porcine circovirus infections
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- porcine circovirus infections
International Common Names
- English: abortions and stillbirths in pigs; atypical porcine reproductive and respiratory syndrome; atypical PRRS; dermatitis - nephropathy syndrome; dermatitis and nephrophy syndrome of pigs; multisystemic wasting syndrome of swine; porcine circovirosis; porcine circovirus associated reproductive disease; porcine circovirus diseases; porcine circovirus type 2, postweaning multisystemic wasting syndrome in pigs; porcine dermatitis and nephropathy syndrome; porcine dermatitis and nephropathy syndrome of pigs; porcine respiratory disease complex; post-weaning multisystemic wasting syndrome; postweaning multisystemic wasting syndrome of pigs; postweaning PRRS; proliferative necrotizing pneumonia; sow abortion and mortality syndrome; systemic necrotizing vasculitis and glomerulonephritis in pigs
Pathogen/sTop of page porcine circovirus 2
OverviewTop of page
Porcine circovirus (PCV) was first recognized as a contaminant of the continuous pig kidney cell line PK/15 (Tischer et al., 1982). This PCV contaminant of PK/15 cells was thought to be non-pathogenic. During late 1990s, an apparently new potentially pathogenic PCV, antigenically and genomically distinct from the previously known one, was recognized, isolated and characterized (Allan et al., 1998a,b; Hamel et al., 1998; Meehan et al., 1998). This latter virus has been associated with postweaning multisystemic wasting syndrome (PMWS) (Segalés et al., 2005). A number of other disease conditions in pigs have also been linked with this virus, including porcine dermatitis and nephropathy syndrome (Rosell et al., 2000b), reproductive disease (West et al., 1999), porcine respiratory disease complex (Thacker and Thacker, 2000) and proliferative necrotizing pneumonia (PNP) (Pesch et al., 2000, Drolet et al., 2003). To distinguish between those two distinct viruses, it was proposed that PCV isolates from diseased pigs should be designated porcine circoviruses type 2 viruses (PCV2), and the original PCV contaminant of PK/15 cell cultures designated porcine circovirus type 1 virus (PCV1) (Allan et al., 1999b). Both porcine circoviruses are small (17 nm), icosahedral, non-enveloped viruses containing a circular, single-stranded DNA genome and classified within the family Circoviridae (McNulty et al., 2000).
The complete nucleotide sequences of approximately 150 PCV2 isolates/strains were reported by September 2005 (GenBank database; http://www.ncbi.nlm.nih.gov/). Analysis of the genomes of PCV2 from isolates from North America and Europe have shown >93% inter-isolate homology (Meehan et al., 1998; Mankertz et al., 2000; Larochelle et al., 2002). However, comparison of the genomic sequence of PCV2 isolates with the genomic sequence of PCV1 showed <80% overall homology (Hamel et al., 1998; Meehan et al., 1998). Potentially, six open reading frames (ORFs) larger than 200 nucleotides have been suggested for PCV2 (Hamel et al., 1998; Meehan et al., 1998), although only ORF1 (replicase proteins; Rep) and ORF2 (capsid protein; Cap) seem to be expressed under in vivo and in vitro conditions. Subsequently, a third viral gene termed ORF3 has been described (Liu et al., 2005). The ORF3 protein appears to be a highly conserved one, with >95% identity at the amino acid level among PCV2 strains (Liu et al., 2005).
Since PCV2 has been associated with a number of diseases in pigs, the terminology porcine circovirus diseases (PCVD) was proposed to include those conditions that have been linked with PCV2 infection (Allan et al., 2002). The most significant PCVD is PMWS. This wasting syndrome was firstly described in western Canada in 1991 in healthy SPF herds (Clark, 1996; Harding, 1996); the authors proposed the acronym PMWS to describe the clinical condition. Since these initial reports of PCV2-associated PMWS, the disease has been reported in almost all pig producing countries around the world, in all 5 continents (Segalés et al., 2005). PMWS histological lesions associated with an abundance of PCV2 antigen have been retrospectively described as early as 1986 in Spain and the UK (Rodríguez-Arrioja et al., 2003b; Grierson et al., 2004) and in 1989 in Japan (Mori et al., 2000). Moreover, the first PCV2 infection in pigs was retrospectively described as early as 1969 (Sánchez et al., 2001b). Consequently, PMWS should not be considered as a new disease and PCV2 should not be considered a new virus. Moreover, PMWS is nowadays defined as a multifactorial disease in which PCV2 infection of pigs is necessary but not sufficient to trigger the disease, and a number of infectious and non-infectious factors, or triggers, are necessary for the development of clinical disease (Segalés et al., 2005).
PMWS is clinically characterized by progressive weight loss, respiratory signs and, sometimes, jaundice in postweaning pigs (usually 6- to 16-week-old animals). Morbidity is usually low <20%), but case fatality high (Segalés et al., 2005). The most significant gross lesions are generalized lymphadenopathy and non-collapsed, rubbery lungs (Segalés et al., 2004b). Histologically, a wide range of lesions can be detected, the most important ones located in lymphoid tissues; lymphocyte depletion and granulomatous inflammation of lymphoid organs is the most characteristic pathology of PMWS (Segalés et al., 2004b). Inflammatory lesions are observed, however, in many tissues, including lung, liver, kidney and intestines (Segales et al., 2004b; Krakowka et al., 2005). PCV2 antigen and/or nucleic acid have been demonstrated in abundance in association with histological lymphoid lesions.
Since PMWS is considered the most important PCVD, significant efforts to control it have been made worldwide during more than a decade. The advent of PCV2 vaccines since 2004 in some parts of the world, and since 2006-07 in a more generalized fashion, has radically changed the perception of veterinarians on this disease (Kekarainen et al., 2010). The use of PCV2 vaccines is now generalized, being the most sold vaccine for piglets worldwide.
