porcine reproductive and respiratory syndrome

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4 th International Symposium on Emerging and Re-emerging Pig Diseases – Rome June 29 th – July 2 nd , 2003 detectable humoral anamnestic response following homologous PRRSV challenge and this seems to be true following repeated injections of MLV. Perhaps this phenomenon is part of what is being reported as failure of seroconversion in the field. Another possibility is that PRRSV can be attenuated by repetitive passage in cell culture to such an extent that the virus may not even be infectious for pigs, even when given intramuscularly at a dose of 2 x 10 6 CCID50 PRRSV (38). Interestingly, highly attenuated PRRSV may not even readily infect fetuses following direct inoculation (34). The mechanism behind the attenuation of PRRSV is unknown. Viremia - Following intramuscular injection of MLV, swine will replicate the virus and produce a viremia that usually lasts less than 4 weeks in young swine and less than 2 weeks in old swine. Transmission - Under experimental conditions swine vaccinated with MLV develop few if any clinical signs. Vaccinated boars can shed vaccine virus in semen and the duration of seminal shedding seems to be shorter when compared to wild-type virus infection (16,43,54). Vaccination of pregnant naive swine can result in transplacental infection and congenitally-infected piglets that appear normal at birth (34). Based on limited studies, the incidence of transplacental infection appears to be lower for MLVvaccinated pregnant sows when compared to pregnant sows infected with wild-type PRRSV (37). There are field reports of vaccinated animals shedding vaccine virus to naïve contacts based on seroconversion of the contacts (55). The potential duration for MLV shedding is not known. There are also reports of vaccine virus transmission between herds where the vaccine virus has been linked to clinical disease recognized mostly as reproductive failure (9). In these cases the clinical disease is attributed to MLV that has been serially passaged in swine and the vaccine virus reverted to a virulent state. There are genetic differences between the MLV and the putative MLV field isolates (42,56), how the genetic changes contribute to a reversion to virulence is not known. The incidence and impact of fetal infection with vaccine virus in the field is unknown. Serology - Under experimental conditions vaccinated animals seroconvert (>0.4 S/P ratio) about 100% of the time using the IDEXX ELISA. Based on this serologic test, the humoral immune response (antibody) will decay or decrease over time with some animals being reported as seronegative (
4 th International Symposium on Emerging and Re-emerging Pig Diseases – Rome June 29 th – July 2 nd , 2003 contact with pigs from different sources, always a potential PRRS disaster. Because of these difficulties most veterinarians try to control PRRS problems in pigs by depopulating the chronically-infected sites and changing animal flow. In addition to changing animal flow, there is another important strategy for PRRS control and prevention, the isolation of replacement animals before their introduction into the breeding herd. The need for isolation is that the introduction of replacement animals is probably the biggest risk faster for importing PRRSV into a herd. Once the decision for isolation has been made, the debate then ensues, How long is long enough for isolation? Duration of isolation can be dependent on the PRRS status of the recipient herd and of the replacement animals. Essentially, the goal of isolating replacement animals is to test them for evidence of seroconversion prior to their introduction into the herd. If the source of the replacement animals is considered to be PRRSV negative, then a few weeks of isolation is adequate to test for evidence of seroconversion. In most countries where PRRS is endemic there is a high percentage of PRRSV-infected herds. This makes the movement of PRRSV-infected swine likely and complicates the concept of isolation for incoming animals. If the replacement pigs are from a PRRS-positive herd more time in isolation is needed since the purpose of isolation is to let the incoming animals recover from any infection and stop shedding the infectious agent prior to their introduction into the herd. As stated previously, in the case of PRRS it could take months for some animals to stop shedding PRRSV and it may not be practical to isolate replacement gilts for extended periods of time. One solution to this problem of long-term isolation is to purchase replacement gilts at the time of weaning. It is assumed that by the time the gilts are of breeding age they will have become infected with PRRSV (via horizontal transmission from penmates), cleared the virus, and will not be shedding virus when they enter the breeding herd. This time frame is adequate most of the time. However, there is probably an occasional time when some gilts introduced into the herd are actively shedding PRRSV. This could be due to the effects of colostrum. Colostrum from a seropositive sow can suppress the clinical effects of a cogenital/neonatal PRRSV infection and