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By J. T. Van Oirschot (auth.), B. Liess (eds.)

The background of study on hog cholera (HC)/classical swine fever (CSF) should be approximately divided into 3 stages that are characterised by means of the tools on hand on the time for demonstrati ng the causati ve agent. section coated the interval sooner than the viral etiology of HC was once chanced on by way of de Schweinitz and Dorset (1904)*. Thereafter (Phase II) the detection of HC virus (HCV) used to be entire by way of arduous, time-consuming and dear pig inoculation experiments. This explains the wide look for tools not just for detection but additionally for actual infectivity titration in addition to for acceptable serological innovations to unravel pressing difficulties in regards to the pathogenesis, analysis, epidemiology and prophylaxis of HC. It used to be now not earlier than the overdue fifties that HC learn entered section III whilst fluorescent antibody concepts provided not just the capability for detection and titration of HCV in porcine telephone cultures but in addition for extra in depth examine on hog cholera and its virus. And but, there are many inquiries to be spoke back, e. g. at the genetic and antigenic relation of HCV to bovine viral diarrhea (BVD) virus. There are symptoms that section IV of HC study will endure the stamp of biotechnology. In view of this improvement it seems that acceptable to provide an up-dating and summarizing account of HC/CSF together with comparative facets of infections attributable to structurally comparable viruses. The version of the current quantity might were very unlikely with no the cooperation of numerous recognized scientists who immediately agreed while requested for contribution.

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Mengeling WL: Endogenous neutralization of virus during fatal hog cholera illness. Am J Vet Res (31 ):91-95,1970. 51. Kom G: Ober eine Abnahme der Serumvirustiter, zur Funktion der virusneutralisierenden sowie der Olymotrypsin prHzipitierenden Antik8rper im Krankheitsverlauf und zum Heilungsvorgang bei der Schweinepestkrankheit. TierHrztl Umschau (35):19-27,1980. 52. Torlone V, Titoli F, Gialetti L: Circulating interferon production in pigs infected with hog cholera virus. Life Sci (4):1707-1713,1965.

Quart (9):92-103,1969. Nat Inst Anim Hlth 71. Van Oirschot JT: Effect of infections with swine fever virus on inmune functions. III. Antibody response to lipopolysaccharide and sheep red blood cells. Vet Microbiol (8):97-103,1983. 72. Corthier G: Cellular and humoral inmune response in pigs given vaccinal and chronic hog cholera viruses. Am J Vet Res (39):1841-1844,1978. 73. Van Oirschot JT, Terpstra C: A congenital persistent swine fever infection. I. Clinical and virological observations. Vet Microbiol (2):121-132,1977.

Rohrer, H. -H. Atlas der pathologischanatomischen und histologischen Diagnostik der Schweinepest. VEB Gustav Fischer VerI. Jena, 1960. 6. K. and Morrill, C. C. Hog cholera in gnotobiotic pigs. Clinical signs and gross pathologic findings in germ-free and monocontaminated pigs. J. Amer. Vet. Med. Ass. 140: 19561961,1962. 7. Matthias, D. und Klaus, H. Pathologisch-physiologische Untersuchungen zum Hamoglobinund Eisenstoffwechsel beiSchweinepest. Arch. expo Vet. Med. 12: 427-443, 1958. 8. J. W. Focal necrosis in the mucosa of the gall bladder in pigs with hog cholera.

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