Host AnimalsTop of page
|Animal name||Context||Life stage||System|
|Sus scrofa (pigs)||Domesticated host, Wild host||Pigs: All Stages|
Hosts/Species AffectedTop of page
Pigs and wild boars are the only recognized naturally affected hosts of PCV1 and PCV2 (Segalés et al., 2005). PCV2 infection is considered ubiquitous in domestic pigs, with a sero-prevalence close to 100% in slaughter-age animals (Rodríguez-Arrioja et al., 2002; Sibila et al., 2004). PCV2 antibodies have been demonstrated in 33 and 37% of wild boars in Belgium, examined in 1993 and 2000, respectively, and 48% in Spain (Sanchez et al., 2001b; Vicente et al., 2004). Besides domestic pigs, PMWS has also been described in wild boar in North America (Ellis et al., 2003) and Europe (Schulze et al., 2004; Vicente et al., 2004).
Although it is assumed that all breeds of domestic pigs are susceptible to infection and can develop disease, some field observations have suggested that certain genetic lines of pigs, specifically in relation to sire lines, differ in susceptibility to PMWS.
Recent serological surveys in cattle, goats, sheep, horses, dogs, cats, mice and humans have shown no evidence of PCV2 infection (Allan et al., 2000; Ellis et al., 2001; Rodríguez-Arrioja et al., 2003a). Serological data on a potentially high risk population, veterinarians, have also been negative .
Systems AffectedTop of page digestive diseases of pigs
multisystemic diseases of pigs
reproductive diseases of pigs
respiratory diseases of pigs
urinary tract and renal diseases of pigs
DistributionTop of page
PCV2 is now considered a ubiquitous virus, both in countries where porcine circovirus diseases (PCVD) have or have not been described (Allan and Ellis, 2000; Segalés et al., 2005). PCV1 is also considered widespread, but its exact prevalence, probably lower than that of PCV2 (Calsamiglia et al., 2002), has not been determined. Moreover, it is possible that early serological investigations on what is now known as PCV1 (Tisher et al., 1986; Dulac and Afshar, 1989; Edwards and Sands, 1994; Allan et al., 1994) may have actually detected cross-reactive antibodies to PCV2 (Pogranichny et al., 2000; Rodríguez-Arrioja et al., 2000). Postweaning multisystemic wasting syndrome (PMWS) and also porcine dermatitis nephropathy syndrome (PDNS) have been described in all continents and in most, if not all, countries where those diseases have been investigated (Segalés et al., 2005).
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Korea, Republic of||Present||Choi et al., 2000|
|Taiwan||Widespread||Choi and Chae, 1999|
|Canada||Widespread||Dulac and Afshar, 1989; Clark, 1997; Ellis et al., 1998|
|-Alberta||Widespread||Harding and, 1997|
|-Ontario||Present||Cottrell et al., 1999|
|-Prince Edward Island||Present||Illanes et al., 2000|
|-Quebec||Widespread||Larochelle et al., 1999|
|USA||Present||Hines and Lukert, 1995|
|-California||Present||Daft et al., 1996|
|-Indiana||Present||Kiupel et al., 1998|
|-Minnesota||Present||Atchison et al., 1999|
|-Nebraska||Present||Atchison et al., 1999|
|-Wisconsin||Present||Atchison et al., 1999|
|Denmark||Present||Allan et al., 1998a; Allan et al., 1998b; Allan et al., 1999a|
|France||Widespread||Allan et al., 1998a; Allan et al., 1998b|
|Germany||Present||Mankertz et al., 2000|
|Ireland||Present||Spillane et al., 1998|
|Italy||Widespread||Marcoto et al., 1999|
|Spain||Widespread||Allan et al., 1998a; Allan et al., 1998b; Segalés et al., 1997; Plana-Durán et al., 1999|
|UK||Widespread||Edwards and Sands, 1994; Gresham et al., 2000; Kennedy et al., 2000|
|New Zealand||Present||Horner, 1991|
PathologyTop of page
The most obvious gross lesions in postweaning multisystemic wasting syndrome (PMWS) are non-collapsed lungs and enlargement of lymph nodes (Clark, 1997; Rosell et al., 1999); however these lesions are not always present. The enlargement of lymph nodes is probably one of the earliest features of PMWS affected pigs; the presence of normal to atrophic lymph nodes have also been observed in pigs affected by this syndrome. In a low proportion, lymph nodes may have the presence of multifocal areas of necrosis that are visible macroscopically (Segalés et al., 2004b). Non-collapsed, tan-mottled lungs, with or without evident interstitial oedema, is a relatively common feature in PMWS. A percentage of PMWS affected animals may also have atrophic, discoloured livers (usually in these cases jaundice is also evident), and/or multifocal white foci in the kidney cortices. Moderate to high numbers of PMWS affected pigs have bronchopneumonia and gastric ulceration of the pars oesophagea, which are not related to the direct effect of PCV2; bronchopneumonia is associated with bacterial infections while gastric ulceration is of multifactorial origin. However, the lesion in the stomach cause internal haemorrhage and it is the cause of death of a number of pigs with PMWS and can be partly responsible for the paleness of skin which has been frequently associated with the disease (Segalés et al., 2000). At the end stage of the disease, cachexia may develop.
The most characteristic microscopic lesions of PMWS affected pigs are found in lymphoid tissues. Moderate to severe of lymphocyte depletion with loss of follicles is present in almost all pigs with PMWS; this finding is usually combined with a multifocal to diffuse, moderate to very intense histiocytic and/or multinucleate giant cell infiltration. Another key finding is the presence of sharply demarcated, spherical, basophilic cytoplasmic inclusions of PCV2 in histiocytic cells (Clark, 1997; Rosell et al., 1999). Mild lymphoid lesions like the ones described above are usually associated with subclinical PCV2 infections and, alternatively, to pigs that have recovered from the disease (Segalés, 2002). Other PMWS microscopic lesions (therefore, associated with PCV2 infection) have been described in many tissues. A subacute interstitial pneumonia is the most usual lung lesion in PMWS affected pigs (Clark, 1997; Rosell et al., 1999). In some cases it is possible to see large histiocytic and multinucleate giant cells in the thickened interalveolar walls and/or within alveoli. In chronic cases, bronchiolitis fibrosa obliterans may be present (Clark, 1997; Segalés et al., 2004b). Hepatic lesions have been described as lymphocytic-histiocytic inflammatory infiltration in portal zones, single cell necrosis of hepatocytes, swelling and vacuolation of hepatocyte cytoplasm and karyomegaly (Clark, 1997). However, in some cases it is possible to detect very severe lesions showing generalized perilobular fibrosis, with disorganization of liver plates and massive loss of hepatocytes; these lesions are associated with jaundice and macroscopic lesions in the liver. Four stages of hepatic damage in PMWS affected pigs have been established based on intensity and distribution of these lesions (Rosell et al., 2000a). Other microscopic lesions detected in PMWS affected pigs include lympho-histiocytic inflammatory infiltrates, which can be potentially present in all tissues (Clark, 1997; Rosell et al., 1999). Sporadically, moderate to severe granulomatous enteritis with blunting of villi have been detected.
