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Histopathological findings in a critically ill patient with avian influenza A (H7N9)

tetano

Editor, Senior Moderator
J Thorac Dis. 2015 Dec;7(12):E672-7. doi: 10.3978/j.issn.2072-1439.2015.11.59.
[h=1]Histopathological findings in a critically ill patient with avian influenza A (H7N9).[/h] Huang JB[SUP]1[/SUP], Li HY[SUP]1[/SUP], Liu JF[SUP]1[/SUP], Lan CQ[SUP]1[/SUP], Lin QH[SUP]1[/SUP], Chen SX[SUP]1[/SUP], Zhang HY[SUP]1[/SUP], Wang XH[SUP]1[/SUP], Lin X[SUP]1[/SUP], Pan JG[SUP]1[/SUP], Weng H[SUP]1[/SUP].
[h=3]Author information[/h]

[h=3]Abstract[/h] To date, data regarding the pulmonary histopathology of human H7N9 disease are scarce. We herein describe a patient with a severe case of avian influenza A (H7N9). A chest computerized tomography (CT) scan showed diffuse ground-glass opacities and consolidation throughout the lungs. A resection of pulmonary bullae in the right middle lobe was performed by video-assisted thoracic surgery (VATS) based on the extracorporeal membrane oxygenation (ECMO) supportive technique on the 23(rd) day after the onset of symptoms because of a right pneumothorax persistent air leak. The histopathological findings of the resected lung tissue revealed pneumocyte hyperplasia and fibroproliferative changes along with diffuse alveolar damage. Bronchoalveolar lavage fluid (BALF) specimens for influenza A (H7N9) virus were continuously positive for more than three weeks, despite oseltamivir treatment, and continuous viral replication significantly prolonged the course of the disease. The patient's clinical status continuously deteriorated, with the development of refractory hypoxemia due to progressive and rapid lung fibrosis, which was confirmed by the final histological changes observed from a limited post-mortem biopsy of lung tissue. Pre-terminally, he developed multi-organ failure and died on the 39(th) day after symptom onset, despite corticosteroid treatment.


[h=4]KEYWORDS:[/h] H7N9; Influenza virus; avian; histopathology; oseltamivir; pneumonia

PMID: 26793388 [PubMed] PMCID: PMC4703663 Free PMC Article
 
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