Complete Genome Sequence of Ureaplasma parvum Serovar 3 Strain SV3F4, Isolated in Japan

Wu, Heng Ning; Nakura, Yukiko; Motooka, Daisuke; Nakamura, Shota; Nishiumi, Fumiko; Ishino, Saki; Kawai, Yasuhiro; Tanaka, Tatsuya; Takeuchi, Makoto; Nakayama, Masahiro; Fujita, Tomio; Yanagihara, Itaru

doi:10.1128/genomea.00256-14

Cited by 10 publications

(12 citation statements)

References 18 publications

(15 reference statements)

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“…genomes have been fully sequenced. However, there is no evidence for the existence of a plasmid in 19 human Ureaplasma genomes (42), nor was any evidence uncovered in our previous study (43). Codon usage by the family Mycoplasmataceae, including ureaplasmas, differs from that of other bacteria, and the GC content of these species is lower than that of other bacteria (43).…”

Section: Discussionmentioning

confidence: 86%

In Vitro Activity of Five Quinolones and Analysis of the Quinolone Resistance-Determining Regions of gyrA , gyrB , parC , and parE in Ureaplasma parvum and Ureaplasma urealyticum Clinical Isolates from Perinatal Patients in Japan

Kawai

Nakura

Wakimoto

et al. 2015

Antimicrob Agents Chemother

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g Ureaplasma spp. cause several disorders, such as nongonococcal urethritis, miscarriage, and preterm delivery with lung infections in neonates, characterized by pathological chorioamnionitis in the placenta. Although reports on antibiotic resistance in Ureaplasma are on the rise, reports on quinolone-resistant Ureaplasma infections in Japan are limited. The purpose of this study was to determine susceptibilities to five quinolones of Ureaplasma urealyticum and Ureaplasma parvum isolated from perinatal samples in Japan and to characterize the quinolone resistance-determining regions in the gyrA, gyrB, parC, and parE genes. Out of 28 clinical Ureaplasma strains, we isolated 9 with high MICs of quinolones and found a single parC gene mutation, resulting in the change S83L. Among 158 samples, the ParC S83L mutation was found in 37 samples (23.4%), including 1 sample harboring a ParC S83L-GyrB P462S double mutant. Novel mutations of ureaplasmal ParC (S83W and S84P) were independently found in one of the samples. Homology modeling of the ParC S83W mutant suggested steric hindrance of the quinolone-binding pocket (QBP), and de novo prediction of peptide structures revealed that the ParC S84P may break/kink the formation of the ␣4 helix in the QBP. Further investigations are required to unravel the extent and mechanism of antibiotic resistance of Ureaplasma spp. in Japan.Ureaplasma spp. are among the smallest self-replicating organisms, in terms of both genome size and cellular dimensions. They lack cell walls and are thus resistant to penicillin and other ␤-lactams. These organisms exist in association with eukaryotic cells, mainly colonizing mucosal surfaces of the respiratory and urogenital tracts (1, 2). Ureaplasma spp. are common inhabitants of the lower genital tract and can be isolated from 40% to 80% of women of child-bearing age (1, 3). Ureaplasma spp. have been associated with a range of pathologies, including nongonococcal urethritis (NGU), miscarriage, preterm delivery, neonatal pneumonia, and chronic lung disease in preterm neonates (4, 5). Many reports have suggested that Ureaplasma parvum and/or Ureaplasma urealyticum may be associated with urogenital infections, infertility, and adverse pregnancy outcomes (6). Regarding the management of ureaplasmal infections, only a limited number of reports are available on the surveillance of antimicrobial resistance in clinical Ureaplasma strains, which is crucial for providing therapy empirically (6). The treatment of ureaplasmal infections is limited to tetracyclines, macrolides, and quinolones (5, 7). Resistance to all the three antibiotic classes in clinical Ureaplasma isolates has been documented, with unique nucleic acid substitutions identified as potential molecular mechanisms for each (5,(8)(9)(10).Quinolones are used for treating urogenital infections and interact in bacteria with the type II topoisomerases DNA gyrase and topoisomerase IV, both of which are composed of two A and two B subunits; these subunits are encoded by the gyrA and gyrB genes for DNA...