PDNS affected pigs are characterized by skin, red-to-dark macules and papules, which correspond microscopically to necrotic tissue associated with necrotizing vasculitis of dermal and hypodermal capillaries and arterioles, and extensive haemorrhages (Hélie et al., 1995; Segalés et al., 1998a; Thibault et al., 1998). Necrotizing vasculitis is, moreover, a systemic feature, since these lesions can be present in any tissue, although they are more prominent in the skin, kidney pelvis, mesenteries and spleen (Thibault et al., 1998). Apart from skin lesions, pigs which die acutely with PDNS have bilaterally enlarged kidneys that are firm in consistency, with fine granular cortical surface and oedema of the renal pelvis (Hélie et al., 1995, Segalés et al., 1998a, Thibault et al., 1998). The renal cortex shows multiple small reddish pinpoint lesions, similar to petechial haemorrhages, which microscopically correspond to enlarged and inflamed glomeruli, with fibrin, necrotic inflammatory cells and erythrocytes within Bowman’s capsules (fibrino-necrotizing glomerulitis). Histologically, a moderate to severe non-purulent interstitial nephritis with dilation of renal tubules is also seen. Pigs with a prolonged disease course may show chronic glomerulonephritis, probably resulting from progression of the initial glomerular damage (Segalés et al., 1998a). Normally, both skin and renal lesions are present in PDNS, but in rare cases, either skin or renal lesions may occur singularly (Segalés, 2002). Renal lymph nodes, as well as other nodes, may be enlarged and of red colour due to blood drainage from affected zones with haemorrhages (skin mainly). Microscopically, lesions similar to PMWS such as lymphocyte depletion and a certain degree of histiocytic and/or multinucleate giant cell infiltration are frequently observed in lymphoid tissues of PDNS affected pigs (Rosell et al., 2000b). Spleen infarcts may also be present (Segalés et al., 1998a), as a result of necrotizing vasculitis of splenic arteries or arterioles.
PCV2-associated reproductive disease is characterized by the delivery of stillborn and non-viable newborn piglets with hepatic chronic passive congestion and cardiac hypertrophy with multifocal areas of myocardium discoloration (West et al., 1999; O’Connor et al., 2001). Fibrosing and/or necrotizing myocarditis is the hallmark of PCV2-associated reproductive disease (West et al., 1999; O’Connor et al., 2001).
A number of methods have been developed to detect PCV2 in tissues to correlate its detection with the presence of lesions. Among them, in situ hybridisation (ISH) and immunohistochemistry (IHC) are the most used tests. PCV2 nucleic acid or antigen in PMWS affected pigs is usually found in the cytoplasm of histiocytes, multinucleate giant cells and other monocyte/macrophage lineage cells such as alveolar macrophages, Kupffer cells and follicular dendritic cells of lymphoid tissues (Rosell et al., 1999; Allan and Ellis, 2000). Sporadically, it is also possible to detect viral nucleic acid or protein in the cytoplasm of renal and respiratory epithelium, vascular endothelium, lymphocytes, pancreatic acinar and ductular cells and nuclei of monocyte/macrophage lineage cells, smooth muscular cells, pancreatic acinar and ductular cells, hepatocytes and enterocytes (McNeilly et al., 1999; Rosell et al., 1999, 2000a; Sirinarumitr et al., 2000).
A strong correlation has been observed between the amount of PCV2 nucleic acid/antigen and severity of microscopic lymphoid lesions (Rosell et al., 1999; Quintana et al., 2001; Krakowka et al., 2005). However, PCV2 nucleic acid/antigen can be found in tissues of clinically healthy pigs; in these cases the amount of virus and the intensity of histopathological lesions are low (Quintana et al., 2001). Positive ISH or IHC results in clinically healthy pigs or diseased pigs without moderate to severe PMWS lesions should be interpreted with caution since subclinical PCV2 infection with viraemia usually occurs in almost all farms; moreover, recently infected pigs or pigs in a convalescent phase from PMWS may not have typical histological lesions or may have very mild lesions, and low levels of PCV2 antigen/nucleic acid can be detected in lymphoid tissues (Quintana et al., 2001; Segalés, 2002). These findings must be taken into account when selecting the animal for establishing diagnosis. The levels of PCV2 nucleic acid/antigen in lung of pigs with porcine necrotizing pneumonia (PNP) (Grau and Segalés, 2006 [submitted, author address available from CABI]) and foetal heart of reproductive failure cases (West et al., 1999) are usually high, but are relatively low in lymphoid tissues of PDNS affected pigs (Segalés et al., 2004b).
One of the most used techniques to detect PCV2 uses polymerase chain reaction (PCR) (Segalés et al., 2005). PCR is the most sensitive technique to detect PCV2. However, since PCV2 is widespread in farms with and without PMWS (Larochelle et al., 2003; Rose et al., 2003; Sibila et al., 2004), the use of PCR alone to diagnose the syndrome is not sufficient. Quantitative PCR methods may help in the diagnosis of the disease in vivo, since the amount of PCV2 is higher in PMWS affected pigs compared with pigs subclinically infected (Liu et al., 2000; Olvera et al., 2004).
DiagnosisTop of page
Diagnostic criteria for postweaning multisystemic wasting syndrome (PMWS) in single animals are now well established (Sorden, 2000; Segalés, 2002). A pig or a group of pigs have PMWS if they fulfill the following criteria:
- Clinical signs: growth retardation and wasting, frequently with dyspnoea and enlargement of inguinal lymph nodes, and occasionally with jaundice
- Histopathological lesions: moderate to severe lymphocyte depletion together with granulomatous inflammation; concomitantly, diseased animals may show presence of intracytoplasmic inclusion bodies
- PCV2 detection: moderate to high amounts of PCV2 within the lesions in lymphoid and other tissues of affected pigs.
