Kensaku Seike

Bacterial loads of Ureaplasma urealyticum contribute to development of urethritis in men.

Ureaplasma urealyticum could be a pathogen of non-gonococcal urethritis (NGU) in men. However, ureaplasma is often detected in men without NGU, and the proportion of cases possibly attributable to this pathogen is still undefined. We attempted to determine the bacterial loads of U. urealyticum significantly associated with NGU. The 16S rRNA genes of U. urealyticum were quantified by a real-time polymerase chain reaction-based assay in first-void urine (FVU) from 26 asymptomatic and 25 symptomatic men positive for U. urealyticum. The leucocyte counts in first-void urine (FVU) were determined as an objective measure of inflammatory response to ureaplasma in the hosts by automated quantitative urine particle analysis. Positive correlations were observed between copies of the 16S rRNA genes of U. urealyticum per ml and the leucocyte counts per µl in FVU (r = 0.49, p = 0.0003). Loads of ≥104 copies of the 16S rRNA gene of U. urealyticum/ml, corresponding to ≥5 × 103 cells of U. urealyticum/ml in FVU, were significantly associated with the presence of urethritis symptoms (p < 0.0001) and with higher leukocyte counts in FVU (p < 0.0001). The bacterial load of U. urealyticum, possibly of ≥5 × 103 cells of U. urealyticum/ml in FVU, could be significantly associated with the development of symptomatic NGU.

Male non-gonococcal urethritis: From microbiological etiologies to demographic and clinical features.

To detect microorganisms responsible for male acute urethritis and to define the microbiology of non‐gonococcal urethritis.

Drug Resistance-Associated Mutations in Mycoplasma genitalium in Female Sex Workers, Japan

Mycoplasma genitalium was detected in 21 (14.1%) of 149 vaginal swab samples and in 1 (0.7%) of 149 throat washing samples from female sex workers during 2013–2014 in Japan. Prevalences of M. genitalium with macrolide resistance–associated 23S rRNA mutations and fluoroquinolone resistance–associated parC alterations were 47.1% and 36.8%, respectively.

Bacterial loads of Ureaplasma parvum contribute to the development of inflammatory responses in the male urethra

Ureaplasma parvum, which has been recognised as a coloniser in the male urethra, is detected in some men with non-gonococcal urethritis. In this study, we quantified the 16 S rRNA genes of U. parvum by a real-time polymerase chain reaction-based assay in first-voided urine from 15 symptomatic and 38 asymptomatic men who were positive only for U. parvum. We also determined the leukocyte counts by automated quantitative urine particle analysis in their first-voided urine. Positive correlations were observed between copies of the 16 S rRNA genes of U. parvum/ml and the leukocyte counts/µl in first-voided urine (p = 0.0019). The loads of ≥104 copies of the 16 S rRNA gene/ml, corresponding to ≥5 × 103 cells of U. parvum/ml, were significantly associated with the presence of ≥12.5 leukocytes/µl in first-voided urine that might document the presence of inflammatory responses in the urethra. However, a large portion of the subjects (83.0%) had bacterial loads of <5 × 103 cells of U. parvum/ml, and 79.5% of them showed <12.5 leukocytes/µl. The ambiguity of the pathogenic role of U. parvum in non-gonococcal urethritis could, in part, be due to its low bacterial loads, which might not give rise to inflammatory responses in the male urethra.

Novel penA mutations identified in Neisseria gonorrhoeae with decreased susceptibility to ceftriaxone isolated between 2000 and 2014 in Japan

OBJECTIVES We examined four clinical strains of Neisseria gonorrhoeae (GU030113, GU110095, GU110332 and GU110362) isolated between 2000 and 2014 in Japan, exhibiting ceftriaxone MICs of 0.5 mg/L, for mutations of the genes associated with penicillin resistance. METHODS The penA, mtrR, porB1b (penB), ponA and pilQ genes of the strains were sequenced. PBP2s of the strains were aligned to the PBP2s associated with decreased susceptibility to oral cephalosporins, and PBP2s of previously reported strains with decreased susceptibility to ceftriaxone. RESULTS GU030113 had PBP2 pattern X with an additional substitution of A502T. GU110095 had PBP2 pattern XXVII. GU110332 had PBP2 pattern XXXIV with an additional substitution of P552S. GU110362 had PBP2 composed of pattern X (amino acid positions 1-291) and pattern V (amino acid positions 292-576). GU030113, GU110095 and GU110332 had deletion of A in the mtrR promoter, G120K and A121D or A121N in PorB1b and L421P in PBP1. GU110362 had A40D in the repressor of MtrR and L421P in PBP1. The strains did not have mutations of pilQ1 and pilQ2. CONCLUSIONS Addition of A502T to PBP2 pattern X in GU030113 and of P552S to PBP2 pattern XXXIV in GU110332 would possibly contribute to decreased susceptibility to ceftriaxone. In GU110095 and GU110362, it was suggested that, in addition to their altered PBP2s, the enhanced efflux pump, reduced permeability in the outer membrane, another altered target of β-lactams and/or other mechanisms not identified in the present study might contribute to decreased susceptibility.

Prediction of the persistence of Mycoplasma genitalium after antimicrobial chemotherapy by quantification of leukocytes in first-void urine from patients with non-gonococcal urethritis

Mycoplasma genitalium is regarded as another pathogen of male non-gonococcal urethritis (NGU). Failure to eradicate this mycoplasma is associated with persistent or recurrent NGU, but this mycoplasma is not routinely examined in clinical practice. In cases of M. genitalium-positive NGU, therefore, some criteria are needed to assess the success or failure of antimicrobial chemotherapy other than microbiological outcomes. We enrolled 49 men with M. genitalium-positive non-chlamydial NGU. At successive visits after treatment, we inquired about their symptoms, observed their urethral meatus for urethral discharge, and examined their first-void urine (FVU) for quantification of leukocytes and for the persistence of M. genitalium. M. genitalium was eradicated in 34 patients after treatment, whereas the mycoplasma persisted in 15. Urethritis symptoms and urethral discharges were not found to be predictors of the persistence of M. genitalium up to the 25th day after the start of treatment. Leukocyte counts in FVU from the patients with persistence of M. genitalium were significantly higher than those from the patients with eradication of the mycoplasma. Leukocyte counts of 10 leukocytes/μl or more between the 18th and 24th day after the start of treatment were most significantly associated with the persistence of M. genitalium. Quantification of leukocytes in FVU would appear to be crucial to judge the outcome of treatment in patients with non-chlamydial NGU and could be helpful to predict the persistence of M. genitalium after treatment when M. genitalium is not routinely examined in clinical specimens in clinical practice.

ALK Gene Translocation in Inflammatory Myofibroblastic Tumor of the Urinary Bladder: A Case Report.

A 26-year-old woman with gross hematuria was seen in a previous hospital. Magnetic resonance imaging (MRI) showed a tumor at the dome of the urinary bladder with invasion outside of the bladder wall. The patient underwent transurethral resection of the bladder tumor (TUR-BT). From the result of the pathological examination, the tumor was suggested to be carcinosarcoma of the bladder. The patient was then referred to our hospital for treatment. We performed radical cystectomy and ileal conduit diversion. Pathological examination of the excised specimen revealed an inflammatory myofibroblastic tumor as the basis for immunostaining of anaplastic lymphoma kinase (ALK).

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.