Mycoplasma hominis, M. genitalium and Ureaplasma spp.

Authors: Sabine Pereyre, Pharm.D., Ph.D., Christiane Bebear, M.D.Cécile M. Bebear, M.D., Ph.D.

Authors (First Edition, 1998 and Second Edition, 2002): Christiane Bebear, M.D.Cécile M. Bebear, M.D., Ph.D. Michel Dupon, M.D.


The main structural characteristic of mycoplasmas is their lack of cell wall that makes them innately resistant to β-lactams and to all antibiotics, which target the cell wall. They are also characterized by smaller cellular and genomic sizes than other bacteria and are considered as the smallest organisms capable of autonomous replication. Mycoplasma genitalium represents the smallest bacterial genome totally sequenced with 580 kpb(21). The consequences of such characteristics are the lack of detection by light microscopy, and complex nutritional requirements. Indeed, they grow on acellular, but rich and complex media with amino acid precursors, serum and yeast extract supplements. Nucleic acid amplification testing (NAAT) techniques are required for very fastidious species such as M. genitalium.


Mycoplasmas are frequently present as commensals in the oropharynx or in the genital tract of healthy subjects. Of the 18 species found in humans, only a few are clearly pathogenic. M. salivarium and M. orale are the commensal species most commonly found in the oropharynx. M. pneumoniae (discussed elsewhere in the textbook) colonizes the lower respiratory tract and is clearly pathogenic. M. amphoriforme is the most recent human mycoplasma species to be recognized and has been detected in the lower respiratory tract of several immunocompromised persons (23). A possible pathogenic role had been proposed for M. fermentans and M. penetrans, genital mycoplasmas, both in immunocompetent and immunosuppressed patients, but without definitive argument (58). Of the seven mycoplasmas that have been detected in the genitourinary tract, only Ureaplasma urealyticum and U. parvum (referred to hereafter as Ureaplasma spp. ), M. hominis, and M. genitalium are clearly associated with disease. However, M. hominis and Ureaplasma spp. are frequently isolated from the lower urogenital tract of healthy adults, men and women. Colonization is linked to younger age, lower economic status, sexual activity with multiple partners, African-American ethnicity, hormonal status, and is greater among women during pregnancy (586263). M. hominiscould be found in the vagina in less than 10% of healthy women while Ureaplasma spp. could be found in up to 50% of them (62). The presence of M. genitalium in the genital tract of asymptomatic people has also been documented (10).

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Four genital mycoplasmas, M. hominisM. genitalium and Ureaplasma spp. have been associated with a large variety of illnesses but have been demonstrated as a cause only for a few clinical conditions (58).

M. hominis

M. hominis has been associated with various pathological conditions (Table 1). The most frequent are genital infections in women but not in men. M.  hominis is not responsible for cervicitis. It can be involved in pelvic inflammatory disease (PID) but PID are usually considered to be a multibacterial infection in which M. hominis is probably acting as a secondary agent (658). The exact proportion of cases of PID related to M. hominis infection is not known and is certainly lower than those due to Chlamydia trachomatisNeisseria gonorrhoeae or M. genitalium.  

M. hominis is one of the organisms that proliferate during the course of bacterial vaginosis, associated with Gardnerella vaginalisand anaerobes, but its contribution to the pathological process is unknown. The treatment of bacterial vaginosis, when indicated, is not specifically directed against M. hominis, but rather against other microorganisms. However the high concentration of M. hominis in that condition can lead to invasion of the endometrium and the upper genital tract. Several studies have reported that M. hominis can survive and replicate in Trichomonas vaginalis cells (16). In this symbiotic relationship between these two human pathogens, it was reported that the presence of M. hominis could enhance the virulence of infected T. vaginalisisolates (55). However, the infection of T. vaginalis by M. hominis is not associated with metronidazole resistance (9). Candidatus Mycoplasma girerdii, uncultived mycoplasma recently identified in the vaginal secretions of women infected with T. vaginalis, was alsoreported to be tightly associated with trichomonasis(20).

