Treatment with protein synthesis inhibitors improves outcomes of secondary bacterial pneumonia after influenza.

Karlström A, Boyd KL, English BK, McCullers JA
J Infect Dis. 2009 199 (3): 311-9

PMID: 19113989 · PMCID: PMC2687083 · DOI:10.1086/596051

Pneumonia occurring as a secondary infection after influenza is a major cause of excess morbidity and mortality, despite the availability and use of antibiotics active against Streptococcus pneumoniae. We hypothesized that the use of a bacteriostatic protein synthesis inhibitor would improve outcomes by reducing the inflammatory response. BALB/cJ mice infected with influenza virus and superinfected with S. pneumoniae were treated with either the cell-wall-active antibiotic ampicillin or the protein synthesis inhibitor clindamycin or azithromycin. In the model, ampicillin therapy performed significantly worse (survival rate, 56%) than (1) clindamycin therapy used either alone (82%) or in combination with ampicillin (80%) and (2) azithromycin (92%). Improved survival appeared to be mediated by decreased inflammation manifested as lower levels of inflammatory cells and proinflammatory cytokines in the lungs and by observation of less-severe histopathologic findings. These data suggest that beta-lactam therapy may not be optimal as a first-line treatment for community-acquired pneumonia when it follows influenza.

MeSH Terms (19)

Ampicillin Animals Anti-Bacterial Agents Bronchoalveolar Lavage Fluid Clindamycin Disease Models, Animal Drug Screening Assays, Antitumor Drug Therapy, Combination Female Inflammation Influenza A virus Lung Mice Mice, Inbred BALB C N-Acetylmuramoyl-L-alanine Amidase Orthomyxoviridae Infections Pneumonia, Pneumococcal Protein Synthesis Inhibitors Tumor Necrosis Factor-alpha

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