Fermentation products as feed additives mitigate some ill-effects of heat stress in pigs.

Heat stress (HS) may result in economic losses to pig producers across the USA and worldwide. Despite significant advancements in management practices, HS continues to be a challenge. In this study, an in-feed antibiotic (carbadox, CBX) and antibiotic alternatives ( [XPC], and [SGX] fermentation products) were evaluated in a standard pig starter diet as mitigations against the negative effects of HS in pigs. A total of 100 gilts were obtained at weaning (6.87 ± 0.82 kg BW, 19.36 ± 0.72 d of age) and randomly assigned to dietary treatments (2 rooms/treatment, 2 pens/room, 6 to 7 pigs/pen). After 4 wk of dietary acclimation, half of the pigs in each dietary group (1 room/dietary treatment) were exposed to repeated heat stress conditions (RHS; daily cycles of 19 h at 25°C and 5 h at 40°C, repeated for 9 d), and the remaining pigs were housed at constant thermal neutral temperature (25°C, [NHS]). Pigs subjected to RHS had elevated skin surface temperature ( < 0.05; average 41.7°C) and respiration rate ( < 0.05; 199 breaths per minute (bpm) during HS, and overall reduced ( < 0.05) BW, ADG, ADFI, and G:F regardless of dietary treatment. Independent of diet, RHS pigs had significantly shorter ( < 0.05) jejunum villi on d 3 and d 9 compared to NHS pigs. Heat stress resulted in decreased villus height to crypt depth ratio (V:C) in pigs fed with control diet with no added feed additive (NON) and CBX diets at d 3, whereas the pigs fed diets containing XPC or SGX showed no decrease. Transcriptional expression of genes involved in cellular stress (, , , ), tight junction integrity (, , ), and immune response (, , and ) were measured in the ileum mucosa. Pigs in all dietary treatments subjected to RHS had significantly higher ( < 0.05) transcript levels of and , and an upward trend ( < 0.07) of mRNA expression. RHS pigs had higher ( < 0.05) transcript levels of and in NON diet, in XPC and CBX diets, and in SGX diet compared to the respective diet-matched pigs in the NHS conditions. Neither RHS nor diet affected peripheral natural killer () cell numbers or NK cell lytic activity. In conclusion, pigs subjected to RHS had decreased performance, and supplementation with fermentation products in the feed (XPC and SGX) protected pigs from injury to the jejunum mucosa.

Characterization of Porcine Epidemic Diarrhea Virus Isolate US/Iowa/18984/2013 Infection in 1-Day-Old Cesarean-Derived Colostrum-Deprived Piglets.

Porcine epidemic diarrhea virus (PEDV) was first recognized in North America in April 2013 and has since caused devastating disease. The objective of this study was to characterize disease and viral detection associated with an original North American PEDV isolate inoculated in neonatal piglets. Thirty-six 1-day-old cesarean-derived and colostrum-deprived piglets were randomly assigned to the control (n = 16) or challenged group (n = 20); the latter were orogastrically inoculated with 1 ml of US/Iowa/18984/2013 PEDV isolate titered at 1 × 10(3) plaque-forming units per milliliter. Rectal swabs were collected from all piglets prior to inoculation and every 12 hours postinoculation (hpi) thereafter, with 4 control and 5 challenged piglets euthanized at 12, 24, 48, and 72 hpi. One piglet had a positive real-time quantitative polymerase chain reaction test on rectal swab at 12 hpi, and all remaining piglets were positive thereafter, with highest viral quantities detected at 24 and 36 hpi. Diarrhea was evident in 30% and 100% of challenged piglets at 18 and 24 hpi, respectively. Viral antigen was detected in enterocytes by immunohistochemistry in the duodenum and ileum of piglets euthanized at 12 hpi and was apparent throughout the small intestine of all piglets thereafter, with villus height:crypt depth ratios consistently below 4:1. Viremia was confirmed in 18 of 20 pigs at euthanasia. Clinical disease was severe and developed rapidly following infection with an original North American PEDV isolate, with lesions, viremia, and antigen detection possible by 12 hpi.