may inhibit the rate of virus transmission among a group of pigs. Instead of PRRSV transmitting rapidly through the group, it "smolders" resulting in a slow rate of transmission with some gilts actively shedding virus upon entry into the breeding herd. In an effort to get around the complications of managing active PRRSV-infections in the isolation barn, it has been stressed to purchase replacement gilts from PRRS-positive herds that are clinically normal or stable. In these herds the incidence of active PRRSV-shedding pigs is lower and the purchase of replacement gilts as weaners has less risk. Although this practice may have less risk, it is difficult for pork producers to make the investment for housing replacement gilts from the time of weaning until breeding age. Some pork producers have had good success with purchasing older gilts from PRRS-stable herds and maintaining them in an 8-weeklong isolation period. Prior to entry into the herd, the gilts are tested for PRRSV antibody and their PRRS status if followed through isolation. If the group of replacement gilts is deemed PRRS stable, then they are kept. Generally, this scheme works well when buying gilts; however, when trying to follow up on these herds to evaluate the success of the isolation strategies, many of the herds have experienced another PRRS epidemic within a couple of years and the herd may end up in the endemic PRRS cycle described earlier. 33 Unfortunately, there are so many variables in these cases that it is difficult to determine the source of the virus for the cyclical PRRS epidemics. For example, the current PRRS epidemic may be due to introduction of new virus or endemic virus that has found a subpopulation of susceptible pigs. When virus is recovered and analyzed, there are at least some genetic changes when compared to virus isolated from previous epidemics. If there is "substantial" genetic change between the viruses, then it is assumed this virus is new to the herd. A different problem exists where the replacement gilts are PRRS-negative and they need to be prepared for entry into a PRRS-positive sow herd. One way to address this issue is combining the practice of isolation with the practice of acclimitization, i.e., exposing incoming replacement animals to the recipient herd’s endemic pathogens. In regards to PRRS, this practice usually involves several strategies. One is the use of cull animals and/or the “feed-back” of certain materials to the replacement animals with the hope that these actions will infect them with PRRSV (20). A concern about this style of acclimatization is if it would consistently work since adult swine do not consistently shed virus for any length of time and PRRSV is readily inactivated outside of living tissue. Another acclimatization plan that can be consistent at infecting replacement gilts with PRRSV involves operating the isolation barn under a continuous animal flow where horizontal PRRSV transmission is maintained by the continual addition of naïve replacements. This concept has merit when the replacement animals are PRRS negative and they are going into a PRRS positive herd. However, this practice is analogous to trying to maintain a fire, sometimes the fire may go out and sometimes the fire might burn out of control. The brakes or controls for this strategy involve another isolation facility that is maintained on an All-In/All-Out pig flow. The plan is to let the replacement animals “cool down” at this second site before they enter the herd. This may be a critical point since in PRRS-positive sow herds that are stable there may be subpopulations of sows that have become susceptible to a PRRSV infection. This strategy of maintaining a continuous flow acclimatization may require monitoring the PRRS status of the replacement gilts to make sure that the virus is still circulating in the isolation barn. A more consistent and perhaps more dangerous version of the continuous flow strategy is to harvest serum from PRRSVinfected pigs and then inject this serum into replacement gilts to establish active infection (6). Another possibility for immunizing PRRS-negative replacement gilts would be the use of PRRSV vaccines. In this situation all replacement gilts are vaccinated at the same time upon entry into the isolation facility. As discussed above, precautions should be taken concerning transmission risks of the MLV virus. Again, the 8 week period of isolation is a commonly used time-frame that reduces the chance of transmitting vaccine virus and allows the vaccinated gilt time to develop an immune response that would confer some clinical protection. The extent of this protection is difficult to predict. Over the years there has been extensive use of MLV and KV in a variety of strategies all designed to control and prevent PRRS. I assume there are proponents and opponents for every vaccine strategy that has been devised. This diverse response to vaccine use points out 1) the difficulty in designing any universal control and prevention plan; 2) the frustrations of trying to reconcile research results (where PRRSV vaccines can be demonstrated to be efficacious) with
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