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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.
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
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.

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:

  • Movement of carrier pigs.
  • Airborne transmission up to 3km (2 miles).
  • Mechanical means via faeces, dust, droplets and contaminated equipment.
  • Contaminated boots and clothing.
  • Vehicles especially in cold weather.
  • Artificial insemination but only if the boar is viraemic. This period is probably only 3-4 days.
  • The mallard duck and probably other species of bird.
PRRS infects all types of herd including high or ordinary health status and both indoor and outdoor units, irrespective of size.

Clinical signs in the breeding herd

Stillborn piglets with PRRS
Stillborn piglets with PRRS

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.

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
When the virus first enters the breeding herd disease is seen in dry sows, lactating sows and sucking piglets.

Clinical signs in dry sows during the first month of infection

  • Short periods of inappetence spreading over 7-14 days - 10-15% of sows at any one time.
  • The body temperature may be elevated from 39-40ºC (103-105ºF).
  • Abortions, often late term, may occur at a 1-6% level. These are often the first signs to be noted.
  • Transient discoloration of the ears may be seen (2% level. Blue ear disease).
  • Some sows farrow slightly early. 10-15% over the first 4 weeks.
  • Increased returns occur 21-35 days post-service.
  • Prolonged anoestrus and delayed returns to heat post-weaning.
  • Coughing and respiratory signs.
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.

Clinical signs in farrowing sows in the first month of infection

  • Inappetence over the farrowing period.
  • A reluctance to drink.
  • Agalactia and mastitis.
  • Farrowings are often 2-3 days early.
  • Discoloration of the skin and pressure sores associated with small vesicles.
  • Lethargy.
  • Respiratory signs.
  • Mummified piglets. 10-15% may die in the last 3-4 weeks of pregnancy.
  • Stillbirth levels increase up to 30%.
  • Very weak piglets at birth.
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.

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
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.

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:

  • A 10-15% reduction in farrowing rate (90% of herds return to normality).
  • Reduced numbers born alive.
  • Increased stillbirths.
  • Poor reproduction in gilts.
  • Early farrowings.
  • Increased levels of abortion (2-3% but rises up to 50% have been reported).
  • Inappetence in sows at farrowing.
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.

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

  • This is aimed at preventing secondary infections, usually either respiratory or enteric until an immunity builds up.
  • Piglets should be injected with either long-acting OTC or amoxycillin on days 3, 7 and 14 after farrowing.
  • Electrolytes should be given to counteract dehydration.
Management control and prevention
  • Raise the farrowing house temperature during the period of farrowing and whilst disease is active to 23ºC (75ºF).
  • Provide extra bedding. Use shavings or other suitable materials to create the best environment for the piglet.
  • Provide an extra heat lamp by the side of the sow.

Signs in boars

  • Inappetence.
  • Increased body temperature.
  • Lethargy.
  • Loss of libido.
  • Lowered fertility.
  • Poor litter sizes.
  • Lowered sperm output.
  • Reduced mortality and acrosomal defects.
Diagnosis
Healthy macrophage
Healthy macrophage
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.

Similar diseases
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.

