Postweaning Multisystemic Wasting Syndrome
Postweaning Multisystemic Wasting Syndrome (PMWS)
In 1982 a novel virus, subsequently named porcine circovirus (PCV), was identified by Tischer et al in 1892 (12). PVC is a DNA virus and member of the Circoviridae family. PCV infections may interfere with normal immune function (11).
The first description of PMWS was in Saskatchewan in 1991 (6); this syndrome has now been described worldwide. Clinically the syndrome is characterized by wasting, paleness of the skin, dyspnea, diarrhea and icterus (jaundice). In 1997, the presence of porcine circovirus (PCV2) antigen was demonstrated in lesions of animals affected by PMWS (2). However, PCV2 is considered a necessary but not sufficient factor to develop PMWS.
Since 1999, PCV2 has been suggested to play a role in reproductive disorders, porcine dermatitis and nephropathy syndrome (PDNS), porcine respiratory disease complex (PRDC), proliferative and necrotizing pneumonia (PNP) and congenital tremors, but it remains a controversial issue (7,9). Dr. SE Sanford from Ontario, Canada presented 5 cases of PCV2 related reproductive failure in startup herds and the common features were:
a) startup gilts herds,
b) large number of mummies plus stillbirths, late-term abortions and NIP sows,
c) gilts flows creating PVC2 naïve populations,
d) nonsuppurative to necrotizing myocarditis in mummies, stillborn and neonates,
e) abundant PCV2 antigen in myocardium (10).
Similar features were found by Harding and Halbur, 2002 (7).
Clinical presentation
PMWS most commonly affects pigs from 2 to 3.5 months of age. The clinical sings include weight loss, emaciation, tachypnea, dyspnea, jaundice, enlarged lymph nodes and pallor. Less common sings are diarrhea, coughing, pyrexia, gastric ulceration, sudden deaths and central nervous system disturbances.
Some trials have fully demonstrated that PCV2 can be itself (without any other apparent triggering factor) the cause of PMWS. PCV infections may interfere with normal immune function.
Some of the clinical sings may be caused in part or exacerbated by secondary infections. In USA the principal clinical sings are: respiratory infections, wasting and diarrhea.
PCV2 has been associated with porcine respiratory and reproductive syndrome (PRRS), Pneumonia (PNP), Reproductive failure, PDNS, PRDC, Porcine parvovirus (PPV), Congenital tremors (CT), Enteritis, Pseudorabies, Glassers disease, Streptococcal meningitis, Salmonellosis and Dietetic hepatosis.
Dr. Gaylan Josephson believes there are four co-factors that work with PCV2 to make a disease outbreak. One is co-infection with another virus, such as PRRS; another is co-infection with bacteria, such as Mycoplasma hyopneumoniae or Haemophilus parasuis. Stress and suppression or stimulation of the immune system also appears to be associated with disease outbreaks. PCV2 and PDNS were first described in the United Kingdom in 1993. Easy detection by presence of necrotizing skin lesions, mainly located on the hind limbs and perineal area.
PCV2 and reproductive disorders, and almost all of these descriptions of reproductive disorders came from Canada. PCV2 can be transmitted vertically and cause reproductive failure (in absence or presence) of other pathogens.
PCV2 and PRCD are characterized by slow and uneven growth, and reduced feed intake, higher feed to gain conversion rates, cough, and clinical pneumonia.
PCV2 and Proliferative and necrotizing pneumonia (PNP) was initially described in 1990 in Canada as a condition associated with respiratory problems in nurseries and finishing barns. PCV2 and congenital tremor (CT) are characterized by tremors of the head and limbs. CT type A has been divided into 5 different subtypes (AI to AV). CT subtype II has been traditionally associated to an unidentified virus. However, the clinical and/or pathologic conditions other than PMWS have only been reported as retrospective studies (PDNS, PNP) and clinical cases (PRDC, CT) (10).
Epidemiology
PMWS has been observed in almost all type of farms. Serologically, PCV2 infections are spread worldwide. Carlos Pijoán, PhD (Pigletter, July 2002) wrote that PMWS seems to be more prominent in regions that have both a high pig density and high level of disease in their pig population; and is not important in North America. But, Harms et al. (4) from ISU-VDL diagnosed 3163 pneumonia cases in 2000 and the most common etiologic diagnosis was PRRSV in 42% of the swine pneumonia cases; porcine circovirus type2 was diagnosed in 22% of the cases; SIV in 17% and M. hyopneumoniae in 14%.
Emergence of PMWS disease, and not the PCV2 virus, may have been caused by changes in management practices, stimulation of the immune system, a change in the genetics of the host, or emergence of other agents that enhance disease severity during mixed infections. Post-weaning mortality is 5-20%.
