As we’ve learnt, Vibrio cholerae is a marine bacterium common in estuarine environments and is the causative agent of cholera. V. cholerae enters the human gastro intestinal (GI) tract through contaminated water, passing the gastric acid barrier and mucin layer of the small intestine and adheres to the epithelial lining. Once here, the bacteria quickly reproduces and becomes pathogenic, secreting the cholera toxin and causing acute diarrhoea in the host. Each diarrheal episode purges huge numbers of V. cholerae, reaching counts of up to 109 CFUs ml-1, leading to cholera epidemics and responsible for over 120,000 fatalities each year. In addition to diarrhoea, cholera also frequently causes vomiting and it is reported that symptoms are more severe in people suffering from malnutrition. It is therefore very unlikely that digested food is a key nutrient source for V. cholerae cells in the human host, begging the question; how does V. cholerae reach such high numbers so quickly?
During the onset of colonisation, energy sources such as the mucus layer coating the GI tract and sialic acids of mucous membranes are likely, however it is not clear whether these would provide sufficient requirements for the rapid multiplication and growth of V. cholerae in between diarrheal purges. Pukatzki & Provenzano (2013) hypothesise that V. cholerae employ a Type VI secretion system (T6SS) to engage in intraguild predation (e.g. predation of neighbouring species or strains competing for the same resources) to supplement their high energy requirements.
Predatory bacteria have been well documented and are best characterised by Bdellovibrionaceae that infiltrate the periplasm of gram negative bacteria and consume the macromolecules as a nutrient source. Myxobacteria have also been shown to illicit bacteriocidal tendencies, killing and converting prey cells into growth straits and T6SS genes have been identified in Myxococcus Xanthus. All V. cholerae strains sequenced to date have genes for a highly conserved TS66 and they have also been found in around 25% of all sequenced Proteobacteria, indicating that the secretion system has ancestral origins that precede the evolutionary divergence of Vibrio lineages.
T6SS was linked to pathogenesis when it was first discovered in V. cholerae in 2007, documented by an effector that crosslinks actin and causes toxicity in another bacterium, Dictyostelium discoideium. Whilst only a small number of strains have expressed T6SS in the lab, T6SS genes have been transcribed in human volunteers (using non-toxigenic strains!) using in vivo expression technology (IVET). During infection of V. cholerae, the host microbiome undergoes a radical transformation, with ‘good’ bacteria rapidly being replaced by ‘bad’ bacteria. Intraguild predation would allow V. cholerae to benefit both directly, through consumption of the prey cells and indirectly, from effectively eliminating the competition occupying the same niche.
This hypothesis appears highly plausible and would explain how V. cholerae are able to grow and multiply so rapidly. In contrast to Roberto’s post (4th March 2014) where Vibrio species are being predated, here it is the Vibrio species predating. Could this be an example of an evolutionary arms race? Interestingly, all gram positive bacteria investigated to date are resistant to the bactericidal attempts of V. cholerae T6SS and understanding why this should be may allow development of treatments for cholera. Exploring the triggers and relationship between V. cholerae and T6SS further should prove to be a promising area for future studies.
Pukatzki, S., & Provenzano, D. (2013). Vibrio cholerae as a predator: lessons from evolutionary principles. Frontiers in microbiology, 4 (384) 1-5 doi: 10.3389/fmicb.2013.00384