Ma, Hok Lun. / Thesis submitted in: December 2008. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2009. / Includes bibliographical references (leaves 233-273). / Abstracts in English and Chinese. / Abstract --- p.i / Abstract (Chinese version) --- p.v / Tables of contents --- p.vi / Acknowledgement --- p.xvi / List of figures --- p.xvii / List of tables --- p.xxi / List of abbreviations and symbols --- p.xxviii / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Respiratory illnesses in children --- p.1 / Chapter 1.1.1 --- Worldwide burden of childhood pneumonia --- p.1 / Chapter 1.1.2 --- Further mortality related to childhood pneumonia --- p.4 / Chapter 1.2 --- Etiology agent of childhood respiratory illnesses --- p.5 / Chapter 1.2.1 --- Difficulties in determining etiological agent --- p.5 / Chapter 1.2.2 --- Overall situation of etiological agents in childhood pneumonia --- p.6 / Chapter 1.2.3 --- Relationship between age and pathogens --- p.9 / Chapter 1.2.4 --- "Relationship between serotypes, carriage and invasiveness" --- p.11 / Chapter 1.2.4.1 --- Carriage and Invasiveness --- p.12 / Chapter 1.2.4.2.1 --- Carriage of S. pneumoniae and H. influenzae in children in Hong Kong --- p.12 / Chapter 1.2.4.2.2 --- "Serotypes, carriage and invasiveness in S. pneumoniae" --- p.14 / Chapter 1.2.4.2.3 --- "Serotypes, carriage and invasiveness in H. influenzae" --- p.17 / Chapter 1.3 --- Epidemiology of antibiotic-resistant pathogens --- p.18 / Chapter 1.3.1 --- Molecular typing methods --- p.18 / Chapter 1.3.2 --- Spread of antibiotic-resistant pathogens --- p.20 / Chapter 1.3.2.1 --- Spread of antibiotic-resistant S. pneumoniae --- p.26 / Chapter 1.3.2.1.1 --- Spread of penicillin-resistant S. pneumoniae --- p.26 / Chapter 1.3.2.1.1.1 --- Spread of Spanish-23F-1 --- p.27 / Chapter 1.3.2.1.1.2 --- Spread of Spanish-6B-2 --- p.28 / Chapter 1.3.2.1.1.3 --- Spread of antibiotic-resistant S. pneumoniae clones in Hong Kong --- p.28 / Chapter 1.3.2.1.2 --- Spread of cephalosporin-resistant S. pneumoniae --- p.29 / Chapter 1.3.2.1.3 --- Spread of macrolide-resistant S. pneumoniae --- p.30 / Chapter 1.3.2.1.4 --- Spread of fluoroquinolone-resistant S. pneumoniae --- p.31 / Chapter 1.3.2.2 --- Spread of antibiotic-resistant H. influenzae --- p.32 / Chapter 1.3.2.2.1 --- Spread of β-lactam-resistant H. influenzae --- p.32 / Chapter 1.3.2.2.2 --- Spread of macrolide-resistant H. influenzae --- p.33 / Chapter 1.3.2.2.3 --- Spread of fluoroquinolone-resistant H. influenzae --- p.34 / Chapter 1.4 --- Mechanism of antibiotic-resistance in respiratory pathogens --- p.36 / Chapter 1.4.1 --- Mechanism of antibiotic-resistance in S. pneumoniae --- p.37 / Chapter 1.4.1.1 --- Mechanism of penicillin- and cephalosporin-resistance in S. pneumoniae --- p.37 / Chapter 1.4.1.1.1 --- Penicillin-binding protein (PBP)-mediated mechanism --- p.37 / Chapter 1.4.1.1.2 --- PBP-independent mechanisms --- p.49 / Chapter 1.4.1.1.2.1 --- "Murine peptide branching genes, murMN operon" --- p.49 / Chapter 1.4.1.1.2.2 --- "Two-component system, CiaRH" --- p.50 / Chapter 1.4.1.1.2.3 --- "Putative glycosyltransferase, CpoA" --- p.52 / Chapter 1.4.1.1.3 --- RNA and protein expression studies on S. pneumoniae for β-lactam-resistance --- p.52 / Chapter 1.4.1.1.3.1 --- RNA expression in penicillin-sensitive S. pneumoniae --- p.53 / Chapter 1.4.1.1.3.2 --- Protein expression in penicillin-resistant S. pneumoniae --- p.53 / Chapter 1.4.1.2 --- Mechanism of macrolide- and lincosamide- resistance in S. pneumoniae --- p.54 / Chapter 1.4.1.3 --- Mechanism of tetracycline-resistance in S. pneumoniae --- p.55 / Chapter 1.4.1.4 --- Mechanism of fluoroquinolone-resistance in S. pneumoniae --- p.55 / Chapter 1.4.2 --- Mechanism of antibiotic-resistant in H. influenzae --- p.56 / Chapter 1.4.2.1 --- Mechanism of β-lactam-resistance in H. influenzae --- p.56 / Chapter 1.4.2.1.1 --- β-lactamase-producing H. influenzae --- p.56 / Chapter 1.4.2.1.2 --- β-lactamase-negative ampicillin-resistant (BLNAR) H. influenzae --- p.58 / Chapter 1.4.2.1.2.1 --- Relationship between amino acid substitutions in PBP3 and β-lactam- resistance --- p.58 / Chapter 1.4.2.1.2.2 --- Relationship between amino acid substitutions in AcrR and β-lactam-resistance --- p.60 / Chapter 1.4.2.2 --- Mechanism of macrolide-resistance in H. influenzae --- p.61 / Chapter 1.4.2.3 --- Mechanism of fluoroquinolone-resistance in H. influenzae --- p.64 / Chapter 1.5 --- Impact of vaccination --- p.65 / Chapter 1.5.1 --- H. influenzae type b vaccination --- p.65 / Chapter 1.5.1.1 --- Efficacy of Hib conjugate vaccine --- p.66 / Chapter 1.5.1.2 --- Herd immunity related to Hib conjugate vaccine --- p.66 / Chapter 1.5.2 --- Pneumococcal vaccination --- p.66 / Chapter 1.5.2.1 --- Vaccine efficacy and herd immunity of pneumococcal vaccines --- p.67 / Chapter 1.5.2.2 --- Development of conjugate vaccines with higher valency --- p.67 / Chapter 1.5.2.3 --- Serotype replacement --- p.67 / Chapter 1.5.2.4 --- Development of pneumococcal vaccines with new targets --- p.69 / Chapter 1.6 --- Objectives of this study --- p.70 / Chapter Chapter 2 --- Materials and methods --- p.72 / Chapter 2.1 --- Collection and Identification of microorganisms --- p.72 / Chapter 2.1.1 --- Collection of S. pneumoniae and H. influenzae --- p.72 / Chapter 2.1.2 --- Identification of S. pneumoniae and H. influenzae --- p.73 / Chapter 2.2 --- Serotyping of S. pneumoniae and H. influenzae --- p.74 / Chapter 2.2.1 --- Serotyping by polymerase chain reaction (PCR) --- p.74 / Chapter 2.2.1.1 --- Preparation of crude DNA extract --- p.74 / Chapter 2.2.1.2 --- Screening for common serotypes by multiplex PCR --- p.74 / Chapter 2.2.1.3 --- Composition of PCR Mix --- p.77 / Chapter 2.2.1.4 --- Serotyping PCR conditions --- p.81 / Chapter 2.2.1.5 --- Gel Electrophoresis --- p.81 / Chapter 2.2.2 --- Serotyping by serum agglutination --- p.82 / Chapter 2.3 --- Antimicrobial susceptibility testing --- p.83 / Chapter 2.4 --- Clonal analysis of penicillin- and cephalosporin-resistant S. pneumoniae --- p.87 / Chapter 2.4.1 --- Pulsed-field Gel Electrophoresis (PFGE) --- p.87 / Chapter 2.4.1.1 --- Preparation of agarose plugs for PFGE --- p.87 / Chapter 2.4.1.2 --- Lysis of bacteria in agarose plugs --- p.89 / Chapter 2.4.1.3 --- Digestion of chromosomal DNA by restriction enzyme --- p.89 / Chapter 2.4.2 --- Multi-locus sequence typing (MLST) --- p.90 / Chapter 2.4.2.1 --- PCR amplification of house-keeping genes in MLST --- p.90 / Chapter 2.4.2.1.1 --- Preparation of DNA from agarose plugs --- p.92 / Chapter 2.4.2.1.2 --- Composition of PCR Mix --- p.92 / Chapter 2.4.2.1.3 --- MLST PCR conditions --- p.92 / Chapter 2.4.2.1.4 --- Gel Electrophoresis of MLST PCR products --- p.92 / Chapter 2.4.2.1.5 --- MLST PCR products purification --- p.93 / Chapter 2.4.2.2 --- Sequencing of housekeeping genes in MLST --- p.93 / Chapter 2.4.2.3 --- Sequencing analysis and sequence type (ST) determination in MLST --- p.94 / Chapter 2.4.3 --- Extended panel of antibiotic susceptibility testing on S. pneumoniae with known STs --- p.94 / Chapter 2.5 --- Analysis on potential penicillin- and cephalosporin-resistance mechanisms in S. pneumoniae --- p.96 / Chapter 