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Variable intertidal temperature explains why disease endangers black abalone.

Tal Ben-Horin1, Hunter S Lenihan, Kevin D Lafferty

  • 1Bren School of Environmental Science and Management, University of California, Santa Barbara, California 93106, USA. tbenhorin@bren.ucsb.edu

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Summary
This summary is machine-generated.

Daily temperature variability increases black abalone susceptibility to rickettsial withering syndrome (WS). However, disease expression and mortality only occur at elevated water temperatures, not temperature variability.

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Area of Science:

  • Marine Biology
  • Ecology
  • Pathogen-Host Dynamics

Background:

  • Infectious diseases can threaten species with local extinction, challenging epidemiological theory.
  • Rickettsiales-like pathogen caused local extinction of black abalone (Haliotis cracherodii) in southern California.
  • Withering syndrome (WS) in black abalone is linked to elevated water temperatures.

Purpose of the Study:

  • Investigate the influence of mean temperature and daily temperature variability on WS epizootiology.
  • Determine how environmental conditions affect black abalone susceptibility and disease expression.
  • Understand the mechanisms driving mass mortality events in black abalone.

Main Methods:

  • Field measurements of abalone body temperatures.
  • Laboratory experiments manipulating intertidal environmental conditions.
  • Testing the impact of temperature variability and mean temperature on WS infection and expression.

Main Results:

  • Daily temperature variability enhanced black abalone susceptibility to infection.
  • Disease expression and mortality were dependent on warm water temperatures, not temperature variability.
  • Infected abalone remained asymptomatic until temperatures exceeded thresholds for WS.

Conclusions:

  • Marine intertidal thermal variation facilitates pathogen infection in black abalone.
  • Warm water temperatures trigger WS expression in infected individuals.
  • Mass mortalities can occur before density-dependent factors limit pathogen spread.