Mårdh P A
Yale J Biol Med. 1983 Sep-Dec;56(5-6):529-36.
The present report is a review of data assuming an etiological relationship between pelvic inflammatory disease (PID) and Mycoplasma hominis. Thus the organism can be isolated from the vagina/cervix more frequently in PID patients than in any other clinical group, i.e., in half to three-fourths of all such cases. One-fourth of PID patients develop a significant antibody response to M. hominis during the course of the disease. The antibody response can be detected by indirect hemagglutination tests. Grivet monkeys infected experimentally with M. hominis develop PID, predominantly parametritis; the infection seems to spread via lymphatics to the parametria. These animals develop a significant antibody response. The animals, like naturally infected women, develop a marked increase in the serum level of IgM. In tissue cell cultures of human fallopian tubes experimentally infected with M. hominis, a decrease of the mucociliary wave activity occurs. So far, few clinical data support an etiological role for Ureaplasma urealyticum in PID. In grivet monkeys, the organism does not produce PID.
本报告是对有关盆腔炎性疾病(PID)与人型支原体之间病因关系的数据的综述。因此,与其他任何临床组相比,PID患者的阴道/宫颈中更常分离出该病原体,即在所有此类病例的一半至四分之三的患者中可分离出。四分之一的PID患者在疾病过程中对人型支原体产生显著的抗体反应。抗体反应可通过间接血凝试验检测到。实验感染人型支原体的猕猴会发生PID,主要是子宫旁炎;感染似乎通过淋巴管扩散到子宫旁组织。这些动物产生显著的抗体反应。与自然感染的女性一样,这些动物的血清IgM水平显著升高。在实验感染人型支原体的人输卵管组织细胞培养中,黏液纤毛波活动会降低。到目前为止,很少有临床数据支持解脲脲原体在PID中的病因学作用。在猕猴中,该病原体不会引起PID。