25 research outputs found

    Human pathogen shown to cause disease in the threatened elkhorn coral Acropora palmata

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    Coral reefs are in severe decline. Infections by the human pathogen Serratia marcescens have contributed to precipitous losses in the common Caribbean elkhorn coral, Acropora palmata, culminating in its listing under the United States Endangered Species Act. During a 2003 outbreak of this coral disease, called acroporid serratiosis (APS), a unique strain of the pathogen, Serratia marcescens strain PDR60, was identified from diseased A. palmata, human wastewater, the non-host coral Siderastrea siderea and the corallivorous snail Coralliophila abbreviata. In order to examine humans as a source and other marine invertebrates as vectors and/or reservoirs of the APS pathogen, challenge experiments were conducted with A. palmata maintained in closed aquaria to determine infectivity of strain PDR60 from reef and wastewater sources. Strain PDR60 from wastewater and diseased A. palmata caused disease signs in elkhorn coral in as little as four and five days, respectively, demonstrating that wastewater is a definitive source of APS and identifying human strain PDR60 as a coral pathogen through fulfillment of Koch\u27s postulates. A. palmata inoculated with strain PDR60 from C. abbreviata showed limited virulence, with one of three inoculated fragments developing APS signs within 13 days. Strain PDR60 from non-host coral S. siderea showed a delayed pathogenic effect, with disease signs developing within an average of 20 days. These results suggest that C. abbreviata and non-host corals may function as reservoirs or vectors of the APS pathogen. Our results provide the first example of a marine “reverse zoonosis” involving the transmission of a human pathogen (S. marcescens) to a marine invertebrate (A. palmata). These findings underscore the interaction between public health practices and environmental health indices such as coral reef survival

    Human Pathogen Shown to Cause Disease in the Threatened Elkhorn Coral Acropora palmata

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    Coral reefs are in severe decline. Infections by the human pathogen Serratia marcescens have contributed to precipitous losses in the common Caribbean elkhorn coral, Acropora palmata, culminating in its listing under the United States Endangered Species Act. During a 2003 outbreak of this coral disease, called acroporid serratiosis (APS), a unique strain of the pathogen, Serratia marcescens strain PDR60, was identified from diseased A. palmata, human wastewater, the non-host coral Siderastrea siderea and the corallivorous snail Coralliophila abbreviata. In order to examine humans as a source and other marine invertebrates as vectors and/or reservoirs of the APS pathogen, challenge experiments were conducted with A. palmata maintained in closed aquaria to determine infectivity of strain PDR60 from reef and wastewater sources. Strain PDR60 from wastewater and diseased A. palmata caused disease signs in elkhorn coral in as little as four and five days, respectively, demonstrating that wastewater is a definitive source of APS and identifying human strain PDR60 as a coral pathogen through fulfillment of Koch\u27s postulates. A. palmata inoculated with strain PDR60 from C. abbreviata showed limited virulence, with one of three inoculated fragments developing APS signs within 13 days. Strain PDR60 from non-host coral S. siderea showed a delayed pathogenic effect, with disease signs developing within an average of 20 days. These results suggest that C. abbreviata and non-host corals may function as reservoirs or vectors of the APS pathogen. Our results provide the first example of a marine \u27\u27reverse zoonosis\u27\u27 involving the transmission of a human pathogen (S. marcescens) to a marine invertebrate (A. palmata). These findings underscore the interaction between public health practices and environmental health indices such as coral reef survival

    Human Pathogen Shown to Cause Disease in the Threatened Eklhorn Coral Acropora palmata

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    Coral reefs are in severe decline. Infections by the human pathogen Serratia marcescens have contributed to precipitous losses in the common Caribbean elkhorn coral, Acropora palmata, culminating in its listing under the United States Endangered Species Act. During a 2003 outbreak of this coral disease, called acroporid serratiosis (APS), a unique strain of the pathogen, Serratia marcescens strain PDR60, was identified from diseased A. palmata, human wastewater, the non-host coral Siderastrea siderea and the corallivorous snail Coralliophila abbreviata. In order to examine humans as a source and other marine invertebrates as vectors and/or reservoirs of the APS pathogen, challenge experiments were conducted with A. palmata maintained in closed aquaria to determine infectivity of strain PDR60 from reef and wastewater sources. Strain PDR60 from wastewater and diseased A. palmata caused disease signs in elkhorn coral in as little as four and five days, respectively, demonstrating that wastewater is a definitive source of APS and identifying human strain PDR60 as a coral pathogen through fulfillment of Koch's postulates. A. palmata inoculated with strain PDR60 from C. abbreviata showed limited virulence, with one of three inoculated fragments developing APS signs within 13 days. Strain PDR60 from non-host coral S. siderea showed a delayed pathogenic effect, with disease signs developing within an average of 20 days. These results suggest that C. abbreviata and non-host corals may function as reservoirs or vectors of the APS pathogen. Our results provide the first example of a marine “reverse zoonosis” involving the transmission of a human pathogen (S. marcescens) to a marine invertebrate (A. palmata). These findings underscore the interaction between public health practices and environmental health indices such as coral reef survival

