Efficacy of Telavancin in Comparison to Linezolid in a Porcine Model of Severe Methicillin-Resistant Staphylococcus aureus Pneumonia.

Current guidelines recommend vancomycin and linezolid as first-line agents against methicillin-resistant Staphylococcus aureus (MRSA) nosocomial pneumonia. Telavancin is a potential new therapeutic alternative, specifically in monomicrobial MRSA pneumonia. This study compared the efficacies of telavancin versus linezolid in a porcine model of severe MRSA pneumonia. In 18 mechanically ventilated pigs (32.11 ± 1.18 kg), 75 ml of 106 CFU/ml of MRSA was administered into each pulmonary lobe. After the onset of pneumonia, pigs were randomized into three groups: a control group, a group receiving 22.5 mg/kg of body weight every 24 h (q24h) of telavancin, and a group receiving 10 mg/kg q12h of linezolid intravenously. Tracheal aspirate and bronchoalveolar lavage (BAL) fluids were cultured every 24 h. After 48 h of treatment, tissue samples were collected from the ventral and dorsal sections of each lobe. Microbiological and histopathological analyses were performed. Lung tissue concentrations differed among the groups (P = 0.019), with the lowest MRSA lung burden in the telavancin group (P < 0.05 versus the control). MRSA was detected in 46.7%, 40.0%, and 21.7% of the lung tissue samples from the control, linezolid, and telavancin groups, respectively (P < 0.001). MRSA concentrations differed among the groups in tracheal aspirate fluid (P = 0.011) but not in BAL fluid. Furthermore, there was no increased risk of kidney injury during telavancin use. Thus, telavancin has higher bactericidal efficacy than linezolid during the first 48 h of treatment in a porcine model of severe MRSA pneumonia. However, studies are needed to confirm the benefits of telavancin in treating MRSA nosocomial pneumonia.

Targeting the Main Anatomopathological Features in Animal Models of Myocardial Infarction.

Cardiovascular disease is the leading cause of human mortality and disability worldwide, primarily due to myocardial infarction (MI) and the resultant heart failure. To address this, animal models of MI have been developed to better understand the pathophysiological process and to enable the discovery and development of new therapies. The most commonly used small and large mammal models of MI accurately reproduce histopathologically the four characteristic post-MI phases: cardiac cell death, inflammation, myocardial repair and remodelling. However, differences between the time of onset of each characteristic phase and the kinetics of various cellular reactions between human MI and animal models, and between animal models, require careful consideration when defining the variables to be analysed and the timepoints of assessment in experimental studies. Typically, the progression of the different phases post-MI occur more rapidly in rodent models compared with large-animal models and man, suggesting the use of large-animal models is more translational for studying human MI. This review provides an overview of the main anatomopathological features of small and large animal models of MI and discusses the key species-specific histopathological similarities and differences.