Disease in coral reef ecosystems has received great attention, particularly in the western Atlantic where coral disease has been incriminated in the marked degradation of reef habitats (Santavy & Peters 1997, Green & Bruckner 2000). The reefs of the Northwestern Hawaiian Islands (NWHI) are considered to be relatively healthy but are not immune to the conditions that have led to the decline of other reef systems. An outbreak of white syndrome on Acropora cytherea was found at French Frigate Shoals (FFS) in 2003 (Aeby 2006) and an unusual disease presenting as skin de-pigmentation was discovered in reef fish (Ctenochaetus strigosus) at FFS in May 2005. It is important for management agencies to have an understanding of the vulnerability of these reefs to disease and the first steps in managing disease are developing an understanding of the causes of disease and assessing its geographic extent. The objectives of our studies are to understand the epizootiology, or disease dynamics, of coral and fish disease within the NWHI.
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Figure 1. Marked colony with Acropora white syndrome at FFS in May 2005. (Click on the image to open a larger version.) |
French Frigate Shoals (FFS) has the highest diversity and abundance of acroporid corals within the NWHI (Maragos et al 2004). Acropora is affected by two diseases of concern (Acropora white syndrome and Acropora growth anomalies) at FFS (Aeby in press) so five permanent sites were set up in May 2005 to follow the temporal and spatial changes in diseases through time. All five permanent sites at FFS were re-surveyed in May 2006 and four other Acropora-rich sites were surveyed for disease either quantitatively (Rapture Reef, CRED site# 8) or qualitatively (La Perouse, CRED site# 28). Seven of the nine sites were found to have colonies infected with Acropora white syndrome (frequency of occurrence = 66.7%). Prevalence of the disease ranged from zero to 4.98%.
Fifty out of 54 marked colonies of Acropora cytherea were re-located and photographed. Analysis of the 41 marked colonies that had Acropora white syndrome (AWS) in 2005, revealed partial to total mortality in 97.6% of the colonies in 2006. Forty-six percent of the colonies suffered complete mortality (case fatality rate) with the remaining colonies exhibiting partial colony mortality that ranged from 10–90%. Twenty-seven new cases of AWS were found and tagged for follow-up surveys. Eight out of nine marked colonies with growth anomalies were also found and re-photographed. Five of the eight colonies (62.5%) had an increased number of growth anomalies that ranged from 2 to 19 new tumors per colony. 57.1% of the colonies had growth anomalies with signs of necrosis. Within the transects, seven new colonies with growth anomalies were found and tagged.
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Figure 2. Same colony in May 2006 showing complete mortality from disease. (Click on the image to open a larger version.) |
Disease can affect coral communities directly through mortality of colonies such as we observed with Acropora white syndrome or indirectly through sub-lethal events such as reduced growth, resilience or reproduction. Acropora growth anomalies probably result in an energy drain on the colony that could affect reproductive output. A. cytherea is known to reproduce during May/June in the NWHI (Kenyon 1992), so we sampled eight tumored and non-tumored A. cytherea colonies. These samples will be examined histologically (studying cells and tissues at the microscopic level) and for reproductive status in the lab. Once a disease of concern has been identified the next step is to understand the disease processes so that management or treatment of the disease can begin. Despite the successful treatment of black-band disease accomplished in the Florida Keys, few other studies have explored the possibility of treating infected corals. The first step in developing a treatment plan would be to determine the etiology, or the cause or origin, of the disease.
Recently, the etiology of Acropora white syndrome in the Marshall Islands was determined and found to be a pathogenic bacterial sp. (Sussman et al personal communication). As a first step in elucidating the etiology of Acropora white syndrome at FFS we conducted basic studies on the ecology of the bacterial communities on infected versus uninfected corals. Bacteria from colonies with signs of Acropora white syndrome and uninfected controls were cultured and colony-forming units per cm3 coral tissue were found to be much higher in the infected tissue (avg. >15,000) as compared to control regions of the colony (avg. 34.8) or healthy colonies (avg. 25.9). This suggests that the disease front of the infected region has an overgrowth of bacteria that could be due to either pathogenic and/or opportunistic bacteria. The low bacterial numbers on the control regions of the infected colony suggests that the increased bacterial response may be limited to the site of infection with no whole colony response.
Johnston Atoll may serve as a stepping-stone for recruitment of organisms into the NWHI including potential pathogens.Acropora white syndrome (AWS) has been documented at Johnston Atoll (Aeby unpublished data) opening up the possibility that Johnston was the pathway from which the disease entered FFS. While we were unable to test this hypothesis through identification and comparison of the pathogens causing AWS at Johnston versus FFS during the May-June 2006 cruise due to logistical issues, we were able to examine the condition of the reefs of Johnston that could reflect the potential for future damage from AWS at FFS. Quantitative and qualitative disease surveys were conducted at several sites at Johnston Atoll. Acropora white syndrome was found at 8 of 12 sites (frequency of occurrence = 66.7%). Prevalence of the disease ranged from zero to 19.2%. One site (JM 1ap: Donovan’s Reef) was found to have high numbers of completely dead table corals with coral cover less than 5%. Coral cover at Donovan’s Reef in 2001 and 2003 was visually estimated from photographs to be greater than 80%. This suggests that this area of the reef has experienced a dramatic decline in coral within the past three years.
Diseases in marine ecosystems are not limited to corals. A number of diseases of reef fish have now been found in the Main Hawaiian Islands (Work et al 2003; Work & Aeby unpublished data) and our objective was to determine whether those diseases also occur in fish in the NWHI. We have examined 336 butterflyfish for cutaneous tumors in the NWHI (May 2005: n=155; May 2006: n=181) and found no signs of disease. Butterflyfish with cutaneous tumors have been found in the MHI (Work & Aeby unpublished. data) but apparently this disease is not found or is extremely rare on the pristine reefs of the NWHI.
In May 2005, reef fish (kole) were found with an obvious skin discoloration. External examination of some of these fish revealed poor body condition and fins with ragged edges. The most significant histological finding in fish with pigment anomalies was excessive growth of skin cells suggestive of pre-cancerous lesions. Other incidental lesions such as muscle parasites or necrosis of the kidney were occasionally found. An additional twenty-three kole were necropsied in May 2006 and will be examined histologically for signs of disease. Ta‘ape were introduced into Hawai‘i in the 1950s (Randall 1987) and have spread all the way to Midway Atoll but have not yet reached Johnston Atoll. Ta‘ape are closely associated with certain native goatfish (Mulloidichthys sp.) (Friedlander et al 2002) and goatfish from the MHI have been found to be infected with some of the same diseases as ta‘ape (Work et al unpublished data). Given that ta‘ape were introduced into Hawai‘i, there is the concern that the recently documented diseases may also have been introduced and are spreading to native fish species. To address this question we sampled goatfish from the NWHI (n=11) where ta‘ape are present and Johnston Atoll (n=26) where no ta‘ape occur. Tissue samples are being processed and will be examined histologically for signs of disease.
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