Activities of Eravacycline and Other Antimicrobial Agents against Human Mycoplasmas and Ureaplasmas.

We performed susceptibility testing for eravacycline in comparison to 4 other antimicrobials against 10 , 40 , 44 , 20 , and 20 isolates. All eravacycline MICs were ≤0.25 μg/ml, except that for one isolate of , for which the MIC was 2 μg/ml.

Evaluation of Commercial Molecular Diagnostic Methods for Detection and Determination of Macrolide Resistance in Mycoplasma pneumoniae.

We evaluated six commercial molecular tests targeting , namely, the BioFire FilmArray respiratory panel (RP), the Meridian Alethia Mycoplasma Direct, the GenMark ePlex respiratory pathogen panel (RPP), the Luminex NxTAG RPP, the ELITech ELITe InGenius MGB research use only (RUO) PCR, and the SpeeDx MP assays. Laboratory-developed PCR assays at the University of Alabama at Birmingham and the Centers for Disease Control and Prevention were used as reference standards. Among 428 specimens, 212 were designated confirmed positives for The highest clinical sensitivities were found with the InGenius PCR (99.

Activities of Gepotidacin (GSK2140944) and Other Antimicrobial Agents against Human Mycoplasmas and Ureaplasmas.

Gepotidacin, a novel first-in-class triazaacenaphthylene topoisomerase II inhibitor, was tested against 85 type strains and clinical isolates of , , , , and in comparison to levofloxacin, moxifloxacin, azithromycin or clindamycin, and tetracycline. Gepotidacin MICs (μg/ml) were 0.125 (), 0.

In Vitro Activities of Lefamulin and Other Antimicrobial Agents against Macrolide-Susceptible and Macrolide-Resistant Mycoplasma pneumoniae from the United States, Europe, and China.

Lefamulin, an investigational pleuromutilin, was tested against a collection of 18 macrolide-susceptible and 42 macrolide-resistant Mycoplasma pneumoniae strains, and the results were compared with those of azithromycin, erythromycin, tetracycline, doxycycline, and moxifloxacin testing. Lefamulin was highly active against all strains tested, with all MICs at ≤0.008 μg/ml.

In Vitro Activities of Omadacycline (PTK 0796) and Other Antimicrobial Agents against Human Mycoplasmas and Ureaplasmas.

In vitro activities of omadacycline, a new aminomethylcycline, were determined for Mycoplasma and Ureaplasma spp. and compared with those of azithromycin, clindamycin, moxifloxacin, tetracycline, and doxycycline. All omadacycline MICs were <2 μg/ml.

In vitro antibacterial activity of AZD0914 against human Mycoplasmas and Ureaplasmas.

In this study, susceptibilities were determined for AZD0914, a spiropyrimidinetrione DNA gyrase inhibitor, azithromycin, doxycycline, and levofloxacin against Mycoplasma and Ureaplasma species. The activity of AZD0914 was comparable to that of levofloxacin and doxycycline against Mycoplasma genitalium and Mycoplasma pneumoniae. The AZD0914 MIC90 against Mycoplasma hominis was 8-fold greater than that for levofloxacin.

Comparison of the illumigene Mycoplasma DNA amplification assay and culture for detection of Mycoplasma pneumoniae.

A loop-mediated isothermal amplification (LAMP) system, the illumigene Mycoplasma DNA amplification assay (Meridian Bioscience, Inc., Cincinnati, OH) was evaluated to determine its analytical sensitivity, specificity, and clinical application in comparison to historic culture in a collection of archived respiratory specimens. The illumigene limit of detection was ≤88 CFU/reaction for 10 Mycoplasma pneumoniae reference strains.

Transplacental transfer of Azithromycin and its use for eradicating intra-amniotic ureaplasma infection in a primate model.

Background: Our goals were to describe azithromycin (AZI) pharmacokinetics in maternal plasma (MP), fetal plasma (FP), and amniotic fluid (AF) following intra-amniotic infection (IAI) with Ureaplasma in pregnant rhesus monkeys and to explore concentration-response relationships.

