This section focuses on the role of mollicutes in the human. While most mycoplasma species are harmless commensals in the human and, where pathogenic, are life-threatening only under exceptional circumstances, one should be aware of the fact that some mycoplasmas exist in animals that cause 100% morbidity and 50% mortality, as e.g. M. mycoides subspecies mycoides, the agent of pleuropneumonia in cattle.
As with other bacteria, mycoplasmas may be considered normal flora in one site, e.g. Ureaplasma colonizing the human vagina, and abnormal when present at other sites, e.g. when found in joint fluid. Such findings may, in fact, be a first sign of immunosuppression in hypogammaglobulinemia. The induction of chronic disease states in patients with normal defense systems is an intriguing feature of mycoplasma infections. Besides the above-mentioned evasive strategies which are common to most mycoplasmas, each pathogenic mycoplasma may present specialized mechanisms of evasion of the immune system.
Although M. pneumoniae resides primarily in the oropharynx and can be isolated from secretions during lower respiratory disease, this organism has occasionally been found in the urethra or cervix of patients attending clinics for sexually transmitted diseases. Aside from causing classical 'atypical pneumonia' in school-age children, younger age groups may exhibit bronchitis, bronchiolitis, pharyngitis and croup. M. pneumoniae and concomitant host reactions can induce hemolytic anemia, Stevens-Johnson syndrome, myo- and pericarditis (9% of cases) and adult respiratory distress syndrome. M. pneumoniae-associated neurologic diseases (encephalitis, meningitis, myelitis, polyradiculitis) are being recognized with increasing frequency (following at least 1/1000 respiratory infections), some with debilitating or fatal outcome. Direct invasion, a neurotoxin, autoimmune complex formation with gang-liosides or vasculopathy are all being discussed as pathomechanisms. Neuropathy, including Guillain-Barre syndrome following M. pneumoniae infection, has been associated with the induction of autoantibodies to galactocerebroside.
U. urealyticum was first isolated from male patients with nongonococcal urethritis (50% of cases). It sometimes causes prostatitis, but may otherwise be found in the male urethra without any symptoms. U. urealyticum is normal flora of the female genital tract after onset of sexual activity (in some populations up to 80% of pregnant women are positive), but in conjunction with anaerobic gram-negative rods, Gardnerella vaginalis and a concomitant depression of protective lactobacilli, it is part of the pathologic bacterial vaginosis and is then present in large numbers. Bacterial vaginosis predisposes to upper genital tract infections (especially endometritis) and an adverse pregnancy outcome, and it doubles the risk of spontaneous preterm delivery. Like other organisms associated with bacterial vaginosis, U. urealyticum and M. hominis are suspected to be involved in intrauterine growth retardation of the fetus. Isolation of U. urealyticum from the chorioamnion with signs of histological chorio-amnionitis rather than colonization of the lower genital tract is associated with prematurity and low birthweight. Mid-pregnancy antimicrobial treatment directed against anaerobes and U. urealyticum reduces the rate of premature delivery in high-risk women with bacterial vaginosis.
The prevalence of U. urealyticum depends on the population studied. In Europe, about one-tenth of mature newborns carry U. urealyticum at birth, whereas one-third of extremely low birthweight infants (prematures of less than 1000 g birthweight) are colonized. In mature newborns, congenital Urea-plasma pneumonia has occasionally been described. Extremely low birthweight infants with Ureaplasma colonization of the lower respiratory tract, however, have a twofold increase in chronic lung disease characterized by the prolonged need for ventilation and/or supplemental oxygen.
M. hominis can be found in male urethritis in 19% of cases, and in the female genital tract as a commensal and as a member of the bacterial vaginosis family. Pelvic inflammatory disease, pyelonephritis, postpartum fever, posthysterectomy wound infection and fetal scalp abscesses may ensue from there. M. hominis has also been isolated from respiratory secretions of premature infants with pneumonia and in adult pharyngitis. In patients with reduced immunity, dissemination of genital mycoplasmas to other sites is possible, e.g. to the cerebrospinal fluid in premature infants, to the joints of hypogamma-globulinemic persons or nosocomially to operative wounds. M. hominis and U. urealyticum have recently been demonstrated in adenotonsillitis in children.
M. genitalium has been found associated with male urethritis (in 14-17% of cases), female urethritis, salpingitis, pelvic inflammatory disease, and arthritis in the immunocompromised state. M. genitalium has also been detected in the respiratory tract, but care must be taken in distinguishing this organism from M. pneumoniae, as both behave similarly in culture and share genetic and antigenic traits.
Mycoplasmas/ureaplasmas and arthritis
Association of mycoplasmas or ureaplasmas with arthritis in animals is an accepted fact and has been thoroughly studied in animal models such as, e.g. that with M. arthritidis in the mouse and rat. Although M. arthritidis may be a special case, as this strain which does not typically infect humans produces a superantigen, an association of mollicutes with human arthritis has long been under debate, and solid evidence in favor of an involvement of mycoplasmas and ureaplasmas in arthritis is increasing. In general, these organisms remain undiscovered unless specifically sought. Thus, mollicutes are taken to be a rare cause of septic inflammatory arthritides. However, mollicutes are responsible for about 40%
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