<i>Mycoplasma hominis</i> and <i>Ureaplasma </i>infections

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Mycoplasma hominis and Ureaplasma infections

Authors: Ken B Waites, MD, F(AAM), Namasivayam Ambalavanan, MD
Section Editors: Daniel J Sexton, MD, Morven S Edwards, MD
Deputy Editor: Allyson Bloom, MD

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Nov 2023. | This topic last updated: Oct 23, 2023.

INTRODUCTION

Mycoplasma hominis and Ureaplasma species have been associated with a number of
urogenital infections and complications of pregnancy. They also cause various infections at
nongenital sites, especially in immunocompromised patients and neonates.

The clinical associations, diagnosis, and treatment of infections caused by M. hominis and
Ureaplasma species will be reviewed here.

Infections caused by other pathogenic mycoplasmas, specifically Mycoplasma pneumoniae

and Mycoplasma genitalium, are discussed separately. (See "Mycoplasma pneumoniae
infection in adults" and "Mycoplasma pneumoniae infection in children" and "Mycoplasma
genitalium infection".)

MICROBIOLOGY

Classification — The term "mycoplasma" is widely used to refer to any organism within
the class Mollicutes, which comprises eight genera (including Mycoplasma, Ureaplasma,
Acholeplasma, Anaeroplasma, Entomoplasma, Spiroplasma, and Asteroleplasma). Over
200 named Mycoplasma species exist. Fourteen Mycoplasma species, one Acholeplasma
species, and two Ureaplasma species have been isolated from humans on multiple
occasions; other species of animal origin have also been rarely detected in humans, usually
in immunocompromised patients, and are considered transient colonizers [1]. Only six
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species, five of which inhabit the genitourinary tract, are established human pathogens:

● M. hominis
● M. genitalium
● Mycoplasma fermentans
● Ureaplasma
• Ureaplasma urealyticum
• Ureaplasma parvum
● M. pneumoniae

Mycoplasma amphoriforme has been detected in the respiratory tracts of persons with
antibody deficiency and chronic bronchitis or bronchiectasis, but its true role as a human
pathogen has not been firmly established.

Characteristics — Mycoplasmas and ureaplasmas are the smallest free-living organisms.

Because they lack a cell wall, neither mycoplasmas nor ureaplasmas can be visualized by
Gram stain. In order to culture these organisms, specialized media containing animal
serum is required. (See 'Diagnosis' below.)

Mycoplasma species typically utilize glucose, arginine, or both as metabolic substrates, but
their metabolic properties cannot be used to distinguish them from one another.
Ureaplasmas are unique because of their ability to hydrolyze urea [1].

Pathogenesis — Although M. hominis and Ureaplasma spp normally exist in a state of

adherence to mucosal epithelial cells of the urogenital tracts, they can disseminate to
other sites and cause infection when there is a disruption of the mucosa (eg,
instrumentation, surgery, trauma) and/or an underlying immaturity in host defenses, such
as in the developing fetus or premature infant or in persons with immunocompromising
conditions, such as antibody deficiencies.

M. hominis and ureaplasmas have surface proteins that facilitate cytadherence [2].
Ureaplasmas can attach to erythrocytes, white blood cells, host mucosal cells, and even
spermatozoa. Ureaplasmas also produce an IgA protease to degrade immunoglobulins
and release ammonia through urealytic activity [1]. The microbiologic burden of
genitourinary mycoplasmas may be higher in HIV-infected individuals than in the HIV-
uninfected population, and immunosuppression, both cellular and humoral, may
contribute to disseminated disease in M. hominis- and Ureaplasma-infected patients [3,4].
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High-rate variation in cell surface protein antigens may facilitate evasion of the host
immune system and their persistence in invasive sites [1].

NORMAL GENITAL AND NEONATAL COLONIZATION

M. hominis and Ureaplasma spp are part of the normal genital flora of many sexually
experienced males and females [5]. The percentage of females with vaginal colonization
with these organisms increases after puberty in proportion to the number of lifetime
sexual partners [6]. Transient neonatal colonization also occurs.

The rate of colonization with M. hominis increases more rapidly with increasing sexual
experience in females than in males, suggesting that females are more susceptible to
colonization [7]. By adulthood, up to 80 percent of healthy females have Ureaplasma spp,
and 50 percent have M. hominis in their cervical or vaginal secretions [2]. Sexually active
men are also frequently asymptomatically colonized with M. hominis (25 percent in one
series of 99 males attending a clinic for sexually transmitted diseases) [8]. Genital
colonization may also be associated with lower socioeconomic status.

Newborns who are colonized with Mycoplasma or Ureaplasma spp are presumed to have
been exposed during passage through the birth canal, since colonization is less common
in infants born by caesarean section. Exposure in utero also occurs [1]. Colonization is
linked to lower birthweight and gestational age at birth [1].

Neonatal colonization is transient, and the proportion of infants colonized decreases

proportionately with postnatal age [9]. Infants more than three months of age are rarely
colonized. M. hominis is seldom recovered from prepubertal boys, whereas a small
percentage of prepubertal girls have been found to be colonized in some studies, even in
the absence of sexual activity or abuse.

GENITOURINARY DISEASE ASSOCIATIONS

Uncertain role in disease — M. hominis and Ureaplasma spp have been associated with
various genitourinary tract infections and complications of pregnancy. However, the
precise roles of Mycoplasma and Ureaplasma spp in such diseases have been difficult to
define accurately for the following reasons [2]:
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● Many healthy asymptomatic adults have genitourinary colonization with M. hominis
and Ureaplasma spp. (See 'Normal genital and neonatal colonization' above.)

● Mycoplasmas are rarely the only organisms isolated from a genitourinary specimen,
so it is sometimes difficult to distinguish whether they are causative pathogens or
simply co-isolates.

● Published studies on the pathogenicity of these organisms commonly have important

design limitations.

● Detection of these organisms has traditionally been difficult and complex. Although
newer nucleic acid amplification assays increase detection, they do not necessarily
contribute to establishing causality.

Vaginitis and bacterial vaginosis — Mollicutes do not cause inflammatory vulvovaginitis;

however, the bacterial load of M. hominis and, to some extent, Ureaplasma spp can be
much higher in females with bacterial vaginosis (BV) than in those without this condition. It
has therefore been suggested that M. hominis acts symbiotically with other BV pathogens
(eg, Gardnerella vaginalis) or possibly as a sole pathogen. The strong association of BV
with preterm birth also raises the possibility that these organisms might play an etiologic
role (see 'Intra-amniotic infection and adverse pregnancy outcomes' below). Nevertheless,
numerous studies performed over several years in various countries have yielded
conflicting results on the significance of M. hominis in BV, and detailed examination of the
vaginal microbiome has not yet provided a definitive answer [1,10].

Pelvic inflammatory disease — Although M. hominis is commonly found in the female

genitourinary tract, including among females with pelvic inflammatory disease (PID), the
role of M. hominis as a cause of PID remains controversial [11]. In one study, M. hominis
was isolated from 4 of 50 fluid samples taken directly from the fallopian tubes of females
with salpingitis versus none of 50 samples from females in the control group [12].
Significant rises or falls in antibody titers to M. hominis occurred in 9 of the 16 females
with salpingitis who had positive lower genital tract cultures for M. hominis. The presence
of infection in the absence of changes in antibody titers may reflect the localized nature of
salpingitis. However, M. hominis is rarely present in patients with salpingitis who do not
also have evidence of concurrent chlamydial or gonococcal infections or BV. As a result, its
role as a primary pathogen in salpingitis is still uncertain. (See "Pelvic inflammatory
disease: Pathogenesis, microbiology, and risk factors".)
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Ureaplasma spp have been isolated directly from affected fallopian tubes, but not in pure
culture. Moreover, negative results of serologic tests, fallopian tube cultures, and non-
human primate studies do not support a causal relationship for ureaplasmas as a sole
pathogen in PID [11].

Neither M. hominis nor Ureaplasma spp cause cervicitis. We are unaware of a significant
association between Ureaplasma spp and chronic pelvic pain syndrome.

