Recognizing and diagnosing postweaning multisystemic wasting syndrome (PMWS)
John C.S. Harding, DVM, MSc; Edward G. Clark, DVM, MVSc, Dipl ACVP
JH: Harding Swine Veterinary Service, Box 2922, Humboldt, Saskatchewan, Canada S0K 2AO; EGK: Western College of Veterinary Medicine
Diagnostic notes are not refereed
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Postweaning multisystemic wasting syndrome (PMWS) is a new disease first described in 1996.1,2 In the past 6-8, months the number of affected herds has grown considerably, and there are now confirmed cases in Alberta, Saskatchewan, Manitoba, Quebec, California, Iowa, Indiana, and Spain. Furthermore, since 1994, a similar syndrome--"wasting disease of piglets"--has been confirmed in as many as 200 herds in France.
Because PMWS is a new disease, it is difficult to recognize and diagnose (particularly, to differentiate it from porcine reproductive and respiratory syndrome (PRRS) or postweaning anorexia/starvation). This paper reviews the clinical and pathological characteristics of the disease to help the veterinarian and pathologist reach a definitive diagnosis.
In our experience, PMWS is most commonly diagnosed in herds free of the major enteric and respiratory diseases affecting swine. Such diseases include Mycoplasma hyopneumoniae, Actinobacillus pleuropneumoniae, progressive atrophic rhinitis, salmonellosis, swine dysentery, transmissible gastroenteritis virus (TGEV), and pseudorabies. Affected herds may be farrow-to-finish, farrow-to-feeder pig, off-site nursery, or grower pig operations. The disease has been diagnosed in herds ranging in size from very small (50-sow) to large (1200-sow) operations. PMWS most commonly affects pigs 2-3 weeks postweaning, or at about 5-6 weeks of age, although this depends somewhat on the characteristics of pig flow within the unit. Drafts, overcrowding, poor air quality, and commingled ages exacerbate the expression and severity of the disease. Based on our experience, areas of stress and commingled ages exacerbate the expression and perhaps the severity of the disease. On affected farms, the morbidity and mortality associated with PMWS appears to be dependent on the degree of compartmentalization within the unit and the stage of the outbreak. In an acute outbreak, the mortality rate associated with PMWS may peak at close to 10% (calculated monthly), whereas endemically infected herds may experience considerably less morbidity and mortality.
Suspect herds should be examined thoroughly, noting the age and number of pigs with characteristic clinical signs (Table 1). Clinical signs, including wasting, dyspnea, and icterus, are particularly suggestive. With the exception of eperythrozoonosis, which is extremely rare in Canada and much of the United States, the development of jaundice in more than a sporadic pig is unusual. Furthermore, the presence of icterus differentiates the syndrome from PRRS. The most common and consistent clinical signs of PMWS are wasting and dyspnea.
Postmortem examination is absolutely essential for PMWS diagnosis at the herd level. Because the lesions characteristic of PMWS vary somewhat, postmortems on several carcasses or euthanized pigs will be required before the full range of lesions is seen. Selecting the appropriate number or type of carcass is usually not a problem, as there is normally an over-abundance of suspect pigs in need of humane euthanasia, especially during acute outbreaks of the disease. Our recommendation is to keep cutting. A group of 8-12 affected pigs will normally support the diverse range of lesions that can be noted grossly. Also unique to PMWS is that typical gross lesions are not always consistent. For instance, kidneys may appear waxy and enlarged, or spotted and of normal size. Lungs can be either non-collapsed or atelectatic, and mottled red or grey (Table 2).
Gross pathology is extremely valuable in ruling out other equally important bacterial and viral diseases, which can cause the wasting of postweaned pigs (Table 3).
Histopathology is required for definitive diagnosis. Although not pathognomonic of the disease, many of the lesions are strongly suggestive (Table 4). Veterinary pathologists who have adequate experience with the disease are very adept at recognizing characteristic lesions if a suitable number of representative tissues are submitted (Table 5), regardless of whether they show gross lesions. Submitting an assortment of live pigs with clinical disease is strongly recommended during early investigations. These pigs provide the pathologist with valuable clinical information which is not normally received with "bits and pieces" submissions. But when the latter is the only alternative, diagnosis can be made on fixed tissue submission only. Fresh tissue for bacterial and/or viral culture may assist in determining the presence or absence of secondary opportunistic or obligate pathogens.
Unique to PMWS is the presence of intensely basophilic staining inclusion bodies on H & E sections. The intracytoplasmic inclusion bodies can be noted in most tissues, but are most prominent in the lymph nodes, tonsils, and Peyer's patches of the ileum. The inclusion bodies appear to be clusters of porcine circovirus, according to EM and other tests.
Adjunct diagnostic tests
The lesions of PMWS are associated with porcine circovirus (PCV) infection based on immunoperoxidase (IP) staining.3 However, at the time of writing, there is no definitive answer regarding the exact role of PCV in the pathogenesis of PMWS. Circoviruses are known to cause other nonmammalian diseases including psittacine beak and feather disease and chicken anemia.4 Recently, a diagnostic polymerase chain reaction has been reported,5 but until the definitive etiology of PMWS is elucidated and Koch's postulates are fulfilled positive IP and PCR results must be interpreted with caution. Furthermore, serologic diagnosis will not be possible until an etiologic agent is identified. It is not yet known whether PCV serologic tests6,7 currently available are useful for the diagnosis of PMWS at the farm level.
1. Harding JC. Postweaning multisystemic wasting syndrome: Preliminary epidemiology and clinical findings. Proc Western Can Assoc Swine Pract. 1996:21.
2. Clark EG. Pathology of postweaning multisystemic wasting syndrome of pigs. Proc Western Can Assoc Swine Pract. 1996:22-25.
3. Clark EG. Postweaning multisystemic wasting syndrome. Proc AASP Ann Meet. 1997:499-501.
4. Studdert MJ. Circoviridae: New viruses of pigs, parrots and chickens. Aust Vet J. 1993;4:121-122.
5. Nayar GPS, Hamel A, Lin L. Detection and characterization of porcine circovirus associated with postweaning multisystemic wasting syndrome in pigs. Can Vet J. 1997;38:385-386.
6. Dulac GC, Afshar A. Porcine circovirus antigens in PK-15 cell line (ATCC-CCL-33) and evidence of antibodies to circovirus in Canadian pigs. Can J Vet Res. 1989;53:431-433.
8. Kyriakis SC, Andersson G. Wasting pig syndrome (WPS) in weaners: Treatment with amperozide. J Vet Pharmacol Therap. 1989;12:232-236.