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Community-acquired Pneumonia Among Children in Taiwan
Pediatrics and Neonatology (2013) 54, 1e2
Available online at www.sciencedirect.com
journal homepage: http://www.pediatr-neonatol.com
EDITORIAL
Community-acquired Pneumonia Among Children in Taiwan Community-acquired pneumonia is a common disease and the leading cause of death among children worldwide. In Taiwan, Streptococcus pneumoniae, Mycoplasma pneumoniae, and viruses are equally common etiologic pathogens in healthy children with community-acquired pneumonia.1 Historically, pneumonia caused by Streptococcus pneumoniae usually resolved completely without destructive sequelae in spite of intense inflammation during pneumococcal infection. However, the incidence of complications of pneumococcal pneumonia, including necrotizing pneumonia and/or empyema, has increased among children in the past decade.2 Before the use of pneumococcal conjugate vaccine 7 in Taiwan, serotype 14 was the most common serotype that caused necrotizing pneumonia and/or empyema.2 Since 2009, there has been a shift from serotype 14 being the predominant serotype to serotype 19A.3 The same shift occurred for the genotype ST46, a clone associated with necrotizing pneumonia and empyema,2,3 being the predominant genotype previously to genotype ST320. Serotype 19A ST320 pneumonia had a significantly higher risk of lung necrosis and air leak.3 The evolution of serotype 19A ST320 into a highly virulent strain with high-level resistance to antimicrobial agents is a great challenge in treating pneumococcal disease. The optimal pneumococcal conjugate vaccine must contain serotype 19A to prevent this serious complication in children in Taiwan and elsewhere. M. pneumoniae is a common pathogen responsible for pediatric community-acquired pneumonia, accounting for 10e40% of cases. The illness is usually self-limiting, with symptoms lasting several weeks, but sometimes it causes severe pneumonia. Although there is still insufficient evidence to show that antibiotics are effective in children with pneumonia caused by M. pneumoniae, macrolides are the drug of choice for treating children with M. pneumoniae infection.4 Since 2000, macrolide resistance in M. pneumoniae strains has been increasing since the report of a pediatric patient infected by macrolide-resistant M. pneumoniae in Japan. Disease caused by macrolideresistant M. pneumoniae has a longer duration of fever than that caused by macrolide-susceptible M. pneumoniae.5 The mechanism of resistance to macrolides in
M. pneumoniae frequently involves mutations in the 23S rRNA including transitions of A2063G and A2064G. The mutation at A2063G is more common than A2064G, but the mutation at A2064G confers resistance to a broader spectrum of other antimicrobial agents. Wang et al reported that M. pneumoniae was the most frequent cause of fatal community-acquired pneumonia in a medical center in Taiwan.6 A proportion of M. pneumoniae pneumonia was noted to present with persistent fever, hypoxemia, and radiographic deterioration in spite of macrolide usage.7 Pleural effusion, necrotizing pneumonitis, lung abscess, bronchiolitis obliterans organizing pneumonia, and acute respiratory distress syndrome have been reported in association with M. pneumoniae pneumonia in children.7 Severe lung injury in M. pneumoniae pneumonia was presumed to be a consequence of overproduction of cytokines and an exuberant cell-mediated immune response. Clinical experiences and animal models suggest that the use of both antimicrobial therapy and immunomodulatory agents is important to improve the outcome of severe M. pneumoniae pneumonia. In contrast, extracorporeal membrane oxygenation therapy could be considered to treat patients with acute respiratory distress syndrome caused by M. pneumoniae.7 The percentage of macrolide-resistant M. pneumoniae strains in Taiwan was 23% in a multicenter study.5 Given the increase of macrolide-resistant M. pneumoniae in recent years, effective antimicrobial treatment should be a critical component of managing severe cases of macrolide-resistant strain infection. More studies to evaluate the optimal treatment in severe cases of M. pneumoniae pneumonia regardless of macrolide resistance are warranted. Yu-Chia Hsieh Department of Pediatrics, Chang Gung Children’s Hospital, Chang Gung Memorial Hospital, Chang Gung University, College of Medicine, 5 Fu-Shin Street, Kweishan 333, Taoyuan, Taiwan E-mail address: [email protected]
1875-9572/$36 Copyright ª 2013, Taiwan Pediatric Association. Published by Elsevier Taiwan LLC. All rights reserved. http://dx.doi.org/10.1016/j.pedneo.2012.12.018
Dec 4, 2012
2
References 1. Chen CJ, Lin PY, Tsai MH, Huang CG, Tsao KC, Wong KS, et al. Etiology of community-acquired pneumonia in hospitalized children in northern Taiwan. Pediatr Infect Dis J 2012;31: e196e201. 2. Hsieh YC, Hsueh PR, Lu CY, Lee PI, Lee CY, Huang LM. Clinical manifestations and molecular epidemiology of necrotizing pneumonia and empyema caused by Streptococcus pneumoniae in children in Taiwan. Clin Infect Dis 2004;38:830e5. 3. Hsieh YC, Wang CW, Lai SH, Lai JY, Wong KS, Huang YC, et al. Necrotizing pneumococcal pneumonia with bronchopleural fistula among children in Taiwan. Pediatr Infect Dis J 2011;30: 740e4.
