Genital Mycoplasmas: Mycoplasma genitalium , Mycoplasma hominis , and Ureaplasma Species

Taxonomy and Microbiology

The clinically important genital mycoplasmas— Mycoplasma hominis, Mycoplasma genitalium, Ureaplasma urealyticum, and Ureaplasma parvum —belong to the Mollicutes class and Mycoplasmataceae family of bacteria. Mycoplasma spp. and Ureaplasma spp. are the only two genera in this family. In this chapter the trivial term genital mycoplasmas is used to refer to these genera collectively. Ureaplasma spp. are most prominently distinguished from Mycoplasma spp. by virtue of their ability to hydrolyze urea for energy production. The two Ureaplasma spp. differ phenotypically and genotypically and were officially designated as separate species in 2002. Originally they were believed to be biovariants of a single species and were first known as T-mycoplasmas and later renamed Ureaplasma urealyticum. This background information is important because textbooks and research papers published before 2002 did not distinguish the two species. The trivial term ureaplasmas is used in this chapter in reference to published research that did not differentiate the two species or in reference to conditions that are associated with both species.

Mollicutes in general have the distinction within the bacterial kingdom for having the smallest genomes of any known self-replicating organisms. The smallest of these is the genome of M. genitalium, which is only 580,000 base pairs in length and therefore is believed to be close to the minimal set of genes necessary for independent life. For this reason, its genome was among the first to be completely sequenced as well as the first to be completely reconstructed in vitro. Mollicutes evolved from Clostridia -like gram-positive bacteria by virtue of extensive gene deletion. M. genitalium is very closely related genetically to Mycoplasma pneumoniae, having evolved away from this organism by additional gene deletions. As with all members of the Mollicutes class of bacteria, the genital mycoplasmas lack a cell wall and thus are osmotically fragile. Reflective of their small genomes, they have limited biosynthetic capacity, which is why complex growth media containing sterols are required for their cultivation in vitro.

The natural habitat of the genital mycoplasmas is the human genitourinary tract, where they adhere to mucosal surface epithelial lining cells, although M. genitalium also can be found intracellularly. They are found outside this environment less frequently, and, when they are, it is often in the setting of immune deficiency such as that found in very-low-birth-weight premature infants. Although the mechanisms differ among species, the genital mycoplasmas all have the ability to vary immunogenic proteins on their cell surface. This appears to be the major mechanism by which they avoid the host immune response and is the reason they are able to persist for months to years in the same host. Mycoplasma fermentans and Mycoplasma penetrans are two other mycoplasmas that have been identified in the human genitourinary tract, but they have not been consistently associated with human disease. These are not discussed further in this chapter.

Epidemiology

All of the genital mycoplasmas are sexually transmitted, although their roles in genital tract disease vary significantly, as discussed in detail in “Clinical Manifestations.” The ureaplasmas are more commonly found in both the male and female genital tracts than either of the two Mycoplasma spp. In a study of healthy college men, ureaplasmas were present in the urethras of 29%, whereas M. hominis was present in 7%. For both organisms, prevalence correlated strongly with the number of sex partners. Among sexually active female nursing students, the same group of investigators found that the prevalence of ureaplasmas varied from 38% to 75% and the prevalence of M. hominis varied from 9% to 17%, depending on the number of lifetime sex partners. In a nationally representative sample of young adults in the United States, the prevalence of M. genitalium was 1.0%, whereas in the same population the prevalence of Chlamydia trachomatis was 4.2%. In this and another survey study, prevalence of M. genitalium was related to the number of reported sex partners. Evidence for sexual transmission of M. genitalium was further strengthened by studies demonstrating high rates of genotype concordance within couples. The epidemiology of M. genitalium closely parallels that of C. trachomatis and Neisseria gonorrhoeae. All are found more frequently in younger sexually active men and women and are more common in African Americans than in other racial groups. Young age is also a risk factor for infection by the ureaplasmas and M. hominis, but racial associations have been less well studied.

Neonates born vaginally are frequently colonized in both the genital and the respiratory tracts by ureaplasmas and less frequently by M. hominis . Colonization after cesarean section occurs less commonly, supporting the hypothesis that exposure to vaginal secretions at birth is the primary risk factor for acquisition in neonates. Boys in general are less likely to be colonized than girls. Colonization of the genital tract in girls persists in some cases and is likely to be a reservoir for infection of boys when sexual intercourse is first initiated. Much less is known about transmission of M. genitalium to neonates at delivery. However, it was reported that 9% of 319 children undergoing bronchoscopy for medical indications at a mean age of 8 years had M. genitalium detected in lavage fluid by polymerase chain reaction (PCR) assay. This was compared with positivity rates of 10% for M. pneumoniae, 5% for M. hominis, and 9% for U. parvum . If these data can be confirmed, it may be that all the genital mycoplasmas have the ability to colonize the respiratory tract and possibly may be present for long periods of time.