You and Your CourseOpportunities
Research and Teaching
Our ResearchResearch Degrees
Partners and Community
Partner with JCU
- Careers and Employability
- Open Day
- Australian Institute of Tropical Health & Medicine
- Student Resources
Q Fever - a local disease
Q fever is a zoonotic disease, first described in 1935 in Queensland, Australia during an outbreak of a febrile illness among abattoir workers. It is caused by Coxiellaburnetii, a bacterium that is capable of developing spore-like structures that are extremely resistant to the effects of the environment. It is highly infectious with a single organism able to cause disease.
Q fever in humans begins as an acute febrile illness. It poses an occupational health risk to persons in contact with a range of domestic and wild animals and their products. As the disease progresses, there may be evidence of pneumonia, hepatitis or endocarditis.
Our work on Coxiella focuses on the production and screening of recombinant antigens which may provide improved diagnostic reagents and ultimately a better vaccine
- Australian wildlife as potential reservoirs of Q fever
The role of domestic animals as reservoirs for human infection is well documented. However, increasing numbers of patients without exposure to traditional animal sources are presenting. The role of native and non-native (feral) animals are being investigated as potential sources of human infection.
- The use of bioinformatics in the design of diagnostic and vaccine antigens
Q-Vax is a formlin fixed whole cell vaccine used only in Australia. Large scale culture and purification of a PC3 level organism such as C. burnetii for vaccine production is expensive and hazardous. Recombinant vaccines using antigens selected via in silico technologies are being investigated as potential alternatives.
- The role of Toll Like Receptors in the response to Coxiella burnetii infection
The resolution of C. burnetii infection relies on an effective adaptive immune response. The role of TLR’s in responses to obligate intracellular bacterial infections is not well characterised, although it has been suggested that TLR-2 and TLR-4 may have varying roles to play. Interactions between the host and the bacterium during infection are being studied.