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- Author or Editor: Thomas R. Famula x
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Abstract
Objective—To assess heritability and mode of inheritance for hypoadrenocorticism in Bearded Collies.
Animals—635 Bearded Collies.
Procedure—Dogs were classified as affected by hypoadrenocorticism or unaffected. Phenotypic and pedigree data were analyzed. Heritability was estimated by use of Bayesian statistical methods. Regressive logistic models for complex segregation analyses were used to characterize mode of inheritance.
Results—Hypoadrenocorticism was diagnosed in 60 (9.4%) dogs. Heritability of hypoadrenocorticism was estimated to be 0.76 with both sexes affected with equal probability. Evaluation of the pedigrees did not support a Mendelian autosomal dominant mode of inheritance. Evidence from the complex segregation analysis for a single locus of large effect on hypoadrenocorticism was not convincing.
Conclusions and Clinical Relevance—Hypoadrenocorticism in Bearded Collies is highly heritable. Although a precise genetic mechanism responsible for inheritance of the disorder remains undetermined, breeding decisions must include consideration of the genetic likelihood of passing on this deleterious disorder to offspring of affected dams and sires. (Am J Vet Res 2002;63:643–647).
Abstract
Objective—To characterize a genetic component to cricopharyngeal dysfunction (CD) in Golden Retrievers.
Animals—117 dogs.
Procedure—The CD phenotype was determined by videofluoroscopy, and dogs were classified as affected if the upper esophageal sphincter (UES) did not open, if there were morphologic abnormalities of the UES, or if opening of the UES was delayed for ≥ 6 videofluoroscopic frames (0.2 seconds) after closure of the epiglottis. All survey radiographic and videofluoroscopic studies were reviewed by the same radiologist.
Results—Of the 117 dogs (47 males and 70 females) with a CD phenotype determined via videofluoroscopy, 21 dogs (18.0%) had abnormalities of the UES (affected). Of these 21 dogs, 9 were males (19.1% of all males) and 12 were females (17.1% of all females). The heritability of CD in a threshold model was estimated as 0.61, which established that CD could be passed from parent to offspring. Results of complex segregation analysis suggested that a single recessive allele of large effect contributed to the expression of this disease in Golden Retrievers.
Conclusions and Clinical Relevance—The determination that CD is inherited in Golden Retrievers is an important step in providing information for veterinarians attending dogs with this disorder. Breeders also require this information to make informed breeding decisions. ( Am J Vet Res 2004;65:344–349)
Abstract
Objective—To assess heritability and mode of inheritance for hereditary equine regional dermal asthenia (HERDA) in Quarter Horses.
Animals—1,295 horses with Quarter Horse bloodlines, including 58 horses affected with HERDA.
Procedure—Horses were classified as affected or unaffected or as undetermined when data were insufficient to assess phenotype. Pedigree data were analyzed to determine the probable mode of inheritance. Heritability was estimated by use of Bayesian statistical methods.
Results—Heritability (mean ± SD) of HERDA was estimated to be 0.38 ± 0.13, with both sexes having an equal probability of being affected. Results for evaluation of the pedigrees were consistent with a single Mendelian autosomal recessive mode of inheritance.
Conclusions and Clinical Relevance—HERDA in Quarter Horses is an inherited disease, and affected horses are more likely to produce affected offspring. An autosomal recessive mode of inheritance should be considered by people making breeding decisions involving Quarter Horses when a first-degree relative has been confirmed with HERDA or has produced affected offspring. In addition, breeders whose horses have produced affected offspring can reduce the likelihood of producing affected horses in the future by avoiding inbreeding. (Am J Vet Res 2005;66:437–442)
Abstract
Objective—To compare the effectiveness of lincomycin and oxytetracycline for treatment of digital dermatitis (DD) in dairy cows through gross visual examination, histologic evaluation, and bacteriologic evaluation.
Design—Randomized controlled clinical trial.
Animals—25 cows with DD lesions from a commercial Holstein dairy herd.
