Macrolide‐resistant Mycoplasma pneumoniae pneumonia in transplantation: Increasingly typical?

Mycoplasma pneumoniae is one of the most common bacterial causes of pneumonia. Macrolide‐resistant M pneumoniae (MRMP) was documented in 7.5% of isolates in the United States. Resistance portends poor outcomes to macrolide therapy, yet patients respond well to fluoroquinolones or tetracyclines such as minocycline. However, MRMP may be under‐appreciated because M pneumoniae generally causes relatively mild infections in non‐immunosuppressed adults that may resolve without effective therapy and because microbiological confirmation and susceptibility are not routinely performed. We report two cases of pneumonia due to MRMP in kidney transplant recipients. Both patients required hospital admission, worsened on macrolide therapy, and rapidly defervesced on doxycycline or levofloxacin. In one case, M pneumoniae was only identified by multiplex respiratory pathogen panel analysis of BAL fluid. Macrolide resistance was confirmed in both cases by real‐time PCR and point mutations associated with macrolide resistance were identified. M pneumoniae was isolated from both cases, and molecular genotyping revealed the same genotype. In conclusion, clinicians should be aware of the potential for macrolide resistance in M pneumoniae, and may consider non‐macrolide‐based therapy for confirmed or non‐responding infections in patients who are immunocompromised or hospitalized.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/163484/2/tid13318.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/163484/1/tid13318_am.pd

Composition for personal growth : program design and evaluation.

<p>Two categories were used for cross-validation of the model, either type 1 or type 2. Clinical isolates were treated as an unknown class and cross-validated sensitivity, specificity, and class error were based on their classification prediction score with their respective reference strain control class. CV, cross-validated.</p><p>Cross-validated PLS-DA modeling statistics for the prediction performance for NA-SERS typing of individual type 1 and 2 <i>M</i>. <i>pneumoniae</i> clinical isolates.</p

Comparative In Vitro Susceptibilities and Bactericidal Activities of Investigational Fluoroquinolone ABT-492 and Other Antimicrobial Agents against Human Mycoplasmas and Ureaplasmas

We determined in vitro susceptibilities for ABT-492 and other antimicrobials against Mycoplasma pneumoniae, Mycoplasma fermentans, Mycoplasma hominis, and Ureaplasma species. ABT-492 MICs were ≤1 μg/ml, and the agent was bactericidal against selected isolates of M. pneumoniae and M. hominis. ABT-492 has potential for treatment of infections due to these microorganisms

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. genitalium, whereas clindamycin was most active against M. hominis. DC-159a MICs were ≤0.5 μg/ml for all Mycoplasma species and ≤4 μg/ml for ureaplasmas. DC-159a was the most active fluoroquinolone tested against M. pneumoniae and M. fermentans, and it was second to moxifloxacin against the other species. It was bactericidal against 10 M. pneumoniae isolates and demonstrated killing of ≥99.9% of the inoculum at 24 h for 2 isolates. The excellent in vitro activity of DC-159a demonstrates its potential for use in the treatment of infections due to mycoplasmas and ureaplasmas

In Vitro Susceptibilities to and Bactericidal Activities of Garenoxacin (BMS-284756) and Other Antimicrobial Agents against Human Mycoplasmas and Ureaplasmas

The in vitro susceptibilities to garenoxacin (BMS-284756), an investigational des-fluoroquinolone, and eight other agents were determined for 63 Mycoplasma pneumoniae, 45 Mycoplasma hominis, 15 Mycoplasma fermentans, and 68 Ureaplasma sp. isolates. Garenoxacin was the most active quinolone, inhibiting all isolates at ≤1 μg/ml. The garenoxacin MIC at which 90% of isolates are inhibited (MIC(90)s; ≤0.008 μg/ml) was at least 4-fold less than those of moxifloxacin and clindamycin, 8-fold less than that of sparfloxacin, and 64-fold less than those of levofloxacin and ciprofloxacin for M. pneumoniae. For M. hominis, the garenoxacin MIC(90) (≤0.008 μg/ml) was 4-fold less than those of clindamycin and moxifloxacin, 8-fold less than that of sparfloxacin, and 64-fold less than those of levofloxacin and ciprofloxacin. All 15 M. fermentans isolates were inhibited by garenoxacin at concentrations ≤0.008 μg/ml, making it the most active drug tested against this organism. For Ureaplasma spp., the garenoxacin MIC(90) (0.25 μg/ml) was equivalent to those of moxifloxacin and doxycycline, 4-fold less than those of levofloxacin and sparfloxacin, 8-fold less than that of azithromycin, and 32-fold less than that of ciprofloxacin. Garenoxacin and the other fluoroquinolones tested were demonstrated to have bactericidal activities against M. pneumoniae and M. hominis by measurement of minimal bactericidal activities and by time-kill studies. Further study of garenoxacin is required, as it has great potential for use in the treatment of infections due to mycoplasmas and ureaplasmas

Comparative In Vitro Activities of Investigational Peptide Deformylase Inhibitor NVP LBM-415 and Other Agents against Human Mycoplasmas and Ureaplasmas

Peptide deformylase inhibitor LBM-415 and seven other drugs were tested against Mycoplasma pneumoniae (100 isolates), Mycoplasma hominis (20 isolates), Mycoplasma fermentans (10 isolates), and Ureaplasma species (50 isolates). LBM-415 was active against M. pneumoniae (MICs, ≤0.008 μg/ml). It showed no activity against M. hominis and M. fermentans and modest activity against Ureaplasma spp

Data from: Specificity and strain-typing capabilities of Nanorod Array-Surface Enhanced Raman Spectroscopy for Mycoplasma pneumoniae detection

Mycoplasma pneumoniae is a cell wall-less bacterial pathogen of the human respiratory tract that accounts for > 20% of all community-acquired pneumonia (CAP). At present the most effective means for detection and strain-typing is quantitative polymerase chain reaction (qPCR), which can exhibit excellent sensitivity and specificity but requires separate tests for detection and genotyping, lacks standardization between available tests and between labs, and has limited practicality for widespread, point-of-care use. We have developed and previously described a silver nanorod array-surface enhanced Raman Spectroscopy (NA-SERS) biosensing platform capable of detecting M. pneumoniae with statistically significant specificity and sensitivity in simulated and true clinical throat swab samples, and the ability to distinguish between reference strains of the two main genotypes of M. pneumoniae. Furthermore, we have established a qualitative lower endpoint of detection for NA-SERS of < 1 genome equivalent (cell/μl) and a quantitative multivariate detection limit of 5.3 ± 1 cells/μl. Here we demonstrate using partial least squares- discriminatory analysis (PLS-DA) of sample spectra that NA-SERS correctly identified M. pneumoniae clinical isolates from globally diverse origins and distinguished these from a panel of 12 other human commensal and pathogenic mycoplasma species with 100% cross-validated statistical accuracy. Furthermore, PLS-DA correctly classified by strain type all 30 clinical isolates with 96% cross-validated accuracy for type 1 strains, 98% cross-validated accuracy for type 2 strains, and 90% cross-validated accuracy for type 2V strains