Researchers in New Mexico have located fungal pathogens that cause disease in humans in the lung tissues of small mammals, including rodents. The findings support the hypothesis that rodents could be a breeding ground for respiratory fungal pathogens.
Like the SARS-CoV-2 virus, host jumps have also allowed fungi to evolve and diversify, contributing to an increase in reports of novel human pathogens over the last four decades.
Using next-generation sequencing, the researchers analyzed fungal DNA in rodent lung tissues from museum specimens. “We wanted to understand if the fungal spores of respiratory pathogens reside in soils because they feed on dead and decaying plant matter, or if they are instead living within small animals and their spores are released into the soil after the rodents die,” says first author Paris Salazar-Hamm, from the University of New Mexico. “We found that many of the rodents we sampled from areas in the Southwestern U.S. were harboring the type of fungi that can cause lung infections in humans, such as the fungus that leads to Valley Fever, a disease that typically causes flu-like symptoms and can be life threatening.”
The team detected the fungus Coccidioides, the cause of Valley Fever, in the lung tissues of animals from Kern County, California, and Cochise and Maricopa Counties in Arizona—areas that have high rates of this disease. “In addition, we detected sequences from Coccidioides in animals from Catron, Sierra, and Socorro Counties in New Mexico, which is the first time this pathogen has been detected in the environment in this region,” says Salazar-Hamm.
The findings—published recently in Frontiers in Fungal Biology—could inform health officials where there is potential for disease to be acquired locally. “Current forecasts of the distribution of Coccidioides, based on climate and soil conditions, predict that Valley fever will expand substantially northward and eastward over the next century because of climate change impacting environmental conditions. Our results will inform these modeling efforts by adding valuable information about animals as reservoirs for pathogens,” adds Salazar-Hamm.
Future studies hope to examine the health of the host animals and how this may impact the spread or virulence of the diseases. “We were not able to assess the health of the mammalian hosts from which the lung tissues were acquired. Despite the presence of pathogens, it was impossible to say conclusively that there was disease,” says Salazar-Hamm. “It would be interesting to further explore the impact of the fungi on the mammals. That effort would require more detailed information about the general health of the animal in question.”