Griffith’s Institute for Glycomics will share in a significant US funded grant awarded by the National Institute for Health (NIH) for a two-year research project investigating the role of Vibrio cholerae (V. cholerae) in causing widespread cholera epidemics.
V. cholerae is a Gram-negative, comma-shaped bacterium/pathogen. The bacterium’s natural habitat is brackish or saltwater. Some strains of V. cholerae cause the disease cholera, which is an important public health problem worldwide, and an indicator of inequity and lack of social development.
Cholera is an acute diarrhoeal infection caused by ingestion of food or water contaminated with this bacterium. Researchers have estimated that every year there are roughly 1.3 to 4.0 million cases, and 21,000 to 143,000 deaths, worldwide due to cholera.
Cholera is an extremely virulent disease that can cause severe acute watery diarrhoea. It takes between 12 hours and 5 days for a person to show symptoms after ingesting contaminated food or water. Cholera affects both children and adults and can kill within hours if untreated.
Professor Victoria Korolik, grant recipient and one of the research leaders at the Institute for Glycomics, will be a Co-Investigator on the project in collaboration with researchers from the University of California, Santa Cruz.
“V. cholerae’s ability to cause infection and epidemics is tied to its dissemination and survival in aquatic habitats and its transmission to human hosts,’’ Professor Korolik said.
“The pathogen’s ability to form biofilms (where it collectively grows on different types of surfaces to form multi-cellular communities) is crucial for its survival in aquatic habitats between epidemics and is advantageous for host-to-host transmission during epidemics.”
In V. cholerae, a signalling molecule called c-diGMP (nucleotide cyclic dimeric guanosine monophosphate), is broadly conserved in bacteria and is a key regulator of biofilm formation. Currently, there is limited understanding of how this signalling molecule controls biofilm formation, which environmental signals modulate its levels and biofilm formation, and the consequences of its signalling in V. cholerae infectivity, transmission and dissemination.
“Through this research project, these information gaps will be addressed by focusing on two specific aims: 1) Analyse c-diGMP signalling pathways that control biofilm formation dynamics; and 2) Analyse the activation of c-diGMP signalling pathways and their consequences in the V. cholerae infection cycle. This research project seeks to further define and determine impacts of these pathways on the V. cholerae infection cycle,” added Professor Korolik.
Professor Mark von Itzstein AO, Director of the Institute for Glycomics, said: a better understanding of these signalling pathways and their role in biofilm formation could potentially lead to the development of new treatments that reduce the effect of V. cholerae biofilm-associated infections, as well as biofilm-associated infections from other pathogenic bacteria.