tetano
Editor, Senior Moderator
Vet Microbiol
. 2021 Dec 7;264:109303.
doi: 10.1016/j.vetmic.2021.109303. Online ahead of print.
Klebsiella pneumoniae infection following H9N2 influenza A virus infection contributes to the development of pneumonia in mice
Li Li-Juan[SUP] 1 [/SUP], Shun Kang[SUP] 1 [/SUP], Li Zhi-Juan[SUP] 1 [/SUP], Li Dan[SUP] 2 [/SUP], Xiao Feng[SUP] 1 [/SUP], Yuan Peng[SUP] 1 [/SUP], Zhang Bo-Shun[SUP] 1 [/SUP], Shijin Jiang[SUP] 1 [/SUP], Xie Zhi-Jing[SUP] 3 [/SUP]
Affiliations
Abstract
In this study, whether H9N2 influenza A virus (IAV) infection contributed to secondary Klebsiella pneumoniae infection was investigated. From post-infection onwards, clinical symptoms were monitored, examined and recorded daily for 11 days. As a result, no clinical signs were observed in the mice infected with single H9N2 IAV, implying that H9N2 IAV was less pathogenic to mice. Compared to single K. pneumonia infection, K. pneumoniae infection following H9N2 IAV infection exacerbates lung histopathological lesions and apoptosis, resulting in more severe diseases. Lung index of the mice with H9N2 IAV and K. pneumoniae co-infection was significantly higher than those in the other groups. Bacterial loads in the tissues in H9N2 IAV and K. pneumoniae co-infection group were significantly higher than those in the single K. pneumoniae infection group at 7 dpi. It demonstrated that prior H9N2 IAV infection contributed to K. pneumonia proliferation and delayed bacterial clearance in mice. Secondary K. pneumoniae infection influences seroconversion of anti-H9N2 antibody titers and the cytokine profiles. The findings demonstrated that H9N2 IAV infection facilitated secondary K. pneumonia infection, causing severe the diseases in mice.
Keywords: H9N2 influenza A virus; Klebsiella pneumoniae serotype K2; Secondary infection.
. 2021 Dec 7;264:109303.
doi: 10.1016/j.vetmic.2021.109303. Online ahead of print.
Klebsiella pneumoniae infection following H9N2 influenza A virus infection contributes to the development of pneumonia in mice
Li Li-Juan[SUP] 1 [/SUP], Shun Kang[SUP] 1 [/SUP], Li Zhi-Juan[SUP] 1 [/SUP], Li Dan[SUP] 2 [/SUP], Xiao Feng[SUP] 1 [/SUP], Yuan Peng[SUP] 1 [/SUP], Zhang Bo-Shun[SUP] 1 [/SUP], Shijin Jiang[SUP] 1 [/SUP], Xie Zhi-Jing[SUP] 3 [/SUP]
Affiliations
- PMID: 34923246
- DOI: 10.1016/j.vetmic.2021.109303
Abstract
In this study, whether H9N2 influenza A virus (IAV) infection contributed to secondary Klebsiella pneumoniae infection was investigated. From post-infection onwards, clinical symptoms were monitored, examined and recorded daily for 11 days. As a result, no clinical signs were observed in the mice infected with single H9N2 IAV, implying that H9N2 IAV was less pathogenic to mice. Compared to single K. pneumonia infection, K. pneumoniae infection following H9N2 IAV infection exacerbates lung histopathological lesions and apoptosis, resulting in more severe diseases. Lung index of the mice with H9N2 IAV and K. pneumoniae co-infection was significantly higher than those in the other groups. Bacterial loads in the tissues in H9N2 IAV and K. pneumoniae co-infection group were significantly higher than those in the single K. pneumoniae infection group at 7 dpi. It demonstrated that prior H9N2 IAV infection contributed to K. pneumonia proliferation and delayed bacterial clearance in mice. Secondary K. pneumoniae infection influences seroconversion of anti-H9N2 antibody titers and the cytokine profiles. The findings demonstrated that H9N2 IAV infection facilitated secondary K. pneumonia infection, causing severe the diseases in mice.
Keywords: H9N2 influenza A virus; Klebsiella pneumoniae serotype K2; Secondary infection.