Factors that trigger PCV2 infection to progress to full blown PMWS may be in the form of coinfecting pathogens (PPRS, PPV, or another virus or bacteria), immune stimulation such as adjuvants and vaccines, environmental factors (ammonia, endotoxins), or the consequence of other stressors such as transportation and mixing of pigs.
Pathological, immunohistological and flow cytometric studies suggest that pigs with PMWS are immunosuppressed. Natural co-infection with PCV2 and PRRSV occurs in a high proportion of affected PMWS pigs ranging from 20-60% in the USA. Although it may be unclear whether PCV2 plays the role of a primary pathogen, synergistic pathogen, secondary, or opportunistic pathogen. The shedding of PCV2 in boar semen has been demonstrated (11).
Diagnosis
The final diagnosis of PMWS is established based on three criteria: 1) presence of a clinical picture compatible with PMWS, 2) presence of characteristic histopathological lesions and 3) detection of PCV2 within the lesions in tissues of affected pigs.
Lymphoid tissues are the most valuable tissues to establish a PMWS diagnosis. The differential diagnosis is dependent on each farm, but the most important is the respiratory form of PRRS. The differentiation between PRRS and PMWS is very difficult. It can be done by appropriate battery of laboratory tests. The most important thing is to know what the pathogens are present and to treat them accordingly (10). Pigs are known to become immune competent at approximately 70 days of gestation. The presence of viral antibodies and DNA in pre-calostral fetuses is a clear indication that vertical transmission and in utero infection of PCV2 occurs regularly in the field. The immunofluorescence test (IFA) detected active antibodies both in PMWS or non PMWS pigs. Hepatocytes and renal epithelial cells may have an important role in PMWS pathogenesis.
Prevention and control
On Feb. 9, 2006, the Veterinary Biologics Section of the Canadian Food Inspection Agency (CFIA) issued a permit authorizing Merial Canada Inc. to import and distribute a sow vaccine, Circovac, for emergency use as an aid in the prevention and control of diseases caused by porcine circovirus type II (PCV2). There is some controversy about this vaccine.
Madec and Waddilove, 2002 (8) described a combined approach based on 20 point emergency plan against PMWS for severely affected farms (table 1).
The main areas to prevent and control:
1. Reduce pig-to-pig contact
2. Improve hygiene and husbandry practices
3. Reduce stressors
4. Provide correct nutrition
5. Control concurrent diseases
| Table 1 20-Point Plan Against PMWS |
|
Farrowing 1. All-in, all-out and empty pit and clean and disinfect between batches
Grower/Finisher Stage
|
| Madec and Waddilove, 2002 |
| Conclusions |
| In the absence of a licensed vaccine, we have to improve management strategies. Although the results are contradictory, the use of immunomodulation products, feedback with viscera and blood of affected animals, and serum-therapy (subcutaneous injection of PCV2 hyperimmune sera from commercial 100 kg pigs at 7 days after weaning) may be effective. To eliminate co-factors such as concurrent diseases, stress, commingling, overcrowding, inadequate feeding programs. Acetaminophen orally administered in feed (30 mg/kg b/w) for 10 days, without antibiotherapy, resulted in a significant improvement of the total morbidity rate of piglets in a heard chronically infected by PMWS (1). |
References
1. Bernard, F. et al., 2003. Proc 17th IPVS 1:205.
2. Clark, E.G. 1997. Proc AASP Meeting 28:499-501.
3. Farnham, M.W. et al., 2002. Detection of PCV2 antibody and DNA in stillborn pig sera from farms with a history of high born-dead pigs. Proc 17th IPVS 1:174.
4. Harms, P.A. et al., 2002. Three cases of PRDC associated with PCV2. J Swine Health Prod 10 (1): 27-30.
5. Harding, J.C. and Halbur, P.G. 2002. PMWS and PCV2 Disease Merial keynotes 17th IPVS: 19-31.
6. Harding, J.C. 1996. Proc Western Can Assoc Swine Pract: 21
7. Lukert, P.D. and Allan, G.M. 1999. Disease of Swine ISUP: 119-124.
8. Madec, F. and Waddilove, J. 2002. PMWS and PCV2 Disease Merial keynotes 17th IPVS: 45-53.
9. Sanford, S.E. 2002. Proc 17th IPVS, 1:171
10. Segalés, J. and Domingo, M. 2002. Proc 17th IPVS, 1:35-42
11. Segalés; J. and Clark, E.G. 2002. PMWS and PCV2 Disease Merial keynotes 17th IPVS: 33- 43.
12. Tischer, I. et al., 1982. A very small porcine virus with circular single stranded DNA. Nature 295: 64-66.
