Sea star wasting (SSW) disease describes a condition affecting asteroids that resulted in significant Northeastern Pacific population decline following a mass mortality event in 2013. The etiology of SSW is unresolved. We hypothesized that SSW is a sequela of microbial organic matter remineralization near respiratory surfaces, one consequence of which may be limited O 2 availability at the animal-water interface. Microbial assemblages inhabiting tissues and at the asteroid-water interface bore signatures of copiotroph proliferation before SSW onset, followed by the appearance of putatively facultative and strictly anaerobic taxa at the time of lesion genesis and as animals died. SSW lesions were induced in Pisaster ochraceus by enrichment with a variety of organic matter (OM) sources. These results together illustrate that depleted O 2 conditions at the animal-water interface may be established by heterotrophic microbial activity in response to organic matter loading. SSW was also induced by modestly (∼39%) depleted O 2 conditions in aquaria, suggesting that small perturbations in dissolved O 2 may exacerbate the condition. SSW susceptibility between species was significantly and positively correlated with surface rugosity, a key determinant of diffusive boundary layer thickness. Tissues of SSW-affected individuals collected in 2013–2014 bore δ 15 N signatures reflecting anaerobic processes, which suggests that this phenomenon may have affected asteroids during mass mortality at the time. The impacts of enhanced microbial activity and subsequent O 2 diffusion limitation may be more pronounced under higher temperatures due to lower O 2 solubility, in more rugose asteroid species due to restricted hydrodynamic flow, and in larger specimens due to their lower surface area to volume ratios which affects diffusive respiratory potential.
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When bacteria meet many arms: Autecological insights into Vibrio pectinicida FHCF-3 in echinoderms
Abstract Sea star wasting (SSW) has been described globally in over 25 species of asteroids. This condition is characterized by body wall lesions, loss of turgor and ray autotomy, which often results in the mortality of specimens. The cause of SSW has remained elusive. A recent report detailing a potential causative agent,Vibrio pectenicidaFHCF-3 (Prentice et al., 2025), inspired an investigation into its occurrence in available genomic and transcriptomic data from 2013-2015 from wild specimens and those enrolled in experimental incubations. WhileVibrio pectenicidaFHCF-3 16S rRNA gene sequences were detected in abnormal body wall tissues ofPycnopodia helianthoidesfrom public aquaria in 2013, they were not detected in grossly normal or abnormal body wall specimens of other species sampled concurrently at sites where mass mortality was observed and from public aquaria. Experimental amendment ofPisaster ochraceuswith organic matter substrates led to enrichment ofV. pectenicidaFHCF-3 16S rRNAs at the animal-water interface, and that they surged in abundance 24h prior to body wall lesion appearance. However, in this experimentV. pectenicidaFHCF-3 16S rRNAs were inconsistently detected in coelomic fluid of abnormal specimens, and their abundance at specimen surfaces was inversely related to coelomic fluid detections. Perplexingly,V. pectenicidaFHCF-3 was detected in abnormalP. helianthoidestreated with 0.2 µm filtrates of homogenized tissues, but absent in grossly normal heat-treated filtrate controls in prior work.Vibriospp, are copiotrophs that experience rapid growth to dominate microbial communities in plankton and tissues when amended to seawater in a mesocosm experiment. These patterns indicateV. pectenicidaFHCF-3 might cause abnormalities inP. helianthoidesunder certain conditions, but its growth might be a secondary rather than primary determinant of disease (i.e. it is saprobic or an opportunistic agent). It remains possible that sea star wasting abnormalities inP. helianthoidesrepresent a generalized response to bacterial infiltration, driven by a diverse set of bacteria which includes but does not require species such asV. pectenicidaFHCF-3. Finally, our data suggest that this taxon is not intimately tied to SSW abnormalities in other species. Hence,V. pectenicidaFHCF-3 may be a driver of a SSW disease inP. heliathoides, but cannot be the cause of all SSW across species.
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- Award ID(s):
- 2049225
- PAR ID:
- 10661355
- Publisher / Repository:
- bioRxiv
- Date Published:
- Format(s):
- Medium: X
- Institution:
- Cornell University
- Sponsoring Org:
- National Science Foundation
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