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To evaluate the possibility of virus transmission through feathers of call ducks, we performed two experiments, intranasal infection study and transmission study, using the Japanese H5N1 highly pathogenic avian influenza virus (HPAIV) A/chicken/Yamaguchi/7/2004 (Ck/Yama/7/04). In Experiment 1, 1-day-old, 2-wk-old, and 4-wk-old birds were inoculated intranasally with Ck/Yama/7/04. Birds in all age groups exhibited necrosis and/or viral antigens in the feather epithelium. Nonpurulent encephalitis and focal necrosis of the pancreas and heart also were common to inoculated birds. In Experiment 2, nine 2-wk-old birds that were orally inoculated with feathers of an infected call duck exhibited the nonpurulent encephalitis, necrosis of the feather epithelium, and focal necrosis of the pancreas and heart, accompanied by viral antigens. These lesions were similar to those in intranasal infection. Some birds were positive for the virus isolation from cloacal swabs and hemagglutination inhibition antibody. The infection was confirmed in seven of nine birds. This study confirmed that the Japanese HPAIV can replicate in the feather epithelium, causing necrosis in call ducks through the natural infection route. It also suggests that feathers of call ducks infected with Ck/Yama/7/04 can be a potential source of infection for unaffected birds in nature.

ABSTRACT. The plasma and urine kinetics of flunixin-meglumin (FNX, 2 mg/kg, i.v.) in rabbits were examined. Unusual pharmacokinetic profiles were obtained, including high binding percentage with plasma protein (> 99%), a short elimination half-life (< 4 hr) and a relatively large Vd-area (0.5 L/kg). These profiles indicate that some active transport mechanisms are involved in FNX disposition. The recovery of FNX from urine was approximately 9 % of the dose within 24 hr following the injection. The estimated renal clearance of the unbound drug nearly corresponded to the renal blood flow rates, indicating that active tubular secretion in the renal re-absorptive tract may be involved in the disposition. The effect of a concomitant administration of pravastatin (PV) on FNX disposition was also examined. PV is a representative substrate of a transporter in human liver cells (OATP-2). After the PV administrations, the Vd-area of FNX and total body clearance markedly decreased, indicating that FNX is actively taken up and metabolized in liver cells by an OATP-2 like transporter. In conclusion, there are at least 2 active transport pathways for FNX pharmacokinetics in rabbits, one is renal tubular secretion and the other is in the sinusoidal section of the liver.

One-day-old, 2-wk-old, and 4-wk-old call ducks (Anas platyrhyncha var. domestica) inoculated intravenously with the H5N1 highly pathogenic avian influenza virus A/chicken/Yamaguchi/7/2004 isolate (Ck/Yama/7/04) were examined clinically, pathologically, and virologically. Clinically, the birds exhibited mild-to-severe neurologic signs and corneal opacity. All birds in the 1-day-old group and one bird in the 4-wk-old group died within 4 days after the virus inoculation. Histologic changes were characterized by severe nonpurulent encephalitis and necrotic lesions of feather epithelium on day 3 postinoculation (PI) or later. Focal necrosis of myocardial cells, pancreatic acinar cells, skeletal myocytes, and corneal epithelial cells was observed. Viral antigens were detected in association with necrotic changes. Viruses were isolated from all examined organs including the skin with many feathers. Serum antibody against the virus was detected in all surviving birds on day 10 PI by hemagglutination-inhibition tests. These results suggest that Ck/Yama/7/04 has a pathogenicity that causes neurologic sign, nonpurulent encephalitis with mortality, and feather lesions for call ducks. Feather lesions with viral antigens and the virus isolation from the skin suggest that Ck/Yama/ 7/04 has a predilection for feathers in call ducks.

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