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 ...

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A n approximately 36-hour-old Morgan/Friesian colt was referred to the large animal hospital at the University of Wisconsin for an evaluation of altered mentation, first noticed shortly after birth. Parturition had been unobserved, but the foal had been found separated from the mare by a fence at a few hours of age. The foal was ambulatory and able to nurse when first discovered but showed progressive disorientation, apparent blindness, and aimless wandering during the following 36-hour period. A Snap immunoglobulin G (IgG) assay a at 24 hours of age had shown an IgG concentration Ͼ800 mg/dL, and a CBC performed at that time was normal. The foal was treated twice with dimethyl sulfoxide 1 g/kg IV, diluted in 5% dextrose before referral.At presentation, the colt wandered aimlessly, bumped into objects, and appeared blind with sluggish but intact pupillary light responses. When positioned under the mare, the foal nursed successfully. Physical examination was unremarkable. A CBC and serum biochemistry were normal, including a serum IgG concentration of 937 mg/dL measured by radioimmunodiffusion.Initial treatment for presumptive hypoxemic, ischemic encephalopathy included a 250-mL loading dose of 20% magnesium sulfate for 1 hour, followed by a constant rate infusion at 42 mL/h and thiamine hydrochloride 2.2 mg/kg IV q24h. Antimicrobial therapy consisted of amikacin 20 mg/kg IV q24h and procaine penicillin G 22,000 U/kg IM q12h. Omeprazole 1 mg/kg PO q24h also was administered to the foal.The foal's mental status remained static during the next 24 hours, and additional treatment with mannitol 1 g/kg IV q24h and dexamethasone sodium phosphate 0.1 mg/kg IV q24h on days 2 and 3 of hospitalization was not associated with improvement. On day 3, the foal underwent general anesthesia for a computerized tomographic scan of the skull and proximal spine, which was normal. A cerebrospinal fluid sample was obtained from the lumbosacral space and was normal on cytologic evaluation and had a normal protein concentration.On day 4 of hospitalization, the foal developed a rightsided head tilt but otherwise remained static through day 5 of hospitalization. Magnesium sulfate therapy was discontinued on day 5, but the remainder of the therapeutic regimen was unchanged. On day 6, the foal had 2 brief, generalized seizures that were controlled with midazolam 0.05 mg/kg IV. Between seizures, the foal was still bright, afebrile, and nursing.On day 7 of hospitalization, the foal became febrile (40ЊC) and developed a mucopurulent nasal discharge and progressive tachypnea with diffuse adventitious crackles and wheezes on auscultation. Fever, mucopurulent nasal discharge, and coughing had been noted in several other mares and foals in the neonatal care unit during the previous 7 days. Antimicrobial therapy was changed to ticarcillin/clavulanic acid 50 mg/kg IV q8h and gentamicin 6.6 mg/kg IV q24h, and the foal was treated with polyionic fluids, although it was still nursing. During days 8-10, the foal's neurologic status continued to improve, wi...

inhalation of LPS resulted in localized pulmonary inflammation characterized by neutrophil influx and increased expression of the endothelial cell adhesion molecule, E-selectin. It may be possible to relate our experimental findings to the clinical consequences of airborne LPS exposure in swine confinement facilities.