Abstract. Three different strains of pseudorabies (Aujeszky's disease) virus were inoculated into ligated closed loops in the jejunum and ileum of five specific-pathogen-free pigs. Infected areas were compared with respect to distribution of histologic lesions and pseudorabies virus antigen. Two wild-type strains of pseudorabies virus produced enteric lesions consisting of necrosis of the subepithelial macrophages in the basilar crypt epithelium, necrosis of the lymphoid follicles in the Peyer's patches, degeneration of the epithelial cells in the crypt and villi, degeneration of the neuronal cells in the myenteric plexuses, and formation of intranuclear inclusion bodies on postinoculation days 2-4. Pseudorabies virus antigen was initially detected in subepithelial macrophages of the dome of Peyer's patches on postinoculation day 2 and subsequently extended to superficial epithelium and deeper into the lymphoid follicles and myenteric plexuses on postinoculation days 3-4. Many pseudorabies virus particles were also detected in the center of their necrotic foci. However, 1 mutant strain (ara-T-resistant) of pseudorabies virus did not produce enteric lesions. The results suggest that the primary target of infection by wild-type strains of pseudorabies virus might be the macrophages distributed in the subepithelial area of the dome Peyer's patches.Pseudorabies (Aujeszky's disease) is an acute and naturally fatal condition of pigs caused by swine herpesvirus. Pseudorabies virus (PRV) is neurotropic in nature and spreads from a peripheral viral replication site to the central nervous system (CNS), producing nonsuppurative encephalitis. 8,9,12,[18][19][20] Lesions caused by PRV infection outside the CNS in pigs have been reported. 15 One mutant (ara-T-resistant) strain of PRV was also pathogenic in swine tracheal organ cultures and produced extensive pneumonia in intranasally infected gnotobiotic piglets. 11,13,14 Some wild strains of PRV have produced necrotic lesions in the gastrointestinal tract and myenteric plexuses. 5,16 However, there is little information how PRV crosses the barrier of the intestinal lining and produces the intestinal lesions.In the present study, ligated closed loops in the jejunum and ileum of pigs inoculated with 3 different strains of PRV were examined. The purpose of this study was to describe the pathogenesis of enteric lesions caused by PRV infection.
Materials and methodsAnimals. Five specific-pathogen-free 6-wk-old (11-12 kg body weight) pigs were used. The animals had no neutralizing antibody against PRV.From the National Institute of Animal Health, Kannondai, Tsukuba, Ibaraki 305, Japan (Narita, Kawashima, Arai, Hirose, Yamada), the Jilin Academy of Agricultural Science, Gongzhuling, Jilin 136100, China (Zhao), and the Tochigi Livestock Sanitary Laboratory, Utsunomia, Tochigi 320, Japan (Ezura).Received for publication May 2, 1996.Virus. Three strains of PRV, Yamagata S-81 (YS-81), ara-T-resistant (YS-81TR), 11,13 and Tochigi-94 (TC-94), 5 were used. Two wild-type strains of PRV, YS...