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Blake Ushijima

Publications and source records attributed to Blake Ushijima.

5 recordsLinked to original sources

Investigating microbial size classes associated with the transmission of stony coral tissue loss disease (SCTLD)

Effective treatment and prevention of any disease necessitates knowledge of the causative agent, yet the causative agents of most coral diseases remain unknown, in part due to the difficulty of distinguishing the pathogenic microbe(s) among the complex microbial backdrop of coral hosts. Stony coral tissue loss disease (SCTLD) is a particularly destructive disease of unknown etiology, capable of transmitting through the water column and killing entire colonies within a matter of weeks. Here we used a previously described method to (i) isolate diseased and apparently healthy coral colonies within individual mesocosms containing filtered seawater with low microbial background levels; (ii) incubate for several days to enrich the water with coral-shed microbes; (iii) use tangential-flow filtration to concentrate the microbial community in the mesocosm water; and then (iv) filter the resulting concentrate through a sequential series of different pore-sized filters. To investigate the size class of microorganism(s) associated with SCTLD transmission, we used 0.8 µm pore size filters to capture microeukaryotes and expelled zooxanthellae, 0.22 µm pore size filters to capture bacteria and large viruses, and 0.025 µm pore size filters to capture smaller viruses. In an attempt to further refine which size fraction(s) contained the transmissible element of SCTLD, we then applied these filters to healthy “receiver” coral fragments and monitored them for the onset of SCTLD signs over three separate experimental runs. However, several factors outside of our control confounded the transmission results, rendering them inconclusive. As the bulk of prior studies of SCTLD in coral tissues have primarily investigated the associated bacterial community, we chose to characterize the prokaryotic community associated with all mesocosm 0.22 µm pore size filters using Illumina sequencing of the V4 region of the 16S rRNA gene. We identified overlaps with prior SCTLD studies, including the presence of numerous previously identified SCTLD bioindicators within our mesocosms. The identification in our mesocosms of specific bacterial amplicon sequence variants that also appear across prior studies spanning different collection years, geographic regions, source material, and coral species, suggests that bacteria may play some role in the disease.

PeerJ

Combining tangential flow filtration and size fractionation of mesocosm water as a method for the investigation of waterborne coral diseases

The causative agents of most coral diseases today remain unknown, complicating disease response and restoration efforts. Pathogen identifications can be hampered by complex microbial communities naturally associated with corals and seawater, which create complicating “background noise” that can potentially obscure a pathogen’s signal. Here, we outline an approach to investigate waterborne coral diseases that use a combination of coral mesocosms, tangential flow filtration, and size fractionation to reduce the impact of this background microbial diversity, compensate for unknown infectious dose, and further narrow the suspect pool of potential pathogens. As proof of concept, we use this method to compare the bacterial communities shed into six Montastraea cavernosa coral mesocosms and demonstrate this method effectively detects differences between diseased and healthy coral colonies. We found several amplicon sequence variants (ASVs) in the diseased mesocosms that represented 100% matches with ASVs identified in prior studies of diseased coral tissue, further illustrating the effectiveness of our approach. Our described method is an effective alternative to using coral tissue or mucus to investigate waterborne coral diseases of unknown etiology and can help more quickly narrow the pool of possible pathogens to better aid in disease response efforts. Additionally, this versatile method can be easily adapted to characterize either the entire microbial community associated with a coral or target-specific microbial groups, making it a beneficial approach regardless of whether a causative agent is suspected or is completely unknown.

