• Vaccine Ontology ID: VO_0011384
• Type: Subunit vaccine
• Status: Research
• Antigen: A. pleuropneumoniae ApxIa and ApxIIa
• apxIIA gene engineering:
  • Type: Recombinant protein preparation
  • Description: The apxIIA gene was cloned from A. pleuropneumoniae serotype 5 isolated from the lungs of Korean pigs with pleuropneumonia. For the oral vaccine, S. cerevisiae expressing ApxIA antigen as well as the ApxIIA antigen were prepared (Shin et al., 2007).
  • Detailed Gene Information: Click Here.
• apxIA gene engineering:
  • Type: Recombinant protein preparation
  • Description: The apxIA gene was cloned from A. pleuropneumoniae serotype 5 isolated from the lungs of Korean pigs with pleuropneumonia. For the oral vaccine, S. cerevisiae expressing ApxIA antigen as well as the ApxIIA antigen were prepared (Shin et al., 2007).
  • Detailed Gene Information: Click Here.
• Adjuvant:
  • VO ID: VO_0000133
• Adjuvant:
  • VO ID: VO_0000139
• Vector: Saccharomyces cerevisiae
• Immunization Route: Oral immunization

• Vaccine Ontology ID: VO_0011356
• Type: Subunit vaccine
• Status: Research
• Antigen: ApxIA (Shin et al., 2007)
• apxIA gene engineering:
  • Type: Recombinant protein preparation
  • Description: The apxIA gene was cloned from A. pleuropneumoniae serotype 5 isolated from the lungs of Korean pigs with pleuropneumonia. For the oral vaccine, S. cerevisiae expressing ApxIA antigen were prepared (Shin et al., 2007)
  • Detailed Gene Information: Click Here.
• Adjuvant:
  • VO ID: VO_0000139
• Vector: Saccharomyces cerevisiae (Shin et al., 2007)
• Immunization Route: Oral immunization

• Vaccine Ontology ID: VO_0004544
• Type: DNA vaccine
• Status: Research
• Host Species as Laboratory Animal Model: Mouse
• apxIA gene engineering:
  • Type: DNA vaccine construction
  • Detailed Gene Information: Click Here.
• apxIIA gene engineering:
  • Type: DNA vaccine construction
  • Detailed Gene Information: Click Here.
• Vector: pcDNA3.1 (Chiang et al., 2009)
• 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

• Vaccine Ontology ID: VO_0002767
• Type: Live, attenuated vaccine
• Status: Research
• ApxIC gene engineering:
  • Type: Gene mutation
  • Detailed Gene Information: Click Here.
• Preparation: To construct an avirulent mutant strain by inactivation of ApxI toxin, the apxIC gene of A. pleuropneumoniae serovar 10 was inactivated by inserting a chloramphenicol resistance gene cassette into the downstream XhoI site of the apxIC gene for constructing the transfer plasmid. The transfer plasmid was introduced into the electrocompetent A. pleuropneumoniae serovar 10 for homologous recombination by electroporation. The mutant strain was obtained and identified by PCR and Southern blotting (Xu et al., 2007).
• Immunization Route: intranasal immunization

• Type: Live, attenuated vaccine
• Status: Research
• ApxIIC gene engineering:
  • Type: Gene mutation
  • Detailed Gene Information: Click Here.
• ApxIVA gene engineering:
  • Type: Gene mutation
  • Detailed Gene Information: Click Here.
• Preparation: Plasmid pENT1 was used to introduce the ΔapxIVA deletion into A. pleuropneumoniae single mutant ΔapxIIC via the single-step transconjugation system. The colonies with the correct PCR profile were confirmed by Southern blot and sequencing assays (Liu et al., 2007).
• Immunization Route: Intraperitoneal injection (i.p.)

• Vaccine Ontology ID: VO_0004607
• Type: Recombinant vector vaccine
• Status: Research
• Host Species as Laboratory Animal Model: Mice
• Vector: A mutant form of Actinobacillus pleuropneumoniae serovar strain HS93, known as HS93Tox- which lacks the genes ApxA (structural toxin) and ApxC (post-translational activating protein) (Prideaux et al., 1998).
• Preparation: The HS93Tox- mutant of the serovar 7 strain of Actinobacillus pleuropneumoniae lacks the genes encoding the toxin ApxA and the post-translational activating protein ApxC, but still has genes required for secretion, making it a good vector. A plasmid vector was created to express the ApxA gene inside the HS93Tox- mutant of A. pleuropneumoniae, so that the bacterium acts as a vector for its own natural toxin (Prideaux et al., 1998).
• Immunization Route: Intramuscular injection (i.m.)
• Virulence: Because the toxin has been attenuated, this greatly decreases the potential virulence of the vaccine.
• Description: The HS93Tox-/pIG-T1K vector strain, using an Actinobacillus pleuropneumoniae to express the AxpA gene, was shown to protect mice against Actinobacillus pleuropneumoniae challenges (Prideaux et al., 1998). ApxA gene encodes an A. pleuropneumoniae structural toxin (Prideaux et al., 1998).

