The Oligonucleotide primers of virulence-associated genes used in this study.

<p>The Oligonucleotide primers of virulence-associated genes used in this study.</p

The prevalence of virulence-associated genes among 74 uropathogenic <i>E</i>. <i>coli</i> isolates from cats.

<p>The 29 virulence-associated genes analysed were: <i>afa/draBC</i>, Dr-binding adhesins; <i>fimH</i>, mannose-specific adhesin of type 1 fimbriae; <i>papA</i>, P fimbriae structural subunit; <i>papE</i>, fimbriae tip pilins; <i>papC</i>, p fimbriae assembly; <i>papG</i>, p fimbriae adhesin (and alleles I, II, and III); <i>sfa/focDE</i>, S and F1C fimbriae; <i>sfaS</i>, S fimbriae; <i>focG</i>, <i>focA</i>, F1C fimbriae; <i>bmaE</i>, blood group M fimbriae; <i>hlyD</i>, <i>hlyA</i>, α-haemolysin; <i>cnf1</i>, cytotoxic necrotizing factor type 1; <i>kpsM</i> II, group 2 capsule in addition to specifically targeting K1 and K5 genes; <i>rfc</i>, O antigen polymerase; <i>fyuA</i>, ferric yersiniabactin receptor; <i>iutA</i>, aerobactin receptor; <i>iroN</i>, almochelin receptor; <i>ireA</i>, iron-responsive element gene; <i>ibeA</i>, invasion of brain endothelium; <i>traT</i>, serum-resistance associated; PAI, pathogenicity island; <i>cvaC</i>, Colicin-V.</p><p>The prevalence of virulence-associated genes among 74 uropathogenic <i>E</i>. <i>coli</i> isolates from cats.</p

Maximum likelihood tree constructed using MEGA 6.0 based on the nucleotide sequences of seven housekeeping genes: <i>adk</i>, <i>gyrB</i>, <i>fumC</i>, <i>icd</i>, <i>mdh</i>, <i>purA</i> and <i>recA</i>, and depicting infrerred phylogency of 74 uropathogenic <i>E</i>. <i>coli</i> (UPCE) from cats.

<p>Resistant phenotype (RP), phylogenetic group (PG), sequence type (ST), ST clonal complex (STcc; “N” indicates No STcc), virulence-associated genes and the prevalence of ESBL were displayed the right of the dendrogram. Virulence-associated genes were arranged in descending order according their corresponding prevalence. Gray square indicates the presence of the virulence-associated genes and ESBL. The sequence types highlighted in red were also found to be associated with both humans and other animals, and sequence types highlighted in blue were identified in humans or animals, or in water.</p

Splits tree decomposition network was obtained using distance matrix obtained from allelic profiles using a web version of Splits-Tree (http://pubmlst.org/analysis/).

<p>Most groups A and B1 isolates had shorter branches, suggesting that they were closely related as the group A and B1 isolates were considered as sister groups.</p

Comparison of predicted intrinsic hepatic clearance of 30 pharmaceuticals in canine and feline liver microsomes

<p>1. Known cytochrome P450 (CYP) substrates in humans are used in veterinary medicine, with limited knowledge of the similarity or variation in CYP metabolism. Comparison of canine and feline CYP metabolism via liver microsomes report that human CYP probes and inhibitors demonstrate differing rates of intrinsic clearance (CL_int).</p> <p>2. The purpose of this study was to utilize a high-throughput liver microsome substrate depletion assay, combined with microsomal and plasma protein binding to compare the predicted hepatic clearance (CL_hep) of thirty therapeutic agents used off-label in canines and felines, using both the well-stirred and parallel tube models.</p> <p>3. In canine liver microsomes, 3/30 substrates did not have quantifiable CL_int, while midazolam and amitriptyline CL_int was too rapid for accurate determination. A CL_hep was calculated for 29/30 substrates in feline microsomes. Overall, canine CL_hep was faster compared to the feline, with fold differences ranging from 2–20-fold.</p> <p>4. A comparison between the well-stirred and parallel tube model indicates that the parallel tube model reports a slighter higher CL_hep in both species.</p> <p>5. The differences in CYP metabolism between canine and feline highlight the need for additional research into CYP expression and specificity.</p