Pathogenesis of porcine epidemic diarrhea virus isolate (US/Iowa/18984/2013) in 3-week-old weaned pigs.

Porcine epidemic diarrhea virus (PEDV) is associated with clinical diarrhea in naïve swine of all ages. This report describes timing of antibody generation and disease progression following infection with a US PEDV isolate by assessing fecal viral shedding, morphometric analysis of intestinal lesions, and magnitude of immunohistochemical staining. Sixty-three, 3-week-old pigs were randomly allocated into control (n=27) and challenged (n=36) groups. Challenged pigs were administered 1 mL of 1 × 10(3) PFU/mL of US/Iowa/18984/2013 PEDV isolate by oro-gastric gavage. Three control and four challenged pigs were necropsied on days post-inoculation (dpi) 1, 2, 3, 4, 7, and weekly thereafter, until study termination on dpi 35. Clinical disease, fecal shedding, body weight, and temperature were monitored during the study period. Diarrhea was observed in challenged pigs beginning for some on dpi 2, affecting a majority of pigs by dpi 6 and subsiding by dpi 10. Average daily gain was significantly lower (P<0.001) for one week post-infection in challenged pigs. PEDV was detected in feces by PCR on dpi 1 and continued in a subset of pigs until dpi 24. PEDV-specific antigen was detected in villous enterocytes of challenged pigs by immunohistochemistry (IHC) on dpi 1, 2, 3, 4, 7, and 14. Microscopic lesions included severe diffuse atrophic enteritis with significantly reduced (P<0.001) villous length observed on dpi 3, 4, and 7. Under the conditions of this study, fecal shedding of PEDV and IHC staining can precede and continue beyond the observation of clinical signs, thus increasing the risk of viral transmission.

Poor weaning transition average daily gain in pigs is not correlated with pathological or immunological markers of enteric disease during a porcine reproductive and respiratory syndrome virus outbreak.

Previous research suggests that enteric disease and poor gut health interact to decrease pig performance. Our objective was to determine if light birth weight pigs or those from the bottom 10th percentile of transition ADG (tADG) have a higher incidence of pathogen presence or enteric lesions than heavier or faster-growing contemporaries. A total of 1,500 pigs were weighed at birth and divided into 5 birth weight (BRW) categories: <1, 1 to 1.25, 1.26 to 1.5, 1.51 to 1.75, and >1.76 kg. At weaning, 1,054 random pigs were moved to a commercial wean-to-finish barn. Pigs were weighed individually at 0 and 3 wk postweaning. Transition ADG was calculated as the ADG between wk 0 and 3 postweaning. One pig from each of the 10th, 30th, and 70th percentiles of tADG was used to create 1 set of 3 pigs with the same litter size and from the same parity sow. Forty pigs from each of the 3 tADG percentiles were matched for sex, litter size, and sow parity but not BRW to create 20 matched sets of 60 pigs. This allowed for the main effects of BRW and tADG to be studied as a 5 × 3 factorial design. At 3 and 22 wk postweaning, pigs were euthanized for organ system tissue evaluation. Lung, lymph node, and digesta were analyzed for presence of pathogens and for severity of microscopic lesions (0 = not present, 1 = present, with slight erosion, 2 = present, with moderate erosion, and 3 = present and severe erosion). Data were analyzed using PROC GENMOD and GLIMMIX, where pig served as the experimental unit. The fixed effects were BRW and tADG and the random effects were pen and set. There were no BRW × tADG interactions (P = 0.16). There was no correlation (P = 0.12) between tADG and pathogen presence at either 3 or 22 wk postweaning. Incidence and severity of microscopic lesions in the large intestine at 3 wk postweaning decreased linearly with increasing tADG (P = 0.01). Lesion incidence and severity were also affected (P < 0.04) by tADG at 22 wk postweaning, with greater stomach incidence in the 10th percentile. Birth weight affected (P = 0.02) haemolytic Escherichia coli and Salmonella spp. B (includes Salmonella typhimurium) isolation at 3 wk postweaning as well as Brachyspira spp. isolation at 22 wk postweaning (P = 0.05) but in mixed directions. There were no effects (P = 0.21) of BRW or tADG on serum or ileum mucosa immune markers. In summary, it is apparent from this research that neither BRW nor tADG are likely causes of pathogen or lesion incidence.

