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Forstchen, M.

Publications and source records attributed to Forstchen, M..

3 recordsLinked to original sources

A Common Agrochemical Mixture Increases Snail Hosts and Ecological Drivers of Schistosomiasis Risk

O_LIAgricultural intensification is accelerating across tropical regions, increasing fertilizer and pesticide inputs into freshwater ecosystems that regulate the transmission of many environmentally mediated diseases. For schistosomiasis, a major neglected tropical disease, transmission risk is strongly governed by the abundance of freshwater snail intermediate hosts and their aquatic habitat, yet most agrochemical studies have focused on single compounds rather than realistic mixtures. C_LIO_LIUsing replicated semi-natural aquatic microcosms, we experimentally tested how nitrogen- urea fertilizer and the widely used herbicide atrazine, applied alone and in combination at environmentally relevant concentrations, alter snail hosts (Biomphalaria glabrata), submerged aquatic vegetation (Ceratophyllum demersum), and algal resources that underpin schistosomiasis transmission. C_LIO_LIFertilizer and atrazine, both singly and together, increased snail habitat (C. demersum) and adult snail abundance. By reducing phytoplankton, atrazine likely alleviated shading on vegetation, thereby promoting habitat that supported snails through indirect bottom-up pathways. Agrochemical mixtures produced non-additive effects on host and habitat dynamics, indicating that transmission-relevant ecological responses cannot be predicted from single-compound exposures alone. Although parasite infection levels were low, the observed increases in snail hosts and habitat represent reliable ecological drivers of schistosomiasis risk. C_LIO_LISynthesis and applications. Our findings demonstrate that common agrochemical mixtures can restructure freshwater food webs in ways likely to elevate disease risk, highlighting the need to incorporate mixture-driven ecological responses into agrochemical risk assessment and agricultural management strategies in disease-endemic regions. C_LI

ecology↗

Rising daptomycin resistance in Enterococcus faecium across a hospital system occurred via rampant recurrent evolution and occasional transmission between patients.

The rise of antibiotic resistance in a population involves two distinct processes: the origin of resistance and its spread. Here we study the contribution of both processes to the increase in daptomycin resistance in Enterococcus faecium in a hospital system. This case-control genomic study includes whole-genome sequencing of 82 isolates obtained from 24 case patients with clinically determined daptomycin-resistance and 24 controls. Among the case patients, the first isolate was resistant in 15 patients (R patients) while in the remaining nine the first isolate was susceptible but was followed by one or more resistant isolates (SR patients). Mutations in a set of candidate daptomycin resistance genes were compared within and between all patients. Additionally, among closely related isolates, mutations were identified across the entire assembled genome. Daptomycin resistance evolved separately multiple times and there was no phylogenetic clustering of the R or the SR groups. Six of the nine SR pairs gained mutations in previously identified candidate loci for daptomycin resistance, with the major cardiolipin synthase (clsA) being mutated most frequently. The hospital-wide increases in daptomycin resistance in E. faecium was the result of recurrent evolution taking multiple evolutionary pathways and occasional transmission of resistant isolates between patients. ImportanceAntimicrobial resistance in healthcare settings presents an important challenge, because infections with resistant organisms are associated with higher cost, longer hospital stays and worse outcomes for patients. However, it can be difficult to identify the factors driving the increase in resistance, specifically the relative contribution of resistance arising anew through mutation versus the transmission of resistant organisms from patient to patient. We study a hospital where resistance to daptomycin was increasing among Enterococcus faecium, an important hospital pathogen. We find the increase in resistance was the results of resistance arising many times independently. We also identify occasional transmission of daptomycin resistant organisms. Thus, control of daptomycin resistance in E. faecium may require interventions that both slow the emergence of resistance within patients and slow its spread. This work sheds light on the complex population dynamics leading to antibiotic resistance in hospitals.

evolutionary biology↗

Global change drivers and the risk of infectious disease

Anthropogenic change is contributing to the rise in emerging infectious diseases, but it remains unclear which global change drivers most increase disease and under what contexts. We amassed a dataset from the literature that includes 1,832 observations of infectious disease responses to global change drivers across 1,202 host-parasite combinations. We found that biodiversity loss, climate change, and introduced species were associated with increases in disease-related endpoints or harm (i.e., enemy release for introduced species), whereas urbanization was associated with decreases in disease endpoints. Natural biodiversity gradients, deforestation, forest fragmentation, and most classes of chemical contaminants had non-significant effects on these endpoints. Overall, these results were consistent across human and non-human diseases. Context-dependent effects of the global change drivers on disease were common and are discussed. These findings will help better target disease management and surveillance efforts towards global change drivers that increase disease. One-Sentence SummaryHere we quantify which global change drivers increase infectious diseases the most to better target global disease management and surveillance efforts.

ecology↗