2.5.1 --- Sequencing of potnetial penicillin- and cephalosporin- resistance determinants in S. pneumoniae --- p.96 / Chapter 2.5.1.1 --- Primer design of penicillin-binding protein (PBP) genes --- p.96 / Chapter 2.5.1.2 --- Primer design of non-PBP resistance determinants --- p.100 / Chapter 2.5.1.3 --- PCR amplification and sequencing of resistant determinants --- p.100 / Chapter 2.5.1.4 --- Sequence analysis --- p.100 / Chapter 2.5.2 --- Study on efflux mechanism of S. pneumoniae --- p.103 / Chapter 2.5.2.1 --- Modification of macrodilution for efflux assay --- p.103 / Chapter 2.5.2.2 --- Cefotaxime MIC determination with efflux inhibitors --- p.104 / Chapter 2.5.2.3 --- Determination of appropriate CCCP concentration --- p.105 / Chapter 2.5.2.4 --- Growth curve with efflux inhibitor --- p.105 / Chapter 2.5.3 --- Heteroresistance assay of S. pneumoniae --- p.106 / Chapter 2.5.4 --- "RNA expression study on penicillin- and cefotaxime-resistance determinants (pbp2x, pbpla and pbp2a) of S. pneumoniae" --- p.107 / Chapter 2.5.4.1 --- Growth of S. pneumoniae for RNA extraction --- p.107 / Chapter 2.5.4.2 --- RNA extraction and DNase digestion --- p.107 / Chapter 2.5.4.3 --- cDNA synthesis and real-time PCR --- p.108 / Chapter 2.6 --- Analysis on cephalosporin- and macrolide-resistance mechanisms in H. influenzae --- p.111 / Chapter 2.6.1 --- β-lactamase production of H. influenzae --- p.111 / Chapter 2.6.1.1 --- Nitrocefin Hydrolysis --- p.111 / Chapter 2.6.1.2 --- Screening for the presence of p-lactamase gene (blaTEM-1 and blaROB-1) by multiplex PCR --- p.111 / Chapter 2.6.2 --- PCR detection and sequencing of β-lactam- and macrolide- resistance determinants in H. influenzae --- p.113 / Chapter Chapter 3 --- Results of S. pneumoniae and H. influenzae children study --- p.116 / Chapter 3.1 --- Patient demographics of children study --- p.116 / Chapter 3.2 --- Serotype distributions --- p.117 / Chapter 3.2.1 --- Serotypes / serogroup distribution in S. pneumoniae --- p.117 / Chapter 3.2.2 --- Serotype distribution in H. influenzae children study --- p.120 / Chapter 3.3 --- Antibiotic susceptibilities and resistance antibiograms --- p.122 / Chapter 3.3.1 --- Antibiotic susceptibilities of S. pneumoniae --- p.122 / Chapter 3.3.2 --- Relationship between antibiotic resistance profiles and serotypes in S.pneumoniae --- p.126 / Chapter 3.3.3 --- Antibiotic susceptibilities of H. influenzae --- p.135 / Chapter 3.3.4 --- Antibiotic resistance profiles of H. influenzae --- p.138 / Chapter 3.4 --- Clonal analysis of penicillin- and cephalosporin-resistant S.pneumoniae --- p.139 / Chapter 3.4.1 --- Pulsed-field gel electrophoresis (PFGE) of S. pneumoniae --- p.139 / Chapter 3.4.2 --- Multi-locus sequence typing of S. pneumoniae --- p.141 / Chapter 3.5 --- Analysis of the penicillin- and cephalosporin-resistance determinants in S. pneumoniae --- p.143 / Chapter 3.5.1 --- "Sequence analysis of major pbp genes (pbp2x, pbpla and pbp2a)" --- p.143 / Chapter 3.5.2 --- "Sequence analysis of other potential penicillin- and cephalosporin- resistance determinants (pbp 1 b, pbp2b, pbp3, cpoA, ciaRH and murMN)" --- p.152 / Chapter 3.5.3 --- Sequence analysis of putative promoter sequences of pbp genes --- p.167 / Chapter 3.5.4 --- Efflux Inhibition Assay --- p.171 / Chapter 3.5.5 --- Heteroresistance Assay --- p.177 / Chapter 3.5.6 --- "RNA expression study on penicillin- and cephalosporin resistance determinants (pbp2x, pbpla and pbp2a)" --- p.179 / Chapter 3.6 --- Analysis of β-lactam-resistance determinants in H. influenzae --- p.185 / Chapter 3.6.1 --- β-lactamase