OBJECTIVES: To investigate the efficacy and safety of prolonged azithromycin (PAZM) versus switching to doxycycline (SDXC) in the treatment of macrolide-unresponsive Mycoplasma pneumoniae pneumonia (MUMPP) in children. METHODS: A total of 173 children with MUMPP who were hospitalized in Baoji Central Hospital, from January to December 2023 were selected as subjects. According to the choice of secondary antibiotic after 72 hours of initial macrolide therapy, they were divided into two groups: PAZM and SDXC. The efficacy and adverse drug reactions were compared between the two groups, and the risk factors for refractory Mycoplasma pneumoniae pneumonia (RMPP) were analyzed. RESULTS: Compared with the PAZM group, the SDXC group had significantly shorter time to defervescence and time to cough relief, a significantly lower proportion of patients using glucocorticoids, and a significantly higher proportion of patients with lung lesion absorption (P<0.05). No adverse reactions such as liver and kidney function impairment and tooth discoloration were observed in either group. RMPP occurred in 47 cases in the PAZM group. The univariate analysis showed that lactate dehydrogenase levels and age were risk factors for RMPP (P<0.05). CONCLUSIONS The efficacy of SDXC is superior to that of PAZM in children with MUMPP, and short-term use of doxycycline is relatively safe.
Humans ; Pneumonia, Mycoplasma/drug therapy* ; Doxycycline/administration & dosage* ; Female ; Male ; Azithromycin/administration & dosage* ; Child ; Child, Preschool ; Anti-Bacterial Agents/administration & dosage* ; Macrolides/administration & dosage* ; Adolescent ; Mycoplasma pneumoniae/drug effects*

OBJECTIVEMutations in 23S rRNA gene are known to be associated with macrolide resistance in Mycoplasma pneumoniae (M. pneumoniae). However, these mutations alone do not fully explain the high resistance rates in Asia. The aim of this study was to investigate other possible mutations involved in macrolide resistance in M. pneumoniae.

METHODSThe whole genomes of 10 clinical isolates of M. pneumoniae with macrolide resistance were sequenced by Illumina HiSeq2000 platform. The role of the macrolide-specific efflux transporter was assessed by efflux-pump inhibition assays with reserpine and carbonyl cyanide m-chlorophenyl-hydrazone (CCCP).

RESULTSA total of 56 single nucleotide polymorphisms (SNPs) were identified in 10 clinical isolates in comparison to the reference strains M129 and FH. Strikingly, 4 of 30 SNPs causing non-synonymous mutations were clustered in macrolide-specific efflux system gene macB encoding macrolide-specific efflux pump protein of the ATP-binding cassette transporter family. In assays of the minimal inhibitory concentrations (MIC) of macrolide antibiotics in the presence of the efflux pump inhibitors caused a significant decrease of MICs, even under detectable levels in some strains.

CONCLUSIONOur study suggests that macrolide efflux pump may contribute to macrolide resistance in M. pneumoniae in addition to the common point mutations in 23S rRNA gene.

Anti-Bacterial Agents ; pharmacology ; Drug Resistance, Bacterial ; genetics ; Genome-Wide Association Study ; Macrolides ; pharmacology ; Microbial Sensitivity Tests ; Mutation ; Mycoplasma pneumoniae ; drug effects ; genetics

OBJECTIVETo investigate the association of drug resistance of Mycoplasma pneumoniae (MP) with DNA load and genotypes in children with MP pneumonia.

METHODSA total of 230 children who were hospitalized and diagnosed with MP pneumonia between January 2012 and December 2016 were enrolled. Throat swabs were collected from the 230 children, and a rapid drug sensitivity assay was used to determine the sensitivity of clinical isolates of MP to nine commonly used antibacterial agents. Quantitative real-time PCR was used to measure MP-DNA load in throat swabs. PCR sequencing was used to determine the genotype of 2063 locus of the MP 23S rRNA V domain.

