Seagrass Wasting Disease

Disease Ecology of Labyrinthula sp.

History in Australia

∗Blue & Bold = Research Gap

Virulence

Summary Citation
Opportunistic Pathogens Typically acts as a saprobe (degrader) of senescent or dead marine plant/algae biomass. However, when isolates can penetrate the epidermis/cell wall of the living host, it can kill the cells, causing black lesions to form. For seagrasses, once enough of the living tissue turns necrotic (i.e. bisect the blade width), nutrient and oxygen resources are blocked and the blade dies. Once enough blades die on a plant or meadow, it may be considered a disease-related die-off.
Abiotic or Biotic Factors More work needs to be done to understand if there are abiotic or biotic triggers for virulence in Labyrinthula and if so, what are the cellular mechanisms behind them.
Genetics Primarily as amplicon sequencing for genetic or phylogenetic surveys and identification. There is ongoing work for whole genome sequencing. NCBI
Vectors & Cross-Infection Known vectors include seagrass blades/wrack as well as the water column. For some Labyrinthula isolates, cross-infection can occur among different seagrass species. Vergeer & den Hartog 1994; Garcias-Bonet et al. 2011; Martin et al. 2016; Trevathan-Tackett et al. 2018

Hosts affected

Reviewed in Martin et al. 2016, Sullivan et al. 2013

Seagrass – Leaves

Macroalgae – Frond/thallus

Mangrove – Leaves

Turf Grass

Ameoba

Fish

 

Host susceptibility

 

Summary Citation
Heathy/Neutral Conditions Labyrinthula has been shown to be present on seagrasses showing no signs of disease, i.e. Older leaves have often been confirmed to be more susceptible to infection than younger leaves. Seagrass leaves that are large and long tend to been shown to have higher incidences of lesions. Bocklemann et al. 2013; Groner et al. 2014; Groner et al. 2016
Degraded Conditions Low salinity Low salinity environments typically act as a refuge against infection due to Labyrinthula intolerance to low salinities (typically <15 psu). Even if seagrasses are stressed by low salinities, it is not expected to result in higher incidences of wasting disease. Jakobsson-Thor et al. 2018
High salinity It is suggested that high salinity alone cannot cause increases in seagrass wasting disease, possibly linked to the metabolic response of seagrass to high salinity (increase respiration and ROS) indirectly slowing Labyrinthula growth and infection. Trevathan et al. 2011
High temperature Presence of Labyrinthula zosterae and symptoms of wasting disease has been shown to be higher in summer months in field studies. High temperature stress, in some cases, has been hypothesised to cause stress in seagrass and potentially higher susceptibility to disease. Bocklemann et al. 2013
Light Insufficient research, although it is hypothesised that reduced photosynthesis would reduce the health of the seagrass and thus cause it to be more susceptible to disease. Vergeer et al. 1995
Eutrophication Insufficient research NA
Depth There is contradictory evidence on the effect of depth on wasting disease. Both relative shallow and deep meadows have been shown to have increased Labyrinthula prevalence. Groner et al. 2014; Jakobsson-Thor et al. 2018
Multiple stressors Temperature + salinity + oxygen sulphide stress The effect of multi-stressor events on seagrass wasting disease are complex. Elevated infection/disease is likely only to occur if the seagrass is immunocompromised and Labyrinthula is not. In some cases, environmental stress can negatively affect both host and pathogen resulting in low infection/disease rate. Bishop et al. 2017
Salinity + depth Infection increased with salinities > 25 psu and with increasing depth. Jakobsson-Thor et al. 2018
Potential for defence or recovery Secondary metabolites Production of biochemical compounds by seagrass has been suggested defence mechanisms for Labyrinthula infection, either directly or indirectly and in vitro. Potential compounds include phenolic acids, tannins, flavone glycosides. It is hypothesised that seagrasses have both constitutive (innate) and induced (produced) biochemical defences. Vergeer & Develi 1997; Arnold & Targett 2002; Steele et al. 2005; Brakel et al. 2014; Trevathan-Tackett et al. 2015; Jakobsson-Thor et al. 2018
Reactive oxygen species Reactive oxygen species (ROS) and the hypersensitive response is a mechanism used seagrasses, likely as a defence response. There is evidence that seagrasses accumulate ROS during infection, but it is unclear if Labyrinthula presence or invasion into the tissues directly triggers this response. Trevathan et al. 2011; Loucks et al. 2013
Limitation to lesion growth Lesion prevalence may be high in seagrass meadows, yet meadows generally do not commonly experience wasting disease-related die-backs. It is not clear the exact mechanism of the limited infection, whether it be linked to seagrass defences or limited capacity of some Labyrinthula isolates to infect living, healthy tissue. NA

Environment

 

