Coral Disease Handbook

7/28/2019 Coral Disease Handbook

http://slidepdf.com/reader/full/coral-disease-handbook 1/124

1

Coral Disease Handboo

Guidelines or AssessmentMonitoring & Managemen



Editors: Laurie J. Raymundo, Courtney S. Couch and C. Drew Harvell

Contributing authors: Laurie J. Raymundo1, Courtney S. Couch2, Andrew W. Bruckner 3, C. Drew Harvell4,Thierry M. Work5, Ernesto Weil6, Cheryl M. Woodley7, Eric Jordan-Dahlgren8, Bette L. Willis9, Yui Sato9, Greta S. Aeby10.

Cover photos: (top) Lyle Vail, Lizard Island Research Station (A acility o the Australian Museum), (bottom) Ernesto Weil,University o Puerto Rico.

The Coral Ree Targeted Research & Capacity Building or Management (CRTR) Program is a leadinginternational coral ree research initiative that provides a coordinated approach to credible, actual

and scientically-proven knowledge or improved coral ree management.The CRTR Program is a partnership between the Global Environment Facility, the World Bank, The Universityo Queensland (Australia), the United States National Oceanic and Atmospheric Administration (NOAA) andapproximately 50 research institutes and other third-parties around the world.

Coral Ree Targeted Research and Capacity Building or Management Program, c/- Centre or MarineStudies, Gerhmann Building, The University o Queensland, St Lucia, Qld 4072, AustraliaTel: +61 7 3346 9942 Fax: +61 7 3346 9987 Email: [email protected] Internet: www.gecoral.org

1University o Guam, 2Cornell University, 3NOAA Coral Ree Conservation Program, 4Cornell University, 5USGS-National Wildlie Health Center,6University o Puerto Rico, 7NOAA Center or Coastal Environmental Health and Biomolecular Research, 8Universidad Nacional Autónomade México, 9James Cook University, 10Hawaii Institute o Marine Biology.

ISBN: 978-1-9213-17-01-9

Product code: CRTR 001/2008

Editorial design and production: Currie Communications, Melbourne, Australia, June 2008.

© Coral Ree Targeted Research and Capacity Building or Management Program, 2008.



3

Contents

1. The Objectives and Scope o This Manual 7

2. A Decision Tree or Describing Coral Lesions in the Field 17

3. Conrming Field Assessments and Measuring Disease Impacts 33

4. Assessment and Monitoring Protocols 47

5. Detecting and Assessing Outbreaks 65

6. Management Issues and Actions 75

Reerences 85

Acknowledgements 95

Appendices 99

Glossary and acronymsRegional contact list o coral disease expertsSupplementary disease and compromised health photographsData sheets currently used or assessment and monitoringSupplementary disease descriptions

Authors 121

A Coral Disease Handbook:Guidelines for Assessment, Monitoring and Management



4



5

Our research careers began in Discovery Bay, Jamaica, in the mid 1970s, where we both studied thebehavior o coral ree organisms, rather than the corals themselves. At that time, living coral covered70 percent o the bottom, and no one worried about the long term persistence o the rees, eventhough the rees were clearly impacted by people via severe overshing. Quite simply, we took therees or granted.

That sunny condence turned out to be totally unounded. In 1980, Hurricane Allen, a categoryve storm, struck and turned much o the ree into a rubble ground. However, rees routinely get hitby hurricanes and typhoons, so they should have recovered. But in 1982 the sea urchin Diademaantillarum was decimated by an as yet unidentied pathogen, and losing this last remaining major grazer contributed to the overgrowth o corals by seaweeds throughout the region. By 1995, coralcover stood at less than 10 percent.

But the loss o grazers was not the only thing happening to these rees. A more subtle and gradualbut no less important killer was also taking its toll – the white band disease o the branching staghornand elkhorn corals. These two species used to be so common that as students we were taught aboutthe “Acropora cervicornis zone” and the “Acropora palmata zone”. Now both species are listed asendangered under the Endangered Species Act, having lost over 90 percent o their numbers in theensuing decades. Like the elms and chestnuts o US orests, they have largely vanished due to disease.

And they are not alone – white plague, yellow band, black band, and many others have since been

documented as major ree killers, not only in the Caribbean but in the Pacic as well. For most o thesediseases we still do not know the causative agent – nor the extent to which pollution and increasedsea surace temperatures may be contributing to disease outbreaks or aecting the ability o corals torecover rom inections. Yet progress is being made, and simply reliably recognizing and documentingthese syndromes and their patterns o inection are important rst steps in addressing this problem.

This handbook makes it much easier to do just that. Designed or managers, it outlines proceduresor describing signs, measuring disease impacts, monitoring disease outbreaks, assessing causes, andmanaging rees to minimize losses due to disease. As the authors note, inormation and expertise oncoral disease are inadequate relative to the scale o the problem. This handbook helps managers notonly to document and manage disease on the rees they are responsible or, but also allows them tocontribute to our scientic understanding o this grave threat.

Nancy Knowlton Marea HatziolosSant Chair in Marine Science Environment Department

National Museum o Natural History The World Bank

Smithsonian Institution


Foreword



6




7

Chapter 1The Objectives and Scope o This Manual

In this chapter you will ind:

A general introduction to infectious diseases in corals – what they are, why they are a growing problem, and

what is currently understood about them.

A look at the current global patterns and hotspots in regard to coral reef diseases.

A summary of the impact of ocean warming and poor water quality on coral reef diseases.



8


The Objectives and Scope o This ManualL. Raymundo and C. D. Harvell

1.1 The state o coral rees and the purpose o this manualCoral rees are the most diverse and among the most productive ecosystems on earth. Millions o people directly rely on the harvest derived rom coral rees as their major source o protein and income.In addition, the revenue coral rees earn rom tourism, recreation, education and research is o major importance to their local and national economies. And nally, current research in such areas as naturalproducts chemistry suggest that coral rees support an unknown number o organisms that may prove tobe o major benet in the treatment o critical human diseases. Yet, in spite o their obvious importance,rees continue to be impacted by “the big our” human activities that threaten their sustainability:climate change, land- and marine-based pollution, habitat degradation and over-shing.

Many o these impacts have obvious and immediate eects, such as smothering or ragmentation o coral to the point o total mortality. However, some eects, such as those rom chemical pollutants,waste or excess nutrients, are more insidious, and their impacts may be more dicult to understandand quantiy. One phenomenon which has recently gained the attention o coral ree scientists andmanagers is disease. Diseases aecting corals, particularly in the Caribbean, have increased in bothrequency and severity within the last three decades and caused major community shits on Caribbeanrees. Yet we are only beginning to understand enough about drivers o disease outbreaks to consider management actions.

While diseases aecting corals have increased since the 1970’s, there are ew individuals throughoutthe world trained to recognize diseases on coral rees. In addition, there are many areas where thereis absolutely no inormation regarding the status o coral health and disease.

Written or coral ree managers, this manual aims to ll the knowledge gap by bringing together what is currently known about coral diseases, how they are studied, and what options are availableor managing them. We rst present some general concepts about disease to put this manual and its

scope in perspective. We then present the most current descriptions o known coral diseases, withinormation to assist in their eld identication. Subsequent chapters are devoted to conrming eldidentications, quantiying impacts o disease to coral communities, assessing disease on rees, andsetting up monitoring programs. We then provide inormation as to what is currently understoodregarding disease outbreaks and how to track and study them. We end with guidelines on managementpractices and suggestions or where to obtain urther inormation and direction.

Included in the appendices are categories o additional inormation which we hope will be useul.Underlined terms throughout the text indicate words listed in the glossary in Appendix 1.

1.2 What is disease?Diseases are a natural aspect o populations, and are one mechanism by which population numbers

are kept in check. For the purposes o this manual, we will use the term disease to mean “anyimpairment to health resulting in physiological dysunction”. Disease involves an interaction betweena host, an agent, and the environment. The ocus o this manual is infectious biotic diseases; thosethat are caused by a microbial agent, such as a bacterium, ungus, virus, or protist, that can be spreadbetween host organisms and negatively impact the host’s health. Other orms o disease that impactcorals may be considered abiotic diseases; they do not involve a microbial agent but impair health,nonetheless. Examples may be those caused directly by environmental agents such as temperaturestress, sedimentation, toxic chemicals, nutrient imbalance and UV radiation. In addition, noninfectiousbiotic diseases are not transmitted between organisms, though they may be caused by a microbialagent. For example, certain microbes secrete a toxin which damages the host animal or plant.A good example o this is botulism; toxins released by the bacterium Clostridium botulinum cause anon-inectious but deleterious disease in organisms that consume it.



9

1.3 Why study inectious diseases o corals?Pathogenic microorganisms, having very short reproductive cycles, evolve more rapidly thanmulticellular organisms. They are also continually transported to new environments in the oceans byruno, shipping vessels, aquaculture, and changing ocean currents. Thereore, we can expect thatnew diseases will continue to emerge. Recent examples o emergent inectious diseases on land thatare threats to humans and wildlie include AIDS, bird fu, and SARS. Under specic conditions, diseaselevels may exceed a population’s ability to cope, resulting in rapid and widespread mortality.

Figure 1.1 Ree in Hanalei Bay, Kauai, Hawaii, which has experiencedextreme sediment stress, resulting in reduced coral coverage and theprolieration o the zooanthids. Photo: G.S. Aeby

A disease is considered an outbreak when the rate at which new hostsbecome inected increases.Technically, an outbreak is denedas R

0>1. R

0is the ratio o new

inections to existing inections (seeChapter 5 and Appendix 1).

Over the past three decades, coralrees worldwide have experienced

major changes in structure andunction due to both anthropogenicand natural impacts (15-18). Virtuallyall o the most pervasive threatsimpacting coral ree ecosystems,including land-based and marinepollution, overshing, global climatechange, and ocean acidication,have been suggested as synergistsor acilitators o inectious disease(Figure 1.1). Inectious disease incorals has increased in requency

and distribution since the early 1970’s when a white band disease outbreak took a heavy toll on

Caribbean acroporids. There has since been an exponential increase in numbers o reported diseases,host species and locations with disease observations. This rate o change is not normal, and hasresulted in signicant loss o coral cover.

Figure 1.2 Students being trained in coral disease assessment methods in theZaragosa Marine Protected Area, Central Philippines. Photo: L. Raymundo

Currently, the study o coral diseaseis in its inancy and those whodevote their time and expertise to itare virtually “learning as they goalong”. However, through theexperience o others who study andmanage diseases in wildlie, armedand cultured animals and plants,and even human populations, we

can adapt methodologies andstrategies to coral diseases thathave been successul in other medical arenas.



10


This manual aims to address an urgent need: to update coral ree managers regarding our currentunderstanding o the basic ecology o coral diseases. This will help improve monitoring eorts andaid in proper recognition o coral diseases and related issues o coral health (Figure 1.2). Although itis important to remember that detailed laboratory investigation remains essential or proper diseasediagnosis and a complete understanding o the impacts to the coral host, we also hope that this

manual will help increase the number o individuals able to provide inormation on the state o healtho the world’s rees. By studying disease and establishing baselines prior to a crisis, we can armourselves with a better knowledge o appropriate management options or a given situation.

1.4 The emergence o coral diseaseDamage to coral by abiotic and biotic actors acting alone or in synergy have led to a global reductionin coral cover (6,18,22-24). To date, the most inectious syndromes o coral or which a causativeagent has been isolated involve bacteria (26). In addition to the loss o coral tissue, disease can causesignicant changes in reproduction rates, growth rates, community structure, species diversity andabundance o ree-associated organisms (28,29). While an unprecedented increase in coral diseasehas been well-documented in the Caribbean over the last decade (11,25,30-32), and some argue

that climate warming has driven part o the increase in damaging outbreaks (Causey, pers. comm.),much less is known about the status o disease throughout the Indo-Pacic (26). However, preliminarysurveys in Australia (33), the Philippines (34), Palau (35), Northwestern Hawaiian Islands (36), AmericanSamoa (37), the central Pacic (38), and East Arica (39,40), have revealed signicant and damagingnew diseases in all locations surveyed. Many o these are suspected or conrmed as inectious.

Figure 1.3 Coral bleaching within the Basdiot Marine Protected Area,Philippines, summer 2006. Photo: K. Rosell

What has prompted this emergenceo coral disease? Current researchsuggests that humans may notonly be introducing new pathogensinto the oceans though aquaculture,runo, human sewage, and ballastwater, but may also be exacerbatingexisting opportunistic inections due to stressors such as poor water quality and climate warming(16,41). Climate warming is nowestablished as an important actor in some current outbreaks(23,32,42). Some experts, suchas Billy Causey (Superintendent,Florida Keys National MarineSanctuary), argue that stressulwarming events may have driveneven more outbreaks than we havedetected to date (Causey, pers.

comm.). Because ree-building corals have a narrow range o thermal tolerance (between 18°C and30°C), they are extremely susceptible to temperature stress. It is well known that corals “bleach” (losetheir symbiotic zooxanthellae) at high temperatures (Figure 1.3). The coral bleaching observedworldwide ollowing the 1998 El Niño was the most massive and devastating recorded up to thatpoint (43), only to be exceeded by another bleaching event in Australia in 2002. The latter part o 2005brought widespread bleaching to the Caribbean, caused by the largest warm thermal anomaly in 100years (Eakin, pers. comm.). The Caribbean thermal anomaly o 2005 was immediately ollowed byoutbreaks o white plague, yellow band disease (42) and white patch disease (32).



11

Our working hypothesis is that, in some cases, the death o coral during hot thermal anomalies isexacerbated by opportunistic inectious pathogens whose virulence is enhanced by increasedtemperatures. Changing environmental conditions could also infuence disease by altering host-pathogen interactions. Increased temperatures could aect basic biological and physiologicalproperties o corals, particularly their ability to ght inection, thus infuencing the balance between

potential pathogen and host (44). In addition, the pathogens themselves could become more virulentat higher temperatures (45). This is particularly challenging to study because o the complexity o the coral holobiont. The animal itsel consists o the coral polyp, the unicellular algae (zooxanthellae)with which it co-exists in a mutualistic relationship, and a bacterial community existing within thesurace mucous layer (SML), the coral tissue itsel and its skeleton. This is very similar to the humanholobiont that has its own unique and critical gastrointestinal mucosal microbiota which producesessential vitamins and amino acids not otherwise available to the human host. The coral SML containsa complex microbial community that responds to changes in the environment in ways that we are justnow beginning to appreciate (46,47). The normal microbial fora within the mucus layer may protectthe coral against pathogen invasion, and disturbances in this normal fora could lead to disease (48).The massive introduction o non-indigenous pathogens, which may occur with aquaculture and ballastwater release, could also disturb the microbial community (16).

1.5 What is our current state o knowledge?The current, and rather urgent, ocus o research is the biology o microorganisms that can bepathogenic to corals. We are working diligently to develop new molecular and biomedical tools toidentiy specic agents and their origins, and determine the role o these agents in causing diseasein corals. In Figure 1.4, we present ve diseases with documented causal agents. The process bywhich causation is veried is explained in detail in Chapter 3. Undoubtedly as we learn more, wewill continue to nd that certain diseases may be caused by more than one microorganism, thoughwhether this may be a matter o location, seasonality or other environmental parameters is unknown.For instance, the species comprising the microbial consortium associated with black band diseaseappears to vary with dierent geographic locations (49). Similarly, there is evidence that Caribbeanyellow band disease (YBD) is caused by a consortium o bacteria (50). Because o inherent diculties in

the process, proving causation may be based on relatively ew corals or disease events. For example,the demonstration o causation or both white plague type II and white patch disease are basedon tests o relatively ew corals, each rom a single location or outbreak event. Our vision is thatcoral disease managers will eventually be equipped with molecular diagnostics to reliably veriy theidentity o a given inectious micro-organism. Thus the process o continuing to veriy these agents isimportant (51).




12

Figure 1.4 The ve coral diseases or which Koch’s postulates have been ullled, showing disease, host coral and microbialpathogen. The classic way to prove a microorganism causes disease is to satisy Koch’s postulates. A microorganism must beisolated rom a diseased individual. That “isolate” is then used to inect a healthy individual. The same disease must develop,and the same organism must be isolated rom the new inection. This classic method is a tough challenge in the ace o unculturable marine microorganisms and polymicrobial syndromes, requiring molecular approaches.

*Originally named white pox, but eld signs or this disease are now termed “white patch disease”; this name will be used inthis book.

1 source: http://commtechlab.msu.edu/sites/dlc-me/zoo/microbes/serratia.html2 source: http://www.cdc.gov/ncidod/dbmd/mdb/images/aspergillos.JPGHarvell et al. (26). Photos by: A. Bruckner and E. Weil.

The last decade has been a time o intense research into causative agents o coral disease. Thoughwe still lack evidence showing the origin o any coral disease, the role o specic pathogens in causingvarious diseases, their pathogenesis, and agent-host interactions, signicant progress is being made in all

o these areas. Some inectious agents that cause disease in marine animals, such as that o aspergillosiso octocorals (Figure 1.5) and toxoplasmosis in sea otters, are thought to originate on land.

Figure 1.5 Caribbean sea an Gorgonia ventalina with multiple aspergillotic lesions. Photo: E.Weil

Others, such as viruses inadvertently introduced romshrimp or abalone arms to wild populations (McCallum,pers. comm.), originate in aquaculture arms (16). Trackingthe origins o pathogenic agents might reveal sources thatcan be controlled beore being introduced into the ocean.For example,Serratia marcescens is a ubiquitous bacteriumintroduced into coastal waters via sewage that may be thecause o white patch, a disease that aects Acroporapalmata (52). There is a very real risk, thereore, that humanactivities may inadvertently introduce environmentalstressors and potential pathogens to marine communities,and will continue to do so unless our understanding o such dynamics improves.

1.6 What are the global patterns and where are the hotspots?The Caribbean has been reerred to as a “hot spot” or disease because o a rapid emergence o new,extremely virulent diseases, increased requency o epizootic events, and rapid spread o emergingdiseases among new species and regions. At least 82 percent o coral species in the Caribbean arehost to at least one disease (21).

In the Pacic, the threat o coral diseases has been regarded as minor, due to the large distancesbetween rees and island nations, ewer potential sources o pathogens, a paucity o epizootiological

Diploria Acropora Acropora Gorgonia Oculinalabyrinthiormis cervicornis palmata ventalina patagonica

Aurantimonas coralicida

(bacterium)

Vibrio carchariae(bacterium)

Serratia marcescens 1 (bacterium)

Aspergillus sydowii 2 (ungus)

Vibrio coralliilyticus (shown) and

V.shiloi (bacterium)

White plague II White band II White pox* Aspergillosis Bacterial bleaching



13

studies and ew recorded outbreaks. However, there were relatively ew comprehensive detailedstudies o coral disease in the Pacic prior to 2000, and most available inormation came rom a handulo locations and researchers. As eorts increase to document coral diseases rom more locationswithin the Pacic, the lists o species aected by disease, locations where diseases are reported, andprevalence o those diseases, are steadily increasing. It is now apparent that certain sites in the

Pacic show a rather high prevalence o disease, and reports o outbreaks that kill a large number o colonies in a relatively short time suggest that the threat o disease impacts can no longer beconsidered minor.

1.7 What do we know about environmental drivers and stress?An understanding o the infuence that the environment plays in disease outbreaks could guide thedevelopment o useul management strategies (Figure 1.6). In this section, we summarize what isknown about the relationship between particular environmental drivers and disease outbreaks.As with most aspects o the management o inectious disease in a marine setting, it is a work inprogress and it is critical to keep in mind that all inectious syndromes are dierent and may respondin dierent ways to environmental change. However, identiying the actors that control the mostimportant inectious syndromes is a key management strategy.

Compromised environmentIncreased pathogen range

and virulence

Normal environment

Host immuno-competentAdequate melanizationand ameobocyte activity

Host immuno-suppressedDecreased melanizationand amoebocyte activity

Normal resistance Lowered resistance

Pathogen

Environmenti.e. changing water

temperature

Figure 1.6 A schematic model showing the eect o an environmental impact – changing temperature – on a gorgoniancoral inected by ungus. The healthy octocoral on the let is immuno-competent and is thus able to mount a normal immuneresponse (melanization and amoebocyte activity). The diseased and dying octocoral on the right shows decreased melanizationand suppressed amoebocyte activity, and is thus susceptible to attack by microorganisms. Modied rom Mydlarz et al. (53).Photos by: C Couch and E. Weil.

Healthy Host Immuno-suppressed hostMelanization

Amoebocytes



14


TemperatureOutbreaks o some diseases are enhanced by ocean warming anomalies. An increase in diseaseollowing warming events may occur because corals are less able to ght disease while under temperature stress, or because pathogens are more virulent at higher temperatures. In three knowncases where the pathogen can be cultured separately (Aspergillus sydowii, Vibrio shiloi and Vibrio

coralliilyticus), pathogen growth and/or virulence increased with rising temperature, up to an optimaltemperature (45,54-57).

Seasonal patterns in disease prevalence in the northeastern Caribbean provide urther support or a link between warming ocean waters and disease outbreaks. Recurrent outbreaks o two virulentand damaging diseases, white plague and yellow band, have developed during seasons o highestwater temperatures or the past our years on Puerto Rican rees (Weil unpubl. data; Hernández-Delgado unpubl. data) and in the US Virgin Islands (42,58). Immediately ollowing the peak o the2005 bleaching event, the most devastating recorded in the North-eastern Caribbean, outbreaks o white plague, yellow band and white patch (32) were even more extensive in these areas and someoutbreaks continued through 2007.

On the Great Barrier Ree, coral disease prevalence increased rom winter to summer in all major amilies o coral (33). Prevalence increased teen-old in acroporids, twelve-old in aviids anddoubled in pocilloporids in summer surveys. In addition, prevalence o three coral diseases increasedsignicantly in summer surveys, with skeletal eroding band increasing more than two-old, black bandand other cyanobacterial inections more than three-old, and white syndrome more than 50-old.

Further work to document a link with temperature was carried out using disease prevalence surveysspanning 500 km o a latitudinal gradient along the Great Barrier Ree. In 1998, the Australian Instituteo Marine Science’s Long-Term Monitoring Program began to systematically monitor white syndrome(WS), which aects more than 15 coral species, including dominant plating acroporids. Diversconducted annual coral disease surveys on 47 rees rom 1998 to 2004 to quantiy the number o cases o WS. Using a weekly our km data set o temperature values derived rom the NOAA AVHRRPathnder (a radiation-detection imager that can determine sea surace temperature), a signicantrelationship was detected between the requency o warm temperature anomalies and the incidence o white syndrome, indicating a relationship between temperature and disease. Interestingly, this

relationship also depended on a high degree o coral cover, as would be expected or transmission o an inectious agent between hosts (23).

Links between outbreaks or increasing prevalence and warm temperature have thus been detectedor black band disease, aspergillosis, yellow band disease, white patch disease and white syndrome.The list will likely grow as the data set expands. We still need to understand the mechanism operatingin each syndrome: can we distinguish whether increased disease transmission during ocean warmingis caused by compromised host immunity or the expansion o geographic range o microorganisms?Understanding these dynamics should aid in developing management strategies during periods o stressul temperatures.

Water QualityAs human populations continue to increase, nutrients, terrigenous silt, pollutants and even pathogens

themselves can be released into nearshore benthic communities (59). While the link betweenanthropogenic stress and disease susceptibility is currently poorly understood, one hypothesis isthat coral disease is acilitated by a decrease in water quality, particularly due to eutrophication andsedimentation. It is an urgent management priority to understand the link between water quality andinectious coral disease, because this is a local actor we can have some hope o managing.



15

Although corals are able to grow in high-nutrient water (60), recent evidence suggests a synergisticeect between elevated nutrients and disease. High nutrients (N, P) were associated with accelerateddisease signs in both yellow band disease- and aspergillosis-inected corals in eld manipulations(61), and in black band disease (62), although high nutrients alone were not associated with increasedtissue loss in healthy corals. This is consistent with the ndings o Kuntz et al. (63) who observed rapid

tissue shedding in healthy corals exposed to elevated carbon sources, but little eect on corals o elevated N and P. Thus, corals seem to thrive under high nutrient conditions, but the combination o an active inection and elevated nutrients increases the disease progression rates o some syndromes.It is unclear whether this eect is due to an impact on host resistance or a positive eect on pathogengrowth or virulence.

Figure 1.7 Tissue loss in a massive Porites in Palau caused by silt deposition.Photo: A. Croquer

Sedimentation oers yet another challenge to host diseaseresistance. The impacts o terrigenous sedimentation onnearshore communities are visibleand well-documented; coralsinhabiting silted rees otenpossess large patches o dead,exposed skeleton bordered byapparently receding margins o healthy tissue (Figure 1.7). Whilecoral tissue mortality was previouslyassumed to be the result o directsmothering, microbial agents mayalso contribute. Early work byHodgson (64) identied silt-associated bacteria as a possiblecause or necrosis in sediment-damaged corals, as antibiotic-treated water reduced the amount

o tissue damage in experimentally-silted corals. More recently, opportunistic terrestrial pathogens(the soil ungus Aspergillus sydowii and the human enterobacterium Serratia marcescens) have beendemonstrated as causal agents or two diseases currently impacting dominant corals in the Caribbean(52,65). Thus, terrigenous silt may not only cause physical stress or shallow, benthic organisms suchas corals, but may also act as a pathogen reservoir.

This evidence suggests that anthropogenic stressors are linked with disease severity in complex ways.It is important to establish and quantiy such linkages, as these actors may be possible to mitigatevia improved ree management and land-use practices. The challenge lies in demonstrating theselinkages in the complex system o diverse stressors acting upon the coral holobiont.



Chapter 2A Decision Tree or Describing

Coral Lesions in the Field


A standardized procedure that will enable you to describelesions in corals that encompasses the range of variation

in colony morphology and geographic location.

Guidance for organizing and collecting data, particularly if you encounter a lesion that is unfamiliar or undescribed.

Descriptions and photos of commonly encountered lesions inthe Western Atlantic, Indo-Pacific, Red Sea and East Africa.



18


A Decision Tree or Describing Coral Lesions in the FieldL. Raymundo, T. Work, A. Bruckner and B. Willis

2.1. IntroductionDisease is the absence o health and is usually maniested by the presence o a lesion (a morphologicabnormality). Three important points should be kept in mind when reading this chapter:

1. Diseases can have many causes; some o these are inectious (such as bacteria, parasites,or viruses) and others are not (such as genetically-based or toxicant-induced disorders).

2. The typical sign o a diseased coral is a lesion; a maniestation o disease that may not provide anyclue regarding causation.

