RESUMEN
BACKGROUND: Antimicrobial resistance (AMR) rates may display seasonal variation. However, it is not clear whether this seasonality is influenced by the seasonal variation of infectious diseases, geographical region or differences in antibiotic prescription patterns. Therefore, we assessed the seasonality of AMR rates in respiratory bacteria. METHODS: Seven electronic databases (Embase.com, Medline Ovid, Cochrane CENTRAL, Web of Science, Core Collection, Biosis Ovid, and Google Scholar), were searched for relevant studies from inception to Jun 25th, 2019. Studies describing resistance rates of Streptococcus pneumoniae and Haemophilus influenzae were included in this review. By using random-effects meta-analysis, pooled odd ratios of seasonal AMR rates were calculated using winter as the reference group. Pooled odd ratios were obtained by antibiotic class and geographical region. RESULTS: We included 13 studies, of which 7 were meta-analyzed. Few studies were done in H. influenzae, thus this was not quantitively analyzed. AMR rates of S. pneumoniae to penicillins were lower in other seasons than in winter with pooled OR = 0.71; 95% CI = 0.65-0.77; I2 = 0.0%, and to all antibiotics with pooled OR = 0.68; 95% CI = 0.60-0.76; I2 = 14.4%. Irrespective of geographical region, the seasonality of AMR rates in S. pneumoniae remained the same. CONCLUSION: The seasonality of AMR rates could result from the seasonality of infectious diseases and its accompanied antibiotic use.
Asunto(s)
Antibacterianos/uso terapéutico , Farmacorresistencia Bacteriana , Infecciones por Haemophilus , Haemophilus influenzae , Neumonía Neumocócica , Estaciones del Año , Streptococcus pneumoniae , Farmacorresistencia Bacteriana/efectos de los fármacos , Farmacorresistencia Bacteriana/genética , Infecciones por Haemophilus/genética , Infecciones por Haemophilus/metabolismo , Infecciones por Haemophilus/patología , Haemophilus influenzae/genética , Haemophilus influenzae/metabolismo , Humanos , Neumonía Neumocócica/tratamiento farmacológico , Neumonía Neumocócica/genética , Neumonía Neumocócica/metabolismo , Sistema Respiratorio/microbiología , Streptococcus pneumoniae/genética , Streptococcus pneumoniae/metabolismoRESUMEN
The aim of the present study was to estimate the relative contribution of immunogenetic and microbiological factors in the development of recurrent tonsillitis in a Mexican population. Patients (n = 138) with recurrent tonsillitis and an indication of tonsillectomy (mean age: 6.05 years ± 3.00; median age: 5 years, female: 58; age range: 1-15 years) and 195 non-related controls older than 18 years and a medical history free of recurrent tonsillitis were included. To evaluate the microbial contribution, tonsil swab samples from both groups and extracted tonsil samples from cases were cultured. Biofilm production of isolated bacteria was measured. To assess the immunogenetic component, DNA from peripheral blood was genotyped for the TNFA-308G/A single-nucleotide polymorphism (SNP) and for the IL1B -31C/T SNP. Normal microbiota, but no pathogens or potential pathogens, were identified from all control sample cultures. The most frequent pathogenic species detected in tonsils from cases were Staphylococcus aureus (48.6%, 67/138) and Haemophilus influenzae (31.9%, 44/138), which were found more frequently in patient samples than in samples from healthy volunteers (P < 0.0001). Importantly, 41/54 (75.9%) S. aureus isolates were biofilm producers (18 weak and 23 strong), whereas 17/25 (68%) H. influenzae isolates were biofilm producers (10 weak, and 7 strong biofilm producers). Patients with at least one copy of the IL1B-31*C allele had a higher risk of recurrent tonsillitis (OR = 4.03; 95% CI = 1.27-14.27; P = 0.013). TNFA-308 G/A alleles were not preferentially distributed among the groups. When considering the presence of IL1B-31*C plus S. aureus, IL1B-31*C plus S. aureus biofilm producer, IL1B-31*C plus H. influenzae or IL1B-31*C plus H. influenzae biofilm producer, the OR tended to infinite. Thus, the presence of IL1B-31*C allele plus the presence of S. aureus and/or H. influenzae could be related to the development of tonsillitis in this particular Mexican population.
Asunto(s)
Portador Sano/microbiología , Infecciones por Haemophilus/etiología , Interleucina-1beta/genética , Infecciones Estafilocócicas/etiología , Tonsilitis/etiología , Adolescente , Adulto , Anciano , Alelos , Biopelículas , Portador Sano/inmunología , Estudios de Casos y Controles , Niño , Preescolar , Femenino , Infecciones por Haemophilus/genética , Infecciones por Haemophilus/microbiología , Haemophilus influenzae/aislamiento & purificación , Humanos , Fenómenos Inmunogenéticos , Lactante , Masculino , México , Microbiota , Persona de Mediana Edad , Recurrencia , Factores de Riesgo , Infecciones Estafilocócicas/genética , Infecciones Estafilocócicas/microbiología , Staphylococcus aureus/aislamiento & purificación , Tonsilitis/genética , Tonsilitis/microbiología , Factor de Necrosis Tumoral alfa/genética , Adulto JovenRESUMEN
PURPOSE: Most pleural effusions are associated with bacterial pneumonia, and the identification of the pathogen will assist the therapeutic decision. A specific method that is not affected by previous antibiotic therapy is sought to detect the main causative agents of pneumonia in infants and children (Streptococcus pneumoniae, Haemophilus influenzae, and Staphylococcus aureus). The aim of the present study was to compare the polymerase chain reaction (PCR) technique with standard culture methods in identifying bacterial infections in infants' and children's pleural effusion. METHODS: Samples obtained from pediatric patients (n = 37) with a diagnosis of pneumonia associated to pleural effusion, submitted to thoracentesis, were analyzed by PCR with specific primers. RESULTS: The PCR technique identified the presence of bacterial infection in a larger proportion (95.2%) than the standard culture method (33.3%) on complicated pleural effusion samples. The microorganism detection on uncomplicated pleural effusion samples was positive only by the PCR method (31.3%). The frequencies of microorganisms identified on complicated pleural effusion were 57.1% of all patients for methicillin-resistant Staphylococcus; 52.4%, S pneumoniae; 28.6%, S aureus; and 23.8%, H influenzae. The previous use of antibiotics interferes with standard culture method, but it did not interfere with the PCR results. CONCLUSIONS: The molecular diagnosis by PCR method could improve the etiologic diagnosis and might help to guide the treatment of parapneumonic effusion in children.
