Lethal acrodermatitis in bull terriers

A lethal syndrome characterized clinically by growth retardation, progressive acrodermatitis, chronic pyoderma and paronychia, diarrhea, pneumonia, and abnormal behavior was observed in 17 related Bull Terrier pups. Median survival time was 7 months. Laboratory evaluation revealed non-degenerative neutrophilia, consistently low activities of serum alkaline phosphatase and alanine transaminase, and frequently, hypercholesterolemia. Lymphocyte blastogenic responses were decreased and there was dysgammaglobulinemia in pups in which quantitative studies of immunoglobulins were made. The mean of plasma zinc concentrations in 5 affected pups was significantly lower than the mean of age- and breed-matched controls. Pathologic findings included parakeratosis, hyperkeratosis, and superficial bacterial infections of the skin. There was severe reduction of lymphocytes in T-lymphocyte areas of lymphoid tissue. Bronchopneumonia and dilatation of the cerebral ventricles were found in most affected pups. Family studies indicated that the syndrome is inherited as an autosomal recessive trait. In spite of its similarities to lethal trait A46 in Black Pied Danish cattle and acrodermatitis enteropathica in man, oral or parenteral treatment with zinc failed to ameliorate the clinical signs of the syndrome.     

Congenital mitral insufficiency in bull terriers

Ten young bull terriers with physical, electrocardiographic and radiological findings suggestive of congenital mitral insufficiency were examined between 1976 and 1987. In four of these animals a definitive diagnosis was confirmed by either cardioangiography or autopsy. Congenital mitral insufficiency would appear to be a common developmental cardiac anomaly in bull terriers in Australia.     

Malassezia and Candida infections in bull terriers with lethal acrodermatitis

In 12 cases of lethal acrodermatitis (LAD), four sampling techniques (brush, swab, scrape and adhesive tape strip) were used to study the distribution of yeasts in various body sites and these results were compared with those from five cases of atopic dermatitis and those of 10 normal dogs. Malassezia was frequently isolated from lesional and non-lesional skin and haircoat, footpads, nails and mucous membranes from dogs with either LAD or atopic dermatitis, although, generally, more Malassezia organisms were isolated from LAD cases. In normal dogs, Malassezia was most frequently recovered from the ear canal and the perianal skin. Candida was isolated frequently from dogs with LAD, but only a single isolate of this yeast was found in the other two groups. Fungal hyphae and pseudohyphae, probably Candida albicans, could be detected in samples collected from the nails and footpads of dogs with LAD. Both Malassezia and Candida could be isolated using all four sampling techniques. The MacKenzie (toothbrush) technique and adhesive tape strip cultures proved simple methods for the semiquantitative evaluation of yeasts. The high recovery rate of Malassezia and Candida from dogs with LAD is probably related to immune dysfunction, particularly T-cell dysfunction, known to be present in these dogs. C albicans infection may in part be responsible for the pathogenic changes of the nails and footpads commonly seen in cases of LAD.     

Familial po1ycystic kidnev disease in bull terriers

Polycystic kidney disease was observed in eight related bull terriers. Two dogs died suddenly, two were presented for haematuria, while the remainder were outwardly normal but detected during ultrasonographic screening programmes. A definitive diagnosis was made at either necropsy or using renal ultrasonography, although affected dogs also had abnormal urinalyses with haematuria, proteinuria, cast formation and sometimes bacterial infection. Valvular heart disease was detected clinically or at necropsy in all the affected dogs. The presence of polycystic kidney disease in several related dogs suggests that this condition is familial. The disease has clinical and pathological similarities with autosomal dominant polycystic kidney disease of humans.     

Serosurvey of antiBabesia antibodies in stray dogs and American pit bull terriers and American staffordshire terriers from North Carolina

Stray dogs (n=359) and kennel dogs (n=149) from North Carolina were tested for evidence of antiBabesia antibodies. AntiBabesia antibodies were detected in 21/359 and 22/149 of the stray and kennel dogs, respectively. A total of 57 dogs from both groups were tested for babesiasis by light microscopy and polymerase chain reaction (PCR). Babesia deoxyribonucleic acid (DNA) was detected in 3/28 of the stray dogs and 14/29 of the kennel dogs. When Babesia DNA was detected by PCR, the species-specific PCR results differed from the Babesia species antibody titer results in 6/17 of the PCR-positive dogs. There was no association between antiBabesia antibodies and the presence of ticks. There are currently Babesia gibsoni epizootics affecting American pit bull terrier kennels.     

Polycystic kidney disease in bull terriers: an autosomal dominant inherited disorder

The prevalence, mode of inheritance and urinalysis findings in Bull Terriers with polycystic kidney disease were assessed by screening 150 clinically normal dogs. The disorder was diagnosed in 39 dogs on the basis of renal ultrasound results and family history of the disease. In equivocal cases confirmation required gross and histopathological renal examination. Necropsy was performed on nine affected dogs and the kidneys from another five affected animals were also examined. Renal cysts were usually bilateral, occurred in cortex and medulla and varied from less than 1 mm to over 2.5 cm in diameter. Cysts were lined by epithelial cells of nephron origin. Abnormal urine sediment and proteinuria were common in affected dogs. The disease appears to be inherited in a highly penetrant autosomal dominant manner.     

