How Microbial Community Composition Regulates Coral Disease Development - From Seminar

In this paper the authors developed mathematical models in order to understand how changes in environmental conditions affects the microbial community dynamics in the coral mucus layer.

Bleaching and disease are both partly to blame for the rapid decline in coral reef cover worldwide and associated with both of these is shift in the composition of the coral mucus layer microbial community from the resident microbes which are critical to the functioning of the coral holobiont to a community of pathogenic microbes, which the authors point out is often a Vibrio. This shift is often after a period of environmental stress, such as a heat wave. The models devised by the authors then aim to understand the mechanisms responsible for the shift in microbial communities, at what point does the resident microbial community become vulnerable to being outcompeted and replaced by the pathogenic microbial community and whether recovery is possible.

The first model described by the authors assumes a spatially homogenous or well-mixed mucus layer. In this model microbial populations are measured in units of the growth limiting substrate provided by the host and its endosymbionts and also assumes that there is no microbial inoculation from external sources. The model produces a nullcline for both the pathogenic and beneficial microbes and just like the Lotka-Volterra model, if one nullcline is completely above the other then whichever nullcline is lower will be subject to competitive exclusion i.e. there are two potential stable states; one dominated by the beneficial microbes and one dominated by the pathogenic microbes. A third possibility is if the nullclines cross, there will still be competitive exclusion but which is excluded depends on initial conditions.

The authors then explain how the model can explain the replacement of beneficial microbes by pathogenic microbes. Colder months are unfavourable to pathogens and so they are outcompeted and excluded by beneficial microbes meaning the pathogen exclusion is the only stable state. During the warmer months, although the pathogenic microbes may have a higher intrinsic growth rate due to higher temperatures, their growth is limited by antibiotics, which keeps the pathogen exclusion stable. During unusually high temperatures however there is a loss of antibiotic activity and so pathogen dominance can become stable. Importantly the model also predicts that the sudden switch of the microbial community will still occur even if the change in conditions is gradual. A further important prediction of the model is that the switch back or recovery from pathogenic communities to beneficial communities will also occur suddenly but the recovery requires different conditions and may not happen until a long time after conditions change back to the conditions more favourable to the beneficial microbes, they require the conditions to be even more favourable to them than they initially were until a switch back happens.

The second model is called the spatially hetrogenous model and aimed to examine whether spatial variability allowed for a broader range of outcomes and particularly whether spatial variability could allow a stable coexistence of both pathogenic and beneficial microbes. The general reasoning of this model was that the well-mixed models prediction of a rapid shift in mucus layer microbial communities may have turned out in part due to not taking into consideration spatial variability, this second model then was expanded to include spatial variability. This was not found to be the case however, the spatially heterogeneous model in fact backed up the results from the well-mixed model that the authors sum up as “once temporary extreme heat allows pathogens to overgrow, their dominance will persist until conditions become highly unfavorable for pathogenic persistence.”

Mao-Jones J, Ritchie KB, Jones LE, Ellner SP (2010) How Microbial Community Composition Regulates Coral Disease Development. PLoS Biol 8(3): e1000345. doi:10.1371/journal.pbio.1000345