RESUMO
INTRODUCTION: Macrolide-resistant Mycoplasma pneumoniae (MRMP) has become prevalent in children. This study investigated the clinical and laboratory variables of MRMP and macrolide-sensitive M. pneumoniae (MSMP) and identified factors associated with prolonged hospital admission in children. METHODS: A prospective multicenter study was conducted in 1063 children <18 years old in July 2018-June 2020. The 454 had a positive M. pneumoniae polymerase chain reaction assay. RESULTS: Most subjects had MRMP (78.4%), and all mutated strains had the A2063G transition. We defined MRMP* (n = 285) as MRMP pneumonia requiring admission and MSMP* (n = 72) as MSMP pneumonia requiring admission. Patients with MRMP pneumonia were older, more likely to have segmental/lobar pneumonia, and had more febrile days than those with MSMP pneumonia. C-reactive protein (CRP), lactate dehydrogenase (LDH), and percentage neutrophils were more strongly associated with MRMP* than MSMP* groups. Percentage neutrophils, CRP, and alanine aminotransferase significantly changed between admission and follow-up measurements in patients with MRMP* (P < 0.05). The duration of admission positively correlated with the number of febrile days after initiation of antibiotic medication and laboratory variables (white blood cell count, CRP, and aspartate aminotransferase [AST]) (P < 0.05). Random forest analysis indicated that the number of febrile days after initiation of antibiotic medication, AST, and percentage neutrophils at admission was over five. CONCLUSIONS: This study indicated that children with M. pneumoniae pneumonia with a higher number of febrile days after initiation of antibiotic medication, AST, and percentage neutrophils at admission were more likely to have prolonged admission duration.
Assuntos
Mycoplasma pneumoniae , Pneumonia por Mycoplasma , Criança , Humanos , Adolescente , Mycoplasma pneumoniae/genética , Estudos Prospectivos , Farmacorresistência Bacteriana , Pneumonia por Mycoplasma/tratamento farmacológico , Pneumonia por Mycoplasma/epidemiologia , Macrolídeos/uso terapêutico , Macrolídeos/farmacologia , Antibacterianos/uso terapêutico , Antibacterianos/farmacologia , Proteína C-ReativaRESUMO
BACKGROUND: Respiratory infections among children, particularly community-acquired pneumonia (CAP), is a major disease with a high frequency among outpatient and inpatient visits. The causes of CAP vary depending on individual susceptibility, the epidemiological characteristics of the community, and the season. We performed this study to establish a nationwide surveillance network system and identify the causative agents for CAP and antibiotic resistance in Korean children with CAP. METHODS: The monitoring network was composed of 28 secondary and tertiary medical institutions. Upper and lower respiratory samples were assayed using a culture or polymerase chain reaction (PCR) from August 2018 to May 2020. RESULTS: A total of 1023 cases were registered in patients with CAP, and PCR of atypical pneumonia pathogens revealed 422 cases of M. pneumoniae (41.3%). Respiratory viruses showed a positivity rate of 65.7% by multiplex PCR test, and human rhinovirus was the most common virus, with 312 cases (30.5%). Two hundred sixty four cases (25.8%) were isolated by culture, including 131 cases of S. aureus (12.8%), 92 cases of S. pneumoniae (9%), and 20 cases of H. influenzae (2%). The cultured, isolated bacteria may be colonized pathogen. The proportion of co-detection was 49.2%. The rate of antibiotic resistance showed similar results as previous reports. CONCLUSIONS: This study will identify the pathogens that cause respiratory infections and analyze the current status of antibiotic resistance to provide scientific evidence for management policies of domestic respiratory infections. Additionally, in preparation for new epidemics, including COVID-19, monitoring respiratory infections in children and adolescents has become more important, and research on this topic should be continuously conducted in the future.
Assuntos
COVID-19 , Infecções Comunitárias Adquiridas , Pneumonia por Mycoplasma , Adolescente , Criança , Infecções Comunitárias Adquiridas/microbiologia , Humanos , Reação em Cadeia da Polimerase Multiplex/métodos , Staphylococcus aureusRESUMO
Plastic bronchitis is an uncommon disorder characterized by the formation of bronchial casts. It is associated with congenital heart disease or pulmonary disease. In children with underlying conditions such as allergy or asthma, influenza can cause severe plastic bronchitis resulting in respiratory failure. A review of the literature showed nine cases of plastic bronchitis with H1N1 including this case. We report a case of a child with recurrent plastic bronchitis with eosinophilic cast associated with influenza B infection, who had recovered from plastic bronchitis associated with an influenza A (H1N1) virus infection 5 months previously. To the best of our knowledge, this is the first case of recurrent plastic bronchitis related to influenza viral infection. If patients with influenza virus infection manifest acute respiratory distress with total lung atelectasis, clinicians should consider plastic bronchitis and early bronchoscopy should be intervened. In addition, management for underlying disease may prevent from recurrence of plastic bronchitis.