M. hominis is responsible for infections related to pregnancy. It has been isolated from the amniotic fluid of women with chorioamnionitis and there is strong evidence of involvement in post-partum or post-abortum fever (4263) generally secondary to endometritis. M. hominis as well as Ureaplasma spp. have  been found in blood cultures, respiratory specimens, and cerebrospinal fluid (CSF) of newborns resulting from in utero infections or mainly from vertical transmission  at birth (62). In many cases, no inflammatory signs can be found in the CSF and recovery does not require a specific treatment. However, in some cases, severe infections with clinical and biological signs of meningitis have been observed, mainly in premature newborns with low birth weight 63

M. hominis has also been associated with extragenital infections (4058). Its frequency is probably underestimated because it is not frequently detected in these specimens. However, it has been demonstrated as responsible for a number of cases including septic arthritis (31).  septicemia, osteitis, retroperitoneal abscesses and peritonitis, hematoma infection, vascular and catheter-related infections, sternal wound infections associated with mediastinitis after thoracic surgery, prosthetic valve endocarditis, pericarditis, brain abscesses, and pneumonia mainly by hematogenous spread (58). 

These types of infection appear to be linked to immunosuppression mainly hypogammaglobulinemia but immunocompetent patient can also be infected (3843).

Ureaplasma spp.

Two species have been found to cause human infections (Table 1), U. parvum and U. realyticum, the latter being more frequently associated with urogenital infections.

Ureaplasmaspp., particularly U. urealyticum, are causes of non-gonococcal urethritis (NGU) in men (58).  They play a minimal and uncertain role in prostatitis and epididymitis as well in cystitis, pyelonephritis and urinary calculi (58).Ureaplasma spp. can be found in the mucosal surfaces of the cervix or vagina of sexually mature asymptomatic women (6263). The vertical transmission rate varies from 18% to 88% according to studies. This rate is higher in low birth weight. Babies can be infected by intrauterine infection or intrapartum transmission (62). Ureaplasmas can cause placental inflammation and may invade the amniotic sac early in pregnancy in the presence of intact fetal membranes, causing persistent infection and adverse pregnancy outcome, including preterm labor, preterm premature rupture of membranes, and chorioamnionitis (2862). Ureaplasma spphave been isolatedfrom the blood of women with postpartum or postabortal fever. Maternal infection can lead to major neonatal complications such as pneumonia, bacteremia, and meningitis. The pulmonary colonization with Ureaplasma spp. was recently significantly associated with the development of bronchopulmonary dysplasia in preterm infants (30).

Ureaplasmas and mycoplasmas can be important pathogens in individuals with immunodeficiency. Ureaplasma spp. can cause invasive disease of the joints, especially in individuals with antibody deficiencies but non only (21825). There is also some evidence that Ureaplasma spp. are involved in reactive arthritis.

M. genitalium

M. genitalium is a sexually transmitted organism (3437). The urogenital tract is the primary site of M. genitalium infection but asymptomatic rectal carriage has been reported in men who have sex with men(7) and in asymptomatic women (25).  Pharyngeal carriage was not reported (25).

In the global population, the rate of M. genitalium infection ranges from 1 to 4% in men and from 1 to 6.4% in women (10).  Carriage may be asymptomatic (47).  M. genitalium carriage is higher in population at high risk of sexually transmitted infections (STI): the prevalence of M. genitalium infections ranges between 4% and 38% in STI testing centers (10). M. genitalium infections are significantly more frequent in HIV-positive men and women (41). Morever, a longitudinal study showed a greater than twofold independent increased risk of HIV-1 acquisition among Sub-Saharan African women infected with M. genitalium (3536).

M. genitalium is responsible for NGU in men independently of the presence of C. trachomatis and Ureaplasma spp(2632). It is responsible for 15-20% of NGU cases and is the second most common cause of NGU after C. trachomatisM. genitalium is also associated with approximately 30% of persistent or recurrent urethritis (325153) and may be associated with post-gonococcal urethritis, balanoposthitis, prostatitis and epididymitis (10) (Table 1).

In women, the pathogenic role of M. genitalium is less definitive than in men (Table 1). M. genitalium can be found in the vagina, cervix, and endometrium but M. genitalium infections are commonly asymptomatic. It can be detected in 10-30% of women with clinical cervicitis (25303133) making of M. genitalium the only human mycoplasma implicated in the genesis of mucopurulent cervicitis and urethritis. There was evidence for association of M. genitalium with PID (323753). One study also reported a substantial increase in risk for post-abortal PID among women with M. genitalium (5).

M. genitalium may cause female infertility, especially tubal infertility, but more studies are needed to confirm this finding (10).

