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Porcine Reproductive and Respiratory Syndrome (PRRS)
PRRS is caused by a virus which was first isolated and classified as an arterivirus as recently as 1991. The disease syndrome had been first recognised in the USA in the mid 1980's and was called Mystery swine disease or blue ear disease.
The virus of PRRS has a particular affinity for the macrophages particularly those found in the lung. Macrophages are part of the body defences. They ingest and remove invading bacteria and viruses. Those present in the lung are called alveolar macrophages. In contrast to most other bacteria and viruses, macrophages do not destroy the PRRS virus. Instead, the virus multiplies inside them producing more virus and kills the macrophages. Up to 40% of the macrophages are destroyed. This removes a major part of the bodies defence mechanism and allows bacteria and other viruses to proliferate and do damage.
.jpg "Ear oedema, a symptom of PRRS in older pigs") Ear oedema, a symptom of PRRS in older pigs |
A common example of this is the noticeable increase in severity of enzootic pneumonia in grower/finisher units when they become infected with PRRS virus. Another example is the alarming increase that can occur in clinical cases of meningitis in herds in which virulent Streptococcus suis type 2 is enzootic. This observation has been used by research workers in the experimental reproduction of streptococcal meningitis. Once it has entered a herd the PRRS virus tends to remain present and active in the herd indefinitely.
The persistence of the virus within a herd is related to a number of factors:
- If sero-negative susceptible gilts are regularly introduced into the herd they may enable the virus to persist.
- Infection is maintained in recently weaned piglets once their maternal antibody disappears. Infection is transmitted to these pigs from older groups previously infected and this procedure is responsible for active enzootic respiratory disease continuing on many farms.
- It may take up to a year for all breeding stock, particularly in large herds, to become infected for the first time and although the virus appears to spread rapidly in a herd it may be some 4-5 months before at least 90% of the sows have become sero-positive. Furthermore, it is not uncommon for sow herds 1-2 years after infection to contain less than 20% of serological positive animals. This does not however necessarily mean they are not still immune nor does it mean that they have stopped passing on immunity to their offspring.
Methods of spread
Adult animals excrete virus for much shorter periods of time (14 days) compared to growing pigs which can excrete for 1-2 months. PRRSV may infect foetuses from mid pregnancy onwards and is excreted in salvia, colostrum and milk.
The following are common methods of spread:
Clinical signs in the breeding herd
The tendency is for any epizootic virus infections to get less virulent e.g. African swine fever and rabbit myxomatosis. Also field observations suggest that the virus destroys the macrophages and this lowers the pigs immunity. The severity of an outbreak in a herd will depend to an extent upon other viruses and bacteria already present in the herd and their capacity to cause disease. Furthermore, when the pigs' immunity is compromised, excessive stocking density and the quality of the environment also become important. For example, PRRS in a minimal diseased pig may cause no detectable pneumonia but if the pigs are already infected with respiratory pathogens and are in circumstances of poor housing and inadequate environments, severe disease may develop and persist.
Acute disease
Clinical signs in dry sows during the first month of infection
Clinical signs in farrowing sows in the first month of infection
In some herds, these may reach up to 30% of the total pigs born. Piglet mortality peaks at 70% in weeks 3 or 4 after the onset of symptoms and only returns to pre-infected levels after 8-12 weeks. The reproductive problems may persist for 4-8 months before returning to normal, however in some herds it may actually improve on the pre-PRRS performance.
Long term effects
The effects of PRRS on reproduction efficiency in herds in which the infection has become enzootic have been observed in the field for up to 12 months after disease has apparently settled. These are as follows:
Field experiences show this is unusual in herds of less than 500 sows provided live vaccination has not been carried out.
