2009 Pandemic Influenza A (H1N1): Pathology and Pathogenesis of 100 Fatal Cases in the United States

[tetano]

Am J Pathol. 2010 May 27. [Epub ahead of print]
2009 Pandemic Influenza A (H1N1): Pathology and Pathogenesis of 100 Fatal Cases in the United States.

Shieh WJ, Blau DM, Denison AM, Deleon-Carnes M, Adem P, Bhatnagar J, Sumner J, Liu L, Patel M, Batten B, Greer P, Jones T, Smith C, Bartlett J, Montague J, White E, Rollin D, Gao R, Seales C, Jost H, Metcalfe M, Goldsmith CS, Humphrey C, Schmitz A, Drew C, Paddock C, Uyeki TM, Zaki SR.

From the Infectious Diseases Pathology Branch,* Division of Viral and Rickettsial Diseases; Epidemiology Branch, Influenza Division, Centers for Disease Control and Prevention, Atlanta, GA; and the Influenza Department, National Institute for Viral Disease Control and Prevention, Centers for Disease Control and Prevention, Beijing, China.
Abstract

In the spring of 2009, a novel influenza A (H1N1) virus emerged in North America and spread worldwide to cause the first influenza pandemic since 1968. During the first 4 months, over 500 deaths in the United States had been associated with confirmed 2009 pandemic influenza A (H1N1) [2009 H1N1] virus infection. Pathological evaluation of respiratory specimens from initial influenza-associated deaths suggested marked differences in viral tropism and tissue damage compared with seasonal influenza and prompted further investigation. Available autopsy tissue samples were obtained from 100 US deaths with laboratory-confirmed 2009 H1N1 virus infection. Demographic and clinical data of these case-patients were collected, and the tissues were evaluated by multiple laboratory methods, including histopathological evaluation, special stains, molecular and immunohistochemical assays, viral culture, and electron microscopy. The most prominent histopathological feature observed was diffuse alveolar damage in the lung in all case-patients examined. Alveolar lining cells, including type I and type II pneumocytes, were the primary infected cells. Bacterial co-infections were identified in >25% of the case-patients. Viral pneumonia and immunolocalization of viral antigen in association with diffuse alveolar damage are prominent features of infection with 2009 pandemic influenza A (H1N1) virus. Underlying medical conditions and bacterial co-infections contributed to the fatal outcome of this infection. More studies are needed to understand the multifactorial pathogenesis of this infection.

PMID: 20508031 [PubMed - as supplied by publisher]


http://www.ncbi.nlm.nih.gov/pubmed/20508031

 

[kent nickell]

Re: 2009 Pandemic Influenza A (H1N1): Pathology and Pathogenesis of 100 Fatal Cases in the United States

excerpts:

This study includes autopsy specimens from confirmed 2009 H1N1 case-patients submitted to the Infectious Disease Pathology Branch, Centers for Disease Control and Prevention (CDC) for evaluation from May 1 to October 1, 2009.

The median age of fatal case-patients was 36 years (range 2 months to 84 years). 80% were aged 20 to 60 years.

Overall, 26 (26%) case-patients had confirmatory test results of bacterial co-infection. (these test included sophisticated pcr assays rather than cultures)

Obesity (body mass index > 30) was the most significant associated underlying condition present in 46%, and 17% of case-patients were extremely obese (body mass index > 40).

Bacterial co-infections with S. pneumoniae and S. aureus were the most frequent identified in this study. The prevalence of invasive S. aureus, either MRSA or MSSA was high among younger patients.

Confirmation of 2009 H1N1 was obtained only by postmortem evaluation in over half of the case-patients. This underscores the important role of medical examiners, coroners, and pathologists in infectious disease surveillance.