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Laboratory diagnosis of mycoplasmal infections is mainly based on direct methods either by culture or NAAT according to the species and type of specimens (60). Except for M. pneumoniae infections, serological diagnosis is not indicated for other mycoplasma species. Mycoplasmas are extremely sensitive to adverse environmental conditions, particularly to drying and heat. Therefore, the use of a suitable transport system is essential to preserve specimen viability until cultures can be inoculated.

Culture is well adapted to species like Ureaplasma spp. and M. hominis, which can be isolated easily and rapidly from urogenital specimens leading to quantitative results and allowing susceptibility testing from isolates. Species identification requires the use of specific rich and complex mycoplasma agar medium that differ from one species to another. Many commercial growth media and diagnostic kits are available (37).  Only NAAT and mass spectrometry methods can differentiate U. urealyticumfrom U. parvum (45). It should be noticed that M. hominis can grow, giving tiny colonies, on standard bacteriologic media such as Columbia agar. Alternative non-culture based tests such as PCR can also be performed to increase the sensibility of detection if the specimen is from an extra-genital site or is a normally sterile body fluid or tissue.

Culture is not adapted for detection of the extremely fastidious M. genitalium species. The M. genitalium detection is obtained by NAAT testing, using either in-house PCR or commercially available diagnostic tests (1056).


Mechanisms of pathogenesis are mostly known for M. pneumoniae. However, adhesins have also been described in M. genitalium, a species phylogenetically close to M. pneumoniae. Like M. pneumoniaeM. genitalium cells harbor a tip terminal structure which mediates attachment to host cells. Spontaneous or in vitro mutants which lack expression of the cytadhesin MgPa lose the ability to hemagglutinate or adhere to cellular structures (6).  The peptide methionin superoxide dismutase MsrA, present in M. genitalium and Ureaplasma spp., is probably a virulence factor (1724). M. hominis adhesin families have been also described (2744). Depletion of arginine, production of ammonia and activity of membrane-bound enzymes phospholipase and aminopeptidase are associated with pathogenesis. In Ureaplasma spp, several iron transporters and the MBA protein, major antigen recognized during infection of humans, have also been proposed as virulence factors (24). 


General Considerations

To address the need for a standard method for performing in vitro susceptibility tests for human mycoplasmas and ureaplasmas, the Clinical and Laboratory Standards (CLSI) subcommittee on antimicrobial susceptibility testing of human mycoplasmas recently reported an international multilaboratory collaborative study. Media and consensus methods for the performance and quality control of antimicrobial testing of M. pneumoniaeM. hominis and U. urealyticum using broth microdilution and agar dilution techniques were standardized. Moreover, MIC breakpoints for selected antimicrobial agents have now been published by the CLSI (61). Susceptibility testing kits using the broth microdilution technique are currently sold in Europe. Some of these kits combine detection and identification in the same product.

Mycoplasma lack peptidoglycan and are thus resistant to all cell wall active antibiotics such as beta-lactams, fosfomycin and glycopeptide antibiotics. They are also resistant to rifampin, polymyxins, nalidixic acid, sulfonamides and trimethoprim.

The most common antimicrobials active against mycoplasmas are included in the three major drug classes: tetracyclines, macrolides-lincosamides-streptogramins-ketolides (MLSK group), and fluoroquinolones (57).  Some differences are observed according to the species, mainly for the macrolides-lincosamides-streptogramins-ketolides group, and acquired resistance has been described. These antibiotics also give high intracellular concentrations. This is of interest because several mycoplasma species such as M. hominis and M. genitalium localize and survive within the cells (12). Other classes of antimicrobials such as aminoglycosides and chloramphenicol sometimes demonstrate activity in vitro. However, due to their toxicity, they are normally not considered as suitable antimicrobial agents in humans except for the occasional use of chloramphenicol for the treatment of systemic infections in neonates caused by M. hominis or Ureaplasma spp. in the setting of antibiotic resistance or clinical failure with other agents (57). No study concerning the in vitro effect of combinations of drugs against mycoplasmas has been reported.

The in vitro susceptibility of M. hominisM. genitalium and Ureaplasma spp. is shown in Table 2.

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M. hominis and Ureaplasma spp.

