Adiaspiromycoses in Wild Rodents from the Pyrenees, Northeastern Spain.

Adiaspiromycosis is a nontransmissible infectious pulmonary disease caused by the inhalation of propagules from fungal species belonging to the family Ajellomicetaceae, especially Emergomyces crescens. Adiaspiromycosis caused by E. crescens has been recorded in a broad number of species worldwide, with small burrowing mammals being considered the main hosts for this environmental pathogen. Only a handful of studies on adiaspiromycosis in European wildlife has been published to date. We assessed the occurrence of adiaspiromycosis in wild rodents (Murinae and Arvicolinae) from the central Spanish Pyrenees (NE Spain). The lungs of 302 mice and 46 voles were screened for the presence of adiaspores through histopathologic examination. Pulmonary adiaspiromycosis was recorded in 21.6% of all individuals (75/348), corresponding to 63/299 wood mice (Apodemus sylvaticus) and 12/40 bank voles (Myodes glareolus). Adiaspore burden varied highly between animals, with a mean of 0.19 spores/mm2 and a percentage of affected lung tissue ranging from <0.01% to >8%. These results show that the infection is present in wild rodents from the central Spanish Pyrenees. Although the impact of this infection on nonendangered species is potentially mild, it might contribute to genetic diversity loss in endangered species.

The bacterial genetic determinants of Escherichia coli capacity to cause bloodstream infections in humans.

Escherichia coli is both a highly prevalent commensal and a major opportunistic pathogen causing bloodstream infections (BSI). A systematic analysis characterizing the genomic determinants of extra-intestinal pathogenic vs. commensal isolates in human populations, which could inform mechanisms of pathogenesis, diagnostic, prevention and treatment is still lacking. We used a collection of 912 BSI and 370 commensal E. coli isolates collected in France over a 17-year period (2000-2017). We compared their pangenomes, genetic backgrounds (phylogroups, STs, O groups), presence of virulence-associated genes (VAGs) and antimicrobial resistance genes, finding significant differences in all comparisons between commensal and BSI isolates. A machine learning linear model trained on all the genetic variants derived from the pangenome and controlling for population structure reveals similar differences in VAGs, discovers new variants associated with pathogenicity (capacity to cause BSI), and accurately classifies BSI vs. commensal strains. Pathogenicity is a highly heritable trait, with up to 69% of the variance explained by bacterial genetic variants. Lastly, complementing our commensal collection with an older collection from 1980, we predict that pathogenicity continuously increased through 1980, 2000, to 2010. Together our findings imply that E. coli exhibit substantial genetic variation contributing to the transition between commensalism and pathogenicity and that this species evolved towards higher pathogenicity.

Experimental Mycobacterium microti Infection in Bank Voles (Myodes glareolus).

Voles are maintenance hosts of Mycobacterium microti. In line with the goal to eradicate tuberculosis (TB) in livestock, the role of this mycobacteria needs to be assessed since it might interfere with current M. bovis/M. caprae surveillance strategies. To better understand the pathogenesis of TB in voles, an experimental infection model was set up to reproduce M. microti infection in laboratory Bank voles (Myodes glareolus). Two infection routes (intragastric and intraperitoneal) and doses (105 and 106 CFU/0.1 mL) were assessed. Voles were culled at different post-infection time points. Serology, histopathology, acid-fast bacilli staining, qPCR, and mycobacterial culture from tissues were performed. In addition, qPCR from feces and oral swabs were conducted to assess bacterial shedding. The model allowed us to faithfully reproduce the disease phenotype described in free-ranging voles and characterize the pathogenesis of the infection. Most animals showed multifocal and diffuse granulomatous lesions in the liver and spleen, respectively. Less frequently, granulomas were observed in lungs, lymph nodes, muscles, and salivary gland. Mycobacterial DNA was detected in feces from a few animals but not in oral swabs. However, one contact uninfected vole seroconverted and showed incipient TB compatible lesions, suggesting horizontal transmission between voles.