NOTE: Some of the following data can be also applied to the chapter “Transmission within herd”.
I. DIRECT TRANSMISSION:
The most frequent routes of PRRS virus transmission between herds are the introduction of infected animals and the use of contaminated semen.
PRRS virus is spread mostly by semen and direct contact with infected animals. In the second case, the highest risk situations are introduction of positive replacements in reproductive herds, or introduction of weaned piglets from different sources (positive and negative) in fattening units. Regarding replacements, besides being a very important source of virus introduction, particularly when they are from an external herd with an unknown or positive PRRS virus status, negative gilts also have a significant role in the circulation of the virus when introduced on a positive/unstable farm; in this last case, they act as a constant flow of susceptible animals, which contributes to the infection being sustained.
Regarding transmission by other species, feral swine can act as a source of the virus, whereas many other species, including dogs, cats, raccoons, rats, mice, etc. are not susceptible to infection.
For more information about the role of semen and direct contact in PRRS virus transmission, please see the section “Transmission between animals”.
II. INDIRECT TRANSMISSION:
As detailed in the section, “Physical and chemical characteristics of PRRS virus”, the virus is fairly labile in the environment. It is important to point out that the virus does not persist in the environment or survive on fomites under dry conditions, and that cold temperatures favour its survival.
Nevertheless, indirect transmission of PRRS virus has been demonstrated by several routes.
Insects and rodents: Experimentally, mechanical transmission of PRRS virus has been demonstrated via houseflies and mosquitoes. The virus can survive for a short period on the exterior surface of the insects and in the gastrointestinal tract being the main site of retention of the virus. Some authors suggest that they may be capable of transporting PRRS virus at least 2.4 km from an infected farm. Regarding rodents, all available data indicate that rats and mice are not a reservoir for the disease.
Personnel: Hands, coveralls, gloves, boots, etc. of personnel (own and external) can serve as mechanical vectors.
Fomites: A number of contaminated fomites can act as mechanical vectors. Examples include any farm supply, external equipment (from electricians, plumbers, carpenters, etc.), needles, etc. It is also worth mentioning the importance of transport vehicles. It has been demonstrated that pigs can be infected through contact with the interior of transport contaminated with PRRS virus. The best solution for eliminating the virus from transport vehicles is washing, disinfecting (peroxygens and glutaraldehyde-quaternary ammonium chloride combinations for two hours are highly effective) and drying.
CONTACT WITH CONTAMINATED RESIDUES AND MEAT:
In lagoon effluents the virus can survive and can remain infectious for up to three or eight days at 20ºC and 4ºC respectively. Consequently, the recycling of lagoon water must be considered as a high risk practice. Also, PRRS virus can survive in water for more than one week. Therefore, it is very important to completely dry all surfaces (equipment, facilities, transport vehicles, etc.) after washing and disinfecting. In pig meat, PRRS virus can be detected for at least one week at 4ºC and for months under frozen conditions (-20ºC); uncooked pig meat should not be allowed into the farm.
Some authors have claimed that long distances (more than 3 or even 9 km) airborne spread of PRRS virus is possible. However, airborne transmission cannot always be demonstrated. In some cases, airborne transmission of PRRS virus cannot be detected in pigs sharing the same air space (in the same unit). In other cases, it has been demonstrated only for short distances (a few meters). In some countries, it has been estimated that over 1 kilometre beyond the initial outbreak, the probability of becoming infected through area spread is extremely low. In conclusion, in given conditions, methods of indirect transmission such as vectors seem to be more important than airborne spread.
Nevertheless, airborne transmission over short or long distances appears to be isolate specific (it is probably more common with type II strains) and, among other factors, depends on meteorological conditions.
Risk factors for airborne transmission. Risk increases depending on:
Strain: related to virulence, more common with type II (?)
Proximity to infected farms actively shedding virus via aerosols.
Winds: directional winds from infected to uninfected farm of low velocity with intermittent gusts.
Temperature: cold temperatures (<5 ºC) increase risk more than warm temperatures.
Relative humidity: high relative humidity (>75 %) increases risk more than low relative humidity.
Infected pigs can shed virus from multiple routes and for a long time; mainly by nasal secretions, saliva and semen; less frequently in milk and colostrum, and rarely in urine and faeces. The amount of virus shed, together with the duration of the shedding, vary significantly among strains.
Routes of exposure:
Swine can be infected by several routes of exposure, including oral, intranasal, percutaneous, and sexual (intrauterine and vaginal). The probability of infection is highly dependent on the route and the dose of virus.
Chronic/persistent infection (carrier animals):
The virus can be detected in blood for long periods of time. The length of viraemia is strongly influenced by the strain and the animal’s age; it may extend to weeks in piglets (up to 90 days), whereas in adult pigs it may last for only a few days. After viraemia, PRRS virus can persist for several weeks, particularly in tonsils and other lymphoid tissues. Although most pigs clear PRRS virus within 90 or 120 days, some may remain persistently infected for several months; virus may be isolated from tonsils up to 150 days post-infection. Persistent infection occurs at all ages, but maximum values have been observed in in utero infected foetuses. It has been suggested that the persistence of PRRS virus involves continuous viral replication; it is not a true steady-state persistent infection.