Comparison of sesion severity, distribution, and colonic mucin expression in pigs with acute swine dysentery following oral inoculation with "Brachyspira hampsonii" or Brachyspira hyodysenteriae.

Swine dysentery is classically associated with infection by Brachyspira hyodysenteriae, the only current officially recognized Brachyspira sp. that consistently imparts strong beta-hemolysis on blood agar. Recently, several strongly beta-hemolytic Brachyspira have been isolated from swine with clinical dysentery that are not identified as B. hyodysenteriae by PCR including the recently proposed species "Brachyspira hampsonii." In this study, 6-week-old pigs were inoculated with either a clinical isolate of "B. hampsonii" (EB107; n = 10) clade II or a classic strain of B. hyodysenteriae (B204; n = 10) to compare gross and microscopic lesions and alterations in colonic mucin expression in pigs with clinical disease versus controls (n = 6). Gross lesions were similar between infected groups. No histologic difference was observed between infected groups with regard to neutrophilic inflammation, colonic crypt depth, mucosal ulceration, or hemorrhage. Histochemical and immunohistochemical evaluation of the apex of the spiral colon revealed decreased expression of sulphated mucins, decreased expression of MUC4, and increased expression of MUC5AC in diseased pigs compared to controls. No difference was observed between diseased pigs in inoculated groups. This study reveals significant alterations in colonic mucin expression in pigs with acute swine dysentery and further reveals that these and other microscopic changes are similar following infection with "B. hampsonii" clade II or B. hyodysenteriae.

Effect of porcine circovirus type 2 (PCV2) infection on reproduction: disease, vertical transmission, diagnostics and vaccination.

Porcine circovirus type 2 (PCV2) causes great economic losses in growing pigs and there are several reviews on disease manifestations and lesions associated with PCV2 in growing pigs. Reproductive failure in breeding herds, predominately associated with increased numbers of mummies and non-viable piglets at parturition, is one of the disease manifestations of PCV2 infection. Boars shed low amounts of infectious PCV2 in semen for extended time periods, and vertical transmission of PCV2 to fetuses during PCV2 viremia of the dam has been experimentally confirmed. However, intrauterine-infected piglets often are clinically normal. Nevertheless, pigs infected with PCV2 by the intrauterine route can be born viremic, possibly contributing to horizontal spread of PCV2 within the breeding herd and into the nursery. Shedding of PCV2 in semen and prevalence of intrauterine-infected piglets can both be greatly reduced by PCV2 vaccination well ahead of expected PCV2 exposure. This review is a discussion on current knowledge on the effects of PCV2 infection in the dam and in in utero fetuses, including clinical signs, lesions, diagnosis and prevention through vaccination. Infection of boars with PCV2, the potential for PCV2 transmission via semen and prevention of PCV2 shedding are also discussed.

Porcine circovirus type 2 (PCV2) vaccination is effective in reducing disease and PCV2 shedding in semen of boars concurrently infected with PCV2 and Mycoplasma hyopneumoniae.

