Vibrio coralliilyticus strain OCN008 is an etiological agent of acute Montipora white syndrome

• Published in: Applied and Environmental Microbiology 2014-04, Vol.80 (7), p.2102-2109
• Main Authors: Ushijima, Blake, Videau, Patrick, Burger, Andrew H, Shore-Maggio, Amanda, Runyon, Christina M, Sudek, Mareike, Aeby, Greta S, Callahan, Sean M
• Format: Article
• Language: English
• Subjects: Animals; Anthozoa - microbiology; Cluster Analysis; DNA, Bacterial - chemistry; DNA, Bacterial - genetics; DNA, Ribosomal - chemistry; DNA, Ribosomal - genetics; Environmental Microbiology; Epidemiology; Genes; Genotype; Gram-negative bacteria; Hawaii; Host Specificity; Molecular Sequence Data; Montipora; Montipora capitata; Pathogens; Phylogeny; Porites compressa; RNA, Ribosomal, 16S - genetics; Sequence Analysis, DNA; Temperature; Tissues; Vibrio; Vibrio - genetics; Vibrio - isolation & purification; Vibrio - physiology; Virulence Factors - genetics
• ISSN: 0099-2240; 1098-5336; 1098-6596
• DOI: 10.1128/AEM.03463-13

Identification of a pathogen is a critical first step in the epidemiology and subsequent management of a disease. A limited number of pathogens have been identified for diseases contributing to the global decline of coral populations. Here we describe Vibrio coralliilyticus strain OCN008, which induces acute Montipora white syndrome (aMWS), a tissue loss disease responsible for substantial mortality of the coral Montipora capitata in Kāne'ohe Bay, Hawai'i. OCN008 was grown in pure culture, recreated signs of disease in experimentally infected corals, and could be recovered after infection. In addition, strains similar to OCN008 were isolated from diseased coral from the field but not from healthy M. capitata. OCN008 repeatedly induced the loss of healthy M. capitata tissue from fragments under laboratory conditions with a minimum infectious dose of between 10(7) and 10(8) CFU/ml of water. In contrast, Porites compressa was not infected by OCN008, indicating the host specificity of the pathogen. A decrease in water temperature from 27 to 23°C affected the time to disease onset, but the risk of infection was not significantly reduced. Temperature-dependent bleaching, which has been observed with the V. coralliilyticus type strain BAA-450, was not observed during infection with OCN008. A comparison of the OCN008 genome to the genomes of pathogenic V. coralliilyticus strains BAA-450 and P1 revealed similar virulence-associated genes and quorum-sensing systems. Despite this genetic similarity, infections of M. capitata by OCN008 do not follow the paradigm for V. coralliilyticus infections established by the type strain.