CCA 0, CFD 1

Corals are important bio-engineers, depositing calcium carbonates and creating vast expenses of reefs which are visible from space. Many of these reefs are colonised by crustose coralline algae (CCA), which can cover up to 50% of living reefs, and consequently act as important sites for coral larval settlement. Although CCA are an important part of reef ecology, very little is known about them or their susceptibility to disease. Disease could potentially cause drastic reductions in CCA populations, with known on effects which promote community shifts to fleshy macro-algal dominance (DDAMnation – Rohwer, 2010). The authors of this paper aim to look at the effects of ocean warming and OA on CCA, and the interaction with coralline fungal disease (CFD), a previously described CCA disease from the Pacific. A combination of field observations and experimental manipulations were used.

Histopathological changes were examined using fragments of CCA which displayed signs of CFD, with Grocott’s methanamine silver being used to confirm the presence of fungal hyphae. To culture the fungus associated with CFD, cellulose agar was used with media containing antibiotics to stop bacterial growth, and a control without antibiotics to preclude any negative effects on fungal growth. Cultures were incubated at 25, 27 or 30 °C, aerated, and left for 21 days. Frozen, ground CFD lesions were thawed, and individual fungal filaments were isolated. DNA was extracted from filaments, and fungal specific 18s rRNA PCR amplification was used from mixed-environmental samples. Phylogenetic analysis was assessed using the National Centre for Biotechnology Information (NCBI), which was used to align the 653bp 18S rRNA gene sequences. A phylogenetic tree was constructed and evolutionary distances were computed.

The quantification of CFD occurrences was done using photo-quadrats, from 12 permanent sites between July- August and October-November, 2008. 40 of the 59 transects surveyed became permanent as part of the Palmyra disease monitoring programme and were surveyed again in 2009 for CFD occurrences and CCA cover. CFA was also measured during El Nino, with 13 CFD cases being photographed weekly, with CFD vital rates (lesion surface area and linear progression rate) were calculated using Image J software.

Temperature and acidification experiments were conducted using C0₂ bubbling and heating, to examine independent and interactive effects of OA and waring on CFD disease dynamics as well as CA growth (net calcification).  OA conditions were mimicked by bubbling pre-mixed air enriched with C0₂ (reflecting atmospheric conditions projected for 2100). Four independent water baths (two ambient and two warmed) held experimental aquaria that were randomly assigned to elevated or present-day C0₂ conditions, in order to create every combination of warming and OA treatment. Aquaria were covered to prevent evaporation and rainwater from affecting salinity, and placed under a shade cloth to mimic the natural light found at 10m on the forereef (where the CCA is found). Controls were also conducted for algal metabolism. Net calcification rates of CCA were quantified to the nearest mg, and CFD disease rates were calculated using ImageJ (e.g lesion progression)

The paper demonstrated that ocean warming and acidification can have complex interactive effects on marine disease dynamics. Habitat difference seemed to have an important role, with some reefs (Palmyra’s forereef) having a CFD occurrence independent of CCA abundance; suggesting that host abundance alone does not explain observed spatial variation in CFD. The authors mention that the results for the experiments may differ if they were in-field (because CFD variation could be a result of the abundance of preferential host species of CCA) but note that CCA taxonomy is difficult and requires microscopic examination making it impossible in the field. The overall results from the experiments indicate that less acidic but warmer conditions characterise the most favourable conditions for CFD occurrence. Regardless of the mechanisms behind fine-scale CFD variations, it is clear that the disease is more abundant and virulent under elevated temperatures. This suggests that the prevalence and virulence of CFD may increase in line with future climate projections. Unsurprisingly, the experiment also showed that elevated pCO₂ contributes to increasing acidity, which leads to the degradation and structural loss of CCA, suggesting net dissolution. This is likely to increase the vulnerability of CCA, and the virulent effect of CFA is only going to exacerbate this.  However, the authors did discover a slowed growth of lesions in more acidic water, but this minor positive is  swamped by the overriding negative effects that increased acidity has on the whole CCA organism.

All in all, this paper is a fascinating look at the effects of OA and increased temperature on the relationship between parasitic CFD and CCA. Unfortunately, it seems that the parasitic fungi is better suited to the future projected oceanic conditions, and therefore is likely to thrive, resulting In potential major losses in CCA ecosystems, and damages to the coral reefs they inhabit.

Reviewed: Williams GJ et al. 2014 Ocean warming and acidification have complex interactive effects on the dynamics of a marine fungal disease. Proc. R. Soc. B 281: 20133069.

http://dx.doi.org/10.1098/rspb.2013.3069