Porcine circovirus 2 replication in colostrum-deprived piglets following experimental infection and immune stimulation using a modified live vaccine against porcine respiratory and reproductive syndrome virus.

Porcine circovirus type 2 (PCV2) infection is now recognized as the major factor in the development of post-weaning multisystemic wasting syndrome (PMWS). Although Koch's postulates have been fulfilled for PCV2 and PMWS, the severe clinical expression of the disease observed in field cases has been difficult to reproduce experimentally. Some studies have demonstrated that immune stimulation associated with the use of some commercially available swine vaccines may trigger progression of PCV2 infection to disease and lesions characteristic of PMWS. Here we describe the effects on PCV2 infection in an experimental model following the use of a commercially available modified live vaccine to porcine respiratory and reproductive syndrome virus (PRRSV). Although none of the piglets infected with PCV2 developed clinical PMWS, the severity of microscopical lesions and the PCV2 antigen load associated with these lesions were higher in the PRRSV-vaccinated piglets compared with those detected in the PCV2 only infected animals.

Experimental infection of 3-week-old conventional colostrum-fed pigs with porcine circovirus type 2 and porcine parvovirus.

This report describes an experimental infection with porcine circovirus type 2 (PCV2) in combination with porcine parvovirus (PPV) in 3-week-old conventional colostrum-fed pigs with maternal antibodies to both viruses. Two groups of four pigs each were inoculated with PCV2 and PPV. One of the groups received also a commercial inactivated vaccine against porcine pleuropneumonia to evaluate possible effects of the stimulation of the immune system of pigs on the infection. Another group of four pigs was kept as uninfected control. Clinical signs, rectal temperatures and body weights were recorded. Serum antibody titers to PCV2 and PPV were determined at weekly intervals. Pigs were killed 42 days after inoculation and tissue samples were examined for the presence of gross and microscopic lesions. Tissues were also analyzed for the presence of PCV2 and PPV DNA by PCR, and for the presence of PCV2 antigen by immunohistochemistry (IHC). All the pigs had serum antibodies to PCV2 and PPV at the beginning of the trial. None of them developed clinical symptoms or pathological lesions typical of post-weaning multisystemic wasting syndrome (PMWS), a disease associated to PCV2 infection. However, IHC and/or PCR analyses showed that clinically silent PCV2 infection developed in five of the eight inoculated pigs, regardless of the administration of the vaccine. In particular, PCV2 DNA and/or antigen were detected in most of the tissues examined in the two pigs with the lowest titer of maternal PCV2 antibodies at the beginning of the trial. PPV DNA was not detected in any of the samples examined. The five pigs with PCR and/or IHC evidence of PCV2 infection had a mean weight gain during the experiment lower than that of the inoculated PCR-negative pigs considered together and that of the control pigs. In conclusion, it would appear that passive immunity against PCV2 can play a role in preventing the development of PMWS, but is not able to prevent the establishing of clinically silent PCV2 infections. The dissemination and persistence of the virus in the tissues may depend on the level of PCV2 antibodies at the time of inoculation.

PMWS: experimental model and co-infections.

Porcine circovirus type 2 (PCV2) is now recognised as the causal agent of porcine multisystemic wasting syndrome (PMWS), an economically important wasting disease of young pigs [J. Vet. Diagn. Invest. 12 (2000) 3]. Gross lesions of PMWS include generalised lymphadenopathy, hepatitis, nephritis and pneumonia and typical histological lesions include lymphocytic depletion and multinucleated giant cell formation in lymph nodes, degeneration and necrosis of hepatocytes, and multifocal lymphohistocytic interstitial pneumonia. This communication will review the results of experimental infections of gnotobiotic (GN), colostrum-deprived (CD) and colostrum-fed (CF) pigs within our group, and elsewhere, with PCV2 and the conclusions that can be drawn from this work.

Lack of antibodies to porcine circovirus type 2 virus in beef and dairy cattle and horses in western Canada.

Porcine circovirus type 2 (PCV2) is a recently recognized agent that is consistently associated with postweaning multisystemic wasting disease in swine. There are conflicting data concerning the ability of this virus to infect and cause disease in other species. To determine if normal cattle, cattle affected with various illnesses, and normal horses in endemic areas of PCV2 infection in swine have had PCV2 infections, 100 randomly selected bovine sera, 100 equine sera, and 100 colostrum samples from clinically normal dairy cattle were examined for the presence of antibodies to porcine circoviruses by using ELISAs. All samples tested were negative for antibodies to porcine circoviruses. As well, a seronegative neonatal Holstein calf and 6 seronegative, 6-month-old beef calves that were experimentally infected with PCV2 failed to develop antibodies to the virus. These results suggest that natural infection of cattle and horses with PCV2 does not occur, or is a rare event, in western Canada.

Experimental infection of colostrum deprived piglets with porcine circovirus 2 (PCV2) and porcine reproductive and respiratory syndrome virus (PRRSV) potentiates PCV2 replication.

