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Vaccine Comparison

A. pleuropneumoniae HS93C-Ampr Actinobacillus pleuropneumoniae apxIA mutant vaccine Actinobacillus pleuropneumoniae apxIIIB and apxIIID double mutant vaccine Actinobacillus pleuropneumoniae ureC and apxIIA double mutant deletion vaccine rS.C-APP-ApxI/ApxII
Vaccine Information Vaccine Information Vaccine Information Vaccine Information Vaccine Information
  • Vaccine Ontology ID: VO_0011385
  • Type: Live, attenuated vaccine
  • Status: Research
  • Antigen: A. pleuropneumoniae ApxII-activating protein, ApxIIC
  • ApxIIC gene engineering:
    • Type: Gene mutation
    • Description: Site-specific mutagenesis of the apxIIC gene utilized the recombination plasmid pEP-CAmpr. Cesium chloride-purified pEP-CAmpr DNA was isolated from E. coli and linearized with ClaI. Following digestion, the DNA was purified by phenol-chloroform extraction and ethanol precipitated. A total of 3 μg of linearized DNA was electroporated (0.2-cm-diameter cuvettes; 400 Ω; 1.25 kV) into A. pleuropneumoniae HS93 (serovar 7, ApxII) (Prideaux et al., 1999).
    • Detailed Gene Information: Click Here.
  • Vector: A. pleuropneumoniae serovar 7 strain HS93
  • Immunization Route: Intramuscular injection (i.m.)
  • Vaccine Ontology ID: VO_0002766
  • Type: Live, attenuated vaccine
  • Status: Research
  • apxIA gene engineering:
    • Type: Gene mutation
    • Description: This apxIA mutant is from Actinobacillus pleuropneumoniae (Xu et al., 2006).
    • Detailed Gene Information: Click Here.
  • Immunization Route: intranasal immunization
  • Type: Live, attenuated vaccine
  • Status: Research
  • apxIIIB gene engineering:
    • Type: Gene mutation
    • Detailed Gene Information: Click Here.
  • apxIIID gene engineering:
    • Type: Gene mutation
    • Detailed Gene Information: Click Here.
  • Preparation: An apxIIIBD mutant (1536∆B∆D) was selected and the correct mutation was verified by PCR using three primer pairs. The X3BD-F2 and X3BD-R2 primer pair was designed to produce products of 3720 and 4365 bps from the wild-type 1536 and 1536∆B∆D genomes, respectively (Park et al., 2009).
  • Immunization Route: intranasal immunization
  • Type: Live, attenuated vaccine
  • Status: Research
  • apxIIA gene engineering:
    • Type: Gene mutation
    • Detailed Gene Information: Click Here.
  • ureC gene engineering:
    • Type: Gene mutation
    • Detailed Gene Information: Click Here.
  • Preparation: To construct the A. pleuropneumoniae serotype 2 isogenic mutant, 12 clinical isolates were tested initially with respect to their amenability to genetic manipulation via conjugation and cointegration of pBMKUΔ1 (Tonpitak et al., 2002).
  • Immunization Route: aerosol immunization
  • Vaccine Ontology ID: VO_0004785
  • Type: Recombinant vector vaccine
  • Status: Research
  • Host Species for Licensed Use: Baboon
  • apxIA gene engineering:
    • Type: Recombinant vector construction
    • Description: S. cerevisiae expressing either ApxI or ApxII (Shin et al., 2013).
    • Detailed Gene Information: Click Here.
  • apxIIA gene engineering:
    • Type: Recombinant vector construction
    • Description: S. cerevisiae expressing either ApxI or ApxII (Shin et al., 2013).
    • Detailed Gene Information: Click Here.
  • Preparation: The surface-displayed ApxIIA#5 expressing S. cerevisiae and the ApxIA expressing S. cerevisiae (Shin et al., 2013).
  • Immunization Route: Oral immunization
Host Response Host Response Host Response Host Response Host Response

Mouse Response

  • Persistence: An apxIA mutant is attenuated in mice (Xu et al., 2006).
  • Efficacy: An apxIA mutant offered a level of cross-serovar protection against A. pleuropneumoniae infection in mice (Xu et al., 2006).

Pig Response

  • Vaccination Protocol: Nine 6-week-old pigs received 109 CFU of the A. pleuropneumoniae vaccine strain in 1 ml of growth medium, via intranasal inoculation on day 0, while nine control pigs received 1 ml of BHI. The vaccine was prepared by inoculating 10 ml of BHI-NAD (10 μg/ml) with a single colony of the vaccine strain and growing with shaking at 37°C until an OD600 of 0.8 was reached. The vaccination schedule was repeated on day 14. On day 28, the nine vaccinated and nine control pigs were divided into groups of six and three (Prideaux et al., 1999).
  • Challenge Protocol: Two groups of six pigs (i.e., vaccinated and unvaccinated) were challenged with 2 × 109 A. pleuropneumoniae HS25 (serovar 1) in 2 ml of growth medium via the intranasal route, while the groups of three were given 2 ml of BHI broth in a similar manner. The challenge strain was prepared by inoculating a single colony of HS25 into BHI-NAD (10 μg/ml) and growing until an OD600 of 0.8 was reached. At this time the viable count was 109 CFU/ml. At 5 days postchallenge, pigs were euthanized, and the number and severity of lung lesions were recorded (Prideaux et al., 1999).
  • Efficacy: Pigs vaccinated with live HS93C- Ampr via the intranasal route were protected against a cross-serovar challenge with a virulent serovar 1 strain of A. pleuropneumoniae (Prideaux et al., 1999).

