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  • Author or Editor: H. D. Lehmkuhl x
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Abstract

Objective

To determine the pathogenic potential of an adenovirus isolated from a goat.

Animals

14 colostrum-deprived, isolation-reared goat kids approximately 3 weeks old.

Procedure

Kids were inoculated with either cell culture fluid containing adenovirus (n = 10) or uninfected cell culture fluid (n = 4): 2 ml transtracheally and 1 ml/nostril. Clinical signs of disease and rectal temperature were recorded daily; nasal secretion and fecal specimens were collected daily. Control kids were necropsied, 2/d, on postinoculation days (PID) 5 and 10. Virus-inoculated kids were necropsied on PID 3, 5, 7, 10, and 28. After necropsy, lung, liver, kidney, and brain specimens were aseptically collected for virus isolation attempts. Tracheal fluid was collected on sterile cotton swabs. Turbinate, trachea, lung, mediastinal lymph node, liver, kidney, duodenum, jejunum, ileum, mesenteric lymph node, colon, and brain specimens were collected for histologic evaluation.

Results

Kids developed mild-to-moderate clinical respiratory tract infection. Virus was recovered consistently from nasal secretion and sporadically from fecal specimens. Grossly, there were multiple areas of atelectasis and hyperemia, principally in the cranioventral portion of the lungs. Microscopically, there was detachment and sloughing of foci of epithelial cells of the terminal bronchioles and alveoli. In kids necropsied late in the disease, these changes were accompanied by hyperplasia of type-II epithelial cells. Viral inclusions were not an obvious feature, but a few cells contained probable inclusions.

Conclusions and Clinical Relevance

The caprine adenovirus reported here is capable of inducing respiratory tract disease and lesions in the lungs of young kids. (Am J Vet Res 1997;58:608–611)

Free access
in American Journal of Veterinary Research

Abstract

Objective

To evaluate blood pressure, renal function, and the renin-angiotensin-aldosterone system (RAAS) in cats with autosomal dominant polycystic kidney disease (ADPKD) and to assess the effect of enalapril on these variables.

Animals

6 cats with ADPKD and 6 age-matched healthy cats.

Procedure

To measure blood pressure and heart rate, a radiotelemetry catheter was placed in the left femoral artery of each cat. Baseline data collection included 24-hour blood pressure, heart rate, and motor activity. Blood was then collected for analysis of RAAS status and renal function. Enalapril (0.5 mg/kg of body weight, PO, q 24 h) was administered for 1 week, and data collection was repeated.

Results

Differences in baseline blood pressure, heart rate, motor activity, RAAS status, and renal function were not detected between cats with ADPKD and control cats. Hypertension was not documented in cats with ADPKD. Blood pressure was significantly reduced for 15 to 17 hours after treatment with enalapril in both groups. Administration of enalapril also resulted in significant increases in plasma renin activity and significant decreases in angiotensin converting enzyme activity and atrial natriuretic peptide concentration but only minimal changes in glomerular filtration rate and effective renal plasma flow in both groups of cats.

Conclusions and Clinical Relevance

Although hypertension is common in humans with ADPKD, cats with ADPKD were normotensive. Treatment with enalapril (0.5 mg/kg, PO, q 24 h) significantly reduced blood pressure in normotensive healthy cats and cats with ADPKD, and resulted in predictable changes in RAAS enzyme activities and hormone concentrations. Enalapril had minimal effects on renal function. (Am J Vet Res 1999;60:1516–1525)

Free access
in American Journal of Veterinary Research

Abstract

Objective—To evaluate the potential importance of dystrophin, α-sarcoglycan (adhalin), and β-dystroglycan, by use of western blot analysis, in several breeds of dogs with dilated cardiomyopathy.

Sample Population—Myocardial samples obtained from 12 dogs were evaluated, including tissues from 7 dogs affected with dilated cardiomyopathy, 4 control dogs with no identifiable heart disease (positive control), and 1 dog affected with Duchenne muscular dystrophy (negative control for dystrophin). Of the affected dogs, 4 breeds were represented (Doberman Pinscher, Dalmatian, Bullmastiff, and Irish Wolfhound).

Procedure—Western blot analysis was used for evaluation of myocardial samples obtained from dogs with and without dilated cardiomyopathy for the presence of dystrophin and 2 of its associated glycoproteins, α-sarcoglycan and β-dystroglycan.

Results—Detectable differences were not identified between dogs with and without myocardial disease in any of the proteins evaluated.

Conclusions and Clinical Relevance—Abnormalities in dystrophin, α-sarcoglycan, and β-dystroglycan proteins were not associated with the development of dilated cardiomyopathy in the dogs evaluated in this study. In humans, the development of molecular biological techniques has allowed for the identification of specific causes of dilated cardiomyopathy that were once considered to be idiopathic. The use of similar techniques in veterinary medicine may aid in the identification of the cause of idiopathic dilated cardiomyopathy in dogs, and may offer new avenues for therapeutic intervention. ( Am J Vet Res 2001;62:67–71)

Full access
in American Journal of Veterinary Research