Methods: Following intra-amniotic inoculation of Ureaplasma parvum, rhesus monkeys received AZI (12.5 mg/kg every 12 hours intravenously for 10 days; n = 10).

Maternal azithromycin therapy for Ureaplasma intraamniotic infection delays preterm delivery and reduces fetal lung injury in a primate model.

Objective: We assessed the efficacy of a maternal multidose azithromycin (AZI) regimen, with and without antiinflammatory agents to delay preterm birth and to mitigate fetal lung injury associated with Ureaplasma parvum intraamniotic infection.

Study Design: Long-term catheterized rhesus monkeys (n = 16) received intraamniotic inoculation of U parvum (10(7) colony-forming U/mL, serovar 1). After contraction onset, rhesus monkeys received no treatment (n = 6); AZI (12.

Standardized methods and quality control limits for agar and broth microdilution susceptibility testing of Mycoplasma pneumoniae, Mycoplasma hominis, and Ureaplasma urealyticum.

An international multilaboratory collaborative study was conducted to develop standard media and consensus methods for the performance and quality control of antimicrobial susceptibility testing of Mycoplasma pneumoniae, Mycoplasma hominis, and Ureaplasma urealyticum using broth microdilution and agar dilution techniques. A reference strain from the American Type Culture Collection was designated for each species, which was to be used for quality control purposes. Repeat testing of replicate samples of each reference strain by participating laboratories utilizing both methods and different lots of media enabled a 3- to 4-dilution MIC range to be established for drugs in several different classes, including tetracyclines, macrolides, ketolides, lincosamides, and fluoroquinolones.

Comparative genome analysis of 19 Ureaplasma urealyticum and Ureaplasma parvum strains.

Background: Ureaplasma urealyticum (UUR) and Ureaplasma parvum (UPA) are sexually transmitted bacteria among humans implicated in a variety of disease states including but not limited to: nongonococcal urethritis, infertility, adverse pregnancy outcomes, chorioamnionitis, and bronchopulmonary dysplasia in neonates. There are 10 distinct serotypes of UUR and 4 of UPA. Efforts to determine whether difference in pathogenic potential exists at the ureaplasma serovar level have been hampered by limitations of antibody-based typing methods, multiple cross-reactions and poor discriminating capacity in clinical samples containing two or more serovars.

Chromosomal mutations responsible for fluoroquinolone resistance in Ureaplasma species in the United States.

We sequenced the full lengths of the gyrA, gyrB, parC, and parE genes in 13 fluoroquinolone-resistant Ureaplasma isolates (levofloxacin MICs, 4 to 32 μg/ml) and 10 susceptible isolates (MICs ≤ 2 μg/ml). Mutations were detected in all resistant isolates but in none of the susceptible isolates. The most prevalent mutation was the S83L substitution in the ParC protein.

Genotypic characterization of ureaplasma serovars from clinical isolates by pulsed-field gel electrophoresis.

Genetic relationships within ureaplasma serovars were investigated by pulsed-field gel electrophoresis (PFGE). One hundred thirteen Ureaplasma parvum isolates and 78 Ureaplasma urealyticum isolates were different from their ATCC serovar type strains and different within the same serovars. The organisms were geographically widespread.

Extensive horizontal gene transfer in ureaplasmas from humans questions the utility of serotyping for diagnostic purposes.

Ureaplasma parvum and Ureaplasma urealyticum are sexually transmitted, opportunistic pathogens of the human urogenital tract. There are 14 known serovars distributed between the two species. For decades, it has been postulated based upon limited data that virulence is related to serotype specificity.

Mutations in ribosomal proteins and ribosomal RNA confer macrolide resistance in human Ureaplasma spp.

Genetic mechanisms of macrolide resistance were investigated in six isolates of Ureaplasma spp. with erythromycin minimum inhibitory concentrations (MICs)≥ 8 μg/mL that were derived from 370 cultures obtained over a several year period. Point mutations in domain V of 23S rRNA and/or mutations in ribosomal protein L4 genes are likely to be responsible for this drug resistance.

