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B J Thacker

Publications and source records attributed to B J Thacker.

27 records · Page 2Linked to original sources

Cross-protection experiments in pigs vaccinated with Actinobacillus pleuropneumoniae subtypes 1A and 1B.

Cross-protection experiments were conducted to determine whether antigenic differences located within the lipopolysaccharides (LPS) of Actinobacillus pleuropneumoniae subtypes 1A and 1B were important with respect to the efficacy of whole cell, formalin-inactivated bacterins. Based on clinical signs, lung lesions scores and mortality rates, pigs immunized with A. pleuropneumoniae subtype 1A were partially protected against severe challenge with both subtypes 1A and 1B. In contrast, 1B vaccinated pigs were not protected against severe challenge with subtype 1A but were partially protected against 1B challenge. Cross-reactive serum antibody levels were measured with an ELISA using outer membranes of subtype 1A or 1B as the coating antigen. Serum antibodies were detected against both subtypes within 2 weeks after the first immunization. Antibody levels increased with time and were generally higher against the homologous subtype coating antigen. We conclude that antigenic variation within a capsular serotype, due to antigenic variation within LPS, can result in the failure of whole cell bacterins to provide protection against challenge with the same capsular serotype. This lack of cross-protection within a capsular serotype provides partial explanation for vaccination failures observed under field conditions.

Actinobacillus Infections↗

Antigenic differences within Actinobacillus pleuropneumoniae serotype 1.

Two distinct antigenic subtypes of Actinobacillus pleuropneumoniae serotype 1 were identified via coagglutination (Co-A) and designated as 1A and 1B. The reference strains, ATCC 27088 (1A) and ISU 158 (1B), were used to prepare hyperimmune rabbit sera for Co-A reagents. Of 75 serotype 1 field isolates tested by Co-A, 35 isolates typed as 1A, 12 as 1B and 28 as 1A/1B. Significant cross-reactivity between the 2 subtypes was found in the Co-A and was eliminated in 20/28 1A/1B strains by using Co-A reagents prepared with rabbit sera absorbed with the heterologous reference strain. However, twelve isolates (5 1A and 7 1A/1B; 16%) showed no reaction with Co-A reagents prepared with absorbed sera. Immunoblots of outer membranes (OM) prepared from APP 1A or 1B reference strains and field isolates indicated that antigenic differences between subtypes 1A and 1B were located within the high molecular weight (MW) region of the gels (40-100 kDa). Hyperimmune rabbit sera against 1A or 1B and sera from pigs vaccinated with whole-cell, formalin inactivated 1A or 1B bacterins reacted with the high MW region only in strains of the homologous subtype. In contrast, 4 of 5 sera from 1B infected pigs and 2 of 5 sera from 1A infected pigs reacted with all APP serotype 1 strains regardless of subtype. Apparently, infection exposed cross-reactive antigenic determinants that were not exposed by immunization with killed bacteria preparations. SDS-PAGE gels with LPS purified from APP 1A, 1B, 9 and 11 showed that 1A, 9 and 11 LPS O-antigens had an identical smooth ladder pattern, while 1B LPS was distinctly different. In immunoblots with OM or LPS and in dot-immunobinding assays with LPS, rabbit antiserum against APP 1A reacted with 1A, 9 and 11. In contrast, rabbit antiserum against APP 1B only reacted with APP 1B and weakly with APP 9 in the OM immunoblot and with LPS from APP 1B, 9 and 11 in the LPS immunoblot and dot-immunobinding assay. We conclude that 2 subtypes of APP serotype 1 can be distinguished based on their antigenic differences. These differences are located, at least in part, within the LPS O-antigens. LPS O-antigens from APP 1B appear more antigenically similar to APP 9 LPS than to either APP 1A or APP 11 LPS. There may also be antigenic differences in the capsular polysaccharides of APP 1A and 1B strains.(ABSTRACT TRUNCATED AT 400 WORDS)

Actinobacillus Infections↗

Polymerase chain reaction amplification of pseudorabies virus DNA from acutely and latently infected cells.

