writings in Julian Sprung's Reef Notes column have given me
some considerable measure of concern, and have been the topic
of numerous threads on The Coral Forum.
In his most recent article (Sprung 2002),
Sprung states that "the" problem with Catalaphyllia
is pathogenic bacteria. Before addressing various issues on
a point-by-point basis, I note that he does not mention what
pathogenic bacteria are to blame, and there are no citations
as to this information's origin. Furthermore, there is no
real indication of what "the" problem is, or if
Catalaphyllia has any other problems that may occur
that are not caused by pathogenic bacteria as supposed. The
acknowledgements given for this discovery are information
gathered from discussions with a public aquarium and a public
aquarist, and, presumably, his own writings.
Not only has he pronounced or suggested
bacterial infection as a cause of death in many questions
in his column regarding an ailing organism, from fish to algae,
but also he has done so without what I consider to be proper
citations as to the documentation of such events. I generally
hold Mr. Sprung's abilities and knowledge in high regard,
but these statements give me pause. Furthermore, Mr. Sprung's
statement is being proposed in aquarium corals where no rigorous
investigations have been done to date, to my knowledge, that
support these disease conditions and mortalities in the organisms
described. Apparently, he has also described a cure for the
disease, yet I question whether any of the problems listed
below attributed to bacterial infections have been accurately
characterized or investigated at all.
In the following list, I have identified
statements from Mr. Sprung's Reef Notes column in which there
seems to be no scientific basis to support them.
Sprung, J. 2000. Reef Notes. FAMA 23(1):
Catalaphyllia problem attributed
to bacterial infection. No reference.
RTN attributed to bacterial infection. No reference.
Goniopora death attributed to bacterial infection.
J. Sprung self-
Bleaching attributed to bacterial infection. No reference.
Virulent Vibrio sp. outbreak diagnosed remotely
in aquarium as cause of death for serpent star, Astraea
snails, and numerous divergent taxa of crabs. No reference.
Sprung, J. 2000. Reef Notes. FAMA 23(6):
Mass coral bleachings attributed
to bacterial disease. Rosenberg and Toren references to
Goniopora death attributed to bacterial infection.
Sprung, J. 2000. Reef Notes. FAMA 23(7):
Bacterial disease is principal
cause of death in captive anemones.
Probably Vibrio spp. and compared to uncharacterized
disease of stony corals. No reference.
Sprung, J. 2000. Reef Notes. FAMA 23(10):
Vibrio spp. and other
bacteria responsible for Tridacnid deaths. Self-reference
and lay reference.
Catalaphyllia harbors a particularly virulent bacteria.
Sprung, J. 2001. Reef Notes. FAMA
Xenia death attributed
to pathogenic bacteria. No reference.
Flatworms and even algae disappearance attributed to microbial
or viral pathogens. No reference.
Sprung, J. 2001. Reef Notes. FAMA
Goniopora death and bleaching
attributed to pathogenic bacteria. No reference.
Spung, J. 2002. Reef Notes. FAMA 25(3):
Antibiotic treatment with doxycycline
and iodine recommended for bleaching, poor growth and
poor polyp expansion in Acropora and bleaching
in unidentified corallimorpharians attributed to unknown
disease, pathogenic bacteria and bacterial infection.
Sprung, J. 2002. Reef Notes. FAMA 25(5):
Catalaphyllia death and
disease attributed to pathogenic bacteria. No reference.
Tridacnid clam mortality attributed to bacterial pathogens,
but admission that little is known. No reference.
Trachyphyllia mortality attributed to bacterial
pathogens. No reference.
Tropical coral bleaching attributed to bacterial pathogens.
While Sprung and Delbeek (1997) state that,
"it is our opinion that most [diseases] are caused by
bacterial infection," Mr. Sprung seems to have foregone
that statement, and now describes such events as proven fact.