    RNA-seq Analysis Reveals That an ECF σ Factor, AcsS, Regulates Achromobactin Biosynthesis in Pseudomonas syringae pv. syringae B728a

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    Iron is an essential micronutrient for Pseudomonas syringae pv. syringae strain B728a and many other microorganisms; therefore, B728a has evolved methods of iron acquirement including the use of iron-chelating siderophores. In this study an extracytoplasmic function (ECF) sigma factor, AcsS, encoded within the achromobactin gene cluster is shown to be a major regulator of genes involved in the biosynthesis and secretion of this siderophore. However, production of achromobactin was not completely abrogated in the deletion mutant, implying that other regulators may be involved such as PvdS, the sigma factor that regulates pyoverdine biosynthesis. RNA-seq analysis identified 287 genes that are differentially expressed between the AcsS deletion mutant and the wild type strain. These genes are involved in iron response, secretion, extracellular polysaccharide production, and cell motility. Thus, the transcriptome analysis supports a role for AcsS in the regulation of achromobactin production and the potential activity of both AcsS and achromobactin in the plant-associated lifestyle of strain B728a

    Treatments and controls used in the challenge experiments.

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    <p>A total of eleven challenge experiments were conducted each within a single aquarium and each with three <i>Acropora palmata</i> coral fragments (F1, F2, F3). Coral colony of origin and number of days to tissue loss is included for each coral fragment. Treatments and controls for which there was no tissue loss are also noted.</p

    Bacterial treatments inoculated onto the <i>Acropora palmata</i> fragments in the challenge experiments.

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    <p>Eight isolates of <i>Serratia marcescens</i> representing three pulsed-field gel electrophoresis (PFGE) strains (PDR60, PDL100, and WWI31) were used. The source, location, and date of collection are included for each treatment.</p

    <i>Acropora palmata</i> colonies used in the challenge experiments.

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    <p>Number of fragments per <i>A. palmata</i> colony, the challenge for each fragment (control or inoculation with a <i>Serratia marcescens</i> test isolate), and the result of each challenge (tissue loss or no tissue loss) are included. Three coral fragments (F1, F2, F3) were used for each challenge.</p

    Time series of white pox affected <i>Acropora palmata</i> at Looe Key Reef in the Florida Keys and average time to tissue loss in the challenge experiments.

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    <p>A. Images of white pox affected <i>A. palmata</i> at Looe Key, from June 2008, to June 2009, to July 2009 (left to right), show colony growth and partial mortality. Scales bars are 3 cm on a side or 3 cm in diameter. (Photographs by JW Porter and MK Meyers) B. Average time (days) to development of disease signs on <i>A. palmata</i> inoculated with <i>Serratia marcescens</i>. Days to tissue loss was averaged for the three <i>A. palmata</i> fragments used in each treatment and each control. The original inoculum was recovered for all seven of the presented <i>S. marcescens</i> inocula, including five isolates of strain PDR60 collected from acroporid serratiosis (APS)-affected <i>A. palmata</i> (isolates 1, 2), non-host coral <i>Siderastrea siderea</i> (isolate 4), corallivorous snail <i>Coralliophila abbreviata</i> (isolate 5), and untreated wastewater (isolate 6). Two additional inocula included <i>S. marcescens</i> strain PDL100 (isolate 7), previously confirmed as an APS pathogen through fulfillment of Koch's Postulates (2) and <i>S. marcescens</i> strain WWI31 from untreated wastewater (isolate 8). The vehicle control exhibited tissue loss beginning at day 15. The <i>E. coli</i>-plus-vehicle control and the isolate 3-plus-vehicle treatment did not exhibit tissue loss and remained apparently healthy for the duration of the 26 day study. Virulent strains (isolates 1, 2, 5, 6, 8) caused tissue loss within 14 days of inoculation and attenuated strains (isolates 4, 7) caused tissue loss after day 14.</p
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