The question is very difficult to answer as the outcome of PRRSV infection in a naïve farm is depending on many factors that differ a lot between farms. Some of the factors are:
Type of farm: farrow to finish, farrow to wean or multisite.
Construction of barn compartments.
Pig flow: continuous flow or all in-all out.
Level of internal biosecurity, including personnel flow, disinfection etc.
PRRSV strain characteristics.
In a single site, farrow to finish farm, with continuous flow and low level of internal biosecurity the spread of virus in a population can be rapid. On the other hand, in a multisite farm with high internal and external biosecurity the virus spread can be limited to a single site or barn. The lower level of general farm management, the easier and faster the PRRSV spread.
It has to be remembered that PRRSV strains differ in a level of viremia and shedding by infected pigs. “Milder” viruses will be easier handled by infected animals, the level of shedding can be lower, so the spread of such strain could be slower even in conditions of farrow to finish farm. Recently in Belgium more aggressive PRRSV type 1 strains were described that efficiently replicate in nasal mucosa that helps shedding in aerosols, and in effect, in virus spread.
Clinical symptoms of PRRSV infection can be from very mild to severe, depending on the strain characteristic and existing co-infections in a population, as well as environmental conditions. The earliest symptoms post infection are not specific and most often transient: depression, lethargy and anorexia. Some animals can be feverish and exhibit dyspnea and cough. The better health status of pigs and better environmental conditions, the milder the course of the disease can be. However, there are strains of PRRSV type 1 and particularly of type 2 that can cause high fever and severe pneumonia, even in specific pathogen free pigs. Usually younger pigs are more affected than older pigs, in which the acute phase of infection can be asymptomatic. This phase will start in a part of a farm population where the virus first enters, end eventually the symptoms will roll over the rest of the population, depending on the aforementioned conditions. As the clinical respiratory symptoms are not specific to PRRSV, they can be confused with other disease conditions. Laboratory detection (PCR) of PRRSV in blood, oral fluid or lungs or lymphoid tissue of symptomatic pigs is necessary for early detection of virus infection in a previously naïve farm.
The most prominent clinical symptoms of PRRSV infection is reproductive failure: late term abortion, premature farrowings, stillborn and weakborn piglets and high preweaning mortality. Often this is when PRRSV is first suspected in a farm. It has to be remembered that these symptoms can be caused by PRRSV only if sows or gilts were infected and become viremic in third trimester of gestation. Only then the virus can infect placenta, cause lesions and cross fetal barrier, inducing reproductive failure. Even then not every litter will be affected in the same way. Some litters can be born apparently healthy but infected, and shedding PRRSV to littermates and between litters. Sows that became infected in first half of gestation, control viremia before the virus can cross placenta, so the litters are protected from in utero infection. Such piglets are protected also by colostral antibodies until several weeks of age. Most of cases of reproductive failure have non-infectious etiology so laboratory diagnosis is necessary to confirm the role of PRRSV. Detection of antibodies to PRRSV in sows that, let say, aborted, and virus by PCR in piglets in affected litters confirms PRRS case in a reproductive herd.
As reproductive herd shows delayed effect of PRRSV circulation in a farm, one has to assume that if the reproductive symptoms are evident and confirmed to be linked to PRRSV, the virus must have circulated in a population already for several weeks, unnoticed.
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