A characteristic of alphaherpesviruses, including pseudorabies virus (PRV), is that the acute phase of the disease is followed by lifelong latency. Latently infected animals are asymptomatic but can transmit reactivated virus. Corticosteroid administration, tissue explanation, blot- and in situ hybridizations have been used to demonstrate the presence of latent PRV infections. The use of blot hybridization as a convenient method for defining the incidence of PRV infections in swine herds has been hampered by the detection limit of this method. The objective of this study was to increase this sensitivity of blot hybridization by polymerase chain reaction (PCR) amplification of target sequences. Two sets of 20-mer primers were synthesized and used to amplify gX and gII glycoprotein gene sequences in two different strains of PRV. The specificity of the amplification was verified by Southern blot hybridization and restriction endonuclease analysis of the amplified fragments. Amplification of target sequences by PRC increased their detection limit by a factor of at least 10(5). Porcine ganglion samples, in which latency had been demonstrated by in vitro explanation, were analyzed by PCR together with positive and negative controls. Duplicate slot blot analyses of a portion of the amplified products were used to demonstrate latency in seven of eight samples. It was concluded that blot hybridization of PCR amplified DNA appears to be both a sensitive and convenient method for the detection of PRV induced latency.

Animals↗

Clinical, virologic, and histopathologic observations of induced porcine parvovirus infection in boars.

Twelve 8- to 12-month-old crossbred boars were inoculated with a virulent strain (NADL-8) of porcine parvovirus (PPV). Hemicastrations were performed on 6 boars 3, 7, 10, 14, 21, and 28 days after an IM injection of 10(8) median cell culture infectious dose (CCID50) of PPV (n = 3) or injection of 10(7.4) CCID50 given intratesticularly (IT, n = 3). Noninfected cell culture medium (0.25 ml) was injected into each testicle of a 7th boar (IT inoculated control). Virus or viral antigen was detected in testicular and epididymal tissues up to 14 days after inoculation. Direct immunofluorescence indicated that viral antigen was mainly associated with the vasculature of the interstitium. Microscopic lesions were not evident in the testicles and epididymides of IM inoculated boars. Acute-to-chronic testicular degeneration was evident in the IT inoculated boars, as well as in the IT inoculated control boar. Six boars were inoculated IM or orally/nasally with 10(7.9) CCID50 of PPV. Semen was collected twice weekly for 8 weeks after inoculation. Virus was not detected in any ejaculates. Semen also was collected from 4 boars for 5 weeks before inoculation, and preinoculation and post-inoculation semen quality was compared. Pronounced changes in sperm output, ejaculate volume, motility, or morphologic defects were not observed. The reproductive consequences of experimental PPV infection in boars were minimal because reproductive function was unaffected and venereal transmission of PPV was not detected.

Animals↗

Potentiating effect of adjuvants on humoral immunity to porcine parvovirus vaccines in guinea pigs.

Fourteen different adjuvants, given either in single or combined form with another compound were compared in guinea pigs for their ability to potentiate humoral immunity to porcine parvovirus (PPV) antigen after 2 vaccinations. Two injections were given, the second 3 weeks following the initial vaccination. Antibody concentrations to PPV in sera from injected animals were measured over a 5-week period by the hemagglutination inhibition test. At the conclusion of the experiment, guinea pigs injected with the following adjuvants and PPV antigen: CP-20 961 (Avridin), 50% aluminum hydroxide gel, ethylene maleic anhydride (EMA), oil and water emulsion (O/W) and dimethyl-dioctadecyl-ammonium bromide (DDA) immunologically responded with high geometric mean HI titers (380, 224 and 427, 602, 512, 1202 respectively), whereas guinea pigs receiving Emulsan, sodium dodecyl sulfate (SDS), L-121, combinations of Emulsan/aluminum hydroxide, SDS/aluminum hydroxide and B. pertussis/aluminum hydroxide responded with low mean titers (54, 64, 18, 27, 11, 64, 14, 20 respectively). Guinea pigs injected with antigen without adjuvant responded weakly with geometric mean titers of 3.3 and 16 for the 2 groups tested. Prior to booster injection, guinea pigs immunized with 13 of the preparations had low (less than 4) or undetectable antibody titers. Antibody titers from guinea pigs receiving DDA adjuvant continued to rise throughout the duration of the experiment and at the conclusion had the highest mean titers of the groups tested (1202). The 2 groups immunized with 50% aluminum hydroxide gel had high mean titers (224, 427), but in both instances there was a wide range of titers within a group evidenced by high standard deviations. In contrast, guinea pigs receiving either DDA, CP-20 961, O/W or EMA had antibody titers within a narrow range and small standard deviation. The significance of aluminum hydroxide gel concentration on immunogenicity is discussed.