A herd case definition has been suggested based on the accomplishment of two different conditions (Grau-Roma et al., 2012). Firstly, a significant increase in postweaning mortality, compared to the historical background in the herd, must be observed in association with presentation of clinical signs compatible with PMWS. Secondly, PMWS must be diagnosed in at least one of three to five necropsied pigs, concurrently with the increase in mortality. Also, diagnostic assessment of other potential concomitant diseases that cause increase of mortality is important.
Case definition for porcine dermatitis and nephropathy syndrome (PDNS) is relatively simple (Smith et al., 1993; Helie et al., 1995) and includes two main criteria (detection of PCV2 is not currently included in the diagnostic criteria for PDNS, since this syndrome is considered an immunocomplex disease and the specific antigen associated to those complexes is still unknown):
- Gross lesions: haemorrhagic and necrotizing skin lesions, mainly located on the hind limbs and perineal area, and/or swollen and pale kidneys with generalized cortical petechia
- Histopathological lesions: systemic necrotizing vasculitis, and necrotizing and fibrinous glomerulonephritis.
Case definition for reproductive problems associated with PCV2 infection, based on clinico-pathological features of the described cases (West et al., 1999), should include three main criteria:
- Clinical signs: late-term abortions and stillbirths, sometimes with evident hypertrophy of the fetal heart
- Histopathological lesions: fibrosing and/or necrotizing myocarditis
- PCV2 detection: moderate to high amounts of PCV2 in the myocardial lesions and other fetal tissues.
During the last 5 years, a significant number of publications have dealt with immunology of PCV2 infection, specifically of PMWS affected pigs. Although the immunological events that occur in diseased pigs are known, very little is known about the early immunological pre-clinical features of pigs that subsequently develop PMWS.
Seroconversion to PCV2 occurs between 14 and 28 days after infection (PI) (Allan et al., 1999b; Balasch et al., 1999; Pogranichny et al., 2000; Krakowka et al., 2001), independently of the disease status of the animal. However, some studies have indicated that pigs that develop PMWS seroconvert later than subclinical PCV2 infected pigs (Bolin et al., 2001; Rovira et al., 2002; Okuda et al., 2003). Under field conditions, colostral antibodies decline during lactating and nursery periods, and an active seroconversion occurs subsequently around 7 to 12 weeks of age (Rodríguez-Arrioja et al., 2002; Larochelle et al., 2003). PMWS is not usually observed in pigs younger than 4 weeks of age (Segalés and Domingo, 2002), which may be associated with protective maternal immunity against PCV2 (McKeown et al., 2005; Ostanello et al., 2005). Although a humoral immune response to PCV2 in the field takes place around 2 to 3 months of age, a variable percentage of growing or finishing pigs may be viraemic, suggesting that the PCV2 antibodies are not fully protective against the infection (Rodríguez-Arrioja et al., 2002; Larochelle et al., 2003; Sibila et al., 2004). This situation may be partly explained by the generation of neutralizing antibodies; pigs with high level of PCV2-replication or with PMWS develop low or non-detectable titres of PCV2 neutralizing antibodies compared with pigs that get subclinical PCV2 infection (Meerts et al., 2006, [submitted, author address available from CABI]).
It has been shown that stimulation and/or activation of the immune system of experimentally PCV2 infected pigs by some viruses or non-infectious factors increase PCV2 replication and viral loads (Allan et al., 1999b; Krakowka et al., 2000, 2001; Harms et al., 2001; Rovira et al., 2002), suggesting that immunostimulation can be a pivotal event for the development of PMWS (Krakowka et al., 2001). Conversely, typical microscopic lymphoid lesions in tissues from PMWS affected pigs (Clark 1997; Rosell et al., 1999), the association of the disease with opportunistic pathogens (Clark 1997; Carrasco et al. 2000; Nuñez et al., 2003; Segalés et al., 2003b), and other changes in immune cell subpopulations of lymphoid tissues and peripheral blood mononuclear cells (PBMC) (Segalés et al., 2001; Darwich et al., 2002, 2003; Chianini et al., 2003; Nielsen et al., 2003) are regular features of PMWS in severely affected pigs, suggesting that immunosuppresion is a feature of PMWS affected pigs (Segalés et al., 2004a).
A significant alteration of the cytokine mRNA expression patterns of different pro-inflammatory and regulatory cytokines in lymphoid tissues has been described in PMWS affected pigs (Darwich et al., 2003, Stevenson et al., 2004), although these results were not further confirmed by other authors (Sipos et al., 2004). Moreover, it has been suggested that the inability of some PCV2-infected pigs to produce interferon in the early stages of the infection may be a key factor for PMWS development (Stevenson et al., 2004). PCV2 infection of blood and plasmacytoid dendritic cells as well as dendritic cells precursors has shown in vitro that the virus does not inhibit these cells differentiation, and the capacity to process and present antigen to T lymphocytes by those cells is maintained (Vincent et al., 2003, 2005). An immunomodulatory effect of PCV2 on natural interferon producing cells has also been described, suggesting that PCV2 infected pigs, or at least those with PMWS, would be more susceptible to concomitant infections (Vincent et al., 2005).
The mechanisms responsible for lymphocyte depletion and immunodeficiency associated with PCV2-infection are not known at present. Some authors have suggested apoptosis as a mechanism for B cell depletion in lymph nodes (Shibahara et al., 2000), although conflicting results have been published (Mandrioli et al., 2004; Resendes et al., 2004a). Moreover, there is evidence that lymphocyte proliferation could be inhibited in the thymus and secondary lymphoid organs (Darwich et al., 2003; Mandrioli et al., 2004).
Very marginal information is available on immunology assoicated with PCVDs other than PMWS. It has been suggested that excessive PCV2 antibody titres may trigger the development of PDNS (Wellenberg et al., 2004a), and that cytokine profiles and haematological data of PDNS-affected pigs support a Th1 bias in these animals (Sipos et al., 2005). However, most of this information has not been repeated and further studies are required. No data on immunology exist regarding PCV2-associated reproductive disease.