M. hominis and Ureaplasma spp. are susceptible to tetracyclines but acquired resistance to tetracyclines has been reported. This resistance is associated with the acquisition of the tet(Mgene. It codes for the tet(M) protein which protects the ribosome from the action of tetracyclines (57).  It confers high-level resistance to all tetracyclines. Glycylcyclines such as tigecycline retain activity against M. hominis containing tet(M) but not Ureaplasma spp (57).  The prevalence of acquired tetracycline resistance among M. hominis and Ureaplasma spp. varies according to the country and the antimicrobial exposure of the population. It was reported to be 19% for M. hominis and 2% for Ureaplasma spp. in France between 1999 and 2002 (14). This low tetracycline resistance rate for Ureaplasma spp. was also reported in the UK and China with less than 5% of isolates being classified as resistant to tetracycline. However, surveillance from different regions in the USA between 2000 and 2004 showed that 45% of Ureaplasma spp. isolates were resistant to tetracyclines (57). 

Ureaplasma spp. are susceptible to macrolide and related antibiotics except lincosamides 57M. hominis is resistant to erythromycin and to all 14-membered macrolides (roxithromycin, clarithromycin, dirithromycin) and 15-membered macrolides (azithromycin), but sensitive to josamycin, a 16-membered macrolide. This intrinsic resistance is associated with a guanine to adenine transition at position 2057 (Escherichia coli numbering) in the domain V of 23S rRNA, the molecular target of macrolides (57). Only a very few cases of acquired resistance to MLSK have been reported for clinical isolates of M. hominis and Ureaplasmaspp . The prevalence of acquired macrolide resistance is unknown but probably very low, except perhaps in China where recent reports suggest that macrolide resistance may be frequent, presumably as a result of selective pressure because of widespread macrolide use (57). 

Ureaplasmas and M. hominis are intrinsically susceptible to fluoroquinolones; however, newer fluoroquinolones such as levofloxacin and moxifloxacin are more active in vitro against human mycoplasmas than older ones such as ofloxacin and ciprofloxacin (Table 2). Mutations in the target genes gyrA and gyrB of DNA gyrase and parC of topoisomerase IV are the main mechanisms conferring fluoroquinolone resistance in human mycoplasmas and ureaplasmas. Resistant clinical isolates of M. hominis and Ureaplasma spp. show cross-resistance to all fluoroquinolones. The level of resistance depends on the number and positions of the mutations. The newest fluoroquinolones like moxifloxacin remain most effective against the mutants although they loose their bactericidal activity in vitro (57). 

The prevalence of fluoroquinolone resistance in genital mycoplasmas is unknown but is certainly very low, estimated at less than 1% for Ureaplasma spp. in France in the 2000’s (3). However, as these drugs have been used much more extensively over the past years, cases of significant infections caused by fluoroquinolone-resistant M. hominis or Ureaplasma spp. are being reported, especially in persons who have previously received fluoroquinolones and those who are immunosuppressed.

M. genitalium

M. genitalium is susceptible to MLSK, levofloxacin and moxifloxacin. Tetracyclines are also potent in vitro but many therapeutic failures are reported even though there is no documented specific acquired resistance (10). Macrolide resistant clinical isolates of M. genitalium were reported a few years ago (8) and are now spreading in several countries. All isolates contained a point mutation at position 2058 or 2059 (E. coli numbering) in the domain V of the 23S rRNA (57).  The prevalence of macrolide resistance in M. genitalium was recently reported to be 14% in France (54), but is rising up to 40% in Denmark, Australia and UK (464952).  Fluoroquinolone resistance-associated mutations were first genetically demonstrated by PCR-based assays on M. genitalium-positive urine of men with NGU treated with levofloxacin (15).  Moxifloxacin treatment failures have now been reported (11). Mutations potentially associated with fluoroquinolone resistance were reported in parC or gyrA genes in up to 15% of clinical specimens from patients attending sexual health clinics in Sydney (52).

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Drugs of Choice

Oral tetracyclines have historically been the drugs of choice for use against urogenital and systemic infections due to M. hominisand Ureaplasma spp. in adults. However, in locations and patient populations where tetracycline resistance or treatment failures are common, other drugs such as fluoroquinolones should be considered guided by in vitro susceptibility data when possible. Newer fluoroquinolones like levofloxacin and moxifloxacin should be preferred to older ones. Clindamycin is an alternative treatment for M. hominis whereas macrolides can be used against ureaplasmas.

Some infections may be treated by a single antibiotic as it is the case for acute NGU. However, combination of drugs is indicated for polymicrobial infections such as PID (64). In other cases such as severe M. hominis infections occurring in immunocompromised patients, combination of drugs usually active against the mycoplasmas (such as clindamycin and doxycycline or a fluoroquinolone and doxycycline) have been recommended. In those cases, guidelines for optimal therapy remain to be established. Current therapeutic considerations are based only upon case reports.