I am not saying or even suggesting that
coral or other organismal disease in our aquariums does not
have a bacterial cause in some cases. However, finding a bacteria,
characterizing it, proving its virulence (and not just "happening
to be present" or part of a secondary infection), and
making sure it is present in ALL cases with a characteristic
set of well-described signs is a huge and difficult task (see
Appendix 1). As far as I know, no aquarium diseases in invertebrates
have ever been properly characterized or assigned a causative
agent. I would be very pleased it if was that easy; or perhaps
more importantly, that such findings could be used to support
or applied to coral disease work in both the aquarium and
Concerning Catalaphyllia, Mr. Sprung
writes that Internet forum discussions have suggested that
this coral starves in captivity, and while I cannot speak
for all possible forums or threads, I believe this statement
to be incorrect. It is my observation that forums tend to
attribute starvation to the demise of Goniopora, not
Catalaphyllia. Mr. Sprung also claims, "the academic
notion put forward is that Catalaphyllia lives in nutrient
rich lagoons and will not thrive in a heavily skimmed 'clean'
aquarium. There are relatively few academia putting forth
notions on aquarium corals, and none of us have, to my knowledge,
Sprung also cites the various locations
where he has seen Catalaphyllia in the wild, and while
interesting, Catalaphyllia isn't being exported from
Australia, the Solomon Islands, Japan, and Palau. Thus, observations
of it from these locations are somewhat irrelevant to aquarists.
I recently described the collection locales for this coral
from its primary sources in Indonesia, and similar to his
findings, I found it in varied habitats (Borneman 2002a).
However, he seems to feel that, because it occurs in varied
habitats, a correlation can be made that it is tolerant of
variant water qualities and lighting in the aquarium as a
Transplantation studies show that this
is indeed not the case. Corals transplanted from low-light
to high-light environments rarely are able to adapt and generally
bleach and die. In contrast, corals transplanted from high-light
to low-light environments tend to survive, but only after
a significant acclimatization period (Pecheux 1995, see below).
In regards to feeding and nutrients, a similar adaptation
seems to exist. Corals found throughout reef zones that exist
in areas with high particulates tend to gain a greater proportion
of their energy from particulate feeding, and those transplanted
from low particulate to high particulate environments tend
to do poorly (Anthony 2000). The same has been found in regard
to temperature and other parameters (some of the many references
available with summary in Pecheux 1995). Sprung correctly
uses some of these same examples in a recent submission to
an annual publication regarding bleaching (Sprung 2002, above),
and yet apparently fails to see their relevance in this case.
In areas where Catalaphyllia are
collected, there is a dramatic difference in the variations
of habitat where they are both found and collected, and depending
on where an individual specimen was originally harvested,
the change to holding tanks and ultimately the home aquarium,
may require significant acclimation periods. As a result,
the coral, like those in transplantation studies, may simply
be unable to adapt and die.
One of the things that needs to be realized, and it was presented
at a meeting of the Coral Disease and Health Consortium in
Charleston earlier in the year (Borneman 2002b), was the need
for accurate reporting and consistent use of terms. We felt
the general lack of knowledge and descriptive language used
(or misused) in coral disease hinders further progress in
coral disease research and reporting.
In the matter of calling this condition
a disease: a disease is defined as any deviation from or interruption
of the normal structure or function of any part, organ, or
system, or combination thereof that is manifested by a characteristic
set of symptoms and or signs and whose etiology, pathology
and prognosis may be known or unknown (Dorland's Medical Dictionary).
For coral disease, the following conditions are generally
accepted in the field:
1. Signs, not symptoms
2. An identifiable group of signs
3. A recognized etiological or causal agent(s)
4. Consistent structural alterations
Can he or anyone define the characteristic
set of signs, a recognized agent, or consistent structural
alterations in the problem affecting Catalaphyllia?
I would ask what studies or works have been done, and how
were they done? Where were they published? Have they been
Regarding the fact that he assumes bacterial
pathogens as a matter of elimination of other viewpoints,
disease can be caused by both biotic and abiotic factors.
Some are as follows:
Biotic factors (living organisms such
as parasites, pathogens)
-associated flora and fauna
have relationships from mutualistic to parasitic.
-infectious agents (spread from host to host) viruses,
bacteria, fungi, protozoans, algae, nematodes and others
are known or possible.
