Biology subjects

Lorch, J.

Publications and source records attributed to Lorch, J..

3 recordsLinked to original sources

bioRxiv2022

Hotspots for snake fungal disease across Europe are maintained by host and pathogen identity

1. Infectious diseases are influenced by interactions between host and pathogen, and are rarely homogenous across the landscape. Areas with elevated pathogen prevalence maintain a high force of infection, can facilitate pathogen spread to new regions, and may indicate areas with impacts on host populations. However, isolating the ecological processes that result in increases in infection prevalence and intensity remains a challenge. 2. Here we elucidate the contribution of pathogen clade and host species in disease hotspots of Ophidiomyces ophidiicola, the pathogen that causes snake fungal disease, in 21 species of snakes infected with multiple pathogen strains across 10 countries in Europe. 3. We found isolated areas of disease hotspots in a landscape where infections were otherwise low. O. ophidiicola clade had important effects on transmission, and areas with multiple pathogen clades had higher host infection prevalence. Snake species identity further influenced infection, with most positive detections coming from the Natrix genus. Most species present in the community only experienced increased levels of infection when multiple strains were present. However, one species, N. tessellata, appeared highly susceptible, having increased infection prevalence regardless of pathogen strain, indicating that this species may be important in pathogen maintenance. 4. Our results suggest that both host and pathogen identity are essential components contributing to increased pathogen prevalence. More broadly, our findings indicate that coevolutionary relationships between hosts and pathogens may be key mechanisms explaining variation in landscape patterns of disease.

ecology↗

bioRxiv2022

Population genetic analysis of Ophidiomyces ophidiicola, the causative agent of snake fungal disease, indicates recent introductions to the USA

Snake fungal disease (SFD; ophidiomycosis), caused by the pathogen Ophidiomyces ophidiicola (Oo), has been documented in wild snakes in North America and Eurasia, and is considered an emerging disease in the eastern USA. However, a lack of historical disease data has made it challenging to determine whether Oo is a recent arrival to the USA or whether SFD emergence is due to other factors. Here, we examined the genomes of 82 Oo strains to determine the pathogens history in the eastern USA. Oo strains from the USA formed a clade (Clade II) distinct from European strains (Clade I), and molecular dating indicated that these clades diverged too recently ([~]2,000 years ago) for transcontinental dispersal of Oo to have occurred via natural snake movements across Beringia. A lack of nonrecombinant intermediates between clonal lineages in Clade II indicates that Oo has actually been introduced multiple times to North America from an unsampled source population, and molecular dating indicates that several of these introductions occurred within the last few hundred years. Molecular dating also indicated that the most common Clade II clonal lineages have expanded recently in the USA, with time of most recent common ancestor mean estimates ranging from 1985-2007 CE. The presence of Clade II in captive snakes worldwide demonstrates a potential mechanism of introduction and highlights that additional incursions are likely unless action is taken to reduce the risk of pathogen translocation and spillover into wild snake populations.

microbiology↗

bioRxiv2022

Mutational footprint of platinum chemotherapy in a secondary thyroid cancer

Although papillary thyroid carcinoma (PTC) is the most frequent endocrine tumor with a generally excellent prognosis, a patient developed a clinically aggressive PTC eleven years after receiving platinum chemotherapy for ovarian endometrioid adenocarcinoma. Germline and somatic analyses of multi-temporal and multi-regional molecular profiles indicated that ovarian and thyroid tumors did not share common genetic alterations. PTC tumors had driver events associated with aggressive PTC behavior, an RBPMS-NTRK3 fusion and a TERT promoter mutation. Spatial and temporal genomic heterogeneity analysis indicated a close link between anatomical locations and molecular patterns of PTC. Mutational signature analyses demonstrated a molecular footprint of platinum exposure, and that aggressive molecular drivers of PTC were linked to prior platinum-associated mutagenesis. This case provides a direct association between platinum chemotherapy exposure and secondary solid tumor evolution, in specific aggressive thyroid carcinoma, and suggests that uniform clinical assessments for secondary PTC after platinum chemotherapy may warrant further evaluation.

genomics↗