Canine cholelithiasis is considered to be an uncommon condition and is frequently cited as being an incidental finding. However, there is a paucity of contemporary literature to support these assertions. The aim of this retrospective cross-sectional study was to report the prevalence, clinical presentation, and long-term follow-up of cholelithiasis in dogs. The electronic database at the Small Animal Hospital, University of Glasgow was searched to identify dogs that were diagnosed with cholelithiasis on ultrasound between 2010 and 2018. Sixty-eight dogs were identified, giving an overall prevalence of cholelithiasis in our hospital of 0.97% (confidence interval 0.76–1.22%). Medical records of 61 dogs were available for review. Cholelithiasis was classified as an incidental finding in 53 (86.9%) dogs, with 8 (13.1%) dogs being classified as symptomatic, having complications of cholelithiasis that included biliary duct obstruction, biliary peritonitis, emphysematous cholecystitis, and acute cholecystitis. Follow-up was available for 39 dogs, with only 3 dogs (7.7%) developing complications attributed to cholelithiasis, including biliary duct obstruction and acute cholecystitis, within the subsequent 2 yr. Cholelithiasis is an uncommon but frequently incidental finding in dogs. Within the follow-up period, few of the dogs with incidental cholelithiasis went on to be become symptomatic.

The generation of homozygous null mutants for the crk1 Cdc2-Related Kinase of Leishmania mexicana was attempted using targeted gene disruption. Promastigote mutants heterozygous for crk1 were readily isolated with a hyg-targeting fragment, but attempts to create null mutants by second-round transfections with a bie-targeting fragment yielded two classes of mutant, neither of which was null. First, the transfected fragment formed an episome; second, the cloned transfectants were found to contain wild-type crk1 alleles as well as hyg and ble integrations. DNA-content analysis revealed that these mutants were triploid or tetraploid. Plasticity in chromosome number following targeting has been proposed as a means by which Leishmania avoids deletion of essential genes. These data support this theory and implicate crk1 as an essential gene, validating CRK1 as a potential drug target. L mexicana transfected with a Trypanosoma brucel homologue, tbcrk1, was shown to be viable in an immcrk1 null background, thus showing complementation of function between these trypanosomatid genes. The expression of crk1 was further manipulated by engineering a six-histidine tag at the C-terminus of the kinase, allowing purification of the active complex by affinity selection on Nl(2+)-nitriloacetic acid (NTA) agarose.