3. Some lesions in corals may have known causes that are not attributable to disease, though theyresult in the coral’s health being compromised. For example, sh bites and crown-o-thorns starsh

eeding scars should be characterized as predation; lesions associated with breakages may becaused by storms or anchor damage and should be characterized as disturbance; and lesionscaused by aggressive interactions between corals or between corals and other sessile organismsshould be characterized as competition. All can lead to tears and breaks in the tissue and partialmortality, and can stress the host coral. In suspected disease cases, it is oten impossible todetermine the cause o the lesion (and, thereore, the cause o the disease) without additionallaboratory or experimental eorts (as discussed in Chapter 3).

Given the diversity o coral morphologies and the potential or environmental stressors to infuencethe progression o a disease, lesions may take on gross morphologies that dier between speciesor that vary temporally or spatially. The rapid growth o literature on coral diseases in the past ewdecades, in the absence o a standardized approach to describing lesions in corals, has resultedin a prolieration o disease names and conusion among researchers. The need or a standardized

approach to describing lesions in corals is clear and urgent.In this chapter we present a scheme that will allow you to describe lesions in corals in a manner thatcan be interpreted by others regardless o colony morphology or geographic location. This schemealso permits you to determine whether or not a lesion has a cause that can be readily determinedwith a high degree o condence ater a rapid assessment o the scene (i.e. predation, competitionsuch as algal overgrowth, invertebrate galls). There are two compelling reasons or including lesionso known cause in your surveys:

1. Certain organisms that interact with corals may be vectors o disease or create potential entrywounds or inectious agents. Recording observations o such associations can lead to greater understanding o how a particular disease is spread, and thus is vitally important.

2. Documentation o such interactions indirectly provides inormation on ecosystem health.

For example, a great number o lesions caused by smothering rom silt may suggest that the ree isaected by land-based sedimentation. Ree managers could make use o this inormation to workwith land managers and local legislators to improve land use practices because o a documentedeect on coral health.



21

2.3 Field assessments o Western Atlanticdiseases and compromised health states

1. Tissue loss: known predation by fshand invertebrates resulting in compromised health

Fish bites• Predominant corallivorous shes including parrotsh, butterysh, lesh, puffersh, triggersh,

and damselsh amilies.

• Corallivores may be in the surrounding area, but often are not observed feeding on coral.

• Most predators create distinctive scars characterized by removal of tissue and underlying skeleton.Butterfysh delicately extract tissue rom individual polyps without abrading the skeleton – theselesions are oten only visible with a hand lens.

Below we describe the most common examples o sh predation encountered on westernAtlantic rees.

Parrotfsh (ocused biting)• Diffuse patterns of tissue loss associated with scrapes or gouges (i.e.

bite marks) by Sparisoma viride (stoplight parrotsh) that removecorallites and underlying skeleton.

• Lesions are large (2-50cm wide), and may be focal, multifocal or diuse. Lesions oten expand rapidly over one to ve days, beginningat a ocal point at the colony margin or within the colony surace andradiating out.

• Sparisoma viride graze predominantly on Montastraea annularis,Montastraea faveolata, Colpophyllia natans and Porites astreoides,and on 18 other species.

• In brain corals (C.natans

andDiploria strigosa

), sh remove tissue ina radiating band starting at one end o the colony. Look or predatorsin the area.

Spot biting• Multifocal, paired lesions associated with removal of corallites,

resulting rom bite marks o parrotsh, puersh and other shes.

• The size and shape of lesions may form a pattern consistent with theupper and lower jaw o the predator.

• Various species leave numerous bite marks on individual colonies.

• Scars include recent lesions lacking tissue and lesions in variousstages o regeneration, as evidenced by pale tissue coveringthe injury.

Damselfsh• Multifocal well-circumscribed, circular, less than 1cm in diameter, acute to

subacute (most species) or diuse (brain corals) associated with tissue lossand removal o corallites by Stegastes planifrons.

• Lesions generally expand outwards, as older lesions are colonizedby algae.




22

• InAcropora, coral growth over time may create chimney-like structuresencircling the algae. In brain corals, bites ollow ridges (previouslymisdiagnosed as “ridge mortality disease”) – lesions progressivelyexpand outwards, but tissue remains in grooves until overgrown byalgae. In M. annularisspecies complex (shown) and Siderastrea siderea,

sh bite at individual polyps in a mosaic pattern.• Look for predators in the area.

Hermodice carunculata (freworm or bristle worm)• Diffuse acute tissue loss beginning from branch tips or colony

projections, revealing intact underlying bare skeleton.

• The amphinomid polychaete H. carunculata eeds on less than 10species o scleractinians, milleporids, anemones and gorgonians.

• Usually active only at night, but sometimes seen during the day.

Gastropod predation• Coralliophila is the only major genus that is predatory on Western

Atlantic corals:

• Focal to multifocal, small, ovoid acute tissue loss. With heavyinestations, a scalloped pattern o shell scars may extend rom thebase or margin o the colony and radiate up and out.

• Two species commonly feed on corals. C. abbreviata (see arrow)eed on scleractinian and hydrozoan corals, while C. caribaea preersgorgonians and zoanthids.

• Small individuals are relatively immobile and may cluster at colony

margins.

• Snails may retreat to the base of the colony during the day.

• Look for predators on colony or at base.

2. Tissue loss: abiotic and biotic diseases

2a. Pigmented band diseases:the presence o a distinct narrow band o pigmented tissue

Black band disease• Black or dark reddish-brown linear, diffuse or annular bands of acute

to subacute tissue loss with a 1mm to 5cm wide margin, less than1mm thick.

• Band is composed of black-red lamentous organisms peppered withwhite laments, separating healthy tissue and white, bare skeleton.

• Band radiates outwards from the colony margin or a focal siteo injury.



23

• In moderate (subacute) infections, denuded skeleton is colonized bylamentous algae and other epibionts.

• May be more than one disease front per colony which may mergeover time. Aects 22 scleractinian corals, one hydrozoan coral andour octocorals.

Red band disease• Diffuse to circular band of red or dark reddish-brown lamentous

organisms lacking white laments, 1mm to 5cm wide.

• Rapid to moderate (acute to subacute) tissue loss reveals intact, bareto algae-covered skeleton.

• Band is linear to annular to irregular, radiating outwards from thecolony margin or a ocal site o injury.

• Common on octocorals, also affects Agaricids, Meandrina andMycetophyllia and other less common scleractinians (see Appendix 4).

Caribbean ciliate inection• Observed infecting coral in two distinct patterns: a diffuse black or

grey band, several mm to 2cm thick, separating healthy tissue rombare skeleton or a diuse scattered patch.

• Both bands and patches have a “salt-and-pepper” speckledappearance caused by the presence o ciliates.

• Patches may be associated with colonizing algae on bare skeleton

2b. Focal or multiocal tissue loss without distinct microbial bandUlcerative white spots

• Multifocal well-circumscribed, distinct white discoloration or acutetissue loss revealing intact bare skeleton.

• Lesions are less than 1cm in diameter with discrete margin and mayeither contain bleached tissue or be devoid o tissue.

• Lesions may coalesce and become colonized by algae, or healand disappear.

White patch disease• Diffuse focal or multifocal lesions, 1-80cm in diameter with a sharply

circumscribed leading edge o tissue loss.

• Lesions may radiate out over time and coalesce (see arrow), or (in Acropora) heal and resheet once mortality stops.

• Frequently, tissue remnants are visible adjacent to the leading edge.

• Corallites may be eroded, but underlying skeleton is intact.

• Formerly called white pox and patchy necrosis in Acropora palmata,but similar signs reported in other massive and plating corals.




24

2c. Annular or linear tissue loss without distinct pigmented bandWhite band disease

• Disease front characterized by linear, discrete band of acute tissueloss, 2-10cm wide, which may circumscribe the branch.

• Band separates healthy tissue from exposed skeleton colonizedby epibionts.

• Disease progresses rapidly (mm-cm/day) from colony base or branch biurcation.

• Tissue adjacent to exposed skeleton may be bleached; snails andreworm predators may colonize the disease ront.

• Only observed in Acropora.

White plague• Lesions are focal or multifocal-to-coalescing, with a linear or annular

margin, depending on colony morphology.

• A discrete band of bare skeleton separates live tissue fromalgal-colonized skeleton.

• Tissue adjacent to exposed skeleton may be bleached.

• Linear tissue loss begins at the base or margin of a colony, or emanatesrom an algal/sediment interace within the colony, and advances1mm to > 10cm/day.

• Closely resembles white band disease, but affects more than 40 spp.o non-acroporid massive and plating corals.

2d. Tissue loss without distinct pigmented bandCaribbean white syndromes• Diffuse patterns of tissue loss with no distinctive pigmented mat or

band at the interace, i.e. tissue loss that is not characteristic o either white band or white plague.

• In acroporids, this can include diseases that start within the colonyand not at the base, and spread in irregular patterns.

3. Discoloration

Dark spots disease• Focal to multifocal lesions with annular to irregular margins, purple to

brown in color and 1cm to more than 45cm in diameter.

• Dark spots may expand over time, coalesce, and form diffuse toannular bands adjacent to or surrounding exposed skeleton.

• Affected tissue may be associated with a depression of the coralsurace and may seasonally disappear.

• Underlying skeleton may retain dark pigmentation when tissue is gone.

• Primarily affects Stephanocoenia, Montastraea and Siderastrea.



25

Yellow band disease• Focal, multifocal, diffuse lesions with annular to linear margins of pale

yellow, bordered by healthy tissue.

• Lesions progress mm to cm per month.

• The leading edge of the band remains pale yellow or lemon colored,while tissue previously aected gradually darkens prior to ull tissueloss; acute tissue loss is rare.

• Primarily affects Montastraea.

Pigmentation response• Multifocal or diffuse areas of white, purple, yellow, brownish or blue

colored tissue discoloration.

• Tissue may appear unhealthy, swollen, and/or peeling away atthe edges.

• Pigmentation may form lines, bumps, spots, patches, bands or

irregular shapes.

• Considered a response of the coral host to a variety of stressors(i.e. unidentied pathogens, competition, predation, boring auna,abrasion, etc.), suggesting that organism health is compromised.

• Common on corals such as Porites, Siderastrea, and Montastraeaand octocorals such as Gorgonia, Pseudoplexaura, Plexaura,Briareum, and Erythropodium.

Aspergillosis• Diffuse lesion(s) of various sizes and shapes distributed throughout

the sea an blade and branch network, resulting in loss o tissueand/or skeleton.

• Tissue surrounding the lesion often becomes dark purple(pigmentation response). Aected colonies may also producepurple nodules or galls near the lesion, which can encapsulateungus, algae or other epibionts in an attempt to connethe inection.

• Lesions recently produced by predation (amingo tongue, reworms)usually do not show purple coloration but instead the dark brownskeletal matrix, devoid o tissue, is clearly seen.

• Some of these lesions along the branches eventually producepurpled edges.

• Lesions from continuous contact with other octocorals, corals,hydrocorals and/or the substrate usually show the pigmentationresponse at the point o contact.

• Only affects octocorals, most commonly Gorgonia, Pseudop-terogorgia, Plexaura, Plexaurella.




26

Ulcerative white spots• Described above under Tissue Loss.

• Also involves loss of pigmentation, as lesions may contain bleachedtissue at certain stages, so it is cross-reerenced here.

Bleaching• Focal, multifocal-to-coalescing, or diffuse areas of tissue discoloration.

• Loss or reduction in the number of endosymbiotic algae (zooxanthellae)rom coral tissue.

• Tissue is present, but with reduced or absent pigmentation.

• Bleaching can affect the entire colony, upper surfaces, the base, or discrete patches.

• Bleached tissue may be associated with irregular patterns of tissue loss.

4. Growth anomaliesGalls

• Focal to multifocal skeletal deformation with presence of organism(crab, barnacle, etc.).

• Deformations caused by skeletal deposition around the resident

invertebrate result in uncharacteristic patterns. Resulting lesions maybe ocal or multiocal, circular to irregularly shaped mass o thickenedcoenosteum (see arrow), elevating polyps 2-4mm above the suraceo the colony or an.

• Also reported as tumor-like growth, tumor, algal tumor, algal gall,gorgonin pearl, and nodules on gorgonians.

Growth anomalies o unknown cause• Focal or multifocal, annular to diffuse lesion consisting of abnormally

arranged skeletal elements (corallites, ridges, valleys), which are visiblylarger or smaller than those o adjacent healthy tissue.

• They may protrude above the colony surface, and may or may not be

covered by intact tissue.• Pigmentation may be normal, lighter (suggesting loss of zooxanthellae),

or completely absent (suggesting an absence o zooxanthellae).

• In some types, corallites may be completely absent, and the growthanomaly resembles a white plaque over the colony surace. In other types, corallites may be highly disorganized and tissue may die inirregular patches and bare skeleton may be colonized by epibionts.

• Also includes conditions referred to as gigantism, accelerated growth,tumors, and chaotic polyp development.



27

2.4 Field assessments o Indo-Pacifc, East Aricanand Red Sea diseases and compromised health states

1. Tissue loss: known predation orstress resulting in compromised health

Fish bites• Look for predators in survey area (though they may actively feed at night) and distinctive scars

on coral skeleton.

• These examples are not exclusive and other sh predators may leave different scars.

• Look for gouging, scraping, or other regular patterns of tissue loss, often clustered oncolony surace.

Below we describe common examples o sh predation encountered in the Indo-Pacic, East Aricaand Red Sea regions.

Parrotfsh

• Diffuse patterns of tissue loss associated with scrapes or gouges(i.e. bite marks or scars) that expose bare skeleton.

• Recent lesions are white and typically have discrete borders.

• Older lesions may be healing or partially or wholly colonized by algae,the latter indicating that tissue loss is not progressing.

• Scars may be focused along exposed ridges of coral.

• Parrotsh are usually in the vicinity and feed by day.

Puerfsh• Multifocal, linear to oblong paired areas of distinct tissue loss with

mild erosion o bare skeleton (see arrows).

• Puffersh may be in vicinity, but may not be observed feeding.

• Less damaging to skeleton than parrotsh bites, and may also beconcentrated along exposed colony ridges.

Damselfsh• Diffuse patterns of tissue loss producing lesions that may be linear,

annular or irregular in shape.

• Lesions are colonized by algae that are farmed by damselsh visible

in the area.• Most frequently observed in branching Acropora thickets.




28

Acanthaster planci (Crown-o-Thorns starfsh; COTS)

• Diffuse morphous area of tissue loss revealing intact, bare skeleton.

• Lesion margin may be scalloped (see arrow) on plating, massive or tabular colonies.

• Lesion border is generally discrete and may have visible strings of tissue and mucus.

• Feeding usually occurs from colony edge (plating massive, tabular orms) or base (branching orms), exposing large areas o whiteskeleton consistent with rapid tissue loss.

• COTS are in vicinity either feeding or under colony by day.

Tube ormers• Focal to multifocal, circular to amorphous areas of tissue loss with

erosion o skeleton and annular thin band o white or pink tissueaccompanied by presence o boring polychaetes (tube worms –see arrow), gastropods (vermetids), or barnacles.

• Feeding structures and gills protrude from the coral surface. Commonon massive Porites.

• Also observed in the western Atlantic.

Gastropod predationThe ollowing two genera are major predators o Indo-Pacic corals (limpets and other molluscs arealso known corallivores):

Drupella• Diffuse areas of tissue loss extending from branch bases or colony

edges, revealing bare, intact skeleton (see arrow).

• Lesion has a discrete border, and strings of mucous and tissue maybe visible.

• Rate of tissue loss typically slower than for A. planci predation, thoughduring outbreaks, numbers per colony may be in the hundreds.

• Drupella in vicinity hiding at colony base by day, oten clustered,

or eeding by night. Empty shells also indicate presence.

Coralliophilia

• Focal to multifocal areas of tissue loss revealing bare eroded skeletonand occasional raised thin pink annular band (pigmented coral tissueencircling lesion).

• Shells are relatively immobile and rmly attached to colony surface;may be heavily ouled and more visible on massive corals.

• May be clustered in colony crevices and show strong preference for massive and branching Porites.

• Old feeding scars may be present (see arrow).



29

Sediment damage• Diffuse amorphous area of tissue loss revealing skeleton covered by

sediment.

• Water is typically highly turbid and sediment visible on benthic

suraces. When it accumulates on live coral, it leaves dead, ouledskeleton underneath.


Algal overgrowth• Colonization and overgrowth of living coral tissue by algae

(various species).

• With heavy overgrowth, underlying coral tissue usually dies, leavingbare skeleton.

• Abrasion may cause a pigmentation response (see below under

Discoloration), but this is not always present.


2. Tissue loss: abiotic and biotic diseasesThis reers to lesions that do not have any o the discrete patterns o tissue loss or skeletal damageconsistent with predation or compromised health states described above.

2a. Pigmented band diseases:presence o a distinct narrow band o pigmented material

Black band disease• Black or dark reddish-brown linear or diffuse annular bands at the

interace between live coral tissue and exposed skeleton (see arrow).

• Band comprises black-red lamentous organisms (cyanobacteria)peppered with white laments which can only be seenmicroscopically.

• Band radiates outwards from the colony margin or a site of injuryon massive, plating or oliose corals, or circumscribes branches onbranching corals.

• In moderately progressing infections, denuded skeleton is colonizedby lamentous algae and other epibionts.

• May be more than one disease band per colony which may mergeover time.

• Affects at least 40 species of corals, particularly Acropora species.





30

Skeletal eroding band• Black or dark green “salt-and-pepper”, speckled, diffuse band.

• May form either a discrete, dark band several mm to cm wide atinterace between healthy tissue and recently exposed skeleton

(1o inection; photo) or a diuse, scattered patch on exposed skeleton(2o inection ollowing predation or other tissue loss).

• Speckled appearance caused by boring ciliates which erode skeleton.

• Common in Acropora and Pocillopora.

Brown band• Brown, linear or annular band at the interface between live tissue and

exposed skeleton, though a thin white band between brown bandand healthy tissue is sometimes also present.

• Lesion border is typically discrete.

• Tissue loss may be rapid and begins from branch base but may

spread to adjacent branches at contact points.

• Band consists of mobile ciliates, which may contain zooxanthellaerom consumed tissue (visible under microscope; gives band itsbrown color).

• Observed most commonly on branching Acropora.

2b. Tissue loss without distinct bandUlcerative white spots

• Multifocal patterns of tissue loss exposing intact, bare white

skeleton.• Lesions are small (<1cm diameter), regularly ovoid, with

discrete margins and may either contain bleached tissueor be devoid o tissue.

• Heavy infections may result in lesion coalescence (see arrow) followedby algal colonization.

• Most common onPorites; also onMontipora, aviids, and the octocoralHeliopora.

• Also present in western Atlantic.

White syndromes

• Diffuse areas of tissue loss exposing bare, intact skeleton.• No band apparent between healthy tissue and bare skeleton;

lesion border may be discrete or diuse, but not pigmented.

• Rate of tissue loss moderate to rapid.

• Lesions behind active disease fronts are white, grading to browndistally as skeleton becomes ouled. Can resemble bleaching,but close inspection reveals absence o tissue.

• Host range wide, aecting at least 15 genera.



31

Atramentous necrosis• Multifocal to irregular pattern of tissue loss exposing bare, white

skeleton subsequently colonized by a distinctive grayish-black, oulingcommunity.

• Lesions typically start as small bleached spots followed by tissueloss and coalescence o adjacent lesions.

• Bare skeleton may be covered by a thin white lm, under whicha black sulurous deposit may accumulate, giving the lesion agrayish appearance.

• Chronic inections result in colonization by epibionts which obscuretypical signs o disease.

• Montipora are most susceptible, but it has also been observed onAcropora, Echinopora, Turbinaria and Merulina.

3. Tissue discolorationPigmentation response

• Multifocal or diffuse areas of pink, purple or blue brightly coloredtissue discoloration.

• Tissue on corallite walls may appear swollen or thickened.Pigmentation may orm lines, bumps, spots, patches or irregular shapes.

• Considered a response of the coral host to a variety of stressors(i.e. competition, boring auna, algal abrasion – see arrow), suggestingthat coral health is compromised.

• Common on Porites, which displays bright pink or purplepigmentation.

Trematodiasis• Multifocal, distinct pink to white, small (1-2mm) areas of

tissue swelling.

• Swelling is a response to presence of an encysted parasitic trematode(fatworm) visible under microscope i tissue is sampled.

• Only observed on massive Porites.

Unusual bleaching patterns• Diffuse focal, or multifocal-to-coalescing amorphous areas of white

tissue with a discrete margin.

• Loss or reduction in the number of endosymbiotic algae(zooxanthellae) rom coral tissue. Note that tissue is present,but with reduced or absent pigmentation.



32


• Distinguished from thermal bleaching which typically affects upper or entire suraces o corals. Unusual bleaching patterns include whitestripes or patches oten with discrete borders.

• The degree of bleaching can vary from pale to white, and indicatescompromised health.

4. Growth anomaliesGalls

• Focal to multifocal skeletal deformation associated with the presenceo an organism (i.e. crab, barnacle, etc.).

• Deformations caused by skeletal deposition around the residentinvertebrate in uncharacteristic patterns. Resulting lesions may be

ocal or multiocal, circular to irregularly shaped masses o thickenedcoenosteum (see arrow), elevating polyps several mm above thesurace o the colony.

• Also present in the western Atlantic.

Growth anomalies o unknown cause• Focal or multifocal, circular to diffusely shaped lesions consisting of

abnormally arranged skeletal elements (corallites, ridges, valleys),which are larger or smaller than those o adjacent healthy tissue.

• They may protrude above the colony surface, and may or may notbe covered by intact normal-appearing tissue.

• Pigmentation may be normal, lighter (suggesting loss of zooxanthellae), or completely absent (suggesting absence o zooxanthellae). In some corallites it may be completely absent,and the growth anomaly resembles a white plaque over the colonysurace. In other types, corallites may be highly disorganized andtissue may die in irregular patches and bare skeleton may becolonized by epibionts.

• Also includes conditions referred to as: gigantism, acceleratedgrowth, tumor, neoplasia, hyperplasia, chaotic polyp development.

• Also present in the western Atlantic.



Chapter 3Conirming Field Assessments and

Measuring Disease Impacts


Key questions to ask when disease is detected: geographic extent, host range, seasonality, and case fatality rate.

Basic methods for describing lesions incorals and confirming field assessmnts.

A summary of current practices used to determinethe causes of unknown lesions in corals.

Information on how to collect, handle and preserve specimensfor histology, microbiology and molecular assays and general

considerations such as safety, permits and labelling.



35

When assessing the geographic extent o disease, managers should address the ollowing questions(listed under the headings “Hosts”, “Place” and “Time”). The answers may provide clues to laboratorydiagnosticians on potential causes o disease.

Hosts

• Does disease primarily affect a particular group or genus of corals?Some diseases, particularly those caused by inectious agents, are very host-specic. On the other hand, i multiple hosts are aected, this may indicate a non-specic cause o disease (i.e. elevatedtemperature, poisoning, etc.).

Figure 3.2 White syndrome spreading to adjacent colonies o Pachyseris in Palau. Photo: L. Raymundo

• Does disease primarily affect a particular sizeclass of coral? Certain diseases aect older colonies morethan younger ones and vice versa.

• Does disease appear to be spreadingbetween adjacent colonies?

Evidence o this is strongly suggestive o a communicable agent (Figure 3.2). Note

that this needs to be conrmed throughadditional laboratory investigations.

Place• Do corals affected by the disease have a particular spatial distribution?

For example, perhaps colonies that are shaded are more prone to disease. Perhaps disease appearsto aect colonies predominantly on the ree fat but those on the ree crest or slope are unaected.Perhaps there is a depth or water circulation gradient associated with disease occurrence.

• Have there been recent changes in the environment?

Answering this could partly explain why disease suddenly occurs at a particular location.For example, have there been recent changes in land use patterns adjacent to the ree (chemicalspills, construction, excessive terrestrial runo) or unusual environmental events (hurricanes,temperature anomalies, resh water infuxes)? It is important to collaborate with local agenciesand other managers who are responsible or monitoring environmental characteristics suchas rainall, water temperature, turbidity and salinity (see Chapter 4 or details). Keeping track o such data, along with changes in disease prevalence or incidence, can oten reveal patternswhich may be exacerbating or inhibiting the impact o the disease.

Time• Does disease occur more frequently during certain times of the year?

Some diseases have a seasonal component. Determining whether a temporal component existscould provide clues to potential causes o disease, and will help to predict uture impacts.



36


2. Geographic spread Visual surveys o geographic extent over time can give an indication o how ast a disease is spreading.However, it is usually more desirable to quantiy the spread o disease in a population, particularlywhen one is comparing multiple regions or sites. One practical way to do this is to measure theincidence o disease. Unlike prevalence, which is a static measure (o disease), incidence measures

the number o new cases o disease over a dened time period and thus can be a useul indicator o whether or not disease is spreading. Increasing incidence suggests a spreading disease. By its verynature, incidence (o disease) can never be greater than prevalence (see Box 3.1). See Chapter 4 or calculations o disease prevalence, incidence and other parameters.

3. Case atality rate

Figure 3.3 Cattle ear tag (see arrow) used to mark and codea coral colony. Photo: T. Work

This is measured as the percent o colonieshaving a disease that actually die rom thatdisease. Managers should be more concernedwith diseases that have a high case atality rate(see Box 3.1). To get a measure o case atalityrate, it is necessary to mark colonies aectedwith disease and to measure the number o colonies with disease that die ater a set timeperiod. Various methods exist to mark coralcolonies (i.e. masonry nails, fagging tape,plastic or stainless steel tags), but we haveound that commercially available cattle ear tags axed to colonies with cable ties will lastor at least one year, even in highly turbulentconditions (Figure 3.3).

One last note on coralsCorals are colonial animals that ragment as a means o asexual reproduction. They can also partially

die and later grow new tissue over this dead skeleton; both processes can slow growth o the colonyas a whole and reduce colony size. The age o a colony may, thereore, be dicult to estimate romcolony size. While it can be assumed that large colonies o a given species are old, small coloniesare not necessarily younger; they could have experienced ragmentation or partial mortality or other actors which have resulted in slow growth rate. While measuring coral colony sizes is reasonablystraightorward, it is important to remember that estimating age rom size should not be attempted.

Another actor which can be challenging when assessing disease in a coral community is colonyboundaries. With extensive monospecic stands, it may be dicult to determine where one colonyends and another begins, particularly when colonies are in physical contact. When aced with thissituation, look or subtle changes in coloration; oten dierent colonies will appear as slightly dierentshades. Also, look or the borders where the colonies abut each other; i a stand or thicket is composedo dierent colonies (rather than a single one), then these colony margins will not use, but will remainseparate, and may be dierentially pigmented or show signs o competition.



37

Box 3.1Examples o prevalence and incidence measures in a chronic disease.

