Baltes Nina, Kyaw Sunn, Hennig-Pauka Isabel, Gerlach Gerald-F
Department of Infectious Diseases, Institute of Microbiology, School of Veterinary Medicine, Infectious Diseases of Animals, Bischofsholer Damm 15, Hannover D-30173, Germany.
Vet Microbiol. 2004 Aug 19;102(1-2):67-72. doi: 10.1016/j.vetmic.2004.05.002.
The genes for the large subunit of [NiFe] hydrogenase 2, (hybB) and for L-1,2 propanediol oxidoreductase (fucO), were identified in an Actinobacillus (A.) pleuropneumoniae serotype 7 strain. Based on the hypothesis that adaptation to anaerobic conditions in damaged lung tissue may play a role in A. pleuropneumoniae persistence in host tissues, deletion mutants with a deletion in the hybB or the fucO gene were constructed and examined in an aerosol infection model. Deletion of the hybB or fucO genes appeared to have no significant effect on A. pleuropneumoniae virulence.
在胸膜肺炎放线杆菌血清型7菌株中鉴定出了[NiFe]氢化酶2大亚基(hybB)和L-1,2-丙二醇氧化还原酶(fucO)的基因。基于受损肺组织中对厌氧条件的适应可能在胸膜肺炎放线杆菌在宿主组织中的持续存在中起作用这一假设,构建了hybB或fucO基因缺失的缺失突变体,并在气溶胶感染模型中进行了检测。hybB或fucO基因的缺失似乎对胸膜肺炎放线杆菌的毒力没有显著影响。