The COVID-19 pandemic has snapped into focus the deep risks that can unfold when an animal pathogen jumps into people. But what about the reverse? What are the potential pathways and risks of human pathogens “spilling back” and making the jump to wildlife?
A team of researchers recently published a literature review in Ecology Letters that assesses cases of human-to-wildlife transmission events and characterizes spillback factors. University of Florida medical geographer Sadie Ryan coauthored the paper. Ryan is a professor in the Department of Geography in the UF College of Liberal Arts and Sciences, and she is a faculty member of the UF Emerging Pathogens Institute.
“Having seen things like the fact that SARS-CoV-2 could spread in mink farms, to tigers in zoos, and into wild white-tailed deer, we went through the literature and found 100 cases where there has been spillback,” Ryan said. “It is likely more common than we think it is, but we are missing a lot of data, due to sampling bias.”
The authors report that most documented cases are skewed to long-lived non-human primates, captive animals, and those that are managed by or habituated to humans. There is a need for studies on animals that with shorter life spans, ungulates, rodents, and bats, they report.
More than 25% of reported cases involved the bacteria that causes tuberculosis. It has been found in elephants, ungulates, captive birds, mesocarnivores, and a rodent. Few reported examples led to disease or death, and even fewer showed evidence of a human pathogen being newly maintained in a wild animal population. This is key because when a human pathogen is maintained in a wild animal population, it has the potential to spillback into people – perhaps with new genetic changes that make it more transmissible and/or able to produce more severe disease.
The researchers examined two major transmission pathways. In the first, a human pathogen spills into wildlife and produces substantial disease or death. But ultimately the animals are an evolutionary dead end for the pathogen, and it is not able to be maintained in the non-human population.
In the second pathway, a human pathogen spills into an animal population and it is maintained but then potentially spills back into people. Additional pathways exist, the researchers note. For example, there may be regular or frequent transmission between hosts of different species, which provides more opportunity of the pathogen to become entrenched or to mutate and gain new features.
In their literature search, the authors found more evidence for the first pathway than the second. This doesn’t mean it is more likely to occur in real life, just that it’s better documented. For example, reports involving captive primates, or primates that are habituated to people – through ecotourism, for example – are likely overrepresented in the literature. They write:
“. . . it seems unlikely that charismatic, long-lived species are truly more susceptible to human-infecting pathogens; instead, these species are probably known to host human pathogens because they more frequently live alongside humans and are therefore more often exposed, or because they have simply been more intensively monitored and sampled.”
By contrast, there may be many instances of animals infected with human pathogens that had few or no symptoms. These cases may go undetected and unreported. The comparative lack of evidence for this pathway is interesting because reservoirs of human pathogens in wildlife pose a problem for efforts to eliminate disease.
“It’s a double-edged problem,” Ryan said. “How do we know when spillback threatens species conservation? When human diseases escape and damage existing animal species. But also, how might then that spillback to us and drive future pandemics? We found little evidence for the reservoir hypothesis. But just because we did not find a lot of it doesn’t mean it’s not happening.”
Acknowledgments: This work grew from a virtual collaboration, the Viral Emergence Research Initiative, or VERENA, which curates open access databases of viral ecology with the goal of predicting future threats.
By: DeLene Beeland