Pig Response

  • Persistence: An apxIA mutant is attenuated in pigs (Xu et al., 2006).
  • Efficacy: An apxIA mutant offered a level of cross-serovar protection against A. pleuropneumoniae infection in pigs (Xu et al., 2006).

Pig Response

  • Persistence: The LD50 of 1536∆B∆D in mice was 6.9 x 108 CFU, while that of the wild-type was 4.0 x 108 CFU, showing that the mutation of the apxIIIBD genes attenuates the lethality of A. pleuropneumoniae in mice (Park et al., 2009).
  • Efficacy: To evaluate the ability of the mutant 1536∆B∆D strain to protect mice against lethal challenge, mice were immunized with 1536∆B∆D twice and challenged with a lethal dose of wild-type A. pleuropneumoniae 1536. Eight of the nine mice immunized with 1536∆B∆D survived for more than 72 hr after lethal challenge (89% protection), while all eight of the unimmunized mice died by 72 hr after challenge (Park et al., 2009).

Pig Response

  • Persistence: In all pigs, an immune response could be detected in the detergent extract enzyme-linked immunosorbent assay (ELISA), and only in the wild-type group six of seven pigs showed elevated levels (>10 ELISA units [EU]) in the ApxIIA ELISA 3 weeks after challenge. These results showed that the A. pleuropneumoniae double-mutant strain is highly attenuated and that the group infected with the mutant strain can be discriminated from the wild-type-infected group based on the ApxIIA ELISA (Tonpitak et al., 2002).
  • Efficacy: A single aerosol application of the attenuated double mutant resulted in protection from clinical disease comparable to that obtained with two applications by using a conventional bacterin vaccine. In addition, immunized pigs were protected significantly from colonization of the lungs (Tonpitak et al., 2002).

Pig Response

  • Vaccination Protocol: Three groups were designated as the untreated pigs (n = 5, control), the pigs fed with the vector-only S. cerevisiae (n = 5, vector control), and the experimental pigs fed with the ApxIA expressing S. cerevisiae and the surface-displayed ApxIIA#5 expressing S. cerevisiae at a time (n = 10, vaccinated group), respectively. The yeast vaccines were followed by three-time administrations with ApxIA (1.5 × 109 CFU) and ApxIIA (1.5 × 109 CFU) with one week interval (Shin et al., 2013).
  • Vaccine Immune Response Type: VO_0003057
  • Challenge Protocol: The pigs were challenged intranasally one week after final vaccination with a dose (1.5 × 109 CFU) of A. pleuropneumoniae serotype 5 Korean isolate from a pig with porcine pleuropneumonia (Shin et al., 2013).
  • Efficacy: The vaccinated pigs showed higher specific IgG- and IgA-related antibody activities than the non-treated control and vector control pigs. Additionally, the induced immune responses were found to protect pigs infected with A. pleuropneumoniae according to the analysis of clinical signs and the gross and microscopic pulmonary lesions (Shin et al., 2013).
References References References References References
Prideaux et al., 1999: Prideaux CT, Lenghaus C, Krywult J, Hodgson AL. Vaccination and protection of pigs against pleuropneumonia with a vaccine strain of Actinobacillus pleuropneumoniae produced by site-specific mutagenesis of the ApxII operon. Infection and immunity. 1999; 67(4); 1962-1966. [PubMed: 10085043].
Xu et al., 2006: Xu F, Chen X, Shi A, Yang B, Wang J, Li Y, Guo X, Blackall PJ, Yang H. Characterization and immunogenicity of an apxIA mutant of Actinobacillus pleuropneumoniae. Veterinary microbiology. 2006; 118(3-4); 230-239. [PubMed: 16930871].
Park et al., 2009: Park C, Ha Y, Kim S, Chae C, Ryu DY. Construction and characterization of an Actinobacillus pleuropneumoniae serotype 2 mutant lacking the Apx toxin secretion protein genes apxIIIB and apxIIID. The Journal of veterinary medical science / the Japanese Society of Veterinary Science. 2009; 71(10); 1317-1323. [PubMed: 19887737].
Tonpitak et al., 2002: Tonpitak W, Baltes N, Hennig-Pauka I, Gerlach GF. Construction of an Actinobacillus pleuropneumoniae serotype 2 prototype live negative-marker vaccine. Infection and immunity. 2002; 70(12); 7120-7125. [PubMed: 12438394].
Shin et al., 2013: Shin MK, Kang ML, Jung MH, Cha SB, Lee WJ, Kim JM, Kim DH, Yoo HS. Induction of protective immune responses against challenge of Actinobacillus pleuropneumoniae by oral administration with Saccharomyces cerevisiae expressing Apx toxins in pigs. Veterinary immunology and immunopathology. 2013; 151(1-2); 132-139. [PubMed: 23206402].