RESUMEN
In 2015, Clostridium difficile testing rates among 30 US community, multispecialty, and cancer hospitals were 14.0, 16.3, and 33.9/1,000 patient-days, respectively. Pooled hospital onset rates were 0.56, 0.84, and 1.57/1,000 patient-days, respectively. Higher testing rates may artificially inflate reported rates of C. difficile infection. C. difficile surveillance should consider testing frequency.
Asunto(s)
Clostridioides difficile , Infecciones por Clostridium/epidemiología , Infecciones por Clostridium/microbiología , Disparidades en el Estado de Salud , Técnicas Bacteriológicas , Clostridioides difficile/genética , Infecciones por Clostridium/diagnóstico , Hospitalización , Hospitales , Humanos , Técnicas de Amplificación de Ácido Nucleico , Vigilancia en Salud PúblicaRESUMEN
Alveolar macrophages and neutrophils mediate innate immune defense against the opportunistic fungal pathogen Aspergillus fumigatus and are believed to be essential for host survival following inhalation of fungal spores (conidia). Although alveolar macrophages are postulated to kill inhaled conidia and neutrophils are believed to act against hyphae, the relative contribution of alveolar macrophages and neutrophils to early defense against A. fumigatus remain incompletely defined. To more precisely characterize the contributions of alveolar macrophages and neutrophils in antifungal host defense, we selectively depleted each cell population at different times following pulmonary challenge with conidia. Mice depleted of alveolar macrophages prior to pulmonary A. fumigatus infection recruited neutrophils normally and restricted hyphal tissue invasion. In contrast, neutrophil depletion prior to or within 3 h after infection was associated with high mortality. Neutrophil depletion at later time points, however, was associated with nearly normal survival rates. Our studies suggest that neutrophils, but not alveolar macrophages, provide essential anticonidial defense and that a brief period of influx into the respiratory tree is sufficient to prevent conidial germination and invasive disease.