Experimental Reproduction of Postweaning Multisystemic Wasting Syndrome in Cesarean-Derived, Colostrum-Deprived Piglets Inoculated with Porcine Circovirus Type 2 (PCV2): Investigation of Quantitative PCV2 Distribution and Antibody Responses

Abstract

Abstract. Sixteen cesarean-derived, colostrum-deprived piglets were inoculated intranasally with porcine circovirus type 2 (PCV2), originally isolated from a pig affected with postweaning multisystemic wasting syndrome (PMWS). At 1 day postinoculation (PI), 3 of the 5 piglets in the uninoculated control group were moved to the room of inoculated piglets for contact exposure. Porcine circovirus type 2 was detected by polymerase chain reaction (PCR) in swabs from inoculated piglets from 1 day PI and from contact piglets from 2 days after cohabitation. Porcine circovirus type 2 was also detected in all serum samples but not in control piglets 7 days PI. Until the end of study, PCV2 was detected in swabs and serum samples by PCR but not in the control piglets. One inoculated piglet died suddenly without clinical signs 19 days PI. Beginning at 14 days PI, 5 piglets, including 1 contact piglet, had clinical signs of depression, anorexia, and icterus, and 1 inoculated piglet died 21 days PI. Most of the piglets exhibiting the above clinical signs became moribund and were necropsied 21 and 28 days PI. In the piglets that showed clinical signs, gross lesions, including icterus of liver and hemorrhage in stomach, and typical histopathological lesions of PMWS, such as lymphoid depletion and basophilic intracytoplasmic inclusion bodies in lymph nodes and other tissues, were observed. Porcine circovirus type 2 was detected by PCR in all tissue samples except in those of the control piglets. Porcine circovirus type 2 was recovered from several tissue samples of the piglets necropsied until 35 days PI. In particular, PCV2 was recovered in high titer from most of the tissue samples of the piglets exhibiting clinical signs. Serum antibody against PCV2 was mostly detected in inoculated piglets and in contact piglets 14 and 21 days PI by an indirect fluorescence antibody test but was not detected in the piglets exhibiting clinical signs until 28 days PI. These results indicate that PCV2 was able to induce clinical PMWS in the absence of other swine pathogens and that there were significant differences in both the quantitative PCV2 distribution in tissues and the antibody response between the piglets that were infected and developed PMWS and those that were infected but remained healthy.

Acute Hepatitis in a Piglet Experimentally Inoculated with Tissue Homogenates from Pigs with Postweaning Multisystemic Wasting Syndrome

“…In previous studies, coinfections with other porcine viruses or immunostimulation have been shown to be important in the development of clinical PMWS [1,7,8]. In contrast, a recent report demonstrated that PCV-2 could induce clinical PMWS in piglets in the absence of other swine pathogens [10]. In the case presented here, the inoculum of tissue homogenates was shown to be free from PCV-1, PPV and PRRSV.…”

The comparative profile of lymphoid cells and the T and B cell spectratype of germ-free piglets infected with viruses SIV, PRRSV or PCV2

“…In this study, we observed this outcome in only one GF animal that was inoculated with the PCV2 688 isolate (Additional file 2) while other investigators report 40% mortality in SPF animals [17] and~50% of conventional animals [18]. The extent of PCV2 viremia may also differ among GF piglets [8], colostrum-deprived piglets [16], and conventional pigs [1]. Clinical PMWS, unlike SIV and PRRSV, is often late to develop and occurs beyond the 5-6 weeks in which GF piglets can be maintained in isolators.…”

“…However, the response of T cells is generally weak [21]. Although the appearance of specific antibodies is delayed [16,21], subclinical PCV2 infection is characterized by the presence of neutralizing antibodies that correlate with protection from PCV2 infection [20].…”

“…It is characterized by weight loss, diarrhea, respiratory distress, enlarged lymph nodes and a generalized lymphopenia and loss of adaptive immunity [14][15][16][17][18]. Microscopic lesions consist of hepatitis, nephritis, damage of lymphoid tissue, and extensive lymphopenia [16][17][18]. Full expression of PMWS appears to require secondary factors such as coinfection, vaccination or other factors that activate the immune system [17][18][19].…”

“…One of these, postweaning multisystemic wasting syndrome (PMWS), is a multifactorial disease complex which develops in weaned 5-12 week-old piglets [15]. It is characterized by weight loss, diarrhea, respiratory distress, enlarged lymph nodes and a generalized lymphopenia and loss of adaptive immunity [14][15][16][17][18]. Microscopic lesions consist of hepatitis, nephritis, damage of lymphoid tissue, and extensive lymphopenia [16][17][18].…”