Research team
Neisseria meningitidis and N. gonorrhoeae are two closely related obligate human pathogens.
N. meningitidis is the causative agent of epidemic meningococcal meningitis and septic shock. It colonises mucosal surfaces of the nasopharynx and in susceptible individuals, the bacterium becomes systemic resulting in fatal bacteremia.
Vaccines based on the polysaccharide capsules have been developed to prevent community spread, and these are therefore are an effective means of reducing meningococcal disease. Serotype B remains prevalent since there is no vaccine against this organism, however.
Neisseria gonorrhoeae on the other hand, is the causative agent of the sexually transmitted disease (STD) gonorrhoea. Each year across the world, some 20-60 million new cases are reported per annum, according to the World Health Organization (WHO).
In males, gonococcal infection is generally acute and resolves rapidly with treatment. In women, however, the infection remains asymptomatic; without treatment it progresses to pelvic inflammatory disease (PID), resulting in infertility in about one-third of patients.
Unlike meningococci, this organism is increasingly resistant to antibiotics, and there are recent reports of the emergence of a “superbug” resistant to all antibiotics. Because the cell surface proteins expressed by this organism are highly antigenically variable, no successful vaccine strategies have been developed to prevent infections.
Dr Kahler’s group is interested in three different facets of these important human pathogens:
- Understanding the biosynthesis pathway and regulatory networks controlling the production of the primary toxin produced by meningococci, the endotoxin.
- Examining the regulatory networks within meningococci that are triggered during attachment to the human nasopharynx.
- The role of stress proteins in the survival of gonococci during intracellular growth in human urethral and cervical cells.
School of Biomedical, Biomolecular and Chemical Sciences
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CRICOS Code: 00126G
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Last updated:
Tuesday, 23 June, 2009 4:35 PM
