Abstract
1 James A. Baker Institute, New York State College of Veterinary Medicine, Cornell University, Ithaca, New York 14853, U.S.A.
2 State Veterinary Institute for Virus Research, Lindholm, 4771 Kalvehave, Denmark
3 Department of Veterinary Microbiology and Pathology, College of Veterinary Medicine, Washington State University, Pullman, Washington 99164, U.S.A.
4 Department of Veterinary Clinical Medicine and Surgery and Washington Animal Disease Diagnostic Laboratory, College of Veterinary Medicine, Washington State University, Pullman, Washington 99164, U.S.A.
and5 National Veterinary Assay Laboratory, Ministry of Agriculture, Forestry and Fisheries, 1-15-1 Tokura, Kokubunji, Tokyo 185, Japan
Canine parvovirus type 2 (CPV-2) became widespread during 1978 and was reported in many countries during 1978 and 1979. Earlier studies showed that CPV-2 was replaced in the U.S.A. around 1980 by an antigenically and genetically variant virus (CPV-2a). Here we show that CPV-2 was present in the U.S.A., Japan, Belgium and Australia prior to 1980, but that between 1979 and 1982 CPV-2 was replaced by CPV-2a in all of those countries as well as in France and Denmark. Examination of sera collected between 1979 and 1984 from wild coyotes (Canis latrans) in the U.S.A. by an agar gel precipitin assay indicated that the coyotes were originally infected by CPV-2, but that after 1980 the juvenile coyotes were being infected with CPV-2a. The natural global replacement of CPV-2 by CPV-2a over a period of 2 to 3 years indicates that CPV-2a has a strong epidemiological advantage over CPV-2, although the mechanism involved remains to be defined.