White circles are live coral colonies; green circles are diseased colonies documented during the previoustime period (prevalence), red circles are new cases o disease (incidence), and black circles are dead colonies

(mortality).

Time Total cases New cases Population Prevalence Incidence

1 5 100 0.05

2 8 3 100 0.08 0.03

3 14 6 100 0.14 0.06

4 24 10 100 0.24 0.1

Time 1 Time 2 Time 3 Time 4

Time Total cases New cases Population Prevalence Incidence1 5 100 0.05

2 8 3 100 0.08 0.03

3 14 5 100 0.14 0.05

4 26 2 100 0.16 0.02


Time Total cases New cases Population Prevalence Incidence

1 5 100 0.05

2 12 11 96 0.12 0.11

3 22 21 85 0.25 0.25

4 35 33 66 0.53 0.5


Example 3: An acute lethal disease spreading quickly through a coral population. Incidence tracksprevalence much more closely. The case atality rate at times 2,3 and 4 would be 80% (4/5), 90% (10/11),and 90% (19/21), respectively. This is very high.

Example 2: Incidence initially rises, refecting increasing new cases. Incidence then decreases, refectinga decline in new cases. Prevalence continues to increase the entire time.

Example 1: Incidence is much lower over time than prevalence, but increases steadily. This indicates thespread o disease in the population.




38

3.2 Basic methods or confrmingfeld assessments and describing disease states

3.2.1 Recognizing disease in the feld

This discussion builds on the inormation presented in Chapter 2, and is meant to provide you with

more decision-making power. The most critical aspect o recognizing disease states in corals is to“know your animal”. While this recommendation may seem trite, recognizing what comprises “normalvariation” in morphologic appearance o a coral is a critical rst step to understanding the role thatdisease plays in a ree ecosystem. For example, some coral species have dierent morphologies or color schemes depending on their geographic location or ree zone. White discoloration is commonin the growing tips o some coral species where tissues have yet to be colonized by zooxanthellae,and this could be misinterpreted as partial bleaching (Box 3.2).

For the eld biologist, diseases in corals are maniested as a change in morphology (via a lesion).When encountering a diseased coral, two important points should be kept oremost in mind:

1. Disease is a continuum between health and death, and this continuum is refected by changesin morphology as disease progresses. Thus, when observing a lesion on a coral, remember thatthis lesion could be in the early, middle, or late stages o the disease. Establishing this requiresdiseased colonies to be marked and monitored over time (see Section 3.1, Case Fatality Rate, or methods). Marking colonies with lesions and documenting the progression o the lesion over timecan provide invaluable data or understanding how a disease impacts host colonies, how ast it killstissue, and whether or not colonies can recover or halt the spread o disease.

2. The causes o most coral diseases are unknown, and except or certain cases (see Section 3.3),you will not be able to determine the cause o a lesion without urther laboratory investigations.

Figure 3.4 A colony o Porites cylindrica exhibiting subacutetissue loss rom white syndrome. Photo: L. Raymundo

Given these two limitations, the rst step todescribing a coral disease is to ormulate agood morphologic description o the lesion.Doing this is critical or two reasons. First, itorces you to ocus on the evidence (i.e. the

lesion) and not the potential cause o the lesion.Second, a good morphologic description o the lesion provides the best tangible objectivedata regarding that disease (pending urther laboratory work). These objective data can thenbe used to communicate acts about thisdisease to others in a standardized manner,thereby allowing or accurate comparisons o disease among geographic regions. Thedecision tree in Chapter 2 (Figure 2.1) o thismanual will help you do this.

3.2.2 Describing a lesion in a hard coralHard corals are relatively simple animals that consist o a thin layer o tissue overlying a calciumcarbonate skeleton. Accordingly, a lesion in corals will maniest in three ways:

1. Tissue lossTissue is missing, revealing underlying skeleton (Figure 3.4). In such lesions, close attention shouldbe paid to the skeleton as this may give clues to the progression or potential cause o the disease.For example, a dened area o bare, intact white skeleton bordered by tissue indicates that tissueloss was recent and relatively rapid (acute). In contrast, a progression rom healthy tissue to a bando bare, white, intact skeleton to algae-covered skeleton would suggest an advancing ront o tissue loss (subacute). I tissue loss is acute, note whether the skeleton is intact or eroded; acute



39

tissue loss with skeletal erosion suggests trauma (i.e. sh bite, anchor damage, etc.), and a visualassessment o the immediate area may provide urther clues as to the origin o that trauma. Whenobserving white skeleton on a coral, it is helpul to look closely to make sure no tissue is overlyingthe area; magniying lenses are helpul or this. Failure to do so may conuse tissue loss with whitediscoloration (bleaching).

2. DiscolorationThis is a deviation rom the “normal” color o tissues. The discoloration most amiliar to manybiologists is white discoloration (bleaching) due to loss o zooxanthellae rom tissues. However,

other types exist and it is important to reiteratehere that many coral species show broad rangesin normal coloration. This must be consideredwhen diagnosing a potential disease state(Figure 3.5). When describing the discolorationo corals, it is important to stick with basic colors(i.e. white, purple, pink, brown, etc.) and avoidobscure terms.

3. Growth anomalyThis is an abnormal conguration o the coral skeleton. Typical growth anomalies orm as nodular or caulifower-shaped growths o the coral skeleton. These oten lack, or have reduced numbers

o, polyps and are discolored white or are distinctlypaler in color than surrounding healthy tissue. Other

corallilte structural irregularities may also be present,but require a microscope to see (Figure 3.6).

The three basic types o lesions described aboveare not mutually exclusive and can occur singly or in various combinations. A nal step to describinga coral lesion is to note the distribution o thatlesion on the colony. A lesion can be ocal (a singleoccurrence on the colony), multiocal (severalscattered or clumped occurrences), or diuse(encompassing more than 25 percent o the colonysurace – Figure 3.7). Additional terms and detailsto systematically describe lesions in corals areavailable in Chapter 2.

Figure 3.7 Lesion types: (A) ocal lesion o a growth anomaly. Photo: D. Burdick; (B) multiocal lesions o trematodiasis.Photo: G. Aeby; (C) diuse lesion o white syndrome. Photo: L. Raymundo

Figure 3.6 Growth anomalies on Goniastrea edwardsi .Photo: D. Burdick

Figure 3.5 Tissue discolouration caused by dark spotsdisease on Stephanocoenia. Photo: E. Weil




40

3.3 Determining causes o lesions: How to collect, handleand preserve specimens or histology, microbiology andmolecular assays

3.3.1 The challenge o determining causation

The goal o this chapter is to provide a summary o current practices employed to determine causation o unknown lesions in corals. As we discussed in Chapter 2, determining the cause o lesions rom predationor certain environmental impacts may be relatively straightorward i the evidence is present and visible inthe immediate environment o the ree. Thereore, an initial assessment o the immediate area surroundingthe coral is essential or such diagnoses. For example, a coral displaying ‘multiocal acute tissue loss withskeleton erosion in a consistent pattern (i.e. linear, elliptical), and with corallivorous sh nearby inducingsimilar lesions’ should be diagnosed as sh bite (predation). Similarly, ‘ocal acute tissue loss and erosiono skeleton bordered by a thin band o pink discoloration with presence o snails’ could be attributed tosnail predation. Other animals may also be visible within the coral skeleton. For example, barnacles willencrust in coral skeleton and be bordered by a thin margin o white discolored tissue, but will be visible inthe center o the lesion upon close scrutiny.

In most cases, however, determining the actual cause o a coral lesion is not possible without

additional laboratory investigations, particularly i involvement o a microbial agent is suspected. Whilewe recognize a ull-on investigation into causation may be beyond the capacity o many managersreading this book, we eel that it is appropriate to provide background inormation that outlines whatcan be done, should this course o action be deemed appropriate. Even i it is not within the capacityo a eld station, local laboratory, or managing organization to take on such work, we believe it isimportant to convey the complex nature o investigating coral disease and determining causation. Tothis end, we oer inormation on current approaches to assessing and testing or causation. Briefy, thisusually involves characterizing the lesion at tissue and cellular levels (histopathology). I an inectiousagent is suspected as a cause o the lesion, additional samples may be needed or microbiology (seeSection 3.4 or sampling protocols). In the end, disease investigations in corals are best done througha partnership between coral biologists and disease diagnosticians amiliar with appropriate laboratorymethods (Figure 3.8).

Figure 3.8. Collaboration with local scientists to assist with microbiologicalanalyses is important. Here students are processing samples rom coral mucus.Photo: T. Lewis

Determining a specic cause o adisease is, o course, o paramountimportance and is a major goal inall disease characterization eorts.However, it is a challenging andlengthy process. I an inectiousagent is suspected, one way toaddress this is by employing astep-by-step process to provewhat is known as Koch’s Postulates(66). The rst step in this processrequires collecting diseased andhealthy tissue samples and

describing the morphology o thelesion at the gross and cellular level which, in some cases, mayreveal the presence o a potentialcausative agent. Various approp-riate laboratory tools are used toculture, isolate and identiysuspected causative agents. These

putative pathogens are then introduced to healthy host tissue under controlled experimental conditionsand the response o the host tissue is observed. I lesions develop, the tissue is sampled to re-isolatethe introduced microbe. I it is re-isolated rom the diseased lesion, then it can be classied as a causalagent or the disease.



41

Koch’s Postulates have been proved or only a handul o coral diseases to date (see Chapter 1, Figure1.4), principally due to the limitations o this method. Black band disease, or instance, is the mostcomprehensively studied disease, but is caused by a microbial consortium dominated by cyanobacteria,Beggiatoa and Desulfovibrio, which collectively have harmul eects on coral tissue and contribute toits death (67,68). Using Koch’s Postulates to prove causation is not an appropriate method in this case,

as more than one agent is involved. In addition, certain diseases may be caused by microbial agents thatare not culturable, and so cannot be tested using this method. This is one reason why the histological,microbial, and molecular characterization or most diseases remains very incomplete and why alternativemethods are currently being developed. Below, we provide some guidelines or collecting and handlingspecimens to assist in this characterization. It should be stressed that such work requires collaborationbetween those in the eld (i.e. ecologists and ree managers) and laboratory scientists (i.e. histologists,microbiologists, toxicologists, molecular and cellular biologists). Please reer to Appendix 2 or a list o experts in the eld who can be contacted should you be interested in pursuing this route. Arrangementsshould be made prior to sampling and specimen preparation, so the scientist or laboratory receivingspecimens can be prepared to process them.

Figure 3.9. Diver collecting coral mucus with a syringerom the surace o a Siderastrea siderea colony.Photo: B. Seymour

Specimens are samples containing material rom adisease site, collected or laboratory analyses.Relevant samples include coral tissue (ragmentsrom diseased and healthy tissue o the same colony,as well as rom an unaected reerence colony), coralsurace mucus and water (collected using a sterilesyringe), and sediment (collected with a sterile tube),as well as other fora or auna associated with thediseased corals (Figure 3.9). Available historical or background inormation surrounding the problemsuch as that discussed in Section 3.1, along withphoto documentation, will assist in the diagnostic

process and should be included with the samples (69,70). The specimens must be handled in amanner that preserves the individual sample’s identity, prevents cross-contamination and avoidsdamage to the sample. The preservation method used will be dictated by the intended analysis

(i.e. histology, microbiology, toxicology, virology).

3.3.2 General considerations

PermitsPermits or collection and/or transport are required or most studies involving coral disease, regardless o the jurisdiction. The number and type o permits required vary rom one location to another. Managersare oten in charge o issuing permits, and thus play a crucial role. It is oten the manager who must setrestrictions on sample size, type and number, and who may be instrumental in establishing proceduresor biocontainment, quarantine, or ree closures. Thereore it is essential that collection permit requestsinclude a clear rationale or the type and number o samples being requested.

SaetyThe primary consideration when collecting diseased tissue o any kind is personal saety andinection control or both human and coral. Here are general considerations or minimizing risk o spreading disease:

• When multiple sites are to be visited, ALWAYS visit the healthy (or apparently healthy) sites beforeentering an area with known disease, to prevent potential spread o inectious agents. Similarly, whensampling within a diseased site, rst sample the apparently unaected (healthy) individuals, ollowedby portions o a diseased colony that appear unaected (healthy) and sample the diseased portion(lesions) o the colony last.

• Each collected sample should be placed into a separate labelled container; live or frozen tissuesshould be transported in double containment to prevent any possible contamination back to theocean at new sites.




42

• Divers should consider themselves and their equipment as potential vectors of disease betweenlocations. I sampling rom multiple rees, ensure that between sites you quickly rinse SCUBA gear and other equipment in ve percent bleach solution (or other suitable disinectant solution) thenrinse in resh water.

3.3.3 Specimen documentation

LabellingLabel collection containers prior to sampling. A small tag o waterproo paper with inormation writtenin pencil can be placed in the container (bag/jar/tube) and allows you to change or add inormationater sampling. Label syringes or mucus collection prior to the dive as well. Basic label inormationshould include the ollowing:

• collection site

• coral genus and species (if known)

• location on coral where sample was collected (reference tissue from healthy colony, unaffectedportion o diseased colony, diseased tissue margin, disease mat)

• date• initials of sampler

PhotographingPhotographing lesions provides a record o color, location and appearance. Both actual size andmacro shots should be taken beore and ater removal o tissue biopsies; include a scale o some sortin each picture (ruler, dive knie, coin, etc). Make sure to document where and when the photo wastaken. Photos o the general ree site are useul additional documentation.

3.3.4 Sampling

For HistologyHistological analyses characterize the microscopic morphology o tissue and may help guide urther investigations (71). Typically, samples are viewed with a light microscope or general tissue organization.Histological data can reveal cellular changes that occur in tissues under normal, stressed or diseasedconditions, and whether oreign organisms (i.e. bacteria, ungi, parasites) are present (Figure 3.10).

Figure 3.10 Histological samples o sea an coral Gorgonia ventalina. (A) tissue rom a healthy coral. (B) tissue rom a lesion o a coral with Aspergillosis; the ungus has spread throughout the skeleton o this coral. This analysis can be useul or conrmingeld assessment. Photo: C. Couch

A B



43

Sampling or histology is straightorward, but involves handling potentially hazardous chemicals, so thesampler needs to be aware o proper procedures. In general, a tissue sample is taken and placed in asuitable xative or preservative. I the analysis is solely or morphology, then 10 percent seawater-bueredormalin is sucient. However, i immunological or DNA-based staining or preparation or electronmicroscopy is needed, additional xatives and procedures are necessary. These preparations should be

done under supervision by personnel rom the laboratory where the samples will be sent or analysis.Histological coral samples can be removed in a number o ways. The most simple is removing a smallragment o the coral using a hammer and chisel, coring devices (i.e. leather punch, pneumatic drill,hand drill), rongeurs, wire cutters, or garden clippers. Light microscopy usually requires approximatelytwo cm2 o apparently healthy tissue taken several centimeters rom the diseased tissue and another sample that includes the disease margin (i.e. bare skeleton and intact, diseased tissue). The samplesshould be placed in labelled plastic bags with resh seawater until returning to the boat. It is importantto completely immerse the sample in xative as soon ater collection as possible (the recommendedratio o xative to sample is 10:1), noting the time interval between collection and xation; cellular changes can begin as soon as a sample is removed rom the coral.

For microbiological analysesMicrobiological analyses are important diagnostic tools i an inectious agent is suspected as a causeo disease. Two approaches are currently used to isolate and identiy possible microbes involvedin disease: culture-dependent methods and culture-independent (DNA-based) techniques. Culture-dependent techniques (Figure 3.11A) are used to isolate, grow and identiy microbes such as bacteriaor ungi rom lesions, tissue, mucus or surrounding water or sediment. While these methods are useul,they are only able to identiy a small raction o the total microbial community, as many such organismsare not culturable. Thereore, culture-independent methods (Figure 3.11B) have been developed thatuse DNA or RNA present in the samples to examine the diversity o microbial communities in samplesor in specic molecular tests (such as polymerase chain reaction assays). Samples are usually taken romhealthy and/or diseased coral tissue and coral mucus, to look or shits in these communities betweenhosts, healthy versus diseased tissue, species, seasons, geographic location or environments.

The viability o bacteria and their community structure within samples change rapidly and unpredictablyater sampling, thus it is critical that samples be processed rapidly. There are two main approaches:

a) sampling specimens or preservation (i.e. DNA extraction, protein analysis,anthropogenic chemical analysis); and

b) sampling specimens that require rapid processing (i.e. live bacterial culture).

Figure 3.11 Examples o approaches to investigating a potential inectious cause o coral disease.A) culture-dependent techniques to isolate and identiy microorganisms. The plates shown representtwo dierent culture media (TCBS and GASW) at two concentrations (10µl and 100µl). B) culture-independent technique wherein the DNA or RNA o various microorganisms in a sample can be used toidentiy the number o dierent organisms present. Photos: C. Woodley

A B




44

Field work oten does not allow or quick processing, so documenting time intervals between samplecollection and processing is essential. Samples or culturing live bacteria must be processed within12 to 24 hours. Although culture-dependent methods are not dicult they do require trainedindividuals to conduct the procedures. Local hospitals or diagnostic laboratories may be able to assistmanagers with sampling, plating and culturing techniques. Culture plates should then be sent to a

marine microbiologist or urther analysis. Some samples, particularly those or international shipments,may require additional permits or documentation or export and/or import, so the collector should beaware o relevant policies and regulations.

Sampling or culture-independent analyses is straightorward but time-sensitive, so while specializedtraining is not required, attention to detail and proper labelling are essential. As this procedurerequires specialized equipment, such work should be undertaken as a collaborative eort betweeneld ecologists and a microbiology laboratory.

Biochemical and molecular analysesMolecular analyses address the ormation, structure, and unction o macromolecules such as lipids,metabolites, nucleic acids and proteins. Several such analyses have been adapted to coral and can beused to dene a cell’s physiological condition or health status (Figure 3.12; 70). The sampling

Figure 3.12 ELISA assay or measuring cellular diagnostic parameters.Photo: Haereticus Environmental Laboratory

protocol or these analyses is identicalto those or collecting tissue biopsiesor histology or culture independentanalyses, but requires equipmentwhich may not be available. Pleaseconsult experts or detailed inormation.

Specimen shipmentPrior to any sample collection, arrangements must be made with the receiving laboratory(ies) or shipment and analyses. Shipping documentation must be considered, particularly with internationalshipments, and proper authorization obtained. A key consideration is the protection o sampleintegrity during shipping. This involves:

• preventing cross-contamination;• preventing decomposition;

• preventing leakage;

• preserving individual specimen identity; and

• proper labeling (69).

Attention to these will ensure sae delivery and avoid nes (which can be considerable, depending onthe inraction). Further regulations and permits (i.e. CITES) may be required depending on the type o sample being collected and shipped, as well as the country o origin and the destination.



45

Box 3.2

Coral disease nomenclature: a current challenge

Much conusion has resulted rom the many reports o new diseases over the last ten years.Several o the names presented in the literature have been assigned on the basis o a ewor single observations, and they lack photographic documentation, detail on gross signs, or evidence o coral tissue destruction. Other conditions were presumed to have been caused bya pathogen, but later shown to result rom predation or competition. Dierent researchers havealso used terminology interchangeably to describe similar signs, such as the various namesgiven to the white syndromes. There is also a growing number o diseases identied in the

Caribbean that have been subdivided (i.e. “Type I” and “Type II”), based on rates or patternso disease spread or species aected. It can be extremely dicult to veriy which “type” o disease is present based on single observations, as initial signs o inection may look dierentrom later stages and rates o spread cannot be determined without monitoring. Furthermore,certain diagnostic eatures, such as the presence o a bleached ront o tissue that advancesahead o the dying tissue, are not readily visible or may be absent depending on the time o observation. For example Caribbean white plague type I and II (6) and white band type I andII (8) dier in rate o progression, a characteristic which is only discernible via monitoring. Darkspot type I and II, dark band syndrome, purple band syndrome and tissue necrosis (11) allbasically reer to the same suite o disease signs, as do white pox, patchy necrosis and necroticpatch syndrome (13). The prolieration o names presents diculties when evaluating hostranges and geographic distribution o coral diseases and can lead to incorrect assumptionsabout causative agents.

This conusion and lack o coordination has resulted in an increased eort to consolidateinormation, build consensus regarding nomenclature, and develop the science o coraldisease research in a coordinated ashion. Such eorts are vastly improving our current stateo knowledge and should continue to do so in the uture. Properly describing lesions anddisease signs and developing new histological and molecular diagnostic tests is crucial to thiseort. It is hoped that the inormation in this book will urther assist in the development o acoordinated approach.



46




47

Chapter 4Assessment and Monitoring Protocols


Objectives and methods for rapid assessment and long-term monitoring.

Designing a valid and reliable sampling protocol.

Quantifying coral disease prevalence,incidence and mortality rate.

Guidelines for measuring basic environmental variables which may impact disease dynamics.



48


Assessment and Monitoring ProtocolsE. Weil, E. Jordán-Dahlgren, A. Bruckner and L. Raymundo

4.1 Rapid assessment versus monitoring –goals and objectives o each

Most protocols used to assess coral ree ecosystems involve characterizing coral cover, speciesdiversity, sh community structure, water quality, and human activities, with an emphasis on detectingchange. While this approach may provide a detailed picture o ree condition at the time o the survey,and how the ree has changed between survey periods, it may ail to identiy actors responsible or the changes observed, or predict uture trends under varying management scenarios. Alternatively,surveys ocusing only on a specic threat to a community, such as disease or bleaching, may providedetailed diagnostic inormation and rigorous data on prevalence, incidence, and impacts, but may missadditional inormation on ree condition that is critical to understanding the impacts o the threat.

Figure 4.1 An integrated approach to obtain quantitative data on a ree community can provide a more complete picture o a ree’s health status thana survey examining only disease states. Here, divers take detailed data on thecoral population. Photo: B. Willis

The ideal approach to studying

coral diseases and their impacts,given sucient unding andqualied personnel, is a well-designed, integrated, multi-component survey. Such a surveywould provide population,community and/or ecosystem-level data on benthic organisms,shes, water quality, environmentalparameters and the humandimension, along with diseasecomponents at dierent spatialand temporal scales (Figure 4.1).

This approach allows assessmento coral ree community structureand unction, temporal changes,and potential links betweenassessed parameters that mightbe responsible or observedchanges in ree condition. It isimportant to understand thatsignicant correlations between

disease prevalence and environmental and/or biological actors do not prove causality. It simplysuggests associations between the variables considered.

Due to the potential or high coral mortality rom disease, estimating the magnitude o disease

impacts should be a undamental management goal. There are two main approaches in current use:rapid assessments and monitoring.

1. Rapid assessments – These characterize the ree area(s) surveyed at the moment o the assessment;a single point in time. This usually estimates relatively static (state) variables about a population or a community and is useul or comparing multiple sites or dierent time periods.



49

2. Monitoring – This detects changes over time within the same ree area(s). The aim o such surveysis to estimate changing (process) variables. For both approaches, a protocol that answers specicquestions must be designed. For instance, initial questions or a protocol that seeks to describe ageneral ree condition would include:

• Are there coral diseases present on the reef? If so, which ones?

• What species are affected?

• Are there reefs, reef zones or reef areas apparently more affected than others?

In this case, a relatively simple sampling eort using qualitative or semi-quantitative rapid assessmentscould provide the answers (see Table 4.1 or surveying techniques). On the other hand, monitoringwould address the questions o changes over time – something rapid assessments cannot do.Thereore monitoring should be the approach considered in any short or long-term managementprogram or Marine Protected Areas and other areas o high conservation value.

Table 4.1 Descriptions o commonly-used surveying techniques. Descriptions taken rom Edmunds (1), Porter & Meier (5),Antonius (7), Kuta & Richardson (9), English et al. (10), Bruckner & Bruckner (12), AGRRA (14), Jaap et al. (19), Santavy et al. (20),Bruckner (21), Weil et al. (25), Feingold (27).

Survey Description Advantage Disadvantage

Manta Tows A diver/snorkeler istowed behind a smallboat at a slow andconstant speed or axed time interval.

Allows rapid coverageo large areas. Providesestimates o coralcover, dominant coraltypes, broad mortalityestimates.

Detailed diagnostic or quantitative data notpossible. Dependenton high water quality.May only be useul toestimate mortalitycause i very visible(i.e. COTS, BBD).

Timed Swims Diver swims or a xedtime in a straight line

along a single depthgradient. All diseasedcorals in a 2m bandnoted: species, diseasetype, lesion number.

Provides semi-quantitative inormation

on abundance o diseaseover large areas.

Not used or prevalenceor incidence (no total

colony count; surveyarea only estimated).Disease count categoriesused: rare (1-3 cases),moderate (4-12 cases),requent (13-25 cases),abundant (26-50 cases),epidemic (51-100 cases),catastrophic (>100 cases)

Circular areas Inected and healthycolonies o all speciescounted within a circular area (10m radius; 314m2). A stake poundedinto substrate is usedto dene the pivotalcenter o the circle;a 10m transect tape isheld by diver as she/heswims around the stake,keeping the tape taut.

Provides quantitativedata on prevalence andincidence o diseases.I size measurementsare included, populationstructure can beestimated. Best onfat ree substrates, instudies o single diseases(BBD, YBD).

Cannot be used on a ree slope because multiplezones may be includedin a single samplingsite. Does not provideinormation on coralcover unless combinedwith other measures.Impractical in areas withhigh cover and density.

Pivot10 Subsurace

FloatRod



50



Radial belt transect Sampling circular areas inconcentric belts (or arcs)around a pivot point. Thearea sampled is either a

contiguous circle (radialsampling) or a series o rings (radial belt transect)around the pivot point.

Counts the total number o inected and healthycolonies o each specieswithin the outer 8-10m o

a circle (314m2 plot) andidenties all diseases.

Assessment o multiplepermanent sites may betime consuming.

Belt transects All corals within apredened area (i.e.2x20m) are countedand disease presencerecorded. 1m or 2m PVCstick is used to dene aquadrat along a transect.May include more

measurements such ascolony size, coral cover,and percent mortality.

Can provide detailed dataon prevalence based on awhole colony assessment,population dynamics, andhealth status. Long termmonitoring o taggedcolonies can provide dataon colony ate (recovered/

dead/stasis, etc.).

Requires multipletransects in each zone.With high diversity, highcover and abundantsmall corals, individualtransects may requiremultiple dives tocomplete.

Line intercept transects Can provide detailed dataon prevalence based on awhole colony assessment,population dynamics, andhealth status. Long termmonitoring o taggedcolonies can provide dataon colony ate (recovered/dead/stasis, etc.).

Allows rapid assessmento coral communitystructure, condition, andprevalence o diseaserom a whole colonyperspective. Providesinormation on sizestructure, colony density,coral cover.

