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Histopathology of crustose coralline algae affected by white band and white patch diseases.

Quéré G, Meistertzheim AL, Steneck RS, Nugues MM - PeerJ (2015)

Bottom Line: Healthy-looking tissue of diseased CCA did not differ from healthy tissue of healthy CCA.Fungal infections associated with the diseased cells were not seen.Further investigations using an integrated approach are needed to carry out the complete diagnosis of these diseases.

View Article: PubMed Central - HTML - PubMed

Affiliation: Leibniz Center for Tropical Marine Ecology (ZMT) , Bremen , Germany ; Laboratoire d'Excellence 'CORAIL' and USR 3278 CRIOBE EPHE-CNRS-UPVD , Perpignan Cedex , France.

ABSTRACT
Crustose coralline algae (CCA) are major benthic calcifiers that play crucial roles in marine ecosystems, particularly coral reefs. Over the past two decades, epizootics have been reported for several CCA species on coral reefs worldwide. However, their causes remain often unknown in part because few studies have investigated CCA pathologies at a microscopic scale. We studied the cellular changes associated with two syndromes: Coralline White Band Syndrome (CWBS) and Coralline White Patch Disease (CWPD) from samples collected in Curaçao, southern Caribbean. Healthy-looking tissue of diseased CCA did not differ from healthy tissue of healthy CCA. In diseased tissues of both pathologies, the three characteristic cell layers of CCA revealed cells completely depleted of protoplasmic content, but presenting an intact cell wall. In addition, CWBS showed a transition area between healthy and diseased tissues consisting of cells partially deprived of protoplasmic material, most likely corresponding to the white band characterizing the disease at the macroscopic level. This transition area was absent in CWPD. Regrowth at the lesion boundary were sometimes observed in both syndromes. Tissues of both healthy and diseased CCA were colonised by diverse boring organisms. Fungal infections associated with the diseased cells were not seen. However, other bioeroders were more abundant in diseased vs healthy CCA and in diseased vs healthy-looking tissues of diseased CCA. Although their role in the pathogenesis is unclear, this suggests that disease increases CCA susceptibility to bioerosion. Further investigations using an integrated approach are needed to carry out the complete diagnosis of these diseases.

No MeSH data available.


Related in: MedlinePlus

Regrowth of living crust.Regrowth of living crust in (A) CWBS and (B) CWPD. Remnant healthy crust (red arrows) regrew upward and laterally over dead/dying crust. Insert in (A) displays enlargement of transition area with cells showing a condensed nucleus or protoplasmic content (black arrows). T, Transition; Ep, epithallial cells.
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fig-4: Regrowth of living crust.Regrowth of living crust in (A) CWBS and (B) CWPD. Remnant healthy crust (red arrows) regrew upward and laterally over dead/dying crust. Insert in (A) displays enlargement of transition area with cells showing a condensed nucleus or protoplasmic content (black arrows). T, Transition; Ep, epithallial cells.

Mentions: The four CCA species presented similar responses towards diseases. For both diseases, we observed no difference in cell structure and organization between healthy tissue of healthy CCA and healthy-looking tissue of diseased CCA. Cell walls and contents in healthy-looking tissue of diseased CCA were intact without any apparent damage (Figs. 2B and 3B). In contrast, the diseased part of the tissue showed distinct histological changes between diseases. Cells affected by both CWBS and CWPD presented no apparent damage of their cell walls, but showed a complete depletion of their protoplasmic content (Figs. 2D and 3D). However, in all cases of CWBS, we observed a transition area between healthy and dead cells consisting of cells that were partially deprived of protoplasmic content (Fig. 2C). Cells containing what appeared to be a condensed nucleus or balled up cytoplasmic materials were also frequently observed (Fig. 4Ainsert). This transition area most likely corresponds to the white band in the gross morphology (Fig. 1A). It did not exist in CWPD tissue where healthy-looking cells were in immediate vicinity of empty dead cells (Fig. 3C). In two cases of CWBS and one case of CWPD, we observed an overgrowth of the diseased/dead surface by the healthy crust, suggesting tissue recovery (Figs. 4A and 4B).