Non-gonococcal urethritis and cervicitis: The recommended regimens for the treatment of NGU includes azithromycin 1 g orally in a single dose or doxycycline 100 mg orally twice a day for seven days (64). Both regimens are active against C. trachomatisand Ureaplasma spp. responsible of NGU but treatment failures with tetracyclines are reported in about 70% of cases of M. genitalium NGU without any documented resistance  (10). The 1 g single dose of azithromycin was significantly more effective against M. genitalium than doxycycline in randomized trials (3950) and is preferred over doxycycline. However, resistance to azithromycin is rapidly emerging and single dose azithromycin therapy may select for resistance. The median cure rate was only 40% in the most recent trial (33).  A longer course of azithromycin (500 mg once plus 250 mg daily for 4 days) may be superior to single dose regimen and should be used as the first line-treatment for M. genitalium NGU as it may prevent the development of resistance (10). However, patients failing the 1 g azithromycin regimen generally do not benefit from retreatment with the extended dose regimen. Moxifloxacin 400 mg for 7 to 10 days has been successfully used to treat M. genitalium treatment failures with cure rates of 100% in a small number of cases(10). However, moxifloxacin treatment failures were recently reported in Australia and were associated with the presence of fluoroquinolone resistance-associated mutations in gyrA and parCgenes (411).  A few cases of moxifloxacin failures were successfuly cured with pristinamycin (4).

Pelvic Inflammatory Disease: The treatment of PID, a polymicrobial condition, must be directed against several pathogens including C. trachomatisN. gonorrhoeaeM. hominis, Gram negative aerobes and anaerobes. Several antibiotic combinations can be used. All include an antibiotic active against M. hominis, doxycycline 100 mg every 12 hours or clindamycin 900 mg every 8 hours (64). Treatment should be reevaluated 72 hours after initiation and total duration is usually 14 days. Currently recommended PID treatment regimens are based on antibiotics that are not effective against M. genitalium, thus M. genitaliummay be considered in cases of treatment failure. When M. genitalium is detected, a regimen of moxifloxacin 400 mg/day for 14 days has been effective in eradicating the bacteria (48).

Post-partum or Post-abortum Fever: Some patients will recover uneventfully without antibiotic treatment. Specific antibiotic therapy against M. hominis or Ureaplasma spp. is indicated only in circumstances such as persistent fever despite beta-lactam antibiotic therapy or if M. hominis has been isolated at the site of infection. Doxycycline is the first choice, while a 16-membered macrolide or a fluoroquinolone can be used if resistance is suspected or documented.

Neonatal Infections: The treatment of mycoplasma infections in newborns is a very difficult problem because the antibiotics potentially active against mycoplasmas such as tetracyclines, fluoroquinolones or chloramphenicol are contraindicated in newborns and no treatment guidelines for neonatal infections with genital mycoplasmas are available. However, in cases of very severe infections, such as meningitis due to M. hominis or Ureaplasma spp., parenteral tetracyclines have been used most often despite contraindications at a dosage of 2-4 mg/kg/day for 10-14 days (59).  Erythromycin or other macrolides for Ureaplasmaspp., clindamycin for M. hominis, or chloramphenicol for either species are alternatives. No single drug has been successful in every instance in eradication of these organisms from CSF of neonates. Overall, treatment for neonates are the same as for urogenital and systemic mycoplasmal infections in adults with appropriate dosage modifications based on weight with a minimum of 10-14 days of therapy (59).

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Special Situations

For wound infections or abscesses, antimicrobial agents such as doxycycline, clindamycin, or fluoroquinolones should be given for at least two weeks. Surgical debridement and drainage of purulent collections may also be necessary.

Joint or bone infection requires prolonged treatment with doxycycline, clindamycin or fluoroquinolones (218). Duration of therapy should last weeks to several months. Replacement of bone prosthesis may be warranted. Fluoroquinolones have a good bone penetration.

For endocarditis, the recognition of mycoplasmal endocarditis is important because beta-lactam and aminoglycoside antibiotics, which are usually used in the treatment of endocarditis, are not effective against mycoplasmas. A few cases of endocarditis due to M. hominis were successfully treated with doxycycline during several weeks (19). 

The optimal treatment is poorly defined for brain abscesses and meningitis. Several regimens have been suggested, mostly containing doxycycline. Clarithromycin, clindamycin, moxifloxacin or chloramphenicol were occasionally included (1132229).