Nongonococcal urethritis — Ureaplasma spp have been associated with nongonococcal

urethritis (NGU) in some studies [13], but not others [14,15]. In a meta-analysis of studies
involving 1507 NGU patients and 1223 controls, U. urealyticum was more common in
males with NGU [16]. In another study, U. urealyticum was significantly associated with
NGU only among males with fewer than 10 lifetime heterosexual partners [17]. The
authors postulated that adaptive immunity may attenuate the clinical manifestations of U.
urealyticum infection, so that older males with more exposure to this organism are less
likely to have symptoms of NGU from it. However, this hypothesis is not proven, and other
explanations are possible. Overall, U. urealyticum may be responsible for approximately 3
to 11 percent of NGU cases [18,19]. Other studies have suggested that U. parvum can
cause NGU, particularly when present in high numbers [18,20]. (See "Urethritis in adult
males", section on 'Nongonococcal urethritis'.)

Ureaplasmas have also been recovered from an epididymal aspirate from a patient
suffering from non-chlamydial, nongonococcal, acute epididymo-orchitis accompanied by
a specific antibody response [21], and they could be an infrequent cause of the disease.

There is no evidence that M. hominis causes NGU.

Urinary tract infection — M. hominis and Ureaplasma spp can frequently be recovered
from the lower genitourinary tract in males and females, but a causal relationship to
cystitis or prostatitis has not been established. M. hominis may be responsible for up to 5
percent of cases of acute pyelonephritis, particularly when prior instrumentation has been
performed or obstruction is present [11,22]. Ureaplasma spp have not been shown to
cause pyelonephritis. However, they produce urease, induce crystallization of struvite and
calcium phosphates in urine in vitro and calculi formation in animal models, and have been
found in urinary calculi of patients with infection-associated stones more frequently than
in those with metabolic-type stones; these features suggest a possible causal association
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with urinary tract infection [23].

In females, there is no evidence that M. hominis is a cause of the urethral syndrome, but
ureaplasmas may be involved [24].

PREGNANCY-RELATED INFECTIONS

Intra-amniotic infection and adverse pregnancy outcomes — M. hominis and

Ureaplasma spp are frequently found in the amniotic fluid of females with spontaneous
preterm labor, preterm premature rupture of membranes, premature rupture of
membranes at term, low birth weight, miscarriage, and stillbirth [25].

Some of these outcomes are the result of obvious infections, such as chorioamnionitis.
Isolation of Ureaplasma spp, but not M. hominis, from the chorioamnion has been
consistently associated with histological chorioamnionitis and is inversely related to
birthweight, even when adjusting for duration of labor, rupture of fetal membranes, and
presence of other bacteria. These organisms may invade the amniotic cavity when fetal
membranes are intact and initiate an inflammatory reaction in the absence of labor [26].
Ureaplasmas are among the most common microorganisms found in inflamed placentas
[1]. (See "Clinical chorioamnionitis", section on 'Microbiology'.)

Other associations with adverse pregnancy outcomes are more tenuous and may relate to
increased colonization rates and titers of the organisms [27,28]. As an example, in a study
of asymptomatic pregnant women who underwent amniocentesis during the second
trimester, detection of ureaplasmas by polymerase chain reaction (PCR) was associated
with a higher rate of subsequent preterm labor and preterm delivery [29]. Maternal
ureaplasma colonization has also been linked to low birth weight, neonatal
bronchopulmonary dysplasia (BPD), intraventricular hemorrhage, and necrotizing
enterocolitis, all of which are associated with prematurity [28,30].

Nevertheless, whether these organisms are causal remains controversial, since

colonization rates of ureaplasmas (35 to 90 percent) and M. hominis (5 to 80 percent) are
high in the normal pregnant female population. An additional unclear factor is the role
that other organisms, such as those that cause bacterial vaginosis, play in concert with
genital mycoplasmas leading to adverse pregnancy outcomes. While PCR-based diagnoses
have yielded more information on colonization rates, they have not shed much light on
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whether these organisms have an etiologic role.

The role of these organisms in female infertility is also highly controversial, and no causal
relationship has been shown convincingly. In one study, colonization rates were higher in
infertile females than in fertile ones, but did not appear to affect pregnancy rates with in
vitro fertilization [31].There also appears to be an association between M. hominis and
ureaplasma colonization rates and male infertility in China [32], but again, no causality has
been demonstrated.

Some studies have reported that treatment of pregnant women at risk for preterm labor
with antimicrobials effective against mycoplasmas and ureaplasmas is associated with
prolongation of gestation, and thus suggest that these organisms are responsible for
adverse pregnancy outcomes of pregnancy [33]. However, some of the antimicrobials
used, such as macrolides, are known to have significant anti-inflammatory effects, and
these effects, not the eradication of the organism, may possibly have played a role in the
improved outcomes with treatment.

Postpartum and postabortal bacteremia — Both M. hominis and Ureaplasma spp can be
detected in the bloodstream of females with postpartum or postabortal fever; M. hominis
is more common at approximately 10 percent of all cases. In one study, M. hominis was
recovered from blood cultures in 4 of 51 females (8 percent) with fever after abortion; in
contrast, blood cultures were negative for M. hominis in all control females who had a
recent abortion without fever and in all 102 normal pregnant controls [34]. Further
evidence in support of M. hominis infection was a fourfold rise in antibody titers in
approximately one-half of all females who had postabortal fever compared with only 2 of
53 controls who experienced abortion without fever. The higher frequency of antibody
production than blood culture recovery suggests that many patients with postabortal fever
develop nonbacteremic M. hominis infection. However, in another study, M. hominis was
isolated from the blood in 10 of 327 females (3 percent) who had blood cultures taken a
few minutes after delivery; none had fever, and all remained well without treatment [35].

NEONATAL DISEASE

Bacteremia — M. hominis and Ureaplasma spp can be isolated from the bloodstream of
newborn infants with bacteremia, particularly in preterm infants. One study found that 23

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percent of 457 consecutive neonates who were born between 23 and 32 weeks of
gestation had positive umbilical blood cultures for M. hominis and/or Ureaplasma spp [36].
Neonates with positive cultures more often had evidence of inflammatory response
syndrome, and their placentas more often had changes compatible with chorioamnionitis
than babies with negative blood cultures.

Bacteremia in neonates due to M. hominis or Ureaplasma spp can also occur in association
with other complications, such as meningitis or pneumonia [2].

Lung disease — M. hominis and Ureaplasma spp have been isolated in association with
congenital pneumonia in neonates [2,37]. M. hominis and Ureaplasma pneumonia usually
occur early in preterm infants but can also affect term neonates. (See "Neonatal
pneumonia".)

However, controversy remains about whether colonization with Ureaplasma spp

contributes to bronchopulmonary dysplasia (BPD), even more than 30 years after the first
reports associating ureaplasma colonization of the lower respiratory tracts of preterm
neonates with BPD. In a 2005 meta-analysis of 23 studies examining this possible
relationship, Ureaplasma colonization was associated with chronic lung infection
manifesting as long-term oxygen requirements and radiographic changes typical of BPD
[38]. A subsequent meta-analysis from 2014 that included 39 studies also found an
association between pulmonary colonization with Ureaplasma spp and development of
BPD in preterm infants at both 36 weeks postmenstrual age and at 28 days of life [39]. (See
"Bronchopulmonary dysplasia (BPD): Clinical features and diagnosis", section on
'Infection'.)

Meningoencephalitis — Neonatal meningoencephalitis in association with M. hominis or

Ureaplasma spp has been described; acquisition is presumed to have been in utero or via
passage through the birth canal [2,40]. The frequency of mycoplasma and ureaplasma
isolates from the central nervous system in neonates may be higher than is generally
appreciated. In one study, Mycoplasma cultures were performed on 100 preterm infants
who underwent lumbar puncture for suspected sepsis or meningitis: M. hominis was
isolated from the cerebrospinal fluid in five, and ureaplasmas were detected in eight [41].
Brain abscess caused by dual infection of M. hominis and Ureaplasma spp has also been
reported in a neonate [42].

Other complications — Abscesses, especially at scalp electrode monitoring sites, in

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neonates due to M. hominis have been described in case reports [43,44].

