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 ...

Avian scavengers, such as American crows (Corvus brachyrhynchos), have potential to translocate infectious agents (prions) of transmissible spongiform encephalopathy (TSE) diseases including chronic wasting disease, scrapie, and bovine spongiform encephalopathy. We inoculated mice with fecal extracts obtained from 20 American crows that were force-fed material infected with RML-strain scrapie prions. These mice all evinced severe neurological dysfunction 196–231 d postinoculation ( = 198; 95% CI: 210–216) and tested positive for prion disease. Our results suggest a large proportion of crows that consume prion-positive tissue are capable of passing infectious prions in their feces ( = 1.0; 95% CI: 0.8–1.0). Therefore, this common, migratory North American scavenger could play a role in the geographic spread of TSE diseases.

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Prion diseases such as bovine spongiform encephalopathy, chronic wasting disease, and scrapie pose serious risks to human and animal health due to a host of disease-specific factors, including the resistance of infectious prions (PrP(Sc)) to natural degradation and to most commercial inactivation procedures. In an attempt to address this concern, a mouse model was used to compare the efficacy of an alkaline hydrolysis process with a simulated continuous-flow rendering treatment for disposal of PrP(Sc)-infected biological material. Female C57/BL6 mice (N = 120) were randomly divided into 4 treatment groups (n = 30), and each mouse was injected intraperitoneally with their designated treatment inoculum. Treatment groups 1 and 2 served as the positive and negative controls, respectively. Group 3 was inoculated with rendered scrapie-positive mouse brain material to investigate the effectiveness of simulated continuous-flow rendering practices to reduce or eliminate PrP(Sc). Group 4 was inoculated with hydrolyzed scrapie-positive mouse brain material to determine the sterilizing effect of alkaline hydrolysis on PrP(Sc). Mice were monitored for overt signs of disease, and those showing clinical signs were killed to prevent undue suffering. Brains were obtained from all mice that died (or were killed) and analyzed with an ELISA for the presence of PrP(Sc). Results indicated that the simulated continuous-flow rendering treatment used for preparing the rendering treatment group inoculum failed to completely eliminate PrP(Sc). Rendering delayed, but did not stop, clinical mouse-adapted scrapie transmission. Compared with positive controls, the rendering treatment group experienced an approximate 45-d average delay in days to death (250 vs. 205 d for positive controls; P < 0.0001) and a death loss of 73.9% (P = 0.0094). Positive controls suffered 100% death loss. The results validated the efficacy of the alkaline hydrolysis treatment to inactivate all PrP(Sc) because no alkaline hydrolysis treatment group mice succumbed to the disease (P < 0.0001). Based on our results, alkaline hydrolysis should be considered by the animal rendering and beef packing industries as an alternative to incineration, landfill burial, and rendering for disposing of biological material potentially infected or contaminated with prion disease.