The objectives were to determine whether the amount of porcine circovirus type 2 (PCV2) shed in semen increased in boars experimentally coinfected with Mycoplasma hyopneumoniae (MHYO), and whether PCV2 vaccination of boars prior to PCV2 exposure reduced PCV2 viremia and virus shedding in semen. Twelve specific-pathogen-free PCV2- and MHYO-naïve boars were randomly and equally assigned to one of four groups. Six boars were vaccinated against PCV2 (VAC) on Day 0; three PCV2 vaccinated and three non-vaccinated boars were inoculated with MHYO on Day 21, and all boars were challenged with PCV2 on Day 35. The four treatment groups included PCV2-Infected (I), VAC-PCV2-I, MHYO-PCV2-Coinfected (CoI), and VAC-MHYO-PCV2-CoI. Semen, blood swabs, feces, and serum samples were collected weekly until Day 70. All vaccinated boars had seroconverted to PCV2 by Day 35. Between Days 28 and 35, MHYO boars developed moderate respiratory disease, characterized by coughing, respiratory distress, mucopurulent nasal discharge and loss of body condition. One MHYO-PCV2-CoI boar died on Day 50. Boars in the PCV2-I and MHYO-PCV2-CoI groups had significantly higher PCV2 DNA loads in blood swabs than the remaining boars. Moreover, PCV2 vaccination significantly reduced the incidence and amount of PCV2 shedding in semen and feces. In summary, although concurrent MHYO infection did not influence PCV2 shedding patterns, coinfection of boars with PCV2 and MHYO resulted in severe clinical disease and viral shedding was significantly decreased by PCV2 vaccination.

Experimental reproduction of porcine circovirus type 2 (PCV2)-associated enteritis in pigs infected with PCV2 alone or concurrently with Lawsonia intracellularis or Salmonella typhimurium.

Porcine circovirus (PCV)-associated disease (PCVAD) has emerged to become one of the most economically important pig diseases globally. One of the less commonly recognized clinical manifestations of PCVAD is PCV2 type 2 (PCV2)-associated enteritis in growing pigs; however, experimental confirmation of the ability of PCV2 alone or PCV2 coinfection with other agent(s) to induce enteritis is lacking. In this study, 120 specific-pathogen-free (SPF) pigs were divided randomly into six groups: controls (negative control pigs), PCV2 (inoculated with PCV2), LAW (inoculated with Lawsonia intracellularis), SALM (inoculated with Salmonella typhimurium), PCV2-LAW (concurrently inoculated with PCV2 and Lawsonia intracellularis) and PCV2-SALM (concurrently inoculated with PCV2 and Salmonella typhimurium). One half of the pigs in each group were subject to necropsy examination 14 days postinoculation (dpi) and the remaining pigs were examined at 28 dpi. The average daily weight gain was not different (P>0.05) between groups. Individual pigs inoculated orally with PCV2 regardless of coinfection status (2/10 PCV2, 1/10 PCV2-LAW, 3/10 PCV2-SALM) developed PCVAD with diarrhoea and reduced weight gain or weight loss between 14 and 28 dpi. Those pigs had characteristic microscopic lesions in lymphoid and enteric tissues associated with abundant PCV2 antigen. Enteric lesions were characterized by necrosuppurative and proliferative enteritis with crypt elongation and epithelial hyperplasia in LAW and PCV2-LAW pigs by 14 dpi, ulcerative and necrosuppurative colitis in SALM and PCV2-SALM pigs by 14 dpi, and lymphohistiocytic enteritis with depletion of Peyer's patches in PCV2, PCV2-SALM and PCV2-LAW pigs by 28 dpi. To the authors' knowledge, this is the first report documenting that under experimental conditions, PCV2 can induce enteritis independently from other enteric pathogens and that oral challenge is a potentially important route and perhaps the natural route of PCV2 transmission in growing pigs.

Shedding and infection dynamics of porcine circovirus type 2 (PCV2) after experimental infection.

The objective of this study was to determine the amount and infectivity of porcine circovirus type 2 (PCV2) shed in nasal, oral and fecal secretions following experimental infection. Fecal, oral and nasal swabs and blood were collected at regular intervals until 69 days post-inoculation (DPI) from five PCV2-experimentally inoculated pigs (Trial 1). To assess the infectivity of the PCV2 present in excretions, secretions, and on a hypodermic needle, 26 PCV2-naïve pigs (Trial 2) were inoculated with various samples obtained from Trial 1 pigs. In Trial 1, PCV2 DNA was detected in all sample types by 69 DPI. There were no differences in the amount of PCV2 DNA present in different sample types over time. In Trial 2, intraperitoneal inoculation with contaminated fecal, nasal and oral samples; intranasal inoculation of nasal secretions; and feces fed to naïve animals resulted in viremia and seroconversion. Viremia and microscopic lesions were noted in one animal injected using a contaminated needle. In conclusion, experimental PCV2 exposure results in a long term infection. PCV2 is shed in similar amounts by nasal, oral and fecal routes and is infectious to naïve pigs confirming that multiple routes of transmission are likely important in spread of PCV2 between pigs.