OTHER EXTRAGENITAL INFECTIONS

The portal of entry for the mycoplasmas and ureaplasmas that cause nongenitourinary
manifestations is almost always the genitourinary tract. Systemic infections caused by M.
hominis and Ureaplasma spp are most often noted in immunocompromised persons,
particularly those with congenital antibody deficiencies and malignancies, and in organ
transplant recipients. Extragenital infections can also occur following instrumentation of
the genitourinary tract or postpartum.

Arthritis and osteomyelitis — Joint infections have mainly been described in patients
with congenital immune defects such as hypogammaglobulinemia, patients with other
immunocompromising conditions (eg, solid organ transplant or lymphoma), and following
trauma [11,45-48]. M. hominis arthritis can also occur in females after childbirth [49]. A few
patients with prosthetic joint infections due to M. hominis have been described [47,50-53].
M. hominis and Ureaplasma spp have also been reported occasionally as causes of
osteomyelitis in immunosuppressed persons [54-56].

M. hominis arthritis is usually characterized by fever, leukocytosis, and a purulent joint

effusion with large numbers of polymorphonuclear cells but a negative Gram stain on
synovial fluid analysis. In a review of 16 cases of septic arthritis due to M. hominis, one-half
had undergone manipulation of the urinary tract before the onset of infection [47]. Delays
in diagnosis were common, ranging from 5 to 37 days. Ureaplasma arthritis may involve
one or multiple joints and, in some cases, has been associated with subcutaneous
abscesses [57].

Wound infections — M. hominis has been associated with infected pelvic hematoma and
infected cesarean wounds, as well as other surgical site infections following maxillofacial,
abdominal, vascular, cardiothoracic, neurosurgical, and plastic surgical procedures [58-64].
An increasing number of sternal wound infections due to M. hominis have been linked to
cardiac and lung transplantation [64]. In several cases, transmission of M. hominis from
donors of transplanted organs or tissue grafts has been supported by genomic sequencing
[65-67]. Ureaplasma spp have also been reported as a cause of postoperative sternal
wound infection in a few cases [68]. These are endogenous infections, and there is no

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evidence for nosocomial transmission. Sterilization of surgical instruments and disinfection

of surfaces kill these organisms.

In almost all cases, the clinical features of Mycoplasma or Ureaplasma wound infection are
nonspecific. Clues to their presence include the finding of abundant polymorphonuclear
leukocytes with a negative Gram stain, negative routine cultures, and a poor response to
beta-lactam or aminoglycoside therapy.

Bacteremia and endocarditis — M. hominis bacteremia has been demonstrated after

renal transplantation, trauma, and genitourinary manipulations. M. hominis is a rare cause
of prosthetic and native valve endocarditis in adults and children [69-71]. U. parvum was
also reported as a cause endocarditis [56,72]. In one of these case reports, U. parvum
caused native aortic valve endocarditis more than two years following orchitis and septic
arthritis caused by the same organism [72]. Because of difficulties in culturing
mycoplasmas and ureaplasmas, such patients present with culture-negative endocarditis.
(See "Clinical manifestations and evaluation of adults with suspected left-sided native valve
endocarditis", section on 'Culture-negative endocarditis'.)

Respiratory tract infection — The significance of M. hominis or Ureaplasma spp in

respiratory secretions of adults must be interpreted with caution, but in some instances,
they can clearly be of pathogenic significance. M. hominis has been isolated from
respiratory secretions in 1 to 3 percent of healthy persons, 8 percent of patients with
chronic respiratory complaints, and 14 percent of persons engaging in orogenital sex [73].
M. hominis can cause pharyngitis in volunteers whose nasopharynxes were experimentally
inoculated with M. hominis. However, attempts to implicate M. hominis as a cause of
naturally occurring pharyngitis have been unsuccessful [74].

One report described seven patients with intensive care unit (ICU)-acquired pneumonia
during a four-year period who had cultures from bronchoalveolar lavage or pleural fluid
that were positive for M. hominis [75]. This report and others describing the recovery of M.
hominis from lower respiratory tract specimens and/or empyema fluid suggest that M.
hominis is rarely capable of causing lower respiratory tract infection [75-77]. A case report
describes a lung transplant recipient with pneumonia and empyema whose bronchial
brush specimen and pleural fluid grew M. hominis [76]. Another case report documents M.
hominis as a cause of necrotizing pleuropneumonia in a previously healthy adolescent [78].
U. parvum has also been proven as a cause of pneumonia following lung transplantation

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[79].

Central nervous system disease — M. hominis infection has been associated with
nonfunctioning central nervous system (CNS) shunts [60], brain abscess [80,81], subdural
empyema [82], and meningitis [83]. U. urealyticum has been detected in the cerebrospinal
fluid (CSF) of an adult with meningitis, which developed 10 weeks after a complicated
kidney transplantation with organ rejection [84], and in a brain abscess of an adult with
congenital hypogammaglobulinemia [85]. Disseminated ureaplasma infection involving
CSF, kidney, pelvic abscess, skin, and subcutaneous tissue has also been reported in
association with hypogammaglobulinemia, underscoring the importance of an intact
immune system to prevent and control systemic infections caused by these organisms [86].

Post-transplant hyperammonemia — Hyperammonemia syndrome is a rare but

potentially fatal post-transplant complication primarily in lung transplant recipients. This
complication has also been demonstrated following hematopoietic cell transplantation.
The cause is not definitively known, but evidence suggests it is associated with Ureaplasma
spp and M. hominis infection. In some instances, infection is donor-derived. Any lung
transplant recipient with elevated ammonia levels should be evaluated for the presence of
these organisms using culture or nucleic acid amplification testing [79,87-90]. This is
discussed in further detail elsewhere. (See "Noninfectious complications following lung
transplantation", section on 'Hyperammonemia'.)

DIAGNOSIS

Clinical suspicion — Although infections with M. hominis or Ureaplasma spp are relatively
uncommon, their possibility should be considered in preterm neonates and
immunocompromised patients who present with evidence of the associated conditions
detailed above, particularly systemic infection (eg, sepsis), pneumonia, central nervous
system infection, or new-onset arthritis (see 'Neonatal disease' above and 'Other
extragenital infections' above). The suspicion for these organisms should be heightened
when initial microbiologic testing (eg, Gram stain and early routine culture) is negative or
uninformative or if the patient does not improve on antimicrobial therapy for more
common pathogens (eg, with beta-lactams). Similarly, they should be suspected in
immunocompromised patients with wound or surgical site infections (including sternal
wound infections) when routine cultures are negative.
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In such cases, microbiologic testing for M. hominis or Ureaplasma spp should be

performed (see 'Microbiologic confirmation' below). Nevertheless, given the difficulty in
obtaining a microbiological diagnosis, empiric antimicrobial therapy is often warranted
based on this clinical suspicion alone in vulnerable patients. (See 'Treatment' below.)

Unfortunately, many infections eventually proven to be caused by these organisms remain

undiagnosed for long periods of time, because specific microbiologic testing is either
unavailable in clinical laboratories or simply has not been requested. Despite the relative
infrequency of these organisms, it is important to maintain a high index of suspicion, since
the patients in whom these infections occur are at high risk for adverse outcomes.

Routine testing for M. hominis or Ureaplasma spp in patients with uncomplicated genital
tract disease is not warranted; it is uncertain whether detection of such organisms in the
genital tract reflects normal colonization or infection [91]. (See 'Uncertain role in disease'
above.)

Microbiologic confirmation — With the exception of M. hominis, which will sometimes

grow in routine bacteriologic media, special procedures and media are required for
detection of these organisms in clinical specimens. Both culture and nucleic acid
amplification tests can be used for their detection; the choice between them generally
depends on availability and turnaround time. Serology is not useful, since many healthy
people have underlying antibodies, and in the United States, there are no standardized
commercial serologic assays available.

Culture — M. hominis and ureaplasmas often grow in broth cultures within 24 to 48

hours. Most hospital microbiology laboratories do not perform cultures for these
organisms, but they are readily available through reference laboratories. The isolation of
M. hominis or Ureaplasma spp in any quantity from normally sterile body fluids or tissues
is diagnostic of infection, particularly in neonates or other immunosuppressed persons.
Susceptibility testing should be performed if these organisms are isolated on culture of
extragenital sites, but it is mainly limited to reference laboratories.

