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.     

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.     

Immunoglobulin levels in Bull terriers suffering from lethal acrodermatitis

An enzyme-linked immunosorbent assay, developed by one the authors (Huang, 1993) was used to measure immunoglobulin levels in previously stored plasma samples from eight dogs suffering from lethal acrodermatitis (LAD) and 10 normal Bull terriers. The aim of the study was to document plasma immunoglobulin levels and to determine if dogs suffering from LAD had low IgA levels. The results showed that dogs suffering from LAD had normal IgG and IgM levels but significantly lower IgA levels than the control group. This finding may in part explain the frequent occurrence of microbial infections recorded in dogs suffering from 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.     

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.     

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.     

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.     

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.     

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.     

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.     

Chronic pulmonary disease in West Highland white terriers.

This paper describes the clinical features, and diagnostic findings of a chronic respiratory condition in 29 West Highland white terriers. Typically, the dogs were coughing chronically, had dyspnoea and tachypnoea of varying severity, and had deteriorated progressively over months to years. The mean (sem) survival time in months from the clinical signs being first noted by the owners was 17.9 (2.3). Most cases had a combination of respiratory signs, but coughing was the predominant sign in 18 cases. Inspiratory crackles were audible on chest auscultation in 28 cases, 10 of which were also wheezing. Rhonchi were the predominant sound in the remaining case. The main radiographic changes were mild to severe increased Interstitial markings in all cases, with additional bronchial markings in 14 of the dogs. Right-sided cardiomegaly (cor pulmonale) was recorded in 15. Bronchoscopic findings in 17 of the dogs were either normal or involved a mild airway mucoid reaction in eight. Chronic mucosal changes were observed in eight, but in two this finding was equivocal. Dynamic changes to the lumen of the airway were present in seven cases. No significant haematological or biochemical changes could be detected in 20 cases, but four cases were hypercholestrolaemic. A histopathological assessment of four cases revealed alveolar septal fibrosis to be the predominant change. Prednisolone, with or without bronchodilators, was the most commonly used therapy, and the response was variable. The condition appears to be associated with significant pulmonary interstitial fibrosis of unknown aetiology and has clinical similarities to idiopathic pulmonary fibrosis (cryptogenic fibrosing alveolitis) in human beings.     

Sick sinus syndrome in nine West Highland white terriers

Sick sinus syndrome is a clinical term used to describe the clinical signs of sinus node dysfunction. This paper describes the clinical data from nine West Highland white terriers, eight females and one male, in which a diagnosis of sick sinus syndrome was made. The most common clinical signs were episodic weakness and presyncope. Electrocardiographic findings included sinus bradycardia, sinus arrest with or without escape complexes, disturbances of atrioventricular conduction, paroxysmal supraventricular tachycardia, or some combination of these dysrhythmias. The main radiographic changes were mild right-sided cardiomegaly in five cases, and a slight increase in bronchial and interstitial markings in four, but there was no evidence of congestive heart failure in any of the dogs. Echocardiography revealed mild to moderate mitral endocardiosis in three cases with no other significant abnormalities. The dogs' responses to parenteral atropine were variable and were not necessarily related to their response to oral anticholinergic agents. Five of the dogs were initially treated with propantheline bromide, but in only two of them were the clinical signs controlled in the long term. Six of the dogs were successfully treated by the implantation of a transvenous pacemaker.