Clinical signs in piglets
In the early stages of acute disease piglets are born in a very weak condition and rapidly become hypoglycaemic because they are unable to get to the teat and suckle. Together with weak pigs there are a high numbers of stillbirths and late mummified ones. Newborn piglets show sticky brown material over the eyelids and very occasionally small blisters on the skin. Scour, pneumonia and coughing are commonly observed but with increasing time the quality and survivability of the piglets improves. Starvation, splay leg, tremors and paddling and doming of heads may also be seen. Haemorrhage associated with trauma and tail docking due to reduce blood thrombocytes is also reported.
Similar diseases
Aujeszky's disease (AD) when it first enters the herd can be confused with PRRS but nervous signs are present with AD but not with PRRS. A serological test will differentiate between the two.
Treatment
Signs in boars
Similar diseases
Treatment
From this information the following possibilities exist :
Immunity
Clinical signs in weaned and growing pigs
Acute disease
Endemic disease
Similar diseases
Chronic respiratory disease is caused by combination of respiratory pathogens including PRRS, SI, EP, App, Hps and pasteurella bacteria, particularly as they become additive. The diagnosis is then of multiple cause.
Treatment
Management control and prevention
The virus is spread by nasal secretions, saliva, faeces and urine and field studies suggest it can be airborne for up to 3km (2 miles). A carrier state exists in the pig that can last for 2-3 months. In some individuals it is thought that it may last longer although the pigs may not be shedding virus. Artificial insemination can be a potential method of spread if semen is used when the virus is present in the blood (viraemia) and particularly during the first 3-4 week period following the breakdown of an AI stud. Outside this period field evidence indicates the risk of spread in semen is very low from previously infected groups of boars. In a study over a 3 year period 32,000 doses of AI, from an AI stud populated with boars from positive herds, were used in 5 large PRRS negative herds. No infection or sero-conversion occurred.
PRRS infects all types of herd including high or ordinary health status and both indoor and outdoor units, irrespective of size.
.jpg "Stillborn piglets with PRRS")
Stillborn piglets with PRRS
.jpg "Mummified PRRS piglet")
Mummified PRRS piglet
The clinical picture can vary tremendously from one herd to another. As a guide, for every three herds that are exposed to PRRS for the first time one will show no recognisable disease, the second would show mild disease and the third moderate to severe disease. The reasons for this are not clearly understood. However the higher the health status of the herd, the less severe are the disease effects. One may be that the virus is continually mutating as it multiplies throwing up some strains that are highly virulent and some that are not. The USA strains appear particularly virulent.
When the virus first enters the breeding herd disease is seen in dry sows, lactating sows and sucking piglets.
The inappetence may be quite short, often no longer than 12-24 hours, and the sow may eat only half her feed. Thus in the dry sow house there may be episodes when up to 10% of sows at any one time will be slightly off their food. In group housing, this inappetence may not be so noticeable. In herds where sows are subjected to wide fluctuations in environmental temperature, or if the management is poor and nutrition marginal, then the signs are likely to be more severe. Furthermore, in these types of herds, abortion levels are often elevated considerably.
This chapter is primarily concerned with the effects of the disease on reproduction. Disease in piglets is discussed in chapter 8 and disease in weaners and finishers in chapter 9. The initial phase of inappetence and fever will often take 3-6 weeks to move through the breeding herd. Cyanosis or blueing of the ears is a variable finding and less than 5% of sows show it. It is transient and may last for only a few hours. Coughing occurs in some sows and a few individual cases of clinical pneumonia may occur. This acute phase lasts in the herd for up to 6 weeks, and is characterised by early farrowings, increases in stillbirths, weak pigs and an increase in the numbers of large mummified pigs that have died in the last three weeks of pregnancy.
Longer term effects of PRRS on reproductive efficiency are difficult to assess, particularly in herds of low health status. In some there are increases in repeat matings, vulval discharges and abortions, all of which may be blamed on PRRS.
Some herds report that PRRS continues to be associated with reproductive failure and increases in repeats (5-10%) on a normal and abnormal cycle for as long as 6 months after the acute episode has subsided.
