scholarly journals Clinical Efficacy of Doxycycline for Treatment of Macrolide-Resistant Mycoplasma pneumoniae Pneumonia in Children

Antibiotics ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 192
Author(s):  
Hyunju Lee ◽  
Youn Young Choi ◽  
Young Joo Sohn ◽  
Ye Kyung Kim ◽  
Mi Seon Han ◽  
...  

In areas with high prevalence of macrolide-resistant Mycoplasma pneumoniae (MRMP) pneumonia, treatment in children has become challenging. This study aimed to analyze the efficacy of macrolides and doxycycline with regard to the presence of macrolide resistance. We analyzed children with MP pneumonia during the two recent epidemics of 2014–2015 and 2019–2020 from four hospitals in Korea. Nasopharyngeal samples were obtained from children with pneumonia for MP cultures and polymerase chain reaction (PCR). Macrolide resistance was determined by the analysis of 23S rRNA gene transition. Time to defervescence and to chest X-ray improvement were analyzed. Of 145 cases, the median age was 5.0 years and MRMP accounted for 59 (40.7%). Among macrolide-susceptible MP (MSMP), 78 (90.7%) were treated with macrolides and 21 (35.6%) in the MRMP group with doxycycline. In MRMP pneumonia, shorter days to defervescence (2 vs. 5 days, p < 0.001) and to chest X-ray improvement (3 vs. 6 days, p < 0.001) in the doxycycline group than in the macrolide group was observed, whereas no differences were observed among children with MSMP pneumonia. Compared to macrolides, treatment with doxycycline resulted in better outcomes with a shorter time to defervescence and to chest X-ray improvement among children with MRMP pneumonia.

2018 ◽  
Author(s):  
Xiujun Tian ◽  
Ran Wei ◽  
Junyan Shao ◽  
Hong Wang ◽  
Jing Li ◽  
...  

Older children especially from seven to thirteen years old are more prone to develop Mycoplasma pneumoniae (MP) infection; in winter children are more susceptible to infect with MP. In Beijing, China in 2016 the rates of macrolide resistance of MP were 69.48% (in total children), 61.59% (in outpatients) and 79.28% (in hospitalized patients), respectively. All the macrolide resistant isolates harbored A2063G or A2064G mutation in the 23S rRNA gene. Seven isolates showed a mixed infection. Susceptibility results showed that 73 isolates with the A2063G mutation demonstrated different levels resistance to erythromycin (MIC=8 to>256μg/ml), azithromycin (MIC=8 to>64μg/ml) and josamycin (MIC=2 to 8μg/ml). No cross-resistance was observed in the in the antibiotics of levofloxacin and tetracycline against MP.


2019 ◽  
Vol 21 (10) ◽  
pp. 749-754 ◽  
Author(s):  
Chen Yuan ◽  
Fang-Mei Min ◽  
Yin-Jie Ling ◽  
Gang Li ◽  
Hong-Zhou Ye ◽  
...  

Aim: To analyze the clinical characteristics and antibiotic resistance of Mycoplasma pneumoniae pneumonia (MP) in Chinese patients, providing valuable information for the management of patients with MP. Methods: A total of 120 children who were hospitalized in The First Hospital of Huzhou between January and December 2016 for respiratory tract infection due to M. pneumoniae were enrolled in this study. Infection with M. pneumoniae was confirmed by ELISA for M. pneumoniae antibody, PCR, and throat culture. Antibiotic resistance was measured from the minimum inhibitory concentrations (MICs) of antibiotics. The 23S rRNA gene of M. pneumoniae was also examined for mutations using DNA sequencing. Patients with MP were classified into antibiotic resistance (n = 98) and no resistance (n = 20) groups. For the 98 patients showing antibiotic resistance, they were further stratified into subgroups based on the antibiotics initially prescribed: azithromycin or erythromycin (n = 78) and cephalosporin or penicillin (n = 20). Clinical characteristics were compared between the patient groups. Results: Antibiotic resistance group presented significantly longer febrile days compared to the no resistance group (P = 0.007). The number of febrile days after macrolide treatment was also longer in antibiotic resistance group than in no resistance group (P = 0.042). MP patients initially treated with azithromycin or erythromycin showed a longer average duration of respiratory symptoms (P = 0.046) and had a fever for more days after macrolide treatment (P = 0.009) compared to those received cephalosporin or penicillin. The average white blood cell count of patients treated with azithromycin or erythromycin was nearly half of those treated with cephalosporin or penicillin (P < 0.001). Nearly 90% of the resistant M. pneumoniae strains showed A to G substitution at position 2063 of the 23S rRNA gene. Conclusion: The clinical characteristics and antibiotic resistance of MP were analyzed in 120 Chinese patients. DNA sequencing revealed a highly prevalent A2063G mutation in the 23S rRNA gene.


