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Abstract Background We have previously described microscopic and electron microscopic alterations in lymphoid organs of PCV2 inoculated mice as apoptosis. In this study we wanted to investigate the molecular pathogenetic mechanism of PCV2-induced apoptosis. Eight-week old BALB/c mice were either sham inoculated (control mice) or inoculated intraperitoneally (ip) and intranasally (in) with a single (sPCV mice) or multiple (mPCV mice) doses of PCV2. Four control mice and 4 sPCV mice were sacrificed 7, 14, 28 and 42 days post inoculation (PI). All 4 mPCV mice were sacrificed 42 days PI. Following necropsy, immunohistochemistry for caspase 3 and in-situ TUNEL assay were performed on sections of spleen, lymph nodes, thymus and ileum from control, sPCV and mPCV mice. In addition, total RNA was extracted from spleens of control, sPCV and mPCV mice for simultaneous detection and semiquantitation of bcl-2 homologues and various caspase mRNAs using a multiprobe RNase protection assay system. Results PCV2 replicated and was associated with apoptosis in spleens, lymph nodes and Peyer's patches of infected BALB/c mice. Upregulation of caspase 1, 2, 3, 6, 7, 8, 11 and 12 and upregulation for the transcripts of apoptosis inhibitors bcl-2, bcl-w and bcl-X and apoptosis promoters' bax, bak and bad was detected in spleens of sPCV and mPCV mice, but not control mice. Apoptosis was further confirmed by light and electron microscopic morphology as well as by positive TUNEL assay and detection of activated caspase 3. PCV2 nucleic acid was detected by in-situ hybridization in the nuclei and cytoplasm of such apoptotic cells. Conclusion The data presented here support the hypothesis that PCV2 induces apoptosis mediated through the activation of caspases 8 and 3 in the spleens of infected mice.

In the past decade, different members of the genus Mamastrovirus have been associated with outbreaks of neurologic disease in humans, cattle, sheep, mink, and, most recently, porcine astrovirus 3 (PoAstV3) in swine. We performed a retrospective analysis of 50 cases of porcine neurologic disease of undetermined cause but with microscopic lesions compatible with a viral encephalomyelitis to better understand the role and pathogenesis of PoAstV3 infection. Nucleic acid was extracted from formalin-fixed paraffin-embedded (FFPE) tissue for reverse transcription quantitative polymerase chain reaction (RT-qPCR) testing for PoAstV3. In addition, 3 cases with confirmed PoAstV3-associated disease were assayed by RT-qPCR to investigate PoAstV3 tissue distribution. PoAstV3 was detected in central nervous system (CNS) tissue via RT-qPCR and in situ hybridization in 13 of 50 (26%) FFPE cases assayed. PoAstV3 was rarely detected in any tissues outside the CNS. Positive cases from the retrospective study included pigs in various production categories beginning in 2010, the earliest year samples were available. Based on these results, PoAstV3 appears to be a recurring putative cause of viral encephalomyelitis in swine that is rarely detected outside of the CNS at the time of clinical neurologic disease, unlike other common viral causes of neurologic disease in swine. [ABSTRACT FROM AUTHOR]

The article shows the function of Bovine viral diarrhea virus (BVDV) in progression of Porcine circovirus-2 (PCV-2). Two studies were performed, where the first one involved vaccination of germ-free pigs vaccinated with different PCV-2 and BVDV viruses. The second study looked at cesarian-derived, colostrum-derived pigs that were vaccinated with the viruses. Results showed that BVDV and PCV-2 hinder growth and caused death of pigs through developing acute respiratory distress.

Porcine circovirus type 2 (PCV2) and swine influenza virus (SIV) are important pathogens for porcine respiratory disease complex, which is economically significant worldwide. The pathogenesis of PCV2-SIV coinfection is unknown. In this study, we focused on establishing a challenge model for PCV2 to determine whether SIV influences PCV2 replication and increases the severity of PCV2-associated disease. Cesarean-derived colostrum-deprived pigs were inoculated intratracheally with cell culture medium only (negative control group), PCV2 only, or PCV2 followed 1 wk later with SIV H1N1. Two pigs from each group were necropsied at 12, 21, 28, and 35 d after inoculation. Coinfection with SIV did not increase the number of PCV2 genomic copies in serum or target tissues or the severity of microscopic lesions associated with PCV2 in lung or lymph node. The antibody titer to PCV2 did not differ significantly between PCV2-SIV- and PCV2-infected groups. In conclusion, SIV H1N1 did not influence PCV2 replication in dually infected pigs in this study.

