Taylor-Robinson D, Furr P M, Webster A D
Pediatr Infect Dis. 1986 Nov-Dec;5(6 Suppl):S236-8. doi: 10.1097/00006454-198611010-00006.
The lack of antibody in hypogammaglobulinemic patients probably results in failure of mycoplasmas to be "neutralized" and accounts for the diminished ability of the patients to cope with these organisms escaping hematogenously from the respiratory and urogenital tracts. Furthermore Ureaplasma urealyticum and other mycoplasmas are ingested by neutrophils in the absence of opsonins, indicated by the fact that they are able to trigger the release of chemiluminescence from these cells; ureaplasmas are not killed during this process and it is possible that carriage occurs within phagocytes to various sites. Several mycoplasmal species have localized in joints and U. urealyticum organisms are no exception. They have been isolated from the purulent synovial fluids of at least three hypogammaglobulinemic patients in Canada, England and the United States, respectively, the arthritides responding to appropriate antibiotic therapy. In one male patient, however, repeated and prolonged episodes of arthritis over several years, associated with antibiotic-resistant ureaplasmas, responded only to the administration of specific hyperimmune serum. Apart from joint involvement subcutaneous abscesses have been seen, and in the latter patient persistent urethritis was caused by ureaplasmas, these being the only organisms recovered from the urethra. Chronic urethrocystitis/cystitis in hypogammaglobulinemic patients has been associated also with ureaplasmal infection. In addition polyarthritis with recovery of both ureaplasmas and Mycoplasma hominis from the joints has been seen in a kidney allograft patient on an immunosuppressive regimen. However, further evidence that ureaplasmas cause a problem in immunosuppressed patients or in those with the acquired immunodeficiency syndrome is lacking.
低丙种球蛋白血症患者缺乏抗体,这可能导致支原体无法被“中和”,并解释了患者应对这些从呼吸道和泌尿生殖道经血行扩散的病原体的能力下降的原因。此外,解脲脲原体和其他支原体在缺乏调理素的情况下会被中性粒细胞吞噬,这一事实表明它们能够触发这些细胞释放化学发光;在此过程中脲原体不会被杀死,并且有可能在吞噬细胞内携带至各个部位。几种支原体已在关节中定位,解脲脲原体也不例外。它们分别从加拿大、英国和美国的至少三名低丙种球蛋白血症患者的脓性滑液中分离出来,关节炎对抗生素治疗有反应。然而,在一名男性患者中,数年来反复出现的持续性关节炎发作,与对抗生素耐药的脲原体有关,仅对给予特异性超免疫血清有反应。除了关节受累外,还可见皮下脓肿,在该患者中,持续性尿道炎由脲原体引起,这些是从尿道中分离出的唯一病原体。低丙种球蛋白血症患者的慢性尿道膀胱炎/膀胱炎也与脲原体感染有关。此外,一名接受免疫抑制治疗的肾移植患者出现了多关节炎,关节中同时分离出脲原体和人型支原体。然而,目前缺乏进一步的证据表明脲原体在免疫抑制患者或获得性免疫缺陷综合征患者中会引发问题。