Clinical and pathologic features of West Nile virus infection in native North American owls (Family strigidae).

Since the initial report of West Nile virus in the northeastern United States in 1999, the virus has spread rapidly westward and southward across the country. In the summer of 2002, several midwestern states reported increased cases of neurologic disease and mortality associated with West Nile virus infection in various native North American owl species. This report summarizes the clinical and pathologic findings for 13 captive and free-ranging owls. Affected species were all in the family Strigidae and included seven snowy owls (Nyctea scandiaca), four great-horned owls (Bubo virginianus), a barred owl (Strix varia), and a short-eared owl (Asio flammeus). Neurologic signs identified included head tilt, uncoordinated flight, paralysis, tremors, and seizures. Owls that died were screened for flaviviral proteins by immunohistochemical staining of formalin-fixed tissues, followed by specific polymerase chain reaction assay to confirm West Nile virus with fresh tissues when available. Microscopic lesions were widespread, involving brain, heart, liver, kidney, and spleen, and were typically nonsuppurative with infiltration by predominantly lymphocytes and plasma cells. Lesions in owls were much more severe than those previously reported in corvids such as crows, which are considered highly susceptible to infection and are routinely used as sentinel species for monitoring for the presence and spread of West Nile virus. This report is the first detailed description of the pathology of West Nile virus infection in Strigiformes and indicates that this bird family is susceptible to natural infection with West Nile virus.

Bacterial endotoxin enhances the hepatotoxicity of allyl alcohol.

Lipopolysaccharide (LPS), or bacterial endotoxin, causes liver damage at relatively large doses in rats. Smaller doses, however, may influence the response to other hepatotoxicants. The purpose these studies was to examine the effect of exposure to relatively all doses of LPS on the hepatotoxic response to allyl alcohol, which causes periportal necrosis in laboratory rodents through an known mechanism. Rats were pretreated with LPS (100 micrograms/kg) 2 hr before treatment with a minimally toxic dose of allyl alcohol mg/kg), and liver toxicity was assessed 18 hr later from activity of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in plasma and from histologic changes in liver sections. Plasma ALT and AST activities were not elevated significantly in rats treated with vehicle, LPS, or allyl alcohol alone, but pronounced increases were observed in rats treated with LPS and allyl alcohol. Significant liver injury occurred as early as 2 hr after allyl alcohol treatment in LPS-pretreated rats and peaked at 6 hr. LPS treatment did not affect the activity of alcohol dehydrogenase and did not affect the rate of production of NADH in isolated livers perfused with allyl alcohol; thus, LPS does not appear to increase the metabolic bioactivation of allyl alcohol into acrolein. On the other hand, pretreatment with 4-methylpyrazole, an inhibitor of alcohol dehydrogenase, abolished the hepatotoxicity of allyl alcohol in LPS-treated rats, indicating that production of acrolein was needed for LPS enhancement of the toxicity of allyl alcohol. Pretreatment of rats with gadolinium chloride (10 mg/kg), a known inactivator of Kupffer cell phagocytic function, decreased LPS augmentation of the response to allyl alcohol. These data indicate that LPS markedly enhances the hepatotoxic response to allyl alcohol. Furthermore, the results suggest that the LPS-induced enhancement of allyl alcohol hepatotoxicity occurs through a Kupffer cell-dependent mechanism.

Experimental inoculation of foals and pigs with an enterotoxigenic E. coli isolated from a foal.

Hemolytic E. coli strain 807-13, O149:NM:K88(STb+, LT+), was isolated from the feces of a neonatal diarrheic foal. E. coli 807-13 was examined for adhesion to brush border membranes (BBM) from foals, adult horses and pigs, and its pathogenicity was assessed in neonatal foals and pigs. E. coli 807-13 did not adhere to equine BBM but adhered to pig BBM. It did not cause diarrhea nor did it colonize the intestinal epithelium of 3 colostrum-deprived and 3 suckled foals challenged at 24 h of age. Acute ulcerative gastritis and acute suppurative gastritis were observed in 2 colostrum-deprived challenged foals, and acute neutrophilic enteritis was observed in 1 colostrum-deprived and in 1 suckled challenged foal. No similar histopathologic lesions were detected in the control foals. Both gnotobiotic and suckled pigs developed diarrhea after challenge exposure to E. coli 807-13 and the intestinal epithelium of the pigs was colonized. Histopathologic evidence of gastritis and enteritis among the foals indicated some complicity of E. coli 807-13 in foal enteric disease.

