Porcine Reproductive and respiratory syndrome virus (PRRSV) are endemic in most swine‐producing regions of the world, and infections (PRRS) initially characterised by outbreaks of severe reproductive losses, respiratory disease, reduction in growth rate, and increased mortality.
Two types (1 & 2) of PRRSV exists. PRRSV1 and PRRSV2 are regarded as two separate species inside the Arteriviridae family. The two prototype genomes (PRRSV‐1 strain Lelystad and PRRSV‐2 strain VR‐2332) were both discovered around 1991 in Europe (PRRSV‐1) and North America (PRRSV‐2) but vary by approximately 44% in nucleotide sequence. Today, both species share worldwide distribution, with PRRSV‐1 being predominant in Europe and PRRSV‐2 predominant in the Americas and Asia. These two small RNA virus species are remarkably diverse. Intra‐type pairwise nucleotide sequence variation up to 30% is present in PRRSV‐1 viruses, and it exceeds 21% in PRRSV‐2 viruses.
Infected animals shed virus in oral and nasal secretions, urine, semen, mammary secretions, and occasionally faces.
These small RNA viruses have very limited environmental survivability except in moist organic material at neutral pH and temperatures ≤4OC. Frozen, at temperatures ≤18OC, survival is almost indefinite. It is highly sensitive to detergents and common disinfectants. However at cold temperatures choices of products and killing time should be carefully considered.
Clinical presentation of PRRS varies between strains, among herds and over time inside herds, ranging from subclinical to devastating. Epidemics occur in populations naïve to the newly introduced strain, but potentially endemic to other strains. All ages are affected, whereas endemic PRRS occurs in herds that have some degree of immunity to the circulating PRRSV strains.
Multiple (+4) PRRSV co-circulating simultaneously is a common feature of a PRRSV endemic farm. Also, recombination between and within wild-type and attenuated virus vaccine viruses is a common finding. Those findings highlight that there is hardly ‘a’ virus circulating in breeding herds. Instead, there is a diverse ‘cloud’ of PRRSV co-circulating and ever evolving. This may be one of the reasons why the virus is a moving target to existing immunologic solutions to build herd immunity. It is also known that the number of diverse strains co-circulating in the herd positively correlate with virulence. In other words, the more PRRSV variants are circulating in the herd, the greater clinical expression is expected in the pig population.
In endemic PRRS, clinical disease is observed in susceptible subpopulations, usually in nursery and/or young finisher pigs when maternal immunity decays, and/or in replacement gilts or sows that have previously escaped infection (naïve sub populations), as well as their congenitally infected progeny.
In the epidemic infection, the introduction of a new strain to the already endemic farm or the recombination of some of the already co-circulating field strains and/or PRRSV MLV vaccine strains is unfortunately a common feature in farms with poor external and internal biosecurity.
The first phase of acute illness, usually two weeks, is characterised by anorexia, lethargy, respiratory clinical signs, and increased mortality, lasts two or more weeks and affects animals of all ages. It begins in one or more stages of production and quickly spreads within few days, depending on size and composition of the site, to all stages of production.
The second phase usually (if not by seminal infection) characterised by reproductive failure may begin before the first phase of acute illness is completed and continues for 1-4(-6) months. This phase is characterized by reproductive failure, and by high preweaning mortality. When reproductive performance and preweaning mortality return to near pre‐outbreak levels, endemic infection of most herds continues.
During the first phase of acute illness, the sow mortality is 1-4%, 1–3% of litters may be lost in sows that are at 21–109 days of gestation, as overt abortions, or irregular returns to oestrus or nonpregnant sows. Less commonly agalactia, incoordination, and/or a dramatic exacerbation of endemic diseases.
