10. Circoviral disease of swine (PMWS, PDNS). Flashcards
Porcine Circoviruses info?
Porcine circoviruses
o PCV1 ʹ Non-pathogenic (present in tissue cultures, Tischer, 1974 ʹ vaccines of babies but no conseq)
o PCV2 ʹ Responsible for PCV associated diseases (PCVD) or is in the background of those ʹ immune suppressive
o PCV3 ʹ In several cases: with PCV2 in PCVD or asymptomatic animals (foetus or respiratory symptoms) ʹ
genome dissimilar with PCV2 with similar clinical signs
o PCV4: similar to mink circovirus 2019
History of PCV2?
History of PCV2
x 1991: Canada, PMWS: Post weaning multisystemic wasting
syndrome, 1996: first description of PMWS - lethargy/anorexia
Æ immune suppression, and have secondary infections
o o 1998: PCV1 & PCV2 distinction
Sequence homology: close, genome organisation ʹ same Pathogenicity: different, antigenicity: different
o 2001: PCV2 responsible for PMWS
o Retrospecific examations: AB/ATG found in the genome present since 1970s
o PMWS: in Asia & Europe: endemic & epidemic; In S. America: sporadic
o (Evolution of PCV)
o Origin unknown? Virus is similar to the
nanovirus (a plant virus) ʹ banana virus is a
close relative of the circovirus
o End of the adaptation: selection of the best
genome BUT! The effect of the vaccination:
Newest genetic diversification (PCV2D)
The virus is constantly changing ʹ mutating (vaccine not
efficient against some strains) DNA virus but becaused doesnt have
replicase enzymes/repair enzymes ʹ easy to mutate
Pathogenesis?
Pathogenesis
o Virus uses cellular polymerase enzyme: reproduction in dividing cells
o Good antigen
o 3-4 genes: responsible for replication, capsid, apoptosis ORF1 = replication protein (+ve strand) ORF2 ʹ Capsid protein (-ve strand) ORF3 ʹ protein for apoptosis
- Stem loop = 11 nucleotid: works as a primer (helps for the replication)
o Intake: PO, nasal route, sexual route
o Spreading: direct contact, respiratory secretion, saliva, urine, faeces, sperm, infected food, water,
iatrogen route
o PMWS (Porcine multisystemic wasting syndrome) pathogenesis - Oronasal infection
o Day 1: nasal mucosa Æ viraemia
o Day 2: lung
o Day 3: thymus, spleen, bronchial & intestinal LN after BM, liver, kidney, heart, brain
o Monocytes/macrophages, dendritic cells, lymphocytes
- Intravenous infection: the virus can be detected from day 1 into the thymus
o Replication: in dividing cells
o Primer replication: tonsils & LNs around it
o After the viremia: thymus, spleen, LNs (day 3), BM, liver, kidney, heart, brain, monocyte/macrophage, dendritic
cell, lymphocyte
o Viraemia: from 7-14 days, but the virus can persist until 6 months. Virus eruption is continuous
o Antibody presents in the end of the 2nd week, colostral antibody lasts for 4-12 weeks ʹ there are lots
of Abs which can cause hypersensitivity
Predisposing factors?
Predisposing factors: Immune activation: vaccines, virus infections, immunomodulators, virus strain?
Genetic background, parasites
o Diseases connected with PCV (PCVD)
o o PCV2 o Subclinical infections o Post weaning multisystemic wasting syndrome PMWS o Dermatitis nephropathia syndrome PDNS
o Respiratory disease complex PRDC
o Reproductive failure PRF (Parvovirus infection?)
o Granulomatous enteritis PGE
o Necrotizing lymphadenitis PNL
o Congenital tremor PCT
o Exudative epidermatitis PEE
o Used nowadays:
o Subclinical infections
Facts about PCV2?
Facts about PCV2
o In addition to PMWS/PDNS a number of other PCVDs were recognised
o The virus is proven to be immunosuppressive
o The activated immune system can help the development of the disease
o PCV2 is endemic all over the world, & it is still spreading
o The pathogen changed genetically & antigenetically & this change is continuous
o Disease control with vaccine protection
o Domestic pigs & reservoir species (wild boar, rodent)
Immunosuppressive virus?
Immunosuppressive virus
o A: small genome 1 gene for structural capsid protein, 1 gene for replication protein, Can only
replicate in dividing cells, activated & dividing B & T lymphocytes
o B: Blocks fusion of endosome & lysosome, Antigen presenting cells (DC)
o C: dsDNA produced during replication binds to TLR9, B cells & NIPC (cells with natural IFN
production)
o Consequences: more frequent & more severe clinical conditions due to other infections, increased use
(cost) of ABs, vaccines against regular diseases are less effective ʹ Also in pigs without PCVD!!!!
PMWS clinical signs?
PMWS clinical signs?
Clinical signs
o Morbidity 20-30%, at 5-12 (18) weeks of
age
o Progressive weight loss
o Cyanosis, coughing, tachypnoea, anaemia, diarrhoea, nervous signs, fever, lethargy, anorexia,
jaundice, rough hair + symptoms of co-infections
Pathology?
Pathology
o LNs: 3-5x enlarged (inguinal, mesenteric), haemorrhages, cut surface: homogenous texture
o Lung: heavy, non-collapsed, tan coloured, dark red areas, interstitial oedema, lung oedema,
pneumonia
Bad condition, flaccid myocardium, ascites, strawberry heart, spleen enlarged, anaemia, hepatic
shrinkage, jaundice, gastric ulceration, enters the foetus (thymic damage, myocardial replication)
PMWS Histopathology?
o Histopathology: Lymphocyte depletion in lymphoid depletion, interstitial nephritis, interstitial lung oedema,
pneumonia, liver atrophy
Diagnosttics of PMWS?
Diagnostics: It is necessary to determine the condition:
o Epidemiological situation, clinical symptoms, pathological/histopathological exams
Laboratory exams of PMWS?
Laboratory exams: detection of the virus (PCR, ELISA, IF, in situ hybridisation, immunohistochemistry),
detection of the antibodies (virus neutralisation, ELISA (IgG/IgM), iIF)
Detection of the virus PMWS?
Detection of the virus: macrophage, giant cells, dendritic cells, tubular cells, kupffer cells, small & large
brain cells, heart endothel
PDNS info?
PDNS (Porcine Dermaitis Nephropathia Syndrome)
o Type III hypersensitivity reaction
- Extreme high PCV specific antibody titers
- IC depositions (skin kidney, BVs)
o Symptoms: At 30-100kg, progressive weight loss, heavy
breathing, paleness, multifocal, circular, red skin lesions,
haemorrhages, oedema, fever, lethargy, anorexia, ataxia
o Similar to - (Classical swine fever!!, African swine
fever!!!)
Pathology of PDNS?
Pathology
- Enlarged brown-greyish kidney with haemorrhages, greyish necrotic areas, enlarged LNs with haemorrhages,
lung oedema, bronchopneumonia, infarct in spleen, gastric ulcer, haemorrhages in skin, oedema, mesenteric
edema
Histopathology of PDNS?
Histopathology:
o thrombosis, lymphohistiocytic vasculitis, fibrinoid necrosis of skin, exudative
glomerulonephritis, interstitial nephritis, lesions like PMWS in LNs
