Bacterial Communities of Two Ubiquitous Great Barrier Reef Corals Reveals Both Site- and Species-Specificity of Common Bacterial Associates

Background: Coral-associated bacteria are increasingly considered to be important in coral health, and altered bacterial community structures have been linked to both coral disease and bleaching. Despite this, assessments of bacterial communities on corals rarely apply sufficient replication to adequately describe the natural variability. Replicated data such as these are crucial in determining potential roles of bacteria on coral

The Ecology of ‘Acroporid White Syndrome', a Coral Disease from the Southern Great Barrier Reef

Outbreaks of coral disease have increased worldwide over the last few decades. Despite this, remarkably little is known about the ecology of disease in the Indo-Pacific Region. Here we report the spatiotemporal dynamics of a coral disease termed ‘Acroporid white syndrome’ observed to affect tabular corals of the genus Acropora on the southern Great Barrier Reef. The syndrome is characterised by rapid tissue loss initiating in the basal margins of colonies, and manifests as a distinct lesion boundary between apparently healthy tissue and exposed white skeleton. Surveys of eight sites around Heron Reef in 2004 revealed a mean prevalence of 8.1±0.9%, affecting the three common species (Acropora cytherea, A. hyacinthus, A. clathrata) and nine other tabular Acropora spp. While all sizes of colonies were affected, white syndrome disproportionately affected larger colonies of tabular Acroporids (>80 cm). The prevalence of white syndrome was strongly related to the abundance of tabular Acroporids within transects, yet the incidence of the syndrome appears unaffected by proximity to other colonies, suggesting that while white syndrome is density dependant, it does not exhibit a strongly aggregated spatial pattern consistent with previous coral disease outbreaks. Acroporid white syndrome was not transmitted by either direct contact in the field or by mucus in aquaria experiments. Monitoring of affected colonies revealed highly variable rates of tissue loss ranging from 0 to 1146 cm−2 week−1, amongst the highest documented for a coral disease. Contrary to previous links between temperature and coral disease, rates of tissue loss in affected colonies increased threefold during the winter months. Given the lack of spatial pattern and non-infectious nature of Acroporid white syndrome, further studies are needed to determine causal factors and longer-term implications of disease outbreaks on the Great Barrier Reef

Host-Directed Evolution of a Novel Lactate Oxidase in Streptococcus iniae Isolates from Barramundi (Lates calcarifer)▿

In Streptococcus iniae, lactate metabolism is dependent upon two proteins, lactate permease that mediates uptake and lactate oxidase, a flavin mononucleotide-dependent enzyme that catalyzes oxidation of α-hydroxyacids. A novel variant of the lactate oxidase gene, lctO, in Australian isolates of S. iniae from diseased barramundi was found during a diagnostic screen using LOX-1 and LOX-2 primers, yielding amplicons of 920 bp instead of the expected 869 bp. Sequencing of the novel gene variant (type 2) revealed a 51-nucleotide insertion in lctO, resulting in a 17-amino-acid repeat in the gene product, and three-dimensional modeling indicated formation of an extra loop in the monomeric protein structure. The activities of the lactate oxidase enzyme variants expressed in Escherichia coli were examined, indicating that the higher-molecular-weight type 2 enzyme exhibited higher activity. Growth rates of S. iniae expressing the novel type 2 enzyme were not reduced at lactate concentrations of 0.3% and 0.5%, whereas a strain expressing the type 1 enzyme exhibited reduced growth rates at these lactate concentrations. During a retrospective screen of 105 isolates of S. iniae from Australia, the United States, Canada, Israel, Réunion Island, and Thailand, the type 2 variant arose only in isolates from a single marine farm with unusually high tidal flow in the Northern Territory, Australia. Elevated plasma lactate levels in the fish, resulting from the effort of swimming in tidal flows of up to 3 knots, may exert sufficient selective pressure to maintain the novel, high-molecular-weight enzyme variant

Two hepcidin-like antimicrobial peptides in Barramundi Lates calcarifer exhibit differing tissue tropism and are induced in response to lipopolysaccharide

