time of 4.9 weeks, in contrast to 29.5 weeks in cats with a squamous cell carcinoma. These data stress the importance of taking thoracic radiographs of cats with digital tumours before surgical intervention.

Familial stomatocytosis--hypertrophic gastritis (FSHG), a newly recognised disease in the dog (Drentse patrijshond).

A newly recognised disease, which we have given the provisional name of familial stomatocytosis-hypertrophic gastritis (FSHG), is described in two families of dogs of the Drentse partrijshond breed. The affected dogs consisted of 3 females and 5 males, 3 to 19 (mean 9.5) months of age at admission. The main clinical problems were diarrhoea, icterus, and ataxia and paresis of the pelvic limbs. Laboratory evaluation revealed abnormal red cell shape (stomatocytosis), increased osmotic fragility, haemolytic anaemia, and increased liver enzymes and serum bilirubin. Gastroscopic and histopathologic examination of the gastric mucosa revealed hypertrophic gastritis resembling Ménétriers disease in man. Histologic findings in the liver were suggestive of progressive liver disease. Cysts were found in the kidneys of the five oldest patients. Electroneurography in 2 dogs revealed polyneuropathy. In the parents of 2 patients (sister and brother), there were no clinical or laboratory abnormalities. An autosomal recessive hereditary defect of lipid metabolism is suspected.

Canine viral enteritis: prevalence of parvo-, corona- and rotavirus infections in dogs in the Netherlands.

Summary After a brief review of the present knowledge about canine viral enteritis, the role played by parvoviral, coronaviral and rotaviral infections in contagious diarrhoea in dogs in the Netherlands is discussed. For this purpose a serologic survey, pathologic findings in dogs, and the demonstration of parvoviral antigen with an immunofluorescence test and with a newly developed haemadsorption-elution-haemagglutination assay (HEHA) are presented. It is concluded that infections with canine parvovirus, coronavirus and rotavirus appear widespread among dog populations in the Netherlands.

Fibrocartilaginous embolism of the spinal cord (FCE) in juvenile Irish Wolfhounds

Summary This study describes the occurrence of fibrocartilaginous embolism of the spinal cord (FCE) in eight juvenile Irish Wolfhounds that were presented within a period of 16 months (1996–1997). The dogs, seven males and one female between eight and 13 weeks of age, were presented because of an acute onset of abnormal locomotion. Five dogs were euthanized and FCE was diagnosed by the histomorphological presence of focal myelomalacia and Alcian blue‐positive‐nucleus‐pulposus material in the spinal cord vasculature. Three dogs, which were thought to have FCE because of their clinical symptoms, improved with partial or almost complete return to normal locomotion. Although the observed high incidence may be a coincidence, oral information from breeders and lay reports of similar cases in journals for dog breeders from various countries suggest that FCE is a common disorder in young Irish Wolfhounds.

Zollinger-Ellison syndrome in a cat.

Zollinger-Ellison Syndrome in a 12-year old castrated male European Shorthair cat is described. The clinical symptoms were vomiting, weight loss, listlessness and alternating diarrhoea and obstipation. An endocrine tumour near the pancreatic duct had metastasised to the liver. Many duodenal ulcers were present. Immunohistochemistry revealed cells positive for gastrin and neuron-specific enolase (NSE) scattered throughout the tumour.

The role of quantitative electromyography (EMG) in horses suspected of acute and chronic grass sickness

REASONS FOR PERFORMING THE STUDY Clinical evidence of motor neuron involvement in equine grass sickness (EGS) has not been reported. HYPOTHESIS Quantitative electromyography (EMG) analysis can elucidate subtle changes of the lower motor neuron system present in horses with EGS, performed ante mortem. METHODS Fourteen horses diagnosed clinically with acute, subacute or chronic EGS were examined and quantitative EMG performed. Previously published data on healthy horses and horses with proven lower motor neuron disease (LMND) were used as controls. In 8 horses post mortem examination was performed, and in 7 muscle biopsies of the lateral vastus muscle underwent histopathology and morphometry. RESULTS Clinical electrophysiological evidence of neuropathy was present in 12 horses. Analysis of data from the first 4 horses resulted in 95% confidence intervals (CI) of nontransformed data for motor unit action potential (MUP) duration in subclavian, triceps and lateral vastus muscle of 11.0-13.7, 14.8-20.3 and 12.2-17.2 msecs, respectively, and for MUP amplitude 291-453, 1026-1892 and 957-1736 microV, respectively. For number of phases the 95% CI was 3.6-4.4, 2.9-3.6 and 2.9-3.4, respectively, and for number of turns 5.0-6.5, 4.3-5.3 and 3.7-4.6, respectively. No changes in duration of insertional activity were measured. Pathological spontaneous activity was observed in all horses. EGS as evidenced by degenerative changes in the autonomic ganglia in combination with minor degenerative changes of the spinal lower motor neurons was observed on post mortem examination in all 8 available autopsies. In muscle biopsies of 4 out of 7 horses changes consistent with slight neurogenic atrophy were found. CONCLUSIONS AND POTENTIAL RELEVANCE EMG results demonstrated the presence of a neuropathy of skeletal muscles in all horses suspected to have EGS. The combination of clinical and electrophysiological evidence may aid differential diagnosis of neurogenic disease in cases of weight loss and colic.

