Are outbreaks and sporadic respiratory infections by Mycoplasma pneumoniae due to two distinct subtypes?
Are outbreaks and sporadic respiratory infections by Mycoplasma pneumoniae due to two distinct subtypes?
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DOI：
10.1007/bf01586183
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发表时间：
1996-01-01
影响因子：
4.5
通讯作者：
Pietsch, K
中科院分区：
文献类型：
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作者：
Jacobs, E;Vonski, M;Pietsch, K
1986年至1994年间，从患者呼吸道物质中培养出37株肺炎支原体临床分离株，通过免疫学方法和聚合酶链反应（PCR）进行分型。对于免疫分型，使用了两种单克隆抗体（mAb），其识别肺炎支原体菌株FH的P1粘附，但其抑制肺炎支原体粘附红细胞的能力不同。不能抑制粘附的mAb P1.58在免疫印迹中显示与所有患者的分离株反应，而粘附抑制mAb P1.62仅与7个患者的分离株反应。由于肺炎支原体组1（肺炎支原体型菌株M129）和组2（肺炎支原体型菌株FH）的P1-粘附素基因组内的变异，设计了两个引物组。根据PCR扩增产物的大小，所有未显示mAb P1.62反应性的临床分离株均属于肺炎支原体第1组，而mAb P1.62阳性反应支原体分离株被表征为第2组菌株。在1992年肺炎支原体疾病爆发期间，所有19株临床分离株在免疫印迹中与mAb P1.62均未显示交叉反应性，并通过PCR分型为肺炎支原体I组菌株。此外，206例肺炎支原体补体结合试验阳性患者血清（滴度> 1：32份血清显示出对第1组支原体的粘附抑制抗体，22份血清显示出对第2组支原体的粘附抑制抗体，只有7份血清显示出对两个肺炎支原体组的粘附抑制抗体，1992年爆发的血清学数据显示，肺炎支原体第1组感染的患者比第2组感染的患者更频繁地产生粘附抑制抗体，这可能与肺炎支原体疾病的发病机制和随后的感染有关。
Thirty-seven clinical isolates of Mycoplasma pneumoniae, cultured from patients' respiratory material between 1986 and 1994, were typed by immunological methods and by polymerase chain reaction (PCR). For immunological typing two monoclonal antibodies (mAb) were used that recognized the P1 adhesion of Mycoplasma pneumoniae strain FH but differed in their ability to inhibit the adherence of Mycoplasma pneumoniae to erythrocytes. The mAb P1.58, which was not able to inhibit adherence, showed reactions with all patients' isolates in immunoblots, whereas the adherence-inhibiting mAb P1.62 reacted with only seven patients' isolates, Due to variations within the P1-adhesin genome of Mycoplasma pneumoniae group 1 (Mycoplasma pneumoniae type strain M129) and group 2 (Mycoplasma pneumoniae type strain FH), two primer sets were designed. According to the size of the PCR-amplification products, all clinical isolates that showed no mAb P1.62 reactivity belonged to Mycoplasma pneumoniae group 1, whereas mAb P1.62-positive-reacting mycoplasma isolates were characterized as group 2 strains. During an outbreak of Mycoplasma pneumoniae diseases in 1992, all 19 clinical isolates showed no cross-reactivity in immunoblots with the mAb P1.62 and were typed by PCR as Mycoplasma pneumoniae group I strains. Furthermore, 206 Mycoplasma pneumoniae complement fixation test - positive patient sera (titer > 1:40) from the study period were tested for adherence-inhibiting antibodies towards both type strains, Thirty-two sera showed adherence-inhibiting antibodies towards group 1 and 22 towards group 2 mycoplasmas, In only seven sera were adherence-inhibiting antibodies directed to both Mycoplasma pneumoniae groups, The serological data of the outbreak in 1992 revealed that patients with Mycoplasma pneumoniae group 1 infections developed adherence-inhibiting antibodies more frequently than did patients infected with group 2, which might have implications for the pathogenesis of n/lycoplasma pneumoniae diseases and subsequent infections.