Shedding and infection dynamics of porcine circovirus type 2 (PCV2) after natural exposure.

The objective of this study was to determine the amount of porcine circovirus type 2 (PCV2) shed in nasal, oral and fecal secretions over time following natural PCV2 infection. Fecal, oral and nasal swabs and blood were collected at regular intervals starting at 28 days post-farrowing (DPF) until 209 DPF from four pigs naturally infected with PCV2. PCV2 DNA was detected in all sample types. There were no differences in the amount of PCV2 DNA present in different sample types over time. PCV2 DNA was detectable in sera and secretions in pigs through 209 DPF. Natural exposure to PCV2 results in a long term infection and PCV2 is shed in similar amounts by nasal, oral and fecal routes.

Efficacy of experimentally produced spray-dried plasma on infectivity of porcine circovirus type 2.

The value of incorporating spray-dried plasma (SDP) into the diet of weanling pigs to improve feed intake and growth performance has been well documented. However, limited work has been done to confirm that the spray-drying process eliminates all viral contaminates including porcine circovirus type 2 (PCV2). To determine the effect of spray-drying on PCV2 infectivity, colostrum-fed, crossbred, specific-pathogen-free (SPF) pigs were inoculated with PCV2-contaminated SDP intraperitoneally (SDP-IP) or by oral gavage (SDP-OG), inoculated intraperitoneally with PCV2-positive plasma (POS), or left uninoculated (NEG). The plasma used for the experimentally produced SDP was collected from a SPF pig experimentally infected with a PCV2b isolate. Pigs in the NEG group remained seronegative, and PCV2 viremia was not detected. All pigs in the POS group became PCV2 viremic by 14 d postinoculation (DPI) and seroconverted by 28 DPI. In the SDP-IP group, all pigs became viremic by 35 DPI and seroconverted by 49 DPI. In the SDP-OG group, all animals became viremic by 35 DPI and 2/3 pigs seroconverted by 35 DPI. There were no significant (P > 0.05) differences between anti-PCV2-IgG antibody sample-to-positive ratios among pigs in the POS, SDP-OG, or SDP-IP groups. This work provides direct evidence that the experimental spray-drying process used in this study was not effective in inactivating PCV2b in the plasma of a PCV2-infected pig based on a swine bioassay using PCV2-naïve pigs. This work suggests that SDP sourced from pigs could represent a biosecurity risk for the industry.

Evaluation of the safety of four porcine circovirus type 2 tissue homogenate vaccines in a pig bioassay.

Ten four-week-old porcine circovirus type 2 (PCV-2) naive piglets were housed individually in a HEPA-filtered isolator and were randomly assigned to one of six treatment groups. Each of the two pigs in groups 1 to 4 received two intramuscular doses of 2 ml of one of four different autogenous tissue homogenate vaccines (THVs) 14 days apart, and the other two pigs received 2 ml of PCV-2 virus or sterile phosphate buffered saline. When the piglets were euthanased 14 days after the second dose, the injection sites were grossly and microscopically free of swelling, an inflammatory response or abscesses. The positive control pig, one of the two pigs in the THV-2 group and both pigs in the THV-3 group became viraemic. The PCV-2 DNA from the positive control pig and the pigs in the THV-3 group was identical to the PCV-2 DNA that they had been administered.

Multicentric T-cell lymphosarcoma in a white-tailed deer (Odocoileus virginianus).