production and blaTEM-1 promoter study --- p.185 / Chapter 3.6.2 --- "Sequence analysis of β-lactam-resistance determinants (ftsl, acrR genes, AcrAB-TolC efflux pump)" --- p.188 / Chapter 3.6.2.1 --- Sequence analysis offtsl --- p.188 / Chapter 3.6.2.2 --- Analysis of acrR and AcrAB-TolC efflux pump --- p.189 / Chapter 3.7 --- "Analysis of macrolide-resistance determinants in H, influenzae (AcrAB-TolC efflux pump, 23SrRNA, Ribosomal proteins L4 and L22)" --- p.199 / Chapter Chapter 4 --- Discussion on S. pneumoniae and H. influenzae children study --- p.204 / Chapter 4.1 --- Carriage rate of S. pneumoniae children collection --- p.204 / Chapter 4.2 --- Serotype distribution --- p.205 / Chapter 4.2.1 --- Serotype distribution and potential vaccine coverage in S. pneumoniae --- p.205 / Chapter 4.2.2 --- Serotype distribution in H. influenzae --- p.209 / Chapter 4.3 --- Antimicrobial resistance --- p.210 / Chapter 4.3.1 --- Antimicrobial resistance in S. pneumoniae --- p.210 / Chapter 4.3.2 --- Antimicrobial resistance in H. influenzae --- p.214 / Chapter 4.4 --- "Clonal analysis of high-level β-lactam-resistant S, pneumoniae" --- p.217 / Chapter 4.5 --- "β-lactam-resistance mechanisms in S, pneunomiae" --- p.220 / Chapter 4.6 --- Antimicrobial resistance mechanisms in H. influenzae --- p.224 / Chapter 4.6.1 --- β-lactam-resistance mechanism in β-lactamase-producing H. influenzae --- p.224 / Chapter 4.6.1.1 --- Variations in blaTEM-1 promoters in β-lactamase-producing H.influenzae --- p.224 / Chapter 4.6.1.2 --- β-lactam-resistance in β-lactamase-nonproducing H. influenzae --- p.225 / Chapter 4.6.2 --- Macrolide-resistance mechanisms in H. influenzae --- p.228 / Chapter Chapter 5 --- Conclusion and future studies --- p.230 / Chapter 5.1 --- "S, pneumoniae children study" --- p.230 / Chapter 5.2 --- H. influenzae children study --- p.231 / Chapter 5.3 --- Future studies --- p.232 / Bibliography --- p.233 / Appendix I 一 Sequence alignments and Tables --- p.274 / Appendix II 一 Materials and Methods --- p.313

The overall aim of the research described in this thesis was to evaluate the effect of vitamin A supplementation on respiratory health, assessed by lung function in children aged 6--9 years. It comprises three studies. / The first study determined the magnitude of vitamin A deficiency in the target population in Wukro wereda, Northern Ethiopia. Of the 1339 eligible children identified by house to house surveys, 824 had complete data for vitamin A indicators and anthropometry. Xerophthalmia was detected in 5.8% of the children, 8.4% had serum retinol levels <0.35 mumol/L and 51.1% between 0.35--0.70 mumol/L. Liver vitamin A reserve was also found to be low in 41.0% of the children using the Modified Relative Dose Response (MRDR) and in about 85% of the children, the daily vitamin A intake was below the FAO/WHO basal requirement (<250 RE/day). / The second study found that in comparison with children with adequate vitamin A reserve (MRDR < 0.06), those with low reserve (MRDR &ge; 0.06) had forced expiratory volume in one second (FEV1) 48.8 ml (p = 0.006) lower when unadjusted, 23.1 ml (p = 0.04) when partially adjusted for age, gender and height and 14.1 ml (p = 0.20) when fully adjusted for demographic, general health, lung function and household related characteristics. / The third study describes the results of a randomized controlled trial (RCT) to evaluate the impact of vitamin A supplementation on respiratory health as assessed by change in FEV1 at 4 months. The average change was 53.3 ml (n = 496) and 53.8 ml (n = 501) in the vitamin A and placebo