Appropriate clinical specimens (eg, blood, cerebrospinal fluid [CSF], synovial fluid, sputum)
depend on the clinical syndrome suspected. Ideally, they should be inoculated immediately
into broth culture media containing animal serum before they are allowed to dry. If this is
not available or if a delay in laboratory receipt or processing is anticipated, the specimen
can be collected in some type of universal transport medium or mycoplasma broth culture
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media that does not contain antibiotics that would be inhibitory [92]. Specimens in
transport media must be refrigerated or frozen prior to shipment, depending on the time
until they are expected to be received in a reference laboratory for processing.

Liquid and solid media used for culturing these organisms, such as 10B broth for
Ureaplasma spp and SP4 broth for Mycoplasma spp, have pH-sensitive dye indicators that
help distinguish the urea splitters (ureaplasmas) and ammonia metabolizers (M. hominis),
which turn media alkaline, from glucose metabolizers (M. pneumoniae), which turn media
acidic. Specimens should be subcultured onto SP4 agar plates for definitive identification
of M. hominis and onto A8 agar plates for Ureaplasma spp. Genital mycoplasma colonies
develop best when incubated in air plus 5% CO2 or under anaerobic conditions.

● M. hominis may take a week to develop discernible colonies. It can escape detection
using automated blood culture detection systems, such as BacT/ALERT [93], unless
cultures are routinely incubated for three to five days using special media and/or
blind subcultures are made from blood cultures [7]. M. hominis colonies look like a
"fried egg," having a denser center and paler outer zone. M. hominis can also show
up on routine bacterial media as pinpoint colonies that cannot be visualized on Gram
stain. An arginine-utilizing mycoplasma that produces fried-egg colonies on SP4 agar
within three to four days is most likely M. hominis, but a polymerase chain reaction
(PCR) assay is necessary for species confirmation, since commensal mycoplasmas
may behave in a similar manner.

● Ureaplasmas may grow in one to two days. They form tiny pinpoint colonies with a
brown granular appearance on A8 agar when viewed under a stereomicroscope.
Their appearance is sufficient for identification to genus level. Differentiation of
Ureaplasma spp requires testing by the PCR assay [94], but this is not necessary for
routine diagnostic purposes.

Nucleic acid-based tests (including PCR) — Nucleic acid-based tests, such as the PCR
assay, are more easily performed and generally more sensitive than culture methods and
can theoretically be completed in a single day [95]. However, they are not available in most
hospital diagnostic laboratories. In the United States, there are no Food and Drug
Administration-cleared nucleic acid-based assays for these organisms, although several
reference labs have developed and validated their own assays using a variety of gene
targets and techniques. Any specimen suitable for culture can also be tested with nucleic

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acid-based tests (eg, throat swabs, tracheal aspirates or sputum, pleural or synovial fluid,
tissue or bone, CSF).

Nucleic acid-based assays can help in assigning causality when material from sites not
ordinarily colonized (eg, joint fluid or tissue, heart valve tissue, CSF) are tested. However,
positive nucleic acid tests on specimens from sites that are frequently colonized with
multiple organisms (eg, genital tract) are less helpful and should not be considered
diagnostic unless other causes of infection have been ruled out.

TREATMENT

Indications — Patients should be treated for a Mycoplasma or Ureaplasma spp infection if

they have a compatible clinical syndrome with detection of Mycoplasma or Ureaplasma
spp from a normally sterile extragenital site, from lower respiratory tract specimens, or
from infected wound specimens. Immunocompromised patients who present with a
compatible clinical syndrome also warrant empiric treatment given the difficulty in
obtaining a timely microbiologic diagnosis. The clinical diagnosis is discussed elsewhere.
(See 'Clinical suspicion' above.)

Treatment is not warranted for patients who are found to be colonized with these
organisms but do not have clinical disease. For infections that are commonly
polymicrobial, such as pelvic inflammatory disease (PID), if M. hominis is one of several
organisms detected, it is reasonable to include coverage for the mycoplasmas as part of
the broader spectrum regimen. However, there is no definitive evidence that this affects
patient outcomes.

In vitro susceptibility — In vitro antimicrobial susceptibility testing has been standardized

for human mycoplasmas and ureaplasmas, and there are interpretive criteria for minimum
inhibitory concentrations (MICs) for several antimicrobial agents used for treatment of
infections caused by these organisms [96].

Acquired resistance to one or more classes of antimicrobial agents has been well
documented in M. hominis and Ureaplasma spp. The extent and frequency of resistance
varies according to geographic area, type of patient population, and previous exposure to
antimicrobial agents.

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Susceptibility testing results are usually not available when selecting an antibiotic regimen,
since treatment is often empiric or infections are detected by molecular tests. In vitro
susceptibility testing is available through reference laboratories and should be pursued
whenever there is treatment failure, in infections in immunocompromised patients, and for
extragenital infections in normally sterile sites.

Mycoplasma hominis — M. hominis is generally susceptible in vitro to the following

agents:

● Tetracyclines (eg, doxycycline) [97-99]. However, in some patient populations,

resistance has been reported in up to 15 to 40 percent [1,97,100]. Resistance results
from ribosomal protection due to the tetM transposon.

● Clindamycin [97-99].

● Fluoroquinolones (eg, levofloxacin and moxifloxacin) [101,102]. Naturally occurring

resistance caused by mutations in parC and parE in the chromosomal quinolone
resistance determining regions can occur in a small percentage of clinical isolates
[103]. In one French study, quinolone resistance was less than 3 percent between
2010 and 2015 [100]. Resistance can also be induced in vitro by increasing
concentrations of fluoroquinolones.

M. hominis is generally resistant in vitro to macrolides (14- and 15-membered agents such
as erythromycin, azithromycin, and clarithromycin), aminoglycosides, sulfonamide,
trimethoprim, and all beta-lactams [92].

Ureaplasma spp — Ureaplasma spp are generally susceptible to the following agents:

● Tetracyclines (eg, doxycycline) [97-99]. Resistance is fairly uncommon, occurring in

approximately 8 percent of clinical isolates from 2010 to 2015 in a French study [100].
In the United States, 33 to 45 percent of clinical isolates were reported to contain the
tetM transposon that confers resistance by ribosomal protection [1,104]. However, a
more recent study from the United States reported doxycycline resistance in only 1 of
202 U. parvum isolates [105].

● Macrolides (erythromycin, azithromycin, clarithromycin). Resistance due to mutations

in 23S ribosomal RNA or ribosomal proteins has been described and is associated
with treatment failures [87]. In the United States, such resistance remains uncommon
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<i>Mycoplasma hominis</i> and <i>Ureaplasma </i>infections

[104,105].

● Fluoroquinolones (eg, levofloxacin and moxifloxacin) [102]. Naturally occurring

resistance caused by mutations in parC and parE in the chromosomal quinolone
resistance-determining regions is known to occur in a small percentage of clinical
isolates [103]. In a study from the United States, levofloxacin resistance rate was 6
percent for U. parvum and 5 percent for U. urealyticum [105]. Resistance can also be
induced in vitro by increasing concentrations of fluoroquinolones.

Ureaplasma spp are generally resistant in vitro to clindamycin, aminoglycosides,

sulfonamides, trimethoprim, and all beta-lactams.

Regimen selection — The choice of drug, route of administration, dosage, and duration of
therapy depend on the type of patient (ie, neonate, child, or adult), clinical condition
(whether a urogenital infection or infection in a sterile site such as bloodstream or
cerebrospinal fluid [CSF]), type of host (normal or immunosuppressed), and severity of
infection.

Regimen selection is based primarily on an understanding of the in vitro susceptibility

patterns of these organisms, although susceptibility testing results have not been
extensively correlated with treatment outcomes beyond individual case reports. There are
no specific treatment guidelines issued by any professional or regulatory organization.
(See 'In vitro susceptibility' above.)

Neonatal infections — Clinical evidence informing the treatment of neonatal M. hominis

and Ureaplasma infections is limited to case reports or small case series.