During the second, reproductive phase, typically, 5–80% of sows have late abortions/early farrowing’s around day 110, or farrow at term and have litters composed of any combination of normal pigs, weak variably sized pigs, and dead pigs that are fresh stillborn, autolytic (brown), partially mummified, or completely mummified foetuses. Typically, pigs born dead comprise 0–100% of each affected litter and 7–50% of the total pigs born in a farrowing group. In time, there is a shift from predominantly stillborn pigs and large partially mummified pigs to smaller more completely mummified pigs, to small weak‐born pigs, and to pigs of normal size and vigour. Sometimes most abnormal pigs are born alive, premature, weak, and small, but few are born dead. Surviving sows on the subsequent breeding often have delayed return to oestrus and low conception rates. Boars may show additional lack libido and have variable reduction in semen quality occurring 2–10 weeks after infection.
During the phase of late‐term reproductive failure, there is high preweaning mortality (up to 60%) in pigs born prematurely and at term associated most consistently with listlessness, emaciation/starvation, splay leg posture, hyperpnea, dyspnoea (“thumping”), and chemosis.
With the increasing appearance of highly virulent PRRSV strains, severe acute cases show up to 80-100% abortions and piglet mortality, >20% sow mortality, and potentially nervous signs such as ataxia, circling, and paresis.
Acute PRRSV infection in nursery or grower-finisher pigs is characterized most consistently by anorexia, lethargy, cutaneous hyperaemia, hyperpnea and/or dyspnoea, variable coughing, rough hair coats, variable reduction in average daily gain, and elevated mortality of 12–20%, in severe highly virulent infections cases, >50% of batches.
Concurrent with acute PRRS, a higher than usual incidence of endemic diseases is often reported. Diseases most commonly including streptococcal meningitis, Glasser’s disease, exudative dermatitis, sarcoptic mange, and bacterial bronchopneumonia.
Once introduced into a herd, PRRSV becomes endemic in nearly all cases. In endemically infected herds, PRRS is most often seen as regular or occasional outbreaks of typical acute PRRS in susceptible nursery and/or finishing pigs and/or groups of susceptible breeding stock subpopulations or replacement gilts and boars exposed after introduction. Acute clinical disease is as described for epidemics.
PRRSV viral infection spreads rapidly to primary sites of replication in lung and lymphoid tissues. Viremia 6–48 hours post exposure, with a duration of 2-4-(8) weeks. The longer the younger. However in lymphatic tissues PRRSV resides for far longer periods of time. This non-age-related, “chronic persistent” infection, which is the most significant epidemiological feature, varies between pigs and strains but can be up to day 250 post exposure.
Once infected, PRRSV tends to circulate within a herd indefinitely. Endemicity is driven by persistent PRRSV infections (carrier animals) and the continual availability of susceptible animals introduced through birth or purchase. The virus is perpetuated by a cycle of transmission from dams to pigs either in utero or postpartum or by commingling susceptible animals with infected animals.
Routs of infection are in increasing sensitivity: oral, vaginal, intrauterine, intranasal, and parenteral (ear notching, tail docking, teeth clipping, tattooing, and inoculations with medications and biologics, plus bites, cuts, scrapes, and/or abrasions). The latter at doses of ≤20 PRRSV particles, the others between 1×105.3-4.0 TCID50.
Indirect transmission involves transmission by: wind over distances>= 10 km (aerosols), inanimate objects (e.g. equipment, instruments, clothing, various vehicles, inventory, rooms, and alleyways) or substances (e.g. water, food), aerosols, and possibly arthropod vectors.
The role of infected pigs, virus‐contaminated semen, and aerosols in herd‐to‐herd transmission is firmly established, as are poor external biosecurity (contaminated vehicles, feed, tools, people etc.).
Vaccination is considered an integral part of PRRSV control together with strict internal biosecurity and hygienic measures, however control viral remains problematic, and economic studies have uniformly shown that PRRSV inflicts major losses on swine health and productivity. The cost of PRRSV impact has been estimated at $6.25–$15.25 USD per pig marketed (Holtkamp et al. 2013; Nathues et al. 2017).
The complementary use of some inactivated vaccines to PRRS-MLV vaccines together with biosecurity, in particular strict age segregated production, has demonstrated a highly reliable strategy. It demonstrates a strong and broad direct and colostral PRRSV protection, capable of full viral control in breeding stock including piglets till end of nurseries.