groups respectively. After adjusting for baseline covariates, the difference between them was -3.6 ml (95%CI: -21.6, 14.4). In sub-analysis of the data, gender and vitamin A status subcategories were found to be effect modifiers. / In conclusion, high dose vitamin A supplementation did not show an effect on change in FEV1 at 4 months in children aged 6--9 years with high prevalence of vitamin A deficiency. Sub-analysis findings suggest that the benefits to vitamin A intervention in the study setting can probably be achieved if the other nutritional deficiencies such as zinc are addressed. Moreover, the results also suggest that the effects of vitamin A supplementation on respiratory health status are complex and these need to be taken into account in future studies to assess the clinical and public health implications of vitamin A supplementation in this age group.

No description available.

He, Qiqiang. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2009. / Includes bibliographical references (leaves 142-154). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstracts in English and Chinese.

published_or_final_version / abstract / toc / Community Medicine / Master / Master of Philosophy

As infecções respiratórias agudas são uma importante causa de morbidade e mortalidade infantil em todo o mundo. Algumas dessas infecções podem resultar em Síndrome Respiratória Aguda Grave (SRAG). Os vírus respiratórios são os principais responsáveis por esta doença. O monitoramento e a vigilância das SRAG e dos vírus respiratórios são importantes para a gestão em saúde minimizando o impacto destas infecções respiratórias. O presente estudo buscou analisar a sazonalidade e impacto clínico das infecções causadas por vírus respiratórios em crianças internadas em hospital pediátrico do Paraná. Foram incluídos no estudo 229 pacientes de 0 até 15 anos de idade, de janeiro de 2012 a dezembro de 2015, com diagnóstico clínico de SRAG e amostra respiratória coletada e enviada ao Laboratório Central do Estado do Paraná para diagnóstico do agente etiológico. A busca dos casos de SRAG foi realizada utilizando o prontuário eletrônico GSUS (Gestão da Assistência de Saúde do SUS), arquivos do setor de fisioterapia e informações do Núcleo de Controle de Infecções hospitalares do hospital do estudo. Dos pacientes incluídos na pesquisa, foi preenchido um formulário de coleta de dados e posteriormente estes foram analisados de acordo com os objetivos da pesquisa. As análises estatísticas foram efetuadas com o pacote estatístico GRAPHPAD PRISM e foi considerado um nível de significância de 5%. A maioria dos pacientes da amostra pertencia à faixa etária de 0 a 6 meses de idade, não houve sexo predominante. No presente estudo as amostras positivas para pelo menos um agente etiológico contabilizaram 76,41%, e o vírus mais prevalente foi o Vírus Sincicial respiratório (VSR). Quanto à sazonalidade da detecção viral, houve predominância no final de outono e início do inverno, mais acentuada para o VSR. Quando analisada as três temperaturas ambientais da região, a incidência de SRAG foi significativamente maior no quartil descendente da temperatura média para mínima. Não foi observada diferença significativa entre os grupos etiológicos pesquisados com relação ao tempo desde o início dos sintomas até a internação. Houve predominância de internamentos em Unidade de Terapia Intensiva. O tempo de internamento foi significativamente maior naqueles pacientes com doença de base e não alterou conforme os agentes etiológicos identificados ou presença de codetecção. Os pacientes que apresentaram