Systemic neonatal infections caused by M. hominis are uncommon. The organism is

variably susceptible to clindamycin, doxycycline, and fluoroquinolones. Dosing of
clindamycin in newborn infants should be based on postmenstrual age. Experience with
doxycycline and fluoroquinolone use in premature infants is limited.

A positive Ureaplasma spp culture does not indicate need for therapy if the infant is
asymptomatic. Although in vitro efficacy against Ureaplasma spp is observed with
azithromycin, clarithromycin, and fluoroquinolones, a lack of benefit precludes
recommendations on treatment for preterm infants. Definitive evidence on efficacy of
antimicrobial agents in the treatment of central nervous system (CNS) Ureaplasma spp

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<i>Mycoplasma hominis</i> and <i>Ureaplasma </i>infections

infections in infants is also lacking. Sterility of CSF can occur without antimicrobial therapy
[106].

If treatment is provided for Ureaplasma spp, azithromycin (10 mg/kg intravenously [IV]
daily) is an option. An association exists between orally administered azithromycin and
pyloric stenosis in infants younger than six weeks of age. Infants treated with azithromycin
should be followed for signs and symptoms of pyloric stenosis. Erythromycin should be
avoided given its association with pyloric stenosis. Experience with doxycycline in
premature infants is limited. In one study of preterm infants, azithromycin was apparently
effective in eradication of ureaplasmas from the respiratory tract [2,107].

There are no specific guidelines, but the duration of antibiotic therapy depends on the type
of infection being treated and is generally 10 to 14 days.

Extragenital infections in other populations — Most extragenital infections occur in

adults with underlying immunocompromising conditions. We suggest a fluoroquinolone as
first-line therapy for extragenital M. hominis or Ureaplasma spp infections, based on
typical in vitro susceptibility and because the fluoroquinolones have the advantage of
being bactericidal. The preferred fluoroquinolones are moxifloxacin (400 mg orally or IV
once daily) and levofloxacin (500 mg orally or IV once daily). Doxycycline (200 mg loading
dose then 100 mg orally or IV twice daily) is an appropriate alternative agent. If possible,
directed regimen selection should be guided by in vitro susceptibility testing. (See 'Culture'
above.)

Although there is no clear evidence that combination therapy (eg, a fluoroquinolone plus
doxycycline) results in better outcomes than monotherapy, it has been described
[53,108,109] and is a reasonable approach in immunocompromised patients. In such
patients, particularly in those with hypogammaglobulinemia, M. hominis and Ureaplasma
spp have the capacity to produce destructive and progressive disease. Furthermore,
infections may be caused by resistant organisms, and combination therapy potentially
increases the likelihood of using an active agent pending susceptibility results.

In severe infections, immunosuppression should be reduced, if possible; patients with

hypogammaglobulinemia should receive replacement immune globulin. Some infections
(eg, bone and joint infections, deep wound infections) also warrant aggressive
debridement and drainage of infected or necrotic tissue.

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The duration of therapy varies with the severity of disease, the site of infection, the
immune status of the patient, and response to therapy. In some cases, such as with bone
infections, several weeks of therapy are warranted [47,50]. Some reports describe
administering antibiotics for up to a year [110].

Even with aggressive therapy, relapses are likely to occur. Repeat cultures of affected sites,
such as synovial fluid, may be necessary to monitor in vivo response to treatment.

Clinical data to support the use of fluoroquinolones are mainly from case reports and
series [111]. Moxifloxacin is more potent than levofloxacin in vitro, but there are no data to
demonstrate that it provides a more efficacious clinical or microbiologic outcome in vivo.
Doxycycline has also been used successfully, including in CNS and bone infections
[42,84,112].

Uncomplicated urogenital infection — If treatment is warranted for an uncomplicated

urogenital infection caused by M. hominis or Ureaplasma spp, doxycycline (100 mg orally
twice daily) is the drug of choice for nonpregnant adults and adolescents. Duration of
therapy is generally seven days for lower urogenital tract infection, whereas for more
extensive infections, such as PID, antibiotics are given for 14 days. We also offer treatment
to sexual partners regardless of symptoms because of the potential of sexual transmission.

Despite in vitro susceptibility, doxycycline or macrolide treatment of vaginal mycoplasmas

and ureaplasmas is not always successful. Furthermore, some populations have a risk of
acquired tetracycline resistance. In cases of treatment failure or resistance,
fluoroquinolones are another option.

For pregnant women and young children, clindamycin is appropriate for M. hominis
infections and a macrolide (such as azithromycin) is appropriate for Ureaplasma infections.
These are also appropriate alternative agents in nonpregnant adults or adolescents who
cannot take doxycycline.

Regimen selection for urogenital infection is based primarily on in vitro susceptibility

patterns (see 'In vitro susceptibility' above) and outcomes of clinical trials of
nongonococcal urethritis and other genital infections that have used doxycycline
successfully. (See "Urethritis in adult males", section on 'Nongonococcal urethritis'.)

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<i>Mycoplasma hominis</i> and <i>Ureaplasma </i>infections

SUMMARY AND RECOMMENDATIONS

● Microbiology – Mycoplasma hominis and Ureaplasma spp are small bacteria that
lack a cell wall and cannot be visualized by Gram stain. They are part of the normal
genital flora of sexually experienced individuals; transient neonatal colonization also
occurs. (See 'Microbiology' above and 'Normal genital and neonatal colonization'
above.)

● Associated genitourinary syndromes – These organisms have been associated with

various genitourinary tract infections (eg, pelvic inflammatory disease for M. hominis
and nongonococcal urethritis for Ureaplasma spp), as well as complications of
pregnancy, but their precise roles in some of these conditions have been difficult to
define. (See 'Genitourinary disease associations' above and 'Pregnancy-related
infections' above.)

● Populations at risk for extragenital infection – M. hominis and Ureaplasma can

cause severe infection in specific populations. Neonatal infections include
meningoencephalitis, bacteremia, and pneumonia, mainly in preterm infants. In
immunocompromised patients, severe systemic infections (eg, bacteremia and bone,
joint, pulmonary, and central nervous system infections) have also been described;
extragenital infections can also occur following trauma or instrumentation of the
genitourinary tract. (See 'Neonatal disease' above and 'Other extragenital infections'
above.)

● Clinical suspicion and diagnosis – Although relatively uncommon, M. hominis or

Ureaplasma spp infection should be suspected in preterm neonates and
immunocompromised patients with extragenital infections when initial microbiologic
testing is negative or if the patient does not improve on therapy for more common
pathogens. Both culture and nucleic acid amplification tests can be used for their
detection; if these organisms are isolated, susceptibility testing should be performed,
if available. (See 'Diagnosis' above.)

● Treatment

• Neonatal infection – For neonates, data on the treatment of M. hominis and

Ureaplasma spp infections are extremely limited. M. hominis is variably
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<i>Mycoplasma hominis</i> and <i>Ureaplasma </i>infections

susceptible to clindamycin, tetracyclines, and fluoroquinolones. Clindamycin

should be dosed according to postmenstrual age; experience with doxycycline and
fluoroquinolones in premature infants is limited. If treatment is warranted for
Ureaplasma spp, azithromycin is an option. (See 'Neonatal infections' above.)

• Extragenital infection in other populations – For extragenital M. hominis and

Ureaplasma spp infections in nonpregnant individuals, we suggest moxifloxacin or
levofloxacin (Grade 2C). Doxycycline is an appropriate alternative, although
resistance may be increasing; it is also reasonable to use combination therapy (eg,
moxifloxacin or levofloxacin plus doxycycline). Clinical data on the optimal
treatment of these organisms are limited; our preference for certain regimens are
based mainly on in vitro susceptibility data and safety in different populations.
(See 'Extragenital infections in other populations' above.)

• Genital infection – Routine testing for M. hominis or Ureaplasma spp in patients

with uncomplicated genital tract disease is not warranted. If these organisms are
detected in patients with a genitourinary syndrome (eg, nongonococcal urethritis
or pelvic inflammatory disease) and are thought to be the cause of the symptoms,
we suggest doxycycline (Grade 2C). (See 'Uncertain role in disease' above and
'Uncomplicated urogenital infection' above.)