Biotic factors include:
Viruses - likely, but none yet
isolated in any coral disease.
Bacteria - proven for several
diseases; important points include:
- normal flora may provide
- change in mucus from abiotic factors may change flora
- secretion of antibiotic substances by host and flora
- compromised health and immunity
- anthropogenic change in exposure
- tendency for pathogens to be gram negative rods, often
Vibrio, Aeromonas, Pseudomonas,
but these are also native flora
- opportunistic pathogens may be part of normal flora
- bacteria may be consortium members
Fungi - proven for several diseases
- endolithic fungi exist that
- non-native fungi cause Aspergillosis
Nematopsis, a sporozoan in
Coccideans - Gemmocystis cylindrus, in
uncharacterized disease signs
Ciliates - found in associations with
uncharacterized signs of disease
- causes SEB (Skeleton Eroding Band) in the Caribbean
Amoebae - unknown role in Siderastrea
Coralline algae - Mesopeyssonelia
corallepida - Causes PEYssonnelia in the Caribbean
Cyanobacteria - proven - Black Band Disease
and Red Band Disease consortium members
Abiotic factors (environmental
- changes in physical condition
(salinity, light, sediment, etc.)
- can act alone or synergistically
with other biotic or abiotic factors
- nutrients, toxins, hypoxia, stress induced apoptosis,
cellular damage, radiation, thermal stress, xenobiotics,
sewage, and noxins are just some of the possible abiotic
agents of disease
(Note: Many of the examples above are referenced
in Borneman (2001). The information given above is a synthesis
of scientific work in the field. I will be happy to provide
direct references to any of the information above, but have
opted to not directly in-line reference all of the applicable
papers in the interests of brevity. An excellent compendium
secondary source now available that covers much of this material
is found in Porter (2001).)
An entire working group was devoted to
the subject of abiotic factors in coral disease at the previously
mentioned coral disease workshop. Both biotic and abiotic
factors may be (and are likely to be) interrelated. For clarification,
stress is defined as the sum of the biological reactions to
any adverse stimulus that tends to disturb the organism's
homeostasis; should these compensating reactions be inappropriate
or inadequate, they may lead to disorders. Therefore, stress
alone can manifest as disease.
In regard to his recommendations for prophylactic
and directed treatment, in addition to the treatment protocol,
I must disagree with the way this information, if true, would
have come about through the relatively blind use of antibiotics.
Furthermore, he has suggested that persons untrained in coral
disease identification, antibiotic therapy, or any sort of
relevant biological training apply non-judicious use of antibiotics
to organisms harboring not only an unidentified pathogen,
if one even exists, but to concurrently subject the vastly
diverse microbial flora of that coral, and indeed the entire
tank, to antibiotics. I consider this to be troublesome advice.
The following is from a public statement
issued by the American Veterinary Medicine Association:
"Resistance to antimicrobials existed
even before antimicrobials were used. However, this intrinsic
form of resistance is not a major source of concern for human
and animal health. The vast majority of drug-resistant organisms
have instead emerged as a result of genetic changes, acquired
through mutation or transfer of genetic material during the
life of the microorganisms, and subsequent selection processes.
Mutational resistance develops as a result of spontaneous
mutation in a locus on the microbial chromosome that controls
susceptibility to a given antimicrobial. The presence of the
drug serves as a selecting mechanism to suppress susceptible
microorganisms and promote the growth of resistant mutants.
Spontaneous mutations are transmissible vertically. Resistance
can also develop as a result of transfer of genetic material
between bacteria. Plasmids, which are small extra-chromosomal
DNA molecules, transposons and integrons, which are short
DNA sequences, can be transmitted both vertically and horizontally
and can code for multi-resistance. It is believed that the
major part of acquired resistance is plasmid-mediated, although
the method of resistance transfer varies for specific drug/bacteria
Resistance depends on different mechanisms
and more than one mechanism may operate for the same antimicrobial.