Management control and prevention
Diagnosis
.jpg "Healthy macrophage")
Healthy macrophage
.jpg "Dead macrophage")
Dead macrophage
If the herd has not been exposed to PRRS then blood sampling a minimum of 12 adult animals (preferably those that have been off their food at least three weeks) provides a reliable means of diagnosis. Serological tests available include the overlay or IPMA test, the fluorescent antibody test and an ELISA test. All these tests can give rise to false positives and false negatives on individual animals, but on a group basis, they are reliable in indicating whether the herd has been infected or not. Where disease persists serum samples should be examined two weeks apart to demonstrate whether the virus is associated with a particular clinical problem. PCR tests on small blood samples taken in the early acute phase will demonstrate evidence of viral DNA. This is a good sensitive test.
When PRRS first enters the herd the clinical picture could be confused with Aujeszky's disease (AD) / Pseudorabies (PR) but the absence of nervous symptoms in piglets and serological tests will differentiate between the two diseases.
A control programme for dry sows during acute disease
A control programme for the sows in the service area during acute disease
A control programme for the farrowing sow during acute disease
If it is suspected that a chronic reproductive problem is associated with PRRS consider the following action plan. (Fig.6-6).
Because our knowledge of this disease is continually improving you are advised to discuss further controls with your veterinarian . Three procedures need to be considered:
Artificial insemination (AI)
Originally it was thought that artificial insemination would not disseminate PRRS but, epidemiological studies have indicated that it has been a major source of spread during acute disease. Boars may remain viraemic for 8-12 weeks after initial infection or become chronic carriers. There is, however, strong evidence to show that if young breeding boars are moved from known positive farms and held in isolation for 8 weeks with negative sentinel pigs and if the sentinels do not seroconvert the boars can be moved relatively safely into the AI stud. However sero-negative boars in the stud should be closely monitored for sero-conversion and signs of inappetence or fever. If there is any doubt semen movements should be stopped until the position is clarified. Large AI data bases have shown that semen from sero-positive, non shedding boars does not appear to transmit infection to sero-negative herds.
Field observations show that the majority of breeding females become immune and do not succumb to further episodes of infection. However, if the virus continues to circulate in young sows or growing pigs the incoming negative gilts will become infected at some stage. Field experiences in the UK have shown that reappearance of major outbreaks of disease in breeding herds is uncommon.
(442) When introduced first into an EP and App free growing herd there is usually a period of slight inappetence and mild coughing but in some herds there are no symptoms at all. If EP and/or virulent App are present in the herd however, clinical signs may become severe with an acute extensive consolidating pneumonia with the gradual formation of multiple abscesses. Disease becomes evident within 1-3 weeks of weaning, pigs loose condition with pale skin, mild coughing, sneezing and increased respiratory rates. Mortality during this period may reach 12-15%.
Once the acute period of disease has passed through the breeding and finishing herd PRRS virus normally then only becomes of significance in the early growing period, where severe endemic pneumonia can persist with periods of inappetence and wasting of pigs. Pigs become infected as maternal antibody disappears and then remain viraemic for 3 to 4 weeks continually excreting virus. Permanently populated houses maintain the virus at high levels, particularly in the first and second stage accommodation. Clinical disease is seen in pigs from 4 to 12 weeks of age and it is characterised by a fairly predictable time of onset, inappetence, malabsorption and wasting, coughing and pneumonia. In this post-weaning period mortality can rise up to 12% or more and persist inspite of antibiotic treatments. Secondary bacterial infections become evident in pigs at a later stage from 12 to 16 weeks of age from abscesses that develop in the lungs. These infections spread to other parts of the body, particularly joints with increased lameness.
