THE RELATIONSHIP BETWEEN FUSOBACTERIUM SPECIES AND OTHER FLORA IN MIXED INFECTION
THE RELATIONSHIP BETWEEN FUSOBACTERIUM SPECIES AND OTHER FLORA IN MIXED INFECTION
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DOI：
10.1099/00222615-21-2-93
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发表时间：
1986-03-01
影响因子：
3
通讯作者：
WALKER, RI
中科院分区：
文献类型：
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作者：
BROOK, I;WALKER, RI
在小鼠皮下脓肿模型中研究了三种梭杆菌属物种和七种其他细菌物种的混合感染。15株梭杆菌（8株F. nucleatum、4个F. necrophorum和3株F. varium）和脆弱拟杆菌B.溶曲霉菌，金黄色葡萄球菌，A β-组溶血性链球菌、大肠埃希菌、肺炎克雷伯菌和铜绿假单胞菌。电子显微镜照片显示，在接种到小鼠之前和之后，在12个分离株中存在薄的粘多糖壁，其中包括所有11个诱导皮下肿胀的梭杆菌分离株。通过与其他菌种共接种和选择性抗菌治疗，可使梭杆菌产生耐药性。aureus和K.在脓肿诱导中，发现肺炎链球菌与梭杆菌分离株具有相同或更大的重要性，而梭杆菌分离株比A组链球菌和E.杆菌在混合感染中，观察到梭杆菌属的微生物数量相互增强。和K.肺炎假单胞菌、铜绿假单胞菌或拟杆菌属（Bacteriodes spp.）梭杆菌属的抑制只有当它们与A组链球菌共同接种时才注意到。梭杆菌属种的累加或协同能力突出了它们在感染中的潜在致病性。
Mixed infections with three Fusobacterium species and seven other bacterial species were studied in a subcutaneous abscess model in mice. Fifteen Fusobacterium isolates (eight F. nucleatum, four F. necrophorum, and three F. varium) and one isolate each of Bacteroides fragilis, B. asaccharolyticus, Staphylococcus aureus, Group A .beta.-haemolytic streptococcus, Escherichia coli, Klebsiella pneumoniae and Pseudomonas aeruginosa were studied. Electron micrographs showed the presence of a thin mucopolysaccharide wall before and after inoculation into mice in 12 isolates which included all of 11 Fusobacterium isolates that induced subcutaneous abscesses. After co-inoculation of Fusobacterium isolates with other species and selective therapy with antimicrobial agents, S. aureus and K. pneumoniae were found to be of equal or greater importance in abscess induction than were Fusobacterium isolates, while Fusobacterium isolates were found to be more important than Group A streptococci and E. coli. Mutual enhancement of the numbers of organisms in mixed infections was observed with Fusobacterium spp. and K. pneumoniae, P. aeruginosa or Bacteriodes spp. Suppression of Fusobacterium spp. was noticed only when they were co-inoculated with Group A streptococci. The additive or synergistic capabilities of Fusobacterium species highlighted their potential pathogenicity in infection.