Acute Non-gonococcal Urethritis Research Articles

Evaluation of Clinical, Gram Stain, and Microbiological Cure Outcomes in Men Receiving Azithromycin for Acute Nongonococcal Urethritis: Discordant Cures Are Associated With Mycoplasma genitalium Infection.

In men with nongonococcal urethritis (NGU), clinicians and patients rely on clinical cure to guide the need for additional testing/treatment and when to resume sex, respectively; however, discordant clinical and microbiological cure outcomes do occur. How accurately clinical cure reflects microbiological cure in specific sexually transmitted infections (STIs) is unclear. Men with NGU were tested for Neisseria gonorrhoeae, Chlamydia trachomatis (CT), Mycoplasma genitalium (MG), Trichomonas vaginalis, urethrotropic Neisseria meningitidis ST-11 clade strains, and Ureaplasma urealyticum (UU). Men received azithromycin 1 g and returned for a 1-month test-of-cure visit. In MG infections, we evaluated for the presence of macrolide resistance-mediating mutations (MRMs) and investigated alternate hypotheses for microbiological treatment failure using in situ shotgun metagenomic sequencing, phylogenetic analysis, multilocus sequence typing analyses, and quantitative PCR. Of 280 men with NGU, 121 were included in this analysis. In the monoinfection group, 52 had CT, 16 had MG, 7 had UU, 10 had mixed infection, and 36 men had idiopathic NGU. Clinical cure rates were 85% for CT, 100% for UU, 50% for MG, and 67% for idiopathic NGU. Clinical cure accurately predicted microbiological cure for all STIs, except MG. Discordant results were significantly associated with MG-NGU and predominantly reflected microbiological failure in men with clinical cure. Mycoplasma genitalium MRMs, but not MG load or strain, were strongly associated with microbiological failure. In azithromycin-treated NGU, clinical cure predicts microbiological cure for all STIs, except MG. Nongonococcal urethritis management should include MG testing and confirmation of microbiological cure in azithromycin-treated MG-NGU when MRM testing is unavailable.

Urethritis-associated Pathogens in Urine from Men with Non-gonococcal Urethritis: A Case-control Study.

The aetiology of non-gonococcal urethritis (NGU) remains unexplained in 30-40% of patients. Urine samples from men attending Swedish sexually transmitted disease clinics were examined by species-specific quantitative PCRs for Chlamydia trachomatis, Mycoplasma genitalium, Trichomonas vaginalis, Ureaplasma urealyticum, U. parvum, adenovirus, herpes simplex virus, Neisseria meningitidis, Haemophilus influenzae, Moraxella catarrhalis and Streptococcus pneumoniae. A total of 187 men with acute NGU (symptoms ≤ 30 days) and 24 with chronic NGU (symptoms < 30 days) were cases, and 73 men without NGU were controls. Number of lifetime sexual partners was negatively associated with U. urealyticum bacterial load. C. trachomatis and M. genitalium were associated with NGU, as was U. urealyticum, with bacterial loads ≥ 1.3 × 103 genome equivalents/ml urine. Virus and H. influenzae might explain a few NGU cases, but the aetiology in at least 24% of patients with acute NGU was unexplained. In multivariate analysis, detection of U. urealyticum was significantly more common in acute NGU (20%) compared with controls (11%).

Usefulness of quantifying leukocytes in first-voided urine to predict positivity for Chlamydia trachomatis in asymptomatic men at high risk for chlamydial infection

Chlamydia trachomatis causes acute non-gonococcal urethritis, but some infected men are asymptomatic. We examined leukocytes in uncentrifuged first-voided urine (FVU) from asymptomatic men at high risk for chlamydial infection by automated urine particle analyzers to assess whether the quantification of urinary leukocytes could predict chlamydial infection in these men. We enrolled 209 asymptomatic men, whose female sexual partners had been diagnosed as having a genital chlamydial infection. Their FVU specimens were examined for quantification of leukocytes with automated urine particle analyzers and tested for Neisseria gonorrhoeae, C. trachomatis, Mycoplasma genitalium, Mycoplasma hominis, Ureaplasma parvum, and Ureaplasma urealyticum by nucleotide acid amplification tests. Eleven men positive for N. gonorrhoeae or M. genitalium were excluded from further analysis. In the remaining 198 men, 84 positive for C. trachomatis (42.4%) had 1.8-1666.9 white blood cells (WBCs)/μl (median, 43.3 WBCs/μl) in their FVU, whereas 114 negative for C. trachomatis had 0.1-1378 WBCs/μl (median, 4.8 WBCs/μl). A receiver operating characteristic (ROC) curve was constructed to examine the sensitivity and specificity of leukocytes counts for predicting chlamydial infection. A cut-off point of leukocyte counts of 12.5 WBCs/μl was determined from the ROC curve, resulting in a sensitivity of 86.9% and specificity of 88.6% for predicting chlamydial infection. Leukocyte quantification in FVU by automated urine particle analyzers showed good performance in predicting the positivity and negativity for chlamydial infection in asymptomatic men. This test could potentially develop into a relevant tool for preselecting asymptomatic men prior to C. trachomatis screening.