Florida

Emerging coral diseases in Kāne'ohe Bay, O'ahu, Hawai'i (USA): two major disease outbreaks of acute Montipora white syndrome

In March 2010 and January 2012, we documented 2 widespread and severe coral disease outbreaks on reefs throughout Kāne‘ohe Bay, Hawai‘i (USA). The disease, acute Montipora white syndrome (aMWS), manifested as acute and progressive tissue loss on the common reef coral M. capitata . Rapid visual surveys in 2010 revealed 338 aMWS-affected M. capitata colonies with a disease abundance of (mean ± SE) 0.02 ± 0.01 affected colonies per m of reef surveyed. In 2012, disease abundance was significantly higher (1232 aMWS-affected colonies) with 0.06 ± 0.02 affected colonies m -1 . Prior surveys found few acute tissue loss lesions in M. capitata in Kāne‘ohe Bay; thus, the high number of infected colonies found during these outbreaks would classify this as an emerging disease. Disease abundance was highest in the semi-enclosed region of south Kāne‘ohe Bay, which has a history of nutrient and sediment impacts from terrestrial runoff and stream discharge. In 2010, tagged colonies showed an average tissue loss of 24% after 1 mo, and 92% of the colonies continued to lose tissue in the subsequent month but at a slower rate (chronic tissue loss). The host-specific nature of this disease (affecting only M. capitata ) and the apparent spread of lesions between M. capitata colonies in the field suggest a potential transmissible agent. The synchronous appearance of affected colonies on multiple reefs across Kāne‘ohe Bay suggests a common underlying factor. Both outbreaks occurred during the colder, rainy winter months, and thus it is likely that some parameter(s) associated with winter environmental conditions are linked to the emergence of disease outbreaks on these reefs.

Diseases of Aquatic Organisms

First record of black band disease in the Hawaiian archipelago: response, outbreak, status, virulence, and a method of treatment

A high number of coral colonies, Montipora spp., with progressive tissue loss were reported from the north shore of Kaua‘i by a member of the Eyes of the Reef volunteer reporting network. The disease has a distinct lesion (semi-circular pattern of tissue loss with an adjacent dark band) that was first observed in Hanalei Bay, Kaua‘i in 2004. The disease, initially termed Montipora banded tissue loss, appeared grossly similar to black band disease (BBD), which affects corals worldwide. Following the initial report, a rapid response was initiated as outlined in Hawai‘i’s rapid response contingency plan to determine outbreak status and investigate the disease. Our study identified the three dominant bacterial constituents indicative of BBD (filamentous cyanobacteria, sulfate-reducing bacteria, sulfide-oxidizing bacteria) in coral disease lesions from Kaua‘i, which provided the first evidence of BBD in the Hawaiian archipelago. A rapid survey at the alleged outbreak site found disease to affect 6-7% of the montiporids, which is higher than a prior prevalence of less than 1% measured on Kaua‘i in 2004, indicative of an epizootic. Tagged colonies with BBD had an average rate of tissue loss of 5.7 cm 2 /day over a two-month period. Treatment of diseased colonies with a double band of marine epoxy, mixed with chlorine powder, effectively reduced colony mortality. Within two months, treated colonies lost an average of 30% less tissue compared to untreated controls.

Hawaii

Ocean warming and acidification have complex interactive effects on the dynamics of a marine fungal disease

Diseases threaten the structure and function of marine ecosystems and are contributing to the global decline of coral reefs. We currently lack an understanding of how climate change stressors, such as ocean acidification (OA) and warming, may simultaneously affect coral reef disease dynamics, particularly diseases threatening key reef-building organisms, for example crustose coralline algae (CCA). Here, we use coralline fungal disease (CFD), a previously described CCA disease from the Pacific, to examine these simultaneous effects using both field observations and experimental manipulations. We identify the associated fungus as belonging to the subphylum Ustilaginomycetes and show linear lesion expansion rates on individual hosts can reach 6.5 mm per day. Further, we demonstrate for the first time, to our knowledge, that ocean-warming events could increase the frequency of CFD outbreaks on coral reefs, but that OA-induced lowering of pH may ameliorate outbreaks by slowing lesion expansion rates on individual hosts. Lowered pH may still reduce overall host survivorship, however, by reducing calcification and facilitating fungal bio-erosion. Such complex, interactive effects between simultaneous extrinsic environmental stressors on disease dynamics are important to consider if we are to accurately predict the response of coral reef communities to future climate change.

Proceedings of the Royal Society B