Focal accumulations of mononuclear cells in the arterial wall of healthy humans at predilection sites for atherosclerotic lesions have been described as 'vascular-associated lymphoid tissue' (VALT). Here we investigated whether pigs (Sus scrofa), a commonly used animal model for studying cardiovascular disease, have VALT. Samples of major arteries were collected from 10 conventional crossbred pigs (age, 2 to 24 mo) and processed for routine light microscopy, immunohistochemistry, and immunofluorescence. Single or small aggregates of mononuclear cells were noted in the intima and occasionally the inner portion of the tunica media and adventitia at branching sites. The infiltrating cells were primarily CD3+CD4+ T cells, with some macrophages. No CD8+ T cells were present. Infiltrating leukocytes and overlying endothelial cells frequently expressed major histocompatibility class II molecules. Two Ossabaw pigs on low-fat diet had similar leukocytic aggregates at locations where animals of the same breed but fed a high-fat and high-cholesterol diet developed atherosclerotic lesions. Further, the densities of CD3+ T lymphocytes and in these areas were decreased in 2 sedentary and 2 exercised Ossabaw pigs on an atherogenic diet compared with conventional crossbred and Ossabaw pigs on a normal diet. This study shows that focal aggregates of lymphocytes occur in the vasculature of pigs at locations predisposed to development of atherosclerotic lesions. These cellular aggregates are similar to the structures described as VALT in human arteries and reinforce the value of the pig as a model for the study of human cardiovascular disease.

The safety and efficacy of methylene blue (MB) coated indwelling jugular vein/cranial vena cava catheter made up of polyurethane material was tested in a rat model, receiving bacterial culture suspension of Pseudomonas aeruginosa, and Staphylococcus aureus. Daily blood samples were collected from the catheter and peripheral vein for bacterial culture. The clinical parameters (rectal temperature, respiratory rate, total white blood cell count, and loss in body weight) were not different between the groups. All the rats became bacteremic with similar changes in the number of colony forming units in the catheter and peripheral samples. Histopathological lesions were not different between the groups. The findings suggest that rats receiving MB coated catheters behaved similar to non-coated catheters. Based on the results it can be concluded that for this type of gross contamination, catheter coating alone may not eliminate infection/bacteremia.

The entire genomes of 7 isolates of porcine circovirus (PCV) from pigs with congenital tremors (CT), type A2, or postweaning multisystemic wasting syndrome (PMWS) were cloned and sequenced. One isolate (CT-PCV-P7) originated from the late 1960s from a neonatal pig with CT, type A2. Two recent PCV isolates (CT-PCV-P5, CT-PCV-P6) were from 2 affected neonatal pigs, from different farms, with unrelated outbreaks of CT; type A2. Four isolates (PMWS-PCV-P1, PMWS-PCV-P2, PMWS-PCV-P3, PMWS-PCV-P4) originated from pigs with PMWS from 4 different farms. A comparative analysis of these PMWS and PCV isolates demonstrated 99% sequence identity with each other, and over 96% sequence identity with previously sequenced PCV2 isolates. The CT-PCV-P5 and CT-PCV-P6 isolates, however, shared 99% of the same identity with each other, and interestingly also with PMWS PCV isolates. There were no consistent genomic differences between PMWS and recent CT isolates. The CT-PCV-P7 showed 98% identity similarity to PK-15-derived PCV1 and demonstrated only 72% identity similarity to either CT-PCV-P5 or CT-PCV-P6. Phylogenetic analysis confirmed that the old isolate (CT-PCV-P7), and the new isolates (CT-PCV-P5, CT-PCV-P6, PMWS-PCV-P1, PMWS-PCV-P2, PMWS-PCV-P3, PMWS-PCV-P4) were correctly classified as PCV1 and PCV2, respectively.