How to manage the chronic pelvic pain syndrome in men presenting to sexual health services

Chronic pelvic pain syndrome (CPPS) in men is an important and common condition in genitourinary medicine (GUM) and other sexual health services. It has a lifetime prevalence of 2%–14%.1–4 The...

Urethral inflammation in male chimpanzees caused by ureaplasmas and Chlamydia trachomatis

Specimens from men with acute non-gonococcal urethritis were tested to determine their microbial content and then given intra-urethrally to male chimpanzees. Two animals received ureaplasmas only and one became infected. The second did so when given a different strain. Both developed a polymorphonuclear leukocyte (PMNL) response. Two chimpanzees received a mixture of ureaplasmas and Chlamydia trachomatis and there was a suggestion that the ureaplasmas delayed or suppressed the chlamydial response. The latter, that is urethral infection with a pronounced PMNL response, was most clearly seen in a chimpanzee given C. trachomatis only. No inflammation was detected in two chimpanzees acting as controls. Three of five chimpanzees given ureaplasmas genitally, and one that had them endogenously, had them transiently in the oropharynx about 2 weeks later. The occurrence of ureaplasmas in the conjunctiva of three chimpanzees inoculated at this site was also transient and without inflammation. The possibility that Mycoplasma genitalium might have been in the inocula and caused urethral inflammation was discounted largely because no animal had antibody to this mycoplasma.

Antimicrobial chemotherapy of Mycoplasma genitalium-positive non-gonococcal urethritis

Mycoplasma genitalium is an important pathogen of acute non-gonococcal urethritis (NGU) in men and plays a significant role in persistent or recurrent NGU. In the management of patients with M. genitalium-positive NGU, eradication of the mycoplasma from the urethra is necessary to prevent persistent or recurrent NGU. Therefore, M. genitalium should be considered for antimicrobial chemotherapy of NGU. This article reviews the in vitro antimicrobial activities of antibiotics against M. genitalium and the efficacies of various antibiotic regimens against M. genitalium-positive NGU, including the doxycycline and azithromycin regimens recommended as first-line treatments for NGU in the guidelines. Selection of macrolide-resistant M. genitalium by treatment with the single-dose regimen of 1-g azithromycin and mechanisms of macrolide resistance in M. genitalium are discussed. The effectiveness of the moxifloxacin regimen against persistent or recurrent NGU, unsuccessfully treated with azithromycin and/or doxycycline regimens, is emphasized.

Association of Mycoplasma genitalium with balanoposthitis in men with non-gonococcal urethritis

ObjectiveTo determine whether Mycoplasma genitalium is associated with balanitis and/or posthitis in a previous study of the role of M genitalium in men with acute non-gonococcal urethritis (NGU).MethodsIn a previous...