Requires multipletransects throughouteach zone to quantiyprevalence. Does notprovide a comparableassessment o areasurveyed i corals varyin size between sites.Colony size based onactual measurements (or

size classes) but percentcolony mortality isestimated and may varybetween observers.

Point intercept transects Requires multipletransects in each zone.With high diversity,high cover andabundant small corals,individual transects mayrequire multiple divesto complete.

Provides inormation oncover o various benthicorganisms includingcoral as well as substratetypes. Faster to use thanLine intercept, i multiplesurvey sites are needed;allows rapid assessments.

Prevalence may beincorrectly assessedbecause relatively smalloverall area is examinedalong each transect.Does not providedetailed inormation oncolony abundance (largecolonies may be counted

twice) or size structure.Chain transects Biotic and abiotic

components identieddirectly under eachlink in chain. Rugosityestimated by determiningratio o the length o chain laid ollowingbottom contours to thestraight-line distancebetween start and endpoints o the transect.

Provides rapidinormation on ree rugosity, species diversityand cover.

Assesses a very narrowband o ree. Diseasesand other actors may bemissed unless the chainlands on the diseasedportion o a colony.

Pivot 10863 SubsuraceFloat

Rod



51

Validity and reliabilityThe importance o proper sampling design cannot be underestimated, particularly i the data are

going to be applied to management. A good assessment must be both valid and reliable. Validity reers to how eectively the assessment refects what we want it to measure, recognizing that we canonly survey a small portion o the entire ree. Adequate sample representation is, thereore, a crucialcomponent. Reliability pertains to how eciently a method measures specied parameters over theentire set o sampling conditions likely to be encountered, and should incorporate valid replicability.Sample representation and replication ensure that statistical power is optimized, a given situation isproperly characterized, and meaningul comparisons can be made in space and time.

Standardized sampling protocolsMany current surveys use a standardized sampling protocol. This acilitates regional comparisonsbut sometimes sacrices a detailed characterization o the complexity o local ree environments.Thereore, it is important to consider what the objectives o an assessment or monitoring schemeare. I the data are to be used locally to address management issues, then it is important to takeinto account the complexity o the local rees. However, i the data are to be deposited into a larger database or regional or global comparisons, then a standardized protocol applied across sites isnecessary. With the general deterioration o ree communities at local and regional levels, it is clear that the best approach combines the two.


Quadrats Quadrats o various sizes

(0.5m2, 1m2) are placedhaphazardly, randomly,or at specic intervals

along transects.Percent cover o allspecies and substrate

types within quadrat areadetermined by counting

number o quadratsubunits occupied byeach category.

Provides quantitativeinormation on

cover o coral andother organismsand substrates, and

qualitative data on typeso disease present.

With exception o large quadrats

(i.e. 100x250m), poorlyestimates diseaseprevalence, abundance,

size or condition o corals; does not capturedisease on the portion o

a coral that alls outsidethe quadrat. Does notwork well or large

thicket-orming corals.

Photo-quadrats Quadrats o varying

sizes (<1m2) are

photographed using highresolution digital cameras

and video.

Accurate assessmento cover and changes

in cover (when usingpermanent quads).Less bottom time; data

are analyzed in the lab,using image analysis

sotware, such as NIH’sree Image J sotware®.

Requires considerablelab work to analyze

images. May ail todetect diseases and smallcolonies. Does not work

well or large branchingcorals that orm thickets.

Resolution too low toidentiy many coralsto species.



52


4.2 Coral disease rapid assessment and monitoring protocols Validity and reliability o all types o quantitative assessments require satisying a undamental condition:an adequate estimation of the natural variation of the chosen parameters (disease prevalence, coral cover, etc .). Imposed upon this critical point is the very real consideration o time, resources andpersonnel limitations. The ollowing recommendations are provided to help address these issues.

What are the goals o the sampling?What questions are to be addressed and at what spatial and temporal scales? Rapid regionalassessments can reveal large-scale processes such as the expansion rate o a particular disease roman inection ‘hot spot’ to nearby rees, and serve as an early warning system to identiy and trackdisease outbreaks. Monitoring targeted to address very specic questions can provide data on thestatus o a particular disease or coral species, seasonality, incidence and eects o diseases at a localscale, and the role o localized stressors on disease processes and impacts. Monitoring individualcolonies will result in the documentation o patterns o spread, rates o tissue destruction, impact o diseases at a colony or population level, and the ate o aected colonies.

How many sites?

Rees can generally be divided into distinct zones, created by strong environmental gradients actingon the benthic community. The back ree, ree fat, ree crest, ore ree or slope are the standard zones,though these can be highly modied by bathymetry and coral growth, and may even be absent.Further, depth can change drastically within a zone and provide even more complexity. Here, wedene “site” as a zone or habitat o distinct structure within a ree.

For descriptive or rapid assessment surveys, logistics and time constraints may make it necessary tolimit sampling to a single zone within a ree (such as the ree crest). In such cases, the same habitator zone should be surveyed at each location. I great variation exists in community structure within adepth range or zone (due to high relie, spur and groove ormations, etc.), there may be more than one“habitat” present and urther within-zone stratication will be required. For space/time comparisons,at least three replicate sampling units per zone/habitat (linear transect, radial arc, etc.; see Table 4.1)are recommended, as dierences between sampling units can only be examined in comparison tovariation within sampling units.

What sampling technique and sampling unit?Consider objectives, logistics, time, and resources, and reer to Table 4.1 or the most commonly usedsampling techniques. Select the technique that best suits the local conditions while addressing theobjectives o the sampling. The same sampling technique should be used in all areas. The samplingunit is dened by the question(s) asked, which should consider appropriate spatial and temporalscales. For example, i the question reers to colony properties, the sample unit will be each colonyand the technique may involve censusing all colonies within a dened area. I the question reers topopulations or communities, then the sampling unit will be an area or length o ree that is surveyed.Belt transects, circular areas, and quadrats are examples o area sample units, while line, chain andpoint intercept transects are examples o linear sampling units. Sampling units should be replicatedwithin each site; this is discussed in the section below on sampling unit number.

What sampling unit size?This depends on the size and type o spatial distribution o the coral colonies and, in practice, onlogistical constraints. A community with large colonies requires larger sampling areas than onedominated by smaller ones. Area-based sampling units (quadrats, belt transects, etc.) bias count data,due to the eect o including or excluding colonies that extend beyond the edges o the sampling unit(i.e. the “edge eect”). The larger the colony size in relation to the size o the sampling unit, the larger this eect, as a greater proportion o colonies will be excluded. To minimize the edge eect, Green(72) recommends that the ratio o colony size to unit sample size should be very small: a sample areashould be 20 times larger than the mean colony size. Zvuloni et al. (73) propose a mid-point criterion:i more than 50 percent o the colony lies within the sampling unit, the colony should be counted. I a ree community contains many single-species stands (i.e. Acropora thickets), then a smaller size is



55

Why is preliminary sampling advisable?Prior to beginning a major rapid assessment or monitoring eort, it may be necessary to conductpreliminary pilot assessments. Such assessments are useul in estimating the amount o variation inthe parameters being monitored (i.e. live coral cover, prevalence, etc.), so appropriate decisions canbe made regarding replication and sampling technique. Preliminary sampling also has an additional,

rather practical benet – most potential problems can be identied early. These include problemsrelating to sampling design decisions (sites, stratication, type, number and size o sampling units,taxonomic level desired, disease types or signs) and eld logistics. Thereore, the nal sampling designwill be based on direct, practical knowledge o the area, rather than on untested assumptions.

4.3 Designing a monitoring programA comprehensive coral disease monitoring program should apply principles o epidemiology andrisk analysis to coral health assessments. This will help identiy predictors (i.e. risk actors) or changesin coral and ecosystem health (such as warm temperatures or increased nutrient loads); quantiy thestrength o those associations; and ocus diagnostic eorts towards identiying etiology (see Chapter3). Standardized disease monitoring programs can be supplemented with the ollowing:

a. detailed disease assessments (see Appendix 4 or sample data sheets);

b. additional population inormation (i.e. abundances, size classes, species diversity, and health status);

c. quantication o species which may indicate potential health risks to corals, or improvement in ree health as a consequence o management (i.e. macroalgae, herbivores, coral predators); and

d. measures o water quality (i.e. sedimentation, nutrient input, bacterial load). Oten, water qualitymonitoring may be undertaken by a dierent local agency or individual, so collaborative agreementsbetween coral disease and water quality monitoring agencies or individuals may result in reducedcost and eort.

Monitoring should be proactive; it can help predict the likelihood o events such as a disease outbreak,responsive changes in community structure, and recovery rates. A combination o rapid random

assessments and long-term monitoring o permanent sites provides the most comprehensive pictureo the impacts o disease on an area.

4.4 Characterizing long-term disease eects on populationdynamics, community structure and ecosystem unction

Monitoring permanent sites (in addition to random surveys) results in data on the rate o occurrence o new inections and disease impacts at dierent scales (colonies, species, populations, communities).Long-term monitoring o individually tagged colonies aected by disease can also provide detailedinormation on the spatial and temporal dynamics o particular diseases. Such inormationmight include:

• the rate of spread of infection within a colony;

• amount and patterns of mortality sustained from an infection;

• change in the number of lesions over time;

• change in lesion spatial distribution;

• lesion dynamics (position of lesions on colony, temporal scale);

• duration of infection;

• host colony fate (recovery, progression, stasis, mortality, re-infection); and

• environmental correlates.



56


A monitoring program implemented or coral diseases at the population/community level shouldaddress the ollowing:

• types of diseases/syndromes, host range, and variation in disease dynamics between species;

• prevalence and incidence of diseases (population or species level), duration of an outbreak,

consequences to host species, and variability at various spatial and temporal scales;• local, regional and global distribution of diseases;

• physico-chemical parameters (depth, water clarity, temperature, nutrient load, etc.), biologicalactors (predators, algal abundance, bacterial load, etc.), and anthropogenic impacts (pollution,runo, sedimentation, etc.) associated with either chronic or acute disease events;

• long-term effects of disease on coral reef community structure and function at local and regionalscales; and

• potential reservoirs and vectors of disease.

4.5 Establishing and relocating permanent monitoring sitesWorking with permanent sampling units can be challenging to begin with, as it involves nding anoriginal marker position ater time has lapsed, doing so in changing environmental conditions, ndingmarkers that are covered with overgrowth, and working with dierent personnel. However, it is importantto do these things properly so the time spent setting up permanent sites does not go to waste.

Once sites are selected and the survey method dened using the guidelines in Section 4.2, a list o materials must be produced (see Table 4.2). This list should include everything needed or:

a) marking and nding the sites;

b) marking and nding the permanent sampling units; and

c) collecting data.

Many o these materials should be available during every survey because re-bars, tags, fagging tape,

buoys, etc. can disappear between surveys and require replacement.When establishing permanent sites, researchers should attempt to minimize human interaction onthe ree and deploy permanent stakes and tags in as discriminate a manner as possible. For example,re-bars and masonry nails should never be inserted into live coral and all foats, cable ties, tags andother materials should be secured such that they do not abrade corals or other sessile invertebrates.A procedure or establishing permanent transects is described below. This method requires insertiono multiple re-bars per transect. Other approaches, such as those or radial or circular sites, require asingle permanent rebar (and submerged buoy or foat to acilitate relocation o the site) and equipmentor subdividing the site into measurable units, which are temporarily deployed only when assessmentsare underway. Ater the study is completed, the markers should be removed.




58

3. Tie fagging tape or a submerged buoy onto the beginningand end re-bars o the transect (Figure 4.5). An additionalbuoy/foater can be tied to the midway transect marker (nail or re-bar). This will acilitate nding the transect inuture surveys.

4. To place the next belt transect haphazardly, use apre-established method such as moving 1m to the right or let o your previous transect and swimming 10 n kicks.Then, hammer in the rst re-bar o the second transect.Repeat this procedure with all transects at all depths.I quadrats are used along the transect, their positionshould be randomized (see Figure 4.2) and recorded.Rebar stakes or nails can be used as reerence points toposition the quadrat in exactly the same position each time(Figure 4.5).

4.6 Calculating prevalence,incidence, and gross disease characteristics

Data collectionData rom any sample unit that surveys a dened area (belts, quadrats, circles) may be applied to thecalculations detailed below. Using the selected sample unit, all colonies larger than 5cm in diameter (or whatever criterion is selected) are counted, identied to whatever taxonomic unit is decided upon(species, genus, morphological type, etc.), and examined or presence o disease or compromisedhealth, using categories outlined in Chapter 2. These data are entered on a data sheet (see Appendix5 or examples in current use). How precise a taxonomic identication is needed depends on the

questions, surveyors and geographic area. In the Caribbean, there are only ~62 zooxanthellate coralspecies, so collecting data at the species level is possible. In the Indo-Pacic, more than 700 specieshave been recorded, so data are normally collected at the genus level, and segregated by morphology(branching, massive, encrusting, etc.). Additional data on colony size and percent mortality can provideuseul inormation on population dynamics, community structure and impacts o disease and other stressors. For example, in the western Atlantic many researchers measure the height and diameter o colonies and record the percent o the colony surace with recently denuded skeleton and older, algalcolonized skeleton.

Disease prevalenceDisease prevalence is the proportion o diseased colonies to the total measured population o colonies. It can be calculated or individual populations, species or genera, or or the coral communityas a whole, as well as or each particular disease/syndrome, similar group o diseases or or all diseases

lumped together. What is calculated depends on the questions asked.

Prevalence (P) = (# diseased colonies/total # o colonies) x 100A prevalence value is estimated or each area-sample unit. An average prevalence value with standarddeviation can then be calculated or habitats, zones or rees (depending on the stratication and thequestions) using the sample unit prevalence value.

Figure 4.5 Flagging tape tied to the end o a re-bar stake provides a visual marker or relocating a transect. Photo: E. Weil



59

Disease incidenceDisease incidence is the number o new inections appearing in the population within a period o time. This is a very important record o the progress o a particular disease in a particular species,population or community; it characterizes the epizootic temporal dynamics. To estimate the incidenceo a particular disease, all inected colonies ound during the rst survey should be tagged and/or

mapped within each sampling area. This is particularly important i the disease is short-lived or seasonal(such as black band disease or white plague). During subsequent surveys o the same sampling units,newly inected colonies are then identied, counted, tagged and mapped. Dead colonies should becounted and caution must be taken to make sure colonies are not counted twice. For example, i acolony is inected during time T

2, and is dead at time T

4, it is only added to incidence calculations

at time T2. Records o dead colonies should be noted separately, as mortality rate. However, i the

colony was healthy (and, thereore, unmapped and untagged) during a previous survey (i.e. time T2),

but dead by the next survey period (i.e. time T3) then it should be counted in both incidence and

mortality calculations at time T3

(but only i cause o death can be veried as the disease in question).It should also be tagged and mapped so that it is not recounted in later surveys. Average incidence iscalculated or the site as a whole ater incidence values are calculated or each sampling unit or thehabitat and/or ree in question. See Chapter 5 or how to use incidence observations to calculate rateo outbreak.

Incidence (I) = number o new inections within a time period, T

MortalityOten, the aspect o most concern is mortality rate, as this can have proound consequences on thestructure o a ree community. Mortality rate can be calculated as ollows:

M = number o colonies dying per census area per unit time

total number o colonies within census area

However, i the dynamics o a particular disease are o interest, such as how this disease is aectinga particular species, or how severe it is, then the case atality rate (Chapter 3, Section 3.1) may beo interest. The case atality rate measures the mortality rate o those susceptible and aected by aparticular disease:

CF = number o colonies dying o a disease per census area per unit time

total number o colonies with the disease per census area per unit time

These calculations can be used on individual coral species, or on the coral population as a whole.

Another aspect that may be o interest is partial mortality. Corals, as colonial animals, can “partiallydie”, i.e. they may lose a certain portion o their tissue, but the remaining tissue may be healthy andcapable o regrowth. Thereore, it may be o value to monitor partial mortality as a percentage o the

colony which dies as a result o a disease. One can then monitor whether or not the tissue regrows andrecovers ater partial mortality has apparently stopped, whether partial mortality continues to progressto ull colony mortality, or whether the disease appears to come to a halt, but with no apparenttissue regrowth over bare skeleton. In these cases, it is necessary to develop a way o determiningthe percent o the colony surace area aected. For branching and oliose morphologies, the totalnumber o branches, as well as dead and dying ones, can be counted and a ‘percent o colonyaected’ calculated. For massive, plating and encrusting orms, the percent o aected surace areacan be calculated rom photographs, (see “using photographs” below), or lesion and colony diameter can be measured by hand using a transect tape or calipers. I hand measurements are to be used it iscustomary to take a measurement at the widest diameter and then one perpendicular to the widest.The mean can then be calculated rom these two, and the ‘percent o colony aected’ calculated asthe ratio o lesion size to colony size.




60

Disease characteristics at the colony levelI colonies are tagged in order to monitor disease characteristics at the colony level over time,representatives o both diseased and healthy colonies must be tagged within or near the sampling

Figure 4.6 A masonry nail (see arrow) hammered into

dead skeleton can provide a useul reerence pointand scale or monitoring disease progression in anactive lesion. Here a massive Porites colony exhibitssigns o white syndrome. Photo: L. Raymundo

unit. I the disease is aecting multiple species, thenreplicate colonies o each species should be monitored.

Logistics and time resources should be considered whendeciding how many replicates to tag, although ve healthyand ve diseased colonies per species would be aminimum number. The inormation obtained through thisprocess (such as that listed in Section 4.4) is useul or characterizing the etiology o particular diseases. Thesediagnostic characteristics help dene the etiology, such asdaily, weekly, monthly or seasonal changes in lesion or band appearance. All inormation should be collected in atemplate sheet already ormatted or this purpose toreduce the amount o underwater time needed, and tostandardize data collection.

Using photographsPhotographs o diseased colonies are important sources o inormation. When taking photos or later analysis, alwaysplace an appropriate scale bar in each photo; a plastic ruler

Figure 4.7 A branch o Acropora with whitesyndrome. The green cable tie marked the originalposition o the band when it was rst observed andwas used to measure disease progression. Photo:L. Raymundo

is the easiest to use. In addition, in massive and encrustingmorphologies, a masonry nail can be hammered into thecolony at the immediate edge o the advancing ront whenthe colony is initially tagged (hammer into dead skeleton,not into live tissue; Figure 4.6).

In subsequent visits, the distance rom the nail to thenew disease ront is measured with a ruler. In many cases,especially in massive corals, you need a minimum o two

nails per colony or common diseases that advance in alinear or annular manner as the distance rom one nailto the disease ront will vary depending on where youtake the measurement. For branching colonies, a coloredcable tie can be used to mark the original position o thedisease ront (again, place the cable tie at the edge o dead skeleton, not on live tissue) and the distance romthe cable tie to the new disease ront can be measuredin uture surveys (Figure 4.7). Average linear advance ratecan be calculated per week or month as ollows:

Linear progression rate = distance rom nail/cable tie to new disease ront

length o time o census (days/weeks/months)Individual colony time-series photographs, those taken at the same angle and distance duringsuccessive monitoring visits, are powerul visual tools or examining the rate o advance o the diseaseront and host colony ate (Figure 4.8). These can greatly reduce bottom time, providing exactly thesame position is used each time. However, you do need to actor in the time needed to processeach photo in the lab. Photographs can be analyzed using image analysis sotware, which will allowaccurate measurements to be taken o lesion size dynamics (increase/decrease) over time. Sotwarepackages provide instructions on how photographs should be taken. The National Institutes o Health(NIH) provides a ree image analysis sotware package, ImageJ, which can be downloaded romtheir website: www.nih.gov. Another suggested package is CPCe, produced by Nova SoutheasternUniversity in Florida, which also provides a method or assessing cover using a series o randompoints. It can be ound on their website: www.nova.edu/ncri/research/a10.html



61

Figure 4.8 Five-day progression o a white syndrome inection on a tagged colony o Lobophyllia.Flagging tape tied to a nail provided both a visual reerence and a scale bar to use a imageanalysis o the rate o tissue loss. Photo: K.Rosell

4.7 Studying links with environmental driversIn Chapter 1, we discussed environmental degradation on global, regional and local scalesand its links (potential and realized) with stress to coral communities. Because o this link, theimportance o monitoring water quality concurrently with benthic monitoring has been recognized.Suggestions or how to do this are outlined below. However, logistical and cost issues may precludea comprehensive plan.

Included in this section are guidelines or measuring some o the basic environmental variables whichmay have potential impacts on disease dynamics. Managers are encouraged to nd out what water quality parameters are regularly monitored by other agencies in their area, and to develop collaborativearrangements so such data can be shared. Correlations between changes in environmental parametersand disease prevalence or incidence, or in the severity or rate o disease progression, can be testedwith simple statistical tools, and by graphing a certain disease parameter against the environmentalparameter in question (Figure 4.9).

Sea water temperature

At present, the only regional/global environmental variable o concern that can be easily monitoredis sea water temperature, but it is an important one or diseases as well as bleaching events. Anecient way o monitoring sea water temperature is by means o submersible continuous recorderssuch as Tidbits (HOBO®) water temperature loggers. These loggers can be preprogrammed

Figure 4.9 Hypothetical data set showing a strong relationship between increasingsea temperatures and total disease prevalence. Simple graphs, such as this one,can illustrate the strength o a relationship between a measured environmentalparameter and disease.

to record data at xed intervalsor a prolonged period o time.Earlier models require calibrationbeore and ater use with a clinicalthermometer, as they can beinaccurate by up to 3ºC. However,new versions (U22-001 units) canbe deployed deeper (to 30m) andprogrammed to record data or upto ve years. Data can bedownloaded and re-launchedunderwater with a shuttle unit, andso can be immediately redeployed.

24 26 28 30 32

Mean Water Temperature, oC

M e a n T o t a l D i s e a s e P r e v a l e n c e10

8

6

4

2

0




62

Two units per sampling site are recommended; one deployed at shallow and one at deep depth limitso the monitored habitat or zone. I a strong environmental gradient exists among sampling sites, moremay be needed. Temperature data can be summarized and plotted against disease prevalence dataso evidence o co-variation between disease prevalence and seasonal changes o specic diseases or disease outbreaks can be detected.

Figure 4.10 Chronic highly turbid conditions rom silt deposition andresuspension can stress corals and other nearshore benthic organisms.Photo: L. Raymundo

Silt and sedimentationSedimentation is problematic in manycoastal regions o the world whereland use practices are poorly regulatedand terrigenous soil and silt aredeposited into nearshore communitiesvia rivers and runo (Figure 4.10).The sedimentation rate refects theprocesses o deposition/delivery andresuspension o silt. It can be measuredby setting replicate sediment trapsin sampling areas and collecting andreplacing the traps on a weekly or monthly basis (Figure 4.11). Sedimentsare processed in the lab ollowingstandard protocols (rinsing, air- or oven-drying, weighing) and sedimentationrates per unit time (day/week/month)are estimated. Sediment composition(i.e. the proportion o calcium carbonateto terrigenous materials) and granule

size composition can also be determined. Such analyses can provide useul inormation regarding thesources o silt, its long-term impacts to benthic community health and structure, seasonality variations

in silt delivery, and covariation with disease prevalence and bleaching events.

Figure 4.11 A sediment trap can be adeployed to quantiy the amount o silt andother particulate matter settling onto a ree.Photo: E.Weil

I sediment traps and laboratory equipment or sedimentanalysis are unavailable, a less sophisticated method o estimating water clarity can be used. A Secchi disc providesqualitative estimations o clarity/turbidity, though it is not useulin shallow, clear water. A Secchi disc is a 30-cm diameter berglass, metal or wooden disc, painted white (Figure 4.12).(Note that those used or reshwater lakes are usually painted inblack and white alternating quadrants.) It is lowered over theside o a boat attached to a weighted rope, and sunk until it isno longer visible. The length o rope deployed is then measured,the disc is pulled up until it is visible again and then loweredagain until it disappears. The water depth at which the discdisappeared is used as an estimate o the depth o lightattenuation. These measurements are rather qualitative and arethereore only used relative to other such measurements (i.e.when irradiance, cloud and wave conditions are similar).Nonetheless, they can provide an easy and inexpensive way tocompare variability o water turbidity between sites and seasons.To standardize Secchi disc readings, always have the sameperson take the measurements, lower the disc on the shadedside o the boat, and always take measurements on sunny days,between 10am and 2pm, and at the same position at each site.



63

Other water quality parameters

Additional water quality parameters that may indicate environmental stress on corals include pH,nutrient load, and bacterial load. These, however, are more dicult to measure continuously i there are no unds or instrumentation and laboratory analyses. Managers are encouraged to linkwith laboratories, local environmental regulatory agencies, and even hospital laboratories, i it isperceived that any o these actors may be an important management issue that requires attentionand monitoring.

Rainall and river dischargeIt has been veried that two diseases in the Caribbean,aspergillosis and white patch disease, are caused byubiquitous terrestrial opportunistic pathogens (a soil ungusand a human intestinal bacterium, respectively) (52,65).While a denitive source o these pathogens has not beenidentied, it is a strong possibility that human activitieswere instrumental in either delivering these pathogens tonearshore ree environments or increasing their concentration

in these environments.In addition to being a source o potential pathogens incoastal waters, river discharge and non-point runo are themain sources o terrestrial-based anthropogenic stressorssuch as ertilizers, pesticides, silt, sewage, and heavymetals rom roads. Rainall varies seasonally and alters river discharge, aecting salinity and pollutant loads in coastalreceiving waters. Thereore, data on rainall patterns mayprovide a proxy or seasonal shits in the delivery o reshwater and pollutants onto ree communities. Oten, rainall ismonitored by a local weather bureau which may also monitor river discharge. Such data are usually easy accessed, and

may reveal links with seasonal changes and the prevalence o specic diseases. Where covariation is

observed, urther investigation is warranted to determine what stressors or pathogens may be linked withthe disease impacts.

Figure 4.12 A Secchi disc is a useul andinexpensive tool or qualitatively comparingwater turbidity between sites, providing it is usedin a standardized manner.



64


Figure 4.13 A map o transect locations at Las Pelotas inPuerto Rico. Additional underwater structures and dataloggers were included or reerence, to assist in relocatingtransects during subsequent visits.

Figure 4.14 A map o a series o transects on the YucatanPeninsula, Mexico. Transects were located by GPS or easein relocation.

Box 4.1

Relocating dicult sites

We will address one dicult, but not uncommon, case here: setting up a sampling area which

meets all criteria o the survey plan, and then relocating it in uture survey trips when there areno convenient external spatial reerences (coastal reerence marking, visible mooring buoys) or when conditions are dicult (strong winds, deep sampling sites, limited underwater visibility).