• Vaccine Ontology ID: VO_0004637
• Type: Recombinant vector vaccine
• Status: Research
• Host Species for Licensed Use: Baboon
• apxIA gene engineering:
  • Type: Recombinant vector construction
  • Description: HS93Tox-/pIG-T1K, expresses the Apx structural protein in a non-activated form (Prideaux et al., 1998).
  • Detailed Gene Information: Click Here.
• Preparation: HS93Tox-/pIG-T1K, expresses the Apx structural protein in a non-activated form (Prideaux et al., 1998).
• Immunization Route: Intramuscular injection (i.m.)

• Type: Recombinant vector vaccine
• Status: Research
• Host Species for Licensed Use: Mouse
• Host Species as Laboratory Animal Model: Mice
• apxIA gene engineering:
  • Type: Recombinant vector construction
  • Description: An attenuated Salmonella Typhimurium was used to express ApxIA (Hur et al., 2016).
  • Detailed Gene Information: Click Here.
• ompA gene engineering:
  • Type: Recombinant vector construction
  • Description: An attenuated Salmonella Typhimurium was used to express OmpA (Hur et al., 2016).
  • Detailed Gene Information: Click Here.
• apxIIA gene engineering:
  • Type: Recombinant vector construction
  • Description: An attenuated Salmonella Typhimurium was used to express ApxIIA (Hur et al., 2016).
  • Detailed Gene Information: Click Here.
• apxIIIA gene engineering:
  • Type: Recombinant vector construction
  • Description: An attenuated Salmonella Typhimurium was used to express ApxIIIA (Hur et al., 2016).
  • Detailed Gene Information: Click Here.
• Immunization Route: intranasal immunization
• Description: (Hur et al., 2016)

• Vaccine Ontology ID: VO_0004786
• Type: Recombinant vector vaccine
• Status: Research
• Host Species for Licensed Use: Baboon
• apxIIA gene engineering:
  • Type: Recombinant vector construction
  • Description: A neutralizing epitope fragment of ApxIIA toxin was expressed on the cell surface of Saccharomyces cerevisiae (Kim et al., 2010).
  • Detailed Gene Information: Click Here.
• Preparation: (Kim et al., 2010) A neutralizing epitope fragment of ApxIIA toxin was expressed and immobilized on the cell surface of Saccharomyces cerevisiae for efficient vaccine development.
• Immunization Route: Oral vaccination

Mouse Response

• Host Strain: BALB/c
• Vaccination Protocol: Briefly, 15 mice per group were subcutaneously injected with 100 µg of protein extract after emulsifying with complete Freund's adjuvant (Sigma, USA). This was then followed by a boost immunization with the same amount of antigens after emulsifying with incomplete Freund's adjuvant (Sigma, USA) at 2 weeks after the initial immunization. The final immunization was performed in the same manner at 2 weeks after the boost immunization. All groups were immunized orally through an oral gavage with 4 doses of Saccharomyces cerevisiae expressing either ApxIA (group C) or ApxIIA (group D) alone or both (group E) at 10-day intervals (Shin et al., 2007).
• Challenge Protocol: Mice in each group were challenged by intraperitoneal injection of a field isolate of A. pleuropneumoniae serotype 5 at 1.45 × 10^6 CFU (minimal lethal dose, MLD) in 10 days after their final immunization, and were then monitored every 6 h for up to 72 h (Shin et al., 2007).
• Efficacy: After the challenge, the mice in group E had a significantly lower infectious burden and a higher level of protection than the mice in the other groups (p < 0.05) (Shin et al., 2007).

Mouse Response

• Host Strain: BALB/c
• Vaccination Protocol: Briefly, 15 mice per group were subcutaneously injected with 100 µg of protein extract after emulsifying with complete Freund's adjuvant (Sigma, USA). This was then followed by a boost immunization with the same amount of antigens after emulsifying with incomplete Freund's adjuvant (Sigma, USA) at 2 weeks after the initial immunization. The final immunization was performed in the same manner at 2 weeks after the boost immunization. All groups were immunized orally through an oral gavage with 4 doses of Saccharomyces cerevisiae expressing either ApxIA (group C) or ApxIIA (group D) alone or both (group E) at 10-day intervals (Shin et al., 2007).
• Challenge Protocol: Mice in each group were challenged by intraperitoneal injection of a field isolate of A. pleuropneumoniae serotype 5 at 1.45 × 106 CFU (minimal lethal dose, MLD) in 10 days after their final immunization, and were then monitored every 6 h for up to 72 h (Shin et al., 2007).
• Efficacy: The immunogenicity of the rApxIA antigen derived from the yeast was confirmed by a high survival rate and an ApxIA-specific IgG antibody response (p <0.01) (Shin et al., 2007).