2009 European Guideline on the Management of Male Non-gonococcal Urethritis

Urethritis, or inflammation of the urethra, in men is characterized by discharge and/or urethral symptoms such as dysuria or urethral itching, but may be asymptomatic. Urethritis is mainly due to sexually transmitted pathogens. The diagnosis of urethritis is confirmed by demonstrating an excess number of polymorphonuclear leukocytes (PMNLs) in the anterior urethra. This is usually assessed using a urethral smear, but a first-pass urine (FPU) specimen can also be used. Urethritis is described as either gonococcal, when Neisseria gonorrhoeae is detected, or non-gonococcal urethritis (NGU), when it is not. Mucopurulent cervicitis is the female equivalent of male NGU with approximately 40% of cases being due to infection with Chlamydia trachomatis, although female NGU due to C. trachomatis and Mycoplasma genitalium has been reported. There are a number of uncertainties with NGU. There is significant inter-observer and intra-observer error in performing and reading urethral slides and counting PMNLs, especially in samples with low-grade inflammation. In many men with urethritis, a known pathogen is not isolated. Up to one-third of men infected with either C. trachomatis or M. genitalium will not have an excess of PMNLs, the sensitivity of smear ( 5 PMNLs) being far better in the case of an overt discharge, variations being furthermore dependent on populations and techniques of sampling. Indeed if a discharge is present, the isolation rate of C. trachomatis or M. genitalium reaches 50%. In 3–20% an undiagnosed C. trachomatis or M. genitalium infection is found in the partner of a patient with non-chlamydial, non-M. genitalium urethritis if he or she is tested. AETIOLOGY † N. gonorrhoeae. The isolation rate varies enormously in different social settings and different European countries. N. gonorrhoeae is more common in inner city urban, deprived areas compared with more affluent neighbourhoods. The prevalence of the common organisms associated with NGU in more recent studies are listed in Tables 1 and 2. Reported isolation rates of pathogens is lower in more recent studies despite the use of more sensitive tests. The commonest organisms implicated are C. trachomatis and M. genitalium with the latter perhaps causing more symptoms; † Chlamydia is more likely to be isolated in younger patients than M. genitalium and the two organisms rarely coexist in the same individual; † In 30–80% of the cases with NGU neither C. trachomatis nor M. genitalium is detected; † The isolation of Trichomonas vaginalis is dependent on the prevalence of the organism in the community, being more common in non-white ethnic groups and Eastern Europe, and greatly increases with the use of more sensitive polymerase chain reaction assays. T. vaginalis isolation is greater in men .30 years; † The exact role of ureaplasmas in NGU has been controversial, due to conflicting observations in clinical studies. Ureaplasmas are ubiquitous microorganisms which can be isolated from 30% to 40% of healthy sexually active young men. They have recently been divided into two species: U. parvum (biovar 1) and U. urealyticum (biovar 2) and in some studies U. urealyticum has been associated to 5–10% of cases of acute NGU;

Association of Mycoplasma genitalium with acute non-gonococcal urethritis in Russian men: a comparison with gonococcal and chlamydial urethritis

Urethral specimens from 172 men who attended sexually transmitted disease clinics in the Moscow Oblast were examined for Neisseria gonorrhoeae, Chlamydia trachomatis and Mycoplasma genitalium by nucleic acid amplification tests. N. gonorrhoeae was detected in the urethra of 41 (24%) of the 172 men and C. trachomatis in 57 (33%). The latter occurred in 15 (36%) of the 41 men who were infected by N. gonorrhoeae and in 42 (32%) of 131 uninfected by gonococci. Of the 42 men uninfected by gonococci but chlamydia infected, 39 (93%) had symptoms and/or signs of urethritis. M. genitalium was detected in 45 (26%) of the 172 men, in nine (22%) of the 41 men infected with N. gonorrhoeae and in 12 (21%) infected with C. trachomatis. M. genitalium was detected alone in 25 (28%) of the 89 men uninfected by either gonococci or C. trachomatis. Of these 25 men, 24 (96%) had urethral symptoms and signs of inflammation, a proportion significantly more than experienced by the 64 men uninfected by any of the microorganisms. Of the 31 men who apparently had no symptoms or signs of urethritis, only three (10%) were infected by M. genitalium. The data provide evidence for the pathogenicity and frequent occurrence of M. genitalium in men in Moscow and presumably elsewhere in Russia.

50. THE MANAGEMENT OF MEN WITH ACUTE CHLAMYDIA-NEGATIVE NON-GONOCOCCAL URETHRITIS: A LACK OF CONSENSUS AMONG AUSTRALIAN SEXUAL HEALTH PHYSICIANS

Objective: In clinical practice, chlamydia-negative non-gonococcal urethritis (NGU) is a common but poorly understood condition. The purpose of this study was to determine how Australian sexual health physicians manage men with this condition. Methods: In July 2006, a survey was mailed to all members of the Australasian Chapter of Sexual Health Medicine. Results: Of 166 surveys mailed out, 111 (67%) were returned completed. The majority of sexual health physicians (73%, n�=�81) indicated that they believed that female partners of men with acute chlamydia-negative NGU were at risk of adverse reproductive health outcomes. However, only 19% (n�=�21) routinely tested men with acute NGU for pathogens other than Neisseria gonorrhoeae and Chlamydia trachomatis. Most commonly, this was for M. genitalium (n�=�16). While 68% of respondents believed that M. genitalium was a cause of acute NGU, only 27% had access to testing for this organism. Other pathogens that were sometimes tested for included herpes simplex virus, Trichomonas vaginalis and adenovirus. Over half of sexual health physicians indicated that they would usually initiate notification of female sexual partners of men presenting with acute NGU, even before confirmatory test results were available. Conclusion: There are substantial differences in how acute, chlamydia-negative NGU is managed by Australian sexual health physicians. In part, these may relate to differences in beliefs around which pathogens are responsible for this condition and the availability of testing for particular pathogens. Notification of female partners is commonplace, even though the underlying cause of urethritis in affected men appears to be poorly defined.