Segregated Disease Control (SDC)
If your herd is in a region where it is unlikely to be infected directly from a neighbour it is important to determine by serology if your herd has or has not been exposed to PRRS. If it is found to be negative the following actions should be considered:
(See Chapter 3 in the Pig Health Database or the Featured Article)
This technique has proved of considerable value in controlling chronic respiratory disease associated with PRRSV. The objective is control and not elimination. The essential components are:
Vaccination
Live vaccines are available for use in weaners and non pregnant females, i.e. gilts, provided they are kept in isolation for 8 weeks. Their use is not recommended in breeding females due to potential side effects. In herds where serious respiratory problems are complexed with PRRSV their use has been of value.
A new killed vaccine for use in breeding animals is also available. This has the advantage of creating a stabilised immune herd without risk and a positive benefit by a reduction in viraemic post weaned pigs.
Eradication
Partial Depopulation
After a period of time the virus may disappear from the sow and finisher population but remain endemic in the first and second stage rearing in pigs 3-12 weeks of age. By blood sampling sows, weaners and finishers the status of the herd in this respect can be established. Where disease is only active in growing pigs up to 12 weeks of age they can all be removed from the farm together with the next two weeks production of new weaners. The houses are cleaned and disinfected and left empty for two weeks. PRRS disease may be eliminated by this method of partial depopulation.
Segregated Early Weaning (SEW)
PRRS free pigs can be obtained in a similar way from a herd in which the virus has become enzootic and in which sow herd immunity is stable and active virus infection is lower. In this process of segregated early weaning the largest suckled piglets are weaned from the farrowing rooms at 5 days of age to be reared in isolated premises. The method, however, is not 100% reliable and occasionally one or more piglets in a litter may come through already infected. To reduce this happening pigs should only be taken from sero-positive mothers. To avoid all the pigs becoming infected, each group of piglets weaned should be kept in isolation until all the pigs have been tested. PCR tests are carried out on blood samples taken form the navels of the piglets at birth. It takes only a few days to get the results. To improve the system further, instead of farrowing the mothers on the farm they can be farrowed in temporary isolated accommodation outside the farm (MEW). See chapter 3 Segregated weaning.
Hysterectomy
Hysterectomies can be carried out on sows from stable herds. Fostering these piglets on to sows from a PRRS negative herd is an effective method of developing PRRS negative stock. It must be remembered, though, that PRRS can cross the placenta in recently infected gilts and sows. Therefore only pregnant sows that have been sero-positive for at least 4 months should be hysterectomised. Each newborn litters should be tested for infections using a PCR. The foster sows and hysterectomy derived piglets should be kept in isolation until the results are known.
Depopulation/Repopulation
A farm can be depopulated cleaned, disinfected and repopulated with PRRS negative stock. Depopulation is very expensive and before considering this investigate how the herd became infected in the first place and assess the chances off it being re infected again. Repopulation should not be attempted in winter because as the temperature drops, the survival of the virus increases, e.g. 24 hours at 37ºC (99ºF), 6 days at 20ºC (68ºF), 1 month at 4ºC (39ºF). The virus is stable when frozen for long periods of time. Control of PRRS in weaners and finishers is discussed in chapter 9.
Test and Removal Procedures (1)
a) These methods are based upon the premise that over a period of 6 months or more and provided no breeding animals are introduced (i.e. the herd is closed) then the sero prevalence of infection in the breeding herd usually drops to less than 15%. At this point the complete herd is tested by ELISA and PCR and any positive breeding stock are removed. Only sows and sucking pigs remain on the farm, weaned pigs being moved to an offsite facility. Only negative gilts and semen are introduced into the herd following its negative achieved status.
During the period it is important that farrowing houses are managed all in all out with no back fostering of piglets.
b) Eradication by partial depopulation has also been reported from Denmark. The basis again is the establishment of a non-viraemic breeding herd by closing the herd for a minimum period of 6 months and using IMPA and ELISA tests to identify viral excretors. Successes are recorded in breeding, growing and finishing herds. Viral excretion is normally maintained in weaned and growing populations. Such areas on the farm therefore, are depopulated, cleaned and disinfected and then repopulated with weaned pigs from the non viraemic sow herd.