ACKNOWLEDGMENT

The UpToDate editorial staff acknowledges Stephen G Baum, MD, who contributed to an
earlier version of this topic review.

REFERENCES

1. Waites KB, Katz B, Schelonka RL. Mycoplasmas and ureaplasmas as neonatal

pathogens. Clin Microbiol Rev 2005; 18:757.
2. Waites KB, Schelonka RL, Xiao L, et al. Congenital and opportunistic infections:
Ureaplasma species and Mycoplasma hominis. Semin Fetal Neonatal Med 2009;
14:190.
3. Redelinghuys MJ, Ehlers MM, Dreyer AW, et al. A cross-sectional study on the
relationship of age, gestational age and HIV infection to bacterial vaginosis and

- Page 20 of 29 -
<i>Mycoplasma hominis</i> and <i>Ureaplasma </i>infections

genital mycoplasma infection. BMJ Open 2015; 5:e008530.

4. Meyer RD, Clough W. Extragenital Mycoplasma hominis infections in adults: emphasis

on immunosuppression. Clin Infect Dis 1993; 17 Suppl 1:S243.
5. McCormack WM, Rosner B, Lee YH. Colonization with genital mycoplasmas in women.
Am J Epidemiol 1973; 97:240.
6. McCormack WM, Almeida PC, Bailey PE, et al. Sexual activity and vaginal colonization
with genital mycoplasmas. JAMA 1972; 221:1375.
7. Taylor-Robinson D, McCormack WM. The genital mycoplasmas (first of two parts). N
Engl J Med 1980; 302:1003.
8. Lee YH, Rosner B, Alpert S, et al. Clinical and microbiological investigation of men with
urethritis. J Infect Dis 1978; 138:798.
9. Foy HM, Kenny GE, Levinsohn EM, Grayston JT. Acquisition of mycoplasmata and T-
strains during infancy. J Infect Dis 1970; 121:579.
10. Taylor-Robinson D. Mollicutes in vaginal microbiology: Mycoplasma hominis,
Ureaplasma urealyticum, Ureaplasma parvum and Mycoplasma genitalium. Res
Microbiol 2017; 168:875.
11. Taylor-Robinson D. Infections due to species of Mycoplasma and Ureaplasma: an
update. Clin Infect Dis 1996; 23:671.
12. Mårdh PA, Weström L. Tubal and cervical cultures in acute salpingitis with special
reference to Mycoplasma hominis and T-strain mycoplasmas. Br J Vener Dis 1970;
46:179.
13. Povlsen K, Bjørnelius E, Lidbrink P, Lind I. Relationship of Ureaplasma urealyticum
biovar 2 to nongonococcal urethritis. Eur J Clin Microbiol Infect Dis 2002; 21:97.

14. Totten PA, Schwartz MA, Sjöström KE, et al. Association of Mycoplasma genitalium with
nongonococcal urethritis in heterosexual men. J Infect Dis 2001; 183:269.
15. Bradshaw CS, Tabrizi SN, Read TR, et al. Etiologies of nongonococcal urethritis:
bacteria, viruses, and the association with orogenital exposure. J Infect Dis 2006;
193:336.
16. Zhang N, Wang R, Li X, et al. Are Ureaplasma spp. a cause of nongonococcal urethritis?
A systematic review and meta-analysis. PLoS One 2014; 9:e113771.
17. Wetmore CM, Manhart LE, Lowens MS, et al. Ureaplasma urealyticum is associated

- Page 21 of 29 -
<i>Mycoplasma hominis</i> and <i>Ureaplasma </i>infections

with nongonococcal urethritis among men with fewer lifetime sexual partners: a case-
control study. J Infect Dis 2011; 204:1274.
18. Cox C, McKenna JP, Watt AP, Coyle PV. Ureaplasma parvum and Mycoplasma
genitalium are found to be significantly associated with microscopy-confirmed
urethritis in a routine genitourinary medicine setting. Int J STD AIDS 2016; 27:861.
19. Couldwell DL, Gidding HF, Freedman EV, et al. Ureaplasma urealyticum is significantly
associated with non-gonococcal urethritis in heterosexual Sydney men. Int J STD AIDS
2010; 21:337.
20. Deguchi T, Shimada Y, Horie K, et al. Bacterial loads of Ureaplasma parvum contribute
to the development of inflammatory responses in the male urethra. Int J STD AIDS
2015; 26:1035.
21. Jalil N, Doble A, Gilchrist C, Taylor-Robinson D. Infection of the epididymis by
Ureaplasma urealyticum. Genitourin Med 1988; 64:367.
22. Thomsen AC, Lindskov HO. Diagnosis of Mycoplasma hominis pyelonephritis by
demonstration of antibodies in urine. J Clin Microbiol 1979; 9:681.

23. Grenabo L, Hedelin H, Pettersson S. Urinary infection stones caused by Ureaplasma

urealyticum: a review. Scand J Infect Dis Suppl 1988; 53:46.

24. Stamm WE, Running K, Hale J, Holmes KK. Etiologic role of Mycoplasma hominis and
Ureaplasma urealyticum in women with the acute urethral syndrome. Sex Transm Dis
1983; 10:318.
25. Romero R, Garite TJ. Twenty percent of very preterm neonates (23-32 weeks of
gestation) are born with bacteremia caused by genital Mycoplasmas. Am J Obstet
Gynecol 2008; 198:1.
26. Cassell GH, Davis RO, Waites KB, et al. Isolation of Mycoplasma hominis and
Ureaplasma urealyticum from amniotic fluid at 16-20 weeks of gestation: potential
effect on outcome of pregnancy. Sex Transm Dis 1983; 10:294.
27. Capoccia R, Greub G, Baud D. Ureaplasma urealyticum, Mycoplasma hominis and
adverse pregnancy outcomes. Curr Opin Infect Dis 2013; 26:231.
28. Viscardi RM. Ureaplasma species: role in neonatal morbidities and outcomes. Arch Dis
Child Fetal Neonatal Ed 2014; 99:F87.
29. Gerber S, Vial Y, Hohlfeld P, Witkin SS. Detection of Ureaplasma urealyticum in second-
trimester amniotic fluid by polymerase chain reaction correlates with subsequent
- Page 22 of 29 -
<i>Mycoplasma hominis</i> and <i>Ureaplasma </i>infections

preterm labor and delivery. J Infect Dis 2003; 187:518.

30. Murtha AP, Edwards JM. The role of Mycoplasma and Ureaplasma in adverse
pregnancy outcomes. Obstet Gynecol Clin North Am 2014; 41:615.
31. Sleha R, Boštíková V, Hampl R, et al. Prevalence of Mycoplasma hominis and
Ureaplasma urealyticum in women undergoing an initial infertility evaluation.
Epidemiol Mikrobiol Imunol Fall; 65:232.
32. Huang C, Zhu HL, Xu KR, et al. Mycoplasma and ureaplasma infection and male
infertility: a systematic review and meta-analysis. Andrology 2015; 3:809.
33. Vouga M, Greub G, Prod'hom G, et al. Treatment of genital mycoplasma in colonized
pregnant women in late pregnancy is associated with a lower rate of premature
labour and neonatal complications. Clin Microbiol Infect 2014; 20:1074.
34. Harwick HJ, Purcell RH, Iuppa JB, Fekety FR Jr. Mycoplasma hominis and abortion. J
Infect Dis 1970; 121:260.
35. McCormack WM, Rosner B, Lee YH, et al. Isolation of genital mycoplasmas from blood
obtained shortly after vaginal delivery. Lancet 1975; 1:596.
36. Goldenberg RL, Andrews WW, Goepfert AR, et al. The Alabama Preterm Birth Study:
umbilical cord blood Ureaplasma urealyticum and Mycoplasma hominis cultures in
very preterm newborn infants. Am J Obstet Gynecol 2008; 198:43.e1.
37. Resch B, Gutmann C, Reiterer F, et al. Neonatal Ureaplasma urealyticum colonization
increases pulmonary and cerebral morbidity despite treatment with macrolide
antibiotics. Infection 2016; 44:323.
38. Schelonka RL, Katz B, Waites KB, Benjamin DK Jr. Critical appraisal of the role of
Ureaplasma in the development of bronchopulmonary dysplasia with metaanalytic
techniques. Pediatr Infect Dis J 2005; 24:1033.
39. Lowe J, Watkins WJ, Edwards MO, et al. Association between pulmonary ureaplasma
colonization and bronchopulmonary dysplasia in preterm infants: updated systematic
review and meta-analysis. Pediatr Infect Dis J 2014; 33:697.
40. Alonso-Vega C, Wauters N, Vermeylen D, et al. A fatal case of Mycoplasma hominis
meningoencephalitis in a full-term newborn. J Clin Microbiol 1997; 35:286.
41. Waites KB, Rudd PT, Crouse DT, et al. Chronic Ureaplasma urealyticum and
Mycoplasma hominis infections of central nervous system in preterm infants. Lancet
1988; 1:17.
- Page 23 of 29 -
<i>Mycoplasma hominis</i> and <i>Ureaplasma </i>infections

