Histopathological, Immunopathological and Electron Microscopic Studies on Pig Liver Inoculated with Pasteurella multocida Dermonecrotic Toxin.

DOI Web Site 参考文献31件
  • Kurotaki Tetsuro
    Research Center for Veterinary Science of The Kitasato Institiute
  • Onuma Hitoshi
    Japanese Red Cross Blood Center, Saitama Prefecture
  • Arai Yasuko
    Research Center for Veterinary Science of The Kitasato Institiute
  • Ike Kazunori
    Research Center for Veterinary Science of The Kitasato Institiute
  • Oyamada Toshifumi
    Department of Veterinary Pathology, School of Veterinary Medicine and Animal Sciences, Kitasato University
  • Yoshikawa Hiroyasu
    Department of Veterinary Pathology, School of Veterinary Medicine and Animal Sciences, Kitasato University
  • Yoshikawa Takashi
    Department of Veterinary Pathology, School of Veterinary Medicine and Animal Sciences, Kitasato University
  • Kume Katsumi
    Research Center for Veterinary Science of The Kitasato Institiute

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Dermonecrotic toxin (DNT) produced by Pasteurella multocida was purified by anion-exchange chromatography, gel filtration, and high-performance liquid chromatography. Pigs were given an intramuscular injection of P.multocida dermonecrotic toxin (Pm-DNA), which produced necrotic lesions of the liver. Liver sections were taken at intervals of 2, 12, and 24 hours after Pm-DNA injection. We examined the sections histopathologically, immunopathologically, and electron microscopically. The earliest alterations observed were loss of glycogen from hepatocytes, which became more severe during later intervals, vacuolation and single-cell necrosis of hepatocytes, as well as desquamation and fragmentation of the sinusoidal endothelium. The vacuoles subsequently increased in quantity and size with the passage of time and found to contain homogeneous fine material and/or fibrillar material. These materials were thought to be fibrin and blood serum. The vacuoles penetrated the cytoplasm of the hepatocytes. We considered that liver necrosis caused by Pm-DNT probably resulted from the principal effects of vascular injury, although the membrane of the hepatocytes was more or less damaged by the toxin.

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