List of Symptoms/SignsTop of page
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Sign|
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Sign|
|Digestive Signs / Diarrhoea||Sign|
|Digestive Signs / Diarrhoea||Sign|
|Digestive Signs / Melena or occult blood in faeces, stools||Sign|
|General Signs / Ataxia, incoordination, staggering, falling||Sign|
|General Signs / Back atrophy, wasting||Pigs:All Stages||Sign|
|General Signs / Cyanosis, blue skin or membranes||Sign|
|General Signs / Dysmetria, hypermetria, hypometria||Sign|
|General Signs / Fever, pyrexia, hyperthermia||Sign|
|General Signs / Forelimb atrophy, wasting||Pigs:All Stages||Sign|
|General Signs / Forelimb swelling, mass in fore leg joint and / or non-joint area||Sign|
|General Signs / Generalized lameness or stiffness, limping||Sign|
|General Signs / Hindlimb atrophy, wasting||Pigs:All Stages||Sign|
|General Signs / Hindlimb swelling, mass in hind leg joint and / or non-joint area||Sign|
|General Signs / Icterus, jaundice||Pigs:All Stages||Sign|
|General Signs / Inability to stand, downer, prostration||Sign|
|General Signs / Lack of growth or weight gain, retarded, stunted growth||Pigs:Weaner||Diagnosis|
|General Signs / Lymphadenopathy, swelling, mass or enlarged lymph nodes||Pigs:Weaner||Diagnosis|
|General Signs / Pale mucous membranes or skin, anemia||Sign|
|General Signs / Pale mucous membranes or skin, anemia||Sign|
|General Signs / Pelvic atrophy, wasting, hips, gluteal region||Pigs:All Stages||Sign|
|General Signs / Petechiae or ecchymoses, bruises, ecchymosis||Sign|
|General Signs / Sudden death, found dead||Sign|
|General Signs / Sudden death, found dead||Sign|
|General Signs / Swelling skin or subcutaneous, mass, lump, nodule||Sign|
|General Signs / Swelling, mass external abdomen||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Pigs:All Stages||Diagnosis|
|General Signs / Weight loss||Pigs:Weaner||Diagnosis|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Sign|
|Nervous Signs / Tremor||Sign|
|Ophthalmology Signs / Chemosis, conjunctival, scleral edema, swelling||Sign|
|Ophthalmology Signs / Conjunctival, scleral, injection, abnormal vasculature||Sign|
|Ophthalmology Signs / Conjunctival, scleral, redness||Sign|
|Reproductive Signs / Abortion or weak newborns, stillbirth||Pigs:Piglet,Pigs:Sow||Sign|
|Reproductive Signs / Mummy, mummified fetus||Pigs:Sow||Sign|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Pigs:All Stages||Sign|
|Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea||Pigs:All Stages||Sign|
|Skin / Integumentary Signs / Hyperkeratosis, thick skin||Sign|
|Skin / Integumentary Signs / Rough hair coat, dull, standing on end||Sign|
|Skin / Integumentary Signs / Scarred skin||Sign|
|Skin / Integumentary Signs / Skin crusts, scabs||Sign|
|Skin / Integumentary Signs / Skin edema||Sign|
|Skin / Integumentary Signs / Skin erythema, inflammation, redness||Pigs:All Stages||Sign|
|Skin / Integumentary Signs / Skin necrosis, sloughing, gangrene||Sign|
|Skin / Integumentary Signs / Skin papules||Sign|
|Skin / Integumentary Signs / Skin plaque||Sign|
|Skin / Integumentary Signs / Skin pustules||Sign|
|Skin / Integumentary Signs / Skin scales, flakes, peeling||Sign|
|Skin / Integumentary Signs / Skin ulcer, erosion, excoriation||Sign|
|Urinary Signs / Palpable enlarged kidney ,renomegaly||Pigs:All Stages||Sign|
Disease CourseTop of page
Postweaning multisystemic wasting syndrome (PMWS) most commonly affects pigs of 2 to 3.5 months of age, although the disease has been described in 1- to 6-month-old pigs. Only one Japanese report has described naturally occurring PMWS in lactating 3-day-old piglets (Hirai et al., 2001). Morbidity and lethality are variable depending on farms and batches; usual rates are 4 to 30% and 70 to 80%, respectively (Segalés and Domingo, 2002). Clinical signs include wasting as major signs but also unthriftness, pallor of the skin, respiratory distress, diarrhoea, and sometimes jaundice (Segalés and Domingo, 2002). PMWS has been described in almost all types of farms, including farrow-to-finish and multi-site operations, and herd numbers from 30 to 10,000 sows (Segalés et al., 2003a). An individual expression of the disease seems to be a key characteristic of this disease; only some individual pigs have clinical signs in a given pen. These pigs tend to die or to develop marked wasting within a few days; no precise data has been published on the percentage of affected pigs that may recover. Antibiotic treatments usually fail to counteract the disease. When PMWS occurs in farrow-to-finish or in farrow-to-nursery herds, no noticeable disturbance is usually observed in other categories than the post-weaned-growing pigs. The reproductive performances in particular are maintained even in those herds with a high incidence of losses due to PMWS. Thus the reproductive function does not seem at all to be altered in these farms (Segalés et al., 2002a). However, reproductive disease associated with PCV2 has been described both in North America (mainly) and Europe (West et al., 1999; Ladekjaer-Mikkelsen et al., 2001; Sanford, 2002), although its importance seems to be very limited; no data on the potential presence of PMWS in these farms experiencing PCV2-associated reproductive failure have been given. The described reproductive failure is characterized by late-term abortions and stillbirths in the absence (West et al., 1999) or presence (O'Connor et al., 2001) of other well established reproductive pathogens.
It has been observed that most of the pigs developing PMWS corresponded to a few litters, suggesting a possible litter effect (Madec et al., 2000). Moreover, it has been showed that castrated male pigs tend to be more susceptible to PMWS than females, and pigs with lower birth and weaning weights tend to develop PMWS at higher frequencies, as do the lighter pigs at the beginning of the fattening period (Corrégé et al., 2001; Rodríguez-Arrioja et al., 2002).
