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Original Research: COMMUNITY-ACQUIRED PNEUMONIA |

Expanded Clinical Presentation of Community-Acquired Methicillin-Resistant Staphylococcus aureus Pneumonia

L. Jason Lobo, MD; Kurt D. Reed, MD; Richard G. Wunderink, MD, FCCP
Author and Funding Information

From the Department of Medicine (Drs Lobo and Wunderink), the Department of Pathology (Dr Reed), and the Division of Pulmonary and Critical Care Medicine (Dr Wunderink), Northwestern University Feinberg School of Medicine, Chicago, IL.

Correspondence to: Richard G. Wunderink, MD, FCCP, 676 North St Clair, Ste 14-044, Chicago, IL 60611; e-mail: r-wunderink@northwestern.edu


Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2010 American College of Chest Physicians


Chest. 2010;138(1):130-136. doi:10.1378/chest.09-1562
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Background:  Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) has been documented to cause community-acquired pneumonias (CAP), notable for necrotizing features. The frequency of occurrence, risk factors, and optimal treatment of CA-MRSA CAP are unclear.

Methods:  This was a retrospective analysis of patients admitted to Northwestern Memorial Hospital from January 2005 to April 2007 with initial clinical presentation of pneumonia and respiratory or blood culture positive for CA-MRSA. Definition of CA-MRSA was based on sensitivity to trimethoprim/sulfamethoxazole and clindamycin.

Results:  Fifteen patients with CA-MRSA CAP were identified during the 28-month period. Only one of the 14 patients tested had evidence of preceding influenza, and no seasonal pattern was seen. Seven patients were never admitted to the ICU. Eight of 14 with chest CT scans had evidence of lung necrosis. Nine of 15 had evidence of pleural effusions early in their hospital course, and five of nine required at least one pleural drainage procedure. Seven of 15 were immunocompromised (three HIV, one acute lymphocytic leukemia [ALL], one high-dose steroids, and two immunoglobulin deficiency) with an additional three patients with diabetes. Mortality was only 13% (two of 15); both deaths occurred in patients with severe immunocompromise (ALL post chemotherapy and AIDS). Fourteen of 15 patients were treated with antimicrobials that inhibit exotoxin production (clindamycin or linezolid).

Conclusions:  CA-MRSA pneumonia is not necessarily a post-influenza infection. Despite necrotizing features in many, the mortality of CA-MRSA pneumonia in our series is lower than previously reported, and patients do not routinely require ICU care. Treatment with antibiotics that inhibit exotoxin production and/or nontoxigenic strains may explain this improved outcome.

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