Procedures—Cows with DD lesions were randomly assigned to 1 of 3 groups: topical treatment with 10 g of lincomycin hydrochloride (n = 11), topical treatment with 10 g of oxytetracycline hydrochloride (11), and no treatment (3) on days 1 and 2 (d1). Biopsy specimens were obtained for histologic examination from DD lesions prior to treatment and 28 or 31 days (d30) after treatment for histologic examination. Cows were clinically examined on d1, days 12 or 14 (d14), and d30.
Results—No difference was evident in clinical responses to lincomycin and oxytetracycline, so data were pooled; at d30, 8 of 11 of lincomycin-treated lesions and 7 of 11 oxytetracycline-treated lesions appeared visually healed, respectively. Gross visual examination suggested 73% (16/22) of treated cows were healed at d14 and 68% (15/22) of treated cows were healed on d30. Of the 15 lesions that appeared healed on d30, 7 of 15 were classified histologically as active (ulceration and bacterial invasion; 2/15) or incipient (5/15).
Conclusions and Clinical Relevance—Clinical responses to lincomycin and oxytetracycline did not differ. Agreement was good between gross visual and histologic assessments of DD lesions before treatment; agreement 1 month after treatment was variable. Histologic evaluation could not distinguish incomplete healing from lesion recurrence.
Abstract
Objective—To assess the heritability of pancreatic acinar atrophy (PAA) in German Shepherd Dogs (GSDs) in the United States.
Animals—135 GSDs belonging to 2 multigenerational pedigrees.
Procedure—Two multigenerational pedigrees of GSDs with family members with PAA were identified. The clinical history of each GSD enrolled in the study was recorded, and serum samples for canine trypsinlike immunoreactivity (cTLI) analysis were collected from 102 dogs. Dogs with a serum cTLI concentration ≤ 2.0 µg/L were considered to have exocrine pancreatic insufficiency (EPI) and were assumed to have PAA.
Results—Pedigree I consisted of 59 dogs and pedigree II of 76 dogs. Serum cTLI concentrations were measured in 48 dogs from pedigree I and 54 dogs from pedigree II. A total of 19 dogs (14.1%) were determined to have EPI, 9 in pedigree I (15.3%) and 10 in pedigree II (13.6%). Of the 19 dogs with EPI, 8 were male and 11 were female.
Conclusion and Clinical Relevance—Evaluation of data by complex segregation analysis is strongly suggestive of an autosomal recessive mode of inheritance for EPI in GSDs in the United States. (Am J Vet Res 2002;63:1429–1434)
Abstract
Objective—To estimate allele frequencies of the hyperkalaemic periodic paralysis (HYPP), lethal white foal syndrome (LWFS), glycogen branching enzyme deficiency (GBED), hereditary equine regional dermal asthenia (HERDA), and type 1 polysaccharide storage myopathy (PSSM) genes in elite performance subgroups of American Quarter Horses (AQHs).
Design—Prospective genetic survey.
Animals—651 elite performance AQHs, 200 control AQHs, and 180 control American Paint Horses (APHs).
Procedures—Elite performance AQHs successful in 7 competitive disciplines (barrel racing, cutting, halter, racing, reining, western pleasure, and working cow horse) were geno- typed for 5 disease-causing alleles. Age-matched control AQHs and APHs were used to establish comparative whole-breed estimates of allele frequencies.
Results—Highest allele frequencies among control AQHs were for type 1 PSSM (0.055) and GBED (0.054), whereas HERDA (0.021) and HYPP (0.008) were less prevalent. Control APHs uniquely harbored LWFS (0.107) and had high prevalence of HYPP (0.025), relative to AQHs. Halter horse subgroups had significantly greater allele frequencies for HYPP (0.299) and PSSM (0.155). Glycogen branching enzyme deficiency, HERDA, and PSSM were found broadly throughout subgroups; cutting subgroups were distinct for HERDA (0.142), and western pleasure subgroups were distinct for GBED (0.132). Racing and barrel racing subgroups had the lowest frequencies of the 5 disease genes.
Conclusions and Clinical Relevance—Accurate estimates of disease-causing alleles in AQHs and APHs may guide use of diagnostic genetic testing, aid management of genetic diseases, and help minimize production of affected foals.