Porcine dermatitis and nephropathy syndrome (PDNS) has been described in both PMWS and non-PMWS affected farms. However, and although no contrasted data is available, it seems that the concomitance of both syndrome in the same farm is rather frequent. PDNS may affect nursery and growing pigs, and, sporadically, adult animals (Drolet et al., 1999). The prevalence of the syndrome in affected herds is relatively low, being usually between 0.05 and 0.5% (Segalés et al., 1998a). However, higher prevalence has been detected in the UK and other countries, with case mortality in affected herds ranging from 0.25 to 20%, or even higher (Gresham et al., 2000). Mortality among pigs aged 3 months or older approaches 100%, while approximately half of affected pigs aged between 1.5 to 3 months die. Pigs with severe, acute disease die within a few days after the onset of clinical signs. Surviving pigs tend to recover and gain weight 7 to 10 days after the beginning of the syndrome (Segalés et al., 1998a). PDNS affected pigs show anorexia, depression, prostration, stiff-gait and/or reluctance to move, and normal temperatures or mild pyrexia (Segalés et al., 1998a; Drolet et al., 1999). However, the most obvious sign in the acute phase of the disease is the presence of irregular, red-to-purple macules and papules on the skin, mainly located on the hind limbs and perineal area, which tend to coalesce, and may be of generalized distribution in the most severely affected animals. With time, the lesions become covered by dark crusts, and fade gradually (2-3 weeks), sometimes leaving scars (Drolet et al., 1999).The cause of death in PDNS affected pigs is an acute renal failure (Smith et al., 1993; Helie et al., 1995; Segalés et al., 1998a), with usually great increases in serum levels of creatinine and urea.
Other infections/diseases may be found in farms experiencing PMWS and/or PDNS (Ellis et al., 2004). Among them are Aujeszky disease, porcine reproductive and respiratory syndrome (PRRS), porcine parvovirus infection, Glässer’s disease, streptococcal meningitis, salmonellosis, postweaning colibacillosis, non-specific diarrhoea, dietetic hepatosis, and suppurative bronchopneumonia (caused by Pasteurella multocida, Bordetella bronchiseptica, Streptococcus suis and other bacteria). From all these diseases and infections, the respiratory form of PRRS has been a major concern for the swine industry because of its clinical similarity with PMWS and the high percentage of farms and/or pigs experiencing PMWS and PRRS virus infection at the same time (Segalés et al., 2002c).
EpidemiologyTop of page
The oro-nasal route is considered the most likely route of PCV2 transmission. This assumption is based on experimental studies of PCV2 infection using the intranasal route for inoculation (Allan et al., 1999a; Balasch et al., 1999; Ellis et al., 1999b; Krakowka et al., 2000, 2001; Rovira et al., 2002). Under commercial conditions, most pigs get PCV2 infection at the age of 2 to 4 months (Larochelle et al., 2003; Sibila et al., 2004), indicating that horizontal transmission of PCV2 between pigs seems to be very efficient. Horizontal transmission of PCV2 has also been demonstrated under experimental conditions (Albina et al., 2001; Bolin et al., 2001).
Transplacental transmission of PCV2 has recently been demonstrated (Park et al., 2005), suggesting that vertical transmission of PCV2 is a real possibility. However, the frequency of affects on reproduction under field conditions is very rare in Europe (Ladekjaer-Mikkelsen et al., 2001; Pensaert et al., 2004; Maldonado et al., 2005), but several cases of reproductive failure have been described in North America (Sanford, 2002) and data from Korea showed PCV2 infection in about 13% of aborted fetuses and stillborn piglets (Kim et al., 2004).
PCV2 can be detected by PCR in nasal cavities, tonsillar and bronchial secretions, faeces and urine of both naturally PMWS and non-PMWS affected pigs (Segalés et al., 2005), although it is known that the virus load present in these potential excretion routes is much higher in diseased pigs. In experimental infections with PCV2, the virus has been isolated and/or PCR-detected from nasal, rectal, urinary, salivary, ocular and tonsillar swabs (Krakowka et al., 2000; Bolin et al., 2001; Shibata et al., 2003).
PCV2 nucleic acid has also been demonstrated in pig semen by PCR (Hamel et al., 2000; Larochelle et al., 2000), although it has never been isolated from this type of sample. Therefore, it is considered that artificial insemination and natural mating may act as potential routes of dissemination of PCV2, but this has not been proven.
PCV2 nucleic acid has been demonstrated in serum from pigs up to 22 weeks of age under field conditions (Rodríguez-Arrioja et al., 2002), although it has not been assessed whether pigs were continuously or intermittently viraemic. Pigs with persistent infection can occur in both PMWS and non-PMWS affected herds (Larochelle et al., 2003; Sibila et al., 2004). Field data are also supported by experimental studies, since PCV2 has been detected in blood and/or tissues of a significant proportion of experimentally inoculated pigs at termination (days 21-71 after inoculation) of experiments (Allan et al., 1999b; Balasch et al., 1999; Krakowka et al., 2000; Magar et al., 2000; Pogranichny et al., 2000; Harms et al., 2001; Rovira et al., 2002; Resendes et al., 2004b). In one experiment, PCV2 nucleic acid was detected in tissues of a single pig killed 125 days after infection (Bolin et al., 2001). The mechanism by which PCV2 persists in pigs is unknown.
Since PCV2 is present in both PMWS and non-PMWS affected pigs, it has been proposed that different viral strains may vary in pathogenicity. A study comparing PCV2 sequences from diseased and healthy pigs from France did not identify any viral pathogenic molecular markers (Boisseson et al., 2004). This result is consistent with experimental evidence in which PMWS was reproduced using PCV2 from both diseased (Allan et al., 1999b) and healthy pigs (Allan et al., 2003). Further ongoing experiments are being performed to assess potential differences in pathogenicity between PCV2 isolates (Opriessnig and Halbur, 2005).
