Jonathan Warawa, Ph.D.

Jonathan Warawa, Ph.D.

Research Interests

Burkholderia pseudomalleiandBurkholderia malleiare closely related bacterial pathogens that have adapted to different ecological niches, yet both produce a similar disease in susceptible hosts.  These pathogens can be acquired through several different routes of infection, leading to a rapidly fatal septicemic disease that may be difficult to treat in part due to antibiotic resistance to several classes of antibiotics. B. pseudomalleiandB. malleihave the potential for use as bioterrorism agents and have therefore been classified as select agents by government agencies, and there is no licensed vaccine currently available.

B. pseudomalleiis the causative agent of the disease known as melioidosis. B. pseudomalleican be cultured from moist soils of tropical areas worldwide and is endemic in northern Australia and Southeast Asia. B. pseudomalleiinfects a wide range of animal hosts – not limited to mammals – and is considered to be an opportunistic pathogen.  Risk factors for disease include diabetes, renal disease, thalassemia, and severe alcoholism.

Unlike its relative,B. malleiis host-adapted to solipeds (e.g. horses, mules, and donkeys), and is an obligate mammalian pathogen requiring zoonotic transfer to other hosts. B. malleicauses the diseases glanders (respiratory) and farcy (cutaneous), and was eradicated from many areas of the world through a program of systematic culling of infected animals.

The primary focus of this laboratory is to study the progression of disease ofB. pseudomalleiandB. malleiin respiratory disease models – the form of the disease most likely to be associated with bioterrorism.  We are using a combination of approaches to better understand the interactions between host and pathogen in mouse models, including:in vivoimaging, targeted mutagenesis of bacterial genes, microscopy of infected tissues, and an investigation of the host immune response.  The findings of studies conducted in this laboratory will contribute to our understanding of how these pathogens successfully colonize the host lung and disseminate to other host tissues, and identify how these pathogens succeed in overcoming the host immune response to cause disease. A better understanding of the disease process will allow us to develop novel therapeutics that will interfere with disease and favour a successful host immune response.

 

Selected Publications

Warawa JM, Long R, Rosenke R, Gardner D, Gherardini FC. “Bioluminescent diagnostic imaging to characterize altered respiratory tract colonization by theBurkholderia pseudomalleicapsule mutant.” Front. Microbio. 2011;2:133. Epub 2011 Jun 16.

Warawa JM. “Evaluation of surrogate animal models of melioidosis.” Front. Microbio.2010 Dec; 1:141. doi: 10.3389/fmicb.2010.00141.

Warawa JM, Long D, Rosenke R, Gardner D, Gherardini FC. “Role for the Burkholderia pseudomallei capsular polysaccharide encoded by the wcb operon in acute disseminated melioidosis.” Infect Immun. 2009 Dec;77(12):5252-61.

Burtnick MN, Brett PJ, Nair V, Warawa JM, Woods DE, Gherardini FC. “Burkholderia pseudomalleiType III secretion system mutants exhibit delayed vacuolar escape phenotypes in RAW 264.7 macrophages.” Infect Immun. 2008 Apr 28; 76(7):2991-3000.

Warawa J, Woods DE. “Type III secretion system cluster 3 is required for maximal virulence of Burkholderia pseudomallei in a hamster infection model.” FEMS Microbiol Lett. 2005 Jan 1;242(1):101-8.

Moore RA, Reckseidler-Zenteno S, Kim H, Nierman W, Yu Y, Tuanyok A, Warawa J, DeShazer D, Woods DE. “Contribution of gene loss to the pathogenic evolution of Burkholderia pseudomallei and Burkholderia mallei.” Infect Immun. 2004 Jul;72(7):4172-87.

Warawa J, Woods DE. "Melioidosis vaccines." Expert Rev Vaccines. 2002 Dec;1(4):477-82.