Obviously, prolonged viraemia and persistent infection increase the possibility of transmission. As with other members of the genus Arterivirus, pigs recovered from viraemia and/or acute phase can shed PRRS virus at low levels or intermittently. Therefore, a negative result for viraemia or serum antibodies in a previously infected pig does not rule out that the animal could be shedding the virus.
Importance of semen in PRRS virus transmission:
Semen can play a crucial role in PRRS virus transmission. This is due to the special features of the virus shedding by this route and the extensive use of artificial insemination.
Though viraemia usually is very short in boars, from few a days to a maximum of two-to-three weeks, they can shed the virus in semen for several weeks after infection. In addition, amount of virus necessary to infect a susceptible sow by sexual exposure tends to be much lower that the amount of virus usually present in semen from an infected boar. Nevertheless, transmission by semen appears more likely to occur at the early stages of infection due to the high titres of virus in the semen. It is also important to note that a high variability in virus shedding among boars is observed, and that boars are intermittent shedders. Consequently, a negative isolated PCR result in serum or semen does not rule out the possibility of shedding by this route; more than one sample from a given boar should be analysed at different time periods.
Pigs are extremely susceptible to infection by parenteral exposure; very few PRRS virus particles are sufficient to infect pigs by this route. Therefore, any event, practice or contaminated material that could result in breaks in the skin barrier can potentially facilitate the transmission of the virus, such as: teeth clipping, ear notching, tail docking, inoculations with medications (needles)… In relation to the latter point, it has been demonstrated that infection can occur following the use of the same needle used to vaccinate infected pigs. In addition, because the virus is present in oral fluids, normal pig social behaviour and aggressive interactions (bites, scrapes, abrasions…) can also result in parenteral infection.
It is well-known that abortions during the first and second third of gestation due to PRRS virus infection are rare. However, the virus can efficiently cross the placental barrier in the last period of pregnancy and it can replicate in the endometrial and placental tissues. As a result, foetal death can occur; alternatively, piglets that survive pregnancy, which are usually weak, succumb to other infections. Otherwise, they will survive and remain infected. As we have stated before, piglets infected during the foetal phase could remain as positive for a long time and infect other piglets as late as three months post-farrowing.
II. INDIRECT TRANSMISION:
Several routes of indirect transmission by fomites and contaminated residues, as well as airborne transmission, have been demonstrated (please see the section “Transmission between herds (introduction into the farm)”. Within the herd, we should pay particular attention to hands/gloves, coveralls, boots, and mainly to needles, since as we have seen, pigs are most susceptible to infection via parenteral exposure.
The final outcome of a PRRS virus infection on a farm will mainly depend on the virulence of the strain and the previous immunisation status of the herd.
Once PRRS is introduced into a farm, it will tend to circulate indefinitely. It is true that spontaneous elimination can occur, especially on small farms, but it is rare. The presence of negative subpopulations in the herd or a continuous flow of susceptible animals can perpetuate the infection; in this case, if no measures are taken, periodic clinical outbreaks are to be expected.
In general, three different situations can be considered:
First introduction of PRRS virus in a negative farm => most probably, PRRS virus infection will cause a serious outbreak (see information on reproductive failure in the section “Pathogenesis, lesions and clinical disease”). Abortions in waves (mostly, last third of gestation) over months, weak-born piglets, splay-leg, increase in preweaning mortality, etc. In small farms, the infection can be self-limiting; however, in most cases, the virus will continue to circulate (see section “I.II. Vertical transmission” in “Transmission within herd”). Under these circumstances, the dissemination of PRRS virus in weaners and growers is usually very fast.
Introduction of a new PRRS virus strain in a positive farm => from no effect to serious outbreak. This will depend on the strain, the immunisation level of the herd and the presence of negative subpopulations.
Re-circulation or re-emergence of previous PRRS virus already present in the farm => probably, temporary impairment of productive and reproductive parameters. Again, presence of negative subpopulations can be crucial.
The answer is quite simple:a priori, there is no limit.
In order to further explore this subject, some of the available data are discussed below.
In the past, it was thought that recombination between different PRRS virus strains was an uncommon phenomenon. However, examination of full-length genome sequences has demonstrated that:
Recombination is very frequent.
It occurs all along the genome, in both type 1 and type 2 strains.
In fact, recent studies have demonstrated that several strains in both genotypes are the result of the recombination; in some cases that recombination implies at least three different strains, or even more. Obviously, for recombination to happen, it is necessary that at least two different strains infect the same pig close in time. There are evidences that two or more PRRS virus strains can infect the same individual pig. Therefore, if recombination is much more common than we thought in the past, we cannot rule out the simultaneous coexistence of more than one strain on the same herd/farm, especially in the biggest ones. In fact, several studies have identified from two to eight strains in a same herd over a period from three months to four years.
Quasispecies. RNA viruses replicate with extremely high mutation rates, causing significant diversity. When this occurs, groups of diverse variants can simultaneously exist; this phenomenon is known as quasispecies. Thus, a quasispecies is a cloud, group or distribution of diverse variant viruses related by a similar mutation or mutations that collectively contribute to the characteristics of the population. In naturally PRRS virus-infected pigs, the virus exists as a quasispecies distribution of related but distinct viral variants. This phenomenon occurs independent of the strain and the host. Immunomodulation and quasispecies generation have been speculated to play a crucial role in PRRS virus infection and its chronic/persistent course.
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