Zoonoses and Food SafetyTop of page
No zoonotic risk has been identified for PCV2 (Ellis et al., 2000a). In a direct form, PCV2 does not really affect food safety issues in pork. However, since this virus is targeting the immune system, apparently causing immunosuppression in diseased animals, affected herds have a greatly increased incidence of secondary bacterial infections (Segalés et al., 2004a), including Salmonella spp., a well-documented foodborne pathogen (Wellenberg et al., 2004b). Consequently, the use of antibiotics in PMWS affected herds usually increases. Therefore, two potential human risks can be detected in this context; personnel working with animals with increased zoonotic load and increased risk of these potential zoonotic agents to enter the food chain. Specific assessment of these risks has not been studied.
Importantly, the use of PCV2 vaccines has caused a decrease of co-infections and use of antibiotics in affected farms (Vigre et al., 2010; Beach and Meng, 2012), therefore, having significant positive benefits regarding the abovementioned risks.
Prevention and ControlTop of page
Since postweaning multisystemic wasting syndrome (PMWS) is considered the most important porcine circovirus disease (PCVD), significant efforts to control it have been made worldwide during more than a decade. The advent of PCV2 vaccines since 2004 in some parts of the world, and since 2006-07 in a more generalized fashion, has radically changed the perception of veterinarians on this disease (Kekarainen et al., 2010). Although PMWS is still a multifactorial disease, which involves infection of pigs with PCV2 and the influence of infectious and non-infectious factors or triggers for the development of clinical disease, PCV2 vaccination by itself has been able to counteract the detrimental effects of the infection. Therefore, the use of PCV2 vaccines is nowadays generalized, being the most sold vaccine for piglets worldwide. Besides the availability of such products, control measures were focused on the understanding, control and elimination of the co-factors and triggers involved in individual farms. Besides vaccination, the most studied factors (from experimental and epidemiological data) in relation to disease triggering/protection are also outlined below.
The advent of PCV2 vaccines has radically changed the perception on the importance of this viral agent. Therefore, it seems clear there exists a ‘before’ and an ‘after’ of PCV2 vaccination in the pig population worldwide as well as in the mentality of producers and veterinarians. Under field conditions, all PCV2 commercial vaccines existing so far have been able to decrease percentages of mortality and number of runts in nursery and/or fattening/finishing pigs (Fachinger et al., 2008; Kixmoller et al., 2008; Horlen et al., 2008; Desrosiers et al., 2009; Segalés et al., 2009; Pejsak et al., 2010; Marteli et al., 2011; Fraile et al., 2012a,b). More importantly, improvement of average daily gain (10 to 40 g/day in vaccinated pigs compared to non-vaccinated controls), feed conversion rate and pig size/weight homogeneity as well as decreasing of co-infections and use of antibiotics have been the most significant benefits of PCV2 vaccination. Therefore, it seems that all commercial vaccines to date exert a very positive effect in those farms affected by PMWS.
Current commercial products are either inactivated, subunit or genetically engineered vaccines (Beach and Meng, 2012). The first ones consist of the traditional approach of an adjuvanted, killed virus vaccine. However, to date, the most used vaccines in the worldwide market are those based on baculovirus expressed PCV2 capsid protein. Finally, there is a product based on the inactivation of a chimeric virus that includes the ORF2 gene of PCV2 (which encodes the capsid protein) and the genomic backbone of PCV1, the non-pathogenic porcine circovirus.
PCV2 vaccines can be applied to the piglet and/or the sow. Average daily gain and mortality improvement is better in the short term when using piglet vaccination. On the other hand, sow vaccination seems to generate some aside advantages, such as better reproductive parameters including fertility, litter homogeneity, number of liveborn piglets and shorter weaning-to-mate period. Therefore, the decision to use one or the other vaccination schedule (pigs or sows) or both (pigs and sows) should be the product of a well-established cost-benefit balance.
Age at vaccination in piglets may vary, since it should avoid the potential interference by maternally derived immunity and generate vaccine immune response before natural infection takes place. Although this vaccination window may vary from farm to farm, vaccination at weaning is the most usual practice all over the world. Sow vaccination, based on the recommendation for the vaccine licensed to be used in sows, should be performed at 6 and 3 weeks before farrowing in gilts and 3 weeks before farrowing in sows.
Prospective on-field studies carried out in France (Madec et al., 2000) showed flaws in the management in farms severely affected by PMWS. Therefore, it was suggested that several environmental conditions might be necessary in association with PCV2 infection to lead to the clinical expression of the disease. The implementation of what is today known as Madec’s 20-point plan (a list of husbandry measures to lower the impact of the disease) significantly decreased the percentage of mortality in severely affected farms (Madec et al., 2001). These measures were directed to reduce the so-called ‘infection pressure’ in regards PCV2 and any other pathogen, as well as to improve hygiene and reduce stress at the different production stages (Madec et al., 2000; Madec and Waddilove, 2002).
These measures include the reduction in mixing pigs, adequate pig flow (strict all in - all out procedures) and pig density, special care with castration, improvement of air quality and comfort during the postweaning and growing periods, cross-fostering (if necessary) only in the first 24 h after birth, to avoid using large pens, to use openwork partitions between pens, good hygiene practices, to segregate sick animals as soon as possible to hospital facilities, to have sick pens located away from the nursery or growing unit, and to only medicate with antibiotics (injectable) sick animals, at least during 3 consecutive days. The suggested measures were not addressing real risk factors because they were not obtained from an epidemiological survey and their individual impact could not be estimated. However, significant positive results have been obtained when these husbandry measures are applied; in a particular study, a significant improvement in loss rates was achieved when the rate of compliance with the recommended measures was higher (Guilmoto and Wessel-Robert, 2000).
Effects of other viral infections
Experimental data have shown that a higher percentage of pigs co-infected with PCV2 and porcine parvovirus (PPV) or porcine reproductive and respiratory syndrome virus (PRRSV) develop PMWS than single PCV2-inoculated pigs (Allan et al., 1999b; Krakowka et al., 2000; Harms et al., 2001; Rovira et al., 2002). Although the mechanism by which this potentiation effect takes place is not known, it has been hypothesized that PPV and PRRSV activate macrophages, favouring the replication of PCV2 (Ellis et al., 1999b). Similarly to these viruses, Mycoplasma hyopneumoniae appear to potentiate the severity of PCV2-associated lung and lymphoid lesions, to increase the levels and prolong the presence of PCV2-antigen, and the incidence of PMWS in PCV2-inoculated pigs. Therefore, certain viral and bacterial co-infections in susceptible PCV2 infected pigs are considered triggering factors for the disease. These experimental results have been further supported by epidemiological data (Rose et al., 2003), although not in all studies (López-Soria et al., 2005).
