African swine fever (ASF) is caused by a virus that is classified as a member of the Iridovirinae family. The disease in the warthog, the natural host, in Africa was described in 1921 by R. E. Montgomery. The reservoir of the vi rus is inti cks. The i ntroduct i on of domestic pi gs into territory occupied by warthogs i nf ected wi th ASF in the 1960's has endangered the pig industry around the world. The domestic pig is highly sensitive to ASF and develops a devastating disease that kills the pig without giving the immune system a chance to defend the animal against the virus infection. The ability of ASF virus to infect and destroy cells of the reticuloendothelial system leaves a defenseless host that succumbs to an infection which may be described as an acquired immune deficiency di sease of domestic pi gs. Introduction of the virus into Iberia in the 1960's led to a series of ASF epidemics in Spain and Portugal . . and later in France, that caused heavy economic losses. Between 1976 and 1960, ASF virus made its appearance in Malta and Sardinia . . as well as in Brazil, The Dominican Republic . . Haiti, and later in Cuba. In 1985-6 . . ASF appeared in Belgium and The Netherlands.

The history of research on hog cholera (HC)/classical swine fever (CSF) can be roughly divided into three phases which are characterized by the methods available at the time for demonstrati ng the causati ve agent. Phase covered the period before the viral etiology of HC was discovered by de Schweinitz and Dorset (1904)*. Thereafter (Phase II) the detection of HC virus (HCV) was accomplished by laborious, time-consuming and costly pig inoculation experiments. This explains the extensive search for methods not only for detection but also for accurate infectivity titration as well as for applicable serological techniques to solve urgent problems concerning the pathogenesis, diagnosis, epidemiology and prophylaxis of HC. It was not before the late fifties that HC research entered Phase III when fluorescent antibody techniques offered not only the means for detection and titration of HCV in porcine cell cultures but also for more intensive research on hog cholera and its virus. And yet, there are a number of questions to be answered, e. g. on the genetic and antigenic relation of HCV to bovine viral diarrhea (BVD) virus. There are indications that Phase IV of HC research will bear the stamp of biotechnology. In view of this development it appears appropriate to give an up-dating and summarizing account of HC/CSF including comparative aspects of infections caused by structurally related viruses. The editIon of the present volume would have been impossible without the cooperation of several known scientists who instantly agreed when asked for contribution.

This book focuses on the “disease aspects” of classical swine fever (CSF). The epidemiological pattern of the reemergence of CSF from wild boars and its spread to neighboring domestic pigs provides useful information for policy makers. The recent advances in diagnostics and vaccines and how each type of vaccine should be appropriately used in various field situations provide useful information for practicing veterinarians and laboratory scientists, for example, whether the vaccine virus attenuated enough to not cross the placenta to avoid sequelae, how innocuous samples like serum should be cautiously treated to avoid risk of virus spread, how various genotypes of the CSF virus evolve and compete to survive in the field, and how the CSF virus molecularly manipulates normal cell biological processes for its own advantage to survive. Phylogenetic analyses help in tracing the origin of the CSF virus responsible for each outbreak. Overall, readers should be impressed by the capabilities of CFS in pigs. We hope that this book can be a useful reference for all colleagues, whether in CSF-free or CSF-affected parts of the world.