Microorganisms resistant to a certain antimicrobial may also
be resistant to other antimicrobials that share a mechanism
of action or attachment. Such relationships, known as cross-resistance,
exist mainly between agents that are closely related chemically
(e.g. neomycin-kanamycin), but may also exist between unrelated
chemicals (e.g. erythromycin-lincomycin). Microorganisms may
be resistant to several unrelated antimicrobials. Use of one
such antimicrobial will therefore also select for resistance
to the other antimicrobials...
...When an animal is treated with an antimicrobial
drug, a selective pressure is applied to all bacteria exposed
to the drug. Bacteria that are sensitive to the antimicrobial
are killed or put at a competitive disadvantage, while bacteria
that have the ability to resist the antimicrobial have an
advantage and are able to grow more rapidly than more susceptible
bacteria. In addition, bacteria can become resistant when
resistance genes are passed from a resistant bacterium to
a sensitive one. Thus, antimicrobial agents may increase the
prevalence of resistant bacteria among both target pathogens
and normal bacterial flora...
... Whenever an animal or human host is
exposed to antimicrobials, there will be some degree of selection
for a resistant bacterial population. Selection will depend
upon the type of antimicrobial used, the number of individuals
treated, the dosage regimen, and the duration of treatment.
Therefore, it is vital to limit therapeutic antimicrobial
use in animals and humans to those situations where they are
The veterinary profession shares the concerns
of the public, governmental agencies, and public health community
regarding the broad issue of antimicrobial resistance and
specifically the potential risk of resistance developing in
animals with subsequent transfer to humans. Because of that
concern and to maintain the long-term effectiveness of antimicrobials
for animal and human use and to increase the possibility of
future antimicrobial drug approvals for the treatment of animals,
the American Veterinary Medical Association committed to judicious
use of antimicrobials by veterinarians for the prevention,
control, and treatment of animal diseases...
...The objectives of the AVMA are to:
support development of a scientific
knowledge base that provides the basis for judicious therapeutic
support educational efforts that promote judicious
therapeutic antimicrobial use,
preserve therapeutic efficacy of antimicrobials,
ensure current and future availability of veterinary
... There are fifteen general principles
which emphasize preventive actions to avoid disease, consideration
of other options before choosing to use antimicrobials, and
consideration of use of less important drugs before using
the drugs of last resort, especially those that are very important
to human or animal medicine.
1) Preventive strategies, such as appropriate
husbandry and hygiene, routine health monitoring, and immunizations,
should be emphasized.
2) Other therapeutic options should be
considered prior to antimicrobial therapy.
3) Judicious use of antimicrobials, when
under the direction of a veterinarian, should meet all the
requirements of a valid veterinarian-client-patient relationship.
4) Prescription, Veterinary Feed Directive,
and extra-label use of antimicrobials must meet all the requirements
of a valid veterinarian-client-patient relationship.
5) Extralabel antimicrobial therapy must
be prescribed only in accordance with the Animal Medicinal
Drug Use Clarification Act amendments to the Food, Drug, and
Cosmetic Act and its regulations.
6) Veterinarians should work with those
responsible for the care of animals to use antimicrobials
judiciously regardless of the distribution system through
which the antimicrobial was obtained.
7) Regimens for therapeutic antimicrobial
use should be optimized using current pharmacological information
8) Antimicrobials considered important
in treating refractory infections in human or veterinary medicine
should be used in animals only after careful review and reasonable
justification. Consider using other antimicrobials for initial
9) Use narrow spectrum antimicrobials whenever
10) Utilize culture and susceptibility
results to aid in the selection of antimicrobials when clinically
11) Therapeutic antimicrobial use should
be confined to appropriate clinical indications. Inappropriate
uses such as for uncomplicated viral infections should be
12) Therapeutic exposure to antimicrobials
should be minimized by treating only for as long as needed
for the desired clinical response.
13) Limit therapeutic antimicrobial treatment
to ill or at risk animals, treating the fewest animals indicated.
14) Minimize environmental contamination
with antimicrobials whenever possible.
15) Accurate records of treatment and outcome
should be used to evaluate therapeutic regimens."
I have not elaborated on each of the fifteen
points, but they are spelled out very clearly and should be
read by all interested parties. It seems, through his advice
concerning prophylactic dipping of Catalaphyllia, that
Mr. Sprung is advocating and or participating in a direct
or indirect contradiction of almost all of the principles
outlined by the AVMA for judicious antibiotic use.
