Circle virus in hogs

Porcine circovirus diseases have traditionally been defined as those associated with porcine circovirus 2 PCV-2 infection. However, this terminology should be revised because the advent of the novel porcine circovirus 3 PCV-3 may expand the clinicopathologic outcome caused by porcine circovirus infections.

Porcine circovirus 1 PCV-1 is still considered a nonpathogenic agent for swine. This agent was later shown to be a small, nonenveloped virus containing a single-stranded, circular DNA genome; it was named porcine circovirus PCV. PCV antibodies in swine were found to be widespread, and experimental infections with this virus in pigs did not result in clinical disease, suggesting that PCV was nonpathogenic. A new disease was described in Western Canada during the early and mid s.

The etiology was unknown, and the condition was named postweaning multisystemic wasting syndrome PMWS. PCV-2 has been further associated with a number of disease syndromes in pigs, so the term porcine circovirus disease PCVD was proposed as a collective name. PCV-3 has been recently linked with reproductive disorders and multisystemic inflammation associated with vasculitis, as well as with PDNS. The strongest evidence of disease association comes from in situ hybridization detection of viral genome associated with histopathologic lesions.

Moreover, PCV-3 has also been found in a number of conditions respiratory, digestive, neurologic , but its true association is still to be determined. Like the other porcine circoviruses, PCV-3 is found worldwide. Circoviruses are small 17—22 nm in diameter , nonenveloped viruses that contain a single strand of circular DNA.

Novel genotypes have been found, and the most recent proposal suggests the existence of at least 8 PCV-2 genotypes. In the past 5—7 years, another genotype shift from b to d has been evidenced epidemiologically. It is not clear whether differences in virulence exist among or within PCV-2 genotypes.

PCV-3 is also widespread based on PCR results from many parts of the world, and it has been found to have existed in the s. Initially, PCVSD was identified in high health herds that were free of most common swine pathogens. Many agents that cause reproductive failure in sows produce a broad spectrum of sequelae, including abortions and weak neonates, as well as stillbirth So far, the conditions by which PCV-3 is able to cause apparent disease are unknown.

Moreover, the frequency of overt disease associated with this novel virus is also not known. Consequently, it was suggested that PCV-2 infection, linked to other cofactors, was necessary for consistent development of full clinical disease. It appears that a number of factors, such as age and source of pigs, environmental conditions, genetics, the nature of the PCV-2 inoculum used, and the immunologic status of the pig at PCV2 infection, play a significant role in consistent experimental reproducibility of the disease.

The more consistent and repeatable PCVSD disease models have been obtained using infectious and non-infectious cofactors as triggers. Also, the coinfection of PCV-2a and b genotypes has been linked to reproduction of clinical disease under experimental conditions.

The mechanisms by which other viruses or immunostimulation may trigger the development of wasting in PCVinfected pigs is still unknown. High loads of PCV-2 in blood, lymphoid, and other tissues and in potential excretion routes are associated with expression of disease. Damage to the immune system is the main feature of PCVSD, suggesting that affected pigs have an acquired immunodeficiency.

Lymphocyte depletion of lymphoid tissues, changes in peripheral blood mononuclear cell subpopulations, and altered cytokine expression patterns have all been demonstrated in pigs naturally and experimentally affected with the condition.

The identification of cells that support PCV-2 replication has been a matter of controversy. The large amount of PCV-2 antigen found in the macrophages and dendritic cells of diseased pigs appears to be the result of accumulation of viral particles. However, epithelial and endothelial cells seem to be the main target for PCV-2 replication, as well as a small proportion of macrophages and lymphocytes. Much less is known regarding the pathogenesis of other PCVDs. PCV-2 is able to replicate in fetuses as well as in zona pellucida—free embryos.

Moreover, an experiment with embryos exposed to PCV-2 and then transferred to receptor sows suggested that infection can lead to embryonic death. Therefore, it is believed that one of the potential outcomes of PCV-2 infection in sows could be return to estrus.

Transplacental transmission of PCV-2 has been demonstrated. However, experiments using pregnant sows inoculated intranasally have yielded variable results. When successful, those studies have shown that PCV-2 may cause fetal death, similar to that of porcine parvovirosis, with live pigs together with dead piglets and mummies of different sizes.

Late abortion has also been described in PCV-2 natural infection. In general, inappropriate innate immune responses do this Indirect evidence exists, such as significantly higher serum antibody titers to PCV-2 in affected pigs compared with healthy or PCVSD-affected pigs. PCV-3 has not yet been isolated, and only one experimental infection with an infectious clone has been published in the peer-reviewed literature.

This report claimed the reproduction of PDNS, but histopathologic- lesions were not convincing. No real data on the pathogenesis of PCV-3 infection exists as yet. Porcine circoviruses are considered ubiquitous in countries with and without PCVDs. Epidemiologic features are almost known only for PCV Transmission of PCV-2 may be by direct contact with infected pigs.

PCV-2 has been detected in almost all potential excretion routes such as nasal, ocular, and bronchial secretions; saliva; urine; and feces. The virus can be found in semen, but the practical importance of this is probably negligible. Artificial insemination AI of sows with PCVinfected semen from experimentally inoculated boars did not result in sow infection or fetal infection. Therefore, it seems that reproductive disease linked to AI is possible, but only when semen has a high virus load, which is unlikely under natural conditions.

