Several recent 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): 14+

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): 132+

Mass coral bleachings attributed to bacterial disease. Rosenberg and Toren references to unrelated events.

Goniopora death attributed to bacterial infection. No reference.

Sprung, J. 2000. Reef Notes. FAMA 23(7): 156+

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): 114+

Vibrio spp. and other bacteria responsible for Tridacnid deaths. Self-reference and lay reference.

Catalaphyllia harbors a particularly virulent bacteria. No reference.

Sprung, J. 2001. Reef Notes. FAMA 24(3): 66+

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 24(9): 26+

Goniopora death and bleaching attributed to pathogenic bacteria. No reference.

Spung, J. 2002. Reef Notes. FAMA 25(3): 40+

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. No reference.

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. No reference.

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 the wild.

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, proposed this.

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 result.

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 repeated?

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 resistance

- 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 are invasive

- non-native fungi cause Aspergillosis

Protozoans -

Nematopsis, a sporozoan in Porites hypertrophy
Coccideans - Gemmocystis cylindrus, in uncharacterized disease signs

Ciliates - found in associations with uncharacterized signs of disease

Halofolliculina corallasia - causes SEB (Skeleton Eroding Band) in the Caribbean

Amoebae - unknown role in Siderastrea calicoblastic epithelium

Coralline algae - Mesopeyssonelia corallepida - Causes PEYssonnelia in the Caribbean

Cyanobacteria - proven - Black Band Disease and Red Band Disease consortium members

Abiotic factors (environmental stress)

- changes in physical condition (salinity, light, sediment, etc.)

- injury

- 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 combinations.

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 needed.

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 antimicrobial use,
• support educational efforts that promote judicious therapeutic antimicrobial use,
• preserve therapeutic efficacy of antimicrobials, and
• ensure current and future availability of veterinary antimicrobials...

... 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 and principles.

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 therapy.

9) Use narrow spectrum antimicrobials whenever appropriate.

10) Utilize culture and susceptibility results to aid in the selection of antimicrobials when clinically relevant.

11) Therapeutic antimicrobial use should be confined to appropriate clinical indications. Inappropriate uses such as for uncomplicated viral infections should be avoided.

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 antibiotic effect.

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 Catalaphyllia "disease."

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" species.

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, however experimentally.

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 the skeleton.

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 bacteria.

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.

If you have any questions about this article, please visit my author forum on Reef Central.


Anthony, K.R.N. 2000. Enhanced particle-feeding capacity of corals on
turbid reefs (Great Barrier Reef, Australia). Coral Reefs 19(1): 59-67.

Borneman, E.H. 2002a. Do You Know Where Your Corals Are Coming
From? Ecological Information For Aquarists From Coral Collection Areas In Indonesia. AAOL 1(3).

Borneman, E.H. 2002b. The Coral Health and Disease Consortium: New
Information on Coral Disease. Reef Keeping 1(2).

Borneman, E.H. 2001. Aquarium Corals. Microcosm Ltd./TFH Publications,
Neptune City. 464 pp.

Hodgson, G. 1990. Tetracycline reduces sedimentation damage to corals.
Mar Biol 104: 493-6

*Pecheux, Martin. 1995. Review on coral reef bleaching.

Porter, James W. 2001. The Ecology and Etiology of Newly Emerging
Marine Diseases. Kuwer Academic Publishers, Dordecht. 228 pp.

Ritchie, K.B., Polson, S.W., and Smith, G.W. 2001. Microbial disease
causation in marine invertebrates: Problems, practices, and future prospects. Hydrobiologia 460: 131-139.

Rowher, F.., Breitbart, M., Jara, J., Azam F.. Knowlton, N. Diversity of
bacteria associated with the Caribbean coral Montastraea franksi. Coral Reefs 20(1): 85-91.

Salyers, A.A. and Whitt, D.D. 2002. Bacterial Pathogenesis: A Molecular
Approach. ASM Press,Washington, DC. 539 pp.

Segel, L. A., and Ducklow, H. W. 1982. A theoretical investigation into
the influence of sublethal stresses on coral-bacterial ecosystem dynamics. Bull Mar Sci 32: 919-35

**Simon-Blecher, N., and Achituv, Y. 1997. Relationhip between the coral
pit crab Cryptochirus coralliodytes Heller and its host coral. J Exp Mar Biol Ecol 215: 93-102

Sprung, Julian and Delbeek, J.C. 1997. The Reef Aquarium,Volume 2.
Ricordea Publishing, Coconut Grove, Florida. p. 444.

Toonen, Rob. 2001. Goniopora. FAMA 24(6): 142+

*Note: This article contains many errors, and was not used in any part of this article. However, Pecheux provides an excellent summary of coral reef literature on this subject, many papers of which I have used and have in my possession. The extremely large literature base on which the referenced sentences in the text are based comprises a set of data that are important, but beyond direct referencing in this work. The Pecheux reference is given as a source of further readings of the primary literature concerning transplantation, habitat variation, and other factors on the health of corals. Readers are encouraged to contact me for more information.

** Note: In this article, it is stated that "The findings reported in the present study suggest that Crytpochirus coralliodytes crabs are parasites on their coral hosts." I have been doing background research on the various pit crabs, and it appears, like so many topics, that the real answer to the role of these crabs is limited by studies and by a lack of knowledge of the full extent of their specificity and identification. It is suggested here and in other sources that the Indo-Pacific species may be far greater in number and in species specificity than is currently known, and that their individual role as parasites is not well determined among their hosts. In light of this, Ron Shimek and I are beginning further investigations into the nature of this presumably parasitic relationship, including an attempt at the identification of this crab.

Appendix 1:

From Ritchie et al. (2001) in Porter (2001)


Diseases of marine organisms appear to be increasing world-wide, but the causes of many of these remain a mystery. Here we outline steps that we have taken to identify various pathogens of marine invertebrates. These methods, however, rely on the successful cultivation of marine pathogens in the laboratory. Although Koch's postulates were established to generate evidence that a microorganism is the cause of an infectious disease, the limitations of these postulates in detecting microbes that are resistant to cultivation renders the sole use of them impossible in some situations. We, therefore, discuss some sensitive and comprehensive methods for detecting human-associated pathogens that can be adapted and applied to marine systems. A set of nucleic acids sequence-based approaches for establishing microbial disease causation in marine invertebrates is outlined that can be used in collaboration with traditional culture-based and histopathological methods to build a compelling case for microbial disease causation. In addition to providing evidence of causation, these same methods can add greatly to the current database of knowledge dealing with marine microbial communities and will ultimately enhance our understanding of emerging diseases in marine systems.

In the introduction, Ritchie et al. note the interplay of environmental factors, combined stresses, and the opportunistic nature of many marine microbes. 'To date, very little has been done to elucidate disease agents in marine invertebrates. To compound this problem, there is a gross lack of information related to marine microbial systems associated with coral reef organisms. These, among other factors, leave scientists ill-prepared to deal with emerging diseases in marine systems."

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