Mouse Response

• Immune Response: Significant humoral immune responses were induced by this DNA vaccine through intramuscular immunization. The IgG subclass (IgG1 and IgG2a) analysis indicates that divalent DNA vaccine induces both Th1 and Th2 immune responses (Chiang et al., 2009).
• Efficacy: Animals immunized with divalent vaccine demonstrated 70% survival after challenge with a dose of 5 × 108 CFU of A. pleuropneumoniae serotype 1 ten days after 2nd boost. Survival was significantly higher than that of the negative control groups (P < 0.05). No protective efficacy was observed for pcDNA3.1 vector immunization group and PBS control group and all mice were died within 24 h (Chiang et al., 2009).
• Host Ighg1 response
  • Description: Both IgG1 and IgG2a responses were induced by divalent DNA vaccine, with IgG1 slightly higher than IgG2a. The levels of IgG1 and IgG2a were also significant compared with the negative control groups (Chiang et al., 2009).
  • Detailed Gene Information: Click Here.
• Host Ighv1-9 response
  • Description: Both IgG1 and IgG2a responses were induced by divalent DNA vaccine, with IgG1 slightly higher than IgG2a. The levels of IgG1 and IgG2a were also significant compared with the negative control groups (Chiang et al., 2009).
  • Detailed Gene Information: Click Here.

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).

Mouse Response

Mouse Response

• Host Strain: BALB/c
• Persistence: The LD50 data shown that the double mutant ΔapxIICΔapxIVA was attenuated by three-fold, compared with the single mutant HB04C− (Liu et al., 2007).
• Efficacy: Two weeks after secondary immunization, all mice were challenged with 10 LD50 of homologous (WF83) (6.0 × 107) and heterologous (1.8 × 106) (S4074) virulent A. pleuropneumonaie by intraperitoneal route. There was no mouse died in groups 1 and 2, which shown a protection efficiency of 100% against homologous challenge (Liu et al., 2007).

Mouse Response

• Vaccine Immune Response Type: VO_0001030
• Immune Response: The inoculation with HS93Tox-/pIG-T1K induced antibodies specific to the Apx gene, and this response was boosted when the mice were re-inoculated (Prideaux et al., 1998).
• Challenge Protocol: The mice inoculated with HS93Tox-/pIG-T1K strain expressing the toxin gene and the HS93Tox- not expressing the toxin gene were challenged with homologous wild-type serovar 7 and heterologous serovar 1 strains of A. pleuropneumoniae (Prideaux et al., 1998).
• Efficacy: The mice vaccinated with the HS93Tox-/pIG-T1K strain were protected against both the serovar 7 and serovar 1 challenges, but the mice only inoculated with the HS93Tox- strain not expressing the gene for the AxpA toxin received no protection against the heterologous serovar 1 challenge (Prideaux et al., 1998).

Mouse Response

• Vaccination Protocol: Mice were vaccinated with alive strain of HS93Tox-/pIG-T1K (Prideaux et al., 1998).
• Vaccine Immune Response Type: VO_0003057
• Challenge Protocol: Mice were challenged with a wild-type serovar 7, and a serovar 1 strain (Prideaux et al., 1998).
• Efficacy: Live vaccination of mice with HS93Tox-/pIG-T1K offered protection against homologous wild-type serovar 7 challenge, and also heterologous challenge with a serovar 1 strain (Prideaux et al., 1998).

Mouse Response

• Immune Response: The splenic lymphocyte proliferation and the levels of IL-4, IL-6 and IL-12 of the inoculated mice were significantly increased, and the T- and B-cell populations were also elevated. Collectively, the candidate may efficiently induce the Th1- and Th2-type immune responses.(Hur et al., 2016)

Mouse Response

• Vaccination Protocol: Oral immunization was preceded by overnight fasting of the mice (water was provided ad libitum). Freshly harvested 2.5 x 10^7 or 2.5 x 10^8 cells were dissolved into 1ml of 0.9% saline and orally administered at 200 µl/mouse through an oral gavage at 10 day intervals, 4 times (Kim et al., 2010).
• Vaccine Immune Response Type: VO_0003057
• Challenge Protocol: The immunized mice were injected intraperitoneally with 200 ml of an A. pleuropneumoniae preparation (about 1 x 10^8 CFU) or buffer control 10 days after the final immunization (Kim et al., 2010).
• Efficacy: The mice fed the recombinant epitope-expressing yeast were protected from injection of a lethal dose of A. pleuropneumoniae (Kim et al., 2010).

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).