Although not demonstrated, it is assumed that contact with contaminated fomites, exposure to contaminated feeds or biologic products, multiple use of hypodermic needles, or biting insects may play a role in transmission. PCV-2 may persist in swine for several months under either experimental or field conditions. Convalescent swine may carry virus for extended periods and be important in disease transmission.

PCV-2 is fairly resistant to commonly used disinfectants and to irradiation, probably allowing it to accumulate in the environment and be infective for new groups of susceptible pigs if rigorous sanitary measures are not followed. The decline of colostral antibody titer in pigs is associated with onset of PCVSD in late nursery or finishing pigs.

Transplacental infection with PCV-2 has been documented, but it is not known whether pigs infected in utero are able to subsequently develop clinical PCV2-SD. However, results of serologic and PCR studies for antibody or genome against PCVs in other livestock species, non-suid wild animals, and pets have been contradictory, and experimental induction of disease using PCV-1 or PCV-2 in species of livestock other than swine has not been successful.

Mice may be able to replicate and harbor PCV PCVSD is characterized by overt weight loss. Porcine circovirus disease PCVD is the term for a viral disease of pigs that has emerged as a major problem in the United States.

Porcine circovirus type 1 PCV1 was first identified in and was recognized as a non-disease-causing agent that frequently occurred in laboratory tissue cultures. In , swine veterinarians in western Canada began reporting cases of nursery pigs falling ill with clinical signs that included a progressive loss of body condition, visibly enlarged lymph nodes, difficulty breathing, and less commonly diarrhea, pale skin, and jaundice.

The name "postweaning multisystemic wasting syndrome" PMWS was applied to the disease. In , a new circovirus PCV2 was isolated from these outbreaks. Since that time, researchers have been able to successfully reproduce the disease by inoculating pigs with PCV2 in the laboratory.

PMWS has now been reported from most pig-producing countries of the world. Additional PCV2-associated diseases have also been described including reproductive failure, respiratory disease in finishing pigs, and an unusual skin and kidney disease referred to as porcine dermatitis and nephropathy syndrome PDNS.

This prolific virus impairs the immune system and leaves pigs susceptible to other swine diseases and pigs affected may experience increased mortality, poor growth and weight loss, progressing to the level of severe thinning, weakness, and a considerable longer time to market.

Exposing pigs to other pigs or boots, clothing, or equipment that have been around other pigs greatly increases the risk for disease transmission. Genomic sequencing and restriction fragment length polymorphism RFLP techniques have defined several distinct viral clades within the PCV2 genotype but the clinical relevance of these distinctions is not completely understood. In , a circovirus was isolated from porcine kidney cell line PK as an adventitious virus.

Circoviruses are small, nonenveloped animal viruses with single-stranded circular DNA. Porcine circoviruses are quite hardy in the environment and in organic substrates. They are sensitive to most disinfectants but chlorhexidine, ethanol, and iodine are less effective.

Two types of circoviruses in swine have been described. There is circumstantial evidence that PCV1 may be involved in congenital tremors but it is generally considered to be nonpathogenic for swine. Antibodies between the two types have low cross-reactivity.

Many but not all field cases of PCVAD have concurrent viral infections or some other evidence of immune stimulation that seems to allow permissive replication and pathologic effects of PCV2 in swine. Herds that are endemically infected with other significant pathogens, are operated on a continuous flow basis, are in swine dense areas, provide a suboptimal environment air quality, hygiene , or practice poor biosecurity have been shown to be more likely to experience an outbreak of PCVAD.

Once affected, these same herds often are presented with a more severe form of the disease. The epidemiology of porcine circovirus infections is speculative. Nearly all US swine herds are seropositive. Seroconversion usually occurs by two to four months of age irrespective of whether clinical signs of PCVAD are observed.

Transmission of the virus and conditions allowing virulence expression are being vigorously studied. Activated macrophages appear to be permissive for viral replication and persistence. Pigs infected with PCV2 develop viremia of variable duration, with replication and persistence most extensive in macrophages and monocytes of lymphoid organs and lung.

Lymphoid depletion at multiple sites, chronic lymphohistiocytic to granulomatous inflammation, and an erosive bronchiolitis with fibrosis are characteristic. Reproduction of typical lesions by inoculation with PCV2 has been inconsistent but there is general agreement among researchers that the virus is at least necessary and perhaps causal in order for PCVAD to be expressed.

Occasionally, pigs may develop blotchy purple skin lesions and nephropathy, likely as an immune mediated sequel to viral infection, which is termed porcine dermatopathy and nephropathy syndrome PDNS.

PCVAD: Clinical signs include gradual wasting, unthriftiness, rough hair coat, polypnea, dyspnea, pallor, diarrhea, and occasionally icterus. Affected pigs usually die; clinical survivors are severely stunted; non-clinical pigs in the same groups perform quite well. Both signs and lesions, as reported by various investigators, vary considerably. PDNS: Is mainly a condition of pigs from weeks of age.