2013 ◽  
Vol 33 (1) ◽  
pp. 65-68 ◽  
Author(s):  
Joo Hee Hong ◽  
Jin Kyong Chun ◽  
Young Uh ◽  
Ki Jin Oh ◽  
Juwon Kim ◽  
...  

PLoS ONE ◽  
2021 ◽  
Vol 16 (10) ◽  
pp. e0258694
Author(s):  
Nobuhisa Ishiguro ◽  
Rikako Sato ◽  
Toshihiko Mori ◽  
Hiroshi Tanaka ◽  
Mitsuo Narita ◽  
...  

Objectives Macrolides are generally considered to be the drugs of choice for treatment of patients with Mycoplasma pneumoniae infection. However, macrolide-resistant M. pneumoniae has been emerging since about 2000. The Smart Gene® system (MIZUHO MEDY Co., Ltd., Tosu, Japan) is a novel fully automated system for detection of pathogens using the method of quantitative polymerase chain reaction (qPCR) with QProbe (QProbe PCR). The entire procedure is completed within 50 min and the size of the instrument is small (15 x 34 x 30 cm). The purpose of this study was to evaluate the usefulness of the Smart Gene® system for detection of M. pneumoniae and detection of a point mutation at domain V of the 23S rRNA gene of M. pneumoniae. Materials Pharyngeal swab samples were collected from 154 patients who were suspected of having respiratory tract infections associated with M. pneumoniae. Results Compared with the results of qPCR, the sensitivity and specificity of the Smart Gene® system were 98.7% (78/79) and 100.0% (75/75), respectively. A point mutation at domain V of the 23S rRNA gene was detected from 7 (9.0%) of 78 M. pneumoniae-positive samples by the Smart Gene® system and these results were confirmed by direct sequencing. The minimum inhibitory concentrations of clarithromycin among the 5 isolates of M. pneumoniae with a point mutation at domain V of the 23S rRNA gene were >64 μg/ml and those among the 33 isolates without a mutation in the 23S rRNA gene were <0.0625 μg/ml. Conclusion The Smart Gene® system is a rapid and accurate assay for detection of the existence of M. pneumoniae and a point mutation at domain V of the 23S rRNA gene of M. pneumoniae at the same time. The Smart Gene® system is suitable for point-of-care testing in both hospital and outpatient settings.


2012 ◽  
Vol 56 (12) ◽  
pp. 6393-6396 ◽  
Author(s):  
Soo Jin Yoo ◽  
Hyo-Bin Kim ◽  
Sang-Ho Choi ◽  
Sang-Oh Lee ◽  
Sung-Han Kim ◽  
...  

ABSTRACTWe investigated the frequency and clinical significance of macrolide resistance in adult and pediatric patients with community-acquired pneumonia from aMycoplasma pneumoniaeinfection. The frequency of the A2063G mutation in the 23S rRNA gene was significantly higher in children than in adults (61.3% [19/31] and 13.3% [8/60], respectively;P< 0.001). Patients with macrolide-resistantM. pneumoniaeinfections showed a longer duration of fever (P= 0.021) and required a longer duration of antibiotic treatment (P= 0.007).


2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Bai Wei ◽  
Min Kang

We investigated the molecular mechanisms underlying macrolide resistance in 38 strains ofCampylobacterisolated from poultry. Twenty-seven strains were resistant to azithromycin and erythromycin, five showed intermediate azithromycin resistance and erythromycin susceptibility, and six showed azithromycin resistance and erythromycin susceptibility. FourCampylobacter jejuniand sixCampylobacter colistrains had azithromycin MICs which were 8–16 and 2–8-fold greater than those of erythromycin, respectively. The A2075G mutation in the 23S rRNA gene was detected in 11 resistant strains with MICs ranging from 64 to ≥ 512μg/mL. Mutations including V137A, V137S, and a six-amino acid insertion (114-VAKKAP-115) in ribosomal protein L22 were detected in theC. jejunistrains. Erythromycin ribosome methylase B-erm(B) was not detected in any strain. All strains except three showed increased susceptibility to erythromycin with twofold to 256-fold MIC change in the presence of phenylalanine arginine ß-naphthylamide (PAßN); the effects of PAßN on azithromycin MICs were limited in comparison to those on erythromycin MICs, and 13 strains showed no azithromycin MIC change in the presence of PAßN. Differences between azithromycin and erythromycin resistance and macrolide resistance phenotypes and genotypes were observed even in highly resistant strains. Further studies are required to better understand macrolide resistance inCampylobacter.


