Friday 22 March 2013

Vibrio cholerae exploits sub-lethal concentrations of a competitor-produced antibiotic to avoid toxic interactions



Vibrio cholerae exploits sub-lethal concentrations of a competitor-produced antibiotic to avoid toxic interactions

Vibrio cholerae a gram negative bacterium known to cause the disease cholera is transported in to the water column and human food mainly via detritus and planktonic organisms. These pathogens are shown to be inhibited by Vibrionales bacterium SWAT3, an exceptionally broad range inhibitor of other pelagic marine bacterial pathogens. It is able to achieve this pelagic inhibition via the secretion of the antibiotic andrimid.

This paper looks at the reaction pattern of V.cholerae to different concentrations of Andrimid, and to what levels pathogen can demonstrate avoidance behaviour before the antibiotic presence becomes lethal and the cells succumb to toxic concentrations.

The Vibrionales bacterium SWAT3 is also known to be a competitor for the same resources as the V.cholerae, this particle colonising competitor and antibiotic producer influence heavily the micro scale distribution of bacterial species. The study by Graff et al (2013) has shown V.cholerae colonising ability to be inhibited in the presence of SWAT3 to be statistically significant.  The antibiotic produced by the SWAT3 blocks the carboxyl-transfer reaction of acetyl-CoA carboxylase which the Andrimid producers show resistance.

In this study by Graff et al (2013) a growth inhibition and minimal inhibitory concentration of andrimid in agar was carried out, this showed that V.cholerae wasn’t able to colonise agar that contained SWAT3, but agar plates containing  SWAT3-III (a non-antibiotic producing mutant of SWAT3) the presence of V.cholerae was observed, demonstrating the effectiveness of SWAT3 Andrimid production on growth inhibition of these pathogenic marine bacterium.

In order to hypothesise whether andrimids function and interaction can work as chemical signal that deters V.cholerae from colonising particles; a chemotaxis assay assay was used to quantify swimming behaviour (speed and turning rates) by use of polydimethylsiloxane (PDMS) microchannels. In natural marine environments Andrimid produced by SWAT3 would act as “interspecific signalling molecules and deter particle colonisation by V.cholerae”.

Results demonstrated that swimming speeds, when exposed to sub-lethal levels of andrimid, were initially increased as a response to the inhibitor, but in lethal doses speed decreased suggesting the pathogens inability to cope, and succumbing to these toxic concentrations. A significant shift of trajectory was seen between control media and the andrimid treated media (P = 0.0006) but no significance was seen when subjected to SWAT3-III (P = 0.18).

This study was interesting in the fact that it looks at a bacteria V.cholerae, a pathogen effecting not only the marine environment but humans as well. The introduction of andrimid in to its life cycle inhibits its growth and demonstrates avoidance behavior. Such chemically mediated cell– cell interaction has direct implications for elemental cycling in the ocean as well as the spread or outbreak of diseases. This interaction has the ability to control harmful algal blooms and could aid useful future applications.

Graff, J. R., Forschner-Dancause, S. R., Menden-Deuer, S., Long, R. A., & Rowley, D. C.. 2013. Vibrio cholerae exploits sub-lethal concentrations of a competitor-produced antibiotic to avoid toxic interactions. Frontiers in microbiology, 4.

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