Beore leaving the dock, tag all re-bars (or long masonry nails) and organize them in groupsor marking each transect. When the ree site has been selected ater preliminary surveydives, its waypoint (i.e. geographic coordinates) should be recorded in the GPS unit and ina eld notebook, along with all reerence inormation to the site (bearing direction rom thedock, distance rom shore, any shore positioning markings, etc.). Ater all transects have beenestablished, construct a map o the survey area with the relative location o transects and anymajor bottom eatures that can help relocate the sampling area (Figure 4.13). Bearings shouldbe taken with a high precision UW compass, and distances between markers estimated to helpdivers nd the transects in subsequent trips.

Placing a mooring buoy to mark the sampling site is the quickest way to relocate the siteand ensure anchor damage is prevented. But when this is not possible, a sub-surace buoycan be used. To avoid problems o limited visibility or to compensate or a less-than-accurateGPS re-positioning, another sampling site waypoint can be obtained to mark the position o avery distinct and large bottom eature within the sampling area. This eature should be clearlyidentiable rom some distance and will be the bottom spatial reerence point, marked in thesampling area map and photographed or uture use.

Obviously, the most practical way to relocate a site is with a GPS unit (Figure 4.14). However,the useulness o this approach is dependent on the amiliarity o the user with its limitations.Care should be taken to obtain the correct rst GPS position, making sure that there are nodriting eects. To avoid this, mark the waypoint with a small anchored buoy with very littlerope slack. Relocating the waypoint also requires counteracting any driting eects, so use the

same principle when returning to the site.



Chapter 5Detecting and Assessing Outbreaks


How to define a disease outbreak in a coral community.

An overview of early warning signsof coral disease outbreaks.

Approaches for determining the extent and impact of a disease outbreak.



66


Detecting and Assessing OutbreaksC.D. Harvell, C. Woodley, L. Raymundo and Y. Sato

5.1 When is a situation an “outbreak”?An inectious disease outbreak is dened as a situation whereby the rate at which new hosts becomeinected increases. In other words, it is an unexpected increase in disease or mortality where it doesnot normally occur, or is at a requency greater than previously observed. In Figure 5.1, we provide anexample o outbreak dynamics or human diseases. As demonstrated in this graph, once the inectedhost population reaches a critical size, the number o new cases increases exponentially. As

Figure 5.1 General example o dynamics o an inectious disease outbreakin a human population. An outbreak begins with random events that inecta small number o hosts. New cases occur exponentially ater the inectedpopulation reaches a critical number. The outbreak dies out when the

susceptible population declines either through death or increased immunity.Redrawn rom Anderson et al. (4).

more individuals within a populationare exposed to the disease, thenumber o new cases eventuallydeclines, either through host recoveryand immunity or death. The diseasethen becomes a long-term aspect o

the population dynamics, becomingendemic and either reachingequilibrium with ew occasional cases,or undergoing periodic outbreaks.Figure 5.2 shows an actual outbreako Bubonic Plague in Sydney in 1903.The epidemic ollowed this generalpattern, becoming endemic aterwardsuntil it was eradicated.

For coral, the situation is dierent;corals are a highly diverse assemblageo immobile, colonial animals that

can only come into contact withother such animals via growth. Thesurrounding water in which they growprovides a means o contact withpotential vectors o disease such assh. In addition, portions o a colonymay die in response to disease, whileother parts may remain disease-ree,providing an avenue or recovery or eventual re-inection. Thereore, weneed to modiy approaches appliedto humans and other vertebratesto manage coral diseases. For

instance, in corals, we may alsoapply the concept o an outbreakto a disease that suddenly aectsa species previously thought to beresistant, or when there are signs o disease which do not correspondwith any described in the literature(i.e. a potentially new or emergingdisease). To develop a table similar tothat o Table 5.1 or a coral diseasewould require catching the outbreakin its early stage, marking all diseased

Figure 5.2 Disease dynamics o Bubonic Plague in Sydney, Australia, 1903.Modied rom Keeling & Gilligan (3).

Establishment

Removal o

Susceptibles

Equilibrium orRecurrent Epizootics

ExponentialGrowth

Endemicity

R a t e o N e w I n e c t i o n s

Time



67

colonies in a dened area o ree, and monitoring the accumulation o new cases through time. Thisbrings to the oreront the importance o long-term monitoring and regular random assessments, asit is during such activities that the early stages o outbreaks may be noticed. I a disease outbreak isobserved early, then as much inormation as possible can be gleaned rom the event, and a number o management options can be undertaken. Reer to Chapter 6 or detailed inormation on strategies

and options or managing coral disease.Technically, an outbreak is dened as an R

0value greater than one (4). R

0is the “average number

o secondary inections produced when one inected individual is introduced into a populationo susceptible hosts”. An estimation o R

0can be calculated i enough inormation about disease

transmission is known: (the number o contacts per unit time) x (transmission probability per contact) x(duration o inectiousness). A more direct approach o estimating R

0rom eld data as the normalized

accumulation o new cases (i.e. newly inected colonies) over time may be more attainable.Because corals are sessile, it is more possible to directly estimate R

0in eld populations than or

most animals.

R0 = (NT2 - NT1) / NT1

Where

NT1 = the number o cases at time T1NT2 = the number o cases at time T2

A disease will increase in a population with R0

> 1; i.e. a diseased individual will more than replaceitsel. A disease will decline with R

0< 1, and is considered endemic when R

0= 1.

Table 5.1 presents some established R0

values or certain wildlie diseases.

Table 5.1 Examples or estimation o the basic reproductive rate (R0) or various pathogens in wildlie species (modied rom

Real and Biek 74).

Pathogen Host species Scientifc name R0

Rabies virus Spotted hyena Crocuta crocuta 1.9

Phocine distemper virus Harbor seal Phoca vitula 2.8

Mycobacterium bovis Feral erret Mustela furo 0.18–1.20

Mycobacterium bovis Eurasian badger Meles meles 1.2

Classical swine ever virus Wild boar Sus scrofa 1.1–2.1

Both R0

and incidence can be estimated rom eld populations o marked corals (see example o incidence calculation in Chapter 3). The ollowing example is provided or Black Band Disease o Montipora near Orpheus Island, Australia. Three 10mx10m quadrats were established in the vicinity,each encompassing 10-30 diseased colonies. Within the quadrats, all diseased colonies were marked.

Quadrats were subsequently censused monthly or two years, and water temperature was recordedsimultaneously. Monthly census intervals were considered sucient as BBD does not spread veryrapidly. In 2006 and 2007, outbreaks coincided with rising summer temperatures rom November through to March, and declined in the cooler months o April through to August (Figure 5.3).R

0was calculated as the average per capita increase in colonies with BBD (Table 5.2). An R

0< 1 in

February 2006 indicated that BBD cases were declining; an R0

> 1 in December 2006 and January2007 showed an increase in disease within the susceptible population. The extremely high R

0value

o 7.5 in December 2006 indicated the outbreak could become epidemic i temperatures remainedhigh. However, by the ollowing month, temperatures had begun to cool and a corresponding declinein the number o new cases was observed.




68

Figure 5.3 The mean number o new cases o black band disease (incidence) aecting Montipora species on the Great Barrier

Ree, Australia. Data are shown only or months when sampling took place. Values taken rom three quadrats monitored over a two-year period. This pattern closely ollows a seasonal temperature trend and also illustrates the disease dynamics typicalo an outbreak. Data printed with permission rom Sato et al. (2).

Census month Jan 06 Feb 06 Oct 06 Dec 06 Jan 07Mean # BBD cases seen 14.00 16.33 0.67 5.67 15.67

Mean recovery 0.67 0.00 1.67

Mean change in # BBD cases 2.33 5.00 10.00

Mean new cases seen 3.00 5.00 11.67

R0

0.21 7.50 2.06

Outbreaks are usually short-lived, and should be treated with some urgency so as much inormationas possible can be collected while it is available. Chronic diseases can have equally devastating eectson populations and communities, particularly due to their potential eect on tness. Yet because theyare less strikingly visible, it is oten more dicult to garner support or an investigation. Nevertheless,it is important to develop sound protocols or investigating and monitoring both transient outbreaksand chronic low-level disease, as both will actor as mechanisms o community change and indicationso impacts to ree health.

Table 5.2 Estimations o R0

rom the change in the number o cases observed during monthly censuses o a black band diseaseoutbreak on the Great Barrier Ree. Mean recovery, change in case number and new cases were calculated as the dierencebetween the sampling months presented (i.e. Jan-Feb, Oct-Dec, Dec-Jan). Mean change in case number refects both recoveryand new inections. Mean calculated rom three 100m2quadrats. Data printed with permission rom Sato et al. (2).

Jan Feb Feb Mar Apr Jun Aug Sep Nov Jan Mar May Jun Aug Oct Dec Jan22- 2- 22- 22- 18- 15- 21- 26- 14- 2- 6- 5- 17- 18- 22- 22- 28-

Mean new cases/7days2.5

2

1.5

1

0.5

0



69

5.2 Early warning systems or coral disease epizooticsDiagnostic tools or coral disease outbreaks lag behind those developed or bleaching events (For detailed guidelines see Marshall and Schuttenberg 75). Though global eorts to ll the knowledgegaps have resulted in great progress, we do not yet have the ability to accurately detect pendingdisease outbreaks beore they happen. However, there are predictive tools available which arecurrently being tested or applicability to disease outbreak investigations. For example, regular monitoring o water quality parameters and environmental actors, as discussed in Chapter 4, canindicate potential stressul conditions or corals. Increased stress can aect resistance and increasesusceptibility to existing pathogens. Over time, we expect to discern links between a change in aspecic parameter and a change in the prevalence o one or more diseases. Thereore, monitoringenvironmental parameters may help to develop an early warning system or certain diseases.

The complex interactions among stressors, and their eects on corals and ree ecosystems, are generallypoorly understood, making it dicult to assign a specic cause to local or regional declines in coralhealth. Persistent high levels o stress can cause sudden whole-colony mortality and disease may or may not be implicated as a direct cause o death. In contrast, chronic low levels o stress are likely toresult in non-acute, sub-lethal eects on corals, which can have measurable (but not necessarily visible)eects on growth, reproduction or survival. Furthermore, chronic stress can reduce a coral’s ability to

resist disease, making a community o stressed corals vulnerable to an outbreak. Identication andmitigation o these stressors (i.e. toxicants, pollutants, sediment, nutrients, temperature) at an earlystage o detection may enable the prevention o a disease outbreak.

Compromised health may maniest itsel through shits in coral physiology which may not be visiblydetectable when surveying corals in the eld. In the absence o acute mortality, biological indictors –or biomarkers – are being developed and tested to identiy delayed or sublethal eects o exposureto stressors in coral. Biomarkers are substances that can be detected, sampled and measured to helpcharacterize specic changes in health or physiological state. Antibodies, which can be sampled romvertebrate blood, are examples o biomarkers that can be used to detect exposure to a particular pathogen. Coral biomarkers can potentially detect cellular physiological changes in a coral beore thecoral develops visible signs o ill health such as tissue loss or partial mortality. This developing scienceis reerred to as cellular diagnostics (70). Biomarkers rom coral are being sought that can:

1. indicate exposure to a stressor or pathogen;

2. pinpoint an eect o stress or disease on coral physiology; or

3. show susceptibility to the stressor or pathogen.

As with human diagnostic assays, inormation about particular cell unctions can be used todiagnose various disease states as a result o exposure to a specic stressor(s), and providean indication o overall health in the coral. As this technology improves, it is hoped that simple,“user-riendly” diagnostic tools can be developed which test or levels o stress in corals and whichmight suggest increased susceptibility to disease beore an outbreak occurs.




70

5.3 Techniques to quantiy the extent and impact o an outbreakWhen almost nothing is known about a disease (as is the case or most coral diseases) or at thetime when a new or emergent disease is discovered, outbreak investigations are vital. An organized,systematic approach helps determine the extent and impact o the event, the causative agent(s), eachagent’s reservoir or source, and transmission routes between hosts. It can also identiy knowledgegaps, help ormulate hypotheses or urther study, ocus research goals, and help identiy control or management strategies. When the cause o an outbreak is known (i.e. when we have identied thepathogen causing the disease which is rapidly increasing in a population), but the source (reservoir) or route o transmission remains unknown, much investigative work is still required (as was the case withVibrio shiloi , the causative agent o one type o bacterial bleaching). In this case, investigations canocus on lling the knowledge gaps with regard to the ecology o the disease to better guide uturecontrol and management eorts.

Managers oten have the most accurate and up-to-date inormation critical or an outbreak investigation.Their knowledge and historical inormation on local rees are invaluable when it comes to inormingthe investigative process and determining the impact o a disease outbreak. The rst objective in thissituation is to create a “denition” o the disease. This includes identiying eatures that distinguishthis particular disease rom others and provides a route to understanding how and why the outbreak

is occurring (76). The questions a manager can begin asking are:

• ‘who’ is aected? (What species?);

• ‘where’ is the outbreak located? (Including descriptions o surrounding environmental actors andinvestigating other possible outbreak sites);

• ‘when’ is the event occurring? (Seasonal trends, the rate o movement through a population andrate o lesion progression on individual colonies);

• ‘what’ eatures do the clinical and pathology analyses provide toward identiying a causative agent?(Protocol or this process is described in Chapter 3); and

• ‘why’ or ‘how’ did this occur? (This is the pathogenesis but can also include environmental actorswhich might have triggered the event, such as a sudden change in temperature or rainall, or a toxin

spill).The initial inormation provided by the manager is critical to developing the case history and anysubsequent investigation and laboratory work. Assistance in determining i an outbreak is occurringand how to respond to it can be obtained by contacting the Coral Disease and Health Consortium(CDHC) via email at [email protected], Dr. Andy Bruckner or Dr. Cheryl Woodley at NOAA (or seeAppendix 2 or a list o regional experts associated with the CRTR Coral Disease Working Group).

Managers who regularly monitor or assess disease will know what the characteristic prevalence levelsare or a given area or each disease that has been documented and observed in that area. I asituation o concern is observed in the course o monitoring or rapid assessments, certain steps canbe taken immediately. The most obvious situation is a much higher number o inected colonies thanis normally observed or a given disease. Although we usually speak o an outbreak as reerring to asingle disease, this may not necessarily be the case. An outbreak in Palau in January 2005 involved

multiple coral species and both white syndrome and black band disease, though the host rangeo the two diseases diered (35). An even more complicated case occurred during a Florida Keys2003 outbreak, where a disease looked visibly identical in three acroporid host species. Extensivehistological and molecular analyses, however, ruled them to be completely dierent pathologies (77).Below are a ew simple steps that can be taken when documenting an outbreak:

1. Make an initial description o the aected site, which should include the ollowing inormation:benthic composition (see Chapter 4 or methods), depth range, ree zone/habitat, dominantbenthic species, water clarity, current direction and relative strength, proximity to potential sourceso stress such as river mouths, coastal construction zones, cities, and any additional inormationavailable that might shed light on why the outbreak is occurring at that place and time. Even i thisinormation is qualitative, it can still be useul.



71

2. Identiy and describe the characteristics o the lesions o the disease(s) you are observing, usingthe decision tree presented in Chapter 2. Photo-document lesions in all species aected. Makea presumptive eld diagnosis o the suspected disease(s) you are dealing with; are you seeing adisease previously described and/or documented rom the aected site? Or do the signs o diseaseyou are observing not correspond with any previous description? This situation may represent a

new or emerging disease in the area.

Figure 5.4. Top view o white syndrome outbreak spreadingamong at least 5 species in the genera Lobophyllia, Mycedium,Merulina, Fungia, Favia in Palau. Photo: B. Willis

3. Develop a host range list – a list o all taxaapparently aected by each disease youare seeing (Figure 5.4). Make sure to noteany colonies aected by more than onelesion type per colony. In addition, note allother taxa within the aected area whichare not inected; resistance to a particular disease is equally important inormation. Itis most helpul to identiy to specieswherever possible; at the very least, coralsshould be identied to genus.

4. Tag colonies or regular monitoring o disease progression. I possible, tagreplicate colonies o each species aectedor each disease observed. Attach tags todead portions o the colony, or to nearbysubstrate, using fagging tape. Photographall tagged colonies, being careul toplace a scale bar or ruler in each picture.Photographs should attempt to includethe entire lesion; depending on the sizeo the colony and the lesion, it may useulto take both a close-up picture, and awhole-colony picture (see Appendix 3 or

additional photos).

5. Using a systematic search swim pattern,(snorkeling or manta tows may be possiblei the area is shallow), determine thephysical boundary o the aected ree area.Mark the perimeter at regular intervalsusing fagging tape tied to corals or other underwater structures (Figure 5.5). Markingthe boundary will allow you to determine therate at which the aected area is spreadingspatially in uture visits to the site. Quantiythis area by measuring maximum width and

width perpendicular to maximum using atransect tape, and determine depth range.

6. Contact a laboratory with which you have a collaborative agreement, and make arrangementsor sample analysis. Collect samples or microbial and histological analysis using the proceduresoutlined in Chapter 3. I you do not have a collaborative agreement with a laboratory, but eel thissituation is urgent and requires resources beyond your capacity, contact the CDHC via email [email protected].

7. Collect all environmental data available or this site, either rom your own agency or others. Thismight include water temperature, rainall, current wave height and tide patterns, sedimentation,and/or bacterial load.

Figure 5.5 Flagging tape tied to a dead portion o acolony or the substrate is an eective temporary meanso marking an outbreak area boundary so that spreadbeyond an initial observation point can be tracked over time. Photo: K. Rosell




72

8. Soon ater you complete steps 1 to 5, perorm rapid surveys (manta tows are particularly goodor this) at increasing distances rom the outbreak site, to look or sites o secondary outbreaks.Remember: do not go straight to “clean” sites rom the outbreak site. Separate trips should beplanned or these surveys, using equipment which has undergone the sterilization proceduresoutlined in Chapter 3. It is vital that those investigating a disease outbreak avoid spreading the

disease to unaected sites.

Figure 5.6 Remeasuring a black band disease ront on Montiporasp. duringa two year-long monitoring eort o a BBD outbreak on the Great Barrier Ree. The ruler in the photo provided a scale bar or both image analysisand measures o linear progression. Photo: Y. Sato.

9. Set up a monitoring schedule torevisit the principle outbreak site atregular intervals. I mortality isoccurring rapidly, then it is advisableto resurvey at weekly or biweeklyintervals, depending on your resources. When you revisit the site,photograph all tagged colonies,measure the linear progression o the disease ront and note the healthstatus o the colony (progressing,stasis, recovering, dead; Figure 5.6).Also look or new inections,either as additional lesions onpreviously-aected colonies or as new hosts. Over time, look or evidence o recovery, either romtissue resheeting over dead skeletonor through the recruitment o newcolonies (Figure 5.7). Finally, atperiodic intervals, repeat step 8, tomake sure that secondary sites o inection are not developing.

And, nally, how is this inormation to be used? Data gleaned rom a comprehensive documentationo an outbreak and subsequent monitoring is likely to include identication o susceptible andresistant species, species-specic mortality rates, species-specic recovery rates rom tissue regrowth/resheeting, community recovery via recruitment, and responses o other ree biota such as macroalgaeor sponges. All o these data can be used to examine changes in ree community structure as aconsequence o the outbreak and coral mortality. Chapter 6 addresses specic management options,where this inormation may be applied.



73

Figure 5.7 Time series photographs o one Montastrea faveolata colony with yellow band disease (YBD) in Puerto Rico monitoredrom 2004 to 2006. Several YBD lesions developed in June 2004, which expanded outwards during the ollwing months.In February 2005, this colony also became inected with white plague (WP). In September 2005, all o the remaining livingtissue bleached (see white area). Ater the bleaching event most o the colony became inected with YBD and by August 2006,the entire colony was dead. The graph shows the rate o this colony’s tissue loss rom summer 2001 to summer 2006, and thecoinciding bleaching events (BL) and disease outbreaks. Photo: E. Weil

S U - 0 1

W 1 - 0 2 S U -

0 2 W I -

0 3 S U -

0 3 W 1

- 0 4 S U - 0 4

W 1 - 0 5 S U -

0 5 W 1

- 0 6 S U - 0 6

Season

BL

BL

YBDWP

L i n e a r t i s s u e m o r t a l i t y ( c m / m t h

) 3.5

3.0

2.5

2.0

1.5

1.0

0.5

0.0



Chapter 6Management Issues and Actions


A summary of the most current and comprehensivecoral disease databases.

Where to go for further assistance and advice.

A look at management options for coral disease – general thoughts, what has been tried and

current research efforts.



76

Management Issues and ActionsL. Raymundo, C. D. Harvell, A. Bruckner and C. Woodley

6.1 Management issues and challenges

Figure 6.1 Disease management or humans and wildlie involves quarantine,vaccination, culling, and education, most o which are not currently viable optionsor marine diseases. www.cdc.gov; www.dailygalaxy.com, www.rabies-vaccination.com; www.leolabs.com

The management o marinedisease is a new rontier.Traditional management toolsor human and wildlie diseasecontrol include quarantine,culling, vaccinating andeducation (Figure 6.1). However,only quarantine and educationare currently viable options or dealing with coral diseases andexamples where they have been

applied are rare. We mustconsider certain undamentaldierences between marine andterrestrial systems when lookingat options or managing coraldisease. Ocean water supportsa rich and diverse microbialcommunity. How many o those

microbes are pathogenic, or potentially so, remains unknown. Because ocean water supports such avast microbial community, marine systems are considerably more “open” and connected to eachother than terrestrial systems. Additionally, our incomplete knowledge o corals, their diseases, their resistance capabilities and the infuence o environmental stressors on their health, pose additionalchallenges to developing workable management options.

However, the impacts that diseases are having on coral populations highlight an urgent need to developmanagement options concurrently with scientic investigation o diseases. Although the science isstill in its inancy, there are practical steps that ree managers can take to manage coral disease. Thecurrent perception that coral diseases are “unmanageable” is untrue and managers are in the uniqueposition o being able to develop and test options or controlling disease spread. However, thesetests should be conducted with careul planning: any potential management tool should be tested viaa properly designed experiment and, most importantly, results should be reported. The authors o thismanual are available as contact persons or advice on this (their contact details are listed in Appendix2). Below we present some areas which could guide coral disease management.

6.2 Global disease databases: options or managing inormationResource management must be based on sound science. In turn, scientic inormation must beinterpreted and communicated eectively so it acilitates meaningul management decisions. As agrowing eld o science and an urgent management issue, coral disease is the ocus o a world-wideresearch eort which is generating an enormous amount o inormation. Due to the global implicationso disease impacts and the pressing need to standardize all aspects o disease investigation, datageneration and management are two very important eatures contributing to this eort.

There are a number o databases, accessible to the public via the internet, which contain various typeso inormation on coral diseases. Such databases are integral to synthesizing inormation rom diversesources and rely heavily on the addition o accurate inormation as it becomes available. A repositoryor global inormation which is accessible, accurate, and helpul is key to developing and testingmanagement options. Below is a brie description o the most current and comprehensive o these.




77

The Global Coral Disease DatabaseThe Global Coral Disease Database (GCDD), available at http://www.unep-wcmc.org/GIS/coraldis/index.cm, is the most comprehensive compilation o coral disease inormation. It was developedby the U.S. National Oceanic and Atmospheric Administration’s (NOAA) Coral Ree ConservationProgram in conjunction with the United Nations Environmental Program’s (UNEP) World Conservation

Monitoring Centre (WCMC). It is a web-accessible GIS database that compiles records o diseaseobservations and tracks their spread over time, by geo-reerencing disease locations and plottingtheir occurrences onto WCMC coral ree distribution maps. The GCDD includes an online mappingtool (a prototype IMAPS tool) that enables users to search and plot data by disease name, year,or country, with zoom capabilities and a ull inormation sheet or each line o data. It also has theoption to separate reports into novice and expert data. For each disease, inormation can be obtainedregarding: its global and regional occurrence and abundance, aected locations (i.e. country, ree,latitude and longitude) and species, and any available site-specic data on prevalence, incidence, andextent o mortality, by querying the database or using the mapping tool.

The database is linked to WCMC’s Protected Areas and Coral Species databases, and contains coraldisease identication tools and a photographic key to western Atlantic diseases. All in situ observationson prevalence, host range, global geographic distribution, and mortality or coral diseases are

compiled or the period 1972-2006 rom peer-reviewed journal articles, technical reports, regionalmonitoring data rom Atlantic and Gul Rapid Ree Assessment surveys, CARICOMP surveys, GlobalRee Check monitoring eorts, and reports submitted by researchers. These datasets refect wider spatial coverage o disease surveys, repeat surveys, and increases in the types o diseases and speciesaected over the last ew years. The GCDD currently contains over 8000 records o disease, andincludes reports o over 40 coral diseases rom the western Atlantic, 28 rom the Indo-Pacic and verom the Red Sea. Contact Dr. Andy Bruckner, [email protected] or more inormation, or tosubmit inormation on coral diseases.

6.3 Where to go or assistance and adviceIt is important to be aware that there is a network o dedicated and qualied scientists and managers

who can be contacted or assistance, inormation, and advice. In many remote locations, managersoten juggle numerous projects and responsibilities with ew resources, and may even be orced totake on responsibilities or which they have no ormal training. One objective o this book is to provideassistance to individuals who may be working in relative isolation. Another objective is to expand thecurrent network o individuals working in the eld o coral disease and coral ree management, andto assist managers who could benet rom additional expert support in obtaining the advice andinormation they need. Further, we wish to convey the importance o communicating research andmanagement experiences in the eld o coral diseases, either through publication or presentation atsymposia. There are many geographic locations or which there is no inormation currently availableon the status o coral diseases; this is particularly true or much o the Indo-Pacic and East Arica. Bylinking managers and scientists with other managers and scientists, inormation can be exchangedand productive collaborations can be orged. Below, we present two organizations whose memberscan be contacted or inormation and can answer specic questions beyond the scope o this book.

The Coral Ree Targeted Research Program, Coral Disease Working GroupThe Coral Disease Working Group (CDWG) as described in Chapter 1 (Box 1.1) is one o six workinggroups o the Global Environment Facility and World Bank’s Coral Ree Targeted Research (CRTR)program, launched in 2005. The CDWG maintains collaborations in support o coral disease researchat each o the CRTR’s our regional Centers o Excellence: the Marine Science Institute/Bolinao MarineLaboratory o the University o the Philippines, Philippines; University o Dar Es Salaam, Instituteo Marine Science, Zanzibar, Tanzania; University o Queensland Heron Island Research Station,Queensland, Australia; and Unidad Académica Puerto Morelos, Instituto de Ciencias del Mar yLimnología, Universidad Nacional Autónoma de México (National Autonomous University o Mexico,Institute o Marine Sciences and Limnology, Puerto Morelos, Mexico). All Centers o Excellence havethe capability to conduct eld assessments o local inectious coral syndromes and can provide



78


inormation on sample collection and where to send samples. The CRTR website can be ound at www.gecoral.org. This site describes current research eorts in coral ree ecology, and provides additionalcontact inormation. Contact inormation or individual members o the Coral Disease Working Groupo the CRTR can be ound in Appendix 2.

