RESUMO
Epidemiological data on CD infection (CDI) in Latin American are scarce. CDI prevalence and strains characterization were prospectively evaluated in 5 Brazilian hospitals from different regions. Prevalence rates of CDI were 15%, ranging from 0 to 37%. ST42 was the most common Sequence Type and hypervirulent strains were not identified.
Assuntos
Clostridioides difficile/classificação , Infecções por Clostridium/epidemiologia , Diarreia/epidemiologia , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Antibacterianos/uso terapêutico , Proteínas de Bactérias/genética , Toxinas Bacterianas/genética , Brasil/epidemiologia , Clostridioides difficile/efeitos dos fármacos , Clostridioides difficile/isolamento & purificação , Infecções por Clostridium/diagnóstico , Infecções por Clostridium/tratamento farmacológico , DNA Bacteriano , Diarreia/microbiologia , Fezes/microbiologia , Feminino , Glutamato Desidrogenase/genética , Hospitais , Humanos , Masculino , Pessoa de Meia-Idade , Prevalência , Estudos Prospectivos , Sequenciamento Completo do Genoma , Adulto JovemRESUMO
Human exposure to methylmercury (MeHg) due to contaminated fish intake as part of a high-fat (HFD), high-carbohydrate diets is a reality today for many populations. HFD is associated with hypertension and hyperlipidemia, primary cardiovascular disease (CVD) risk factors. Some studies suggest that MeHg induces those risk factors. We evaluated the effect of MeHg exposure in mice fed with HFD or control diet for eight weeks. In the last experimental 15 days, the half group received a MeHg solution (20 mg/L) replacing water. Blood pressure (BP), heart rate, lipoprotein concentrations, and paraoxonase activity were evaluated. Liver cholesterol, triacylglycerol, and IBA-1+ cells, as well as transcriptional levels of genes related to lipid metabolism and inflammatory response, were also assessed. HFD and both MeHg groups presented increased BP and total cholesterol (TC). In the liver, HFD but not MeHg was related to an increase in TC. Also, MeHg intoxication reduced paraoxonase activity regardless of diet. MeHg intoxication and HFD increased steatosis and the number of IBA-1+ cells and modified some gene transcripts associated with lipid metabolism. In conclusion, we demonstrated that MeHg effects on CVD risk factors resemble those caused by HFD.