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Host size and proximity to diseased neighbours drive the spread of a coral disease outbreak in Hawai'i.

ABSTRACT: Understanding how disease risk varies over time and across heterogeneous populations is critical for managing disease outbreaks, but this information is rarely known for wildlife diseases. Here, we demonstrate that variation in host and pathogen factors drive the direction, duration and intensity of a coral disease outbreak. We collected longitudinal health data for 200 coral colonies, and found that disease risk increased with host size and severity of diseased neighbours, and disease spread was highest among individuals between 5 and 20 m apart. Disease risk increased by 2% with every 10 cm increase in host size. Healthy colonies with severely diseased neighbours (greater than 75% affected tissue) were 1.6 times more likely to develop disease signs compared with colonies with moderately diseased neighbours (25-75% affected tissue). Force of infection ranged from 7 to 20 disease cases per 1000 colonies (mean = 15 cases per 1000 colonies). The effective reproductive ratio, or average number of secondary infections per infectious individual, ranged from 0.16 to 1.22. Probability of transmission depended strongly on proximity to diseased neighbours, which demonstrates that marine disease spread can be highly constrained within patch reefs.

SUBMITTER: Caldwell JM

PROVIDER: S-EPMC5784196 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature

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Host size and proximity to diseased neighbours drive the spread of a coral disease outbreak in Hawai'i.

Caldwell Jamie M JM Donahue Megan J MJ Harvell C Drew CD

Proceedings. Biological sciences 20180101 1870

Understanding how disease risk varies over time and across heterogeneous populations is critical for managing disease outbreaks, but this information is rarely known for wildlife diseases. Here, we demonstrate that variation in host and pathogen factors drive the direction, duration and intensity of a coral disease outbreak. We collected longitudinal health data for 200 coral colonies, and found that disease risk increased with host size and severity of diseased neighbours, and disease spread wa ...[more]

PMID: 29321299

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Project description:Disease epidemics typically begin as an outbreak of a relatively small, spatially explicit population of infected individuals (focus), in which disease prevalence increases and rapidly spreads into the uninfected, at-risk population. Studies of epidemic spread typically address factors influencing disease spread through the at-risk population, but the initial outbreak may strongly influence spread of the subsequent epidemic.We initiated wheat stripe rust Puccinia striiformis f. sp. tritici epidemics to assess the influence of the focus on final disease prevalence when the degree of disease susceptibility differed between the at-risk and focus populations.When the focus/at-risk plantings consisted of partially genetic resistant and susceptible cultivars, final disease prevalence was statistically indistinguishable from epidemics produced by the focus cultivar in monoculture. In these experimental epidemics, disease prevalence was not influenced by the transition into an at-risk population that differed in disease susceptibility. Instead, the focus appeared to exert a dominant influence on the subsequent epidemic.Final disease prevalence was not consistently attributable to either the focus or the at-risk population when focus/at-risk populations were planted in a factorial set-up with a mixture (~28% susceptible and 72% resistant) and susceptible individuals. In these experimental epidemics, spatial heterogeneity in disease susceptibility within the at-risk population appeared to counter the dominant influence of the focus.Cessation of spore production from the focus (through fungicide/glyphosate application) after 1.3 generations of stripe rust spread did not reduce final disease prevalence, indicating that the focus influence on disease spread is established early in the epidemic.Synthesis and applications. Our experiments indicated that outbreak conditions can be highly influential on epidemic spread, even when disease resistance in the at-risk population is greater than that of the focus. Disease control treatments administered shortly after the initial outbreak within the focus may either prevent an epidemic from occurring or reduce its severity.

Project description:Until recently, subtropical Hawai'i escaped the major bleaching events that have devastated many tropical regions, but the continued increases in global long-term mean temperatures and the apparent ending of the Pacific Decadal Oscillation (PDO) cool phase have increased the risk of bleaching events. Climate models and observations predict that bleaching in Hawai'i will occur with increasing frequency and increasing severity over future decades. A freshwater "kill" event occurred during July 2014 in the northern part of K?ne'ohe Bay that reduced coral cover by 22.5% in the area directly impacted by flooding. A subsequent major bleaching event during September 2014 caused extensive coral bleaching and mortality throughout the bay and further reduced coral cover in the freshwater kill area by 60.0%. The high temperature bleaching event only caused a 1.0% reduction in live coral throughout the portion of the bay not directly impacted by the freshwater event. Thus, the combined impact of the low salinity event and the thermal bleaching event appears to be more than simply additive. The temperature regime during the September 2014 bleaching event was analogous in duration and intensity to that of the large bleaching event that occurred previously during August 1996, but resulted in a much larger area of bleaching and coral mortality. Apparently seasonal timing as well as duration and magnitude of heating is important. Coral spawning in the dominant coral species occurs early in the summer, so reservoirs of stored lipid in the corals had been depleted by spawning prior to the September 2014 event. Warm months above 27 °C result in lower coral growth and presumably could further decrease lipid reserves, leading to a bleaching event that was more severe than would have happened if the high temperatures occurred earlier in the summer. Hawaiian reef corals decrease skeletal growth at temperatures above 27 °C, so perhaps the "stress period" actually started long before the bleaching threshold of 29 °C was reached. Hawai'i is directly influenced by the PDO which may become a factor influencing bleaching events in subtropical Hawai'i in much the same manner as variations in the El Niño Southern Oscillation (ENSO) influences bleaching events at low latitudes in the tropical Pacific. Records show that offshore temperatures measured by satellite will not always predict inshore bleaching because other factors (high cloud cover, high wind and wave action, tidal exchange rate) can limit inshore heating and prevent temperatures in the bay from reaching the bleaching threshold. Low light levels due to cloud cover or high turbidity can also serve to prevent bleaching.

Dataset Information

Host size and proximity to diseased neighbours drive the spread of a coral disease outbreak in Hawai'i.

Publications

Host size and proximity to diseased neighbours drive the spread of a coral disease outbreak in Hawai'i.

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