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Clinical Characteristics and Antibiotic Resistance of Mycoplasma Pneumoniae Pneumonia in Hospitalized Chinese Children.
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.
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.
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