J Infect Dis. 2008 Dec 29. [Epub ahead of print]
Treatment with Protein Synthesis Inhibitors Improves Outcomes of Secondary Bacterial Pneumonia after Influenza.
Karlstr?m A, Boyd KL, English BK, McCullers JA. - 1Department of Infectious Diseases and the 2Veterinary Pathology Core, St. Jude Children's Research Hospital, 3Department of Pediatrics, Division of Infectious Diseases, Le Bonheur Children's Medical Center, Memphis, Tennessee.
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.
PMID: 19113989 [PubMed - as supplied by publisher]
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Treatment with Protein Synthesis Inhibitors Improves Outcomes of Secondary Bacterial Pneumonia after Influenza.
Karlstr?m A, Boyd KL, English BK, McCullers JA. - 1Department of Infectious Diseases and the 2Veterinary Pathology Core, St. Jude Children's Research Hospital, 3Department of Pediatrics, Division of Infectious Diseases, Le Bonheur Children's Medical Center, Memphis, Tennessee.
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.
PMID: 19113989 [PubMed - as supplied by publisher]
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