The Coral Disease and Health ConsortiumThe Coral Disease and Health Consortium (CDHC) was created in 2003 as a cooperative eort linkingrepresentatives rom U.S. agencies involved in coral ree management. Partners include the U.S.NOAA, the U.S. Environmental Protection Agency (EPA), the U.S. Department o Interior (primarily,National Park Service and Geological Survey), U.S. Coral Ree Task Force agencies, not-or-protorganizations and academia, both national and international. Currently, the group is involved in healthassessments; outbreak responses within the U.S. and associated territories; research and developmentor diagnostics and pathology; an International Registry or Coral Pathology; and capacity buildingeorts that include training, technology transer, and strategic research planning. For a downloadablecopy o the statement o purpose o the CDHC, reer to: www.coralree.gov/library/pd/FInal%20CDHC%20plan.pd. You may contact the CDHC directly at this email address: [email protected], or either Dr. Andy Bruckner or Dr. Cheryl Woodley at NOAA. Please see Appendix 2 or their contact inormation.

6.3 Management options in the ace o incomplete knowledge

6.3.1. Some general thoughts and options

Management strategies or coral disease must develop as a result o careul and rigorous testing andreporting o results. As we stated earlier, the traditional methods o culling and vaccination or diseasecontrol currently have limited application or coral disease management. However, certain aspects o coral lie history may lend themselves to disease control i they are incorporated into a managementstrategy: corals, unlike most other wildlie species o concern, are immobile; once a diseased colonyhas been located, it will remain in that location and can be counted and revisited (and potentiallytreated, i viable methods are developed). Furthermore, corals have the potential to regrow over deadskeleton by resheeting. In these ways, corals unction more like plants. Keeping these characteristicsin mind may help managers to “think outside the box” and develop management strategies uniqueor corals and other sessile, benthic organisms. Experiences rom the agriculture and plant diseaseliterature may provide guidance to management o coral diseases.

As mentioned previously, proving the cause o a disease is a dicult, lengthy process, beyond thescope o most managers and their laboratories or eld stations. However, one does not need toknow the causal agent o a disease to take management steps. A rst important step is to develop aworking knowledge o the diseases and compromised health states present in a given managementarea (i.e. to know what is normally present, and at what levels, in the coral community). It is only byunderstanding what represents ‘baseline’ conditions that one is able to assess what represents above-normal disease levels and their potential or increased mortality.

Building on this idea, long-term monitoring data sets should be viewed as valuable tools or local

management agencies. Responses to natural phenomena such as seasonally warm sea suracetemperatures or periodic corallivore outbreaks can be observed both in the long-term and in alarger geographic context to identiy sites that show greater or lesser resilience to such impacts. It isnow considered good policy to identiy particularly vulnerable sites (as well as those that show highresilience and resistance) or increased protection and management (78). Such data sets can alsobe used to bring about policy change (such as guidelines or coastal development) and to assessthe impacts o events such as ship groundings and chemical spills. In many jurisdictions, there maynot be a legal ramework in place to orce the perpetrators o such events to remediate damage.A comprehensive data set which quanties “beore and ater” impacts can be used as a basis or developing laws and regulations to guide remediation.



79

Figure 6.2 Intensive aquaculture, such as this sh pen, candeliver high concentrations o organic nutrients, antibiotics andpesticides to coastal ecosystems, with unknown impacts to health.Photo: L. Raymundo

This, then, is another important manage-ment tool: by controlling the input o anthropogenic stressors on rees, we canoptimize conditions avorable or ree health and coral growth. Ultimately, this

might be the most powerul and successulmanagement strategy, one with multiplepositive consequences on all coastalecosystems, and one whereby localmanagement agencies can exert somecontrol. Demonstrated links between coraldisease and specic anthropogenic inputscan be used as political leverage to improvewater quality, particularly in those localeconomies dependent on diving tourismand ree health. To date, it appears thatmany inectious syndromes o corals arecaused by opportunistic bacteria, with

many representatives o the genus Vibrio.Vibrio spp. are among the most common bacteria in the ocean (79), and members o this genus arealso responsible or certain important water-borne human diseases such as cholera (Vibrio cholerae;80). Similarly, the ciliate inections, such as brown band disease (BrB), skeletal eroding band (SEB) andCaribbean ciliate inection (CCI) are likely to be opportunistic. For these inections, the bestmanagement option is to control or reduce the stress in the environment, thereby improving thecorals’ chance o resisting or recovering rom inections (Figure 6.2).

6.3.2. What has been tried?

There is evidence to suggest corals that survive a bleaching episode may later succumb to anopportunistic inection, as their resistance is lowered by the stress o bleaching (42,81). In such cases,

Figure 6.3 Applying putty to a yellow band diseaseront slowed the progress o disease. Photo: A.Bruckner

imposing a quarantine on a ree acutely impacted by either bleaching or disease may be a viable option. The ree canbe closed to human activity by prohibiting diving andsnorkelling or a period o time. This was successullyundertaken in Florida in 2003 during a disease outbreak.A Florida Keys ree was closed to all human activity exceptapproved research and investigation or 60 days (B.Causey, pers. comm. and Federal Registrar 82). Thismanagement approach has a number o potentiallypositive consequences. First, when dealing with anoutbreak o an apparently unknown disease, the possiblerisk to humans is very real; closing access can prevent animpact on human health. Second, not only can diversbreak and abrade corals, they can also potentially transmit

pathogens between rees via contaminated gear. Manydive operations take large numbers o divers to severalrees in a single day, which could greatly acilitate thespread o inection between rees via dive gear. Closing aree can isolate an inection and limit its damage.



80


More direct management actions to alleviate inections may be possible in the case o a ew pathogens.For example, there has been some success in controlling the spread o black band disease (BBD)during warming anomalies by aspirating the band using large syringes or pumps. Clay or underwater epoxy putty can then be placed directly over the band. These methods were rst developed by HaroldHudson in 1986, and since then have been adapted by other scientists (Causey, pers. comm.). I clay

is used, all cyanobacterial laments must be removed; it does not persist long and, the laments willeventually emerge rom within the clay (83). Putty is harder to work with as it does not adhere as well.However, it is more permanent and eectively halts any cyanobacterial growth let in underlying coralskeleton ater aspiration. This has also been successully attempted with yellow band disease, whiteplague and white band disease. Preliminary results showed that band progression was slowed, andin more than 60 percent o cases, the disease was arrested (Bruckner, pers. comm.; Figure 6.3). I thisapproach is to be attempted, it should be done with great care to avoid spreading cyanobacteria andother microorganisms comprising a diseased band to surrounding corals.

Another practice that has been attempted is shading highly susceptible rees during bleaching events.It necessitates deploying shade cloth that eliminates approximately 60 percent o incoming irradianceand requires 10 to 12 days to take eect. However, shading corals or this length o time may alsoexacerbate bleaching, so this practice is not recommended.

Finally, experiments have shown that black band disease can be eliminated and the rate o appearanceo new inections can be reduced through re-introduction o herbivorous urchins Diadema antillaruminto habitats where they were ormally abundant (83). Through grazing behavior, these urchins reducethe potential or algal competition with corals, thereby reducing the likelihood o injuries that mayacilitate an invasion by pathogens, and directly removing the substrate that cyanobacterial lamentsrequire or attachment.

While antibiotics are successul in treating systemic inections o humans and wildlie, it is notrecommended to apply antibiotics in open marine ecosystems, and especially to corals. The coralholobiont is an extremely complex consortium involving benecial surace bacteria and indiscriminateuse o antibiotics without proper understanding o this complexity may do more harm than good.

One nal point: currently, the “treatment” o coral diseases in the traditional sense is not consideredeasible or eliminating disease during an outbreak. It is costly and time consuming, and inections

tend to be in varying states o progression at any given point in time. However it may be a viableapproach to save certain high-value colonies, such as massive ree building corals, or rare species thatare viewed as particularly important.

6.3.3 Current research eorts

One experimental program underway at the University o Tel Aviv involves phage therapy o corals.Bacteriophages are viruses that kill bacteria and many are extremely specic in the bacteria they kill.

Figure 6.4 A population explosion o the gastropodcorallivore Drupella cornus. This population killed aseveral hundred-year-old massive Porites colony, amongmany others, in the central Philippines. Note the whitepatches o recently-killed tissue and the brown patchescovered with recruiting macroalgae. Little healthy tissueremains on this colony. Photo: L. Raymundo

This program involves the isolation o specic phagesthat prey on bacteria pathogenic to corals. In testcases, the bacteria treated were Vibrio coralliilyticus and Thalosomonas loyaeana. Scientists were able tosuccessully isolate phages, introduce them to tankswith inected corals and increase the survival rate o the corals. However, transerring such a technologyto a ree system has serious logistical and ethicalissues, and to date, this has not been attempted.

Another potentially important area o research isthe identication and removal o vector organisms. Vectors can transmit pathogens between hosts bycontacting the hosts during predatory, commensal or competitive interactions. Recent research eorts haveuncovered a number o links between host coralsand organisms that transmit a pathogen. The marine



81

corallivorous reworm, Hermodice carunculata, or example, is thought to transmit Vibrio shiloi , whichcauses bleaching (84). The green calcareous alga Halimeda opuntia can transmit the causal agent or white plague, Aurantimonas coralicida, to host corals it brushes against (85). The Caribbean gastropodCoralliophila abbreviata is a vector or a white syndrome that aects Acropora (86) and the three spotdamselsh (Stegastes planifrons) has been shown to transmit black band disease between colonies

via predation (87). However, we do not advocate the indiscriminate removal o all corallivores, asthere is ample evidence rom terrestrial systems o unpredictable consequences resulting rom either the addition or removal o species to and rom ecosystems. That said, there are certain species thatcause an inordinate amount o destruction because their populations go through “boom and bust”cycles. I it was established that any o these highly destructive corallivores, such as the Crown-o-Thorns starsh (COTS), Acanthaster planci , or the gastropods Drupella spp. (Figure 6.4), transmitteda pathogen, then removal o these predators could potentially control the spread o disease. Indeed,in the case o COTS, removal eorts during outbreaks are regularly attempted. Caution must beexercised, however, as there may be other impacts to the ecosystem o such practices. For example,prior to a ull understanding o COTS biology, it was a common practice or volunteer divers to cutthe starsh into pieces. Due to the regenerative powers o starsh, this acted as an asexual means o reproduction and virtually created more starsh. When this practice was stopped, volunteers beganeviscerating the starsh and leaving them on the ree. However, trauma to the gut initiates spawning

in COTS, and so created the next generation o starsh. Today, it is understood that the most eectivemeans o controlling COTS during an outbreak is simple removal rom the ree.

Figure 6.5 Here, college students developed hands-on activities toteach grade school students about the importance o coral rees andthe organisms that depend on them. Photo: B. Baldwin.

Finally, one cannot underestimate theimportance o education and publicawareness eorts (Figure 6.5). Managersshould make every eort to disseminateto the public locally-relevant inormationon coral diseases and their potentialimpacts. Managers may also ocus their attention on target groups who interactregularly with the ree: shers, recreationaldivers, and diving tourism operators and

their clients. In places where divingtourism is a major source o revenue,there may be hundreds o visitors to asingle ree each day. Poorly-trained diveinstructors and tourist dive guides canwreak havoc on a ree by encouragingphysical contact with corals and other benthic organisms (Figure 6.6). However,educating and involving such individuals

in conservation eorts can have productive results. Many dive operators would like to know howthey can adopt an eco-tourism approach to their operations, and many are enthusiastic aboutparticipating in monitoring activities. Harnessing such enthusiasm will provide managers withadditional observers underwater, and the only eorts that are necessary are some initial training and

regular communication.



82


6.4 Procedures and practices to promote better managementDetails o some o these procedures have been outlined elsewhere in this book, but to apply themspecically in a management context, we summarize them here as well.

1. Restrict translocation o corals to prevent movement o disease.Corals are translocated locally, regionally, and globally or a variety o reasons (rehabilitation,aquaculture, and the aquarium trade, to name a ew). Such practices should only be allowedi quarantine conditions are possible. No corals with visible signs o disease or compromisedstates should be collected and transported to other eld locations, no matter what the purpose.Transport to quarantine acilities should be under strict biocontainment conditions that preventrelease o diseased materials or water into the environment.

2. Provide guidance or proper handling andcontainment regimes during coral disease experiments.Chapter 3 o this book discussed such procedures in detail. Managers may be in a position tocreate regulations and enorce rules locally, and it is hoped that the inormation provided in thisbook will be used or this purpose. I additional guidance is necessary, please consult the list o

experts in Appendix 2.3. Monitor proposed coral management and research activities,

as well as rehabilitation or remediation activities, to minimizeor avoid ethical and legal problems with the potential spread o disease.Again, managers are in a unique position to understand the ethical and legal issues involvedwith the use and transport o coral, and the manipulation o coral ree communities. Ensuring theproper procedural controls on these activities will help manage disease.

4. Promote the use o universal precautionmeasures when dealing with diseases in the feld.The suggestions outlined in Chapter 3 and 4, such as working rom uninected to inected areas,and sanitizing SCUBA gear and equipment when moving between rees etc. can be worked into

a ormal regulation and permitting procedure, to ensure compliance.

Figure 6.6 Many dive operations run by poorly-trained instructors encourage their clientsto touch and handle corals. The potential or abrasion and breakage, as well as diseasespread, is very high with such practices. Photo: D. Burdick



84




85

Reerences



86

Reerences

1. Edmunds, P.J. (1991). Extent and eect o black band disease on a Caribbean ree. Coral Rees10 (3):161-165.

2. Sato, Y., D. Bourne, and B.L. Willis. (in prep). Dynamics o a black band disease outbreak atPelorus Island on the Great Barrier Ree.

3. Keeling, M.J. and C.A. Gilligan. (2000). Bubonic plague: a metapopulation model o azoonosis. Proceedings o the Royal Society o London Series B-Biological Sciences 267(1458):2219-2230.

4. Anderson, R.M., C. Fraser, A.C. Ghani, C.A. Donnelly, S. Riley, N.M. Ferguson, G.M. Leung,T.H. Lam, and A.J. Hedley. (2004). Epidemiology, transmission dynamics and control o SARS:the 2002-2003 dynamics. Philosophical Transactions o the Royal Society o London B 359(1447):1091-1105.

5. Porter, J.W. and O.W. Meier. (1992). Quantication o loss and change in Floridian ree coralpopulations. American Zoologist 23:625-640.

6. Richardson, L.L. and R.R. Aronson. (2002). Inectious diseases o ree corals. Proceedings o theNinth International Coral Ree Symposium, Bali 2:1225-1230.

7. Antonius, A. (1995). Coral diseases as indicators o ree health: Field methods. Proceedings o the Second European Meeting o International Society o Ree Studies, Publications du ServiceGeologique du Luxembourg, 29:231-235.

8. Ritchie, K.B. and G.W. Smith. (1998). Type II white-band disease. Revista de Biologia Tropical46 (Suppl. 5):199-203.

9. Kuta, K.G. and L.L. Richardson. (1996). Abundance and distribution o black band disease oncoral rees in the northern Florida Keys. Coral Rees 15 (4):219-223.

10. English, S., C. Wilkinson, and V. Baker. (1997). Survey Manual or Tropical Marine Resources,

2nd Ed., Australian Institute o Marine Science, Townsville. 390 pp.11. Weil, E. (2004). Coral ree diseases in the wider Caribbean. In: E. Rosenberg and Y. Loya (eds).

Coral Health and Disease. Springer-Verlag, Berlin, pp.35-68

12. Bruckner, A.W. and R.J. Bruckner. (1997a). The persistence o black-band disease inJamaica: impact on community structure. Proceedings o the Eighth International Coral Ree Symposium, Panama, 1:601-606.

13. Sutherland, K.P., J.W. Porter, and C. Torres. (2004). Disease and immunity in Caribbean andIndo-Pacic zooxanthellate corals. Marine Ecology-Progress Series 266:273-302.

14. AGRRA. (1998). Atlantic and Gul Rapid Ree Assessment Protocol. http://coral.aoml.noaa.gov/agra/method.htm

15. Bellwood, D.R., T.P. Hughes, C. Folke, and M. Nystrom. (2004). Conronting the coral ree crisis. Nature 429 (6994):827-833.

16. Harvell, C.D., R. Aronson, N. Baron, J. Connell, A. Dobson, S. Ellner, L. Gerber, K. Kim,A. Kuris, H. McCallum, K. Laerty, B. McKay, J. Porter, M. Pascual, G. Smith, K. Sutherland, andJ. Ward. (2004). The rising tide o ocean diseases: unsolved problems and research priorities.Frontiers in Ecology and the Environment 2 (7):375-382.

17. Hoegh-Guldberg, O., P.J. Mumby, A.J. Hooten, R.S. Steneck, P. Greeneld, E. Gomez, C.D.Harvell, P.F. Sale, A.J. Edwards, K. Caldeira, N. Knowlton, C.M. Eakin, R. Iglesias-Prieto, N.Muthiga, R.H. Bradbury, A. Dubi, and M.E. Hatziolos. (2007). Coral rees under rapid climatechange and ocean acidication. Science 318 (5857):1737-1742.




87

18. Hughes, T.P., A.H. Baird, D.R. Bellwood, M. Card, S.R. Connolly, C. Folke, R.K. Grosberg,O. Hoegh-Guldberg, J.B.C. Jackson, J.A. Kleypas, J. Lough, P. Marshall, M. Nystrom, S.R.Palumbi, J.M. Pandol, B. Rosen, and J. Roughgarden. (2003). Climate change, humanimpacts, and the resilience o coral rees. Science 301 (5635):929-933.

19. Jaap, W.C., J.W. Porter, J. Wheaton, K. Hackett, M. Lybolt, M. Callahan, C. Tskos, G. Yeanev,

and P. Dustan. (2000). Coral ree monitoring project executive summary EPA Science AdvisoryPanel Key Colony Beach, December 5-6, 2000. 16.

20. Santavy, D.L.E., E. Mueller, E.C. Peters, L. MacLaughlin, J.W. Porter, K.L. Patterson, and J.Campbell. (2001). Quantitative assessment o coral diseases in the Florida Keys: Strategy andmethodology Hydrobiologia (460):39-52.

21. Bruckner, A.W. (2002). Priorities or eective management o coral diseases. NOAA TechnicalMemorandum NMFS-OPR-22, 54 pp. http://www.coral.noaa.gov/coral_disease/cdhc/man_priorities_coral_diseases.pd

22. Green, E. and A.W. Bruckner. (2000). The signicance o coral disease epizootiology or coralree conservation. Biological Conservation 96 (3):347-361.

23. Bruno, J.F., E.R. Selig, K.S. Casey, C.A. Page, B.L. Willis, C.D. Harvell, H. Sweatman, and A.M.Melendy. (2007). Thermal stress and coral cover as drivers o coral disease outbreaks. PLoSBiology 5 (6):1220-1227.

24. Mydlarz, L.D., S.F. Holthouse, E.C. Peters, and C.D. Harvell. (2008). Cellular responses insea an corals: Granular amoebocytes react to pathogen and climate stressors. PLoS One 3(3):e1811.

25. Weil, E., I. Urreiztieta, and J. Garzón-Ferreira. (2002). Geographic variability in the incidenceo coral and octocoral diseases in the wider Caribbean. Proceedings o the Ninth Coral Ree Symposium, Bali, 2:1231–1237.

26. Harvell, C.D., E. Jordán-Dahlgren, S. Merkel, E. Rosenberg, L. Raymundo, G.W. Smith, E. Weil,and B.L. Willis. (2007). Coral disease, environmental drivers and the balance between coraland microbial associates. Oceanography 20 (1):58-81.

27. Feingold, J.S. (1988). Ecological studies o a cyanobacterial inection on the Caribbean seaplume Pseudopterogorgia acerosa (Coelenterata: Octocorallia). Proceedings o the SixthInternational Coral Ree Symposium, Townville, 57-162. 3

28. Hughes, T.P. (1994). Catastrophes, phase shits, and large scale degradation o a Caribbeancoral ree. Science 265 (5178):1547-1551.

29. Kim, K. and C.D. Harvell. (2004). The rise and all o a six-year coral-ungal epizootic. AmericanNaturalist 164 (5):S52-S63.

30. Porter, J.W., P. Dustan, W.C. Jaap, K.L. Patterson, V. Kosmynin, O.W. Meier, M.E. Patterson,and M. Parsons. (2001). Patterns o spread o coral disease in the Florida Keys. Hydrobiologia460:1-24.

31. Weil, E., G.W. Smith, and D.L. Gil-Agudelo. (2006). Status and progress in coral ree diseaseresearch. Diseases o Aquatic Organisms 69:1-7.

32. Muller, E.M., C.S. Rogers, A.S. Spitzak, and R. van Woesik. (2008). Bleaching increaseslikelihood o disease on Acropora palmata (Lamark) in Hawksnest Bay, St John, US VirginIslands. Coral Rees 27 (1):191-195.

33. Willis, B.L., C.A. Page, and E.A. Dinsdale. (2004). Coral Disease on the Great Barrier Ree. In:E. Rosenberg and Y. Loya (eds). Coral Health and Disease. Springer-Verlag, Berlin, pp.69-104

34. Raymundo, L.J., K.B. Rosell, C. Reboton, and L. Kaczmarsky. (2005). Coral diseases on Philippinerees: genus Porites is a dominant host. Diseases o Aquatic Organisms 64 (3):181-191.



89

53. Mydlarz, L.D., L.E. Jones, and C.D. Harvell. (2006). Innate immunity environmental drivers anddisease ecology o marine and reshwater invertebrates. Annual Review o Ecology Evolutionand Systematics 37:251-288.

54. Alker, A.P., G.W. Smith, and K. Kim. (2001). Characterization o Aspergillus sydowii (Thom etChurch), a ungal pathogen o Caribbean sea an corals. Hydrobiologia 460:105-111.

55. Israely, T., E. Banin, and E. Rosenberg. (2001). Growth, dierentiation and death o Vibrio shiloi in coral tissue as a unction o seawater temperature. Aquatic Microbial Ecology 24 (1):1-8.

56. Banin, E., T. Israely, A. Kushmaro, Y. Loya, E. Orr, and E. Rosenberg. (2000). Penetration o thecoral-bleaching bacterium Vibrio shiloi into Oculina patagonica. Applied and EnvironmentalMicrobiology 66 (7):3031-3036.

57. Ben-Haim, Y., F.L. Thompson, C.C. Thompson, M.C. Cnockaert, B. Hoste, J. Swings, andE. Rosenberg. (2003a). Vibrio coralliilyticus sp nov., a temperature-dependent pathogeno the coral Pocillopora damicornis. International Journal o Systematic and EvolutionaryMicrobiology 53:309-315.

58. Rogers, C.S. and J. Miller. (2006). Permanent ‘phase shits’ or reversible declines in coralcover? Lack o recovery o two coral rees in St. John, US Virgin Islands. Marine Ecology-Progress Series 306:103-114.

59. Fabricius, K.E. (2005). Eects o terrestrial runo on the ecology o corals and coral rees:review and synthesis. Marine Pollution Bulletin 50 (2):125-146.

60. Atkinson, M.J., B. Carlson, and G.L. Crow. (1995). Coral growth in high-nutrient, low-pHseawater: A case study o corals cultured at the Waikiki Aquarium, Honolulu, Hawaii. CoralRees 14 (4):215-223.

61. Bruno, J.F., L.E. Petes, C.D. Harvell, and A. Hettinger. (2003). Nutrient enrichment can increasethe severity o coral diseases. Ecology Letters 6 (12):1056-1061.

62. Voss, J.D. and L.L. Richardson. (2006). Nutrient enrichment enhances black band diseaseprogression in corals. Coral Rees 25 (4):569-576.

63. Kuntz, N.M., D.I. Kline, S.A. Sandin, and F. Rohwer. (2005). Pathologies and mortality ratescaused by carbon and nutrient stressors in three Caribbean coral species. Marine Ecology-Progress Series 294:173-180.

64. Hodgson, G. (1990). Sediment and the settlement o larvae o the ree coral Pocilloporadamicornis. Coral Rees 9 (1):41-43.

65. Geiser, D.M., J.W. Taylor, K.B. Ritchie, and G.W. Smith. (1998). Cause o sea an death in theWest Indies. Nature 394 (6689):137-138.

66. Koch, R. (1891). Ueber bakteriologische Forschung. Verh. X Int. Congr. Med., Berlin 1890.1-35.

67. Richardson, L.L. and K.G. Kuta. (2003). Ecological physiology o the black band diseasecyanobacterium Phormidium corallyticum FEMS Microbiology Ecology 43 (3):287-298.

68. Viehman, S., D.K. Mills, G.W. Meichel, and L.L. Richardson. (2006). Culture and identication o Desulfovibrio spp. rom corals inected by black band disease on Dominican and Florida Keysrees. Diseases o Aquatic Organisms 69 (1):119-127.

69. Friend, M. and J.C. Franson. (1999). Field Manual o Wildlie Diseases: General FieldProcedures and Diseases o Birds. Madison, WI, U.S. Geological Survey, Inormation andTechnology Report 1999-001, 426 pp. www.emtc.usgs.gov/nwhchome.html

70. Downs, C.A. (2005). Cellular diagnostics and its application to aquatic and marine toxicology.In: G. Ostrander (ed). Techniques in Aquatic Toxicology, Vol 2. CRC Press, Inc., Boca Raton,pp.301-313



91

89. Brusca, R. and G. Brusca. (2003). Invertebrates, 2nd Ed., Sinauer Associates, Inc.,Sunderland. 936 pp.

90. Carpenter, R.C. (1997). Invertebrate predators and grazers. In: C.E. Birkeland (ed).Lie and Death o Coral Rees. Chapman and Hall, New York, pp.198-229

91. Wobeser, G.A. (1981). Diseases o Wild Waterowl Plenum Press, New York. 300 pp.92. Gordis, L. (1996). EpidemiologyW.B. Saunders Company, Philadelphia. 277 pp.

93. Martin, A.H., A.H. Meek, and P. Willerberg. (1987). Veterinary epidemiology.Principles and methods, 1st Ed., Iowa State University Press 343 pp.