Summary Citation
Disease Inhibition Low salinity Low marine/estuarine salinities are not suitable conditions for Labyrinthula; typically, salinities below 10-15 psu. McKone & Tanner 2009
High salinity Short-term hypersalinity events (> 40-45 psu) have been shown to suppress Labyrinthula proliferation and infection. Trevathan-Tackett et al. 2011; Bishop et al. 2017
Disease Proliferation Virulence genes Mechanisms behind Labyrinthula virulence is a topic still undergoing research. NA
Seagrass density Seagrass meadows with high leaf density have been show to exhibit higher degree of lesions and diseases, likely due to the great chance of leaf-to-leaf transference of pathogenic Labyrinthula Groner et al. 2016; Irving et al. 2016
Climate Change & Future Predictions There has been some work predicting the effects of climate change on seagrass wasting disease. Most are laboratory experiments simulating shifts in environmental conditions (see above), while some papers have taken a modelling approach to predict disease and transference. Irving et al. 2016

Identification
Examples of lesion formation after seagrasses Zostera muelleri and Heterozostera nigricaulis were infected with Labyrinthula for three days. Arrows point to black lesions caused by Labyrinthula infection that can bisect the leaf width or spread along the leaf edge. Insets highlight the lesion details. First (1°), second rank (2°) and third (3°) rank blades indicate youngest and second- and third-oldest leaf blades, respectively. Scale bars= 1 cm.

Photo credit: Trevathan-Tackett et al. 2018
An example of what Labyrinthula looks like when isolated from a seagrass leaf. The seagrass leaf blade (right) was placed of serum-seawater agar petri dish for a couple days prior to a Labyrinthula colony growing onto the agar. Photo was taken with a microscope under phase contrast and the scale bar represents 1 mm. Photo credit: B. Sullivan & S. Trevathan-Tackett
Representative types of culture morphologies of Labyrinthula sp. isolated from seagrasses along the Victoria coastline of Australia. Asterisks highlight visible ectoplasmic network between cells. Scale bars represent 1 mm (a, c, d), 0.1 mm (d, e) or 0.01 mm (f).

Photo credit: Trevathan-Tackett et al. 2018

Monitoring

 

Method of detection Pros of Method Cons of Method Notes Citation
Lesions Easy; Technically inexpensive Manually intensive; Assumes all lesions are caused by Labyrinthula infection Still used for initial ID with other methods to confirm disease Burdick et al. 1993
Culturing Best standardised way to ID Labyrinthula presence; Best way to build up culture for genetic sequencing or laboratory research; Media can be made inexpensively Isolation and maintaining cultures is labour intensive; Some media recipes are expensive; Need to have training in Labryinthula identification and sterile technique; Cultures can be prone to die-off or have fungal contamination if frequent sub-culturing is not maintained Cryopreservation can be used to keep stock cultures but still unknown how genetics or virulence is affected Martin et al. 2009; Muehlstein et al. 1991; Trevathan et al. 2011; Trevathan-Tackett et al. accepted in Disease of Aquatic Organisms
Pathogenicity/Koch’s Postulates Best standardised way to ID virulence characteristics of Labyrinthula and host susceptibility in a controlled environment Requires living Labyrinthula cultures, mesocosm facilities and proper waste methods to prevent spread of pathogenic Labyrinthula beyond test subject Need to consider natural Labyrinthula presence (and infection) on the healthy seagrass hosts used in testing (i.e. acclimation period prior to infection) Short et al. 1987; Martin et al. 2016
(q)PCR Rapid identification and/or quantification of Labyrinthula on host Requires specific laboratory facilities and instrumentation; Knowledge of genetics and PCR techniques needed; Methodology and primer development are still being optimised Primers used for L. zosterae (q)PCR may need to be tested and adapted to local Labyrinthula isolates Bocklemann et al. 2013

Prevention

Tested Method of Prevention: TBD

 

 

Management

Tested Method of Prevention: TBD

 

Risk Assessment

∗Blue & Bold = Research Gap

Natural Occurrence in Australia

Introduction into new areas, cultures, stocks

Sources

 

Vectors

Spread of disease

How to read the Risk Tables

 

Risk Marix1:

1Levels of Consequence:

Minor: measurable, but minor levels w low/no impact

Moderate: some impact

Major: reduction and impact on reproduction

Severe: significant reductions in size and reproduction

 

Risk Evaluation1:

1Levels of Likelihood:

Remote: Consequence not hear of but plausible

Unlikely: Not likely, unless in special circumstance

Possible: May occur in some circumstances

Likely: Consequence is expected to occur

 

1Assuming no management methods are taken. Modified from Department of Fisheries Western Australia, ‘Threat Identification, Hazard Pathway Analysis and Assessment of the Key Biosecurity Risks presented by the establishment of the Mid-West Aquaculture Development Zone in Western Australia, August 2015