Autopsies reveal H1N1 virus can damage entire airway

12/9/2009

NEW YORK Researchers from the National Institutes of Health and the New York City Office of Chief Medical Examiner on Monday reported that the H1N1 virus can damage cells throughout the respiratory airway, similar to the pandemics occurring in 1918 and 1957.

"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," stated Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases. "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. While most deaths from seasonal influenza occur in adults over 65 years old, deaths from 2009 H1N1 influenza occur predominately among 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 scientists reviewed autopsy reports, hospital records and other clinical data from 34 people who died of 2009 H1N1 influenza infection between May 15 and July 9, 2009. All but two of the deaths occurred in New York. A microscopic examination of tissues throughout the airways revealed that the virus caused damage primarily to the upper airway — the trachea and bronchial tubes — but 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.

Nine-out-of-ten of those autopsied had underlying medical conditions, such as heart disease or respiratory disease, including asthma, before becoming ill with 2009 H1N1 influenza; and 72% of the adults and adolescents who died were obese.

The findings are reported in the Archives of Pathology & Laboratory Medicine, now available online and scheduled to appear in the February 2010 print issue.

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