Poster Presentation Australian Society for Microbiology Annual Scientific Meeting 2019

Causal factors contributing to host immune system change in koalas immunized against chlamydial infection. (#202)

David Lizarraga 1 2 , Peter Timms 2 , Bonnie Quigley 2 , Scott Carver 1
  1. School of Natural Sciences, University of Tasmania, Sandy Bay, Tasmania, Australia
  2. School of Science and Engineering, University of Sunshine Coast, Sippy Downs, Queensland, Australia

The koala (Phascolarctos cinereus) is an iconic Australian marsupial currently experiencing localized extinctions in areas of Queensland and New South Wales. Disease is one factor contributing to this decline of this species, and arguably the most prevalent diseases in koalas are caused by infection with the intracellular pathogen, Chlamydia. Antibiotics can clear chlamydial infection, but their use is complicated by potentially eliminating beneficial bacteria in the koala gut. A chlamydial vaccine is one promising alternative to antimicrobial treatment for koalas that does not yet exist. Recent studies show that wild koalas infected with Chlamydia have a reduced chlamydial load and a lower prevalence of disease after vaccination with a multi-subunit vaccine as compared to unvaccinated koalas. Measurements of cytokine and antibody (IFNγ, IgA, IgG, IL-10, IL-17A and TNFα) abundance are available from these studies, however the effects of vaccination on these immune parameters are less understood. In this study we first created a priori hypotheses to make biologically relevant structural equation models to determine the causal factors in chlamydial load change in immunized koalas. We tested whether the data fit each a priori model using three fit indices: a Bollen-Stine bootstrap, a comparative fit index, and a root mean square of error of approximation. If multiple models fit, we chose the best fitting model based on Akaike’s information criterion relative to sample size (AICc). We found that the best model at time 0 (pre-immunization) fit IFNγ, chlamydial load, and chlamydial disease. Our model at 6 months post vaccination also supports these variables, and indicates vaccination had a strong negative effect on chlamydial load. It was not surprising that IFNγ was a core component of our models, as previous studies found IFNγ inhibits chlamydial growth in vivo and mechanisms for this have been described. Determining the effect of vaccination on IFNγ and chlamydial load will be useful to evaluate the effectiveness of future koala vaccine trials.