Mycoplasma genitalium infection and host antibody immune response in patients infected by HIV, patients attending STD clinics and in healthy blood donors.

Prevalence of Mycoplasma genitalium in humans is still not clear. We have developed a sensitive and specific serological assay for M. genitalium using lipid-associated membrane proteins (LAMPs) as antigens. Antibodies to LAMPs from M. genitalium showed little cross-reactivity to LAMPs from antigenically similar M. pneumoniae. For validity testing, urines from 104 patients were tested by PCR for M. genitalium. All 15 PCR+ patients had M. genitalium-LAMPs antibodies. Moreover, none of 64 antibody-negative patients were PCR+. Serological study of 1800 patients of various diseased groups and healthy blood donors showed M. genitalium was primarily a sexually transmitted microbe that infected patients with AIDS (44.0%), intravenous drugs users with or without HIV infection (42.5%), and also HIV- patients attending STD clinics (42.6%). Only 5.5% HIV- healthy blood donors and 1.3% HIV+ hemophiliacs tested positive. M. genitalium has been associated with acute non-gonococcal urethritis in male patients. However, many sexually active men and women appear to be chronically infected or colonized by the microbe without apparent clinical symptoms and may continue to transmit the organism through sexual contacts.

Mycoplasma genitalium urethritis in men

Mycoplasma genitalium was first isolated from two men with non-gonococcal urethritis (NGU) and thereafter shown to produce urethritis in subhuman primates, inoculated intraurethrally. This mycoplasma has been detected significantly more often in patients with acute NGU, particularly in patients with non-chlamydial NGU, than in subjects without urethritis. The prevalence of M. genitalium-positive non-chlamydial NGU ranges from 18 to 46% of all non-chlamydial NGU cases. In addition, the persistence of M. genitalium in the urethra after antimicrobial chemotherapy is associated with persistence or recurrence of NGU. The various results reported to date tend to support the proposition that M. genitalium is a pathogen of NGU. M. genitalium is highly susceptible to tetracyclines, macrolides, and some new fluoroquinolones, but the clinical data on the chemotherapy in M. genitalium-positive NGU is extremely limited. Because of the possible association between the post-treatment presence of M. genitalium in the urethra and persistent or recurrent NGU, the eradication of this mycoplasma from the urethra is essential in the management of patients with M. genitalium-positive NGU. Further studies are required to establish the optimal chemotherapy for M. genitalium-positive NGU.

Asymptomatic non-chlamydial, non-gonococcal urethritis &amp;mdash; an iatrogenic disease?