Experimental infection of colostrum-deprived (CD) pigs with a combined inoculum of porcine circovirus 2 (PCV2) and porcine reproductive and respiratory syndrome virus (PRRSV) potentiated the replication and distribution of PCV2 virus, when compared with pigs inoculated with PCV2 alone. The replication and distribution of PRRSV in dually infected pigs was not enhanced, when compared to pigs inoculated with PRRSV alone. The mechanisms involved in the potentiation of PCV2 replication in PCV2/PRRSV and PCV2/porcine parvovirus (PPV) dually infected pigs may relate to the fact that monocyte/macrophage cell types are common targets of these 3 viruses.

Distribution of cytopathic and noncytopathic bovine viral diarrhea virus antigens in tissues of calves following acute experimental infection.

The distribution of cytopathic and noncytopathic biotypes of bovine viral diarrhea virus (BVDV) in the tissues of colostrum-fed and colostrum-deprived calves was investigated. Colostrum-fed (group A) and colostrum-deprived (group B) calves were experimentally infected with the BVDV isolate 80/1, which contains both BVDV biotypes. Colostrum-deprived calves were also experimentally infected with a noncytopathic BVDV (group C) or with a cytopathic BVDV (group D) cloned from the 80/1 isolate. All calves were sequentially euthanized, and a wide range of tissue samples were processed for immunofluorescent and virus isolation studies. In group A, consistent immunofluorescent staining for BVDV was detected in vascular smooth muscle of numerous blood vessels in the tissues examined, mainly at 11 and 13 days postinoculation. A predominance of samples containing cytopathic BVDV was observed in the calves of this group, following virus isolation studies. Both cytopathic and noncytopathic BVDV were detected/recovered from a larger range of specimens in the calves in group B than from the calves in group A. In the calves in all the experimental groups, large amounts of BVDV antigen were detected mainly in tissue samples from the lymphoid and gastrointestinal systems, whereas only minimal amounts of BVDV were detected in the respiratory tract. Abundant noncytopathic BVDV antigen was also detected in pituitary gland and in Langerhans islets in pancreases of colostrum-deprived calves infected with the cloned noncytopathic BVDV. Noncytopathic BVDV was isolated from a wider range of tissues from calves in group C than in the colostrum-deprived calves infected with both BVDV biotypes. A cytopathic BVDV was isolated/detected in retropharyngeal, mesenteric, and abomasal lymph nodes and in thymus of 2 calves in group C. Cytopathic BVDV was detected/isolated mainly from mesenteric lymph nodes and Peyer's patches of the calves in group D.

A sequential study of experimental porcine paramyxovirus (LPMV) infection of pigs: immunostaining of cryostat sections and virus isolation.

La Piedad Michoacan Paramyxovirus (LPMV) is a recently recognized paramyxovirus infecting pigs throughout Mexico. Disease syndromes observed in field cases associated with LPMV infection include neurologic, respiratory, and reproductive disorders. Clinical signs and the distribution of LPMV virus and antigen in tissue samples from pigs experimentally infected with LPMV by natural routes were studied. Severe neurologic disease and death occurred following experimental inoculation of 3- and 17-day-old pigs. All of the pigs inoculated at 3 days of age were either dead or moribund by 8 days after inoculation, whereas 30% of the pigs inoculated at 17 days of age were affected. Virus was consistently recovered from or demonstrated in tissues from the respiratory tract of both groups of pigs. LPMV and antigen were also demonstrated in central nervous system (CNS) tissues from these pigs; however, differences in virus distribution within the CNS were demonstrated in the 2 groups. In the pigs inoculated at 17 days of age, isolation of LPMV was restricted to the olfactory bulb and midbrain. In contrast, in the pigs inoculated at 3 days of age, isolation of LPMV was more widespread throughout the CNS tissue examined. Virus excretion studies indicated that nasal spread of LPMV was more important than fecal spread. Comparatively large quantities of infectious LPMV were consistently recovered from urine samples of experimentally infected pigs.

Pathogenesis of porcine circovirus; experimental infections of colostrum deprived piglets and examination of pig foetal material.

The results of virus and antigen distribution following experimental infection of colostrum deprived pigs with pig circovirus (PCV) by oral/nasal and intravenous routes are reported. PCV and antigen were detected using virus isolation and indirect immunofluorescence on cryostat sections respectively. PCV antigen was detected in tissues throughout the body but primarily in spleen thymus, and lung. No PCV antigen or virus was detected in tissue samples from the central nervous system. Examination of pig foetal material from field cases of abortion/stillbirth resulted in 3 PCV isolates from 2 sera and a spleen sample from 2 groups of stillborn piglets from the same farm. No antibody to PCV alone was detected in 160 foetal sera tested. These results suggest that transplacental infection with PCV does occur, possibly prior to foetal immunocompetance. However, it is probably not a significant cause of reproductive disorders in pigs in Northern Ireland.