42. Rao RP, Ghanayem NS, Kaufman BA, et al. Mycoplasma hominis and Ureaplasma
species brain abscess in a neonate. Pediatr Infect Dis J 2002; 21:1083.
43. Abdel-Haq N, Asmar B, Brown W. Mycoplasma hominis scalp abscess in the newborn.
Pediatr Infect Dis J 2002; 21:1171.
44. Sacker I, Walker M, Brunell PA. Abscess in newborn infants caused by Mycoplasma.
Pediatrics 1970; 46:303.
45. Steuer A, Franz A, Furr PM, et al. Common variable immunodeficiency presenting as a
Mycoplasma hominis septic arthritis. J Infect 1996; 33:235.
46. McDonald MI, Moore JO, Harrelson JM, et al. Septic arthritis due to Mycoplasma
hominis. Arthritis Rheum 1983; 26:1044.
47. Luttrell LM, Kanj SS, Corey GR, et al. Mycoplasma hominis septic arthritis: two case
reports and review. Clin Infect Dis 1994; 19:1067.
48. George MD, Cardenas AM, Birnbaum BK, Gluckman SJ. Ureaplasma septic arthritis in
an immunosuppressed patient with juvenile idiopathic arthritis. J Clin Rheumatol 2015;
21:221.
49. Taylor-Robinson D, Thomas BJ, Furr PM, Keat AC. The association of Mycoplasma
hominis with arthritis. Sex Transm Dis 1983; 10:341.

50. Méchaï F, Le Moal G, Duchêne S, et al. Mycoplasma hominis osteitis in an

immunocompetent man. Eur J Clin Microbiol Infect Dis 2006; 25:715.
51. Roerdink RL, Douw CM, Leenders AC, et al. Bilateral periprosthetic joint infection with
Ureaplasma urealyticum in an immunocompromised patient. Infection 2016; 44:807.
52. Qiu HJ, Lu WP, Li M, et al. The infection of Mycoplasma hominis after total knee
replacement: Case report and literature review. Chin J Traumatol 2017; 20:243.
53. Xiang L, Lu B. Infection due to Mycoplasma hominis after left hip replacement: case
report and literature review. BMC Infect Dis 2019; 19:50.
54. Noska A, Nasr R, Williams DN. Closed trauma, Mycoplasma hominis osteomyelitis, and
the elusive diagnosis of Good's syndrome. BMJ Case Rep 2012; 2012.
55. Mohiuddin AA, Corren J, Harbeck RJ, et al. Ureaplasma urealyticum chronic
osteomyelitis in a patient with hypogammaglobulinemia. J Allergy Clin Immunol 1991;
87:104.
56. Frangogiannis NG, Cate TR. Endocarditis and Ureaplasma urealyticum osteomyelitis in

- Page 24 of 29 -
<i>Mycoplasma hominis</i> and <i>Ureaplasma </i>infections

a hypogammaglobulinemic patient. A case report and review of the literature. J Infect

1998; 37:181.
57. Gassiep I, Gore L, Dale JL, Playford EG. Ureaplasma urealyticum necrotizing soft tissue
infection. J Infect Chemother 2017; 23:830.
58. Ti TY, Dan M, Stemke GW, et al. Isolation of Mycoplasma hominis from the blood of
men with multiple trauma and fever. JAMA 1982; 247:60.
59. Cuchí E, Cherta I, Garau J. Mycoplasma hominis catheter-related infection in a patient
with multiple trauma. Clin Microbiol Infect 2000; 6:115.
60. Madoff S, Hooper DC. Nongenitourinary infections caused by Mycoplasma hominis in
adults. Rev Infect Dis 1988; 10:602.
61. Lee YH, Nersasian RR, Nguyen-Kim-Lan, et al. Wound infection with Mycoplasma
hominis. JAMA 1971; 218:252.
62. Mossad SB, Rehm SJ, Tomford JW, et al. Sternotomy infection with Mycoplasma
hominis: a cause of "culture negative" wound infection. J Cardiovasc Surg (Torino)
1996; 37:505.
63. Mori N, Takigawa A, Kagawa N, et al. Pelvic abscess due to Mycoplasma hominis
following caesarean section. JMM Case Rep 2016; 3:e005059.

64. Hopkins PM, Winlaw DS, Chhajed PN, et al. Mycoplasma hominis infection in heart and
lung transplantation. J Heart Lung Transplant 2002; 21:1225.
65. Sampath R, Patel R, Cunningham SA, et al. Cardiothoracic Transplant Recipient
Mycoplasma hominis: An Uncommon Infection with Probable Donor Transmission.
EBioMedicine 2017; 19:84.
66. Smibert OC, Wilson HL, Sohail A, et al. Donor-Derived Mycoplasma hominis and an
Apparent Cluster of M. hominis Cases in Solid Organ Transplant Recipients. Clin Infect
Dis 2017; 65:1504.
67. Novosad SA, Basavaraju SV, Annambhotla P, et al. Mycoplasma hominis Infections
Transmitted Through Amniotic Tissue Product. Clin Infect Dis 2017; 65:1152.
68. Walkty A, Lo E, Manickam K, et al. Ureaplasma parvum as a cause of sternal wound
infection. J Clin Microbiol 2009; 47:1976.
69. Blasco M, Torres L, Marco ML, et al. Prosthetic valve endocarditis caused by
Mycoplasma hominis. Eur J Clin Microbiol Infect Dis 2000; 19:638.

- Page 25 of 29 -
<i>Mycoplasma hominis</i> and <i>Ureaplasma </i>infections

70. Fenollar F, Gauduchon V, Casalta JP, et al. Mycoplasma endocarditis: two case reports
and a review. Clin Infect Dis 2004; 38:e21.
71. Dominguez SR, Littlehorn C, Nyquist AC. Mycoplasma hominis endocarditis in a child
with a complex congenital heart defect. Pediatr Infect Dis J 2006; 25:851.
72. Korytny A, Nasser R, Geffen Y, et al. Ureaplasma parvum causing life-threatening
disease in a susceptible patient. BMJ Case Rep 2017; 2017.
73. MUFSON MA, LUDWIG WM, PURCELL RH, et al. EXUDATIVE PHARYNGITIS FOLLOWING
EXPERIMENTAL MYCOPLASMA HOMINIS: TYPE 1 INFECTION. JAMA 1965; 192:1146.