Fish represent the most diverse and abundant extant vertebrate infraclass. They are also one of the earliest divergent phyla with adaptive immunity based on antigen recognition by MHC and immunoglobulin. The aquaculture industry, which currently provides more than half of the fish for human consumption globally, has successfully exploited the adaptive immune system of fish through mass vaccination programs. However, vaccination against highly diverse antigens, mostly carbohydrates, such as capsular polysaccharides and lipopolysaccharide (LPS) is challenging. Fish have a subdued innate response to LPS, but adaptive response is generally high and type-specific. To better understand the link between initial innate response and early onset of adaptive immunity to carbohydrate antigens in the perciform barramundi (Lates calcarifer), an immune transcriptome was prepared from pronephros and spleen following vaccination with LPS and peptidoglycan. From 163,661 transcripts derived by Illumina mRNA-Seq, most grouped in neuronal, endocrine or immune system categories, suggesting a close relationship between the three systems. Moreover, digestive enzyme transcripts in spleen appeared to be highly inducible in barramundi. Most of the known TLRs were transcribed in the barramundi spleen and HK transcriptome, with the notable exception of TLR4, which is primarily responsible for LPS recognition in mammals. Several C-type lectin receptors were also identified, including CD209, CD205, and CLEC4E (Mincle). As Mincle has been shown to bind LPS and is abundant on dendritic cells, its role in response to LPS in barramundi was further investigated. A high dose of LPS induced TNF-alpha expression via Mincle. However, IL-6 regulation, whilst still regulated in response to LPS, did not depend upon the Mincle pathway, suggesting other routes of activation. This study thus suggests that Mincle acts as a partial substitute for TLR4 in barramundi in the processing of LPS

Analysis of evolutionarily conserved innate immune components in coral links immunity and symbiosis

Reef-building corals are representatives of one of the earliest diverging metazoan lineages and are experiencing increases in bleaching events (breakdown of the coral-Symbiodinium symbiosis) and disease outbreaks. The present study investigates the roles of two pattern recognition proteins, the mannose binding lectin Millectin and a complement factor C3-like protein (C3-Am). in the coral Acropora millepora. The results indicate that the innate immune functions of these molecules are conserved and arose early in evolution. C3-Am is expressed in response to injury, and may function as an opsonin. In contrast, Millectin expression is up-regulated in response to lipopolysaccharide and peptidoglycan. These observations, coupled with localization of Millectin in nematocysts in epidermal tissue, and reported binding of pathogens, are consistent with a key role for the lectin in innate immunity. Furthermore, Millectin was consistently detected binding to the symbiont Symbiodinium in vivo. indicating that the Millectin function of recognition and binding of non-self-entities may have been co-opted from an ancient innate immune system into a role in symbiosis. (C) 2010 Elsevier Ltd. All rights reserved

Location and regional setting of Heron and Wistari Reefs (Capricorn Bunker Group, Southern Great Barrier Reef).

<p>White circles indicate initial broad-scale sites surveyed for white syndrome presence (<i>n = </i>25), red circles indicate belt transect surveys for community structure and white syndrome prevalence (<i>n = </i>8).</p

Temporal patterns of tissue loss in Acroporid white syndrome.

<p>Lesion progression (cm⁻² ± SE) and average temperature (°C ± min/max) recorded during summer months (March–April) and winter months (July–August).</p

Initiation, formation and progression of white syndrome lesion in a colony of <i>Acropora cytherea</i>.

<p>Photographs taken during weekly monitoring in the summer months of 2004 (a–g) and winter (h).</p

Size frequency distributions of healthy and white syndrome affected tabular <i>Acropora</i> spp.

<p>Grey columns = healthy colonies, black columns = white syndrome affected colonies. Histograms fitted with normal distributions (solid line = healthy colonies, dashed line = white syndrome affected colonies).</p

Acroporid White Syndrome in Tabular <i>Acropora</i> spp.

<p>a) size class I [0–80 cm] (Scale = 5 cm) b) class II [80–160 cm] (Scale = 25 cm), c) class III [>160 cm] (Scale = 50 cm).</p