Post-weaning multisystemic wasting syndrome (PMWS)

calendar icon 8 November 2018
clock icon 10 minute read

Background and history

PMWS has during the past year or so become of significance and considerable concern in many countries particularly Canada, the US, Europe and the Far East. It is manifest as the name implies by wasting in pigs from 5 weeks of age to around 14 weeks and is now considered a primary disease.

The disease is associated in part with a porcine circovirus (PCV), so called because its DNA is in the form of a ring. It is extremely small and hardy. There are two serotypes, Type 1 causes no known disease. Type 2 can be found in the lesions and can be isolated in pure culture. There are several different strains (biotypes and genotypes). Antibodies to circovirus type 2 have been detected in pig sera collected in Belgium in 1985 but the clinical disease was not described until 1991 in Western Canada. It has since become widespread in North America and Europe.

Young experimentally inoculated colostrum deprived pigs given Type 2 alone sometimes, develop typical lesions. However, they are more likely to develop lesions if another virus, such as porcine parvovirus (PPV) or porcine reproductive and respiratory syndrome virus (PRRSV), is inoculated at the same time. Naturally occurring clinical cases in the field seem always to have a dual infection with PCV Type 2 and some other virus but most pigs which are infected with PCV and PRRS do not develop clinical PMWS.

Serum surveys in Europe and North America have shown that infection has spread widely through the pig population but only a small proportion of seropositve herds have a history of clinical disease. It seems that most infections are sub-clinical. It is not known why some infections result in disease. Piglets may become infected before weaning.

In Western Canada the disease is often reported in high health herds.

Pigs with PMWS
A typical wasting weaner with PMWS

Similar diseases

Many conditions, such as starvation, malnutrition, lack of water, gastric ulcers, enzootic pneumonia, coliform enteritis, swine dysentery, PRRS and other diseases, can cause similar signs. These all have to be eliminated if a specific diagnosis of PMWS is to be made. One disease deserves special mention here, porcine dermatitis and nephrosis syndrome (PDNS) because it can precede, occur at the same time or follow PMWS. The relationship between these two diseases is not known but each can occur in herds without the other being present. (See the latest on PDNS).

Clinical signs

Weaners and growers

  • PMWS tends to be a slow and progressive disease with a high fatality rate in affected pigs.
  • Starting usually at about 6 - 8 weeks of age, weaned pigs lose weight and gradually become emaciated. Their hair becomes rough, their skins become pale and sometimes jaundiced.
  • Sudden death.
  • Enlarged peripheral lymph nodes.
  • May show diarrhoea.
  • May show respiratory distress caused by interstitial pneumonia.
  • Incoordination.
  • Post weaning mortality is likely to rise to 6 - 10% but is sometimes much higher.
  • Clinical cases may keep occurring in a herd over many months. They usually reach a peak after 6 - 12 months and then gradually decline.

Sows and piglets

  • N/A


PMWS Dead Pig

Pig which has died from PMWS
  • Since most herds have antibodies to PCV, blood testing a herd usually does not help.
  • The clinical signs are not specific (although the picture may be highly sugestive) and to make a diagnosis it is often necessary to post mortem several pigs.
  • Diagnosis is based upon the presence of PCV type 2 histological lesions in lung, tonsil, spleen, liver and kidney tissues. Immunohistochemistry is used to demonstrate PCV in tissues. Probably many small mild outbreaks go undiagnosed.

Post-mortem findings

  • The gross post-mortem lesions are variable.
  • The carcass is emaciated and may be jaundiced.
  • The spleen and many lymph nodes are usually very enlarged, however, the clinical picture with enlarged lymph glands is highly suspicious.
  • Kidneys may be swollen with white spots visible from the surface.
  • The lungs may be rubbery and mottled with oedema. Microscopically these lesions are characteristic and diagnostic particularly if the circovirus is demonstrated in them. If affected pigs are suspended by their back legs the inguinal lymph nodes appear enlarged often the size of large grapes.
  • Oedema or fluid may be seen in the chest and abdominal organs and tissues.


  • Infected faeces.
  • Mechanical means via clothing, equipment, trucks etc.
  • Possibly birds and rodents.
  • Circovirus has also been detected in semen from apparently healthy boars.
  • It is not known what other ways the virus spreads between pigs or between herds.
  • Mixing and stress.
  • Continual production.
  • High stocking densities.


  • Control of the disease is based on pig flow, particularly all-in, all-out systems. Do not move pigs from one batch to another.
  • Virkon S has been shown to be effective in killing the virus. PCV is a very persistent virus in the environment.
  • Pay attention to good husbandry, ventilation and temperature.
  • Avoid high stocking density and reduce mixing of pigs.
  • Avoid fostering pigs after 48 hours of age.
  • Early recognition of sick pigs and segregation is essential.
  • If other diseases are present treatment and control of them may help overall.
  • Closure of the herd to build up a herd immunity has been tried but without much success. The suggestion has been made that, since the virus cycles in the nurseries their temporary emptying may break the cycle. It has been shown that groups of young pigs that are removed from the farm and reared elsewhere do much better than those left in the herd.
  • Keep similar age groups of pigs segregated to separate buildings or sections and reduce faecal transfers as far as is practicable.
  • Use solid partitions between pens.
  • It may be worthwhile considering the use of segregated disease. See Chapter 3 - Segregated Disease Control - page 96.
  • Vaccinate for parvovirus (PPV) and control PRRS.
  • Only purchase breeding stock from herds with no history of the disease or close the herd and use AI only.
  • Only use semen from AI studs where all the boar sources have no history of disease.
  • Check the biosecurity of the herd, including isolation of incoming stock, entry procedures for people and general hygiene. See Chapter 2 - How Infectious Agents are Spread.
  • Pay particular attention to the possibility of faecal transmission particularly by lorries.


  • Antibacterial medication is usually ineffective unless given preventively for a long time in advance of when the start of the disease is anticipated. However, recent reports from Eastern England report good responses to controlling secondary infections using stabilised amoxycillin in feed. (Not a cure).
  • There is no vaccine but if a pasteurella is isolated it would be possible to produce an autogenous vaccine.
  • Recent reports have indicated that where secondary enteric infections occur the use of tiamulin by both injection and in feed may be useful.
  • Pigs are also reported to respond well to injections of corticosteroids (2mg/kg) with improved growth rates and reduced mortalities.

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