Researchers from the National Institutes of Health (NIH) and the New York City Office of Chief Medical Examiner report that in fatal cases of 2009 H1N1 influenza, the virus caused damage to cells throughout the respiratory airway, much like the viruses that caused the 1918 and 1957 influenza pandemics.
A microscopic examination of tissues throughout the airways of 34 people who died of 2009 H1N1 influenza infection between May 15 and July 9, 2009 (all in New York City except 2) revealed that the virus caused damage primarily to the upper airway—the trachea and bronchial tubes. However, the researchers found that tissue damage in the lower airway, including deep in the lungs, was present as well. Evidence of secondary bacterial infection was seen in more than half of the victims.
In all cases, the uppermost regions of the respiratory tract (trachea and bronchial tubes) were inflamed, with severe damage in some cases. In 18 cases, evidence of lower damage in the finer branches of the bronchial tubes, or bronchioles, was noted. In 25 cases, the researchers found damage to the small globular air sacs, or alveoli, of the lungs.
"This study provides clinicians with a clear and detailed picture of the disease caused by 2009 H1N1 influenza virus that will help inform patient management," said NIAID director Anthony S. Fauci, MD, in the study’s announcement. "In fatal cases of 2009 H1N1 influenza, it appears the novel pandemic influenza virus produces pulmonary damage that looks very much like that seen in earlier influenza pandemics."
The new report also underscores the impact 2009 H1N1 influenza is having on younger people. The majority of deaths (62%) in the 34 cases studied were among those 25 to 49 years old; two infants were also among the fatal cases.
The researchers note that 91% of those autopsied had underlying medical conditions, such as heart disease or respiratory disease, including asthma, before becoming ill with 2009 H1N1 influenza. Seventy-two percent of the adults and adolescents who died were obese. According to an announcement about the study, this finding agrees with earlier reports, based on hospital records, linking obesity with an increased risk of death from 2009 H1N1 influenza.
Thirty-three of the 34 cases were studied for evidence of pulmonary bacterial infections. Of these cases, 55% were positive for such infections. According to the study announcement, not all of those individuals who had bacterial pneumonia along with 2009 H1N1 virus infection had been hospitalized, however, indicating that some had acquired their bacterial infections outside of a health-care setting. This raises the possibility, say the authors, that community-acquired bacterial pneumonia is playing a role in the current pandemic.
The findings are reported online in the Archives of Pathology & Laboratory Medicine and will appear in the February 2010 print issue.