Treatment

  • There is no treatment as yet available in animals against virus infections. With PRRS however, it is essential during the acute phase to prevent the multiplication of bacteria that normally would have been destroyed by macrophages. Antibiotic treatment should be given for 3-4 weeks to all sows and boars immediately the disease is diagnosed or suspected. If necessary commence with water soluble antibiotics followed by in-feed medication. Prompt treatment usually reduces abortions, stillbirths, mummified pigs and early farrowings caused by secondary bacteria.
A control programme for dry sows during acute disease
  • Raise the sow house temperature to 21º (72ºF).
  • Avoid night temperature drops.
  • Avoid draughts.
  • Medicate the sow's feed immediately with 500g/tonne of tetracycline either CTC or OTC.
  • If sows are inappetent, medicate the water with OTC or CTC at the onset.
  • Apply the medication to both gilts and boars.
  • Maintain this for a four week period.
  • Increase feed intake by at least 0.5kg per day over the four weeks.
  • Inject individual sows with long-acting OTC or penicillin during periods of inappetence or as advised by your veterinarian.
A control programme for the sows in the service area during acute disease
  • Apply the same procedures as for dry sows.
  • Do not cull any sows for the next six weeks, (at least) to increase the mating programme.
  • Accept that you will have a 10-15% drop in the farrowing rate, and therefore plan to increase the mating programme by more gilts and retention of sows that would have been culled.
  • Buy in gilts if possible from a previously exposed herd, most if not all will be immune. If home bred gilts are kept, introduce these to the infection as early as possible.
  • To do this always move gilts into weaner or finisher accommodation for 3-4 days to expose them to the virus.
  • Consider vaccinating incoming gilts whilst in isolation if one is available. Seek veterinary advice.
  • Do not serve gilts until at least six weeks after exposure to infection or vaccination.
  • Use one dose of AI to compliment each natural mating for an 8 week period.
A control programme for the farrowing sow during acute disease
  • Inject sows 2 days before farrowing with antibiotics. Continue this in succeeding sows for a period of six weeks.
  • Repeat three days later or until farrowed.
  • Use long-acting preparations of antibiotics. Oxytetracycline or semi-synthetic penicillins are medicines of choice.
  • Top dress the sows food daily with in-feed antibiotics premixes. Use OTC, CTC or TMS. (Give 15-20g of a 10% premix per day).
  • Continue this for 10-21 days post-farrowing.
  • Raise the farrowing house temperature to 22ºC (75ºF)
  • Deep bed the pens with straw, shavings or paper if this is possible.
  • Provide extra heat for piglets.
  • Continue the above programme for 4 - 6 weeks as advised by your veterinarian.
If it is suspected that a chronic reproductive problem is associated with PRRS consider the following action plan. (Fig.6-6).

Fig 6.6 - PRRS Action Plan

From this information the following possibilities exist :

  • The herd is negative.
  • There is no infection taking place in the sow herd and no evidence of infection in weaners. In other words the virus has died out and PRRS is not a problem.
  • The sow herd is serologically negative but there is evidence of persistent viral infection in younger growing pigs. Such animals will show evidence of rising titre levels. This continually exposes susceptible breeding stock to disease.
  • Negative gilts become infected and disseminate the virus.
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:
  1. Vaccination if a vaccine is available.
  2. Removal of the infected group of pigs, usually the first and second stage growers from the farm to eliminate the virus.
  3. Expose gilts to maintain an immune breeding herd.
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.

Immunity
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.

Clinical signs in weaned and growing pigs

Acute disease
(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%.

Endemic disease
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.

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

  • In the acute disease when PRRS first enters the farm it is important to cover the period at risk, which is usually six to eight weeks, with in-feed antibiotics or by individual injections and water medication.
  • The broad spectrum antibiotics, tetracyclines, trimethoprim/sulpha, or synthetic penicillins are the medicines of choice but if EP alone is involved tiamulin or lincomycin may be used. If App is active ceftiofur could be a medicine of choice for individual treatments.
  • In endemic disease preventive medication over the period at risk using 500 to 800g of tetracycline or trimethoprim/sulpha 400g/tonne in-feed may be used but it would be advisable to identify the major bacteria involved and determine their antibiotic sensitivities.

    Management control and prevention

    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:

  • Purchase breeding stock from herds believed free of PRRS.
  • Set up a quarantine system to hold pigs for a minimum of eight weeks.
  • As pigs arrive in quarantine, add 6 of your own known negative pigs and mix with the incoming stock.
  • After five weeks of direct contact, blood sample the 6 sentinel pigs and 6 of the incoming stock.
  • Check with the donor herd that it is still believed free.
  • Make sure lorries do not come onto your farm with other pigs already on board.
  • Provide boots and coveralls for all visitors.
  • Do not borrow equipment from other pig farms.
  • Review herd biosecurity.
  • In known infected herds one of two breeding strategies can be adopted. If the virus is not circulating it may be advisable to buy in gilts and boars from negative herds and vaccinate them in isolation. Alternatively gilts and boars from known infected sources should be purchased and acclimatised for at least six weeks before mating. The method should be determined by the performance of the gilts. Both live and killed vaccines are available in some countries and control strategies will be determined by their known safety and efficacy. Seek advice from your veterinarian.
Segregated Disease Control (SDC)
(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:

  • Removal of pigs at weaning (more than 21 days of age) on a weekly batch basis to totally separate housing for a period of 8 weeks (SDC).
  • Vaccination of piglets at one and 3 weeks of age against Mycoplasma hyopneumoniae.
  • Removal of all remaining weaners/growers/finishers.
  • Adaptation of buildings to all in all out and no droplet contact between batches.
  • Return of the SDC pigs.
  • Control/eradication of disease in the sow herd by vaccination/medication.
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.

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