Histopathology of crustose coralline algae affected by white band and white patch diseases.

Quéré G, Meistertzheim AL, Steneck RS, Nugues MM - PeerJ (2015)

Regrowth of living crust.Regrowth of living crust in (A) CWBS and (B) CWPD. Remnant healthy crust (red arrows) regrew upward and laterally over dead/dying crust. Insert in (A) displays enlargement of transition area with cells showing a condensed nucleus or protoplasmic content (black arrows). T, Transition; Ep, epithallial cells.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4493676&req=5

fig-4: Regrowth of living crust.Regrowth of living crust in (A) CWBS and (B) CWPD. Remnant healthy crust (red arrows) regrew upward and laterally over dead/dying crust. Insert in (A) displays enlargement of transition area with cells showing a condensed nucleus or protoplasmic content (black arrows). T, Transition; Ep, epithallial cells.
Mentions: The four CCA species presented similar responses towards diseases. For both diseases, we observed no difference in cell structure and organization between healthy tissue of healthy CCA and healthy-looking tissue of diseased CCA. Cell walls and contents in healthy-looking tissue of diseased CCA were intact without any apparent damage (Figs. 2B and 3B). In contrast, the diseased part of the tissue showed distinct histological changes between diseases. Cells affected by both CWBS and CWPD presented no apparent damage of their cell walls, but showed a complete depletion of their protoplasmic content (Figs. 2D and 3D). However, in all cases of CWBS, we observed a transition area between healthy and dead cells consisting of cells that were partially deprived of protoplasmic content (Fig. 2C). Cells containing what appeared to be a condensed nucleus or balled up cytoplasmic materials were also frequently observed (Fig. 4Ainsert). This transition area most likely corresponds to the white band in the gross morphology (Fig. 1A). It did not exist in CWPD tissue where healthy-looking cells were in immediate vicinity of empty dead cells (Fig. 3C). In two cases of CWBS and one case of CWPD, we observed an overgrowth of the diseased/dead surface by the healthy crust, suggesting tissue recovery (Figs. 4A and 4B).

Bottom Line: Healthy-looking tissue of diseased CCA did not differ from healthy tissue of healthy CCA.Fungal infections associated with the diseased cells were not seen.Further investigations using an integrated approach are needed to carry out the complete diagnosis of these diseases.

View Article: PubMed Central - HTML - PubMed

Affiliation: Leibniz Center for Tropical Marine Ecology (ZMT) , Bremen , Germany ; Laboratoire d'Excellence 'CORAIL' and USR 3278 CRIOBE EPHE-CNRS-UPVD , Perpignan Cedex , France.

ABSTRACT
Crustose coralline algae (CCA) are major benthic calcifiers that play crucial roles in marine ecosystems, particularly coral reefs. Over the past two decades, epizootics have been reported for several CCA species on coral reefs worldwide. However, their causes remain often unknown in part because few studies have investigated CCA pathologies at a microscopic scale. We studied the cellular changes associated with two syndromes: Coralline White Band Syndrome (CWBS) and Coralline White Patch Disease (CWPD) from samples collected in Curaçao, southern Caribbean. Healthy-looking tissue of diseased CCA did not differ from healthy tissue of healthy CCA. In diseased tissues of both pathologies, the three characteristic cell layers of CCA revealed cells completely depleted of protoplasmic content, but presenting an intact cell wall. In addition, CWBS showed a transition area between healthy and diseased tissues consisting of cells partially deprived of protoplasmic material, most likely corresponding to the white band characterizing the disease at the macroscopic level. This transition area was absent in CWPD. Regrowth at the lesion boundary were sometimes observed in both syndromes. Tissues of both healthy and diseased CCA were colonised by diverse boring organisms. Fungal infections associated with the diseased cells were not seen. However, other bioeroders were more abundant in diseased vs healthy CCA and in diseased vs healthy-looking tissues of diseased CCA. Although their role in the pathogenesis is unclear, this suggests that disease increases CCA susceptibility to bioerosion. Further investigations using an integrated approach are needed to carry out the complete diagnosis of these diseases.

No MeSH data available.


Related in: MedlinePlus