PurposeThe aim of this study was to investigate the change in macrolide resistance rate in pediatric Mycoplasma pneumoniae pneumonia and to evaluate the influence of macrolide-resistant M. pneumoniae (MRMP) on the clinical course of disease, by comparing 2 recent, consecutive epidemics in Korea.MethodsA total of 250 patients with M. pneumoniae pneumonia admitted to a single tertiary hospital were enrolled in this study. Detection of MRMP was based on specific point mutations in domain V of the 23S rRNA gene. The medical records of enrolled patients were reviewed retrospectively, and the clinical courses and laboratory data were compared.ResultsThe macrolide resistance rate of M. pneumoniae was 51.1% (48/94) in the 2011 epidemic, and 87.2% (136/156) in the 2015 epidemic. All MRMP isolates had the A2063G point mutation. In comparison of 2 epidemics, the mean age of patients with M. pneumoniae pneumonia was increased, and the total febrile days and febrile days after initiation of macrolides were prolonged in the 2015 epidemic. Overall severity of MRMP or macrolide-susceptible M. pneumoniae (MSMP) pneumonia over 2 epidemics was not significantly changed. However, the proportion of patients who had a fever lasting more than 72 hours after initiation of macrolides and who received corticosteroid treatment were higher in MRMP pneumonia during 2 epidemics.ConclusionsThe macrolide resistance rate of M. pneumoniae has risen rapidly over 2 recent, consecutive epidemics, and this has been associated with a prolonged clinical course and increased use of corticosteroids to treat pediatric M. pneumoniae pneumonia.

A total of 39 water samples from 23 different groundwater wells in Korea were collected and analyzed in order to monitor the occurrence of norovirus (NoV) and other indicator microbes as the first part of a national survey of groundwater. More than 500 L of untreated groundwater were filtered through 1MDS filters. Following elution and concentration by organic flocculation, PCR and sequence analysis were employed to detect and identify NoV, enterovirus, rotavirus, hepatitis A virus and adenovirus (Adv). Somatic and F-specific phages, heterotrophic bacteria, total coliforms and Escherichia coli were also analyzed to infer possible fecal contamination. NoVs were detected in 18% of the 39 samples. Five out of seven NoV-positive samples (71%) were identified as GI while the other two (29%) were GII. Enteroviruses and Advs were detected in two and three samples, respectively. Rotavirus and hepatitis A virus were not detected. Total coliforms, E. coli and coliphages were detected in 49, 15 and 13% of the samples, respectively, but did not appear to be suitable indicators of enteric virus contamination in groundwater. These results suggest that additional treatment may be needed for a significant number of groundwaters prior to use as drinking water.

The presence of human norovirus in the aquatic environment can cause outbreaks related to recreational activities and the consumption of norovirus-contaminated clams. In this study, we investigated the prevalence of norovirus genogroups I (GI) and II (GII) in the coastal aquatic environment in South Korea (March 2014 to February 2015). A total of 504 water samples were collected periodically from four coastal areas (total sites = 63), of which 44 sites were in estuaries (clam fisheries) and 19 were in inflow streams. RT-PCR analysis targeting ORF2 region C revealed that 20.6% of the water samples were contaminated by GI (13.3%) or GII (16.6%). The prevalence of human norovirus was higher in winter/spring than in summer/fall, and higher in inflow streams (50.0%) than in estuaries (7.9%). A total of 229 human norovirus sequences were identified from the water samples, and phylogenetic analysis showed that the sequences clustered into eight GI genotypes (GI.1, 2, 3, 4, 5, 6, 7, and 9) and nine GII genotypes (GII.2, 3, 4, 5, 6, 11, 13, 17, and 21). This study highlighted three issues: 1) a strong correlation between norovirus contamination via inflow streams and coastal areas used in clam fisheries; 2) increased prevalence of certain non-GII.4 genotypes, exceeding that of the GII.4 pandemic variants; 3) seasonal shifts in the dominant genotypes of both GI and GII.