Sick of Quorum Sensing? So are Corals (…maybe)

It’s no secret that coral reef health worldwide is on the decline. A significant contributing factor to this is the increase in incidences and severity of epizootics in the last 30 years. These diseases have the potential to decimate coral populations and yet little is known of their etiology and ecology. White band disease (WBD) for instance, a phenotype prevalent throughout the Caribbean, has destroyed 95% of regional Acropora populations since 1979 and yet many of the virulence factors that cause it are still poorly understood.

White band disease typifies most coral diseases in that it is characterized by tissue degradation along a coral branch. The disease, among many others, is thought to be the result of opportunistic pathogenesis by existing coral holobiont microbiota and so in a study by Rebecca Certner and Steven Vollmer the role of quorum sensing in WBD associated microbes was examined in order to further understand the etiological factors driving the infection.

The investigation of quorum sensing mechanisms was achieved by inoculating both healthy and diseased corals with cell-free culture fluid from healthy or diseased to coral homogenates to examine the resulting effect on the transmission and progression of WBD. In addition to this N-Hexanoyl-DL-homserine (AHL), a common autoinducer used by virulence-associated microbes, was added to coral samples and the resulting shift in host microbial composition examined to assess whether the AHL would induce or amplify WBD-like symptoms.

Interestingly the results showed that CFCF from diseased corals appear to cause significantly greater yield of Cytophaga-Flavobacteria in both healthy and diseased samples which would suggest an induction of WBD-like shift in community composition due to the CFCF addition Cytophaga-Flavobacteria. Healthy CFCF however appears to inhibit Cytophaga-Flavobacteria growth which implies it may contain antimicrobial molecules, a phenomenon often referred to as coral-probiotic hypothesis. In fact, because Cytophaga-Flavobacteria are known opportunistic pathogens the result appears to corroborate the compromised-host hypothesis as it implies that the disease symptoms may be induced by increased vulnerability of the coral host that allows such potential pathogens to outcompete commensal microbes.

The addition of AHL meanwhile, resulted in tissue loss and total mortality of all samples, both healthy and diseased, whereas the healthy control sample remained healthy and alive for the duration of the study. This strongly evidences that AHL plays a pivotal role in disease virulence. This acyl-homoserine lactone quorum sensing system is well characterised in many suspected marine pathogens from the Vibrio genus but has not previously been demonstrated in coral-associated Cytophaga-Flavobacterium. In many Vibrios virulence is positively and negatively controlled by quorum sensing in order to regulate virulence-associated genes and so it is likely that this system is also involved in the repression of host immunity. It is possible therefore that such a ability to disrupt host immunity is also present in Cytophaga-Flavobacteria.

Overall this study provides a vital insight to the mechanisms via which disease-causing agents are able to influence holobiont microbial population. It is obvious that N-Hexanoyl-DL-homserine has a significant influence on the growth of coral-associated bacteria and therefore its presence around coral hosts could act as an early warning for the pathogenesis and infection of diseases.

Certner, R. H. and Vollmer, S. V.. (2015). Evidence for Autoinduction and Quorum Sensing in White Band Disease-Causing Microbes on Acropora cervicornis. Scientific Reports. 5, 11134.