An adult female white-tailed deer (Odocoileus virginianus) with a history of shaking, ataxia, and severe debilitation was submitted for examination. Macroscopic lesions included severe emaciation, severe abdominal and mesenteric lymphadenopathy, and several rumen-associated masses. Microscopically, the ruminal masses and lymph nodes were infiltrated by pleomorphic neoplastic lymphocytes. Similar lymphoblasts were associated with the leptomeninges, choroid plexus, and the intestinal mucosa; these cells were intensely positive for CD3 antigen, indicating their T-cell origin. Lymphoproliferative viruses (bovine leukemia virus and malignant catarrhal fever virus) or epizootic hemorrhagic disease virus were not detected by polymerase chain reaction. To our knowledge, this case represents the first report of the immunophenotype of a multicentric lymphosarcoma, metastasis involving the brain, and epitheliotropic lymphoblasts in a white-tailed deer.

Effect of natural or vaccine-induced porcine circovirus type 2 (PCV2) immunity on fetal infection after artificial insemination with PCV2 spiked semen.

The objectives of this study were to determine if vaccination against porcine circovirus type 2 (PCV2) or previous PCV2 infection of the dam are sufficient to prevent fetal infection when dams are artificially inseminated with PCV2-spiked semen. Nine sows (Sus domestica) were allocated into three groups of three dams each: The PCV2 naïve negative control Group 1 was artificially inseminated with extended PCV2 DNA negative semen during estrus, whereas the extended semen used in the vaccinated Group 2 (PCV2 vaccine was given 8 wk before insemination) and PCV2-exposed Group 3 (infected with PCV2 12 wk before insemination) was spiked with 5 mL of PCV2 inoculum with a titer of 10(4.2) tissue culture infectious dose (TCID(50)) per milliliter at each breeding. The dams in the vaccinated and PCV2-exposed groups were positive for PCV2 antibody but negative for PCV2 DNA in serum at the time of insemination. Three negative control dams, two vaccinated dams, and three dams with previous PCV2 exposure became pregnant and maintained pregnancy to term. After artificial insemination, viremia was detected in one of three vaccinated dams and in two of three dams with previous PCV2 exposure. At farrowing, PCV2 infection was not detected in any piglets or fetuses expelled from the negative control dams or from dams with previous PCV2 exposure. In litters of the vaccinated dams, 15 of 24 live-born piglets were PCV2 viremic at birth, with 6 of 26 fetuses having detectable PCV2 antigen in tissues. In conclusion, vaccine-induced immunity did not prevent fetal infection in this sow model using semen spiked with PCV2.

Effect of porcine circovirus type 2 (PCV2) vaccination of the dam on PCV2 replication in utero.

The aims of this study were to determine if porcine circovirus type 2 (PCV2) vaccination of the dam is effective in preventing fetal PCV2 infection and reproductive failure. Twelve pregnant, PCV2-naïve sows were randomly divided into four groups, with three sows in each group. Group 1 sows served as noninoculated, nonvaccinated negative controls, group 2 sows were vaccinated with a commercially available PCV2 vaccine at 28 days of gestation and were not inoculated, group 3 sows were vaccinated at 28 days of gestation and inoculated with PCV2b at 56 days of gestation, and group 4 sows were inoculated with PCV2b but were not vaccinated. Serum samples from all sows were collected weekly throughout the gestation period, and sows were allowed to farrow naturally. At parturition, sow colostrum samples, presuckle serum samples, and tissues from the piglets were collected. Reproductive failure was not observed under the study conditions. PCV2 vaccination induced PCV2-specific immunoglobulin G and serum neutralizing antibodies in sows from groups 2 and 3 and prevented detectable PCV2 viremia in the dams after challenge. In group 3, PCV2 DNA was detected in colostrum samples, fetuses, and live-born pigs; however, microscopic lesions and PCV2-specific antigen were not present in any of the fetuses in this group. The results from this study indicate that vertical transmission of PCV2 can occur in PCV2-vaccinated dams.

Reproductive failure experimentally induced in sows via artificial insemination with semen spiked with porcine circovirus type 2.