74. Mufson MA. Mycoplasma hominis: a review of its role as a respiratory tract pathogen
of humans. Sex Transm Dis 1983; 10:335.
75. García C, Ugalde E, Monteagudo I, et al. Isolation of Mycoplasma hominis in critically
ill patients with pulmonary infections: clinical and microbiological analysis in an
intensive care unit. Intensive Care Med 2007; 33:143.
76. Lyon GM, Alspaugh JA, Meredith FT, et al. Mycoplasma hominis pneumonia
complicating bilateral lung transplantation: case report and review of the literature.
Chest 1997; 112:1428.
77. Vogel U, Lüneberg E, Kuse ER, et al. Extragenital Mycoplasma hominis infection in two
liver transplant recipients. Clin Infect Dis 1997; 24:512.
78. Pascual A, Perez MH, Jaton K, et al. Mycoplasma hominis necrotizing pleuropneumonia
in a previously healthy adolescent. BMC Infect Dis 2010; 10:335.
79. Fernandez R, Ratliff A, Crabb D, et al. Ureaplasma Transmitted From Donor Lungs Is
Pathogenic After Lung Transplantation. Ann Thorac Surg 2017; 103:670.
80. Bergin SM, Mendis SM, Young B, Binti Izharuddin E. Postoperative Mycoplasma
hominis brain abscess: keep it in mind! BMJ Case Rep 2017; 2017.
81. Kupila L, Rantakokko-Jalava K, Jalava J, et al. Brain abscess caused by Mycoplasma
hominis: a clinically recognizable entity? Eur J Neurol 2006; 13:550.
82. Chong JS, Tseung SY, Lam HS, et al. Successful treatment of multiple subdural
empyemata caused by Mycoplasma hominis in a newborn. Neonatology 2009; 95:179.

83. Hata A, Honda Y, Asada K, et al. Mycoplasma hominis meningitis in a neonate: case
report and review. J Infect 2008; 57:338.
84. Geissdörfer W, Sandner G, John S, et al. Ureaplasma urealyticum meningitis in an adult

- Page 26 of 29 -
<i>Mycoplasma hominis</i> and <i>Ureaplasma </i>infections

patient. J Clin Microbiol 2008; 46:1141.

85. Deetjen P, Maurer C, Rank A, et al. Brain abscess caused by Ureaplasma urealyticum in
an adult patient. J Clin Microbiol 2014; 52:695.
86. Cordtz J, Jensen JS. Disseminated Ureaplasma urealyticum infection in a hypo-
gammaglobulinaemic renal transplant patient. Scand J Infect Dis 2006; 38:1114.
87. Bharat A, Cunningham SA, Scott Budinger GR, et al. Disseminated Ureaplasma
infection as a cause of fatal hyperammonemia in humans. Sci Transl Med 2015;
7:284re3.
88. Wylam ME, Kennedy CC, Hernandez NM, et al. Fatal hyperammonaemia caused by
Mycoplasma hominis. Lancet 2013; 382:1956.
89. Graetz R, Meyer R, Shehab K, Katsanis E. Successful resolution of hyperammonemia
following hematopoietic cell transplantation with directed treatment of Ureaplasma
parvum infection. Transpl Infect Dis 2018; 20:e12839.
90. Nowbakht C, Edwards AR, Rodriguez-Buritica DF, et al. Two Cases of Fatal
Hyperammonemia Syndrome due to Mycoplasma hominis and Ureaplasma
urealyticum in Immunocompromised Patients Outside Lung Transplant Recipients.
Open Forum Infect Dis 2019; 6:ofz033.
91. Horner P, Donders G, Cusini M, et al. Should we be testing for urogenital Mycoplasma
hominis, Ureaplasma parvum and Ureaplasma urealyticum in men and women? - a
position statement from the European STI Guidelines Editorial Board. J Eur Acad
Dermatol Venereol 2018; 32:1845.
92. Waites KB, Taylor-Robinson D. Mycoplasma and Ureaplasma. In: Manual of Clinical Mic
robiology, 11th ed, Jorgensen J, Pfaller M, Carroll K, et al (Eds), ASM Press, Washington
DC 2015. p.1088.
93. Waites KB, Canupp KC. Evaluation of BacT/ALERT system for detection of Mycoplasma
hominis in simulated blood cultures. J Clin Microbiol 2001; 39:4328.
94. Xiao L, Glass JI, Paralanov V, et al. Detection and characterization of human
Ureaplasma species and serovars by real-time PCR. J Clin Microbiol 2010; 48:2715.
95. Waites KB, Xiao L, Paralanov V, et al. Molecular methods for the detection of
Mycoplasma and ureaplasma infections in humans: a paper from the 2011 William
Beaumont Hospital Symposium on molecular pathology. J Mol Diagn 2012; 14:437.
96. Clinical and Laboratory Standards Institute. M43-A: Methods for Antimicrobial Suscepti
- Page 27 of 29 -
<i>Mycoplasma hominis</i> and <i>Ureaplasma </i>infections

bility Testing for Human Mycoplasmas; Approved Guideline. October 2011. https://clsi.
org/media/1451/m43a_sample.pdf (Accessed on December 11, 2018).
97. Krausse R, Schubert S. In-vitro activities of tetracyclines, macrolides, fluoroquinolones
and clindamycin against Mycoplasma hominis and Ureaplasma ssp. isolated in
Germany over 20 years. Clin Microbiol Infect 2010; 16:1649.
98. Pónyai K, Mihalik N, Ostorházi E, et al. Incidence and antibiotic susceptibility of genital
mycoplasmas in sexually active individuals in Hungary. Eur J Clin Microbiol Infect Dis
2013; 32:1423.
99. Valentine-King MA, Brown MB. Antibacterial Resistance in Ureaplasma Species and
Mycoplasma hominis Isolates from Urine Cultures in College-Aged Females.
Antimicrob Agents Chemother 2017; 61.
100. Meygret A, Le Roy C, Renaudin H, et al. Tetracycline and fluoroquinolone resistance in
clinical Ureaplasma spp. and Mycoplasma hominis isolates in France between 2010
and 2015. J Antimicrob Chemother 2018; 73:2696.
101. Bebear CM, Bové JM, Bebear C, Renaudin J. Characterization of Mycoplasma hominis
mutations involved in resistance to fluoroquinolones. Antimicrob Agents Chemother
1997; 41:269.
102. Bébéar CM, de Barbeyrac B, Pereyre S, et al. Activity of moxifloxacin against the
urogenital mycoplasmas Ureaplasma spp., Mycoplasma hominis and Mycoplasma
genitalium and Chlamydia trachomatis. Clin Microbiol Infect 2008; 14:801.
103. Xiao L, Crabb DM, Duffy LB, et al. Chromosomal mutations responsible for
fluoroquinolone resistance in Ureaplasma species in the United States. Antimicrob
Agents Chemother 2012; 56:2780.
104. Xiao L, Crabb DM, Duffy LB, et al. Mutations in ribosomal proteins and ribosomal RNA
confer macrolide resistance in human Ureaplasma spp. Int J Antimicrob Agents 2011;
37:377.
105. Fernández J, Karau MJ, Cunningham SA, et al. Antimicrobial Susceptibility and Clonality
of Clinical Ureaplasma Isolates in the United States. Antimicrob Agents Chemother
2016; 60:4793.
106. American Academy of Pediatrics. Red Book: 2018 Report of the Committee on Infectio
us Diseases, 31st ed, Kimberlin DW, Brady MT, Jackson MA, Long SS (Eds), American Ac
ademy of Pediatrics, Itasca, IL 2018. p.867.

- Page 28 of 29 -
<i>Mycoplasma hominis</i> and <i>Ureaplasma </i>infections

107. Merchan LM, Hassan HE, Terrin ML, et al. Pharmacokinetics, microbial response, and
pulmonary outcomes of multidose intravenous azithromycin in preterm infants at risk
for Ureaplasma respiratory colonization. Antimicrob Agents Chemother 2015; 59:570.
108. Hagiya H, Yoshida H, Yamamoto N, et al. Mycoplasma hominis periaortic abscess
following heart-lung transplantation. Transpl Infect Dis 2017; 19.
109. Mian AN, Farney AC, Mendley SR. Mycoplasma hominis septic arthritis in a pediatric
renal transplant recipient: case report and review of the literature. Am J Transplant
2005; 5:183.
110. Myers PO, Khabiri E, Greub G, Kalangos A. Mycoplasma hominis mediastinitis after
acute aortic dissection repair. Interact Cardiovasc Thorac Surg 2010; 11:857.
111. Eilers E, Moter A, Bollmann R, et al. Intrarenal abscesses due to Ureaplasma
urealyticum in a transplanted kidney. J Clin Microbiol 2007; 45:1066.
112. Gerber L, Gaspert A, Braghetti A, et al. Ureaplasma and Mycoplasma in kidney
allograft recipients-A case series and review of the literature. Transpl Infect Dis 2018;
20:e12937.

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