Description

Vibrio vulnificus is a gram-negative bacterium that is pathogenic to humans and capable of causing wound infections and primary septicemia (Gulig et al. 2005). Growth of C. elegans on pathogenic bacteria reduces their lifespan in a manner that recapitulates some aspects of the natural pathogenicity of many disease agents (for review, see Aballay and Ausubel 2002). C. elegans grown on V. vulnificus have reduced lifespans and this pathogenicity is diminished when worms are grown on V. vulnificus mutant strains defective in known virulence factors (Dhakal et al. 2006).  We set out to use this host-parasite model to better understand the role of iron transport systems in V. vulnificus pathogenicity. Normal iron transport is required for full pathogenicity in mice due to the typically iron-limiting conditions in the host environment. V. vulnificus has three paralogs of the TonB iron transport system, known as the TonB1, TonB2, and TonB3 systems, and strains with deletion mutations in tonB1 and tonB2 (ΔtonB1 ΔtonB2) are defective in iron transport (Kustusch et al. 2012). We tested whether this double mutant V. vulnificus strain would have reduced pathogenicity in C. elegans, as it does in mice. We confirmed that C. elegans grown on wildtype V. vulnificus reduced the median lifespan of animals from 12 days to 9 days. However, animals grown on the ΔtonB1 ΔtonB2 strain also had a median lifespan of 9 days and there was no statistically significant increase in survival of worms grown on the mutant strain (Fig. 1). It is possible that the iron transport systems were not essential for pathogenicity in these experiments because there was sufficient residual iron present despite the use of iron-limited CM9 plates. Further experiments with iron chelators introduced into the media are required to clarify whether the lack of dependence on iron transport is due to residual iron or a result of physiological differences between V. vulnificus infection of C. elegans intestine and its infection of the bloodstream of mice.