Porcine circovirus type 2 (PCV2) is associated with reproductive failure in female pigs. However, the association of PCV2-positive semen in the pathogenesis has not been elucidated. The objectives of this study were to determine whether semen spiked with PCV2 causes infection in PCV2-naïve, mature female pigs and whether delivery of PCV2 via artificial insemination causes reproductive failure or fetal infection. Nine sows were randomly allocated into 3 groups of 3 sows each and artificially inseminated with PCV2 DNA-negative semen (group 1), PCV2 DNA-negative semen spiked with PCV2a (group 2), or PCV2b (group 3). All sows in groups 2 and 3 developed PCV2 viremia 7 to 14 days after insemination. None of the group 2 sows became pregnant, whereas all group 3 sows (3/3) farrowed at the expected date. At parturition, presuckle serum samples were collected, and live-born piglets, stillborn fetuses, and mummified fetuses were necropsied. All live-born piglets (n = 8) in group 3 were PCV2 viremic at birth. Stillborn fetuses (n = 2) had gross lesions of congestive heart failure. Mummified fetuses (n = 25) varied in crown-rump length from 7 to 27 cm, indicating fetal death between 42 and 105 days of gestation. PCV2 antigen was detected in the myocardium by immunohistochemistry of 7/8 (88%) live-born piglets, 2/2 (100%) of the stillborn fetuses, and 25/25 (100%) of the mummified fetuses. In addition, 4/25 mummified fetuses had PCV2 antigen associated with smooth muscle cells and fibroblasts. The results of this study indicate that intrauterine administration of PCV2 causes reproductive failure in naïve sows.

Difference in severity of porcine circovirus type two-induced pathological lesions between Landrace and Pietrain pigs.

Anecdotal information from the field suggests that there are host genetic differences in susceptibility to porcine circovirus type 2 (PCV2) associated disease among Landrace and Pietrain breeds. The objective of this study was to determine if a difference exists in PCV2 susceptibility between Landrace and Pietrain pigs under experimental conditions. Thirty-nine Landrace pigs and 39 Pietrain pigs were blocked by breed, sire, dam, and litter and randomly divided into the following 4 groups: Landrace noninoculated negative control (Landrace-NEG; n = 13), Pietrain noninoculated negative control (Pietrain-NEG; n = 13), Landrace-PCV2 (n = 26; Landrace), and Pietrain-PCV2 (n = 26; Pietrain). After waning of passively acquired anti-PCV2 antibodies, Landrace-PCV2 and Pietrain-PCV2 groups were inoculated with PCV2 isolate ISU-40895. The Landrace-NEG and Pietrain-NEG groups were housed in a separate room, remained noninoculated, and served as negative controls. All pigs in all groups were necropsied at 21 d post PCV2-inoculation. Onset of seroconversion and concentrations of anti-PCV2-IgM, anti-PCV2-IgG, and anti-PCV2 neutralizing antibodies were similar in Landrace-PCV2 and Pietrain-PCV2 groups. Furthermore, the amount of PCV2 DNA and cytokine concentrations in serum and plasma samples were not different between the 2 PCV2-inoculated groups. The severity of PCV2-associated microscopic lesions was different between Landrace and Pietrain pigs; Landrace-PCV2 pigs had significantly (P < 0.05) more severe lymphoid lesions than the Pietrain-PCV2 pigs. Although the pigs originated from the same farm where their dams were commingled, passively acquired anti-PCV2-antibodies waned in Pietrain pigs by approximately 12 wk of age, whereas the majority of the Landrace pigs remained PCV2 seropositive until 18 wk of age and beyond. The results from this study indicate that a genetic difference exists between these 2 breeds of pigs in susceptibility to PCV2-associated lesions.

Comparison of efficacy of commercial one dose and two dose PCV2 vaccines using a mixed PRRSV-PCV2-SIV clinical infection model 2-3-months post vaccination.

