Concurrent to reports of zoonotic and nosocomial transmission of methicillin-resistant Staphylococcus aureus (MRSA) in veterinary settings, recent evidence indicates that the environment in veterinary hospitals may be a potential source of MRSA. The present report is a cross-sectional study to determine the prevalence of MRSA on specific human and animal contact surfaces at a large veterinary hospital during a nonoutbreak period. A total of 156 samples were collected using Swiffers Ò or premoistened swabs from the small animal, equine, and food animal sections. MRSA was isolated and identified by pre-enrichment culture and standard microbiology procedures, including growth on Mueller-Hinton agar supplemented with NaCl and oxacillin, and by detection of the mecA gene. Staphylococcal chromosome cassette mec (SCCmec) typing and pulsed-field gel electrophoresis profile were also determined. MRSA was detected in 12% (19/157) of the hospital environments sampled. The prevalence of MRSA in the small animal, equine, and food animal areas were 16%, 4%, and 0%, respectively. Sixteen of the MRSA isolates from the small animal section were classified as USA100, SCCmec type II, two of which had pulsed-field gel electrophoresis pattern that does not conform to any known type. The one isolate obtained from the equine section was classified as USA500, SCCmec type IV. The molecular epidemiological analysis revealed a very diverse population of MRSA isolates circulating in the hospital; however, in some instances, multiple locations/surfaces, not directly associated, had the same MRSA clone. No significant difference was observed between animal and human contact surfaces in regard to prevalence and type of isolates. Surfaces touched by multiple people (doors) and patients (carts) were frequently contaminated with MRSA. The results from this study indicate that MRSA is present in the environment even during nonoutbreak periods. This study also identified specific surfaces in a veterinary environment that need to be targeted when designing and executing infection control programs.

Objective:To determine the feasibility, degree of respiratory support, and safety of high flow nasal cannula (HFNC) oxygen therapy in sedated and awake healthy dogs, when compared to traditional nasal cannula (TNC) oxygen administration.Design: Randomized experimental crossover study.Setting: University research facility. Animals: Eight healthy dogs.Interventions: Variable flow rates (L/kg/min) were assessed, TNC: 0.1, 0.2, and 0.4 and HFNC: 0.4, 1.0, 2.0, and 2.5. HFNC was assessed in sedated and awake dogs.Measurements: Variables measured included: inspiratory/expiratory airway pressures, fraction of inspired oxygen (FiO 2 ), end-tidal oxygen (ETO 2 ), end-tidal carbon dioxide (ETCO 2 ), partial pressure of oxygen (PaO 2 ), partial pressure of carbon dioxide (PaCO 2 ), temperature, heart/respiratory rate, arterial blood pressure, and pulse oximetry. Sedation status, complications, and predefined tolerance and respiratory scores were recorded.Main results: Using HFNC, continuous positive airway pressure (CPAP) was achieved at 1 and 2 L/kg/min. CPAP was not higher at 2.5 than 2 L/kg/min, with worse tolerance scores. Expiratory airway pressures were increased when sedated (P = 0.006). FiO 2 at 0.4 L/kg/min for both methods was 72%. FiO 2 with TNC 0.1 L/kg/min was 27% and not different from room air. The FiO 2 at all HFNC flow rates ≥1 L/kg/min was 95%. PaO 2 for HFNC 0.4 L/kg/min was lower than at other flow rates (P = 0.005). The only noted complication was aerophagia. PaCO 2 was increased with sedation and use of HFNC when compared to baseline (P = 0.006; P < 0.01). Conclusions:Use of HFNC in dogs is feasible and safe, provides predictable oxygen support and provides CPAP, but may cause a mild increase in PaCO 2 . Flow rates of 1-2 L/kg/min are recommended. If using TNC, flow rates above 0.1 L/kg/min may attain higher FiO 2 .

ObjectiveTo determine the effect of high‐flow nasal cannula (HFNC) oxygen therapy on cardiorespiratory variables and outcome in dogs with acute hypoxemic respiratory failure.DesignProspective, sequential clinical trial.SettingUniversity veterinary teaching hospital.AnimalsTwenty‐two client‐owned dogs that failed to respond to traditional oxygen support.InterventionsInitiation of HFNC therapy after traditional oxygen supplementation failed to increase Spo2 > 96% and Pao2 > 75 mm Hg or improve respiratory rate/effort.Measurements and Main ResultsPhysiological variables, blood gas analyses, and dyspnea/sedation/tolerance scores were collected prior to HFNC initiation (on traditional oxygen support [time 0 or T0]), and subsequently during HFNC oxygen administration at time 30 minutes, 60 minutes, and 7 ± 1 hours. Relative to T0, use of HFNC resulted in a decreased respiratory rate at 1 hour (P = 0.022) and 7 hours (P = 0.012), a decrease in dyspnea score at all times (P < 0.01), and an increase in Spo2 at all times (P < 0.01). There was no difference in arterial/venous Pco2 relative to T0, although Paco2 was correlated with flow rate. Based on respiratory assessment, 60% of dogs responded to HFNC use by 30 minutes, and 45% ultimately responded to HFNC use and survived. No clinical air‐leak syndromes were observed.ConclusionsHFNC use improved oxygenation and work of breathing relative to traditional oxygen therapies, without impairing ventilation. HFNC use appears to be a beneficial oxygen support modality to bridge the gap between standard oxygen supplementation and mechanical ventilation.

The imaging findings in two miniature schnauzers with acute necrotizing pancreatitis are described. Both dogs were treated previously for diabetes mellitus and hyperlipidemia. Vomiting, anorexia, and lethargy were observed in both dogs at presentation. Laboratory evaluations supportive of pancreatitis included left shift, abnormally high serum amylase and lipase activities, hypocalcemia, and abnormally high serum activities of liver enzymes. Sonographically, both dogs had diffusely enlarged hypoechoic pancreatic tissue with anechoic foci compatible with necrosis, abscessation, phlegmon, and pseudocysts formation. Contrast-enhanced computed tomography (CT) findings in both dogs were compatible with pancreatic necrosis. Dog 1 was managed medically for 11 days. Follow-up CT scan in this dog disclosed decreased pancreatic size and increased contrast enhancement compatible with partial resolution of pancreatitis.

Objective: To review the current understanding of mechanisms involved in normal hemostasis and to describe the changes associated with pro-inflammatory disease processes such as sepsis. Data sources: Original research articles and scientific reviews. Human data synthesis: Organ damage caused by sepsis is created in part by the interdependent relationship between hemostasis and inflammation. Markers of coagulation have been found to have prognostic value in human patients with sepsis and there are both experimental and clinical investigations of the therapeutic potential of modulating the hemostatic system in sepsis. Improvement of 28-day all-cause mortality in severe sepsis by treatment with recombinant human activated Protein C strongly supports the interdependence of hemostasis and inflammation in the pathophysiology of sepsis. Veterinary data synthesis: Publications reporting clinical evaluation of the hemostatic changes occurring in septic dogs or cats are minimal. Experimental animal models of sepsis reveal significant similarity between human and animal sepsis and may provide relevance to clinical veterinary medicine until prospective clinical evaluations are published. Conclusions: It is now apparent that inflammation and the coagulation system are intimately connected. Understanding this relationship provides some insight into the pathogenesis of the hemostatic changes associated with sepsis. This new updated view of hemostasis may lead to the development of novel therapeutic approaches to sepsis and disseminated intravascular coagulation in veterinary medicine.