Volume 31, Number 1, January-February 2000
|Page(s)||86 - 87|
|How to cite this article||Vet. Res. (2000) 86-87|
History, occurrence, dynamics and current status of PRRS in EuropeV.F. Ohlinger, S. Pesch and C. Bischoff
bioScreen European Veterinary Disease Management Center GmbH, Mendelstr. 11, Build. L1, 48149 Münster, Germany
Abstract - Late in 1990, veterinarians and farmers in the northwestern part of Germany observed a tremendous increase of late abortions in sows with high numbers of still born and weak born piglets. Within a short time, the disease was also detected in the Netherlands, Belgium, Italy, Spain and with some delay in Great Britain, France, Denmark and other countries, mainly in western Europe. In February 1999, the Porcine Reproductive and Respiratory Syndrome (PRRS) was reported in the Republic of Ireland for the first time. In June 1991, researchers at the ID-DLO Lelystad isolated the so called "Lelystad virus", a member of the arterivirus family, as the causative agent of PRRS. This was the breakthrough necessary for the study of the pathogenesis and epidemiology of the Porcine Reproductive and Respiratory Syndrome. After anti-PRRS virus serology became available, seroepidemiological studies were performed to investigate early outbreaks. Whereas no anti-PRRSV antibodies had been detected in western European countries before 1990, positive results were first obtained with sera taken in the German Democratic Republic in 1987. Further studies revealed an increasing prevalence of anti-PRRSV antibodies in sera from the eastern German swine industry in 1989 and 1990. Before outbreaks occurred in the northwestern part of Germany, a prevalence of about 48% anti-PRRSV antibody positive sera was found in a pool out of 1480 sera received from eastern Germany. Interestingly, no clinical symptoms had been observed in the eastern German swine production. Additionally, only very few outbreaks were found in eastern German swine herds during the period of very severe outbreaks in western European countries, indicating some status of immunity. Despite the unclear origin of the first PRRS outbreaks, two different populations were present during the initial outbreaks: herds with a high level of antibodies in the eastern part of Germany and a totally susceptible seronegative population in western European countries. During the same time the "iron wall" between the two populations broke down. During the initial outbreaks, most herds showed increased numbers of late term abortions with up to 90% weak and stillborn piglets. Reproductive failure was observed for about 4 to 10 weeks in the individual farms. Thereafter no or only few reproductive failures were detected. Whereas most of the farrow-to-finisher herds remained stable, other herds showed waves of PRRSV abortions at 2 to 5 month intervals. Studies on the presence of humoral immunity by profiling the different groups of animals within the herds showed that PRRSV infections usually take place in weaned piglets producing a high pressure of infection. No clinical symptoms have been observed in sow populations with post-infection immunity. However, immunity decreases over time which results in increased numbers of sows that are susceptible to PRRSV infections and have clinical symptoms. These findings indicate that herd structure, herd management and the prevalence of non-immune pigs strongly influence the clinical course of PRRSV infections. Serological studies on different PRRS virus isolates using field sera and monoclonal antibodies have revealed differences in their antigenicity. More detailed information became available after cDNA sequence analysis of European and North American PRRS virus isolates was performed. Nucleotide alignment clearly showed two different genotypes. The European pathotype is represented by the European genotype, only. Molecular epidemiological studies showed, however that PRRS viruses like other RNA viruses undergo phylogenetic drift. cDNA analyses of initial isolates showed nearly complete homology in the genome regions that code for structural proteins, indicating a single origin of western European outbreaks. Variant strains were only observed in Denmark and Spain during the initial outbreaks, pointing towards an additional source of PRRS in those two countries. Isolates obtained in 1991 did show a 97.1% homology in ORF5. An additional antigenetic drift resulted in a decreasing homology of about 81.2% within ORF5 in recent isolates taken in 1999. With regard to highly conserved and highly variable genomic regions, several genotypes or quasispecies do exist in the European swine industry. Since 1996, a single North American genotype based PRRSV modified live vaccine was introduced into some European countries. Up to now, no further North American PRRSV genotypes have been found in the western European swine industry. As expected, studies on modified live vaccine viruses showed some genetic drift, too. However, the speed and level of nucleotide exchanges have been found to be strongly restricted to the potency of spreading to and the level of replication in recent numbers of susceptible pig populations. Only few nucleotide exchanges could be detected in populations with a high prevalence of field virus or vaccine virus induced antibodies. It could be shown by experimental studies as well as by field observations that maintaining a high level of immunity within sow populations will result in the elimination of PRRS viruses. This has been proven by RT-PCR and by PRRSV serology. The situation varies between different countries with regard to virus prevalence, disease control mechanisms and structures in herd management and the swine industry. New outbreaks could be expected to be more frequent in countries with a significant number of susceptible pigs. However problems of decreasing amplitude could be estimated in currently highly affected countries or in populations with a high level of protective immunity. Nevertheless, the development of new antigenic PRRSV variants cannot be excluded. Furthermore, new pathogens like the porcine circovirus type II (PCV 2), which is suspected to be involved in the so called Post weaning and Multisystemic Wasting Syndrome (PMWS), seem to interact with the PRRS virus, its pathogenicity and with anti-viral immunity. PRRSV infections in PCV 2 infected pigs cause a severe respiratory disease that is similar to proliferative necrotizing pneumonia (PNP) followed by PMWS symptoms. Whereas an 88% correlation is shown between PRRSV and PCV2, no significant correlation has been detected for M. hyopneumoniae. Thus PRRSV infections have gained an increasing relevance in the respiratory disease complex in Europe. Nevertheless, total herd immunity has been shown to be an efficient tool for the control and maybe for the eradication of PRRSV. Besides innovative diagnostic tools and efficient vaccines, a strong improvement in herd management and structure seems to be one of the major success factors in PRRSV control.
Corresponding author: V.F. Ohlinger Tel.: (49) 251 980 1900; fax: (49) 251 980 1901;
© INRA, EDP Sciences 2000