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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.


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Gross lesions of CCA diseases.(A) CWBS in Paragoniolithon solubile and (B) CWPD in Hydrolithon boergesenii from Curaçao in 2012. Black arrow shows the white band in CWBS.
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fig-1: Gross lesions of CCA diseases.(A) CWBS in Paragoniolithon solubile and (B) CWPD in Hydrolithon boergesenii from Curaçao in 2012. Black arrow shows the white band in CWBS.

Mentions: In Curaçao, CCA species are affected by the Coralline White Band Syndrome (CWBS) and the Coralline White Patch Disease (CWPD) (Quéré, Steneck & Nugues, 2015). Both pathologies have the potential to reduce the survivorship and settlement of coral planulae and thus may have important implications for the maintenance and recovery of coral reefs (Quéré & Nugues, 2015). They differ in gross symptoms, spatio-temporal variations and lesion spread, suggesting that they may have different causations (Quéré, Steneck & Nugues, 2015). CWBS lesions are defined by a white-band that appears centrally or peripherally and advances slowly but steadily on the healthy tissue, while CWPD manifests by the presence of distinct white patches on the healthy crust, suggesting sudden losses of tissue (Figs. 1A and 1B). Both diseases result in tissue loss with subsequent colonization by endophytic algae often leading to the death of the diseased patch in the case of CWBS (Quéré, Steneck & Nugues, 2015). Visible symptoms may have a biotic or abiotic origin. On one hand, thermal stress has been shown to cause bleaching in both corals and CCA in the laboratory (Anthony et al., 2008) and algal necroses appear on CCA crust under elevated temperature in aquaria (Martin & Gattuso, 2009). On the other hand, bacterial pathogens can also cause bleaching disease in the marine red algae Delisea pulchra (Fernandes et al., 2011). Gross symptoms in the shape of rings are known to be caused by a bacterial infection in the case of CLOD (Littler & Littler, 1995) and by fungi in the case of CFD (Williams et al., 2014). The aim of this study was to describe CWBS and CWPD at the microscopic level in order to better understand these diseases and their effects on coralline algal tissues.


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

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

Gross lesions of CCA diseases.(A) CWBS in Paragoniolithon solubile and (B) CWPD in Hydrolithon boergesenii from Curaçao in 2012. Black arrow shows the white band in CWBS.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig-1: Gross lesions of CCA diseases.(A) CWBS in Paragoniolithon solubile and (B) CWPD in Hydrolithon boergesenii from Curaçao in 2012. Black arrow shows the white band in CWBS.
Mentions: In Curaçao, CCA species are affected by the Coralline White Band Syndrome (CWBS) and the Coralline White Patch Disease (CWPD) (Quéré, Steneck & Nugues, 2015). Both pathologies have the potential to reduce the survivorship and settlement of coral planulae and thus may have important implications for the maintenance and recovery of coral reefs (Quéré & Nugues, 2015). They differ in gross symptoms, spatio-temporal variations and lesion spread, suggesting that they may have different causations (Quéré, Steneck & Nugues, 2015). CWBS lesions are defined by a white-band that appears centrally or peripherally and advances slowly but steadily on the healthy tissue, while CWPD manifests by the presence of distinct white patches on the healthy crust, suggesting sudden losses of tissue (Figs. 1A and 1B). Both diseases result in tissue loss with subsequent colonization by endophytic algae often leading to the death of the diseased patch in the case of CWBS (Quéré, Steneck & Nugues, 2015). Visible symptoms may have a biotic or abiotic origin. On one hand, thermal stress has been shown to cause bleaching in both corals and CCA in the laboratory (Anthony et al., 2008) and algal necroses appear on CCA crust under elevated temperature in aquaria (Martin & Gattuso, 2009). On the other hand, bacterial pathogens can also cause bleaching disease in the marine red algae Delisea pulchra (Fernandes et al., 2011). Gross symptoms in the shape of rings are known to be caused by a bacterial infection in the case of CLOD (Littler & Littler, 1995) and by fungi in the case of CFD (Williams et al., 2014). The aim of this study was to describe CWBS and CWPD at the microscopic level in order to better understand these diseases and their effects on coralline algal tissues.

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