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Dive into the research topics where Drew Harvell is active.

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Featured researches published by Drew Harvell.


Frontiers in Ecology and the Environment | 2004

The rising tide of ocean diseases: unsolved problems and research priorities

Drew Harvell; Richard B. Aronson; Nancy Baron; Joseph H. Connell; Andrew P. Dobson; Steve Ellner; Leah R. Gerber; Kiho Kim; Armand M. Kuris; Hamish McCallum; Kevin D. Lafferty; Bruce McKay; James W. Porter; Mercedes Pascual; Garriett Smith; Katherine Sutherland; Jessica Ward

New studies have detected a rising number of reports of diseases in marine organisms such as corals, molluscs, turtles, mammals, and echinoderms over the past three decades. Despite the increasing disease load, microbiological, molecular, and theoretical tools for managing disease in the worlds oceans are under-developed. Review of the new developments in the study of these diseases identifies five major unsolved problems and priorities for future research: (1) detecting origins and reservoirs for marine diseases and tracing the flow of some new pathogens from land to sea; (2) documenting the longevity and host range of infectious stages; (3) evaluating the effect of greater taxonomic diversity of marine relative to terrestrial hosts and pathogens; (4) pinpointing the facilitating role of anthropogenic agents as incubators and conveyors of marine pathogens; (5) adapting epidemiological models to analysis of marine disease.


Hydrobiologia | 2001

Coral bleaching and disease: contributors to 1998 mass mortality in Briareum asbestinum (Octocorallia, Gorgonacea)

Drew Harvell; Kiho Kim; Craig Quirolo; Julianna Weir; Garriet W. Smith

High sea surface temperature associated with the recent El Niño was responsible for widespread coral bleaching and mortality around the globe in 1998. In addition to mortality caused by temperature and bleaching associated stresses, some of the coral mortality could be due to the outbreak of diseases among already weakened hosts. One possible example of this is the October 1998 epizootic affecting Briareum asbestinum in the Florida Keys, USA. At Carysfort, Sand Key and Western Dry Rocks, between 75 and 90% of B. asbestinum colonies were bleached with prevalence of necroses on bleached colonies ranging from 18 to 70%. Between October 1998 and January 1999, 18 to 91% of colonies on seven 25 × 2 m transects died (mean=68%). In addition, at Carysfort Reef, 65% of necrotic colonies that were tagged in October 1998 were dead by January of the following year. A grafting experiment revealed that lesion-causing infections were transmissible: lesions occurred on 50% of recipient colonies treated with diseased grafts whereas none of the grafts with healthy tissue resulted in disease. Preliminary work to isolate a causative agent yielded a cyanobacterium Scytonema sp., although work to confirm its role in the mass mortality is still on-going. By January 1999, when surviving colonies had regained their color and many lesions had healed, the cause of the Briareum asbestinum mass mortality or even whether a mass mortality had occurred, would have been difficult to ascertain. By any measure, this was a significant epizootic that would have gone undetected or been attributed to bleaching stress in the absence of our evaluation of the role of an infectious disease.


Ecology | 1984

WHY NUDIBRANCHS ARE PARTIAL PREDATORS: INTRACOLONIAL VARIATION IN BRYOZOAN PALATABILITY'

Drew Harvell

Intraindividual variations in morphology as well as variations in population density of bryozoan colonies (Dendrobeania lichenoides) affect foraging patterns of their nudibranch predators in the field and laboratory in Puget Sound, Washington. Three nudibranch species characteristically graze Dendrobeania lichenoides colony perimeters and leave the center unconsumed: = 50% of surveyed colonies showed evidence of nudibranch predation. The proportion of a colony consumed is density dependent. When prey density was low, nudibranchs could consume entire colonies, but ate less per colony as prey density increased in laboratory experiments. Nudibranchs apparently assess intraco- lonial variations in quality, and when prey are abundant, select the preferred parts (perimeter) of each colony. In paired palatability tests, nudibranchs rejected strips cut from colony centers, yet readily ate pieces from other regions. Three features of the colonies were associated with the nonpalatable center of the colony: attachment rhizoids, brown bodies, and embryos. The attachment rhizoids do not account for the decreased palatability observed, which thus may result from either distasteful embryos or brown bodies, which both occur in highest numbers in the colony center. Brown bodies are products of degenerated polypides retained within zooecia in some bryozoan taxa. The function of brown body retention has never been established, despite considerable debate among invertebrate biologists. This study indicates that colonial invertebrate colonies are not necessarily homogeneous resources. Intracolonial palatability may generally vary with ontogeny which, in a colonial animal (or plant) results in intracolonial variation. Nudibranchs primarily eat colonial invertebrates (coelenterates, ascidians, and bryozoans), and consequently their foraging patterns may generally reflect intracolonial variations in the palatability of their resources.


The American Naturalist | 2004

Ecology and Evolution of Host‐Pathogen Interactions in Nature

Drew Harvell

The rates of new diseases outbreaking in natural ecosystems are on the rise. Although work on pathogens in natural ecosystems always lags far behind human and agricultural systems, substantial progress has been made in understanding these interactions. This special issue presents studies across a range of natural ecosystems, including terrestrial, freshwater, and marine. Theory of host‐pathogen interactions drives the focus on questions about natural controls on epizootics in nature, the source of new variant disease strains, the nature of host resistance and parasite virulence, the effects of host species diversity on pathogen prevalence, and the speed of evolution of hosts and pathogens. Studying these interactions in nature brings us to the heart of prominent issues in the evolution and maintenance of biodiversity. These studies pinpoint future priorities in understanding natural dynamics of host resistance and pathogen virulence and factors controlling infectious spread in multispecies communities.


Science | 2015

Emergency response for marine diseases

Maya L. Groner; Rachel Breyta; Andrew P. Dobson; Carolyn S. Friedman; Brett Froelich; Melissa Garren; Frances M. D. Gulland; Jeffrey A. Maynard; Ernesto Weil; Sandy Wyllie-Echeverria; Drew Harvell

Marine diseases can decimate populations and can have substantial ecological, economic, and social impacts. Recent disease outbreaks in marine mammals, shellfish, sponges, seagrasses, crustaceans, corals, and fishes demonstrate the potential for catastrophic effects, including reduced biodiversity,


Trends in Ecology and Evolution | 2003

Rapid evolutionary dynamics and disease threats to biodiversity

Sonia Altizer; Drew Harvell; Elizabeth Friedle


Oceanography | 2007

Coral disease, environmental drivers, and the balance between coral and microbial associates

Drew Harvell; Eric Jordán-Dahlgren; Susan Merkel; Eugene Rosenberg; Laurie Raymundo; Garriet W. Smith; Ernesto Weil; Bette L. Willis


Ecology | 2009

Climate change and wildlife diseases: When does the host matter the most?

Drew Harvell; Sonia Altizer; Isabella M. Cattadori; Laura C. Harrington; Ernesto Weil


Ecology Letters | 2003

Rates of spread of marine pathogens

Hamish McCallum; Drew Harvell; Andrew P. Dobson


Journal of Indonesian Coral Reefs | 2012

Coral Health and Disease in the Spermonde Archipelago and Wakatobi, Sulawesi

Erinn M. Muller; Laurie Raymundo; Bette L. Willis; Jessica Haapkylä; Syafyudin Yusuf; Joanne R. Wilson; Drew Harvell

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Maya L. Groner

University of Prince Edward Island

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Ernesto Weil

University of Puerto Rico at Mayagüez

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Garriet W. Smith

University of South Carolina Aiken

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