Editorial 4. Mulholland S, Gavranich JB, Chang AB. Antibiotics for communityacquired lower respiratory tract infections secondary to Mycoplasma pneumoniae in children. Cochrane Database Syst Rev 2010; CD004875. 5. Wu PS, Chang LY, Lin HC, Chi H, Hsieh YC, Huang YC, et al. Epidemiology and clinical manifestations of children with macrolide-resistant Mycoplasma pneumoniae pneumonia in Taiwan. Pediatr Pulmonol 2012. http://dx.doi.org/10.1002/ ppul.22706 [Epub ahead of print]. 6. Wang LJ, Mu SC, Lin CH, Lin MI, Sung TC. Fatal communityacquired pneumonia: 18 years in a medical center. Pediatr Neonatol 2013;54:22e7. 7. Hsieh YC, Tsao KC, Huang CG, Tong S, Winchell JM, Huang YC, et al. Life-threatening pneumonia caused by macrolide-resistant Mycoplasma pneumoniae. Pediatr Infect Dis J 2012;31:208e9.
Available online at www.sciencedirect.com
journal homepage: http://www.pediatr-neonatol.com
EDITORIAL
Community-acquired Pneumonia Among Children in Taiwan Community-acquired pneumonia is a common disease and the leading cause of death among children worldwide. In Taiwan, Streptococcus pneumoniae, Mycoplasma pneumoniae, and viruses are equally common etiologic pathogens in healthy children with community-acquired pneumonia.1 Historically, pneumonia caused by Streptococcus pneumoniae usually resolved completely without destructive sequelae in spite of intense inflammation during pneumococcal infection. However, the incidence of complications of pneumococcal pneumonia, including necrotizing pneumonia and/or empyema, has increased among children in the past decade.2 Before the use of pneumococcal conjugate vaccine 7 in Taiwan, serotype 14 was the most common serotype that caused necrotizing pneumonia and/or empyema.2 Since 2009, there has been a shift from serotype 14 being the predominant serotype to serotype 19A.3 The same shift occurred for the genotype ST46, a clone associated with necrotizing pneumonia and empyema,2,3 being the predominant genotype previously to genotype ST320. Serotype 19A ST320 pneumonia had a significantly higher risk of lung necrosis and air leak.3 The evolution of serotype 19A ST320 into a highly virulent strain with high-level resistance to antimicrobial agents is a great challenge in treating pneumococcal disease. The optimal pneumococcal conjugate vaccine must contain serotype 19A to prevent this serious complication in children in Taiwan and elsewhere. M. pneumoniae is a common pathogen responsible for pediatric community-acquired pneumonia, accounting for 10e40% of cases. The illness is usually self-limiting, with symptoms lasting several weeks, but sometimes it causes severe pneumonia. Although there is still insufficient evidence to show that antibiotics are effective in children with pneumonia caused by M. pneumoniae, macrolides are the drug of choice for treating children with M. pneumoniae infection.4 Since 2000, macrolide resistance in M. pneumoniae strains has been increasing since the report of a pediatric patient infected by macrolide-resistant M. pneumoniae in Japan. Disease caused by macrolideresistant M. pneumoniae has a longer duration of fever than that caused by macrolide-susceptible M. pneumoniae.5 The mechanism of resistance to macrolides in