padrão misto na radiografia de tórax tiveram um tempo de internamento significativamente maior do que aqueles que apresentaram o padrão infiltrado intersticial. O tempo total foi significativamente menor no grupo Metapneumovírus em relação aos grupos Bordetella pertussis, Influenza, Rinovírus e grupo dos pacientes sem agentes infecciosos detectados. O tempo de ventilação mecânica não apresentou diferenças significativas entre os grupos etiológicos nem com relação à presença ou não de codetecção. A maior parte dos pacientes recebeu alta hospitalar, mas ocorreram três óbitos devido a SRAG, todos em pacientes com alguma doença de base ou condições de risco. / Acute respiratory infections are the most important cause of children morbidity and mortality worldwide. Some of these infections can result in Severe Acute Respiratory Syndrome (SARS). Respiratory viruses are primarily responsible for SARS. The monitoring and surveillance of SARS and respiratory viruses are important for health management, minimizing the impact of these respiratory infections. The present study was about the seasonality and clinical impact of respiratory viruses in children admitted to a pediatric reference hospital. The study included 229 children from 0 to 15 years old, from January 2012 to December 2015, with clinical diagnosis of SARS and respiratory sample collected and sent to the Central Laboratory of the State of Paraná for etiological agent analysis. The search for SARS cases was performed using the GSUS (Health Care Management of SUS) electronic filesystem, records of the center of physiotherapy and information of the Hospital Infection Control Center of the studied hospital. Of the patients included in the research, data collection forms were filled out and later analyzed according to the research objectives. Statistical analyzis were performed with the statistical package GRAPHPAD PRISM and a significance level of 5% was considered. The majority of patients in the sample belonged to the age group 0-6 months of age, and there was no predominant sex. Regarding the risk factors for viral infection, the presence of comorbidity or underlying disease was the most prevalent factor. In the present study, the positive samples for at least one etiological agent accounted for 76.41%, and the most prevalent virus was Respiratory Syncytial Virus (RSV). As for the seasonality of viral detection, there was a predominance in the late fall and early winter, which was more pronounced for RSV. When the environmental temperatures of the region were analyzed, the incidence of SARS was significantly higher in the descending quartile of the average minimum temperature. No significant difference was observed between the studied etiological groups in relation to the time from the beginning of the symptoms until the hospitalization. There was a predominance of hospitalizations in the Intensive Care Unit. The hospitalization time was significantly higher in patients with underlying disease or comorbidities and did not change according to the identified etiological agents or the presence of codetection. Patients who presented a mixed pattern on chest radiography had a significantly longer hospitalization time than those who had the interstitial infiltrate pattern. The total time was significantly lower in the Metapneumovirus group than in the Bordetella pertussis, Influenza, Rhinovirus and group of patients without detected infectious agents. Most patients were discharged from hospital, but there were three deaths due to SARS, all in patients with some underlying disease or risk conditions.

