Pathology in Practice.

In collaboration with the American College of Veterinary Pathologists.

Histological and dermatoscopic description of sphynx cat skin.

BACKGROUND: Histological and hair coat abnormalities of the alopecic sphynx cat have not been described in detail. The hairless allele (hr) in sphynx cats represents a mutation in the gene for keratin 71, a protein expressed in the inner root sheath of humans and mice. HYPOTHESIS/OBJECTIVES: To describe the histological and dermatoscopic abnormalities of sphynx cat skin. ANIMALS: Skin biopsies were collected from 14 sphynx cats and five cats with normal coats. Dermatoscopic examinations were performed on 11 sphynx cats and six additional control cats. METHODS: Vertical and horizontal sections of skin biopsy samples from sphynx and control cats were reviewed. Dermatoscopic images were compared between sphynx and control cats. RESULTS: Sphynx cat hair follicles were often small, curved and kinked and demonstrated infundibular hyperkeratosis and dilatation. Changes in the inner root sheath of sphynx cats included a poorly defined Henle's layer in addition to vacuolar-like changes and eosinophilic globules in Huxley's layer. Dermal papillae in sphynx cat anagen bulbs lacked the normal flame shape and were surrounded by epithelial cells arranged in a disorderly manner. The degree of follicular abnormalities varied between follicles. Follicular density was similar for both sphynx cats and control animals. Sphynx cat hair shafts were misshapen, smaller in diameter and rarely medullated. Dermatoscopy revealed similar hair coat density in sphynx and control cats. CONCLUSIONS AND CLINICAL IMPORTANCE: Sphynx cats demonstrated hair follicle dysplasia, with abnormal shaft production but without a decrease in follicle quantity. Abnormalities in sphynx cat follicles are similar to those in murine KRT71 mutants and suggest abnormal hair shaft keratinization.

Procedure times, complication rates, and survival times associated with single-chamber versus dual-chamber pacemaker implantation in dogs with clinical signs of bradyarrhythmia: 54 cases (2004-2009).

OBJECTIVE: To compare procedure times and major and minor complication rates associated with single-chamber versus dual-chamber pacemaker implantation and with 1-lead, 2-lead, and 3-lead pacemaker implantation in dogs with clinical signs of bradyarrhythmia. DESIGN: Retrospective case series. ANIMALS: 54 dogs that underwent pacemaker implantation because of clinical signs of bradyarrhythmia. PROCEDURES: Medical records of dogs that received pacemakers between July 2004 and December 2009 were reviewed for information regarding signalment, diagnosis, pacemaker implantation, pacemaker type, complications, and survival time. Analyses were performed to determine significant differences in anesthesia time, procedure time, and outcome for dogs on the basis of pacing mode and number of pacing leads. RESULTS: 28 of 54 (51.9%) dogs received single-chamber pacemakers and 26 (48.1%) received dual-chamber pacemakers. Mean ± SD procedural time was significantly longer for patients with dual-chamber pacemakers (133.5 ± 51.3 minutes) than for patients with single-chamber pacemakers (94.9 ± 37.0 minutes), and procedure time increased significantly as the number of leads increased (1 lead, 102.3 ± 51.1 minutes; 2 leads, 114.9 ± 24.8 minutes; 3 leads, 158.2 ± 8.5 minutes). Rates of major and minor complications were not significantly different between dogs that received single-chamber pacemakers and those that received dual-chamber pacemakers or among dogs grouped on the basis of the number of pacing leads placed. CONCLUSIONS AND CLINICAL RELEVANCE: Although dual-chamber pacemaker implantation did result in increased procedural and anesthesia times, compared with single-chamber pacemaker implantation, this did not result in a higher complication rate.

Methylphenidate toxicosis in dogs: 128 cases (2001-2008).

OBJECTIVE: To determine clinical signs and outcomes of methylphenidate hydrochloride (MPH) toxicosis in dogs; to assess effects of amount (ie, dose) and formulation (immediate or extended release) of ingested MPH on onset, duration, and severity of clinical signs; and to describe management of MPH intoxication. DESIGN: Retrospective case series. ANIMALS: 128 dogs with MPH toxicosis or exposure. PROCEDURES: Data from an Animal Poison Control Center (APCC) database from November 1, 2001, to November 30, 2008, were reviewed. Records of dogs were searched for APCC classifications of confirmed (n = 71) or suspected (39) MPH toxicosis; dogs (18) that ingested MPH but did not develop clinical signs of toxicosis were also included. Signalment, dose, clinical signs, treatment, and outcome were evaluated. RESULTS: Clinical signs of toxicosis were reported in 107 of 128 (84%) dogs that ingested MPH; these included hyperactivity in 42 (33%), tachycardia in 27 (21%), vomiting in 19 (15%), agitation in 16 (13%), and hyperthermia in 13 (10%). Doses ranged from 0.36 mg/kg (0.164 mg/lb) to 117.0 mg/kg (53.18 mg/lb). Severity of clinical signs was not strongly associated with dose. More severe and prolonged clinical signs were associated with ingestion of extended-release formulations of MPH; 3 dogs that consumed these formulations (doses, 10.2 mg/kg [4.64 mg/lb], 15.4 mg/kg [700 mg/lb], and 31.1 mg/kg [14.14 mg/lb]) died. Favorable outcomes were reported for most (31/34 [91%]) dogs. CONCLUSIONS AND CLINICAL RELEVANCE: Ingestion of even small amounts of MPH can cause severe clinical signs in dogs. Monitoring and supportive care are recommended regardless of dose.