Abstract & Commentary

By Stan Deresinski, MD, FACP Clinical Professor of Medicine, Stanford; Associate Chief of Infectious Diseases, Santa Clara Valley Medical Center. Dr. Deresinski serves on the speaker’s bureau for Merck, Pharmacia, GlaxoSmithKline, Pfizer, Bayer, and Wyeth, and does research for Merck.

This article originally appeared in the July 2006 issue of Infectious Disease Alert. It was peer reviewed by Connie Price, MD. Dr. Price is Assistant Professor, University of Colorado School of Medicine. Dr. Price reports no financial relationships relevant to this field of study.

Synopsis: Seventeen cases of community acquired pneumonia due to Staphylococcus aureus are described. Most were methicillin resistant and caused severe disease with high mortality.

Source: Hageman JC, et al. Severe Community-Acquired Pneumonia Due to Staphylococcus aureus, 2003-04 Influenza Season. Emerg Infect Dis. 2006; 12:894-899.

The CDC identified 17 patients with community-acquired pneumonia (CAP) due to S. aureus by following up on reports from the Emerging Infections Network of the Infectious Disease Society of America during the 2003-2004 influenza season. The patients ranged in age from 3 months to 62 years (median, 21 years), and 5 (29%) had underlying diseases. All patients had an initial influenza-like illness, and 12 (71%) had laboratory-confirmed acute influenza virus infection. Only one had documented receipt of influenza vaccine during 2003-2004. Twelve (93%) of 13 patients for whom data was available were hypotensive. One-fourth of patients had involvement of multiple lobes of the lung, and one-fourth had radiographic evidence of cavitation or necrosis; 31% had effusions/empyema. ICU admission was required by 81%; 62% required mechanical ventilation and 46% required chest tube placement. Five (29%) died, a median of 7 days (range, 3 to 73 days) after the onset of symptoms; one was dead on arrival at hospital.

Of the 13 S. aureus isolates available, 13 (76%) were methicillin-resistant (MRSA). All contained one or more toxin genes, but 11 of these had only the genes encoding the Panton-Valentine leukocidin. All the isolates were found to be of community-associated pulsed field types; 85% were USA300 (most subtype 0114) and the remainder were USA400.


This study is important in bringing 2 epidemiological strands together—the known increased risk of S. aureus as a cause of CAP complicating influenza virus infection and the emergence of novel strains of MRSA in the community. The cases described here were of remarkable severity, indicating a need for early initiation of appropriate antibiotic therapy and, thus, require awareness of the problem of community-acquired MRSA (CA-MRSA) among clinicians. These cases also demonstrate the importance of procuring specimens, including sputum for microbiological evaluation and examination of Gram stains, something which appears to be increasingly neglected.

Hageman and colleagues point out a warning published in 1959 that during influenza epidemics antibiotic therapy should included coverage of relatively antibiotic-resistant staphylococci.1 At the time, of course, they were referring to penicillin-resistant organisms not MRSA, which had not yet been described (methicillin became available in 1959-1960). This warning remains valid at a time when virulent CA-MRSA are increasingly prevalent and, at the same time, acquiring resistance to additional antibiotics, including the respiratory fluoroquinolones.


1. Martin CM, et al. Asian Influenza A in Boston, 1957-1958. II. Severe Staphylococcal Pneumonia Complicating Influenza. AMA Arch Intern Med. 1959;103:532-542.