Around the middle of the twentieth century, specialist services began routinely screening asymptomatic men with a urethral smear for gram staining. The practice persists in over 90% of United Kingdom services in line with national guidelines.1 If the smear reveals ≥5 polymorphs in five or more oil-immersion fields then a diagnosis of non-gonococcal urethritis (NGU) is made, despite the absence of symptoms or a specific pathogen. Some will even fish out threads or debris from an asymptomatic man’s first-void urine and stain these, in this case looking for ≥10 polymorphs/oil-immersion field. An alternative is a leucocyte esterase test on the urine. Thus (arbitrarily) a new disease was created; necessitating counselling, antibiotic treatment, contact tracing, and frequent psychosocial dilemmas. The Americans generally go easy on the tracing of contacts of cases of asymptomatic NGU in the absence of a specific organism (C. trachomatis) being documented.2 While agreeing on the microscopic criteria for asymptomatic urethritis, in contrast to the UK neither the American nor the Australian guidelines advocate urethral smears for microscopy for asymptomatic men, though neither guidelines actually advise against the practice.3,4 Perhaps technology has advanced to the point where this time-consuming and often problematic diagnosis of asymptomatic non-chlamydial, non-gonococcal urethritis (NCNGU) (and its active pursuit in the clinic) needs to be reappraised. First, we need to ask why did the practice start in the first place? After glancing over their shoulders, a few senior UK genitourinary physicians have intimated their sceptical view that the process was devised ‘to keep the statistics up in the clinics’. By the 1950s, the introduction of penicillin had made large inroads into the major concerns of the time — gonorrhoea and syphilis. The tactic worked. NGU filled the gap and the comprehensive network of UK clinics was preserved. In the meantime, in the USA, the practice did not become as widespread and much of their clinical network was de-funded. But these days the UK clinics are straining under a massive and growing clinical burden— yet more reason to question a traditional practice with a fading rationale. Second, therewas a strong hunch (confirmed by the 1970s) that NGU often indicated an important infection (namely C. trachomatis) with serious consequences for sexual partners, and chlamydial urethritis is commonly asymptomatic. At the time (in the absence of any other test for C. trachomatis infection) this provided a compelling argument for screening for asymptomatic NGU. However, these days, a specific test for C. trachomatis is part of the routine work-up in specialist services,1 so all the urethral smear now contributes is the diagnosis of asymptomatic NCNGU. Additionally, as control programmes take effect, C. trachomatis tends to contribute shrinking proportions (typically< 20%) of acute NGU cases and even smaller proportions of asymptomatic NGU cases.2 The only consistently documented causes of NCNGU are Mycoplasma genitalium5 and Trichomonas vaginalis6 [the latter largely confined to areas of high prevalence (Table 1)] but we don’t routinely test for these organisms. The reasons that we don’t screen for these infections are because the pathogenicity ofM. genitalium has been unclear until recently5 while T. vaginalis tends to be uncommon in those services that can afford to test for it. There may be a scattering of other specific causes of NCNGU (Table 2)7−11 but there is no debate that we don’t know the cause of most cases. Thus we find ourselves in the odd predicament of having constructed and been required to manage an asymptomatic condition with generally no known cause and no known consequences. Some may chose to continue the practice of urethral smears with the justification that a sinister (as yet undiscovered) pathogen is lurking in the urethrae of thesemen and that they wouldn’t otherwise get treated. But the treatments most commonly used for NGU or NCNGU in the public sectors in the UK and the USA (tetracyclines) have no effect on T. vaginalis and, on preliminary experience, a

Urinary tract infection in patients with acute non-gonococcal urethritis - 2

Urinary tract infection in patients with acute non-gonococcal urethritis - 2

Urinary tract infection in patients with acute non-gonococcal urethritis.

Urinary tract infection in patients with acute non-gonococcal urethritis.

Antibodies to Chlamydia trachomatis heat-shock protein 60 kDa and detection of Mycoplasma genitalium and ureaplasma urealyticum are associated independently with chronic nongonococcal urethritis.

Chronic nongonococcal urethritis (NGU) is a well-recognized clinical problem in genitourinary medicine clinics, but its etiology and optimal management are poorly understood. The authors showed previously that antibody to chlamydial hsp60 is associated with urethritis 30 to 92 days after treatment of acute NGU (chronic NGU) and that the detection of ureaplasmas or is associated with chronic NGU in which symptoms or signs are present. The aim was to determine whether these associations are independent of each other. This was a longitudinal prospective follow-up study over a 3-month period of 86 men with acute NGU. Men were tested for, ureaplasmas, and antibody to chlamydia hsp60 at presentation and during follow-up. The detection of either ureaplasmas or (OR, 29.45; 95% CI, 1.78-487) and the occurrence of hsp60 antibody at 30 to 92 days' follow-up (OR, 26.45; 95% CI, 1.34-523) were associated independently with the development of chronic NGU 30 to 92 days after treatment of acute NGU. The presence of chlamydial hsp60 antibody at 30 to 92 days was not associated with the development of chronic NGU in which symptoms or signs were present (P= 0.363). Chlamydial hsp60 antibody associated, however, with chronic NGU in which there were no symptoms or signs (P = 0.01). The results suggest that the immune response to chlamydial hsp60 may have a role in the etiology of chronic NGU in asymptomatic men who have no discharge on examination. The clinical relevance of this is unknown.

Urinary tract infection in patients with acute non-gonococcal urethritis

In young sexually active male patients, clinical differentiation between non-gonococcal urethritis (NGU) and urinary tract infection (UTI) can be difficult. UTI as a cause of NGU has been suggested before, but the prevalence of UTI among acute NGU patients has not been evaluated. We conducted a prospective cross-sectional study of 156 male patients with clinical features of acute urethritis. The prevalence of UTI among acute NGU patients was 6.4% (CI: 1.5-11.3%). There was a possible association between UTI and NGU but this was not statistically significant. The sensitivity and specificity for combining leucocyte esterase and nitrite tests were 83.3% and 89.8%, respectively, with a negative predictive value of 98.8%. We conclude that a mid-stream urine specimen should routinely be collected in patients with symptoms of urethritis. This should be analysed by dipsticks incorporating nitrite and leucocyte esterase tests. Those with a positive dipstick should then be confirmed by culture.