I must emphasize that I am neither friend
nor foe of bacterial causes for coral disease. In fact, it
is probably likely many have direct or secondary causes by
bacteria. But, one must be sure that bacteria are the etiological
agent and this requires difficult and often elaborate scientific
study and technique. To even begin to advise a treatment dosage
should, at the very least, involve trials with the organism
in question. Even then, antibiotic treatment is a dangerous
thing. Sadly, this is still the case even if treatment helps
in some instances.
Even if this were accomplished, I would
still have two simple questions: Why doxycycline? Doxycycline
is a broad spectrum antibiotic similar to tetracycline that
interferes with bacterial protein synthesis. Why does he propose
this drug and not other equally or more effective and/or targeted
antibiotics? Second, because calcium and other ions, like
magnesium, bind doxycycline and render it ineffective, and
with seawater and coral tissue nearly saturated with calcium
and magnesium, how and why does it work so well? I have attempted
to use various antibiotics in trials with corals, and found
that chloramphenicol often works with certain aquarium coral
diseases. It is not always helpful, even in conditions I believe
to show signs of the same disease. Perhaps more difficult
to explain is why the same coral species from the same disease
event fail to respond to other targeted or broad spectrum
antibiotics, including ones known to be more effective against
various potential bacterial species suspected of causing disease
or that are part of the normal surface microbial flora. I
suspect that the action of some of these drugs may be targeting
other molecular pathways and not always acting by their direct
Coral disease is extremely hard to recognize,
even when it is established in the scientific literature and
possesses a characteristic set of signs. How will the average
- or even the highly experienced - aquarist be able to look
at a coral and determine that bacteria are to blame? Any time
a coral is withdrawn, looks bad, has been injured, or for
any number of reasons, its appearance may look grossly similar.
The number of factors that could contribute to individual
cases and produce similar signs are almost uncountable. An
epizootic cannot be pronounced without data, and one cannot
assume that all corals that have a certain appearance have
the same condition.
I am concerned that by using his column's
advice, along with its international distribution, many aquarists,
retailers, wholesalers, exporters, and even collectors unable
to figure out why a Catalaphyllia is failing to thrive,
and even when it may not be failing to thrive if treated prophylactically,
may begin purchasing antibiotics and "treating"
their corals for unknown or even non-existent reasons. I think
history has shown that the previous trend of dipping corals
in iodine - and apparently now, due to information provided
by other sources, malachite green - sometimes helps, sometimes
hurts, and sometimes does nothing. This is because we simply
don't know the root cause of any perceived problem, and we
definitely cannot tell what it is by the gross appearance
of a coral.
Scientists often can't identify what bacterial
species are found on a living coral, and one similarly will
have great difficulties determining which, if any, microscopic
bacteria are present as putative pathogens. This is to say
nothing of the bacterial flora normally present. Even with
a known pathogen, Aspergillis sydowii, the fungi causing
seafan disease, it is known that despite characteristic purple
lesions and erosion, one absolutely cannot make a determination
of Aspergillosis until fungal hyphae have been isolated from
the lesion, because too many other things can produce the
same gross signs.
There is a well-referenced science article
(Hodgson 1990) that describes protocol use of antibiotics
in stress-mediated conditions. Another one of the classic
papers in coral disease is one that proposes disease caused
by opportunistically pathogenic surface microbial flora (Segel
and Ducklow 1982). The authors note that normal coral surface
flora can cause problems for corals under stressful conditions,
if not only by their metabolic activities, but from direct
opportunistic pathogenicity. Antibiotic effectiveness and
unidentified pathogenic bacteria are therefore not necessarily
at the foundation of either of his proposed evidences for
As an example, Psuedomonas aeruginosa
is a ubiquitous surface colonizing bacteria. It's everywhere.
