Widespread human SARS-CoV-2 infections combined with human–wildlife interactions create the potential for reverse zoonosis from humans to wildlife. We targeted white-tailed deer (Odocoileus virginianus) for serosurveillance based on evidence these deer have angiotensin-converting enzyme 2 receptors with high affinity for SARS-CoV-2, are permissive to infection, exhibit sustained viral shedding, can transmit to conspecifics, exhibit social behavior, and can be abundant near urban centers. We evaluated 624 prepandemic and postpandemic serum samples from wild deer from four US states for SARS-CoV-2 exposure. Antibodies were detected in 152 samples (40%) from 2021 using a surrogate virus neutralization test. A subset of samples tested with a SARS-CoV-2 virus neutralization test showed high concordance between tests. These data suggest white-tailed deer in the populations assessed have been exposed to SARS-CoV-2.

Human monkeypox has never been reported in Ghana, but rodents captured in forested areas of southern Ghana were the source of the monkeypox virus introduced into the United States in 2003. Subsequent to the outbreak in the United States, 204 animals were collected from two commercial trapping sites in Ghana. Animal tissues were examined for the presence of orthopoxvirus (OPXV) DNA using a real-time polymerase chain reaction, and sera were assayed for antibodies against OPXV. Animals from five genera (Cricetomys, Graphiurus, Funiscirus, and Heliosciurus) had antibodies against OPXV, and three genera (Cricetomys, Graphiurus, and Xerus) had evidence of OPXV DNA in tissues. Additionally, 172 persons living near the trapping sites were interviewed regarding risk factors for OPXV exposure, and their sera were analyzed. Fifty-three percent had IgG against OPXV; none had IgM. Our findings suggest that several species of forest-dwelling rodents from Ghana are susceptible to naturally occurring OPXV infection, and that persons living near forests may have low-level or indirect exposure to OPXV-infected animals, possibly resulting in sub-clinical infections.

Widespread human SARS-CoV-2 infections combined with human-wildlife interactions create the potential for reverse zoonosis from humans to wildlife. We targeted whitetailed deer (Odocoileus virginianus) for serosurveillance based on evidence these deer have ACE2 receptors with high affinity for SARS-CoV-2, are permissive to infection, exhibit sustained viral shedding, can transmit to conspecifics, and can be abundant near urban centers. We evaluated 624 pre- and post-pandemic serum samples from wild deer from four U.S. states for SARS-CoV-2 exposure. Antibodies were detected in 152 samples (40%) from 2021 using a surrogate virus neutralization test. A subset of samples was tested using a SARS-CoV-2 virus neutralization test with high concordance between tests. These data suggest white-tailed deer in the populations assessed have been exposed to SARS-CoV-2.

In August 2020, outbreaks of coronavirus disease were confirmed on mink farms in Utah, USA. We surveyed mammals captured on and around farms for evidence of infection or exposure. Free-ranging mink, presumed domestic escapees, exhibited high antibody titers, suggesting a potential severe acute respiratory syndrome coronavirus 2 transmission pathway to native wildlife.

Raccoons (Procyon lotor) are common, widely distributed animals that frequently come into contact with wild waterfowl, agricultural operations, and humans. Serosurveys showed that raccoons are exposed to avian infl uenza virus. We found antibodies to a variety of infl uenza virus subtypes (H10N7, H4N6, H4N2, H3, and H1) with wide geographic variation in seroprevalence. Experimental infection studies showed that raccoons become infected with avian and human infl uenza A viruses, shed and transmit virus to virus-free animals, and seroconvert. Analyses of cellular receptors showed that raccoons have avian and human type receptors with a similar distribution as found in human respiratory tracts. The potential exists for co-infection of multiple subtypes of infl uenza virus with genetic reassortment and creation of novel strains of infl uenza virus. Experimental and fi eld data indicate that raccoons may play an important role in infl uenza disease ecology and pose risks to agriculture and human health.T he primary reservoirs of avian infl uenza (AI) are wild birds in the orders Anseriformes (ducks, geese, and swans) and Charadriiformes (gulls, terns, and shorebirds). In these hosts, low-pathogenic forms of the virus typically cause little or no apparent disease, however, large quantities of virus are shed in fecal matter. AI virus is relatively stable in water and can remain viable for up to 200 days, depending on temperature and other environmental factors (1). Thus, bodies of water and adjacent shorelines that wild birds use can become potentially contaminated, increasing the likelihood of subsequent exposure of avian and nonavian species to AI virus.The preference of infl uenza viruses for different cellular receptors and the presence and distribution of those receptors in the host are important factors involved in determining host range and tissue tropism (2). Humans are not typically infected by AI virus because receptors for this virus are distributed in tissues that are located predominantly in the lower respiratory tract. As such, these receptors are not as accessible as human type receptors found in the upper respiratory tissues and require more intimate contact for transmission. Swine are considered important intermediate hosts between birds and humans because they are frequently infected by avian and human infl uenza viruses (3). This fi nding underscores the potential for genetic reassortment that can create new, possibly more virulent subtypes.Other non-avian hosts of AI virus include mink, harbor seals, pilot whales, dogs, cats, and horses (4). These species were found to be competent hosts only after attracting attention because of severe death or illness (4). Wild mammals often reside in the same habitats as waterfowl, feed in the same agricultural areas, wallow and swim in the same bodies of water, and prey on and scavenge dead birds for food. Therefore, ample opportunities exist for free-ranging wild mammals to be exposed to AI by contact with waterfowl and their environment. Many of these species ...

