Objective—To determine whether Tritrichomonas foetus infection resides in reproductive tract tissues from cats housed for breeding and for which a high prevalence of colonic T foetus infection has been reported.
Animals—61 purebred cats in 36 catteries undergoing elective ovariohysterectomy or castration and for which reproductive tract tissues, feces, and a reproductive history were obtained.
Procedures—Reproductive tract tissues were examined for T foetus via light microscopy, immunohistochemical analysis, and PCR assay. History of reproductive tract disease was examined to detect statistical associations with identified or reported exposure to colonic T foetus infection.
Results—15 of 61 (25%) cats and 22 of 33 (67%) catteries were identified with active or reported T foetus infection. Light microscopic, immunohistochemical, or molecular evidence of T foetus infection of the reproductive tract was not detected in any cats, including 15 cats with colonic T foetus infection, 29 cats residing in a cattery in which T foetus–infected cats were identified, and 8 cats for which gross or light microscopic evidence of reproductive tract disease was identified. There were no differences in total number of litters, number of litters per breeding, kitten mortality rate, or birth defects between cats or catteries infected with T foetus and those for which T foetus infection was not identified.
Conclusions and Clinical Relevance—No evidence of reproductive tract colonization by T foetus was detected in this study. Accordingly, it is unlikely that reproductive tract infection with T foetus plays an important role in overall disease transmission.
Case Description—A 4-year-old spayed female mixed-breed dog with a history of allergic skin disease was examined because of regurgitation, coughing, and dysphagia that began 15 days after abdominal surgery for correction of gastric dilatation and volvulus.
Clinical Findings—Severe diffuse esophagitis, esophageal dysmotility, and a benign esophageal stricture at the level of the base of the heart were identified via contrast videofluoroscopy and esophagoscopy. Severe diffuse eosinophilic ulcerative esophagitis was confirmed by histologic examination of esophageal biopsy specimens and cytologic evaluation of specimens obtained by use of a cytology brush. Esophageal eosinophils were evident (14% to 50% of the inflammatory cell population and > 25 eosinophils/hpf).
Treatment and Outcome—No clinical or endoscopic improvement was evident after treatment with antireflux medications, including a proton-pump inhibitor, following an initial esophageal bougienage procedure. An excellent response characterized by resolution of dysphagia and regurgitation with marked improvement of the esophageal mucosa was evident following intralesional and systemic administration of glucocorticoids, 2 additional esophageal bougienage procedures, and feeding of an elimination diet.
Clinical Relevance—To our knowledge, the information reported here is the first description of eosinophilic esophagitis (EE) in a dog. Many similarities exist between the condition in the dog reported here and EE in humans. This clinical report highlights the need to consider EE as a differential diagnosis for esophagitis and esophageal strictures in dogs. When appropriate, esophageal biopsy or cytologic specimens should be obtained and examined to investigate the possibility of EE.
Objective—To determine whether a mutation in the fibrillin 2 gene (FBN2) is associated with canine hip dysplasia (CHD) and osteoarthritis in dogs.
Procedures—Hip conformation was measured radiographically. The FBN2 was sequenced from genomic DNA of 21 Labrador Retrievers and 2 Greyhounds, and a haplotype in intron 30 of FBN2 was sequenced in 90 additional Labrador Retrievers and 143 dogs of 6 other breeds. Steady-state values of FBN2 mRNA and control genes were measured in hip joint tissues of fourteen 8-month-old Labrador Retriever–Greyhound crossbreeds.
Results—The Labrador Retrievers homozygous for a 10-bp deletion haplotype in intron 30 of FBN2 had significantly worse CHD as measured via higher distraction index and extended-hip joint radiograph score and a lower Norberg angle and dorsolateral subluxation score. Among 143 dogs of 6 other breeds, those homozygous for the same deletion haplotype also had significantly worse radiographic CHD. Among the 14 crossbred dogs, as the dorsolateral subluxation score decreased, the capsular FBN2 mRNA increased significantly. Those dogs with incipient hip joint osteoarthritis had significantly increased capsular FBN2 mRNA, compared with those dogs without osteoarthritis. Dogs homozygous for the FBN2 deletion haplotype had significantly less FBN2 mRNA in their femoral head articular cartilage.
Conclusions and Clinical Relevance—The FBN2 deletion haplotype was associated with CHD. Capsular gene expression of FBN2 was confounded by incipient secondary osteoarthritis in dysplastic hip joints. Genes influencing complex traits in dogs can be identified by genome-wide screening, fine mapping, and candidate gene screening.