It's all over our skin. It may actually help our defenses
because it competes with other "non-native" bacteria
and probably keeps real pathogens from colonizing us to a
greater extent. But, given an immunocompromised person, or
someone put in a hospital setting with many strains present,
or those having an organ transplant or surgery with catheterization,
P. aeruginosa is the cause of 10% of nosocomial infections
and is a leading cause of death. The same is true with Staphylococcus
aureus and S. epidermis (Salyers and Whitt 2002).
One further problem Mr. Sprung doesn't
mention is the fact that identifying marine bacteria, much
less establishing a role in disease in a tremendously hard
to control environment, is nearly impossible. Until very recently,
most attempts at identifying coral flora and putative pathogens
become simply listed as unidentified, or perhaps a vague Psuedomonas
sp., or even more often, "most closely resembles
xxxxxx." That's why every time there has been a report
of a new disease bacteria, it is almost always a "new"
However, authors of a recent paper confirmed
something already well recognized (Rowher, et al. 2001); that
many, if not most, of these bacteria are non-culturable. If
you try and grow them to establish causality, it can't be
done. The culturing attempts tend to result either in the
identification of non-pathogens, or completely miss any real
pathogenic strain or species. Furthermore, bacteria that are
amenable to culture are often lumped into non-specific categories
such as "Vibrio-like organisms." The problem
is that when molecular techniques such as PCR have been used
to amplify genes and the results compared to a database, the
species found are possibly quite different and probably far
more accurately identified than what is obtained by traditional
culture. Therefore, these "Vibrio-like" bugs
might not be at all Vibrio, but as this article showed,
catalogued alpha-proteobacteria and other well-known types.
Getting any kind of concrete results at
any level of pathogen identification is an exceedingly difficult
process, fraught with hundreds of obstacles and unknowns,
and remains a mystery to dozens of expert scientists in the
field for almost every coral disease that exists. Coral disease
researchers struggle year after year to try and be able to
identify pathogens, if they are responsible at all, for various
coral diseases. Where there has been a causative agent found,
the majority have not been bacteria, but consortiums and non-bacterial
agents consisting of bacteria, cyanobacteria, fungi, ciliates,
and other organisms. There are three diseases that have been
reported as being caused by a single bacterial pathogen. Two
of these might not be correct, since there were possibly methodological
problems. Most diseases remain mostly or totally uncharacterized
and often despite searching for microbial pathogens. The rest
of the world, outside the aquarium world, is largely unaware
that such a problem exists with Catalaphyllia, and
there is no one studying it to my knowledge in any regard.
In his article Mr. Sprung asks for other
possibilities to explain the problem with Catalaphyllia.
I would like to propose the following possibilities.
All the aforementioned notwithstanding,
there is indeed a difference in the survival of some Catalaphyllia
compared to years ago. However, there are dozens of possible
explanations for this problem, and their survival is not uniformly
dismal; not all Catalaphyllia show a similar set of
signs of a problem, and the incidence of mortality to this
set of signs seems to be decreasing, as well. Unfortunately,
when we surveyed areas of Catalaphyllia collection,
no examples of this condition were seen in the wild, and only
two were seen at exporters, both at a single facility. Similarly,
no specific wholesaler or retailer seems to be the source
of the proposed pathogenic bacteria. Thus, we must assume
that either a) a latency period exists where virulence does
not occur (or occurs very rarely) in the wild, and that it
is only when placed in aquariums that virulence is expressed
or b) that the proposed pathogenic bacteria exist only in
aquariums. Neither scenario has much likelihood of being correct.
For almost the first ten years I was an
aquarist, Catalaphyllia were hardy corals, barring
gross negligence or injury, they could be maintained easily.
They were "a beginner coral" by many accounts, and
to my observations, they never had the problems apparent today.
Then, a few years ago, some began appearing in the aquarium
trade with an abnormal appearance: grossly swollen oral disc
with shrunken tentacles. The oral disc eventually shrank,
as well. The affected corals died, no matter what was tried,
Bacteria can do all sorts of things, and
this is possibly one of them, but it is not normally what
one sees when bacteria invade coral tissue. Bacteria generally
form plaques, webs, create necrotic masses of gel-like tissue,
cause distinct progressing band lines of healthy tissue and
bare skeleton, cause bleaching, or (even less frequently described)
tissue lysis. As Mr. Sprung mentions, in some cases, but not
in all by any means, a white plaque or film is evident on
affected Catalaphyllia. This type of white film may
be a Beggiatoa species. It has been identified in other
corals, and implicated as a sole agent or consortium member
in some coral diseases. However, Beggiatoa are ubiquitous
marine microbes and cannot be eliminated, and their presence
or role in those certain affected Catalaphyllia remains
to be determined.
