Australian Institute of Marine Science

Australian Institute of Marine Science

 
 

Copyright ©1996-2008

 

Coral Diseases on the Great Barrier Reef
Patterns of distribution and changes in abundance
of Hard Coral Disease

 

White Syndrome

"White" type diseases were first described in the Caribbean as far back as the late seventies with the initial discovery of White Plague Type I disease in 197720. This was soon followed by an ever-growing list of other "white" type diseases identified by differing signs of mortality on affected corals. These include Shut Down Reaction21 (1977), White Band Type I22 (1982), White Pox23 (1996), White Plague Type II24 (1998), White Band Type II25 (1998), Skeleton Eroding Band26 (1999) and White Plague Type III27 (2001). With the exception of skeleton eroding band disease, these were all described from the Caribbean.

At present there is no known relationship between the "white" diseases described from the Caribbean and those encountered on the GBR.

This is because pathogens infecting GBR corals have not been isolated and compared to those producing white syndromes in the Caribbean.

The term ‘white-syndrome" (WS) was coined by the AIMS LTMP in recognition of the difficulty in diagnosing a disease(s) of unknown pathology based simply on visual field characters or signs. Typically WS is expressed on a coral as a white band sharply cutting across live coral tissue with a clear area of necrosis where the dead white coral skeleton and the living coral colony meet (Image 4).

The progression of the band is generally slow enough that an area of coral with an increasing density of turf algae is seen, as you look further away from the freshly dead white part of the colony. Within this general pattern the symptoms can vary considerably depending on the progression of the disease and the amount of the colony it infects.

The LTMP has been collecting data on WS since 1999 and despite the fact that many "white" diseases had been described from the Caribbean, a lack of research into diseases of corals on the GBR means that there remains great difficulty relating symptoms observed on corals on the GBR with their counterparts in the Caribbean.

In contrast to BBD, WS is relatively common on the GBR and is usually associated with the fast growing Acropora spp. hard corals (pers obbs). LTMP data shows a fluctuation in the presence of the disease on the GBR over time and that in 2003 there was a large spike in the occurrence of WSD on the GBR (Graph 5).

Hard coral colony showing the typical signs associated with White Syndrome

Image 4 Tabulate Acropora sp. hard coral colony showing the typical signs associated with White Syndrome. These are in order, a line of recently dead necrotic tissue where the disease is active, a line of white denuded coral skeleton that has been recently killed, and a following area of increasingly darkened dead coral as filamentous algae begins to grow on the dead part of the colony.
Photograph AIMS LTMP
Click here for a larger view

Hard coral showing the typical signs of white syndrome

Image 5 Photograph of a massive Goniastrea sp. hard coral showing the typical signs of white syndrome.
Photograph AIMS LTMP
Click here for a larger view

Fortunately this increase was short lived and has not continued in subsequent years. The exact reason(s) for this apparent increase in the incidence of the disease is not known though it was apparent in all sectors of the reef surveyed with the exception of the Townsville sector that has historically recorded the lowest incidence of WS.

Analysis of data collected by the LTMP since 1999 indicates that there is clear evidence for a significant relationship between the occurrence of white syndrome on the log scale and coral cover in each year (i.e. increases in coral cover are associated with a proportional increase in white syndrome disease). Given this result it is not surprising that much of the observed mortality was observed in areas characterised by a high cover of tabulate Acropora spp. hard corals particularly in the Cooktown/Lizard Island sector to the north and Capricorn –Bunker sector to the south (Graph 6).

Of particular interest is the strong cross-shelf pattern in occurrence of WS that is far more common on outer shelf reefs than midshelf and inshore reef (Graph 7). This is in complete contrast to the distribution of BBD. The lack of anthropogenic impacts to these relatively isolated reefs suggests that changes in WS abundance are unlikely to be driven by terrestrial sources of pollution or other human activities. Rather changes in abundance would appear to be driven by simple changes in coral cover. For instance increasing coral cover would be reflected in increased occurrence of WS through easier disease transmission or susceptibility through crowding or as colonies age6. In terms of presence around the reef the reef perimeter analysis showed no evidence for differences in the occurrence of WS among zones (Graph 8). This is despite the fact that coral cover is generally lower on the back reef.

Graph 5. Mean (SE) number of colonies recorded as showing signs of WSD per survey reef from 2000 to 2005.

Graph 6. Mean (SE) number of colonies recorded as showing signs of WSD per survey reef for each of the six LTMP survey sectors. CL = Cooktown/Lizard Island, CA = Cairns, TO = Townsville, WH = Whitsunday, SW = Swain, CB = Capricorn-Bunker.

Graph 7. Mean (SE) number of colonies recorded as showing signs of WSD per shelf position.

Graph 8. Presence absence data recorded during manta tow surveys. Although WSD appears to be more commonly encountered on the front reef slope this is not significant (Pearson Chi-square P = 0.91).

 

 


 CONTENTS
   Introduction | Black Band DiseaseWhite Syndrome | Skeletal Eroding Band
  Brown Band | Skeletal tumours | Atramentous necrosis
  Porites Pinking | Vibrio Induced Bleaching
  References | Content navigation
 

For further information contact
Ian Miller
, AIMS
Telephone: +61 7 4753 4471
Email:
i.miller@aims.gov.au


December 18, 2008