Recent 16S rRNA gene sequencing studies of the duodenal and fecal microbiota have revealed alterations in the abundance of specific bacterial groups in dogs with gastrointestinal (GI) disorders. The aim of this study was to establish a panel of quantitative real-time PCR (qPCR) assays for the evaluation of specific bacterial groups in fecal samples of healthy dogs, dogs with chronic enteropathies (CE), and dogs with acute hemorrhagic diarrhea (AHD). Fecal samples from 242 healthy dogs, 118 dogs with CE, and 57 dogs with AHD were analyzed using qPCR assays targeting Faecalibacterium spp., Turicibacter spp., Bifidobacterium spp., Lactobacillus spp., Streptococcus spp., Ruminococcaceae, C. perfringens, E. coli, gamma-Proteobacteria, Bacteroidetes, and Firmicutes). Differences in bacterial abundance among the three groups were evaluated using a Kruskal-Wallis test followed by a Dunn's post-test. A Bonferroni correction was used to correct for multiple comparisons and an adjusted p<0.05 was considered for statistical significance. Faecalibacterium spp., Turicibacter spp., and Ruminococcaceae were significantly decreased in CE and AHD compared to healthy dogs (p<0.001 for all). Lactobacillus spp. and Streptococcus spp. were significantly increased in dogs with CE (p<0.001 for both) when compared to the healthy dogs. In contrast, Lactobacillus spp. and Streptococcus spp. were significantly decreased in dogs with AHD compared to healthy dogs (p<0.01 and p<0.05, respectively) and also when compared to the dogs with CE (p<0.001 for both). C. perfringens and E. coli were significantly increased in dogs with AHD (p<0.001 and p<0.01, respectively), when compared to healthy dogs. E. coli was also significantly increased in dogs with CE when compared to the healthy dogs (p<0.001). Bacteroidetes were significantly lower in dogs with CE compared to healthy dogs (<0.001). Firmicutes were significantly higher in healthy dogs in comparison to dogs with AHD (p<0.05). Bifidobacterium spp. and gamma-Proteobacteria were not significantly different among all three groups of dogs. In conclusion, the qPCR panel employed here revealed a fecal dysbiosis in dogs with CE and AHD when compared to healthy dogs. These results are similar to recently reported findings using molecular sequencing approaches. Quantification of these bacterial groups by qPCR may be a useful adjunct for the diagnosis or monitoring of gastrointestinal disease in dogs.

No description available.

Thesis (M.S.)--Auburn University, 2008. / Abstract. Includes bibliographical references (p. 33-36).

Thesis--University of Florida. / Description based on print version record. Typescript. Vita. Includes bibliographical references (leaves 92-98).

Thesis (MMedVet (Medicine)) - University of Pretoria, 2002. / Includes bibliographical references.

Thesis (MSc (Veterinary Tropical Diseases, Veterinary Science))--University of Pretoria, 2008. / Includes bibliographical references. Also available in print format.

Thesis (M.S.)--University of Missouri-Columbia, 2006. / Title from title screen of research.pdf file (viewed on December 22, 2006). "May 2006" The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Includes bibliographical references.

Veterinarians in Tucson and Phoenix were surveyed by mail, requesting information about their patients recently diagnosed or treated for Valley Fever. Information obtained included risk factors and outcome.

Diminazene is a drug that is commonly used in the treatment of canine babesiosis. Most of the pharmacokinetic work on diminazene has been undertaken in healthy individuals, while the influence of disease on diminazene pharmacokinetics has been investigated to a limited degree. Population pharmacokinetics allows for the investigation of factors (covariates) that influence pharmacokinetic parameters. The aim of this study was to provide a descriptive model of the population pharmacokinetics of intramuscularly administered diminazene in dogs naturally infected with Babesia canis. Thirty-nine dogs had 142 plasma samples collected. Another 56 samples from 8 healthy dogs, from a previous study, were added to the data set. Population pharmacokinetics was performed using WinNonMix® (Pharsight, Cary, NC). A one-compartment model was fitted to the data. Health status (presence or absence of babesiosis), packed cell volume (PCV), serum albumin concentrations, mental status (a marker for the severity of illness) and the presence of splenomegaly significantly influenced the population pharmacokinetics model. The PCV lost its significance when these covariates were modelled concurrently, due to its correlation to the health status. In the final model, the volume of distribution (health status and albumin) and K01 (health status) was significantly influenced by covariates. / Dissertation (MMedVet)--University of Pretoria, 2007. / Companion Animal Clinical Studies / MMedVet / Unrestricted

Low-dose aspirin therapy in dogs inconsistently inhibits platelet function, termed ‘aspirin resistance’. There are no established diagnostic tests that can predict aspirin resistance in dogs prior to therapy. Platelet function was evaluated in healthy dogs prior to and during low-dose aspirin therapy using turbidimetric and impedance aggregometry, PFA-100, and urine 11-dehydro-thromboxane-B2 concentration. Following a washout, platelet-rich plasma from the dogs was incubated with aspirin and evaluated via turbidimetric aggregometry. After aspirin, the majority of dogs were classified as ‘aspirin responders’ with 81% responding after 7 days. Platelet dysfunction was not consistent in all dogs at all times. Compared to turbidimetric, impedance and PFA-100 results were inconsistent when run concurrently, suggesting turbidimetric is the preferred technique. There was poor agreement between in vitro aspirin incubation and all other tests. Unlike in people, platelet function in dogs is consistently inhibited by aspirin incubation, making this a poor technique for predicting aspirin resistance.