Antimicrobial Susceptibility Testing of
            <i>Chlamydia trachomatis</i>
            Using a Reverse Transcriptase PCR-Based Method

Cross, Neil; Kellock, D J; Kinghorn, G R; Taraktchoglou, Maria; Bataki, Efthalia L.; Oxley, K. M.; Hawkey, Peter M.; Eley, A.

doi:10.1128/aac.43.9.2311

Cited by 26 publications

(11 citation statements)

References 21 publications

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“…However, no data were presented on the sensitivity of the flow-cytometric method in detecting aberrant inclusions. Molecular techniques for identifying infected cells (e.g., real-time polymerase chain reaction or detection of messenger RNA) may be more useful than methods relying on inclusion staining [28].…”

Section: Trachomatis Antimicrobial Susceptibility Test Methodologiesmentioning

confidence: 99%

Evaluation of Antimicrobial Resistance and Treatment Failures forChlamydiatrachomatis: A Meeting Report

et al. 2005

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Each year, Chlamydia trachomatis causes ~3 million new infections and results in more than 1 billion dollars in medical costs in the United States. Repeat or persistent infection occurs in 10%-15% of women who are treated for C. trachomatis infection. However, the role played by antimicrobial resistance in C. trachomatis treatment failures or persistent infection is unclear. With researchers in the field, we reviewed current knowledge and available approaches for evaluating antimicrobial resistance and potential clinical treatment failures for C. trachomatis. We identified key research questions that require further investigation. To date, there have been no reports of clinical C. trachomatis isolates displaying in vitro homotypic resistance to antimicrobials, but in vitro heterotypic resistance in C. trachomatis has been described. Correlation between the results of existing in vitro antimicrobial susceptibility tests and clinical outcome after treatment for C. trachomatis infection is unknown. Animal models may provide insight into chlamydial persistence, since homotypic resistance against tetracycline has been described for Chlamydia suis in pigs. Evaluating C. trachomatis clinical treatment failures, interpreting laboratory findings, and correlating the 2 clearly remain extremely challenging undertakings.

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Section: Trachomatis Antimicrobial Susceptibility Test Methodologiesmentioning

confidence: 99%

Evaluation of Antimicrobial Resistance and Treatment Failures forChlamydiatrachomatis: A Meeting Report

et al. 2005

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“…The main advantage of the RT-PCR technique are corresponding (but consistently higher) MIC values when compared with cell culture method followed by immunofluorescent staining, as showed by Cross and his colleagues on the example of erythromycin and amoxicillin, which points to the improved sensitivity of this method (61). This can be explained by the adequately suppressed chlamydial growth in concentrations exceeding the MIC values measured in cell culture, but with a presence of lowlevel replication and the detection of RNA produced only by viable organisms (62).…”

Section: Main Methods Of Appraising Antimicrobial Resistance Of Chlammentioning

confidence: 99%

Molecular mechanisms of i Chlamydia trachomatis i resistance to antimicrobial drugs

Meštrović

Ljubin‐Sternak

2018

Front Biosci

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() is a leading cause of bacterial sexually transmitted infections in developed and undeveloped countries, and therefore a global public health issue. In an era of increasing bacterial resistance to antibiotics, resistance has been an exceedingly rare phenomenon in ; however, clinical treatment failures attributed to multidrug-resistant strains have been described on several occasions. Cell culture systems using McCoy cells and subsequent immunofluorescent staining are still the most common methodology used for antimicrobial susceptibility testing, but the presence of resistance markers should be appraised by further genetic analysis. Azithromycin resistance of is often a result of the mutations in the peptidyl transferase region of 23S rRNA genes, tetracycline resistance is usually linked to the presence of foreign genomic islands integrated in chlamydial chromosome, whereas a predominant mechanism of fluoroquinolone resistance is a point mutation in the quinolone-resistance-determining region. A nucleotide substitution in gene is responsible for rifampin resistance, and different mechanisms have been involved in the development of resistance to aminoglycosides, lincomycin and sulphonamide/trimethoprim combinations.

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“…Minimal inhibitory concentrations (MIC) of antibiotic substances against C. trachomatis are generally difficult to assess. In one attempt using a RT-PCR method, MIC ranges of moxifloxacin were 0.015-0.25 mg/L, and were remarkably lower than those of ofloxacin 0.25-8 mg/L and ciprofloxacin 0.5-8 mg/L [72].…”

Section: Fluoroquinolonesmentioning

confidence: 99%

Antimicrobials in urogenital infections

Wagenlehner

Wullt

Perletti

2011

International Journal of Antimicrobial Agents

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Antimicrobial Susceptibility Testing of Chlamydia trachomatis Using a Reverse Transcriptase PCR-Based Method

Cited by 26 publications

References 21 publications

Evaluation of Antimicrobial Resistance and Treatment Failures forChlamydiatrachomatis: A Meeting Report

Evaluation of Antimicrobial Resistance and Treatment Failures forChlamydiatrachomatis: A Meeting Report

Molecular mechanisms of i Chlamydia trachomatis i resistance to antimicrobial drugs

Antimicrobials in urogenital infections

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