Abstract

It is difficult to discuss the year in review for pulmonary infections without starting with the 2009 novel H1N1 influenza pandemic. Although excess deaths were reported for pediatric (1) and pregnant patients (2) from the prior year, the most surprising thing about the year 2010 is actually the lack of clinical infection with influenza. This resulted from a combination of factors. The first is that the novel 2009 H1N1 strain was the only circulating influenza strain during the 2009 to 2010 influenza season. The second is the dramatic effect of large-scale immunization against this particular strain. As can be seen in Figure 1, shortly after the vaccine became available, the rate of positive cultures reported to the CDC dropped dramatically (3). A similar pattern was seen with pediatric deaths, another CDC marker of influenza severity. The combination of vaccination and prior exposure during the spring of 2009 resulted in sufficient herd immunity to almost completely block new cases of influenza. Despite the ominous start, the 2009 to 2010 influenza season was actually associated with fewer deaths than in nonpandemic years. One of the lasting effects of this pandemic is a change in the standards of the Advisory Committee on Immunization Practices regarding eligibility for influenza vaccination; the committee now recommends seasonal influenza vaccination or all persons 6 months of age or older (4). The lung pathology of fatal cases of the novel H1N1 infections was reviewed by Mauad and colleagues (5). They describe three distinct pathologic findings: diffuse alveolar damage, necrotizing tracheobronchitis, and diffuse alveolar damage with diffuse alveolar hemorrhage. A subsequent letter suggests that most of the patients who had purulent tracheobronchitis also had concomitant bacterial pneumonia (6). This association supports the concept that viral damage to the airway mucosa may be important in the pathogenesis of secondary pneumonia. Documented bacterial pneumonia at onset of the H1N1 infection is uncommon, but ventilatorassociated pneumonia (VAP) often occurs as a consequence of the severe acute lung injury and prolonged mechanical ventilation (7). Therefore, the purulent tracheobronchitis may be part of the spectrum of VAP previously described in other autopsy series (8). COMMUNITY-ACQUIRED PNEUMONIA

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