Critical role of macrophages and their activation via MyD88-NFκB signaling in lung innate immunity to Mycoplasma pneumoniae.

Mycoplasma pneumoniae (Mp), a common cause of pneumonia, is associated with asthma; however, the mechanisms underlying this association remain unclear. We investigated the cellular immune response to Mp in mice. Intranasal inoculation with Mp elicited infiltration of the lungs with neutrophils, monocytes and macrophages.

Detection and characterization of human Ureaplasma species and serovars by real-time PCR.

We designed primers and probes for the detection and discrimination of Ureaplasma parvum and U. urealyticum and their 14 serovars by real-time PCR. The analytical sensitivity and specificity of the multiplex species-specific PCR were determined by testing corresponding American Type Culture Collection (ATCC) type strains, 47 other microbial species, and human genomic DNA.

Emerging macrolide resistance in Mycoplasma pneumoniae in children: detection and characterization of resistant isolates.

Background: Epidemiologic data from Asia have documented the rapid and extensive emergence of macrolide resistance in Mycoplasma pneumoniae. This drug resistance has also been documented in Europe and recently in the United States, but there is very little information currently available on its prevalence. A rapid technique to identify macrolide-resistant M.

Deficient immune response to Mycoplasma pneumoniae in childhood asthma.

Prospective studies have suggested that some individuals have a persistent IgM response to Mycoplasma pneumoniae infection with relatively little IgG production over many months. Persistence of the organism in patients with an allergic phenotype might predispose to the development of asthma. This study was designed to analyze the prevalence of M.

Comparative in vitro susceptibilities of human mycoplasmas and ureaplasmas to a new investigational ketolide, CEM-101.

MICs were determined for an investigational ketolide, CEM-101, and azithromycin, telithromycin, doxycycline, levofloxacin, clindamycin, and linezolid against 36 Mycoplasma pneumoniae, 5 Mycoplasma genitalium, 13 Mycoplasma hominis, 15 Mycoplasma fermentans, and 20 Ureaplasma isolates. All isolates, including two macrolide-resistant M. pneumoniae isolates, were inhibited by CEM-101 at < or = 0.

Comparative in vitro activities of the investigational fluoroquinolone DC-159a and other antimicrobial agents against human mycoplasmas and ureaplasmas.

The in vitro susceptibilities of 151 unique clinical isolates of Mycoplasma pneumoniae, Mycoplasma hominis, Mycoplasma fermentans, Mycoplasma genitalium, and Ureaplasma species to DC-159a, an investigational fluoroquinolone, in comparison with those to other agents were determined. Macrolides were the most active agents against M. pneumoniae and M.

Inhibition of message for FcepsilonRI alpha chain blocks mast cell IL-4 production induced by co-culture with Mycoplasma pneumoniae.

We have previously described the activation of RBL-2H3 mast cells for IL-4 production by Mycoplasma pneumoniae but the mechanism remains unclear. M. pneumoniae binds eukaryotic cells primarily through sialoglycoproteins on the target cell surface.

Antimicrobial susceptibility among pathogens collected from hospitalized patients in the United States and in vitro activity of tigecycline, a new glycylcycline antimicrobial.

The activities of tigecycline and comparators against isolates collected from 76 U.S. centers between January 2004 and September 2005 were assessed.

A role for the Mycoplasma pneumoniae adhesin P1 in interleukin (IL)-4 synthesis and release from rodent mast cells.

Mycoplasma pneumoniae is a respiratory tract pathogen associated with exacerbations in patients with chronic asthma, yet relatively little is known about the potential role of this organism in asthma pathogenesis. Our previous studies demonstrated that RBL-2H3 mast cells co-cultured with M. pneumoniae released preformed inflammatory mediators, synthesized multiple cytokine mRNA species, and released IL-4 protein.