Do all men attending departments of genitourinary medicine need to be screened for non-gonococcal urethritis?

We investigated the influence of symptoms and signs on the detection of Chlamydia trachomatis, Mycoplasma genitalium and Ureaplasma urealyticum organisms (ureaplasmas) in men with non-gonococcal urethritis (NGU). Two hundred and forty-two men attending the Jefferiss Wing at St Mary's Hospital for a sexual health assessment were evaluated, of whom 169 had NGU. Urethral inflammation was diagnosed if there were either > or =5 polymorphonuclear leucocytes (PMNLs) per high-power field (HPF) in five or more microscope fields of a Gram-stained urethral smear, or > or =10 PMNLs per HPF in five or more fields of a Gram-stained thread from 15-20 mL of a first-passed urine (FPU) specimen. C. trachomatis was diagnosed by direct immunofluoresence, M. genitalium by a polymerase chain reaction assay and ureaplasmas by culture. On multivariate analysis, to control for potential confounding by age, ethnicity, sexual lifestyle and co-infection, an urethral discharge remained significantly associated with the detection of C. trachomatis and M. genitalium in men with acute urethritis [OR 12.3, 95% CI (2.39-63.5) and OR 35.2, 95% CI (3.9-319.6), respectively], but dysuria or penile irritation did not. The detection of ureaplasmas was not associated with any clinical feature. In addition, on multivariate analysis men with NGU who were either symptomatic or had an observable discharge were more likely to have C. trachomatis or M. genitalium detected [(OR 6.92, 95% CI 1.41-33.9) and (OR 5.18, 95% CI 0.99-27.1), respectively], but not ureaplasmas (OR 1.19, 95% CI 0.33-4.35). The findings suggest that in men with acute NGU, symptoms or signs, and in particular a urethral discharge, are associated with the detection of C. trachomatis and M. genitalium, but not ureaplasmas. Currently, there is no precise answer to the question of whether all men attending a GUM clinic need to be screened for NGU, but if clinically asymptomatic NGU is found not to be associated with a sexually transmitted pathogen, the UK clinical guidelines requiring the preparation of a urethral smear from such men would need to be revised.

Mycoplasma genitalium - an up-date

Mycoplasma genitalium was first isolated from men with non-gonococcal urethritis (NGU) more than 20 years ago. Use of polymerase chain reaction technology has shown it to be a cause of acute NGU and probably chronic NGU, almost independently of Chlamydia trachomatis, but there is no substantial evidence that it causes acute or chronic prostatitis. In women, M. genitalium is not associated with bacterial vaginosis, but it is strongly associated with cervicitis and endometritis and serologically with salpingitis and tubal factor infertility. Further studies may show M. genitalium to be associated, perhaps causally, with epididymoorchitis, neonatal disease and reactive arthritis. Furthermore, its potential for enhancing HIV transmission needs to be explored. M. genitalium is susceptible to various broad-spectrum antibiotics, but M. genitalium-associated diseases are probably best treated with azithromycin.

Role of Mycoplasma genitalium and Ureaplasma urealyticum in acute and chronic nongonococcal urethritis.

One hundred fourteen heterosexual men with acute nongonococcal urethritis (NGU) and 64 patients without NGU were studied. We determined that Chlamydia trachomatis and Mycoplasma genitalium were strongly associated with acute NGU after controlling, by means of multivariate analysis, for age, race, sexual lifestyle, and coinfection (odds ratio [OR], 13.0, 95% confidence interval [CI], 2.6-64.5; and OR, 17.9, 95% CI, 2.0-160, respectively). Eighty-six men with acute NGU reattended at least once 10-92 days after treatment; 59 (69%) of these 86 men had urethritis. Seven men had M. genitalium detected during 10-92 days of follow-up, and all had urethritis. Ureaplasmas were not associated with acute NGU in multivariate analysis, but their detection was associated with the presence of urethritis during follow-up (P=.014). Ureaplasmas or M. genitalium were associated with both chronic NGU, which was defined as urethritis that occurred 30-92 days after the commencement of treatment (P=.028), and chronic NGU with symptoms or signs (P=.005).