Anury in two Cairn terriers

Congenital anury (taillessness) was observed in 2 Cairn Terriers. Fecal staining of the hind limbs was evident in both dogs. A mating of the affected dogs produced a litter of 2 apparently normal pups. The small litter size may have been attributable to lethal gene combinations similar to those described in mice. The radiographic appearance of the caudal and sacral vertebrae was atypical in both tailless dogs. Results of myelography and electrodiagnostic testing of anal sphincter function were normal in one of the dogs. One of the tailless dogs was euthanatized and was found to lack specific muscles and muscle parts responsible for normal defecation, which resulted in fecal staining of the hind limbs. Pedigree analysis revealed the tailless dogs to be closely related and slightly inbred, suggesting a hereditary etiologic factor for anury.     

Hepatitis and copper accumulation in Skye terriers

Livers of nine related Skye terriers with liver disease were evaluated for histological changes and copper content. Lesions ranged from hepatocellular degeneration and necrosis (zone 3) with intracanalicular cholestasis and mild inflammation, to chronic hepatitis with cholangioplasia and cirrhosis. Excess copper (801-2,257 micrograms/g) was related to the severity of cholestasis. Skye terrier hepatitis is a distinct disease entity and may be derived from a disorder of intracellular bile metabolism culminating in disturbed bile secretion and the accumulation of copper.     

Inherited copper toxicosis in Bedlington terriers

SUMMARY Chronic hepatitis and increased hepatic copper concentrations, from 1,600 to 6,361 fig/g dry tissue were found in 4 related, Australian-bred Bedlington terriers. Two dogs were asymptomatic and 2 were clinically ill with signs referable to liver dysfunction. Two dogs were treated with d-penicillamine. After one year there was no improvement in the histopathological liver changes in either dog or significant lowering of hepatic copper level in one dog.     

Progressive retinal atrophy in Tibetan terriers

Progressive retinal atrophy was studied in 17 Tibetan Terriers. The diagnosis was made on the basis of clinical signs of the disease, retinal histopathologic findings, or both. Affected dogs were the progeny of matings of affected or ophthalmoscopically normal dogs. Results of the mating supported a simple autosomal recessive mode of inheritance. The disease initially could be diagnosed by findings of night blindness and ophthalmoscopic signs of tapetal hyperreflectivity in affected dogs that were approximately 1 year old. Electroretinograms recorded from affected dogs, compared with those of clinically normal dogs of the same age, did not reveal appreciable abnormalities until affected dogs were 10 months old, at which time a reduction in the amplitude of the b wave was seen in response to a Ganzfeld white-light stimulus. The peak times of the response were unaffected. With progression of the disease, the electroretinographic b-wave amplitude was gradually reduced, and the electroretinographic response was extinguished in affected dogs by the time they were 30 months old. Early in the disease, rod and cone functions were affected equally, with more rapid loss of rod function developing only later in the disease. Fluorescein angiography of affected dogs did not reveal abnormalities earlier than could be detected by ophthalmoscopy. Despite the electroretinographic findings, histopathologic findings included patchy disorientation and disorganization of the outer segments of rods and cones in affected dogs as young as 9 weeks. With progression of the disease, rods were lost at a faster rate than cones, and atrophy of the inner retinal layer was observed.     

Hereditary copper toxicosis in West Highland white terriers

Histologic, histochemical and atomic absorption studies on liver tissue from 71 West Highland white terriers are reported. Twenty-seven dogs had histologically normal liver and copper concentration comparable to mongrel control dogs. Forty-four dogs had hepatic copper concentrations up to 22 times the mean copper concentration found in clinically normal mongrel dogs. Hepatitis, hepatic necrosis and cirrhosis were associated with the increased copper concentration in some dogs. Matings between dogs with high liver copper concentration produced pups with high liver concentration. The copper storage defect is inherited.     

Myokymia and neuromyotonia in 37 Jack Russell terriers

The clinical and clinicopathological characteristics, treatment and outcome of vermicular muscle contractions (myokymia) and generalized muscle stiffness (neuromyotonia) in 37 Jack Russell terriers were evaluated retrospectively. Thirty dogs were affected by both disorders, whereas seven were presented with myokymia and never developed neuromyotonia. Clinical signs started at the mean age of 8 months. Except for signs of myokymia and neuromyotonia, clinical and neurological examination was normal in all dogs. Thirty dogs demonstrated typical signs of hereditary ataxia.Changes in serum chemistry included increased creatine kinase, aspartate aminotransferase and alanine aminotransferase concentrations. Electromyographic abnormalities, especially in muscles showing macroscopically visible myokymia, consisted of semirhythmic bursts of doublet, triplet, or multiplet discharges of a single motor unit. The amplitudes varied between 80 μV and 1 mV and occurred with an interburst frequency between 10 and 40 Hz and an intraburst frequency between 150 and 280 Hz.Most dogs were treated with a sodium channel blocker with variable results. Seven dogs died (most likely because of hyperthermia) or were euthanased during a neuromyotonic attack; 15 dogs were euthanased due to worsening of clinical signs, or lack of or no long-lasting effect of medication, and three were euthanased for unknown or unrelated reasons. Nine dogs were lost to follow-up and three were still alive 5–10.5 years after the start of clinical signs. In conclusion, young Jack Russell terriers with myokymia and neuromyotonia should undergo a complete blood and electrophysiological examination. Long-term prognosis is not favourable.     

西杂牛与哈萨克牛育肥对比试验

对14~17月龄12头西杂牛一代公牛和12头哈萨克公牛进行120 d育肥,西杂一代公牛平均日增重986.5 g±120.45 g,屠宰率55.2%,净肉率44.2%,哈萨克公牛日增重498.2 g±96.3 g,屠宰率46.5%,净肉率36.4%。西杂一代牛比哈萨克牛日增重提高98.0%(P<0.01),屠宰率和净肉率分别提高8.7和7.8个百分点。