Ciliate and bacterial communities associated with White Syndrome and Brown Band Disease in reef‐building corals

Michael Sweet,John Bythell

doi:10.1111/j.1462-2920.2012.02746.x

Abstract

White Syndrome (WS) and Brown Band Disease (BrB) are important causes of reef coral mortality for which causal agents have not been definitively identified. Here we use culture-independent molecular techniques (DGGE and clone libraries) to characterize ciliate and bacterial communities in these diseases. Bacterial (16S rRNA gene) and ciliate (18S rRNA gene) communities were highly similar between the two diseases. Four bacterial and nine ciliate ribotypes were observed in both diseases, but absent in non-diseased specimens. Only one of the bacteria, Arcobacter sp. (JF831360) increased substantially in relative 16S rRNA gene abundance and was consistently represented in all diseased samples. Four of the eleven ciliate morphotypes detected contained coral algal symbionts, indicative of the ingestion of coral tissues. In both WS and BrB, there were two ciliate morphotypes consistently represented in all disease lesion samples. Morph1 (JN626268) was observed to burrow into and underneath the coral tissues at the lesion boundary. Morph2 (JN626269), previously identified in BrB, appears to play a secondary, less invasive role in pathogenesis, but has a higher population density in BrB, giving rise to the visible brown band. The strong similarity in bacterial and ciliate community composition of these diseases suggests that they are actually the same syndrome.

Highlights

The emerging ‘damage-response’ framework of microbial pathogenesis (Casadevall and Pirofski, 2003) suggests that diseases in general arise from complex host–Received 12 September, 2011; revised 9 March, 2012; accepted 16 March, 2012. *For correspondence
As a first step towards understanding disease causation in White Syndrome (WS) (Fig. 1A) this study provides a comprehensive, culture-independent molecular analysis of both ciliate and bacterial communities associated with the disease
Significant differences in denaturing gradient gel electrophoresis (DGGE) banding patterns of bacterial 16S rRNA gene diversity were shown between non-diseased colonies (ND; n = 10), the apparently healthy tissues adjacent to the disease lesion (AH; n = 10) and the disease lesion (DL; n = 10) in Acropora muricata from Heron Island, GBR [one-way analysis of similarity (ANOSIM), R = 0.937, P < 0.001]

Summary

Introduction

The emerging ‘damage-response’ framework of microbial pathogenesis (Casadevall and Pirofski, 2003) suggests that diseases in general arise from complex host–Received 12 September, 2011; revised 9 March, 2012; accepted 16 March, 2012. *For correspondence. It is vital that, in addition to the identification of pathogens via tests of Koch’s postulates: (i) an analysis of the microbial community of healthy and diseased hosts is undertaken to comprehensively identify potential pathogens involved in disease, and (ii) increases in activity of these suspected pathogens are linked to sites of active pathogenesis. These need to be studied in combination to fully understand disease causation. We must be able to distinguish between pathogens that are capable of causing damage, those that are directly involved in a specific pathogenesis and heterotrophs that colonize dead and decaying tissues following disease

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Discussion

Conclusion