RESULTSOf the 230 children, 86 (37.4%) had genotype A in 2063 locus, 134 (58.3%) had genotype G, 8 (3.5%) had genotype C, and 2 (0.9%) had genotype T. Mutant strains (genotype G+C+T) had a significantly higher MP-DNA load than wild-type strains (genotype A) (P<0.05). The strains resistant to erythromycin, azithromycin, clarithromycin, and clindamycin had a significantly higher MP-DNA load than non-resistant strains (P<0.05). MP had a high drug resistance rate to macrolide antibiotics. More than 60% of the cases with resistance to macrolides were found to have A2063G mutations. MP was rarely resistant to quinolones (less than 2%).

CONCLUSIONSMutations in 2063 locus of the MP 23S rRNA V domain may result in the resistance of MP to macrolides and the change in DNA load and can be used as a basis for selecting drugs for MP.

Child ; Child, Preschool ; DNA, Bacterial ; analysis ; Drug Resistance, Bacterial ; Female ; Genotype ; Humans ; Infant ; Male ; Mycoplasma pneumoniae ; drug effects ; genetics ; Pneumonia, Mycoplasma ; drug therapy ; microbiology

No abstract available.
Acute Kidney Injury/microbiology ; Anti-Bacterial Agents/therapeutic use ; Biopsy ; Humans ; Kidney/*microbiology ; Male ; Middle Aged ; Mycoplasma pneumoniae/drug effects/*isolation & purification ; Nephritis/diagnosis/drug therapy/*microbiology ; Pneumonia, Mycoplasma/diagnosis/drug therapy/*microbiology ; Skin Diseases, Bacterial/diagnosis/drug therapy/*microbiology ; Steroids/therapeutic use ; Treatment Outcome ; Vasculitis/diagnosis/drug therapy/*microbiology

Acquired pure red cell aplasia (PRCA) can be induced by various factors such as viral infection, thymoma, connective tissue disease, lymphoma, and adverse drug reactions. PRCA has not been reported in an adolescent in Korea for the past several decades. We recently experienced a case of acquired PRCA in an adolescent. A 14-year-old girl presented with pallor, dizziness, and mild fever. She had isolated normocytic normochromic anemia with reticulocytopenia in the peripheral blood and erythroblastopenia in the bone marrow. She was diagnosed with secondary acquired PRCA presumably induced by Mycoplasma pneumoniae infection during her clinical course, and she experienced spontaneous remission 11 weeks after initial diagnosis. Her clinical and hematologic statuses were normal as far as 20 months after her diagnosis.
Adolescent ; Anemia ; Bone Marrow ; Connective Tissue Diseases ; Diagnosis ; Dizziness ; Drug-Related Side Effects and Adverse Reactions ; Female ; Fever ; Humans ; Korea ; Lymphoma ; Mycoplasma Infections ; Mycoplasma pneumoniae ; Pallor ; Pneumonia, Mycoplasma ; Red-Cell Aplasia, Pure ; Remission, Spontaneous ; Thymoma

Anti-Bacterial Agents ; administration & dosage ; therapeutic use ; Anti-Inflammatory Agents ; therapeutic use ; Azithromycin ; administration & dosage ; therapeutic use ; Biomarkers ; blood ; Child ; Eyelids ; pathology ; Humans ; Immunoglobulin M ; blood ; Lip ; pathology ; Male ; Methylprednisolone ; administration & dosage ; therapeutic use ; Mucositis ; diagnosis ; drug therapy ; microbiology ; Mycoplasma pneumoniae ; drug effects ; isolation & purification ; Pneumonia, Mycoplasma ; complications ; diagnosis ; drug therapy

Anti-Bacterial Agents ; therapeutic use ; Child ; Child, Preschool ; Drug Resistance, Bacterial ; Humans ; Mycoplasma pneumoniae ; drug effects ; pathogenicity ; Pneumonia ; drug therapy ; microbiology