Diagnosis of secondary hyperparathyroidism in a pony using intact parathyroid hormone radioimmunoassay

N. A. Benders, DVM, J. H. van der Kolk, DVM, PhD, Department of Equine Sciences, K. Junker, DVM, Th. S. G.A. M. van den hIngh, DVM, PhD, Department ofVeterinary Pathology, Th. Wensing, PhD, Department of Farm Animal Health, Faculty of Veterinary Medicine, Utrecht University, 3508 TD Utrecht, The Netherlands SINCE Estepa and others (1998) validated a human radioimmunoassay for intact parathyroid hormone (iPTH) for use in the equine species, this method has contributed considerably to the diagnosis of secondary hyperparathyroidism and should be used in preference to the carboxyl-terminal assay (C-terminal PTH) (Capen 1989). High iPTH concentrations are often seen in primary or secondary hyperparathyroidism; Frank and others (1998) described a pony with primary hyperparathyroidism confirmed on the basis of a high iPTH concentration. Secondary hyperparathyroidism can be due to renal failure, which is rare in horses, or to nutritional secondary hyperparathyroidism (NSH). NSH is related to a persistent unbalanced diet causing hypocalcaemia (Krook and Lowe 1964, Krook 1968, Joyce and others 1971, Schryver and others 1971, 1974, Argenzio and others 1974, Walthall and McKenzie 1976, Capen 1989, Palmer 1993). This short communication describes a case in which the iPTH concentration was measured to support the diagnosis of secondary hyperparathyroidism. A five-year-old Shetland pony mare was referred to the Department of Equine Sciences, Utrecht University, because ofweight loss, anorexia and a stiff gait over the previous three days, for which it had been treated with vedaprofen (Quadrisol; Janssen-Cilag BV) and corticosteroids. The mare was pastured with 10 other clinically normal ponies and fed a free choice of maize silage and hay. The owner had bought the mare three months previously. On physical examination the pony was in poor body condition. It had bilateral forelimb shifting-leg lameness, seemed dull and showed a great reluctance to move. The upper face had a swollen appearance with bilateral firm enlargement of the maxilla and mandible, not associated with any clinical signs of pain. The mare had a respiratory rate of 100 breaths/minute, a regular pulse of 96 beats/minute and a body temperature of 38-6°C. The mucous membranes were reddish, moist and some haemorrhages were present. The sclerae were yellow. There was an increased digital pulse. Laboratory evaluation included a complete blood count and serum biochemical analysis; the findings are shown in Table 1. Haematology revealed a slightly decreased packedcell volume (Pcv). The plasma calcium concentration was normal and the plasma ionised calcium concentration was slightly decreased, whereas the plasma phosphorus concentration was increased. Alkaline phosphatase activity was high, probably due to the increased bone resorption. Urinalysis revealed a low normal calcium concentration and hyperphosphaturia. For reference, the calcium and phosphorus concentrations in the urine were determined in 11 clinically healthy warmbloods. The creatinine concentration in the urine was not available for calculation of the fractional excretion of calcium and phosphorus due to FIG 1: Lateral radiograph of the left front foot showing a generalised loss of bone density with a clear number and loss of definition of bone trabeculae

Dietary Management of Labrador Retrievers with Subclinical Hepatic Copper Accumulation

Background Genetic and environmental factors, including dietary copper intake, contribute to the pathogenesis of copper‐associated hepatitis in Labrador retrievers. Clinical disease is preceded by a subclinical phase in which copper accumulates in the liver. Objective To investigate the effect of a low‐copper, high‐zinc diet on hepatic copper concentration in Labrador retrievers with increased hepatic copper concentrations. Animals Twenty‐eight clinically healthy, client‐owned Labrador retrievers with a mean hepatic copper concentration of 919 ± 477 mg/kg dry weight liver (dwl) that were related to dogs previously diagnosed with clinical copper‐associated hepatitis. Methods Clinical trial in which dogs were fed a diet containing 1.3 ± 0.3 mg copper/Mcal and 64.3 ± 5.9 mg zinc/Mcal. Hepatic copper concentrations were determined in liver biopsy samples approximately every 6 months. Logistic regression was performed to investigate effects of sex, age, initial hepatic copper concentration and pedigree on the ability to normalize hepatic copper concentrations. Results In responders (15/28 dogs), hepatic copper concentrations decreased from a mean of 710 ± 216 mg/kg dwl copper to 343 ± 70 mg/kg dwl hepatic copper after a median of 7.1 months (range, 5.5–21.4 months). Dogs from a severely affected pedigree were at increased risk for inability to have their hepatic copper concentrations normalized with dietary treatment. Conclusions and Clinical Importance Feeding a low‐copper, high‐zinc diet resulted in a decrease in hepatic copper concentrations in a subset of clinically normal Labrador retrievers with previous hepatic copper accumulation. A positive response to diet may be influenced by genetic background. Determination of clinical benefit requires further study.