In November 2014, a Eurasian strain H5N8 highly pathogenic avian influenza virus was detected in poultry in Canada. Introduced viruses were soon detected in the United States and within six months had spread to 21 states with more than 48 million poultry affected. In an effort to study potential mechanisms of spread of the Eurasian H5 virus, the United States Department of Agriculture coordinated several epidemiologic investigations at poultry farms. As part of those efforts, we sampled synanthropic birds and mammals at five infected and five uninfected poultry farms in northwest Iowa for exposure to avian influenza viruses. Across all farms, we collected 2,627 samples from 648 individual birds and mammals. House mice were the most common mammal species captured while house sparrows, European starlings, rock pigeons, swallows, and American robins were the most commonly captured birds. A single European starling was positive for Eurasian H5 viral RNA and seropositive for antibodies reactive to the Eurasian H5 virus. Two American robins were also seropositive. No mammal species showed evidence of infection. These results indicate synanthropic species merit further scrutiny to better understand potential biosecurity risks. We propose a set of management practices aimed at reducing wildlife incursions.

ABSTRACT:We used long-term data collected for up to 10 yr (1994)(1995)(1996)(1997)(1998)(1999)(2000)(2001)(2002)(2003)(2004) at 23 trapping arrays (i.e., webs and grids) in Arizona, Colorado, Montana, and New Mexico to examine demographic factors known or suspected to be associated with risk of infection with Sin Nombre virus (SNV) in its natural host, the deer mouse (Peromyscus maniculatus). Gender, age (mass), wounds or scars, season, and local relative population densities were statistically associated with the period prevalence of antibody (used as a marker of infection) to SNV in host populations. Nevertheless, antibody prevalence and some of the risk factors associated with antibody prevalence, such as relative population density, gender bias, and prevalence of wounding, varied significantly among sites and even between nearby trapping arrays at a single site. This suggests that local micrositespecific differences play an important role in determining relative risk of infection by SNV in rodents and, consequently, in humans. Deer mouse relative population density varied among sites and was positively and statistically associated with infection prevalence, an association that researchers conducting shorter-term studies failed to demonstrate. Both wounding and antibody prevalence increased with mass class in both males and females; this increase was much more pronounced in males than in females and wounding was more frequent in adult males than in adult females. Prevalence of wounding was greatest among seropositive deer mice, regardless of mass class, but many deer mice without detectable wounds or scars eventually became infected. Many of these patterns, which will be useful in the development of predictive models of disease risk to humans, were only detected through the application of data collected over a long (10-yr) period and with abundant replication.

Background Avian influenza viruses are known to productively infect a number of mammal species, several of which are commonly found on or near poultry and gamebird farms. While control of rodent species is often used to limit avian influenza virus transmission within and among outbreak sites, few studies have investigated the potential role of these species in outbreak dynamics. Methodology/Principal Findings We trapped and sampled synanthropic mammals on a gamebird farm in Idaho, USA that had recently experienced a low pathogenic avian influenza outbreak. Six of six house mice ( Mus musculus ) caught on the outbreak farm were presumptively positive for antibodies to type A influenza. Consequently, we experimentally infected groups of naïve wild-caught house mice with five different low pathogenic avian influenza viruses that included three viruses derived from wild birds and two viruses derived from chickens. Virus replication was efficient in house mice inoculated with viruses derived from wild birds and more moderate for chicken-derived viruses. Mean titers (EID 50 equivalents/mL) across all lung samples from seven days of sampling (three mice/day) ranged from 10 3.89 (H3N6) to 10 5.06 (H4N6) for the wild bird viruses and 10 2.08 (H6N2) to 10 2.85 (H4N8) for the chicken-derived viruses. Interestingly, multiple regression models indicated differential replication between sexes, with significantly (p<0.05) higher concentrations of avian influenza RNA found in females compared with males. Conclusions/Significance Avian influenza viruses replicated efficiently in wild-caught house mice without adaptation, indicating mice may be a risk pathway for movement of avian influenza viruses on poultry and gamebird farms. Differential virus replication between males and females warrants further investigation to determine the generality of this result in avian influenza disease dynamics.