Proceedings
`
`American Association of Swine Practitioners
`
`28th Annual Meeting
`March 1·4, 1997
`Quebec City, Quebec
`
`CEV Exhibit 1009_001
`
`

`

`Post-Weaning Multisystemic Wasting
`Syndrome (PMWSJ:
`Preliminary Epidemiology and Clinical Presentation
`
`]ohn C. Harding, DVM
`Animal Management Services
`Humboldt, Saskatchewan, CANADA
`
`Post wea.ning ~ultisystemic. wasting syndrome is a new
`
`and umque disease of swme. At the present time, it
`has been diagnosed in 25-30 herds in Saskatchewan and
`Alberta, and is thought to be undiagnosed in some addi(cid:173)
`tional herds across the prairies. Retrospective necropsy data
`indicates the disease was evident in 1991 , but it was not
`recognized as a wide spread disease until early 1996.
`The disease is thought to be viral induced because of its
`epidemic spread in naive herds. It primarily affects nursery
`and grower pigs and rarely affects suckling pigs. Affected
`pigs develop clinical signs between 6-8 weeks of age. There
`may possibly be evidence of a long incubation period, as it
`is able to be transferred via SEW to downstream nurseries
`weaning at 1 0-14 days of age. However, SEW appears to
`be successful at reducing the incidence and severity of the
`syndrome. In most affected herds it is a chronic, insidious
`and sometimes protracted disease. It has been diagnosed in
`both PRRS positive and negative herds, but clinical diag- .
`nosis in PRRS positive herds is complicated by overwhelm(cid:173)
`ing secondary infections. Therefore, histopathologic
`diagnosis is essential in PRRS positive herds.
`The most predominant clinical signs include weight
`loss/emaciation, tachypnea, dyspnea and jaundice. En(cid:173)
`larged lymph nodes are consistently noted on physical ex(cid:173)
`amination. Less common clinical signs are diarrhea,
`productive coughing, and central nervous system distur(cid:173)
`bances. Morbidity is usually low, but case fatality high. In
`rare instances, post weaning mortality due to PMWS has
`been very high (>50%) and suggests that the severity of
`PMWS in a population is affected by triggering factors,
`
`more common to some herds. Furthermore, it is commonly
`observed that PMWS affected pigs are spread diffusely in
`a population rather than being concentrated in specific pens
`or groups. It is not uncommon for severely affected and
`unaffected pigs to coexist in the same pen. This implies that
`there are yet unknown reasons why individual pigs develop
`disease when larger numbers are probably exposed.
`A causative agent has not yet been identified although it
`is believed to be a virus. Until such time that the causative
`agent is identified, herd diagnosis is based on the presence
`of suspicious clinical signs and the pathognomonic his(cid:173)
`topathologic lesions. The unique gross and histopathologic
`lesions have been noted in virtually all tissues, but are most
`common in the lung, lymph system, liver, and kidney. A
`detailed description of pathologic lesions has been prepared
`by Dr. Ted Clarke, in this proceedings.
`There are no magical treatments for the disease, although
`good management practices do facilitate the control within
`a population. Affected herds should therefore attempt to
`maintain stric-AO pig flow, excellent hygiene and segregate
`sick pigs. Numerous feed grade and injectable antibiotics
`have been used, all with poor success. Long term control is
`likely dependent on the development of a solid herd immu(cid:173)
`nity, balanced with a reduction in challenge and viral spread.
`Gaining a better understanding of the etiology, epidemiol(cid:173)
`ogy and pathogenesis of the disease is a priority. Collabora(cid:173)
`tive studies are in progress in Saskatoon, Canada involving
`the Veterinary Infectious Disease Organization, Western
`College ofVeterinary Medicine and several swine practitio(cid:173)
`ners in western Canada. The results of a descriptive
`epidemiologic survey will be presented at the 1997 AASP
`Annual Meeting.
`
`American Association of Swine Practitioners, 1997
`
`503
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`CEV Exhibit 1009_002
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`