Autopsies Show H1N1 Virus Damages Entire Respiratory Airway
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Autopsies Show H1N1 Virus Damages Entire Respiratory Airway

BETHESDA, Md -- December 7, 2009 -- Autopsies of the lungs of people who died of influenza A(H1N1) show that the virus can damage cells throughout the respiratory airway, much like the viruses that caused the 1918 and 1957 influenza pandemics, according to findings published early online and appearing in the February 2010 print issue of Archives of Pathology & Laboratory Medicine.

Researchers reviewed autopsy reports, hospital records, and other clinical data from 34 people who died of H1N1 between May 15 and July 9, 2009. All but 2 of the deaths occurred in New York.

Microscopic examination of tissues throughout the airways revealed that the virus caused damage primarily to the upper airway, but tissue damage to the lower airway was also present. Evidence of secondary bacterial infection was seen in more than half of the victims.

“This study provides clinicians with a clear and detailed picture of the disease caused by 2009 H1N1 virus that will help inform patient management,” said Anthony S. Fauci, MD, National Institutes of Health, Bethesda, Maryland. “In fatal cases of H1N1, it appears the novel pandemic influenza virus produces pulmonary damage that looks very much like that seen in earlier influenza pandemics.”

While most deaths from seasonal influenza occur in adults aged over 65 years, the report indicates that deaths from H1N1 occur predominately among younger people. The majority of deaths (62%) in the 34 cases studied were among those aged 25 to 49 years; 2 infants were also among the fatal cases.

Of those autopsied, 91% had underlying medical conditions, such as heart disease or respiratory disease, including asthma, before becoming ill with H1N1. Seventy-two percent of the adults and adolescents who died were obese. This finding is consistent with earlier reports, based on hospital records, linking obesity with an increased risk of death from H1N1.

The researchers examined tissue samples from the 34 deceased individuals to assess how the H1N1 virus damaged various parts of the respiratory system.

“We saw a spectrum of damage to tissue in both the upper and lower respiratory tracts,” said investigator Jeffery K. Taubenberger, MD, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland.

In all cases, the uppermost regions of the respiratory tract -- the trachea and bronchial tubes -- were inflamed, with severe damage in some cases. In 18 cases, evidence of damage lower down in the bronchioles was noted. In 25 cases, the researchers found damage to the alveoli.

“This pattern of pathology in the airway tissues is similar to that reported in autopsy findings of victims of both the 1918 and 1957 influenza pandemics,” noted Dr. Taubenberger.

The researchers also examined 33 of the 34 cases for evidence of pulmonary bacterial infections. Of the cases, 18 (55%) were positive. Not all of those individuals who had bacterial pneumonia alone with H1N1 had been hospitalised, indicating that some had acquired their bacterial infections outside of a healthcare setting. This raises the possibility that community-acquired bacterial pneumonia is playing a role in the current pandemic. Even in an era of widespread and early antibiotic use, bacterial pneumonia remains an important factor for severe or fatal influenza,” the authors wrote.

Computerized tomography (CT) scans of the lungs available for 4 cases of pulmonary bacterial infection showed ground-glass opacity. According to the authors, it is not known whether the abnormalities detected by CT also occur in people who have milder H1N1 infections. They call for additional investigation into the utility of CT scans as a tool to help clinicians identify and better treat severe H1N1 infections.

SOURCE: National Institutes of Health

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