Assuntos
Bronquite/diagnóstico , Vírus da Influenza A Subtipo H1N1/genética , Influenza Humana/diagnóstico , Administração por Inalação , Corticosteroides/uso terapêutico , Antivirais/uso terapêutico , Bronquite/complicações , Bronquite/tratamento farmacológico , Broncoscopia , Criança , DNA Viral/análise , Dispneia/etiologia , Humanos , Hipersensibilidade/patologia , Vírus da Influenza A Subtipo H1N1/isolamento & purificação , Vírus da Influenza B/genética , Vírus da Influenza B/isolamento & purificação , Influenza Humana/complicações , Influenza Humana/tratamento farmacológico , Masculino , Oseltamivir/uso terapêutico , Atelectasia Pulmonar/diagnóstico por imagem , Atelectasia Pulmonar/tratamento farmacológico , Reação em Cadeia da Polimerase em Tempo Real , Taquipneia/etiologia , Tomografia Computadorizada por Raios XRESUMO
Although the prevalence and causes of food allergy (FA) vary by geographic location, large well-designed epidemiological studies in Asia are lacking. The purpose of this study was to evaluate the prevalence of immediate-type FA in the general population of Korean schoolchildren. A population-based, cross-sectional study was conducted in 2010 using a stratified two-stage cluster-sampling design. In this survey, children aged 6-7 years and 12-13 years were randomly selected, and the presence of FA was determined by a questionnaire survey and assessment of specific IgE. After adjustment for missing data, 3907 children aged 6-7 years and 3975 students aged 12-13 years who completed the questionnaire were included in this study. In children aged 6-7 years, the prevalence of confirmed immediate-type FA was 0.3%, and the prevalence of possible immediate-type FA was 0.3%. By contrast, 0.6 and 1.0% of children aged 12-13 years had confirmed immediate-type FA and possible immediate-type FA, respectively. In 6- to 7-year-old children, egg was the most frequent causative food associated with a confirmed or possible immediate-type FA. In 12- to 13-year-old children, crustaceans were the most frequent cause of confirmed immediate-type FA, and fruit was most frequently involved in possible immediate-type FA. This is the first nationwide population-based study of FA in Korean schoolchildren. Unlike in western countries, the prevalence of immediate-type FA seems to be low. In 12- to 13 year-old children with confirmed immediate-type FA, peanuts/tree nuts are not common causes, whereas crustaceans are frequent triggers.
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Hipersensibilidade Alimentar/epidemiologia , Hipersensibilidade Imediata/epidemiologia , Vigilância da População , Adolescente , Criança , Estudos Transversais , Feminino , Hipersensibilidade Alimentar/diagnóstico , Humanos , Hipersensibilidade Imediata/diagnóstico , Imunoglobulina E/efeitos adversos , Masculino , Prevalência , República da Coreia/epidemiologia , Saúde da População Rural , Saúde da População UrbanaRESUMO
RATIONALE: There is conflicting information about the development and resolution of airway inflammation and airway hyperresponsiveness (AHR) after repeated airway exposure to allergen in sensitized mice. METHODS: Sensitized BALB/c and C57BL/6 mice were exposed to repeated allergen challenge on 3, 7, or 11 occasions. Airway function in response to inhaled methacholine was monitored; bronchoalveolar lavage fluid inflammatory cells were counted; and goblet cell metaplasia, peribronchial fibrosis, and smooth muscle hypertrophy were quantitated on tissue sections. Bone marrow-derived dendritic cells were generated after differentiation of bone marrow cells in the presence of growth factors. RESULTS: Sensitization to ovalbumin (OVA) in alum, followed by three airway exposures to OVA, induced lung eosinophilia, goblet cell metaplasia, mild peribronchial fibrosis, and peribronchial smooth muscle hypertrophy; increased levels of interleukin (IL)-4, IL-5, IL-13, granulocyte-macrophage colony-stimulating factor, transforming growth factor-beta(1), eotaxin-1, RANTES (regulated on activation, normal T-cell expressed and secreted), and OVA-specific IgG1 and IgE; and resulted in AHR. After seven airway challenges, development of AHR was markedly decreased as was the production of IL-4, IL-5, and IL-13. Levels of IL-10 in both strains and the level of IL-12 in BALB/c mice increased. After 11 challenges, airway eosinophilia and peribronchial fibrosis further declined and the cytokine and chemokine profiles continued to change. At this time point, the number of myeloid dendritic cells and expression of CD80 and CD86 in lungs were decreased compared with three challenges. After 11 challenges, intratracheal instillation of bone marrow-derived dendritic cells restored AHR and airway eosinophilia. CONCLUSIONS: These data suggest that repeated allergen exposure leads to progressive decreases in AHR and allergic inflammation, through decreases in myeloid dendritic cell numbers.
