Gonococci causing disseminated gonococcal infection are resistant to the bactericidal action of normal human sera.
Gonococci causing disseminated gonococcal infection are resistant to the bactericidal action of normal human sera.
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引起播散性淋球菌感染的淋球菌对正常人血清的杀菌作用具有抵抗力。
DOI：
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发表时间：
1976
影响因子：
15.9
通讯作者：
K K Holmes
中科院分区：
文献类型：
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作者：
G K Schoolnik;T. M. Buchanan;K K Holmes
对来自播散性淋球菌感染和单纯性淋病患者的分离株测定了淋病奈瑟菌菌株对正常人血清杀菌作用的敏感性。血清敏感性与青霉素敏感性和缺陷型相关。来自西雅图播散性淋球菌感染患者的 39 株淋病奈瑟菌中有 38 株 (97%) 对正常人血清的补体依赖性杀菌作用具有抵抗力。其中 36 种可被小于或等于 mug/ml 的青霉素 G 抑制，并需要精氨酸、次黄嘌呤和尿嘧啶在化学成分确定的培养基（Arg-Hyx-Ura- auxotype）上生长。来自无并发症淋病患者的 43 株分离株中有 12 株也属于 Arg-Hyx-Ura 缺陷型，可被小于或等于 0.030 μg/ml 的青霉素 G 抑制，并且具有血清抗性。从无并发症的淋病患者中分离出的其余 31 株其他基因型菌株中，有 18 株（58.1%）对正常人血清敏感，滴度范围为 2 至 2,048。正常人血清的杀菌作用可以防止血清敏感淋球菌的传播。然而，由于只有一小部分被血清抗性菌株感染的个体发生播散性淋球菌感染，因此血清抗性似乎是传播的必要但不是充分的毒力因素。月经和咽部淋球菌感染等宿主因素可能有利于血清抗性菌株的传播。由于血清抗性 Arg-Hyx-Ura 菌株从播散性淋球菌感染患者中分离出来的频率远高于其他 auxotype 的血清抗性菌株，因此除了血清抗性之外，Arg-Hyx-Ura 菌株可能还具有其他毒力因子。
The susceptibility of strains of Neisseria gonorrhoeae to the bactericidal action of normal human sera was determined for isolates from patients with disseminated gonococcal infection and uncomplicated gonorrhea. Serum susceptibility was correlated with penicillin susceptibility and auxotype. 38 of 39 strains (97%) of N. gonorrhoeae from Seattle patients with disseminated gonococcal infection were resistant to the complement-dependent bactericidal action of normal human sera. 36 of these were inhibited by less than or equal to mug/ml of penicillin G and required arginine, hypoxanthine, and uracil for growth on chemically defined medium (Arg-Hyx-Ura- auxotype). 12 of 43 isolates from patients with uncomplicated gonorrhea were also of the Arg-Hyx-Ura-auxotype, inhibited by less than or equal to 0.030 mug/ml of penicillin G, and serum resistant. Of the 31 remaining strains of other auxotypes isolated from patients with uncomplicated gonorrhea, 18 (58.1%) were sensitive to normal human sera in titers ranging from 2 to 2,048. The bactericidal action of normal human sera may prevent the dissemination of serum-sensitive gonococci. However, since only a small proportion of individuals infected by serum-resistant strains develop disseminated gonococcal infection, serum resistance appears to be a necessary but not a sufficient virulence factor for dissemination. Host factors such as menstruation and pharyngeal gonococcal infection may favor the dissemination of serum-resistant strains. Since serum-resistant Arg-Hyx-Ura strains are far more frequently isolated from patients with disseminated gonococcal infection than serum-resistant strains of other auxotypes, Arg-Hyx-Ura-strains may possess other virulence factors in addition to serum resistance.