Other Mycoplasma Species

Mycoplasma Hominis

M. hominis commonly colonizes the lower genitourinary tract of healthy men and women. Women are more likely to be colonized than men and the likelihood of colonization increases with the number of sexual partners. M. hominis is found in <5% of asymptomatic men and in as many as 20% of men attending sexually transmitted disease clinics. The rate of colonization in asymptomatic women ranges from 10%–30%; ^, the rate of isolation may be higher in women with bacterial vaginosis, ^, urethritis, or cervicitis. Adolescent girls and boys are colonized infrequently, with reported rates of approximately 5% and 2%, respectively. M. hominis seldom colonizes the upper respiratory tract; it has been recovered from the oral or respiratory tracts of 1%–3% of healthy adults and in a greater proportion of those adults who engage in oral-genital sexual practices. M. hominis was also identified in 4.7% of 319 children undergoing bronchoscopy, with the prevalence decreasing with increasing age; the clinical relevance of this finding is uncertain.

The respiratory and genitourinary tracts of neonates can also be colonized (incidence 2%–7%), particularly after birth complicated by prolonged rupture of amniotic membranes or amnionitis.

Isolation of the organism from normally sterile sites and documentation of immunologic response to infection have implicated M. hominis as a cause of the conditions listed in Table 197.2 . Numerous case reports implicate M. hominis as a cause of amnionitis, post-partum fever, and other postpartum infections. However, the clinical importance of neonatal M. hominis infection is less clear. Neonatal central nervous system infections attributed to M. hominis include ventriculitis, meningitis, meningoencephalitis ^, and subdural empyema. M. hominis was isolated from the cerebrospinal fluid (CSF) of 5 (5%) of 100 preterm infants 1–6 days of age; the one infant with CSF pleocytosis had 71 white blood cells/μL and a mononuclear cell predominance. Valencia et al. isolated M. hominis from 9 (13%) of 69 neonates undergoing lumbar puncture; the CSF white blood cell count ranged from 0–28 white blood cells/μL. M. hominis was also isolated from the CSF in 9 (2.8%) of 318 infants evaluated by lumbar puncture in the peripartum period at 4 community hospitals; the one infant who died had concomitant Haemophilus influenzae sepsis. Neonates who did not receive specific therapy for M. hominis in these studies did not appear to have any apparent clinical consequence of infection. In contrast, Wolthers et al. reported a term infant with early onset meningoencephalitis attributed to M. hominis identified by both culture and polymerase chain reaction (PCR) performed on the CSF; this infant had improvement in CSF parameters that coincided with the administration of ciprofloxacin.

Recovery of M. hominis from the respiratory or urinary tract of neonates generally has not been associated with clinical infection. ^, However, neonates with M. hominis isolated from sterile sites appear to have worse clinical outcomes. In a study of 351 preterm infants (23–32 weeks gestational age), M. hominis was isolated from cord blood cultures alone (n = 21, 6.0%) or in combination with Ureaplasma urealyticum (n = 18, 5.1%). Earlier gestational age correlated with a higher rate of positive umbilical cord blood cultures. Furthermore, infants with positive cord blood cultures were more likely to have systemic inflammatory response syndrome compared with infants with negative cord blood cultures.

Numerous anecdotal reports have recorded M. hominis infection occurring outside the genitourinary system in other populations, including immunocompromised patients and patients undergoing intracranial operations. ^, In a series of 36 adult patients with extragential M. hominis infection, patients most commonly had abdominal wound infections following genitourinary tract operations.

M. hominis infection should be suspected when specimens from localized purulent infection, especially following genitourinary tract exposure (e.g., neonate) or manipulation, fails to yield a pathogen by conventional laboratory methods. Isolation and identification of M. hominis require inoculation and initial incubation in beef heart infusion broth containing horse serum and yeast extract, available commercially as pleuropneumonia-like–organism (PPLO) broth. Arginine, which is metabolized by M. hominis , is added to the broth, along with phenol red. Metabolism of arginine increases the pH, so that growth can be detected by a change in the color of the broth, usually within 24–48 hours. Subculture onto solid agar and incubation in 95% nitrogen and 5% carbon dioxide yields, within 7 days, colonies of 200–300 μm, which develop the characteristic “fried egg” appearance. M. hominis (but not M. pneumoniae or U. urealyticum ) also grows on conventional blood agar and in most broth media used for blood culture. Laboratory personnel should be alerted to look for pinpoint, translucent colonies that develop within 2–3 days on blood agar that should be subcultured as described. Recognition of M. hominis growth in blood culture broth depends on blind subculture, even if results of Gram stain of broth are negative. Growth causes little turbidity in broth, but radiometric assays show a positive growth index within 5–7 days. Automated, continuous-monitoring blood culture systems do not permit reliable recovery of M. hominis. Multiplex PCR and PCR-based microtiter plate hybridization assays also have been described; their accuracy and usefulness in the clinical setting remain to be determined.

Generally, M. hominis is susceptible to tetracyclines, fluoroquinolones, and clindamycin. The minimum inhibitory concentration required to inhibit the growth of 90% of organisms (MIC ₉₀ ) values are lower for levofloxacin (0.19–0.5 μg/mL), gatifloxacin (0.063 μg/mL), and moxifloxacin (0.063 μg/mL) than for ciprofloxacin (0.5–1 μg/mL). ^{, ,} Chloramphenicol, rifampin, and linezolid (MIC ₉₀ , 8.0 μg/mL) demonstrate modest in vitro activity. Up to 20% of M. hominis clinical isolates can be resistant to tetracycline and doxycycline, but antibiotic resistance patterns vary by country. ^, One infant received doxycycline to treat M. hominis ventriculitis after whole genome sequencing of the culture isolate failed to identify mutations known to cause resistance to tetracyclines but did identify mutations now to confer lincosamide and macrolide resistance. Fluoroquinolone resistance occurs occasionally. ^, Unlike the other pathogenic mycoplasmas, M. hominis is often resistant to macrolides, azalides, and ketolides, including erythromycin, azithromycin, clarithromycin, and telithromycin. ^{, , ,} The benefit of intravenous immunoglobulin therapy in patients with hypogammaglobulinemia and M. hominis infection is not known.