Prevalence of Mycoplasma agassizii and Chelonian herpesvirus in captive tortoises (Testudo sp.) in the United Kingdom.

During the months of April to August in 1999 and 2002, oral swabs were collected from 146 tortoises (Testudo sp.) in private collections in the United Kingdom and tested by polymerase chain reaction (PCR) for the presence of Mycoplasma agassizii and Chelonian herpesvirus (ChHV). The presence of M. agassizii was confirmed by restriction digestion of the PCR product. A 307-bp fragment of the ChHV UL5 homologue gene was sequenced and found to show most similarity to equine herpesvirus type 1. A prevalence of 15.8 and 8.2% was found for M. agassizii and ChHV, respectively. Comparison of the carriage of both M. agassizii and ChHV in different species of tortoises correlated the presence of M. agassizii with Testudo horsfieldii and ChHV with Testudo marginata and Testudo graeca iberia. An association of ChHV with stomatitis was also found. Mixed infections with both agents were detected. The findings further demonstrate this pathogen-tortoise association and the cross transmission of these infections if different tortoise species are housed together.     

Evidence for genetic distinction among sympatric ecotypes of Arctic char (Salvelinus alpinus) in south‐western Alaskan lakes

Resource polymorphism may play an important role in the process of speciation. The Arctic char (Salvelinus alpinus) exhibits great phenotypic and genetic diversity across its range, making it an ideal species for studies of resource polymorphism and divergence. Here, we investigated genetic variation at 11 microsatellite loci among 287 Arctic char from five isolated yet proximate postglacial lakes in south‐western Alaska that were previously examined for resource polymorphism. Significant differences in pairwise F_ST were detected among all lakes (range from 0.05 to 0.28, all P < 0.02). In one lake (Lower Tazimina Lake), we found evidence for two genetic groups of char and for significant differences in the distribution of microsatellite variability among at least two of the three previously described body size morphotypes (‘large’‐, ‘medium’‐, and ‘small’‐bodied char; maximum F_ST = 0.09; differences in admixture proportions). We also found a significant association between genetic admixture proportions and gill raker counts among body size morphs (r = ?0.73, P < 0.001). Our data represent the first record of genetically distinct sympatric morphs of Arctic char in Alaska and provide further evidence that differences in morphology associated with feeding (gill rakers) and growth trajectories reflect niche diversification and promote genetic divergence in Holarctic populations of Arctic char.     

Sialidase activity in Mycoplasma synoviae

Eleven strains of the avian pathogen Mycoplasma synoviae were evaluated for the presence of sialidase activity with the use of the fluorogenic substrate 2'-(4-methylumbelliferyl)-alpha-D-N-acetylneuraminic acid and the sialidase inhibitor 2-deoxy-2,3- didehydro-N-acetylneuraminic acid. The kinetics of in vitro growth in modified Frey medium were also assessed for each strain. Five strains had been isolated from clinically symptomatic chickens, and strains WVU 1853T and K3344 have been demonstrated to be capable of reproducing disease in specific-pathogen-free chickens. All strains exhibited sialidase activity, although the amount varied 65-fold among strains (P < 0.0001) from 1.3 x 10(-7) to 2.0 x 10(-9) activity units per colony-forming unit. Strains originally isolated from clinically symptomatic birds had more (P < 0.05) sialidase activity than strains from asymptomatic birds. Strain WVU1853T exhibited the most sialidase activity (P < 0.0001) and grew to the highest culture density (P < 0.0001) among strains, but across strains, the rank correlation of growth rate with sialidase activity was not significant. Negligible activity was detected in conditioned culture supernatant fluid. This is the first report of sialidase activity in pathogenic strains of M. synoviae, which suggests a potential enzymatic basis for virulence of the organism.     

