Marine Head and
Lateral Line Erosion, also known by the acronym MHLLE, is
truly an anomaly among ornamental marine fish diseases. While
most other ailments have been studied enough to have reached
a consensus on their exact causes and proven cures, the hobby
has reached no such consensus about MHLLE. Unfortunately,
MLLE is not a problem in aquacultured fish, and as a result,
little research money has been allocated to discovering its
definitive cause(s). This leaves us with primarily the speculation
in the hobby and limited (and often conflicting) scientific
studies as to its cause. Consequently, there are a number
of theories regarding MHLLE's cause making some sense and
showing some promise, but no one cause has been proven conclusively
to be the cause of MHLLE; therefore, there is
no consistent treatment to correct the problem. In this article,
I will discuss and evaluate some of the speculated causes
Note that I am using the phrase "Marine
Head and Lateral Line Erosion" instead of simply "Head
and Lateral Line Erosion." This is because a similar
freshwater ailment exists, which I want to differentiate from
the marine version during later discussions. Although most
authors refer to the freshwater affliction as "Hole in
the Head disease," some confusion remains because other
authors use the two phrases interchangeably. I have even heard
the term "face rot" used to describe either ailment.
In this article, I will draw a clear distinction and use either
"Marine Head and Lateral Line Erosion" or its acronym
"MHLLE" for this particular disorder throughout
Description of the Condition:
This ailment's initial
manifestation is usually the development of small pits around
the eye and on the head and adjacent area. As it progresses,
the holes grow larger, eventually connecting to become larger
lesions, additionally extending back along the fish's lateral
line. In advanced cases, the fins and gill covering begin
to erode. While this condition is seldom fatal, it can horribly
disfigure a once beautiful fish. In my experience, minor cases
that are stopped can allow a reversion to a normally appearing
specimen, but once it has progressed too far, the fish may
be permanently scarred.
One species is a common exception to this syndrome's usual
manifestation. Yellow tangs (Zebrasoma flavescens)
do not appear to be afflicted in the same manner as other
fish (Hemdal, 2003). They first tend to lose their vibrancy
and lighten in overall color. Then their fins erode, usually
beginning with the soft tissue between the dorsal fin's rays.
If there is any erosion around the head or down the lateral
line, it is usually only minor. This is not, however, the
case for all species of the genus Zebrasoma. I have
witnessed purple (Z. xanthurus), sailfin (Z. veliferum)
and brown (Z. scopas) tangs all exhibiting the classic
signs of this condition, while every Yellow tang I have seen
with MHLLE has always exhibited this atypical symptomology.
A Yellow tang (Zebrasoma flavescens) with a typical
manifestation of MHLLE. Notice the relatively minor
pitting around the eye and down the lateral line while
the dorsal fin is showing significant erosion.
There is some question as to whether or not these atypical
instances in yellow tangs can rightly be called MHLLE. And,
I will freely admit that since we don't know for sure what
causes MHLLE, we also cannot say for sure that these disfigured
yellow tangs are suffering from the same thing. But, in my
opinion and that of others (Hemdal, 2003), it would be awfully
strange if they were not related. The common factor being
that fish held in captivity, in many instances in sub-optimal
environments, develop tissue erosion of one type or another.
Surgeonfishes and angelfishes are
the two fish groups most commonly afflicted with MHLLE (Blasiola,
1990 & Hemdal, 2003), although other fish also are susceptible
to this ailment. Groupers and damsels are known to have problems
with MHLLE, even if it is not as commonly encountered. Of
all the fish I have ever seen with this condition, blue regal
tangs (Paracanthurus hepatus) are by far the most frequently
observed to have MHLLE. After them, various species of Zebrasoma
seem to be the next most common, followed by Acanthurus,
Centropyge and Pomacanthus species. On the other
hand, some families of fish, such as wrasses, appear to be
immune although they sometimes do suffer from other mysterious
ailments that may be related to MHLLE, as I will mention later.
A Pacific blue regal tang (Paracanthurus hepatus)
showing a severe case of MHLLE.
THEORIZED POTENTIAL CAUSES
Dietary deficiencies are one of the
most commonly cited factors in outbreaks of MHLLE. When a
discussion comes up on a message board regarding a fish afflicted
with MHLLE, one of the first questions typically asked is
what food is being offered to the affected fish. That is usually
shortly followed by recommendations of various vitamins and
other additives, as well as changes to its nutritional regime.
