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Unit 2: PRRS - causes and predisposing factors

Porcine reproductive and respiratory syndrome was first described in the US in the late 1980s as a reproductive mystery. Clinical signs seen include severe reproductive failure, post-weaning pneumonia, reduced growth and increased mortality. Later in the 1990s a similar syndrome was described in Germany. Nowadays PRRS is widespread in most of the world. However, some countries in Europe (Finland, Norway, Sweden and Switzerland) claim to be free of the disease, and in South America, Chile claims to have eradicated the disease in 2007 (we will explain the approach taken by Chile in the unit 'Alternative strategies for managing PRRS and PMWS'). New Zealand and Australia have never reported the disease.

PRRS is caused by a virus of the Arterivirus family. It has two main subtypes: PRRS virus type 1 (European genotype) and type 2 (North-American genotype) and within each type there are a number of strains. Although the strains are to some extent similar, each has different (genetic) properties that distinguish them and makes them quite unique. The main reason why different strains exist is because PRRS virus can mutate quite rapidly (this is explained in the box 'what is virus recombination?'). The significance of this for vaccine development will become clearer at the end of the section.

Piglet mortality due to PRRS virus

How does the body defend itself against pathogens?

Normally, when an individual gets infected with a pathogen the body reacts by producing antibodies which fight the pathogen (e.g. virus) causing the disease. Antibodies are like an army and protect the body against pathogens; the response of this 'army' is called the immune response. Antibodies are pathogen specific, which means that a pathogen that has already invaded the body will be remembered, so the immune system is prepared to identify it (if the same pathogen enters the body again) and then quickly attack it. In fact this is the principle used in some vaccination procedures, where the vaccine mimics a specific pathogen infection, without causing the disease but developing an immune response, so the immune system is prepared to defend the individual when a "real" pathogen attacks.

If a pig is infected with one PRRS strain, it will be protected against re-infection with the same strain in the future, but it will not be protected against other PRRS strains; in other words, there is no so called 'cross protection' between PRRS strains. The main reason why different strains exist is because PRRS virus can mutate quite rapidly with virus recombination.

What is virus recombination? Why is it important in PRRS control?

The viruses use individual cells in the pig's body to reproduce. The PRRS virus uses mainly cells in the pig's lungs.

Briefly, when the lung cell splits into two it adopts the genetic material of the virus instead of its own material. During this process, mutations in the virus genetic material can occur. The changes during mutation are, most of the time, very small but even though the virus is similar it is not exactly the same. Sometimes the mutations are quite significant and a new different strain emerges.

PRRS virus has a particularly high mutation rate (i.e. changes very quickly) and this is a challenge for herd immunity and vaccine manufacture.

PRRS virus has developed some tricks which interfere with the ability of the pig to respond to infection. They can delay the immune response and, in some cases, the virus can persist in the blood stream for long periods producing a persistent infection. However, experimental work has shown that after an infection, PRRS virus can be eliminated from the pigs and persistent infection rarely lasts more than 200 days. Thus veterinarians often recommend "herd closure" as part of a strategy to eliminate the virus from a herd. This concept is explained in detail in the unit "Alternative strategies for managing PRRS and PMWS"