Adjuvants, Immunologic↗

Swine diseases transmissible with artificial insemination.

The transport of fresh and frozen semen to be used for artificial insemination creates a mode of disease transmission between farms. Normally, semen contains a number of nonpathogenic bacterial contaminants; however, excessive bacterial contamination can result in infertile matings. Contamination with a known pathogen, eg, Brucella suis, could initiate a serious outbreak of disease in a recipient herd. Methods to minimize bacterial contamination of semen include sanitary collecting and processing of semen, isolation of boards from certain pathogens, and the addition of appropriate broad spectrum or combination antibiotics to the semen. Mycoplasmas also have been isolated from semen, although transmission by this route is unlikely. The addition of an appropriate antimycoplasmal antibiotic to semen may be warranted in some situations. Numerous viruses have been detected in semen. Their exclusion from semen is especially critical because of their ability to survive in frozen semen. These viruses include pseudorabies virus, porcine parvovirus, enterovirus, adenovirus, vesicular disease virus, and African swine fever virus. The likelihood of disease transmission is greater with the introduction of a boar into a herd than through the use of fresh or frozen semen. We believe that artificial insemination allows for the introduction of new genetics into a breeding program, with minimal risk of disease transmission.

Animals↗

In utero infection of swine fetuses with infectious bovine rhinotracheitis virus (bovine herpesvirus-1).

The pathogenesis of infectious bovine rhinotracheitis (IBR) virus (bovine herpesvirus-1) was studied in porcine fetuses after in utero inoculation. Laparotomies were performed on 8 seronegative pregnant sows at 34 to 86 days of gestation, and all fetuses in 1 uterine horn of each sow were exposed to IBR virus via inoculation into the amniotic sacs. Fetuses in the other horn served as controls. Clinical signs of infection were not observed in the sows, except for 2 sows that aborted at postinoculation days (PID) 11 and 15. Fetuses of the remaining 6 sows were collected at slaughter on PID 15 to 28. Fetuses were examined for gross abnormalities, presence of IBR virus in tissues, and the formation of neutralizing antibodies to IBR virus. Of 33 inoculated fetuses from 6 sows, 10 were mummified, 11 were hemorrhagic and/or edematous, and 12 were alive. Necrotic lesions were observed on the skin and in the liver of dead and live fetuses. Virus was recovered from 29 of 33 inoculated fetuses. Infectious bovine rhinotracheitis virus was isolated from fetal skin, liver, lungs, kidney, spleen, stomach contents, brain, amniotic fluid, and placenta. Virus was isolated from 4 of 11 fetuses recovered from 1 aborting sow. Antibodies to IBR virus were not detected in sera from the sows. However, antibodies were detected in 6 of 15 fetuses inoculated at 63 to 86 days of gestation and collected at slaughter at 86 to 112 days of gestation. The youngest fetus with detectable IBR antibody was estimated to be 74 days of gestation by measuring crown-rump length of the fetus.

Abortion, Veterinary↗

Survey of porcine parvovirus infection in swine fetuses and their dams at a Minnesota abattoir.

Reproductive tracts were recovered from 209 sow and 32 gilt carcasses at slaughter; animals had been pregnant not less than 27 days. Of 241 litters examined, 28 (11.6%) contained one or more porcine parvovirus (PPV)-infected fetuses, as determined by immunofluorescent microscopy. The frequencies in sow and gilt litters were 12.0% and 9.4%, respectively. The PPV antigen was detected in 219 of 334 (65.6%) dead or mummified fetuses and in 12 of 2,172 (0.5%) live fetuses examined. The 18 litters which contained only dead or mummified fetuses were infected with PPV. As the percentage of litter mummification increased, the likelihood of finding PPV increased. The PPV antibody was detected in ovarian follicular fluids of 94.3% of the sows and 78.1% of the gilts. These findings indicate that PPV is highly associated with fetal mummification and that some pregnant gilts and sows are susceptible to infection.

Abattoirs↗