Background Human adenoviruses (HAdVs) cause a wide range of diseases. However, the genotype diversity and epidemiological information relating to HAdVs among hospitalized children with respiratory tract infections (RTIs) is limited. Here, we describe the epidemiology and genotype distribution of HAdVs associated with RTIs in Beijing, China. Methods Nasopharyngeal aspirates (NPA) were collected from hospitalized children with RTIs from April 2017 to March 2018. HAdVs were detected by a TaqMan-based quantitative real-time polymerase chain reaction (qPCR) assay, and the hexon gene was used for phylogenetic analysis. Epidemiological data were analyzed using statistical product and service solutions (SPSS) 21.0 software. Results HAdV was detected in 72 (5.64%) of the 1276 NPA specimens, with most (86.11%, 62/72) HAdV-positives cases detected among children < 6 years of age. HAdV-B3 (56.06%, 37/66) and HAdV-C2 (19.70%, 13/66) were the most frequent. Of the 72 HAdV-infected cases, 27 (37.50%) were co-infected with other respiratory viruses, most commonly parainfluenza virus (12.50%, 9/72) and rhinovirus (9.72%, 7/72). The log number of viral load ranged from 3.30 to 9.14 copies per mL of NPA, with no significant difference between the HAdV mono- and co-infection groups. The main clinical symptoms in the HAdV-infected patients were fever and cough, and 62 (86.11%, 62/72) were diagnosed with pneumonia. Additionally, HAdVs were detected throughout the year with a higher prevalence in summer. Conclusions HAdV prevalence is related to age and season. HAdV-B and HAdV-C circulated simultaneously among the hospitalized children with RTIs in Beijing, and HAdV-B type 3 and HAdV-C type 2 were the most frequent.

Fifty clinical Mycoplasma pneumoniae strains were isolated from 370 children with respiratory tract infections. Four strains were susceptible to macrolides, while the other 46 (92%) were macrolide resistant. The molecular mechanism of resistance was shown to be associated with point mutations in 23S rRNA at positions 2063 and 2064.Mycoplasma pneumoniae is a common pathogen found in respiratory tract infections of children and teenagers and is commonly treated with macrolides. In recent years, strains which are resistant to common drugs have been isolated from patients (1,(3)(4)(5)(6)(7)(8). In order to evaluate the prevalence of macrolide resistance, we collected clinical samples during 2003 to 2006, cultured M. pneumoniae isolates, and screened for macrolide drug resistance. We investigated the mechanism of resistance by examining the erythromycin target site in the 23S rRNA gene of these strains.Throat swab specimens were collected from 300 inpatient and 70 outpatient children with respiratory tract infection at the Pediatric Department of Beijing Friendship Hospital, affiliated with Capital Medical University, during June 2003 to June 2006. Modified Hayflick medium was used for the isolation and growth of M. pneumoniae. Nested PCR was carried out to verify the identity of M. pneumoniae, using primers which amplify part of the 16S rRNA gene as described previously (2). The MICs of erythromycin, azithromycin, and josamycin required to inhibit M. pneumoniae growth were determined by the microdilution method (1). A reference strain, FH, was used as a drug-sensitive control. Erythromycin resistance was defined as having a MIC of Ն32 g/ml in accordance with the 2006 standards recommended by the CLSI (formerly NCCLS). To examine the molecular mechanisms of drug resistance, the 23S rRNA gene was amplified by nested PCR and the product was sequenced as described previously (8). The DNA sequences were compared with the sequence of M. pneumoniae M129 (GenBank accession no. X68422).Fifty clinical M. pneumoniae strains (44 of them from inpatients) were isolated from the 370 specimens collected. Four strains were susceptible to macrolides, and the other 46 (92%) strains were macrolide resistant. MICs of resistant strains to erythromycin, azithromycin, and josamycin were higher than that of the reference strain and higher than the CLSI guidelines (especially in the case of erythromycin and azithromycin). Table 1 shows the MIC range, MIC 50 , and MIC 90 of clinical isolate strains and the M. pneumoniae reference strain.The 23S rRNA gene sequences of four susceptible strains and the reference strain FH were identical to that of the M.

Background Acute respiratory tract infections (ARTIs) causes high amounts of morbidity and mortality worldwide every year. Human metapneumovirus (HMPV) is a major pathogen of ARTIs in children. In this study, we aimed to investigate the epidemiology and genotypic diversity of HMPV in children hospitalized with ARTIs in Beijing, China. Methods Hospitalized children aged < 14 years with ARTIs were enrolled from April 2017 to March 2018; nasopharyngeal aspirates were collected and subjected to real-time polymerase chain reaction tests for HMPV. HMPV-positive samples were genotyped based on a partial N gene. Whole genome sequences were determined for samples with high viral loads. Results 4.08% (52/1276) enrolled paediatric patients were identified as having HMPV infection. The epidemic season is winter and early spring, children aged ≤ 4 years were more susceptible to HMPV infection (47/52, 90.38%). The co-infection rate were 36.54% (19/52), the most common co-infected virus were influenza and respiratory syncytial virus. The main diagnoses of HMPV infection were pneumonia (29/52, 55.77%) and bronchitis (23/52, 44.23%), while the main clinical manifestations were cough, fever, rhinorrhoea, and sneeze. Among 48 HMPV-positive specimens, A2b (19/48, 39.58%) and B1 (26/48, 54.17%) were the main epidemic subtypes. Patients with HMPV genotype A infection had a higher viral load compared to genotype B patients (6.07 vs. 5.37 log10 RNA copies/ml). Five complete sequences of HMPV were obtained. This is the first report of a whole genome sequence of HMPV-B1 isolated in China. Conclusions HMPV is an important respiratory pathogen in paediatric patients. Cases of HMPV infection could burden hospitals in the epidemic season. HMPV viral loads and genotypes have no correlation with co-infection or clinical characteristics.