94. Wobeser, G.A. (2006). Essentials o Disease in Wild Animals Blackwell Publishing Ltd,Oxord. 243 pp.

95. Rudin, N. (1997). Dictionary o Modern BiologyBarron’s Educational Series

96. Dorland, W.A.N. (2000). Dorland’s Illustrated Medical Dictionary, 29th ed., W.B. Saundersand Company

97. Kim, K. and C.D. Harvell. (2002). Aspergillosis o sea an corals: disease dynamics in the Florida

Keys. In: J.W. Porter and K.G. Porter (eds). The Everglades, Florida Bay, and Coral Rees o theFlorida Keys: An Ecosystem Sourcebook. CRC Press, Boca Raton, pp.813-824

98. Gladelter, W.B., E.H. Gladelter, R.K. Monahan, J.C. Ogden, and R.F. Dill. (1977). Coraldestruction, environmental studies o Buck Island Ree National Monument, St Croix US VirginIslands. Biosphere Reserve Research Report No. 6, National Park Service US Department o Interior, 29 pp.

99. Smith, G.W. and K.B. Ritchie. (1995). Bacteriological studies on white-band disease o Acropora cervicornis. European Meeting o the International Society or Ree Studies,September 5-9, 1995.

100. Gil-Agudelo, D.L., G.W. Smith, and E. Weil. (2006). The white band disease type IIpathogen in Puerto Rico. Revista de Biologia Tropical 54 (Suppl. 3):59-67.

101. Richardson, L.L., W.M. Goldberg, K.G. Kuta, R.B. Aronson, G.W. Smith, K.B. Ritchie, J.C. Halas,J.S. Feingold, and S.M. Miller. (1998). Florida’s mystery coral-killer identied.Nature 392:557-558.

102. Antonius, A. (1973). New observations on coral destruction in rees. Tenth Meeting o the Association o Island Marine Laboratories o the Caribbean, University o Puerto Rico(Mayaguez), 10:3.

103. Rützler, K. and D.L. Santavy. (1983). The black band disease o Atlantic ree corals. I.Description o the cyanophyte pathogen. PSZNI: Marine Ecology 4 (4):301-319.

104. Rützler, K., D.L. Santavy, and A. Antonius. (1983). The black band disease o Atlantic ree corals. III. Distribution, ecology, and development. PSZNI: Marine Ecology 4 (4):329-358.

105. Bruckner, A.W. and R.J. Bruckner. (2006). Consequences o yellow band disease (YBD) on

Montastraea annularis (species complex) populations on remote rees o Mona Island,Puerto Rico. Diseases o Aquatic Organisms 69 (1):67-73.

106. Foley, J.E., S.H. Sokolow, E. Girvetz, and C.W.F. Foley, P. (2005). Spatial epidemiology o Caribbean yellow band syndrome in Montastraea spp.coral in the eastern Yucatan, Mexico.Hydrobiologia 548:33-40.

107. Reeves, L. (1994). Newly discovered: Yellow band disease strikes Keys Rees.Underwater USA 11 (8):16.

108. Dustan, P. (1977). Vitality o ree coral populations o Key Largo, Florida: recruitment andmortality. Environmental Geology 2 (1):51-58.



92

109. Gil-Agudelo, D.L., G.W. Smith, J. Garzon-Ferreira, E. Weil, and D. Petersen. (2004).Dark spot disease and yellow band disease, two poorly known coral disease with highincidence in Caribbean rees. In: E. Rosenberg and Y. Loya (eds). Coral Health and Disease.Springer-Verlag, Berlin, pp.337-349

110. Cervino, J.M., R.L. Hayes, S.W. Polson, S.C. Polson, T.J. Goreau, R.J. Martinez, and G.W.

Smith. (2004). Relationship o Vibrio species inection and elevated temperatures to yellowblotch/band disease in Caribbean corals. Applied and Environmental Microbiology 70(11):6855-6864.

111. Gil-Agudelo, D.L. and J. Garzon-Ferreira. (2001). Spatial and seasonal variation o Dark Spots Disease in coral communities o the Santa Marta area (Colombian Caribbean).Bulletin o Marine Science 69 (2):619-629.

112. Gocheld, D.J., J.B. Olson, and M. Slattery. (2006). Colony versus population variation insusceptibility and resistance to dark spot syndrome in the Caribbean coral Siderastrea siderea.Diseases o Aquatic Organisms 69 (1):53-65.

113. Croquer, A., C. Bastidas, and L. Lipscomb. (2006). Folliculinid ciliates : a new threat toCaribbean corals? Diseases o Aquatic Organisms 69 (1):75-78.

114. Loya, Y., G. Bull, and M. Pichon. (1984). Tumor ormations in scleractinian corals.Hegolwiss Meeresunters 37:99-112.

115. Peters, E.C., J.C. Halas, and H.B. McCarty. (1986). Calicoblastic neoplasms inAcropora palmata, with a review o reports on anomalies o growth and ormin corals. Journal o the National Cancer Institute 76 (5):895-912.

116. Nagelkerken, I., K. Buchan, G.W. Smith, K. Bonair, P. Bush, J. Garzon-Ferreira, L. Botero,P. Gayle, C.D. Harvell, C. Heberer, K. Kim, C. Petrovic, L. Pors, and P. Yoshioka. (1997b).Widespread disease in Caribbean sea ans: II. Patterns o inection and tissue loss.Marine Ecology-Progress Series 160:255-263.

117. Nagelkerken, I., K. Buchan, G.W. Smith, K. Bonair, P. Bush, J. Garzon-Ferreira, L. Botero,P. Gayle, C.D. Harvell, C. Heberer, K. Kim, C. Petrovic, L. Pors, and P. Yoshioka. (1997a).

Widespread disease in Caribbean sea ans. I. Spreading and general characteristics.Proceedings o the Eighth International Coral Ree Symposium, Panama, 1:670-682.

118. Santavy, D. and E.C. Peters. (1997). Microbial pests: coral disease in the Western Atlantic.Proceedings o the Eighth International Coral Ree Symposium, Panama, 1:607-612.

119. Richardson, L.L. (1992). Red band disease: a new cyanobacterial inestation o corals.Proceedings o the American Academy o Underwater Sciences Tenth Annual ScienticDiving Symposium:153-160.

120. Miller, I. (1996). Black band disease on the Great Barrier Ree. Coral Rees 15 (1):58-58.

121. Antonius, A. (1987). Survey o Red Sea coral ree health I. Jeddah to Jizan.Proceedings o the Saudi Biological Society, 10:149-163.

122. Chesher, R. (1985). Practical problems in coral ree utilization and management: A Tongancase study. Proceeding o the Fith International Coral Ree Symposium, Tahiti 213-218.

123. Glazebrook, J.S. and H.M. Streiner. (1994). Pathology associated with tumours and black banddisease in corals rom Agincourt Ree. Joint Scientic Conerence on Science, Managementand Sustainability o Marine Habitats in the 21st Century, Townsville, Australia

124. Littler, M.M. and D.S. Littler. (1996). Black band disease in the South Pacic.Coral Rees 15 (1):20.

125. Korrûbel, J.L. and B. Riegl. (1998). A new coral disease rom the Arabian Gul.Coral Rees 17:22.




93

126. Jordan, I.E. and M.J. Samways. (2001). Recent changes in coral assemblages o aSouth Arican coral ree, with recommendations or long-term monitoring.Biodiversity and Conservation 10 (7):1027-1037.

127. Dinsdale, E.A. (2002). Abundance o black-band disease on corals rom one locationon the Great Barrier Ree: a comparison with abundance in the Caribbean region.

Proceedings Ninth International Coral Ree Symposium, Bali, 2:1239-1243

128. Kaczmarsky, L. (2006). Coral disease dynamics in the central Philippines.Diseases o Aquatic Organisms 69 (1):9-21.

129. Dalton, S.J. and S.D.A. Smith. (2006). Coral disease dynamics at a subtropical location,Solitary Islands Marine Park, eastern Australia. Coral Rees 25 (1):37-45.

130. Burdick, D., V. Brown, J. Asher, M. Gawel, L. Goldman, A. Hall, T. Leberer, J. Kenyon,E. Lundlad, J. McIlwain, J. Miller, D. Minton, M. Nadon, N. Pioppi, L. Raymundo, B. Richards,R. Schroeder, P. Schupp, E. Smith, and B. Zgliczynski. (2008). The State o the Coral Ree Ecosystems o Guam. J. Waddell (ed). The State o the Coral Ree Ecosystems o the UnitedStates and Pacic Freely Associated States: 2008, NOAA Technical Memorandum NOSNCCOS X. NOAA/NCCOS Center or Coastal Monitoring and Assessment Biogeography

Team, Silver Spring, MD, 413-456 pp.131. Raymundo, L.J.H., C.D. Harvell, and T.L. Reynolds. (2003). Porites ulcerative white spot

disease: description, prevalence, and host range o a new coral disease aectingIndo-Pacic rees. Diseases o Aquatic Organisms 56 (2):95-104.

132. Rosenberg, E. (2002). The Oculina patagonica-Vibrio shiloi model system o coral bleaching.Prepared or Workshop Coral Health and Disease: Developing a National Research Plan CoralHealth and Disease Consortium, Charleston, South Carolina, January 22-25, 2002.

133. Jones, R.J., J. Bowyer, O. Hoegh-Guldberg, and L.L. Blackall. (2004). Dynamics o atemperature-related coral disease outbreak. Marine Ecology-Progress Series 281:63-77.

134. Cheney, D.P. (1975). Hard tissue tumors o scleractinian corals.Advances in Experimental Medicine and Biology 64:77-87.

135. Coles, S.L. and D.G. Seapy. (1998). Ultra-violet absorbing compounds and tumorousgrowths on acroporid corals rom Bandar Khayran, Gul o Oman, Indian Ocean.Coral Rees 17:195-198

136. Yamashiro, H., M. Yamamoto, and R. van Woesik. (2000). Tumor ormation on thecoral Montipora inormis. Diseases o Aquatic Organisms 41 (3):211-217.

137. Kaczmarsky, L.T., M. Draud, and E.H. Williams. (2005). Is there a relationship betweenproximity to sewage efuent and the prevalence o coral disease. Caribbean Journalo Science 41 (1):124-137.

138. Aeby, G.S. (1991). Behavioural and ecological relationship o a parasite andits hosts within a coral ree system. Pacic Science 45:262-269.

139. Antonius, A. (1999). Halofolliculina corallasia, a new coral-killing ciliate on Indo-Pacic rees.Coral Rees 18 (3):300.

140. Winkler, R., A. Antonius, and A.D. Renegar. (2004). The skeleton eroding band diseaseon coral rees o Aqaba, Red Sea. PSZNI: Marine Ecology 25 (2):129-144.

141. Riegl, B. and A. Antonius. (2003). Haloolliculina skeleton eroding band (SEB): a coraldisease with ossilization potential? Coral Rees 22 (1):48.



94




95

Acknowledgements



96




97

AcknowledgementsIn 2007, at the CRTR’s Coral Disease Working Group annual workshop at the Bolinao MarineLaboratory in the Philippines, the idea o a coral disease handbook tailored or ree managerswas rst discussed. From July 2007, the group collaborated with the Coral Disease & Health

Consortium (CDHC) so that additional commonly used eld and laboratory methods couldbe incorporated into the handbook, along with a larger network o disease experts.

We are grateul to Esther Peters or her helpul eedback on nomenclature discussions and toDave Burdick, Billy Causey and Paul Marshall, who reviewed this book as potential users andalso provided valuable eedback. We would also thank the CRTR Program’s Synthesis Panel– a partnership between the Global Environment Facility, the World Bank, the University o Queensland, and NOAA – or their support and unding to make this publication possible.We are indebted to the entire sta o Currie Communication or their inspiring creativity,antastic care with detail and many long nights. Most o all, we thank Andy Hooten or thegood idea to write this manual, and support and advice along the way.

Photograph creditsWe thank the ollowing people or use o images or this handbook: Greta Aeby, BradBaldwin, Roger Beeden, Andy Bruckner, Dave Burdick, Ciemon Caballes, Courtney Couch,Aldo Croquer, Teresa Lewis, Cathie Page, Laurie Raymundo, Kathryn Rosell, Yui Sato, Peter Schupp, Brett Seymour, Lyle Vail, Lizard Island Research Station (A acility o the AustralianMuseum), Ernesto Weil, Bette Willis and Thierry Work.

acknowledgements



98




100




101

Appendix 1:Glossary and acronyms

Glossary(Terms dened in the glossary are bold in the text)

Acute disease – A disease that has a relatively rapid onset (i.e. infuenza or ood borne-diarrhea; 88).

Agent – A actor capable o producing an eect (i.e. a cause o disease; 88).

Biomarker – a substance that indicates the status or condition o a specic biological property (70).

Case history – A chronological record o signicant events and observations made during adisease investigation.

Chronic disease (inection) – A disease or inection that has a relatively slow onset (i.e. cancer; 88).

Coenosteum – Skeleton deposited outside and between the corallite walls o the polyps o acolonial scleractinian (71).

Corallite – The calcium carbonate skeleton deposited by and around a single polyp (89).

Corallivore – An animal that eats live coral tissue; certain parrot sh, gastropods such asDrupella and Cyphoma, reworms, and the starsh Acanthaster planci (90).

Diagnosis – The determination o the nature o a disease (88).

Disease – Any impairment that intereres with or modies the perormance o normal unction,including responses to environmental actors such as nutrition, toxicants, and climate; or inectiousagents, congenital deects, or combinations o these actors (91).

Endemic – Present in a susceptible community at all times, but in low requency (92).

Environment – An area where agent and host interact to produce disease (93).

Emergent disease – Any resurging disease that was previously at low levels in a population,or a new disease in a population (94).

Epidemiology – The study o the distribution and determinants o health-related states or eventsin specied populations, and the application o this study to the control o health problems.For non-human animals, the term epizootiology is used (92).

Epizootic – Occurrence o disease at levels above what is expected in a population (88).Applies to non-human animals.

Histology – The study o tissues and cells on the microscopic level (95).

Holobiont – The animal-plant complex ormed by interactions between a coral polyp,

its endosymbiotic algae (zooxanthellae), and its associated bacterial community (44).

Host – An organism that harbors the agent causative o disease (93).

Host range – The collection o species which are susceptible to a given pathogen.

di



102


Immunity – Non-susceptibility to inectious or toxic agents (96).

Incidence – The number o new cases o disease over a specied time period in a population at riskor developing the disease (92).

Inectious – Capable o causing inection (88).

Lesion – Morphologic changes that accompany disease; maniestation o disease (88).

Necrosis – Cell death characterized by irreversible damage, the earliest o which occurs inmitochondria (modied rom Stedman 88).

Octocoral – Corals with polyp tentacles and mesenteries in multiples o 8; includes sot corals,sea ans, Heliopora, and sea pens (89).

Opportunistic inection – Inection caused by existing microorganisms not normally pathogenic (88).For instance, this may occur i environmental conditions change, thereby stressing the hostand increasing its susceptibility to the microorganism.

Outbreak (see epizootic)

Pathogen – Any disease-producing agent (96).

Prevalence – The number o diseased colonies relative to the total number o colonies presentwithin a dened area o survey at a given point in time. Usually expressed as a percent:(no. disease cases/total no. colonies) *100 (modied rom Gordis 92).

Progression – Increasing in severity (96).

R0 – “R naught”; the average number o secondary cases generated by one primarycase in a susceptible population (4).

Reservoir – An alternate host or passive carrier o a disease-causing organism (96).

Resistance (see Immunity)

Scleractinian – Polyps with mesenteries and tentacles in multiples o 6; true stony corals;Acroporidae, Poritidae, Pocilloporidae, etc. (89).

Severity – The percent o a colony aected by a disease (97).

Sign – Any objective evidence o a disease perceptible to an observer (96).

Stress – The sum o biological reactions to an adverse stimulus that disturbs an organism’shomeostasis (96).

Syndrome – A set o signs or a series o events occurring together that oten point to a singledisease or condition as the cause (Dept. o Oncology, University o Newcastle Upon Tyne).

Transmission – A passage or transer o a disease rom one individual to another (96).

Vector – An animal that transers an inectious agent rom one host to another (96).

Virulence – The relative pathogenicity o a microorganism (95); how easily it causes damageto host tissue.



103

General acronym listAGRRA: Atlantic and Gul Rapid Ree Assessment Program

ARC: Australian Research Council

CARICOMP: Caribbean Coastal Marine Productivity Program

CDHC: Coral Disease & Health Consortium

CDWG: CRTR Coral Disease Working Group

CRCP: NOAA’s Coral Ree Conservation Program

CRTR: GEF’s & World Bank Coral Ree Targeted Research Program

EPA: US Environmental Protection Agency

GCDD: Global Coral Disease Database

GEF: Global Environment Facility

NCCOS: National Centers or Coastal Ocean Science

NOAA: US National Oceanic and Atmospheric AdministrationNMFS: NOAA’s National Marine Fisheries Service

UNEP: United Nations Environmental Program

USGS: United States Geological Survey

WCMC: World Conservation Monitoring Centre

Disease/health state acronymsASP: Aspergillosis BBD: Black band disease

BrB: Brown band disease CCI: Caribbean ciliate inection

COTS: Crown-o-thorns starsh DSD: Dark spots disease

GA: Growth anomaly PR: Pigmentation response

RBD: Red band disease SEB: Skeletal eroding band

UWS: Ulcerative white spots WBD: White band disease

WP: White plague WS: White syndrome

YBD: Yellow band disease

di



104




105

Appendix 2:Regional contact list o coral disease experts(For a ull list o experts, see www.gecoral.org)

di

Caribbean

Bruckner, Andrew W. Ph.D. (CDHC)(coral ree ecology, coral diseases,conservation)National Marine Fisheries ServiceOce o Habitat ConservationNOAA Coral Ree Conservation Program1315 East-West HighwaySilver Springs, Maryland 20910 [email protected]

Gil-Agudelo, Diego L. Ph.D.(coral microbiology)Instituto de Investigaciones Marinas yCosteras (INVEMAR)PO Box 1016Cerro Punta de Betín,Santa Marta, Magdalena, [email protected]

Harvell, C. Drew Ph.D. (CRTR: CDWG, Chair)(coral immunology, environmental stress,ecology)

Department o Ecology andEvolutionary BiologyCornell UniversityCorson HallIthaca, New York 14853, [email protected]

Jordan-Dahlgren, Eric Ph.D. (CRTR: CDWG)(coral ree ecology, coral disease)Instituto de Ciencias del Mar y LimnologíaUniversidad Nacional Autónoma de México,Apartado Postal 1152

77500 Cancún, Quintana Roo, México [email protected]

Peters, Esther C. Ph.D. (CDHC)(coral histopathology, ecotoxicology)Tetra Tech, Inc.10306 Eaton PlaceSuite 340Fairax, Virginia 22030, [email protected]

Richardson, Laurie L. Ph.D. (CDHC)(coral microbiology)Florida International University

Dept o Biological Sciences11200 SW Eighth StUniversity Park CampusMiami, Florida 33199, [email protected]

Ritchie, Kim B. Ph.D.(coral microbiology)Center or Coral Ree ResearchMote Marine Laboratory1600 Ken Thompson ParkwaySarasota, Florida 34236, USA

[email protected]

Rohwer, Forest Ph.D.(microbiology, virology)Department o Biology & Center or Microbial SciencesSan Diego State UniversitySan Diego, Caliornia 92182, [email protected]




106

Santavy, Deborah Ph.D. (CDHC)(coral microbiology, Florida Keys)Gul Ecology DivisionOne Sabine Island DriveGul Breeze, Florida 32561, USA

[email protected]

Smith, Garriet W. Ph.D.(CRTR: CDWG, Co-chair)(microbial ecology)University o South Carolina at AikenDepartment o Biology and Geology471 University ParkwayAiken, South Carolina 29801 [email protected]

Weil, Ernesto Ph.D. (CRTR: CDWG)

(coral ecology, reproduction, disease ecology)University o Puerto RicoDepartment o Marine ScienceP.O. Box 908Lajas, Puerto [email protected]

Woodley, Cheryl M. Ph.D. (CDHC, Chair)(microbiology, ecotoxicology)DOC/NOAA/NOS/NCCOSCenter or Coastal EnvironmentalHealth and Biomolecular Research

Hollings Marine Laboratory331 Fort Johnson RdCharleston, South Carolina 29412, [email protected]

Indo-Pacifc

Aeby, Greta S. Ph.D. (CDHC)(coral ree ecology, coral disease ecology)Hawaii Institute o Marine BiologyP.O. Box 1346Kaneohe, Hawaii 96822, USA

[email protected]

Azam, Farooq Ph.D. (CRTR: CDWG)(microbial ecology, microbiology)Scripps Institution o OceanographyUniversity o Caliornia at San Diego9500 Gilman Dr. La Jolla,Caliornia 92093, [email protected]

Jacobson, Dean M. Ph.D.(marine ecology, coral disease, oceanography)College o the Marshall IslandsPO Box 1258Majuro, MH 96960, Marshall Islands

[email protected]

Raymundo, Laurie J. Ph.D. (CRTR: CDWG)(ree ecology, coral disease ecology, MPAs)University o Guam Marine LabUOG StationMangilao, Guam 96923, [email protected]

Rohwer, Forest Ph.D.(microbiology, virology)See Caribbean regional list or contact inormation

Vargas-Ángel, Bernardo Ph.D. (CDHC)(histopathology, ree ecology)Joint Institute or Marine andAtmospheric ResearchUniversity o Hawai’i at Manoa1000 Pope Road, Marine Science Building 312Honolulu, HI 96822, [email protected]

Willis, Bette L. Ph.D. (CRTR: CDWG)(coral ecology, reproduction, disease ecology)

ARC Centre o Excellence or Coral Ree StudiesSchool o Marine and Tropical BiologyJames Cook UniversityTownsville Queensland, 4811, [email protected]

Work, Thierry M. D.V.M. (CDHC)(wildlie disease, epizootiology, pathogenesis)USGS-National Wildlie Health Center Hawaii Field StationPO Box 50167Honolulu, Hawaii 96850, USA

[email protected]



107

Red Sea/East Arica

Kushmaro, Ariel Ph.D.(coral microbiology)Department o Biotechnology EngineeringBen-Gurion University o the NegevPO Box 653Be’er-Sheva 84105, [email protected]

McClanahan, Timothy R. Ph.D.(coral ree ecology, coral disease, MPAs)Coral Ree ProgramsWildlie Conservation SocietyKibaki Flats no. 12Bamburi, Kenyatta BeachP.O. Box 99470Mombasa 80107, [email protected]

Rosenberg, Eugene Ph.D. (CRTR: CDWG)(microbial ecology)Department o Molecular Microbiology andBiotechnologyTel Aviv University, Ramat Aviv 69978, [email protected]

Coral Ree Targeted ResearchProgram Centres o Excellence

Australasia Centre o ExcellenceChair: Proessor Ove Hoegh-Guldberg, Ph.D.Australasia Centre o ExcellenceCentre or Marine StudiesHeron Island Research Station (HIRS)The University o QueenslandQueensland 4072, AustraliaTel: +61 7 3346 [email protected]

East Arica Centre o Excellence

Chair: Alonse Dubi, Ph.D.Institute o Marine ScienceUniversity o Dar Es SalaamP.O. Box 668,Zanzibar, TanzaniaTel: +255 24 2230741/ [email protected]

Mesoamerica Centre o Excellence

Chair: Roberto Iglesias-Prieto, Ph.D.Unidad Académica Puerto Morelos (UAPM)Instituto de Ciencias del Mar y LimnologíaUniversidad Nacional Autónoma de MéxicoApartado Postal 1152Cancún 77500, QRMéxicoTel : +52 (998) 871 02 [email protected]

South-East Asia Centre o Excellence

Chair: Emeritus Proessor Edgardo Gomez,Ph.D.The Marine Science InstituteUniversity o the Philippines

Diliman, Quezon City1101 PhilippinesTel: +63 2 435 [email protected]

di




108



109

Appendix 3Indo-Pacic Coral Health – Decision Tree

1

2

3

4

5

6

7

8

Tissue Loss – Predation1a. Predation (PRD) – e.g. fsh, snail, starfsh eeding scars

Tissue Loss – Non-Predation – Coloured Band Diseases 2a. Skeletal Eroding Band (SEB)

2b. Black Band Disease (BBD)2c.Brown Band Disease (BrB)

Tissue Loss – Non-Predation – No overlying band o coloured material 3a. Ulcerative White Spots (UWS) – ocal tissue loss

3b. White Syndromes (WS) – irregular tissue loss3c.

Atramentous Necrosis (AtN) –grey-black material overlies irregular area o tissue loss

Tissue Discolouration – White 4a. Bleaching (BL) – environmentally induced partial or whole colony bleaching

4b. Focal Bleaching (FBL) – early stage o UWS or unexplained spots4c.Non Focal Bleaching (NFBL) – unusual bleaching patterns, e.g. patches, stripes

Tissue Discolouration – Non White 5a. Pigmentation Response (PR) – coral response to a challenge (not a disease)

5b. Trematodiasis (TR)

Growth Anomalies 6a.Explained Growth Anomalies

6b.Unexplained Growth Anomalies

Compromised Health 7a. Pigmentation Response (see 5a. above)

7b. Unusual Bleaching Patterns (see 4c. above)

7c.Competition – Aggressive Overgrowth – e.g. cyanobacteria,Terpios andCliona sponges, red flamentous algae

7d. Sediment Damage7e. Flatworm Inestation

Diseases in Other Ree Organisms8a. Examples or Crustose Coralline Algae & Gorgonians

di



110


di

Tissue Loss – Predation1. Fish Predation (FPR)2. Invertebrate Predation (IPR)

Tissue Loss – Non-Predation – Colored Band Diseases 3. Black Band Disease (BBD) 4. Caribbean Ciliate Inection (CCI) 5. Aspergillosis (ASP) 6. Purple Spots (PS) 7. Red Band Disease (RBD)

Tissue Loss –Caribbean

White Syndromes8. White Band Disease (WBD)9. White Plague (WP)

10.White Patch Disease (WPA) 11.Caribbean White Syndromes (CWS)

Tissue Discoloration – White 12.Bleaching (BL)

Tissue Discoloration – Non White 13.Dark Spots Disease (DSD) 14.Caribbean Yellow Band Disease (CYBD)

Growth Anomalies 15. Growth Anomalies (GAN)

Compromised Health 16.Compromised Health in Hard Corals (CHC) 17.Compromised Health in Octocorals (CHO) 18.Competition – Overgrowth (CO)

Diseases in Other Ree Organisms 19.Coralline White Band Syndrome (CWBS)

20.Other Ree Organisms – Sponges 21.Other Ree Organisms – Zoanthids & Hydrocorals

Appendix 3Caribbean Coral Health – Decision Tree



111

Appendix 3Supplementary disease and compromised health state photographs

di

Western AtlanticFish bites Black band disease

Porites astreoides spot biting

Montastraea annularis spotbiting lesions lacking tissue(on right) and lesions thathave begun to heal (let)

Whole colony view o Siderastrea siderea with

black band disease

Close up o blackcyanobacterial mat on

Siderastrea siderea

Acropora cervicornis withchimney-like structures rom

damselsh bites

Stephanocoenia interceptawith a damselsh territory

(predation), oten conusedwith white syndrome

Meandrina meandriteswith red band disease mat

(arrow)

Close up o cyanobacterialmat on Agaricia sp.