Therefore, the control of concurrent viral/bacterial infections such as PRRSV, PPV and Mycoplasma hyopneumoniae in the postweaning area should decrease the incidence of PMWS. From a practical point of view, attempts to control PMWS with PPV vaccination on finishing sites in the USA with confirmed PPV circulation have been repeatedly successful (Halbur, 2001). However, this positive effect of PPV vaccination in reducing the clinical incidence of PMWS has not been experimentally proven (Opriessnig et al., 2004b). On the other hand, to date, no published results on the control of PRRSV or Mycoplasma hyopneumopniae infection (by vaccination or other systems) to mitigate the effects of PMWS are available.
Stimulation of the immune system
Results of PCV2 inoculation together with other viruses led to a new hypothesis on the pathogenesis of PMWS. It was hypothesized that a local and/or systemic immunostimulation with a non-infectious irrelevant immunogen incorporated into a strong adjuvant may potentiate PMWS (Krakowka et al., 2001). This hypothesis was tested using gnotobiotic piglets infected with PCV2 and injected with keyhole limpet haemocyanin in incomplete Freund's adjuvant (KLH/ICFA). KLH/ICFA was injected intramuscularly with or without thioglycollate (glycan) intraperitoneally. All systemically immunised, PCV2 infected piglets developed moderate to severe PMWS, whereas none of the piglets infected with the virus alone developed PMWS (Krakowka et al., 2001).
These experimental data have also been supported by a number of on-farm studies, where the PCV2 infection and the use of products that stimulate the pig’s immune system (vaccines, immunomodulators), have acted as triggering factors for PMWS (Allan et al., 2001; Kyriakis et al., 2002). Besides, other experimental studies have failed in demonstrating that non-infectious stimulation of the immune system using KLH/ICFA (Ladekjaer-Mikkelsen et al., 2002) or a vaccine adjuvant (Resendes et al., 2004b) in PCV2 infected pigs result in PMWS. Other experimental trials have demonstrated that, although no overt disease occurred in immunostimulated pigs, the use of bacterins at certain ages may cause longer PCV2 viraemia and more severe lymphoid lesions than pigs that did not receive vaccine products (Opriessnig et al., 2003, 2006).
Altogether, these results indicate that immune activation of any origin (infectious or non-infectious) might be a triggering factor of PMWS and a pivotal event in the pathogenesis of PCV2-associated disease in pigs under certain circumstances not yet fully determined. However, these data should do not indicate that vaccine application is inappropriate, since the benefit of effective vaccinations may be greater than the risk of inducing PMWS in a low percentage of pigs in a given pig population. Therefore, based on the available results, producers with PMWS affected herds should consider determining the approximate timing of PCV2 infection, with the final objective to re-schedule the timing of vaccination as a potential plan to minimize the disease.
PCV2 status and the serological titres to PCV2 of the sow at farrowing
It has been suggested that a significant proportion of the pigs developing PMWS correspond to a few litters, suggesting a possible litter effect (Madec et al., 2000). This observation has been further studied and characterized (Calsamiglia et al., 2007): PCV2 infected sows at farrowing yielded a higher proportion of week-old PCV2 infected pigs and a higher proportion of these pigs died in the nursery and fattening periods, when compared with piglets from non-infected sows, and a greater proportion of animals died from sows that had low or no antibody titres against PCV2. Therefore, measures that increase maternal immunity and decrease sow viraemia at farrowing would presumably diminish PMWS impact on piglet mortality.
Role of nutrition on PMWS
Partial control of epizootic PMWS has been achieved on some farms from the United Kindgom by changes in the diet from affected pigs (Donadeu et al., 2003). These changes included the increase of nutrient density of young pig diets and addition of commercial feed additives, most of them with anti-oxidant effects. The mode of action of these additives is unknown. It has been observed that diet changes do not have a positive effect on all diseased farms. However, it is noteworthy to say that when they appear to have a positive effect on disease, it is almost always in combination with other management changes. Therefore, the particular effect of nutrition on PMWS development is still an open question.
On the other hand, a recent study has shown that conjugated linoleic acid (CLA) ameliorates PCV2 experimental infection (Bassaganya-Riera et al., 2003). Pigs supplemented during 42 days with CLA before the day of viral challenge had reduced microscopic lesions in lymph nodes and lung, increased proliferation of blood CD8 T cells and reduced production of PCV2-specific IFN-gamma by blood CD4 T cells. Therefore, the use of CLA can be considered as another factor that may have some positive effect on PMWS prevention.
Subcutaneous injection of PCV2 hyperimmune sera from commercial abattoir age pigs in suckling or nursery pigs has been successful in substantially reducing the mortality in several PMWS affected batches (Ferreira et al., 2001; Waddilove and Marco, 2002). Strict precautions must be taken in performing serum therapy: blood must be collected from the same farm in which it is to be used, to avoid any risk of introducing other pathogens, and to perform bleeding and injections with maximum hygiene. However, success of this procedure has been variable, and while some farms experienced a pronounced decrease of the incidence of clinical signs due to PMWS (Ferreira et al., 2001; Waddilove and Marco, 2002), others did not report any significant effect. The mechanism of action of serum-therapy has not yet been identified.
Genetics and susceptibility
Several field observations from farmers and veterinarians have suggested that certain genetic lines, especially regarding boars, were associated with lesser PMWS affects. This observation has been supported by recent experimental studies where Landrace pigs were apparently more susceptible to PMWS lesions than Duroc and Large White pigs (Oppriessnig et al., 2004a). Other studies have shown contradictory results with the use of Pietrain boar lines; while the use of this genetic line did not seem to have any effect on the offspring in one study (Rose et al., 2005), another study showed lower general postweaning and PMWS associated mortalities (López-Soria et al., 2011). It is unlikely that a specific breed can be identified as intrinsically resistant, but with a combined epidemiological, genetic and immunological approach, it is more likely that some lines, families or traits of pigs with some degree of innate resistance could be identified if such innate resistance exists.
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