M. pneumoniae frequently involves mutations in the 23S rRNA including transitions of A2063G and A2064G. The mutation at A2063G is more common than A2064G, but the mutation at A2064G confers resistance to a broader spectrum of other antimicrobial agents. Wang et al reported that M. pneumoniae was the most frequent cause of fatal community-acquired pneumonia in a medical center in Taiwan.6 A proportion of M. pneumoniae pneumonia was noted to present with persistent fever, hypoxemia, and radiographic deterioration in spite of macrolide usage.7 Pleural effusion, necrotizing pneumonitis, lung abscess, bronchiolitis obliterans organizing pneumonia, and acute respiratory distress syndrome have been reported in association with M. pneumoniae pneumonia in children.7 Severe lung injury in M. pneumoniae pneumonia was presumed to be a consequence of overproduction of cytokines and an exuberant cell-mediated immune response. Clinical experiences and animal models suggest that the use of both antimicrobial therapy and immunomodulatory agents is important to improve the outcome of severe M. pneumoniae pneumonia. In contrast, extracorporeal membrane oxygenation therapy could be considered to treat patients with acute respiratory distress syndrome caused by M. pneumoniae.7 The percentage of macrolide-resistant M. pneumoniae strains in Taiwan was 23% in a multicenter study.5 Given the increase of macrolide-resistant M. pneumoniae in recent years, effective antimicrobial treatment should be a critical component of managing severe cases of macrolide-resistant strain infection. More studies to evaluate the optimal treatment in severe cases of M. pneumoniae pneumonia regardless of macrolide resistance are warranted. Yu-Chia Hsieh Department of Pediatrics, Chang Gung Children’s Hospital, Chang Gung Memorial Hospital, Chang Gung University, College of Medicine, 5 Fu-Shin Street, Kweishan 333, Taoyuan, Taiwan E-mail address: [email protected]
1875-9572/$36 Copyright ª 2013, Taiwan Pediatric Association. Published by Elsevier Taiwan LLC. All rights reserved. http://dx.doi.org/10.1016/j.pedneo.2012.12.018
Dec 4, 2012
2
References 1. Chen CJ, Lin PY, Tsai MH, Huang CG, Tsao KC, Wong KS, et al. Etiology of community-acquired pneumonia in hospitalized children in northern Taiwan. Pediatr Infect Dis J 2012;31: e196e201. 2. Hsieh YC, Hsueh PR, Lu CY, Lee PI, Lee CY, Huang LM. Clinical manifestations and molecular epidemiology of necrotizing pneumonia and empyema caused by Streptococcus pneumoniae in children in Taiwan. Clin Infect Dis 2004;38:830e5. 3. Hsieh YC, Wang CW, Lai SH, Lai JY, Wong KS, Huang YC, et al. Necrotizing pneumococcal pneumonia with bronchopleural fistula among children in Taiwan. Pediatr Infect Dis J 2011;30: 740e4.
Editorial 4. Mulholland S, Gavranich JB, Chang AB. Antibiotics for communityacquired lower respiratory tract infections secondary to Mycoplasma pneumoniae in children. Cochrane Database Syst Rev 2010; CD004875. 5. Wu PS, Chang LY, Lin HC, Chi H, Hsieh YC, Huang YC, et al. Epidemiology and clinical manifestations of children with macrolide-resistant Mycoplasma pneumoniae pneumonia in Taiwan. Pediatr Pulmonol 2012. http://dx.doi.org/10.1002/ ppul.22706 [Epub ahead of print]. 6. Wang LJ, Mu SC, Lin CH, Lin MI, Sung TC. Fatal communityacquired pneumonia: 18 years in a medical center. Pediatr Neonatol 2013;54:22e7. 7. Hsieh YC, Tsao KC, Huang CG, Tong S, Winchell JM, Huang YC, et al. Life-threatening pneumonia caused by macrolide-resistant Mycoplasma pneumoniae. Pediatr Infect Dis J 2012;31:208e9.