Assuntos
Alérgenos/imunologia , Hiper-Reatividade Brônquica/imunologia , Células Dendríticas/imunologia , Ovalbumina/imunologia , Animais , Células da Medula Óssea , Líquido da Lavagem Broncoalveolar/imunologia , Células Cultivadas , Modelos Animais de Doenças , Feminino , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BLRESUMO
BACKGROUND: IL-13 is a central mediator of allergen-induced airway hyperresponsiveness (AHR), but its role in respiratory syncytial virus (RSV)-induced AHR is not defined. The combination of allergen exposure and RSV infection is known to increase AHR and lung inflammation, but whether IL-13 regulates this increase is similarly not known. OBJECTIVE: Our objective was to determine the role of RSV infection and IL-13 on airway responsiveness and lung inflammation on sensitized and challenged mice. METHODS: Using a murine model of RSV infection and allergen exposure, we examined the role of IL-13 in the development of AHR and lung inflammation in IL-13 knockout mice, as well as using a potent IL-13 inhibitor (IL-13i). Mice were sensitized and challenged to allergen, and 6 days after the last challenge, they were infected with RSV. IL-13 was inhibited using an IL-13 receptor alpha(2)-human IgG fusion protein. AHR to inhaled methacholine was measured 6 days after infection, as was bronchoalveolar lavage fluid and lung inflammatory and cytokine responses. RESULTS: RSV-induced AHR was unaffected by the IL-13i, despite prevention of goblet cell hyperplasia. Similar results were seen in IL-13-deficient mice. In sensitized and challenged mice, RSV infection significantly increased AHR, and after IL-13i treatment, AHR was significantly reduced, but to the levels seen in RSV-infected mice alone. CONCLUSIONS: These results indicate that despite some similarities, the mechanisms leading to AHR induced by RSV are different from those that follow allergen sensitization and challenge. Because IL-13 inhibition is effective in preventing the increases in AHR and mucus production in sensitized and challenged mice infected with RSV, IL-13i could play an important role in preventing the consequences of viral infection in patients with allergic asthma.
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Alérgenos/imunologia , Hiper-Reatividade Brônquica/etiologia , Interleucina-13/imunologia , Infecções por Vírus Respiratório Sincicial/imunologia , Vírus Sincicial Respiratório Humano/patogenicidade , Animais , Líquido da Lavagem Broncoalveolar/citologia , Líquido da Lavagem Broncoalveolar/imunologia , Citocinas/biossíntese , Citocinas/imunologia , Modelos Animais de Doenças , Feminino , Humanos , Interleucina-13/biossíntese , Camundongos , Camundongos Endogâmicos BALB C , Ovalbumina/administração & dosagem , Ovalbumina/imunologia , Infecções por Vírus Respiratório Sincicial/virologiaRESUMO
The lung collectin surfactant protein D (SP-D) is an important component of the innate immune response but is also believed to play a role in other regulatory aspects of immune and inflammatory responses within the lung. The role of SP-D in the development of allergen-induced airway inflammation and hyperresponsiveness (AHR) is not well defined. SP-D levels progressively increased up to 48 hours after allergen challenge of sensitized mice and then subsequently decreased. The levels of SP-D paralleled the development of airway eosinophilia and AHR. To determine if this association was functionally relevant, mice were administered rat SP-D (rSP-D) intratracheally. When given to sensitized mice before challenge, AHR and eosinophilia were reduced by rSP-D in a dose-dependent manner but not by mutant rSP-D. rSP-D administration resulted in increased levels of interleukin (IL)-10, IL-12, and IFN-gamma in bronchoalveolar lavage fluid and reduced goblet cell hyperplasia. Culture of alveolar macrophages together with SP-D and allergen resulted in increased production of IL-10, IL-12, and IFN-gamma. These results indicate that SP-D can (negatively) regulate the development of AHR and airway inflammation after airway challenge of sensitized mice, at least in part, by modulating the function of alveolar macrophages.