PubMed · 12466398
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Brian Henderson, Michael Wilson, Lindsay Sharp, John M Ward. 2002. Actinobacillus actinomycetemcomitans.. https://doi.org/10.1099/0022-1317-51-12-1013
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The role of antibodies to the outer membrane protein PalA of Actinobacillus pleuropneumoniae in protective immunity was studied in pigs vaccinated with purified PalA alone and PalA in combination with toxoids of the RTX toxins ApxI and ApxII using an established challenge model with the virulent serotype 1 of A. pleuropneumoniae. Pigs that developed antibody titers against PalA after immunization were more significantly affected by challenge with A. pleuropneumoniae serotype 1. Following challenge, pigs that were immunized with PalA showed more severe respiratory symptoms, had a higher mortality rate and died faster. They also displayed much more severe lung lesions after necropsy than animals not immunized with PalA. Pigs that were immunized with toxoids of the two cytotoxins ApxI and ApxII were protected against challenge with A. pleuropneumoniae. In contrast, the protective efficacy of the ApxI and ApxII vaccine was completely lost when it was supplemented with PalA. Hence, antibodies induced against the outer membrane protein PalA of A. pleuropneumoniae aggravated the consequences of infection and counteracted the protective effect of anti-ApxI and anti-ApxII antibodies. Due to the high similarity between protein analogues of PalA from various bacteria of the Pasteurellaceae family such as P6 of Haemophilus influenzae or 16kDa Omp of Pasteurella multocida, this deleterious effect of PalA in vaccination should be taken into consideration in the development of vaccines against infections with other Pasteurellaceae.
The possibility to use acute phase proteins to monitor the elimination of a bacterial infection in pigs would facilitate an objective assessment of treatment with various antimicrobial substances. To examine this possibility, the acute phase response (IL-6, serum amyloid A (SAA), and haptoglobin) elicited by Actinobacillus pleuropneumoniae and its reduction on treatment with various antibiotics was studied in serum from specific pathogen free (SPF) pigs. Pigs were infected intranasally with A. pleuropneumoniae serotype 2, and either left as non-treated control pigs or treated with different antibiotics intramuscularly at onset of respiratory disease (20h post-infection). Pigs responded to the infection with prominent increases in activity and concentrations of IL-6, SAA, and haptoglobin. These responses were to a certain extent overlapping and covered the time span from a few hours after infection until development of detectable levels of specific antibodies (7-10 days post-infection in untreated pigs). The haptoglobin response lasted until the end of the study on day 17 and thereby partly coincided with the antibody response. Treatment with antimicrobials that effectively reduced establishment of the infection with A. pleuropneumoniae also reduced the duration of all three acute phase responses, and reduced the concentration of serum haptoglobin. In contrast, less efficacious treatments did not reduce these acute phase responses. Thus, acute phase reactants can be applied to monitor therapeutic effects of antimicrobial drugs in the pig and measurements of IL-6, SAA and haptoglobin could add valuable information about the stage of infection during a disease outbreak.
This paper describes a methodology to quantify the transmission of Actinobacillus (A.) pleuropneumoniae from subclinically infected carrier pigs to susceptible contact pigs, and to test the effect of possible interventions on the transmission. The methodology includes the design of a transmission experiment, and a method with which A. pleuropneumoniae transmission can be quantified and with which the effect of an intervention on the transmission can be tested. The experimental design consists of two parts. First, subclinically infected carrier pigs are created by contact exposure of specific-pathogen-free pigs to endobronchially inoculated pigs. Second, transmission is observed from the group of carrier pigs to a second group of susceptible contact pigs after replacing the inoculated pigs by new contact pigs. The presented analytical method is a generalised linear model (GLM) with which the effect of an intervention on the susceptibility and infectivity can be tested separately, if the transmission is observed in heterogeneous populations. The concept of the experimental transmission model is illustrated by describing an A. pleuropneumoniae transmission experiment in which the effect of vaccination on the susceptibility is quantified. Although it could not be demonstrated that vaccination has an effect on the susceptibility of pigs, it was demonstrated that nasal excretion of A. pleuropneumoniae is related to the infectivity of pigs.