Porcine Circovirus Associated Disease

From Wikipedia, the free encyclopedia
Jump to: navigation, search

Porcine Circoviral Disease (PCVD) and Porcine Circovirus Associated Disease (PCVAD), is a disease seen in domestic pigs. This disease causes illness in piglets, with clinical signs including progressive loss of body condition, visibly enlarged lymph nodes, difficulty in breathing, and sometimes diarrhea, pale skin, and jaundice.[1][2] PCVD has been reported from most pig-producing countries of the world at huge cost to agriculture. PCVD is caused by porcine circovirus type 2 (PCV2).[3]

PCVD was formerly named Postweaning multisystemic wasting syndrome ("PMWS") .[1] Because PCVD can cause other diseases other than PMWS and the "waste" may has negative impact on perceptions of the industry from consumers. The North American industry[clarification needed] endorses "PCVAD" and European use "PCVD" to describe this disease.[4][5]

PMWS & PCV2[edit]

PCV-2 (first isolated in 1997) causes PMWS.[1] PCV2 has a near universal distribution – present in most pig herds. In contrast, PMWS is more sporadic in its distribution. Experimental induction of PMWS has not been achieved by PCV2 infection alone, using infectious DNA clones of the virus or a pure form of PCV2 derived from infectious DNA clones. Therefore it is assumed that PMWS is a multifactorial disease. PCV-2 is necessary but not sufficient for the development of PMWS. However, viral infection by itself tends to cause only mild disease, and co-factors such as other infections or immunostimulation seem necessary for development of severe disease.[1] For example, concurrent infection with porcine parvovirus or PRRS virus, or immunostimulation lead to increased replication of PCV-2 and more severe disease in PCV-2-infected pigs.[1] There is no significant correlation of the disease with virus sequence variation with affected and control pigs.

Clinical Signs[edit]

Both PMWS and porcine dermatitis and nephropathy syndrome (PDNS) are associated to PCV2.[6] Many pigs affected by the circovirus also seem to develop secondary bacterial infections, like Glässer disease (Haemophilus parasuis), pulmonary pasteurellosis, colibacilosis, salmonellosis and others.[7] Postmortem lesions occur in multiple organs, especially in lymphoid tissues and lung, giving rise to the term "multisystemic".[1][2][8] Lesions may also affect the skin, kidney, reproductive tissue, brain, or blood vessels.[1]

Wasting pigs is the most common sign of PMWS infection, increasing the mortality rate significantly.

Management practices to decrease severity of PMWS[edit]

François Madec, a French author, has written many recommendations on how reduce PMWS symptoms. They are mostly measures for disinfection, management, and hygiene, referred to as the "20 Madec Points" [Madec & Waddilove, 2002].

These measures have recently been expanded upon by Dr. David Barcellos, a professor at the Veterinary College in the Universidade Federal do Rio Grande do Sul, Rio Grande do Sul, Brazil. He presented these points at "1st Universidade Federal do Rio Grande do Sul Symposium about swine management, reproduction, and hygiene".

He divided his points by pig growth stage, and they can be loosely summarized as:

  • keep the gutters clean
  • increase feeder space
  • use pens or small cages with solid dividers
  • avoid mixing pigs from different origins
  • improve the quality of air
  • decrease maximum capacity, giving each pig more room
  • separate sick animals as soon as possible, and treat them in a hospital pen. If they do not respond to antibiotics in three days, they should be culled
  • control access of people and other animals
  • reduce invironmental stress factors such as gases and air currents
  • use immunizations and preventive medications for secondary agents commonly associated with PMWS

See also[edit]

Notes[edit]

  1. ^ a b c d e f Ellis, J (March 2014). "Porcine Circovirus: A Historical Perspective". Veterinary Pathology 51 (2): 315–327. doi:10.1177/0300985814521245. PMID 24569612. Retrieved 21 March 2014. 
  2. ^ a b Opriessnig, T; Langohr I (January 2013). "Current state of knowledge on porcine circovirus type 2-associated lesions". Veterinary Pathology 50 (1): 23–38. doi:10.1177/0300985812450726. PMID 22692624. 
  3. ^ Mankertz P (2008). "Molecular Biology of Porcine Circoviruses". Animal Viruses: Molecular Biology. Caister Academic Press. ISBN 978-1-904455-22-6. 
  4. ^ Harding, John C. S. (16–19 Jan 2007), "History of Porcine Circoviral Disease (PCVD) and Current Western Canadian Situation", in Ball, Ronald O.; Ruurd T. Zijlstra, Proceedings of the 2007 Banff Pork Seminar (PDF), Banff: University of Alberta, Department of Agricultural, Food and Nutritional Science, p. 27, retrieved 2012-11-25 
  5. ^ Desrosiers, Robert (16–19 Jan 2007), "Overview of PCVD - The Disease in Eastern Canada & US vs. Europe", in Ball, Ronald O.; Ruurd T. Zijlstra, Proceedings of the 2007 Banff Pork Seminar (PDF), Banff: University of Alberta, Department of Agricultural, Food and Nutritional Science, p. 35, retrieved 2012-11-25 
  6. ^ Barcellos & Pescador, 2003 and Segalés & Domingo, 2000
  7. ^ David Barcellos, 2006
  8. ^ Harding & Clark, 1997

References[edit]

  • Ellis J. Porcine circovirus: a historical perspective. Vet Pathol. 2014 Mar;51(2):315-27.
  • Opriessnig T, Langohr I. Current state of knowledge on porcine circovirus type 2-associated lesions. Vet Pathol. 2013 Jan;50(1):23-38.
  • Grierson S.S., King D.P., Wellenberg G.J. & Banks M.; "Genome sequence analysis of 10 Dutch porcine circovirus type 2 (PCV-2) isolates from a PMWS case-control study." Res Vet Sci. 2004 Dec; 77(3):265-8).