For a while, almost all the Catalaphyllia
I saw in stores had this appearance. Ron Shimek, with the
incredibly good photography, reports, and help of some aquarists,
identified a pit crab, possibly a Cryptochirus species,
that resides below the tissue, between the tissue and the
skeleton. To my knowledge, this crab has been found in almost
every case of Catalaphyllia with signs of this problem.
Also, the animal can apparently leave that host and invade
a new host. If indeed this crustacean is parasitic, and it
does appear to be the case (Simon-Blecher and Achituv 1997
and others. See notes at end of references), then it would
be feeding on the tissue from the underside, and would certainly
be able to cause the signs of the problem: no real external
damage, irritation, loss of tissue mass, and detachment from
Because we did find at least two affected
Catalaphyllia at an export facility with this condition,
it is obvious some specimens are being collected from somewhere
with this condition. We also found some evidence of significant
overharvest of these corals, and that they are very site specific
and are not collected from all collection sites. Does it make
sense then that a Catalaphyllia collection site was
harvested and collection moved to another site where there
were affected corals, and then those were either abandoned
or harvested, and collection again moved to other sites? It
fits very well with observations we made, and also fits in
with the sporadic nature of the affected imports.
For Mr. Sprung's theory to be reasonable
and correct, there would have to be a local or regional epizootic
of some novel unidentified pathogenic bacteria that only affects
Catalaphyllia, and apparently is not contagious to
other Catalaphyllia. This same pathogen wasn't seen
for ten years or more and it is a bacterium that would only
be found in certain areas. Bacteria do not usually localize
themselves in marine environments like this. Coral parasites
are a different matter. It is very possible that an area has
a locally high level of a parasite. They often live and breed
in their host, and are often species and sometimes site-specific.
Is it possible that the stress of collection
(initial harvest, three or four different intermediate tanks,
shipping, cold, hot, and stagnant water), having an active
parasite present, and/or being placed in a tank environment
drastically unlike the collection locale (for example, being
collected from 130 feet down in a muddy environment and then
being placed under 400 watt metal halides) weakens the coral
enough that bacteria can do the rest? I believe so. It's also
possible the stress alone does them in, and bacteria are there
to clean up the dying tissue. Perhaps other microbes besides
bacteria are present. There are many possible pathogens besides
Mr. Sprung has made some significant contributions
to this hobby, is experienced with coral husbandry, and I
am aware he has extensive experience in diving and with maintaining
coral in the home aquariums. However, the recommendation for
wholesale treatment of corals whose normal surface flora contain
known human pathogens presents a serious and significant potential
risk to the aquarist, the public, the coral, the aquarium
and the wild. The use of antibiotics, especially prophylactically,
can create a true problem when healthy corals then become
the cause for resistant strains passed around the hobby every
time we trade a fragment or buy a coral from a store. Perhaps
it has already happened and this is the real reason for the
problem. I very much appreciate his experimental treatment
of these corals to ensure their survival, and his concern
over the problem. I would be pleased to work with him to discover
the true nature of the problem, and to ascertain if and what
bacterial pathogens are the etiological agent of the problem
affecting Catalaphyllia. However, I also urge him to
investigate these various coral problems carefully, or report
information as fact only when such evidence is available.
Upon writing to the editors of FAMA and
Mr. Sprung regarding this subject, I have received a response
from the magazine (Steele, pers. comm.). They responded by
saying they appreciate my concern, have forwarded the letter
to Mr. Sprung, and have hopes that he will further research
the matter and respond to my concerns. They further stated
that they do not want information stated that cannot be backed
up by scientific research and studies. I have not yet heard
from Mr. Sprung.