Extragenital or respiratory infections caused by genital mycoplasmas occur often in immunocompromised patients. In these patients the risk of multidrug-resistant mycoplasmas is higher, leading to the necessity of in vitro susceptibility testing of these microorganisms. In hypogammaglobulinemic patients, administration of immunoglobulin may be useful. Discontinuation or reduction of immunosuppressive drugs might also be useful.


The method of administration of the treatment and its duration will depend on the location and the severity of the infection. Since tetracyclines and macrolides have only bacteriostatic activity against mycoplasmas, the course of the treatment must be sufficiently long. Clinical improvement is the first element and major criterion for evaluation. Cultures that are negative for mycoplasmas are a valid criterion only for normally sterile sites.   In addition, in case of M. genitalium infections, management of sex partners should follow guidelines of patients with NGU or cervicitis. Partner testing and treatment of identified infections should be considered.


No vaccines are available for the prevention of mycoplasma infections.


A major problem concerning genital mycoplasmas is to determine whether they are responsible of the infection. For instance, isolation of M. hominis may only represent colonization of the lower genital tract of women or the respiratory tract of neonates. When the organism is isolated from a normally sterile site, its presence is more likely related to an infection. M. genitalium is now recognized a cause of sexually transmitted infection; however because of a lack of readily available diagnostic tests, there are no clear testing recommendations and no specific guidance on treatment for M. genitalium infection to date.

A high index of suspicion for mycoplasma is important. Clinicians should be aware of the possibility of mycoplasma infections in some specific situations such as PID, infections related to pregnancy, neonatal infections in premature low-birth weight newborns, wound infections after thoracic or abdominal surgery, joint infections in patients with prostheses or various infections in immunosuppressed patients. Failure of beta-lactam antibiotic therapy may be a useful clue.

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Table 1. Relationship between urogenital mycoplasmas and various clinical presentations, adapted from (10).

Disease M. hominis Ureaplasma spp. M. genitalium
Genital infections in men      
Acute NGU - + +
Chronic NGU - +/- +
Post-gonococcal urethritis - - +
Balanoposthitis - - +/-
Epididymitis, prostatitis - +/- +/-
Gynecological infections      
Bacterial vaginosis + +/- +/-
Cervicitis - - +
Urethritis - + +
Endometritis + - +
Salpingitis + - +
Pregnancy related disorders      
Chorioamnionitis +/- + ?
Post-partum fever + + ?
Ectopic pregnancy - - ?
Spontaneous abortion +/- +/- +/-
Premature delivery - + +/-
Tubular infertility - +/- +/-
Neonatal infections + + ?
Extragenital infections      
Septic arthritis + + +
Reactive arthritis - + +
Other localizations + + ?

+ = proved relationship or cause; +/- = non-proved relationship; - = no documented relationship; 
? = not determined; NGU = non gonococcal urethritis

Table 2. MIC Ranges (µg/ml) for various antimicrobials against genital mycoplasmas*

Antibiotics M. genitalium M. hominis Ureaplasma spp.
Doxycycline ≤0.01-0.3 0.1-2 0.02-1
Minocycline ≤0.01-0.2 0.03-1 0.06-1
 MLS group      
Erythromycin ≤0.01 32->1 000 0.02-16
Roxithromycin <0.01 >16 0.1-2
Clarithromycin ≤0.01-0.06 16->256 ≤0.004-2
Azithromycin ≤0.01-0.03 4->64 0.06-4
Josamycin 0.01-0.02 0.05-2 0.03-4
Clindamycin 0.2-1 ≤0.008-2 0.2-64
Pristinamycin ≤0.01-0.02 0.1-0.5 0.1-1
Quinupristin/ Dalfopristin 0.05 0.03-2 0.05-0.5
Telithromycin ≤0.015 2-32 ≤0.015-0.25
Solithromycin ≤0.000000063-0.000125 0.002-0.008 0.002-0.063
Ciprofloxacin 2 0.1-4 0.1-16
Ofloxacin 1-2 0.1-4 0.2-4
Levofloxacin 0.5-1 0.1-2 0.2-2
Moxifloxacin 0.03-0.06 0.06-0.125 0.125-1
Other agents      
Chloramphenicol 0.5-25 4225 0.4-8
Gentamicin ND 2-16 0.1-13

*Data were compiled from published studies in which different methods were used (57).

**Susceptible strains. ND, not determined.

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