2020 ◽  
Vol 22 (4) ◽  
pp. 306-312
Author(s):  
O.V. Ivanova ◽  
Inna A. Edelstein ◽  
O.I. Romashov ◽  
Roman S. Kozlov

Objective. To evaluate effect of 23S rRNA gene mutations in Mycoplasma pneumoniae on severity of community-acquired pneumonia (CAP) in young adult patients. Materials and Methods. A total of 42 case histories of young adult patients with CAP treated at the Smolensk military hospital over the period of 25 October 2017 to 25 December 2019 were reviewed. «AmpliSens® Mycoplasma pneumoniae/Chlamydophila pneumoniae-FL» real-time PCR kit was used to detect M. pneumoniae from nasopharyngeal swabs collected prior to antimicrobial therapy. Testing for 23S rRNA gene mutations conferring macrolide resistance was performed by real-time PCR melt curve analysis (patent no. 2646123) and confirmed by DNA sequencing. Results. All patients had a clinical picture of non-severe CAP on hospital admission. All patients were treated with standard doses of azithromycin or clarithromycin. No respiratory failure or any other complications were observed. Macrolide-resistant genotype of M. pneumoniae was detected in 4 (9.5%) patients. Clinical, laboratory and radiological resolution of pneumonia in all cases occurred on day 10– 16, regardless of the presence of macrolide-resistant genotype. Conclusions. There were no differences in clinical course of severity between CAP caused by M. pneumoniae with 23S rRNA gene mutation and CAP caused by wild-type M. pneumoniae The presence of mutations in the 23S rRNA gene of M. pneumoniae did not worsen the clinical course of CAP.


2005 ◽  
Vol 49 (7) ◽  
pp. 2753-2759 ◽  
Author(s):  
Amera Gibreel ◽  
Veronica N. Kos ◽  
Monika Keelan ◽  
Cathy A. Trieber ◽  
Simon Levesque ◽  
...  

ABSTRACT A collection of 23 macrolide-resistant Campylobacter isolates from different geographic areas was investigated to determine the mechanism and stability of macrolide resistance. The isolates were identified as Campylobacter jejuni or Campylobacter coli based on the results of the hippurate biochemical test in addition to five PCR-based genotypic methods. Three point mutations at two positions within the peptidyl transferase region in domain V of the 23S rRNA gene were identified. About 78% of the resistant isolates exhibited an A→G transition at Escherichia coli equivalent base 2059 of the 23S rRNA gene. The isolates possessing this mutation showed a wide range of erythromycin and clarithromycin MICs. Thus, this mutation may incur a greater probability of treatment failure in populations infected by resistant Campylobacter isolates. Another macrolide-associated mutation (A→C transversion), at E. coli equivalent base 2058, was detected in about 13% of the isolates. An A→G transition at a position cognate with E. coli 23S rRNA base 2058, which is homologous to the A2142G mutation commonly described in Helicobacter pylori, was also identified in one of the C. jejuni isolates examined. In the majority of C. jejuni isolates, the mutations in the 23S rRNA gene were homozygous except in two cases where the mutation was found in two of the three copies of the target gene. Natural transformation demonstrated the transfer of the macrolide resistance phenotype from a resistant Campylobacter isolate to a susceptible Campylobacter isolate. Growth rates of the resulting transformants containing A-2058→C or A-2059→G mutations were similar to that of the parental isolate. The erythromycin resistance of six of seven representative isolates was found to be stable after successive subculturing in the absence of erythromycin selection pressure regardless of the resistance level, the position of the mutation, or the number of the mutated copies of the target gene. One C. jejuni isolate showing an A-2058→G mutation, however, reverted to erythromycin and clarithromycin susceptibility after 55 subcultures on erythromycin-free medium. Investigation of ribosomal proteins L4 and L22 by sequence analysis in five representative isolates of C. jejuni and C. coli demonstrated no significant macrolide resistance-associated alterations in either the L4 or the L22 protein that might explain either macrolide resistance or enhancement of the resistance level.


2003 ◽  
Vol 47 (10) ◽  
pp. 3053-3060 ◽  
Author(s):  
Kevin A. Nash

ABSTRACT High-level, acquired macrolide resistance in mycobacteria is conferred by mutation within the 23S rRNA gene. However, several mycobacteria are naturally resistant to macrolides, including the Mycobacterium smegmatis group and Mycobacterium tuberculosis complex. Thus, the aim of this study was to characterize this resistance. Intrinsic macrolide resistance in M. smegmatis was inducible and showed cross-resistance to lincosamides but not to streptogramin B (i.e., ML resistance). A similar phenotype was found with Mycobacterium microti and macrolide-resistant Mycobacterium fortuitum. A search of the DNA sequence data for M. smegmatis strain mc2155 identified a novel erm gene, erm(38), and expression analysis showed that erm(38) RNA levels increased >10-fold after a 2-h incubation with macrolide. Inducible ML resistance was not expressed by an erm(38) knockout mutant, and complementation of this mutant with intact erm(38) in trans resulted in high-level ML resistance (e.g., clarithromycin MIC of >512 μg/ml). Thus, the results indicate that erm(38) confers the intrinsic ML resistance of M. smegmatis. Southern blot analysis with an erm(38)-specific probe indicated that a similar gene may be present in macrolide-resistant M. fortuitum. This finding, with the presence of the erm(37) gene (Rv1988) in the M. tuberculosis complex, suggests that such genes are widespread in mycobacteria with intrinsic macrolide resistance.


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