Postweaning Multisystemic Wasting Syndrome (PMWS)

Posted by Dr. Steve Dudley on July 14 2009 15:53

History

• PCV1: a non pathogenic contaminant of PK-15
• PMWS: first described in Canada (1991) and related with porcine circovirus
• PCV2: cause of PMWS

Type 2 Porcine Circovirus (PCV2)

• First isolated/characterized 1997/1998
• Stable in environment (similiar to parvo)
• Ubiquitous
  • High prevalence (PCR)
  • High seroprevalence: most pigs lose maternal Ab at 6-12 weeks, seroconvert in finishing period
  • Antibodies in sera from at least mid 1970's

PMWS:

Diagnostic Criteria

1. Clinical signs: Wasting/failure to thrive, +/- dyspnea, diarrhea, pallor, icterus.
2. Microscopic Lesions: Depletion of lymphoid organs/tissues and/or lymhohistiocytic to granulomatous inflammation in any organ (predominantly lung, lymphoid tissue, liver, kidney, intestine, pancreas).
3. PCV2 antigen or genome within characteristic lesions.

Symptoms

• Wasting
• Paleness
• Dyspnea
• Diarrhea
• Icterus
• Increased mortality
• Increased bacterial infections

PMWS

• GROSS LESIONS: enlarged lymph nodes, non collapsed lungs, white dots in kidney.
• MICROSCOPIC LESIONS: lymphocyte depletion with histiocytic and syncytial infiltration of the lymphoid organs

Microscopic Lesions

• Lymphocyte depletion with histiocytic and syncytial infiltration of the lymphoid organs.
• Presence of ICIB
• Interstitial pneumonia
• Interstitial nephritis

Implications of this definition of PMSW:

• Clinical signs are not diagnostic...
• Gross lesions are not diagnostic..
  • Differential Diagnosis of PRRS, Salmonella
  • PCV2 infections is not PMWS....
  • Healthy pigs with histologically normal lymphoid tissues may have low numbers of PCV2-positive cells in lymphoid follicles. Diagnosis of PMWS requires both the lesion and PCV2 within the lesion.
  • Serology and PCR are of questionable value.

Porcine Respiratory Disease Complex (PRDC)

• Respiratory disease in growing pigs
• Agents typically involved in chronic PRDC:
  • PRRSV, SIV, M. hyopneumoniae, P. multocida, Strep. suis, S. cholerae-suis.
• Since most PMWS cases involve respiratory disease, most of our PMWS cases would be considered PRDC.

Distinguishing PMWS from Chronic PRDC

• PMWS is clinically indistinguishable from chronic PRDC
  • Both usually have wasting and respiratory disease
  • Both often have PRRSV + PCV2 + other primary or opportunistic pathogens
  • Gastric ulcers/pale pigs common in both
• Confirmation by histopathology and IHC stains
  • presence or absence of characteristic PMWS lymphoid lesions
  • presence or absence of abundant PCV2 antigen in lungs and/or lymphoid tissues

PCV2 and Chronic PRDC

• Clinical impression that PRDC outbreaks in which PMWS is diagnosed are often of greater severity and duration than would otherwise be expected (uncomplicated influenza)
• Particularly severe PMWS/PRDC is associated with seroconversion to porcine parvovirus
  • Parvovirus vaccination has been used to prevent severe PMWS/PRDC

What can We Conclude?

• PCV2 is necessary for the development of PMWS lesions.
• PCV2 is generally not sufficient for the development of clinical PMWS in conventional pigs. PCV2 causes PMWS, but in most cases PCV2 requires "help" to do so.
• Co-infection with PPV or PRRSV or "immune stimulation" (macrophage activation?) can cause PCV2 infection to progress to clinical PMWS.

Control Strategies

• The disease is very much stress related and minimizing stress by whatever means possible is essential
• Minimize exposure to PCV2 through all-in-all-out technology and appropriate disinfection of buildings and vehicles
• Remove pigs that don't respond to treatment.
• Eliminate or minimize the effects of PRRSV (if present) by breeding herd stabilization, pig flow changes, and/or vaccination.
• Eliminate or minimize the effects of SIV with breeding herd vaccination and possibly pig vaccination
• Minimize the effect of Mycoplasma pneumonia with vaccination and strategic pulse medication
• Determine if PPV is present in tissues (by FA or PCR) from PMWS affected pigs and if the population seroconverts to PPV during the period of time where PMWS occurs. If there is evidence of PPV and PCV2 coinfection, consider strategies to induce immunity to PPV.
• Consider the use of anti-inflammatory drugs and enhanced diets on pigs that are slow to respond.
• If it is an option, consider changing pig scources if the problem occurs repeatedly.

Missing Pieces

• What exactly causes PCV2 infection to progress to PMWS in the field? More work is needed on the suspected factors (lack of passive immunity, level of exposure, infection with PPV or PRRSV or other forms of immune stimulation, host genetics) that may cause this progression in a subset of a group of pigs.
• Why has PCV2 started to become a problem within the last decade when it has (apparently) been circulating in the swine population for years prior to this?
• Why is PMWS in the US a relatively minor problem (compared to PRRSV, SIV, M. hyo.) and why has PMWS suddenly become a devastating problem for the British swine industry?
• Why is the incidence of PCV2-associated disease relative to the incidence of PCV2 infection so low (2-10%)?
• Are there significant differences among PCV2 strains with regard to virulence and tissue tropism?