title: [Histopathologic study of avian influenza H5N1 infection in humans].
abstract: OBJECTIVE
  To identify histopathologic changes of major organs and to correlate clinical symptoms in patients infected by avian influenza H5N1.
  
  
  METHODS
  Autopsy study was performed in two patients died of avian influenza HSN1 infection, following conventional protocols and strict safety procedures. Tissue samples from all major organs of two cases and lung samples of one case were collected and fixed in 4% formaldehyde. Histopathologic changes were evaluated by light microscope.
  
  
  RESULTS
  Diffuse alveolar damage (DAD) of the lung was seen in both cases. Lesions at various stages of development were seen involving different areas of the lung. At the early stages, the lungs exhibited exudative changes, including capillary congestion, necrosis of alveolar epithelial cells, and intra-alveolar edema. Hyaline membranes were prominent and diffusely distributed along alveoli. In the middle-late stages of the disease, the lungs exhibited proliferative and fibrotic changes, including proliferation of pneumocytes and bronchial epithelium, fibrosis of the interstitium and alveolar spaces. Lung biopsy tissue of one case showed DAD and interstitial fibrosis in a background of bronchiectasis. Lymph nodes and spleens showed quantity reduction of lymphocytes and active hemophagocytosis. Other changes in major organs included interstitial carditis in one case and acute renal tubular necrosis in one case. In one case, the brain showed edema with cytoplasmic eosinophilia, loss of structure, axon welling and focal necrosis around ventricle. Multiple foci of trophoblastic necrosis with dystrophic calcification were observed in placenta of one pregnant patient. Acute necrotizing deciduitis was found focally. Sections of fetal lung showed edema and scattered interstitial neutrophils were consistent with acute interstitial pneumonitis.
  
  
  CONCLUSIONS
  The respiratory tract is the major target of avian influenza A H5N1 virus infection. The changes of DAD in the lungs resulted in hypoxia, leading to multiple organ failure and death.
authors.affiliation: Department of Pathology, Peking University Health Science Center, Beijing 100083, China.
authors.forename: Min
authors.initials: M
authors.lastname: Lu
authors.forename: Zhi-Gang
authors.initials: ZG
authors.lastname: Xie
authors.forename: Zhan-Cheng
authors.initials: ZC
authors.lastname: Gao
authors.forename: Chen
authors.initials: C
authors.lastname: Wang
authors.forename: Ning
authors.initials: N
authors.lastname: Li
authors.forename: Min
authors.initials: M
authors.lastname: Li
authors.forename: Hong-Quan
authors.initials: HQ
authors.lastname: Shao
authors.forename: Yu-Ping
authors.initials: YP
authors.lastname: Wang
authors.forename: Zi-Fen
authors.initials: ZF
authors.lastname: Gao
mesh_terms: D000328:Adult; D056809:Alveolar Epithelial Cells / Q000473:pathology*; D000818:Animals; D001717:Birds; D017809:Fatal Outcome; D005260:Female; D006801:Humans; D053124:Influenza A Virus, H5N1 Subtype / Q000472:pathogenicity*; D005585:Influenza in Birds / Q000473:pathology* / Q000503:physiopathology / Q000821:virology; D007251:Influenza, Human / Q000473:pathology*; D008297:Male; D011247:Pregnancy; D011658:Pulmonary Fibrosis / Q000209:etiology / Q000473:pathology*