Is Avian Influenza Infecting Mammals Cause for Concern?
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On February 9th, Colorado Parks and Wildlife (CPW) released information about various wildlife species testing positive for avian influenza. Among the critters found carrying the virus were a skunk, mountain lion, and black bear. All had died from the virus.
“All three of the confirmed cases showed signs of [avian influenza] before or after death including neurologic symptoms such as seizures or circling, general signs of illness such as weakness or lack of responsiveness to human presence, and organ damage including encephalitis, hepatitis, and pneumonia”, reported Travis Duncan with CPW.
The current strain of avian influenza is highly transmissible and was first detected in North America in wild geese in March 2022. In the past year, the virus has readily jumped from avian to mammalian species, which sounds alarming, but this phenomenon is not news.
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Zoonotic diseases – diseases transmissible between humans and other animal species – are due to infectious agents that more than one species is susceptible to. Nearly every big game hunter is aware of disease transmission between livestock and elk – brucellosis and elk hoof disease are common examples. Transmissible spongiform encephalopathies cause diseases like scrapie in sheep, chronic wasting disease in deer and elk, mad cow disease, and Creutzfeldt-Jakob in humans. While these diseases are all different, the pathogenic vectors among species are typical and often include contact with bodily fluids or respiratory droplets.
The 2009 “swine flu” outbreak in the US was caused by the H1N1 influenza virus – the same virus that caused the “Spanish flu” in 1819. The swine flu virus appeared to be a new strain of H1N1 that resulted from a previous triple reassortment of bird, swine, and human flu viruses, which further combined with a Eurasian pig flu virus. Miller et al. (2017) identified 87 percent of swine pathogens listed by the World Organization for Animal Health cause clinical disease in livestock, poultry, wildlife, and humans.
Humans have contributed to zoonotic diseases through industrialization and the expansion of communities to accommodate the global population explosion. Landscape development encroaches on wildlife and exposes species to pathogens through close contact with humans and livestock, etc.
Caserta et al. (2022) tested white-tailed deer harvested by hunters for SARS-CoV-2 (COVID-19) during the 2020 and 2021 hunting seasons in New York State. Test results found only 0.6 percent virus occurrence in 2020, but 21.1 percent occurrence in 2021, including all three variants (Alpha, Gamma, and Delta). The variants were present in deer long after they had subsided in the local human population. This presents an example of wildlife acting as a “reservoir” for a virus that can infect other species. Still, it seems odd that a specific disease or pathogen can infect mammals, including humans, as well as birds.
Aquatic birds of the world are the reservoirs for all influenza A viruses, and the virus is spread by fecal-oral transmission in untreated water. Transmission involves mutational or recombinational events and can occur through fecal contamination of unprocessed avian protein, e.g. animals preying upon infected birds or drinking contaminated water. The transmission of avian influenza viruses or virus genes to humans is postulated to occur through pigs that act as the intermediate host5. Once avian influenza viruses are established in mammals, they are transmitted from animal to animal by the respiratory airborne route.
While disease outbreaks and spread may be somewhat manageable among livestock and poultry populations, controlling disease spread in wildlife is complicated due to the free movement of wild animals. Brucellosis presents a textbook case study.
Cattle introduced brucellosis to the Yellowstone area in the early 1900s and transmitted it to local wildlife populations. The disease has supposedly been eliminated from domestic livestock in the US, yet it remains in the bison and elk populations of the Greater Yellowstone Area6. Like many zoonotic diseases, brucellosis has not significantly threatened wildlife populations.
Understanding animal travel and contact networks is imperative to understanding the potential movement and risk of a disease – information that is not readily available for wild animals, particularly when facing a novel disease.
Researchers have studied ecological niche modelling as a means of predicting disease spread within and among wildlife populations, but data on levels of infection in wildlife are often scarce, open to bias, and insufficient for the assessment of cross-species transmission. Complexities in wildlife populations including host movement, variation in host population size, density, and contact rates, unpredictable variation in climate, and species differences in the host–pathogen relationship lead to low model predictability. Johnson et al. (2019) found that adapting the traditional biotic, abiotic, and movement framework of ecological niche models by summarizing the interaction of three factors – dynamically linked biotic interactors, unlinked abiotic stressors, and dispersal capacity – improves model prediction capability. A practical application for common wildlife species seems unlikely; however, modelling disease spread
with high predictability may allow wildlife managers to avoid significant population-level effects from novel and highly virulent pathogens for known distributions of threatened and endangered species.
The complexities involving host-pathogen interactions are utterly fascinating, but in the grand scheme of life and potential impacts on species at the population level, the discussion may be academic. Animals and pathogens evolve continually together, each modifying their defense or attack strategy in a game of win, lose, or draw – the draw being the common outcome when an animal endures symptoms from the pathogen, recovers, and builds immunity.
Although unnerving, the cross-species spread of pathogens rarely leads to significant population-level effects. These interactions represent the pathology continuum that ebbs and flows through time. Take caution when handling game that appears to be sick and cook it thoroughly if it must be consumed.
You can read more about the effects of avian influenza on wild birds at Harvesting Nature.
Avian influenza – Unprecedented Spread Among Wild Birds – Harvesting Nature
 Trifonov V, H Khiabanian, and R Rabadan. 2009. Geographic dependence, surveillance, and origins of the 2009 influenza A (H1N1) virus. The New England Journal of Medicine 361 (2): 115–19.
 Miller, RS, SJ Sweeny, C Slootmaker, DA Grear, PA Di Salvo, D Kiser, and SA Shwiff. 2017. Cross-species transmission between wild pigs, livestock, poultry, wildlife, and humans: implications for disease risk management in North America. Scientific Reports 7:7821 | DOI:10.1038/s41598-017-07336-z.
 Fong, IW. 2017. Animals and mechanisms if disease transmission. In Emerging Zoonoses: Emerging Infectious Diseases of the 21st Century. Springer International Publishing DOI 10.1007/978-3-319-50890-0_2.
 Caserta, LC, M Martins, SL Butt, NA Hollingshead, LM Covaleda, S Ahmed, MRR Everts, KL Schuler, and DG Diel. 2022. White-tailed deer (Odocoileus virginianus) may serve as a wildlife reservoir for nearly extinct SARS-CoV-2 variants of concern. Proceedings of the National Academy of Science 120(6), https://doi.org/10.1073/pnas.2215067120.
 Webster, RG. 1997. Influenza virus: transmission between species and relevance to emergence of the next human pandemic In O Kaaden, C Czerny, and W Eichhorn, eds., Viral zoonoses and food of animal origin. Springer Vienna. https://doi.org/10.1007/978-3-7091-6534-8.
 Brucellosis – Yellowstone National Park (U.S. National Park Service) (nps.gov)
 Morgan, ER, M Lundervold, GF Medley, BS Shaikenov, PR Torgerson, EJ Milner-Gulland. 2006. Biological Conservation 131:244-254.
 Johnson, EE, LE Escobar, and C Zamrana-Torrelio. 2019. An ecological framework for modeling the geography of disease transmission. Trends in Ecology and Evolution 34(7):655-668. https://doi.org/10.1016/j.tree.2019.03.004.