Inheritance, mode of inheritance, and candidate genes for primary hyperparathyroidism in Keeshonden

BACKGROUND: Primary hyperparathyroidism (PHPT) is caused by inappropriate secretion of parathyroid hormone (PTH) by autonomously functioning neoplastic or hyperplastic parathyroid "chief" cells. Keeshonden are thought to be over-represented in studies on canine PHPT, but no proof of heritability or mode of inheritance has been published. The canine disease clinically resembles human familial isolated hyperparathyroidism (FIHP). HYPOTHESIS: Primary hyperparathyroidism in Keeshonden is genetically transmitted and is caused by a mutation in 1 of 4 genes implicated in human FIHP: MEN1, CASR, HRPT2, or RET. ANIMALS: Pedigrees consisting of 1647 Keeshonden were created including 219 Keeshonden with known PHPT phenotypes (69 positive). DNA samples were obtained from 176 of the 219 Keeshonden (34 positive). METHODS: Heritability and mode of inheritance were determined by segregation analysis. Canine homologs to the human genes were identified. Exons and surrounding intron regions were sequenced and scanned for sense-altering polymorphisms or polymorphisms that segregated with the disease. Messenger RNA from a parathyroid tumor of an affected Keeshond was analyzed for polymorphisms and splice alterations. RESULTS: PHPT follows an autosomal dominant mode of inheritance in Keeshonden with possible age-dependent penetrance. No polymorphisms identified in the genes analyzed were associated with a change in predicted protein or in hypothesized splice sites. CONCLUSIONS AND CLINICAL IMPORTANCE: PHPT is an autosomal dominant, genetically transmitted disease in Keeshonden. Once the mutation locus is identified, genetic testing should quickly decrease the incidence of PHPT in this breed. It is unlikely that mutations in MEN1, CASR, HRPT2, or RET cause PHPT in Keeshonden.     

Day-to-Day variation of the urine protein: creatinine ratio in female dogs with stable glomerular proteinuria caused by X-linked hereditary nephropathy

BACKGROUND: Interpretation of serial urine protein:creatinine (UPC) values is confounded by a lack of data regarding random biologic variation of UPC values in dogs with stable glomerular proteinuria. HYPOTHESIS: That there is minimal day-to-day variability in the UPC of dogs with unchanging proteinuria and the number of measurements needed to reliably estimate UPC varies with the magnitude of proteinuria. ANIMALS: Forty-eight heterozygous (carrier) female dogs with X-linked hereditary nephropathy (XLHN) causing stable proteinuria. METHODS: Urine samples were obtained daily by cystocentesis for 3 consecutive days on 183 occasions (549 samples). The UPC was measured for each sample with a single dry-film chemistry auto-analyzer. Data were analyzed retrospectively by a power of the mean model because the variance of UPC values within the 3-day evaluation periods increased as the magnitude of proteinuria increased. RESULTS: To demonstrate a significant difference (P < .05) between serial values in these proteinuric dogs, the UPC must change by at least 35% at high UPC values (near 12) and 80% at low UPC values (near 0.5). One measurement is adequate to reliably estimate the UPC when UPC <4, but 2-5 determinations are necessary at higher UPC values. CONCLUSIONS AND CLINICAL IMPORTANCE: These guidelines for interpretation of serial UPC values in female dogs with XLHN may also be helpful for interpretation of UPC values in dogs with other glomerulopathies.     

Prevalence of antimicrobial resistance among Salmonella on midwest and northeast USA dairy farms

The objective of this study was to determine the prevalence of antimicrobial resistance among Salmonella isolated from dairy herds in New York, Minnesota, Michigan, and Wisconsin, USA. Serogroup and antimicrobial susceptibility characteristics were determined for Salmonella from cattle and environmental samples collected during August 2000–October 2001 as part of a longitudinal study where 129 herds were visited at 2-month intervals. Salmonella isolates were tested (using a broth microdilution method) for susceptibility to amoxicillin/clavulanic acid, ampicillin, ceftiofur, ceftriaxone, cephalothin, chloramphenicol, ciprofloxacin, gentamicin, kanamycin, nalidixic acid, streptomycin, sulfamethoxazole, tetracycline, and trimethoprim/sulfamethoxazole. Of the 1506 isolates tested for minimum inhibitory concentrations to these 14 antimicrobial agents, 81.2% were pan-susceptible and for most herds (81.6%) the predominant antimicrobial resistance pattern was pan-susceptible. At least 1 Salmonella isolate resistant to 5 or more antimicrobial agents was found on 23.6% of herds. This resistance phenotype was most common among serogroups B and E1 and among samples from calves and farmer-designated sick cows. Resistant samples most frequently exhibited resistance to tetracycline, streptomycin, and/or ampicillin. No samples were resistant to ceftriaxone (though 13 were in the intermediate range), and very few samples were resistant to ciprofloxacin (n = 1), nalidixic acid (n = 5), or trimethoprim/sulfamethoxazole (n = 7).