Search Results

You are looking at 1 - 4 of 4 items for

  • Author or Editor: Mary O. Smith x
  • Refine by Access: All Content x
Clear All Modify Search
in Journal of the American Veterinary Medical Association

Abstract

Objective

To develop a robust molecular genetic test for α-l-fucosidosis in English Springer Spaniels and to screen dogs from the United Kingdom and United States for the mutant allele.

Animals

35 English-bred English Springer Spaniels, 60 American-bred English Springer Spaniels, and 1 affected dog and its parents from a family of English Springer Spaniels in Colorado.

Procedure

Polymerase chain reaction analysis was used to amplify the mutated region in the gene encoding α-l-fucosidase. High guanine-cytosine (GC) content of the region required use of an amplification buffer with high pH. Mutant and normal alleles were separated by polyacrylamide gel electrophoresis. Molecular genetic test results were compared with enzyme data.

Results

A 262-bp PCR product was amplified from normal dogs and compared with a 248-bp product from affected dogs. Carriers had 1 copy of each allele, distinguishable by the 14-bp size difference. Two carriers among the English-bred dogs were identified by use of enzyme and genomic DNA analyses. The molecular defect in dogs from Colorado was proven to be the same as that in British and Australian dogs. None of the other 60 American-bred dogs carried the mutant allele.

Conclusions and Clinical Relevance

A PCR method that can be used to identify dogs affected with or carriers of the autosomal recessive disease fucosidosis was established. Amplification was achieved within a GC-rich region, using a method that may be useful in overcoming amplification problems in GC-rich areas within other genes. Using this test, fucosidosis can be controlled and ultimately eradicated from the English Springer Spaniel population. (Am J Vet Res 1999;60:726-729)

Free access
in American Journal of Veterinary Research

Abstract

Objective—To determine effects of various diets on the pharmacokinetics of phenobarbital and the interactive effects of changes in body composition and metabolic rate.

Design—Prospective study.

Animals—27 healthy sexually intact adult female Beagles.

Procedure—Pharmacokinetic studies of phenobarbital were performed before and 2 months after dogs were fed 1 of 3 diets (group 1, maintenance diet; group 2, protein-restricted diet; group 3, fat- and protein-restricted diet) and treated with phenobarbital (approx 3 mg/kg [1.4 mg/lb] of body weight, PO, q 12 h). Pharmacokinetic studies involved administering phenobarbital (15 mg/kg [6.8 mg/lb], IV) and collecting blood samples at specific intervals for 240 hours. Effects of diet and time were determined by repeated-measures ANOVA.

Results—Volume of distribution, mean residence time, and half-life (t1/2) of phenobarbital significantly decreased, whereas clearance rate and elimination rate significantly increased with time in all groups. Dietary protein or fat restriction induced significantly greater changes: t1/2 (hours) was lower in groups 2 (mean ± SD; 25.9 ± 6.10 hours) and 3 (24.0 ± 4.70) than in group 1 (32.9 ± 5.20). Phenobarbital clearance rate (ml/kg/min) was significantly higher in group 3 (0.22 ± 0.05 ml/kg/min) than in groups 1 (0.17 ± 0.03) or 2 (0.18 ± 0.03). Induction of serum alkaline phosphatase activity (U/L) was greater in groups 2 (192.4 ± 47.5 U/L) and 3 (202.0 ± 98.2) than in group 1 (125.0 ± 47.5).

Conclusions and Clinical Relevance—Clinically important differences between diet groups were observed regarding pharmacokinetics of phenobarbital, changes in CBC and serum biochemical variables, and body composition. Drug dosage must be reevaluated if a dog's diet, body weight, or body composition changes during treatment. Changes in blood variables that may indicate liver toxicosis caused by phenobarbital may be amplified by diet-drug interactions. (J Am Vet Med Assoc 2000;217:847–852)

Full access
in Journal of the American Veterinary Medical Association

Abstract

Objective

To investigate potential sources of an epizootic of listerial encephalitis, using molecular diagnostic and typing methods.

Sample Population

A flock of about 655 sheep.

Procedure

An epizootiologic investigation was performed. Clinical, feed, and environmental samples were tested for Listeria monocytogenes, using polymerase chain reaction and culture methods; recovered isolates were “fingerprinted,” using an automated ribotyping system.

Results

Listeria monocytogenes was recovered from brain specimens of 7 sheep with clinical signs of listerial encephalitis. All clinical isolates had fingerprints identical to those of isolates from farm equipment used to transport silage. Corn silage, which was not fed to the sheep, also contained L monocytogenes of the same pattern type as defined by ribotyping. Listeria monocytogenes was not isolated from the stored haylage designated for feeding the sheep (the cut-off point for isolation being < 102 colony-forming units/g).

Conclusions

Corn silage was implicated as the source of a listeriosis epizootic. It appears to have cross-contaminated the haylage destined for the sheep during handling with a front-end loader. Suspension of silage feeding coincided with cessation of listeriosis cases.

Clinical Relevance

Use of advanced molecular techniques can help to identify the sources and restrict the scope of an epizootic. In epizootics, a single L monocytogenes strain can lead to infection of multiple animals, with rapid progression of the disease. (Am J Vet Res 1997;58:733–737)

Free access
in American Journal of Veterinary Research