Red band disease

Carribean ciliate inection Yellow band disease

Whole colony view o Diploria labyrinthiformis withprogressing band o ciliates

(arrow), dead skeletonovergrown by algae

Close up o Diplorialabyrinthiformiswith band

o ciliates to traveling to theright over healthy tissue

Whole colony view o Montastraea faveolata with

multiple yellow band lesions

Close up o Montastraeaannularis new yellow

band lesion

Ciliates, Halofolliculina sp.rom CCI mag. 50X




112

White patch disease White band disease

White plague Dark spots disease

Indo-Pacifc/East Arica/Red Sea

Fish bites Gastropod predation

Whole colony view o Montastraea annularis with

white plague

Close up o progressingront o white plague in

Montastraea franksi

Siderastrea radians with darkspots disease

Acropora palmata withmultiple white patch lesions,

including acute (upper let andlower right), subacute (upper

right) and an older, algalcolonized lesion (middle) that

has begun to heal

Close up o white patchlesion on Acropora palmata

Whole colony view o Acropora palmata with

white band disease

Close up o progressingront o white band in

Acropora palmata

Porites sp. with numerousparrotsh bite scars

concentrated along ridges

Close up o Porites sp. withpuer sh bites, showing

regular paired scrape marks

Acropora sp. inested withDrupella cornus

Close up Acropora sp. tissueremoved by Drupella cornus

(white region)

Close up o progressionront o dark spots inSiderastrea radians

Carribean white syndromes

Whole colony view o Montastraea cavernosa

with multiple whitesyndrome lesions

Close up Montastraeafranksi white syndrome



113

di

Black band disease Skeletal eroding band

Whole colony view o Coeloseris mayeri with black

band disease. The entirecolony was dead one monthater this photo was taken

Close up o Echinoporalamellosa with black band

Acropora sp. with speckledband o ciliates. Dead

skeleton colonized by algae

Close up o Acroporaintermedia with speckled

band o ciliates

Black band disease ront,showing lamentous

cyanobacteria adjacent todead coral skeleton (white)

on Montipora sp., mag. 45X

Ciliates, Halofolliculinacorallasia (arrow) rom

Acropora sp. with skeletaleroding band, mag. 32X

Brown band disease

Acropora sp. with brownband disease (arrow)

Close up o the brown bando ciliates (arrow)on Acropora sp.

Acropora with brown banddisease inested with ciliates

Ulcerative white spots

Whole colony view o Poritescylindrica with ulcerative

white spots disease

Porites cylindrica showingtwo active lesions; the oneon the let is completely

devoid o tissue; the lesionon the right is bleaching,

mag. 35X



114


White Syndrome

Pigmentation Response

Whole colony view o a massive Porites sp.

pigmentation response tomacroalgae abrasion

Close up o Porites sp.tissue swelling and

pigmentation response tomacroalgae abrasion

Pachyseris speciosa withwhite syndrome

Porites cylindrica with anearly white syndrome lesion

(arrow)

An active disease ront o white syndrome spreading

within Lobophylliahemprichii

Trematode cyst (~1mm)removed rom a

trematodiasis lesionon Porites compressa,

mag 40X

Skeleton o Porites sp. withgrowth anomaly, mag. 10X

Trematodiasis

Growth Anomalies o a unknown cause

Whole colony view o Poritescompressa with numerous

trematodiasis lesions

Massive Porites sp. with agrowth anomaly

Close up Porites compressa showing active pink nodules

rom trematodiasis

Massive Porites with agrowth anomaly o adierent morphology.This type appears as awhite to pink plaque



115

Appendix 4Data sheets currently used or assessment and monitoring

B l e a c h i n g : P a l e , M o t t l e d , W h i t e .

P r e d a t i o n : S n a i l s , F i r e w o r m , P a r r o t s h , D a m s e

l s h .

O v e r g r o w t h : S p o n g e , A l g a e , T u n i c a t e ,

M i l l e p o r a .

W e s t e r n A t l a n t i c d a t a s h e e t t e m p l a t e

–

C o l o n y m e a s u r e m e n t s , m o r t a l i t y , d i s e a s e p r e v a l e n c e a n d c o

m p r o m i s e d h e a l t h s t a t e s

R e c o r d e r :

S i t e :

T r a n s e c t :

D e

p t h :

D a t e :

% L i v e

S p e c i e s

% M o r t a l i t y

O l d

R e c e n t

S i z e

D i a

H

e i g h t

P r e d a t i o n

S / W / P / D

B l e a c h i n g

P / M / W

%

B l e a c h e d

O v e r g r o w t h

S / A / T / M

D i s e a s e

C o m m e n t s



116

A c r o p o r a

t a b u l a r

s t a g h o r n / b u s h y

b o t t l e b r u s h / d i g i t a t e

c o r y m b o s e

i s o p o r a

A n a c r o p o r a / A s t r e o p o r a

M o n

t i p o r a

P o c i l l o p o r a

S t y l o p

h o r a / S e r i a

t o p o r a

S t y l o c o e n

i e l l a / M a

d r a c i s

P o r i t e s

m a s s i v e

b r a n c h i n g

s u b m a s s i v e

G o n

i o p o r a

/ A l v e o p o r a

F a v i a

/ M o n

t a s t r e a

F a v i t e s / E c h

i n o p o r a

P l a t y g y r a / G o n

i a s t r e a

C y p

h a s t r e a / L e p

t a s t r e a

O t h e r f a v i i d s ( g e n e r a )

F u n g

i d s ( g e n e r a )

G a

l a x e a / S

i m p

l a s t r e a

P e c t i n

i a / O x y p o r a

E c h

i n o p

h y l l i a

/ M y c e

d i u m

L o b o p

h y l l i a

/ S y m p

h y l l i a

o t h e r M u s s i d s ( g e n e r a )

H y d n o p

h o r a

M e r u

l i n a

P a r a c l a v / S c a p o p

h y l l i a

P a v o n a

L e p

t o s e r i s / C o e

l o s e r i s

P a c h y s e r i s / G a r d

i n e r o

P s a m m o c o r a

/ C o s c i n a r e a

S i d e r a s t r e a

/ P s e u

d o s i d e r

E u p

h y l l i a / C a t a l / T r a c h y

P l e r o g y r a / P

h y s o g y r a

T u r b

i n a r i a / T u

b a s t r e a

H e

l i o p o r a / T u

b i p o r a

M i l l e p o r a

P r e d a t i o n : 1 D r ( D r u p e

l l a ) 1 C o ( C o r a l l

i o p

h i l i a ) 1 C T ( C O T ) 1 F ( F i s h ) A l g a l o v e r g r o w t h / a b r a s i o n : 2 C y ( c y a n o b a c t e r i a ) 2 M a ( m a

c r o a l g a e ) 2 R F ( r e d l a m e n t o u s ) S i l t s m o t h e

r i n g / a b r a s i o n : S I

I n d o - P a c i f c d a t a s h e e t t e m p l a t e – D

i s e a s e p r e v a l e n c e &

c o m p r o m i s e d h e a l t h s t a t e s

R e c o r d e r :

S i t e :

T r a n s e c t :

D e p t h :

T r a n s e c t P o s i t i o n :

D a t e :

T o t a l

C o l o n y C o u n t

G r o w t h

a n o m a l y

P a t c h y

b l e a c h

B B

D

B r B

W S

U W S

S E B

P R




117

A c r o p o r a

t a b u l a r

c o r y m b o s e

d i g i t a t e

b o t t l e b r u s h

s t a g h o r n / b u s h y

I s o p o r a n

M o n

t i p o r a

A n a c r o p o r a

/ A s t r e o p o r a

P o c i l l o p o r a

S t y l o p

h o r a

/ S e r i a t o p o r a

P o r i t e s m a s s i v e

P o r i t e s b r a n c h i n g

P o r i t e s s u b m a s s i v e

G o n

i o p o r a

/ A l v e o p o r a

F a v i a / F a v i t e s / M o n

t a s t r e a

P l a t y g y r a

/ G o n

i a s t r e a

C y p

h a s t r e a

/ L e p

t a s t r e a

o t h e r F a v i i d s

F u n g

i d s

O c u

l i n i d s / P e c t i n

i d s

M u s s i d s / M e r u

l i n i d s

A g a r i i c i d

/ S i d e r a s t r e

i d s

D e n

d r o p

h y l l i d s

C a r y o p

h y l s ,

T r a c h y p

h y l s

S o t c o r a l s / G o r g o n i a n s

H e

l i o p o r a

/ T u b i p o r a

/ M i l l e p o r a

m a c r o a l g a e / f e s h y a l g a e

r o c k w i t h t u r n g a l g a e

s a n d / s i l t

r e c e n t l y d e a d s t a n d i n g c o r a l

r u b b l e

o t h e r ( s p o n g e s , a s c i d i a n s )

I n d o - P a c i f c d a t a s h e e t t e m p l a t e – L i n e i n t e r c e p t t r a n s e c

t d a t a

R e c o r d e r :

S i t e :

D e p t h :

D a t e :

T 2

T 1

T 3

T 4

T 5

T 6





118

118 D a t a s h e e t t e m p l a

t e – L e s i o n c h a r a c t e r i z a t i o n d a t a s h e e t

R e c o r d e r :

S i t e :

T r a n s e c t :

D a t e :

S p e c i e s

D i s t r i b u t i o n :

L o c a t i o

n :

S e v e r i t y

m l / m d / s / x

L o c a t i o n

B / M / A

D i s t r i b u t i o n

F / M / C / D / L

L e s i o n

C o l o r

M a r g i n

( S / I )

L e s i o n

D i a m

L e s i o n

# / c o l

C o l d i a m

( c m )

T i m i n g

A / S / C

D i a g n o s i s / C o m m e n t s

M a r g i n :

S e v

e r i t y :

T i m i n g :

S m o o t h

M i l d

< 1 0 %

A c u t e ( c u r r e n t ; b a r e s k e l e t o n )

( S )

M o d e r a t e

1 0 - 2 4 %

S u b a c u t e ( r e c e n t ; g r e e n

l a m e n t o u s a l g a e )

I r r e g u l a r

S

e v e r e

2 5 - 4 9 %

C h r o n i c

( I )

E x t r e m e

5 0 - 1 0 0 %

( e p i b i o n t c o m m u n i t y )

o c a l

d i u

s e

l i n e a r

b a s a l

m e d i a

l

a p i c a l

m u l t i o c a l c o a l e s c i n g




119

Appendix 5Supplementary disease descriptions

T a b l e 1 . M a j o r d i s e a s e s o t h e W e s t e r n

A t l a n t i c , r o m p u b l i s h e d l i t e r a t u r e

S y n d r o m e

S

y n o n y m

H o s

t r a n g e

P r e s u m e d c a u s e

R

e f e r e n c e

W h i t e b a n d d i s e a s e ( W B D )

W

h i t e l i n e

d i s e a s e ,

w h i t e d e a

t h ,

w

h i t e p

l a g u e

W h i t e l i n e

d i s e a s e ,

w h i t e d e a t h , w

h i t e

p l a g

u e

U n k o

w n ;

b a c t e r i a

l a g g r e g a

t e s o

t e n p r e s e n

t ( 9 8 )

W B D t y p e I I

W

B D t y p e

I I

A . c

e r v i c o r n

i s

V i b r i o c h a r c h a r i a

b a c t e r i u m

( 1 1

, 9 9

, 1 0 0 )

W h i t e p l a g u e

P

l a g u e

t y p e

I I , w

h i t e p

l a g u e

t y p e

I I I ,

p

l a g u e ; w

h i t e b a n

d d i s e a s e ,

w h i t e

l i n e

d i s e a s e

D i p l o r i a s t o

k e s i +

4 0 s p p .

o n o n -

A c r o

p o r a p

l a t i n g

& m a s s i v e c o r a

l s

A u r a

n t i m o n a s c o r a l i c i d a

( 3 1

, 1 0 1 )

W h i t e p a t c h d i s e a s e

W

h i t e p o x , p a

t c h y n e c r o s i s

A . p

a l m a

t a

S e r r a t i a m a r c e s c e n s

( 1 3

, 5 2 )

B l a c k b a n d d i s e a s e ( B B D )

B

l a c k

l i n e

d i s e a s e

2 4 s c

l e r a c t i n

i a n c o r a

l s , 1 h y d r o z o a n ,

6

g o r g

o n

i a n s

M i c r o

b i a l c o n s o r t i u m o

c y a n o

b a c t e r i a ,

B e g g

i a t o a

& D e s u

l f o v i b r i o

( 1 0 2 - 1

0 4 )

Y e l l o w b a n d d i s e a s e ( Y B D )

Y e

l l o w

b l o t c h d i s e a s e ; r i n g

b l e a c h

i n g ,

y e

l l o w p o x

d i s e a s e ; y e

l l o w

b a n

d

s y n

d r o m e ; y e

l l o w

b a n

d / b l o t c h

M o n

t a s t r a e a .

a n n u

l a r i s s p p .

c o m p

l e x ,

o t h e

r a v i i d s ;

A g a r i c i a a g a r i c

i t e s

P o s s

i b l y V i b r i o ; m a y

b e a

d i s e a s e o

z o o x

a n

t h e

l l a e

( 1 3

, 1 0 5 - 1

1 0 )

D a r k s p o t s d i s e a s e ( D S D )

D

a r k s p o

t d i s e a s e ,

d a r k s p o

t

s y n

d r o m e ,

R i n g

d i s e a s e ,

D S D t y p e

I I ,

P

u r p

l e b a n

d s y n

d r o m e ,

d a r k

b a n

d s

M . a

n n u

l a r i s

M .

f a v e o

l a t a , M

. c a v e r n o s a ,

S i d e

r a s t r e a . s i d

e r e a ,

S . i n

t e r s e p

t a , A

.

a g a r

i c i t e s

F u n g

a l o r i g

i n ; a s s o c i a

t e d w

i t h V i b r i o s p p .

( 1 1

, 1 0 9

, 1 1 1

, 1 1 2 )

C a r i b b e a n c i l i a t e i n f e c t i o n s ( C C I ) S

k e l e t a l e r o

d i n g

b a n

d ( S E B )

> 1 0 s p e c

i e s

i n c l u

d i n g D i c h o c o e n

i a ,

M o n

t a s t r a e a ,

A c r o p o r a

H a l o

f o l l i c u l i n a s p c i l i a

t e

( 3 1

, 1 1 3 )

G r o w t h a n o m a l i e s ( G A )

H

y p e r p

l a s i a ,

N e o p

l a s i a ,

t u m o r s ,

G

i g a n

t i s m ,

a c c e

l e r a

t e d g r o w

t h ,

c h a o

t i c p o

l y p d e v e

l o p m e n

t ,

c a

l i c o b l a s t i c e p

i t h e

l i o m a

D i p l o r i a , C

o l p o p

h y l l i a ,

P o r i t e s

M o n

t a s t r a e a ,

A g a r i c i a ,

A .

p a

l m a

t a ;

D i c h

o c o e n

i a , M

a d r a c i s

U n k n

o w n ; g e n e

t i c o r

t r i g g e r e

d b y

e n v i r o n m e n

t a l s t r e s s o r s

( 1 1 4

, 1 1 5 )

A s p e r g i l l o s i s ( A S P )

S

e a

a n

d i s e a s e

G o r g o n

i a s p p .

& 6 o

t h e r o c

t o c o r a

l s

A s p e r g

i l l u s s y d o w

i i u n g u s

( 2 9

, 5 4

, 1 1 6

, 1 1 7 )

R e d b a n d d i s e a s e ( R B D )

R

e d b a n

d d i s e a s e

t y p e

I , R B D t y p e

I I

G o r g o n

i a , C o

l p o p

h y l l i a , A

g a r i c i a ,

M y c e

t o p

h y l l i a

S t e p

h a n o c o e n

i a ;

T y p e

I I

r e p o

r t e d o n

D . s t i g

o s a ,

M .

a n n u

l a r i s , M

.

c a v e

r n o s a

S .

r a d i a n s ,

P . a s t r e o

i d e s

M i c r o

b i a l c o n s o r t i u m

d o m

i n a

t e d b y

C y a n

o b a c t e r i a S c h

i z o t h r i x m e x i c a n a a n

d S

.

c a l c i c o

l a ; s e c o n

d t y p e

d o m

i n a

t e d b y

t w o

s p e c

i e s o

O s c i l l a

t o r i a

( 1 0 4

, 1 1 8

, 1 1 9 )



120

Appendix 5Supplementary disease descriptions

T a b l e 2 . M a j o r d i s e a s e s o I n d o - P a c i c , E a s t A r i c a n a n d R e d S e a c o r a l s ,

r o m p u b l i s h e d l i t e r a t u r e

S y n d r o m e

L

o c a t i o n

H o s

t s p e c i e s

P r e s u m e d c a u s e

R

e f e r e n c e

B l a c k b a n d d i s e a s e ( B B D )

A

u s t r a

l i a ,

E g y p

t , F i j i , I n d i a

, J o r d a n ,

P

a p u a

N e w

G u

i n e a ,

P h i l i p p

i n e s ,

S

a u

d i A r a

b i a

, T o n g a ,

S o u

t h A r i c a

,

C

N M I , P a

l a u

1 9 g e n e r a ,

4 9 s p e c i e s ; P o c i l l o p o r a a n

d

A c r o

p o r a m o s t

r e q u e n

t l y a

e c t e

d

M i c r o

b i a l c o n s o r t i u m

d o m

i n a

t e d b y c y -

a n o b

a c

t e r i a ,

s u l a t e - r e

d u c i n g

b a c

t e r i a a n

d

s u l d

e - o x

i d i z i n g

b a c t e r i a

( 3 3

, 1 2 0 - 1

2 8 )

W h i t e s y n d r o m e ( W S )

E

g y p

t , A u s t r a

l i a ,

S o

l i t a r y

I s l a n

d s ,

P

h i l i p p

i n e s ,

G u a m

M u l t

i p l e s p p .

o T u r b

i n a r i a ,

A c r o p o r a ,

G o n

i a s t r e a ,

F a v i i d a e ,

P o c i l l o p o r a ,

P o r i

t e s ,

P a v o n a ,

S t y l o p

h o r a ,

M o n

t i p o r a

U n k n

o w n

( 3 3

, 3 4

, 1 2 9

, 1 3 0 )

U l c e r a t i v e w h i t e s p o t d i s e a s e

( U W S )

P

h i l i p p

i n e s ,

G u a m

P o r i

t e s ;

E c h

i n o p o r a ,

G o n

i a s t r e a ,

H e l i o p o r a ,

F a v i a ,

M o n

t i p o r a

P o s s

i b l y a V i b r i o ; n o r m a

l l y c a

l l e d P o r i t e s

U l c e r a

t i v e W h i t e S p o

t D i s e a s e

( 3 4

, 1 2 8

, 1 3 0

, 1 3 1 )

B a c t e r i a l B l e a c h i n g

M

e d i t e r r a n e a n ,

I s r a e

l , T a n z a n

i a

O c u

l i n a p a

t e g o n

i c a ; P o c i l l o p o r a

V i b r i o c o r a l l y l i t i c u s ,

V . s h

i l o i

( 1 3 2 )

A t r a m e n t o u s n e c r o s i s

G

r e a

t B a r r i e r

R e e

, A u s t r a

l i a

M o n

t i p o r a a e q u

i t u b e r c u

l a t a

U n k n

o w n

( 1 3 3 )

G r o w t h A n o m a l i e s ( G A )

C

N M I , O m a n ,

P h i l i p p

i n e s ,

G u a m ,

A

u s t r a

l i a ,

H a w a

i i , P a

l a u ,

E n e w a

t a k ,

F

r e n c h

P o

l y n e s i a ,

N e w

C a

l e d o n

i a ,

M

a l d i v e s ,

M i c r o n e s i a ,

M a r s h a

l l

I s

l a n

d s ,

J a p a n ,

C h i n a

A c r o

p o r a , P

o c i l l o p o r a ,

P a v o n a ,

F u n g

i a ,

M a d

r e p o r a , M

o n

t i p o r a , P

l a t y g y r a ,

P o r i

t e s ,

G o n

i a s t r e a

U n k n

o w n ; g e n e

t i c o r e n v i r o n m e n

t a l s t r e s s

t r i g g

e r s .

A l s o k n o w n a s

h y p e r p

l a s i a ,

n e o p

l a s i a ,

t u m o r s , c a

l i c o b l a s t i c

e p i t h

e l i o m a s

F u n g a l s y n d r o m e

E

a s t

A r i c a n

C o a s t

A s t r e o p o r a ,

M o n

t i p o r a , E

c h i n o p o r a ,

A c r o

p o r a , G

o n

i o p o r a ,

P l a t y g y r a ,

m a s s i v e

P o r i t e s ,

P o c i l l o p r a ,

G o n

i a s t r e a

H y d n o p

h o r a , C

y p h a s t r e a

U n k n

o w n

( 3 9 )

T r e m a t o d i a s i s

H

a w a

i i

P o r i

t e s c o m p r e s s a ,

P . l o b a t a

M e t a c e r c a r i a o

a

d i g e n e

t i c t r e m a

t o d e

( p a r a

s i t i c f a

t w o r m

)

( 1 3 8 )

S k e l e t o n e r o d i n g b a n d ( S E B )

A

u s t r a

l i a ,

E g y p

t , J o r d a n ,

P N G

,

M

a u r i t i u s ,

A u s t r a

l i a ,

G u a m

2 1 g e n e r a o

s c l e r a c

t i n i a ; m o s t c o m m o n

o n A

c r o p o r a

& P o c i l l o p o r a ,

1 h y d r o z o a n

H a l o

f o l l i c u l i n a c o r a

l l a s i a ,

a c o

l o n

i a l

h e t e r o

t r i c h c i l i a

t e

( 3 3

, 1 3 0

, 1 3 9 - 1

4 1 )

Y e l l o w b a n d d i s e a s e

U

n i t e d A r a

b E m

i r a t e s ,

A r a

b i a n

G u

l ,

I r

a n

4 g e n e r a ,

1 2 s p e c i e s o

s c l e r a c t i n

i a

A s s o

c i a t e d w

i t h a c y a n o

b a c

t e r i a

( 1 2 5 )

B r o w n b a n d d i s e a s e ( B r B )

A

u s t r a

l i a ,

G u a m

A c r o

p o r a , P

o c i l l o p o r a ,

E c h

i n o p o r a ,

1 6

s p p .

H e l i c o s t o m a n o n a

t u m c i l i a

t e s

( 3 3

, 1 3 0 )



121

Authors

th

Laurie Raymundo (CDWG)University o Guam

Ernesto Weil (CDWG)University o Puerto Rico

Bette Willis (CDWG)James Cook University

Courtney Couch (CDWG)Cornell University

Cheryl Woodley (CDHC)NOAA Center or CoastalEnvironmental Health and

Biomolecular Research

Greta Aeby (CDHC)Hawaii Institute o

Marine Biology

Andy Bruckner (CDHC)NOAA Coral Ree

Conservation Program

Thierry Work (CDHC)USGS-National Wildlie

Health Center

Yui SatoJames Cook University

Drew Harvell (CDWG)Cornell University

Eric Jordan-Dahlgren(CDWG)

Universidad NacionalAutónoma de México



Disclaimer The inormation contained in this publication is intended or general use, to assist public knowledge and discussionand to help improve the sustainable management o coral rees and associated ecosystems. It includes general statementsbased on scientic research. Readers are advised and need to be aware that this inormation may be incomplete or unsuitableor use in specic situations. Beore taking any action or decision based on the inormation in this publication, readers shouldseek expert proessional, scientic and technical advice.

To the extent permitted by law, the Coral Ree Targeted Research & Capacity Building or Management Program and itspartners, (including its employees and consultants) and the authors do not assume liability o any kind whatsoever resultingrom any person’s use or reliance upon the content o this publication.

NOAA Disclaimer This publication does not constitute an endorsement o any commercial product or intend to be an opinionbeyond scientic or other results obtained by the National Oceanic and Atmospheric Administration (NOAA). No reerenceshall be made to NOAA, or this publication urnished by NOAA, to any advertising or sales promotion which would indicate or imply that NOAA recommends or endorses any proprietary product mentioned herein, or which has as its purpose an interestto cause the advertised product to be used or purchased because o this publication.



The Coral Disease Handbook: Guidelines or Assessment, Monitoring and Management summarizes the relevant known science or managing coral disease. Produced by the CoralRee Targeted Research and Capacity Building or Management Program and its partners, it isdesigned to be used in conjunction with the Underwater Cards or Assessing Coral Health onIndo-Pacifc Rees and the Underwater Cards or Assessing Coral Health on Caribbean Rees.

These tools will help managers and eld scientists identiy and monitor inectious syndromes o coral and take the next step o implementing new management approaches.

The handbook includes three chapters on identiying inectious syndromes and their impactsin the eld; a chapter on coral disease monitoring protocols; a chapter detailing methodsor detecting and assessing new outbreaks o disease; and a chapter on developing newmanagement options or coral disease. It emphasizes the synergies between inectious diseaseand the rapidly changing acilitators o disease outbreaks, like global warming. These actorsmake coral disease management a moving target requiring cooperation and knowledgeexchange between microbiologists, molecular biologists, ecologists and managers.Thishandbook aims to integrate critical, current scientic inormation about coral disease tosupport and strengthen coral ree management.

Coral disease outbreaks have continued to increase and take out the major ree-builders in the

Caribbean during the last two decades. White band hugely aected Acropora palmata in the1970s and in the Keys we started having major impacts o black band in 1986. We are in the throes o several destructive outbreaks in the wider Caribbean now. Both in terms o coral bleaching and the residual outbreaks o coral diseases, I think the Pacifc is lagging about 12 to 14 years behind the Wider Caribbean. This manual flls a critical gap in moving us to the next level in developingincreasingly ambitious management approaches or coral disease.

Billy Causey, Director Southeast Region, Oce o National Marine Sanctuaries

Overall, it is a very impressive compilation, and is sure to be a signifcant contribution to progress in the feld. These types o “state-o-play reviews” are invaluable, in my opinion, or capturing thestate o knowledge, acilitating coordination and cooperation among researchers, and setting theagenda or uture work. There should be more o them.

Paul Marshall, Director Cli t Ch G t B i R M i P k A th it

Coral Disease Handbook

Documents

Transcript of Coral Disease Handbook