As infecções respiratórias agudas são uma importante causa de morbidade e mortalidade infantil em todo o mundo. Algumas dessas infecções podem resultar em Síndrome Respiratória Aguda Grave (SRAG). Os vírus respiratórios são os principais responsáveis por esta doença. O monitoramento e a vigilância das SRAG e dos vírus respiratórios são importantes para a gestão em saúde minimizando o impacto destas infecções respiratórias. O presente estudo buscou analisar a sazonalidade e impacto clínico das infecções causadas por vírus respiratórios em crianças internadas em hospital pediátrico do Paraná. Foram incluídos no estudo 229 pacientes de 0 até 15 anos de idade, de janeiro de 2012 a dezembro de 2015, com diagnóstico clínico de SRAG e amostra respiratória coletada e enviada ao Laboratório Central do Estado do Paraná para diagnóstico do agente etiológico. A busca dos casos de SRAG foi realizada utilizando o prontuário eletrônico GSUS (Gestão da Assistência de Saúde do SUS), arquivos do setor de fisioterapia e informações do Núcleo de Controle de Infecções hospitalares do hospital do estudo. Dos pacientes incluídos na pesquisa, foi preenchido um formulário de coleta de dados e posteriormente estes foram analisados de acordo com os objetivos da pesquisa. As análises estatísticas foram efetuadas com o pacote estatístico GRAPHPAD PRISM e foi considerado um nível de significância de 5%. A maioria dos pacientes da amostra pertencia à faixa etária de 0 a 6 meses de idade, não houve sexo predominante. No presente estudo as amostras positivas para pelo menos um agente etiológico contabilizaram 76,41%, e o vírus mais prevalente foi o Vírus Sincicial respiratório (VSR). Quanto à sazonalidade da detecção viral, houve predominância no final de outono e início do inverno, mais acentuada para o VSR. Quando analisada as três temperaturas ambientais da região, a incidência de SRAG foi significativamente maior no quartil descendente da temperatura média para mínima. Não foi observada diferença significativa entre os grupos etiológicos pesquisados com relação ao tempo desde o início dos sintomas até a internação. Houve predominância de internamentos em Unidade de Terapia Intensiva. O tempo de internamento foi significativamente maior naqueles pacientes com doença de base e não alterou conforme os agentes etiológicos identificados ou presença de codetecção. Os pacientes que apresentaram padrão misto na radiografia de tórax tiveram um tempo de internamento significativamente maior do que aqueles que apresentaram o padrão infiltrado intersticial. O tempo total foi significativamente menor no grupo Metapneumovírus em relação aos grupos Bordetella pertussis, Influenza, Rinovírus e grupo dos pacientes sem agentes infecciosos detectados. O tempo de ventilação mecânica não apresentou diferenças significativas entre os grupos etiológicos nem com relação à presença ou não de codetecção. A maior parte dos pacientes recebeu alta hospitalar, mas ocorreram três óbitos devido a SRAG, todos em pacientes com alguma doença de base ou condições de risco. / Acute respiratory infections are the most important cause of children morbidity and mortality worldwide. Some of these infections can result in Severe Acute Respiratory Syndrome (SARS). Respiratory viruses are primarily responsible for SARS. The monitoring and surveillance of SARS and respiratory viruses are important for health management, minimizing the impact of these respiratory infections. The present study was about the seasonality and clinical impact of respiratory viruses in children admitted to a pediatric reference hospital. The study included 229 children from 0 to 15 years old, from January 2012 to December 2015, with clinical diagnosis of SARS and respiratory sample collected and sent to the Central Laboratory of the State of Paraná for etiological agent analysis. The search for SARS cases was performed using the GSUS (Health Care Management of SUS) electronic filesystem, records of the center of physiotherapy and information of the Hospital Infection Control Center of the studied hospital. Of the patients included in the research, data collection forms were filled out and later analyzed according to the research objectives. Statistical analyzis were performed with the statistical package GRAPHPAD PRISM and a significance level of 5% was considered. The majority of patients in the sample belonged to the age group 0-6 months of age, and there was no predominant sex. Regarding the risk factors for viral infection, the presence of comorbidity or underlying disease was the most prevalent factor. In the present study, the positive samples for at least one etiological agent accounted for 76.41%, and the most prevalent virus was Respiratory Syncytial Virus (RSV). As for the seasonality of viral detection, there was a predominance in the late fall and early winter, which was more pronounced for RSV. When the environmental temperatures of the region were analyzed, the incidence of SARS was significantly higher in the descending quartile of the average minimum temperature. No significant difference was observed between the studied etiological groups in relation to the time from the beginning of the symptoms until the hospitalization. There was a predominance of hospitalizations in the Intensive Care Unit. The hospitalization time was significantly higher in patients with underlying disease or comorbidities and did not change according to the identified etiological agents or the presence of codetection. Patients who presented a mixed pattern on chest radiography had a significantly longer hospitalization time than those who had the interstitial infiltrate pattern. The total time was significantly lower in the Metapneumovirus group than in the Bordetella pertussis, Influenza, Rhinovirus and group of patients without detected infectious agents. Most patients were discharged from hospital, but there were three deaths due to SARS, all in patients with some underlying disease or risk conditions.