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 ...

BackgroundStriped skunks (Mephitis mephitis) are susceptible to infection with some influenza A viruses. However, the viral shedding capability of this peri-domestic mammal and its potential role in influenza A virus ecology are largely undetermined.Methodology/Principal FindingsStriped skunks were experimentally infected with a low pathogenic (LP) H4N6 avian influenza virus (AIV) and monitored for 20 days post infection (DPI). All of the skunks exposed to H4N6 AIV shed large quantities of viral RNA, as detected by real-time RT-PCR and confirmed for live virus with virus isolation, from nasal washes and oral swabs (maximum ≤106.02 PCR EID50 equivalent/mL and ≤105.19 PCR EID50 equivalent/mL, respectively). Some evidence of potential fecal shedding was also noted. Following necropsy on 20 DPI, viral RNA was detected in the nasal turbinates of one individual. All treatment animals yielded evidence of a serological response by 20 DPI.Conclusions/SignificanceThese results indicate that striped skunks have the potential to shed large quantities of viral RNA through the oral and nasal routes following exposure to a LP AIV. Considering the peri-domestic nature of these animals, along with the duration of shedding observed in this species, their presence on poultry and waterfowl operations could influence influenza A virus epidemiology. For example, this species could introduce a virus to a naive poultry flock or act as a trafficking mechanism of AIV to and from an infected poultry flock to naive flocks or wild bird populations.

BackgroundWild raccoons have been shown to be naturally exposed to avian influenza viruses (AIV). However, the mechanisms associated with these natural exposures are not well-understood.Methodology/Principal FindingsWe experimentally tested three alternative routes (water, eggs, and scavenged waterfowl carcasses) of AIV transmission that may explain how raccoons in the wild are exposed to AIV. Raccoons were exposed to 1) water and 2) eggs spiked with an AIV (H4N6), as well as 3) mallard carcasses experimentally inoculated with the same virus. Three of four raccoons exposed to the high dose water treatment yielded apparent nasal shedding of >102.0 PCR EID50 equivalent/mL. Little to no shedding was observed from the fecal route. The only animals yielding evidence of serologic activity during the study period were three animals associated with the high dose water treatment.Conclusions/SignificanceOverall, our results indicate that virus-laden water could provide a natural exposure route of AIV for raccoons and possibly other mammals associated with aquatic environments. However, this association appears to be related to AIV concentration in the water, which would constitute an infective dose. In addition, strong evidence of infection was only detected in three of four animals exposed to a high dose (e.g., 105.0 EID50/mL) of AIV in water. As such, water-borne transmission to raccoons may require repeated exposures to water with high concentrations of virus.