BACKGROUND: This study aimed to evaluate the prevalence of Mycoplasma pneumoniae in primary and tertiary care hospitals and its macrolide resistance rate. METHODS: Nasopharyngeal swabs were collected from 195 pediatric patients in primary and tertiary care hospitals from October to November 2010. The AccuPower MP real-time PCR kit (Bioneer, Korea) was used for the detection of M. pneumoniae. Direct amplicon sequencing was performed to detect point mutations conferring resistance to macrolides in the 23S rRNA gene. RESULTS: Among the 195 specimens, 17 (8.7%) were M. pneumoniae positive, and 3 of the strains (17.6%) obtained from these 17 specimens displayed the A2063G mutation in 23S rRNA. Three macrolide-resistant M. pneumoniae isolates were isolated from patients hospitalized at the primary care hospital. The positive rates of M. pneumoniae for the primary and tertiary care hospitals were 12.1% (15/124) and 2.8% (2/71), respectively (P=0.033). CONCLUSIONS: The positive rate of M. pneumoniae in the primary care hospital was higher than that in the tertiary care hospital. Simultaneous detection of M. pneumoniae and macrolide-resistant mutation genes in the 23S rRNA by real-time PCR is needed for rapid diagnosis and therapy of M. pneumoniae infections.
Anti-Bacterial Agents/*pharmacology ; Child, Preschool ; Drug Resistance, Bacterial/*drug effects ; Female ; Humans ; Infant ; Infant, Newborn ; Macrolides/*pharmacology ; Male ; Mycoplasma pneumoniae/genetics/*isolation & purification ; Nasopharynx/microbiology ; Pneumonia, Mycoplasma/epidemiology/microbiology ; Primary Health Care ; RNA, Ribosomal, 23S/analysis ; Reagent Kits, Diagnostic ; Real-Time Polymerase Chain Reaction ; Tertiary Healthcare

BACKGROUNDMycoplasma pneumoniae is a common pathogen that caused community-acquired pneumonia (CAP). P1 protein served as major adhesion and immunodominant protein in Mycoplasma pneumoniae, but little about P1 gene was learned and the relationship between P1 genotype and macrolide resistance has yet to be explored.

METHODSThe DNA sequence of the entire P1 gene from 35 strains isolated from clinical specimens collected in Beijing, China, in 2010 was determined. The resulting sequences were checked for known macrolide resistance mutations, such as A2063G, A2064G, C2617G in domain V of 23S rRNA. Antibiotic susceptibility test was done to further identify macrolide resistant strains.

RESULTSThirty-four clinical strains were type 1, and were identical to type 1 reference strain MP129. Only one clinical strain, MpYYM22, was type 2, and proved to be variant 2c. One synonymous point mutation in the P1 type 1 gene from two isolates was identified relative to the MP129 P1 sequence at nucleotide position (nt) 552 (C>A), while another two isolates had missense mutations at nt 2504 (G>A). This point mutation caused an amino acid change from glycine to glutamic acid. An AGT tri-nucleotide variable-number tandem repeat (VNTR), coding for serine and repeating 6-11 times, up to 15-16 times, was found in the region between the RepMP4 and RepMP2/3 elements in the 35 isolates examined. All 35 clinical strains, including MpYYM22, demonstrated macrolide resistance with the range of minimum inhibitory concentration (MIC) of erythromycin from 64 to 256 µg/ml, having an A2063G transition in domain V of the 23S rRNA gene.

CONCLUSIONSP1 type 1 was the dominant type of Mycoplasma pneumoniae in Beijing in 2010, although variant 2c strains were present. More samples are needed to determine whether there is a relationship between the P1 genotype and macrolide resistance, as the 35 strains examined did not allow a conclusive result. However, the AGT tri-nucleotide VNTR may be a more informative locus for multi-locus VNTR analysis.

Anti-Bacterial Agents ; pharmacology ; DNA, Bacterial ; Drug Resistance, Bacterial ; Genotype ; Humans ; Macrolides ; pharmacology ; Microbial Sensitivity Tests ; Mycoplasma pneumoniae ; drug effects ; genetics ; metabolism

We describe 2 cases of pneumonia caused by the same macrolide-resistant Mycoplasma pneumoniae in siblings. M. pneumoniae was identified using real-time PCR. Direct sequence analysis of the 23S rRNA gene revealed a point mutation in V domain (A2063G) of the 23S rRNA gene.
Anti-Bacterial Agents/pharmacology ; Child ; Child, Preschool ; Drug Resistance, Bacterial/drug effects ; Humans ; Macrolides/pharmacology ; Male ; Mutation ; Mycoplasma pneumoniae/*genetics/isolation & purification ; Pneumonia, Mycoplasma/*diagnosis/microbiology/radiography ; RNA, Ribosomal, 23S/*analysis ; Real-Time Polymerase Chain Reaction ; Sequence Analysis, RNA ; Siblings