The study objectives were to compare the duration of immunity of commercially available, one and two dose, killed porcine circovirus type 2 (PCV2) vaccines. Sixty, 3.5-week-old pigs were randomly divided into six treatment groups: one dose vaccines (FDAH-1, BIVI-1), two dose vaccines (Intervet-2, FDAH-2), and non-vaccinated negative and positive controls. Tissue homogenate challenge was conducted 63 (two doses) or 84 (one dose) days post vaccination. Viremia was reduced by 78.5% in pigs vaccinated with one dose and by 97.1% in pigs vaccinated with two dose products and overall microscopic lymphoid lesions were reduced by 78.7% and 81.8%, respectively.

Differences in virulence among porcine circovirus type 2 isolates are unrelated to cluster type 2a or 2b and prior infection provides heterologous protection.

Porcine circovirus type 2 (PCV2) is divided into two genetic clusters designated PCV2a and PCV2b. The objectives of this study were to determine whether isolates from different clusters vary in virulence and to determine whether infection with PCV2a isolates induces protective immunity against subsequent infection with a recent PCV2b isolate. One-hundred and thirteen conventional specific-pathogen-free (SPF) pigs were assigned randomly to treatment groups and rooms: pigs inoculated with PCV2a cluster isolates (ISU-40895 or ISU-4838), pigs inoculated with PCV2b cluster isolates (NC-16845 or Can-17639) and uninoculated pigs. Necropsies were performed at 16 or 51 days post-inoculation (p.i.). There were no significant differences in PCV2-associated lymphoid lesions between PCV2a and PCV2b clusters; however, within the same cluster, significant differences were found between isolates: ISU-4838- and Can-17639-inoculated pigs had significantly (P<0.05) less severe lesions compared with ISU-40895- and NC-16845-inoculated pigs. To evaluate cross-protection, six pigs within each group were challenged at 35 days p.i. with an isolate from the heterologous cluster and were necropsied 51 days p.i. The severity of PCV2-associated lesions was reduced in pigs with prior exposure to an isolate from the heterologous cluster in comparison with singly inoculated pigs. Results indicate that the virulence of PCV2a and PCV2b isolates is not different in the conventional SPF pig model; however, the virulence of isolates within the same cluster differs. Increased virulence as reported to be associated with PCV2b isolates in the field was not observed under the conditions of this study. Moreover, cross-protection between PCV2a and PCV2b exists.

Effect of porcine circovirus type 2 (PCV2) vaccination on porcine reproductive and respiratory syndrome virus (PRRSV) and PCV2 coinfection.

The objectives were to determine if PCV2 vaccination is effective in reducing disease and lesions associated with PRRSV and PCV2 coinfection and if there is a difference between intradermal (ID) and intramuscular (IM) route of PCV2 vaccination. Seventy-four, 21-day-old pigs were randomly allocated into one of six groups. On day 0, pigs were vaccinated with 2ml Suvaxyn PCV2 One Dose (Fort Dodge Animal Health, Inc.) by intramuscular (VAC-M-COINF) or intradermal (VAC-D-COINF) routes. On day 28, pigs were either singularly (PRRSV-only, PCV2-only) or coinfected (COINF) with PRRSV and PCV2. All pigs in all groups were necropsied on day 42. All vaccinated pigs seroconverted (IgM, IgG, and neutralizing antibodies) to PCV2 between 14 and 28 days post-vaccination. After challenge, all groups inoculated with PRRSV had reduced average daily gain compared to CONTROLS and PCV2-only (P<0.001). COINF pigs had significantly (P<0.05) reduced anti-PCV2-IgG antibody levels and neutralizing antibody levels compared to both vaccinated groups. COINF pigs had more severe lung lesions compared to VAC-M-COINF (P<0.05). COINF pigs had higher amounts of PCV2 DNA in serum samples and feces (P<0.05) and increased amounts of PCV2 in lymphoid tissues (P<0.05) compared to both vaccinated groups. In summary, PCV2 vaccination was effective at inducing a neutralizing antibody response and significantly reducing PCV2-associated lesions and PCV2 viremia in pigs coinfected with PCV2 and PRRSV. Differences between intradermal and intramuscular routes of vaccine administration were not observed.