Characterization of Escherichia coli isolated from foals.

Serotype, biotype, antibiogram, hemolysin production, fimbrial hemagglutinins, select toxin genes (STb, STaP, LT, slt1 and slt2) and the attaching effacing (eae) gene were determined for 99 foal strains of E. coli. E. coli from diarrheic and normal foals could not be distinguished by serotype, biotype, or antibiogram. Differences (P < or = 0.05) were observed in hemolysin production (11.5% vs 0%) and the expression of mannose-resistant hemagglutinins (23% vs 13%) among E. coli from diarrheic and healthy foals, respectively. Three of the E. coli strains from diarrheic foals were positive with probes for slt genes and one was positive for STb and LT genes. One strain from a healthy foal possessed the STb gene. As determined by the polymerase chain reaction, 8 strains possessed the eae gene. Seven of the 8 strains were from diarrheic foals and one eae-positive strain was from a healthy foal. The slt-positive strains did not possess eae genes and the eae-positive strains did not possess slt genes. These results indicate that enterotoxigenic strains of E. coli are not implicated in any substantial degree in sporadic foal diarrhea. However, the identification of slt-positive and eae-positive strains in foal feces indicate the presence of potentially virulent strains among foals.

Malabsorption of vitamin A in preruminating calves infected with Cryptosporidium parvum.

Serum retinol, retinyl palmitate, and total vitamin A concentrations, and jejunoileal morphology were examined in neonatal calves infected with Cryptosporidium parvum. Group-1 calves served as noninfected controls and, after an adjustment period, were given 50 ml of saline solution i.v. every 12 hours for 6 days. Group-2 calves were inoculated with 10(7) C parvum oocysts and, after the onset of diarrhea, were given 50 ml of saline solution i.v. every 12 hours for 6 days. Group-3 calves were inoculated with 10(7) C parvum oocysts and, after the onset of diarrhea, were treated with difluoromethylornithine (DFMO, 200 mg/kg of body weight i.v., q 12 h) for 6 days. Group-4 calves were naturally infected with C parvum. Jejunoileal biopsy specimens were excised from calves of groups 1-3 at 3 and again at 15 to 16 days of age. During the course of diarrhea and 3 days after saline or DFMO administration, water-miscible retinyl palmitate was administered orally (2,750 micrograms/kg) to each calf in each group. Cryptosporidium parvum infection was associated with significant (P < or = 0.05) reduction in postadministration serum retinol, retinyl palmitate, and total vitamin A concentrations in calves of groups 2, 3, and 4. Cryptosporidium parvum infection caused significant (P < or = 0.05) reduction in villus height. Decreased villus height, villus blunting and fusion, and attenuation of the intestinal mucosa were associated with reduced absorption of vitamin A, as indicated by lower peak postadministration retinyl palmitate concentration in C parvum-infected calves. Intravenous administration of DFMO to group-3 calves did not improve retinol absorption.(ABSTRACT TRUNCATED AT 250 WORDS)

Adhesion of K99-positive Escherichia coli to intestinal brush borders of pigs.

Ileal samples from 242 pigs, collected at 3 Michigan slaughterhouses, were studied to determine the prevalence of intestinal receptors for K99-positive Escherichia coli. A brush border adhesion test was used to identify the receptors. Of the 242 samples examined, receptors were demonstrated in 230 (95%). After storage of brush border preparations at 4 C, bacterial aggregates lacking identifiable brush border fragments were present in samples tested for adhesion, indicating that K99 receptors may be released from brush border membranes. Seemingly, most, if not all, pigs have intestinal receptors for K99 pili, and an inheritance pattern similar to that observed for K88 receptors probably does not exist for K99 receptors.