Influenza infection in wild raccoons.

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 influenza virus. We found antibodies to a variety of influenza 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 influenza 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 influenza virus with genetic reassortment and creation of novel strains of influenza virus. Experimental and field data indicate that raccoons may play an important role in influenza disease ecology and pose risks to agriculture and human health.

Effect of inhaled endotoxin on cardiopulmonary function and E-selectin expression in pigs.

OBJECTIVE: To evaluate the effect of controlled exposure to inhaled lipopolysaccharides (LPS) on the pulmonary inflammatory response of anesthetized pigs. ANIMALS: Forty-seven 8- to 12-week-old domestic pigs. PROCEDURE: Pigs were anesthetized with pentobarbital, instrumented for measurement of cardiopulmonary function, and randomly assigned to receive saline (0.9% NaCI) solution or 0.25, 0.5, or 1.0 microg of LPS/kg/h for 2 or 6 hours via nebulization through the endotracheal tube. Cardiopulmonary variables were measured, ex vivo neutrophil superoxide production determined, and postmortem assessment for pulmonary neutrophil influx and modulation of adhesion molecule (E-selectin) expression was done. RESULTS: Mild changes in cardiopulmonary function were observed in response to inhaled LPS in the 2-and 6-hour groups. In pigs inhaling LPS (0.5 or 1.0 microg/kg/h) for 6 hours, there was significant pulmonary neutrophil influx observed postmortem. An increase in expression of E-selectin on pulmonary endothelial cells after 6 hours of LPS inhalation (0.5 microg/kg/h) was also observed. In contrast, there was no significant influx of neutrophils or expression of E-selectin in lungs from pigs inhaling LPS for 2 hours. CONCLUSIONS AND CLINICAL RELEVANCE: 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.