Asunto(s)
ADN Bacteriano/genética , Derrame Pleural/etiología , Derrame Pleural/microbiología , Neumonía Bacteriana/complicaciones , Neumonía Bacteriana/diagnóstico , Reacción en Cadena de la Polimerasa/métodos , Niño , Preescolar , Estudios Transversales , Cartilla de ADN , Femenino , Infecciones por Haemophilus/diagnóstico , Infecciones por Haemophilus/genética , Humanos , Lactante , Masculino , Infecciones Neumocócicas/diagnóstico , Infecciones Neumocócicas/genética , Sensibilidad y Especificidad , Infecciones Estafilocócicas/diagnóstico , Infecciones Estafilocócicas/genéticaRESUMEN
OBJECTIVE: Despite penicillin prophylaxis and vaccination, infection with encapsulated organisms remains a leading cause of morbidity and death in children with sickle cell disease. The role of Fc receptors in the clearance of encapsulated organisms is well documented. The His(H)-Arg(R) polymorphism at amino acid 131 of the Fc gamma RIIA receptor alters binding affinity for human IgG2 and influences infection with encapsulated organisms in children without sickle cell disease. We hypothesized that the genotype for high-affinity human IgG2 binding (H/H131) is underrepresented in children with sickle cell disease who had encapsulated organism infection. DESIGN: We studied 60 black children with sickle cell disease from four participating centers who had a history of encapsulated organism infection. Genomic DNA from peripheral blood was subjected to amplification by polymerase chain reaction and to sequence analysis for identification of the Fc gamma RIIA genotype, and the genotype distribution was then compared with our data from ethnically matched control subjects. RESULTS: Contrary to our hypothesis, the H/H131 genotype was overrepresented in all individuals (p = 0.046) and in particular in the 11 individuals with a history of Haemophilus influenzae type b infection (64% H/H131, 27% H/R131, 9% R/R131; p = 0.002), in comparison with ethnically matched control subjects (14% H/H131, 60% H/R131, 26% R/R131). In the 51 individuals with a history of Streptococcus pneumoniae infection, the genotype distribution was not statistically significantly different from that of the control population. CONCLUSIONS: The H/H131 Fc gamma RIIA genotype is overrepresented in black children with sickle cell disease and a history of H. influenzae type b infection but not in those with S. pneumoniae infection.
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Anemia de Células Falciformes/genética , Antígenos CD/genética , Población Negra/genética , Infecciones por Haemophilus/genética , Infecciones Oportunistas/genética , Infecciones Neumocócicas/genética , Polimorfismo Genético/genética , Receptores de IgG/genética , Adolescente , Adulto , Anemia de Células Falciformes/inmunología , Niño , Preescolar , Femenino , Genotipo , Infecciones por Haemophilus/inmunología , Humanos , Lactante , Masculino , Infecciones Oportunistas/inmunología , Infecciones Neumocócicas/inmunología , Reacción en Cadena de la Polimerasa , Factores de Riesgo , Rasgo Drepanocítico/genética , Rasgo Drepanocítico/inmunologíaRESUMEN
Because Alaskan Eskimos have the greatest known endemic risk of Haemophilus influenzae type b (Hib) disease and represent a comparatively homogeneous population, we selected this population to evaluate the presence or absence of an association of 35 genetic markers (alleles or allotypes) at 12 chromosomal loci with susceptibility to both invasive Hib disease risk and level of Hib anticapsular antibody. We studied nearly all Alaskan Eskimo children who had had invasive Hib disease between 1971 and 1982 in southwestern Alaska (n = 103) and an equivalent number of controls matched for age, race, and village of residence, and verified not to have had proved or suspected Hib disease. We found no significant associations with Hib disease for the single alleles of HLA-A, -B, -C, -DR, Gm, Km, Am, Kidd, MNSs, ABO, esterase D, or glutamate pyruvate transaminase loci. However, we observed a significant interaction of two loci, Gm(a;..;g,s,t) allotype and HLA-DR8 (P = 0.002), with increased Hib disease susceptibility, and an interaction of the same Gm allotype and HLA-DR5 with decreased disease susceptibility (P = 0.01). We also compared the level of anticapsular antibody to Hib with each genetic marker and two-locus interactions, but no genetic association with antibody level was found. We conclude that some genetic factors contribute to the susceptibility to invasive Hib disease in this population.