In most countries, PRRS is not a notifiable disease and control programs are not in force. Therefore, accurate estimates of the prevalence of infection with wild-type virus in specific countries or regions are not readily available.
Epidemiological situation
When and where PRRSV came from is still a mystery. Even though there were no reports of clinical outbreaks of PRRS before 1987 in North America and 1990 in Europe, antibodies against PRRSV has been detected in archive serum samples originated from East German herds in 1988 and as early as 1979 in Canadian herds.
Nonetheless it can be said that PRRSV is present in most swine-producing regions of the world, with a few exceptions. In Europe, countries free of PRRSV include at present Switzerland, Sweden, Norway and Finland.
Within pig-dense infected regions, it is generally assumed that 60-80% of herds are typically infected. All studies indicate a huge genetic diversity of PRRSV isolates. Most European countries only have genotype 1 strains, but some others like Denmark, Germany, Hungary or Poland have both genotype 1 and 2 isolates. Even though some Type 1 isolates have been found in some areas, Type 2 PRRS is predominant throughout North America and most of Asia.
Within herd prevalence
The majority of the herds will either be endemically infected or free from the infection with only a small fraction of herds in a transient acutely infected state at any point in time. Typically, the herd will experience an acute disease episode lasting 2-4 months (acute phase) followed by a gradual return to an apparently normal production (endemic phase) that can suffer periodic outbreaks of smaller intensity as a result of recirculation of the virus in nonimmune subpopulations of sows and pigs. The infection usually persists in a herd indefinitely, unless specific measures are taken to eliminate the infection.
Within herd seroprevalence may vary, dependent on a number of factors including the type of farm, pig density, herd size and husbandry.
In unstable farrow-to-finish farms, namely those where the virus is circulating among adult sows, the virus spreads in the farrowing crates either because of the birth of viraemic pigs (resulting from transplacental infections) or because of the contamination of farrowing facilities with materials inadvertently brought from other parts of the farm. In this case – when the breeding stock is unstable and viraemic piglets are born - the virus spreads rapidly in weaners. As some reports showed, in most infected farms the majority of seroconversions take already place either by 8 or 14 weeks of age. By the end of the finishing period, most pigs (around 80-100%) are usually seropositive; however, the proportion of infected weaners varies between herds.