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Section: Discussionmentioning

confidence: 86%

In Vitro Activity of Five Quinolones and Analysis of the Quinolone Resistance-Determining Regions of gyrA , gyrB , parC , and parE in Ureaplasma parvum and Ureaplasma urealyticum Clinical Isolates from Perinatal Patients in Japan

Kawai

Nakura

Wakimoto

et al. 2015

Antimicrob Agents Chemother

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“…19 Recently, the sequence of a U. parvum serovar 3 clinical strain SV3F4 revealed a putative new virulence factor serine/threonine kinase and protein phosphatase (STK/STP). 20 In Mycoplasma genitalium , an STP protein is required for host cell cytotoxicity and mutant strains lacking the STP gene produce less hydrogen peroxide than wild-type strains. 21 Recently, Xiao et al 22 demonstrated that Ureaplasma spp.…”

Section: Ureaplasma Speciesmentioning

confidence: 99%

Role of Ureaplasma Respiratory Tract Colonization in Bronchopulmonary Dysplasia Pathogenesis

Viscardi

Kallapur

2015

Clinics in Perinatology

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SYNOPSIS Respiratory tract colonization with the genital mycoplasma species Ureaplasma parvum and U. urealyticum in preterm infants is a significant risk factor for BPD. Recent studies of the ureaplasmal genome, animal infection models, and human infants have provided a better understanding of specific virulence factors, pathogen-host interactions, and variability in genetic susceptibility that contribute to chronic infection, inflammation, and altered lung development. This review will provide an update on the current evidence supporting a causal role of Ureaplasma infection in BPD pathogenesis. The current status of antibiotic trials to prevent BPD in Ureaplasma-infected preterm infants is also reviewed.

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“…commonly colonize the human urogenital tract [ 10 ]. Their genome is 0.72–0.95 megabase pairs and contains 571–711 predicted coding DNA sequences (CDSs), of which 30% have been deduced as hypothetical proteins [ 11 , 12 ]. Their genome contains five putative virulence factors: urease [ 13 ], multiple-banded antigen (MBA) [ 14 ], hemolysin [ 15 ], serine/threonine kinase, and protein phosphatase [ 16 – 18 ].…”

Section: Introductionmentioning

confidence: 99%

“…parvum serovar 3 type strain ATCC700970 was isolated from a patient with nongonococcal urethritis [ 15 ], and the clinical strain SV3F4 of U . parvum serovar 3 was isolated from a Japanese patient with history of an infectious abortion [ 12 ]. In our previous study, the complete genome of the SV3F4 clinical strain was sequenced, and its genome was found to be the smallest among all 14 other human pathogenic serovars of Ureaplasma spp.…”

Section: Introductionmentioning

confidence: 99%

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Type II restriction modification system in Ureaplasma parvum OMC-P162 strain

Nakura

Yoshimura

et al. 2018

PLoS ONE

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Ureaplasma parvum serovar 3 strain, OMC-P162, was isolated from the human placenta of a preterm delivery at 26 weeks’ gestation. In this study, we sequenced the complete genome of OMC-P162 and compared it with other serovar 3 strains isolated from patients with different clinical conditions. Ten unique genes in OMC-P162, five of which encoded for hypothetical proteins, were identified. Of these, genes UPV_229 and UPV_230 formed an operon whose open reading frames were predicted to code for a DNA methyltransferase and a hypothetical protein, respectively. DNA modification analysis of the OMC-P162 genome identified N4-methylcytosine (m4C) and N6-methyladenine (m6A), but not 5-methylocytosine (m5C). UPV230 recombinant protein displayed endonuclease activity and recognized the CATG sequence, resulting in a blunt cut between A and T. This restriction enzyme activity was identical to that of the cultivated OMC-P162 strain, suggesting that this restriction enzyme was naturally expressed in OMC-P162. We designated this enzyme as UpaP162. Treatment of pT7Blue plasmid with recombinant protein UPV229 completely blocked UpaP162 restriction enzyme activity. These results suggest that the UPV_229 and UPV_230 genes act as a type II restriction-modification system in Ureaplasma OMC-P162.

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Complete Genome Sequence of Ureaplasma parvum Serovar 3 Strain SV3F4, Isolated in Japan

Abstract: Here, we present the complete genome sequence of Ureaplasma parvum serovar 3, clinical strain SV3F4, isolated from a Japanese patient with a history of an infectious abortion.

Cited by 10 publications

References 18 publications

In Vitro Activity of Five Quinolones and Analysis of the Quinolone Resistance-Determining Regions of gyrA , gyrB , parC , and parE in Ureaplasma parvum and Ureaplasma urealyticum Clinical Isolates from Perinatal Patients in Japan

In Vitro Activity of Five Quinolones and Analysis of the Quinolone Resistance-Determining Regions of gyrA , gyrB , parC , and parE in Ureaplasma parvum and Ureaplasma urealyticum Clinical Isolates from Perinatal Patients in Japan

Role of Ureaplasma Respiratory Tract Colonization in Bronchopulmonary Dysplasia Pathogenesis

Type II restriction modification system in Ureaplasma parvum OMC-P162 strain

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