This theory, besides being popular also has some evidence
to back it up. Blasiola (1990) conducted a small study in
which he compared two groups of blue regal tangs, Paracanthurus
hepatus. One group was fed a flake food diet low in vitamin
C while a second group was fed a flake food diet supplemented
with live algae. After only three weeks, the fish in the first
group began to exhibit small areas of discoloration around
their eyes. The condition continued and progressively worsened
throughout the testing phase. After 95 days the testing was
stopped because of the severity of the disease's advancement.
At that time the afflicted fish were switched to a diet that
included algae and supplemental vitamin C. In just ten short
days, the fish began to demonstrate improved color.
This would seem to suggest a link between vitamin C deficiency
and MHLLE. Unfortunately, not all cases can be traced to a
mere vitamin C shortage in the diet. For example, Collins
(1995) reported experiencing an outbreak of MHLLE in Atlantic
blue tangs (Acanthurus coeruleus) in a display at the
Indianapolis Zoo. These fish were fed a diet rich in vitamin
C, but suffered from MHLLE nonetheless. After some adjustment
to their diet, which revolved around ensuring they received
a sufficient amount of vitamin A, they recovered so much that
only those that initially had been most severely affected
retained some scarring; no further MHLLE events were experienced.
One more note about these two reports: in the subsequent
Q&A session after Blasiola reported his study at a conference,
there was some discussion about whether or not activated carbon
could have played a role in the outbreak that his test subjects
experienced. On the other hand, the display at the Indianapolis
Zoo, where Steve Collins was curator, had experienced MHLLE
problems that he believed were tied to vitamin A deficiencies,
yet the system did not use any activated carbon (Collins,
1995). Please keep these comments in mind when I revisit activated
carbon in subsequent sections of this article.
I have read some discussions on various message boards that
implicated a lack of iodine as a possible cause of MHLLE.
Usually, the iodine deficiency theory was offered as an explanation
with some other related factors; namely, that iodine and/or
other beneficial elements were removed by protein skimming
or activated carbon. Alternatively, some argued that the iodine
was not available because it simply had been all used up,
and that more was needed and should be supplied via direct
dosing or increasing the frequency and/or amounts of water
changes. Lastly, a lack of iodine in the diet is known to
cause goiters in some fish and at least one authority (Michael,
2003) believes that such a lack may somehow be related to
cases of MHLLE. In my opinion, the entire iodine argument
is moot. I perform and recommend to others that they do regular
water changes, not as a method of maintaining iodine concentrations,
but in an effort to dilute the myriad noxious compounds produced
in reef aquariums that are not easily tracked by standard
test kits (Borneman, 2003). As there are no accurate means
of measuring all the forms iodine may take in aquaria (Holmes-Farley,
2003), and I am adamantly against adding anything to my display
that cannot be measured accurately and consistently, I don't
use iodine and don't encourage its use by most hobbyists.
Poor Water Quality:
Poor water quality is the other culprit
for MHLLE cases most frequently discussed on the internet
and in print (Blasiola, 1990; Frakes, 1988; Fry, 2003; Hemdal,
2003 and Michael, 2003). Factors such as high nitrate levels
or perhaps dissolved organics in the water have all been implicated
at one time or another as potential contributing factors causing
MHLLE. Let's examine each of these in more detail.
"High" (whatever that is) nitrate levels have long
been thought to be problematic. There are as many recommendations
of maximum healthy nitrate levels as there are books on the
subject of marine aquarium keeping. Everyone has an opinion
and the major point I want to make is that these recommendations
are simply opinions. While it may be beneficial to
target a low nitrate level, a definitive answer as to what
is acceptable and what is harmful will require additional
study, although a few studies have been done on nitrate toxicity.
Juvenile common clownfish (Amphiprion ocellaris) were
shown to have slower growth rates when housed in 100 mg/l
of NO3-N than those kept in 15 mg/l
(Frakes, 1993). Also in that same article, Frakes cited information
from a study showing that a concentration of 500 mg/l NO3-N
caused a 50% mortality rate in planehead filefish (Monacanthus
hispidus) and a level of 2,400 mg/l had the same effect
on Beau Gregory damsels (Stegastes leucostictus). So
clearly, nitrate can cause problems, but those all are rather
high values, in some cases astronomically high, and unlikely
to occur in typical aquaria. As none of these tests showed
any connection to MHLLE, whether or not nitrate levels can
cause MHLLE, remains unknown.
An Atlantic blue tang (Acanthurus coeruleus)
showing the typical signs of MHLLE.
So what if the measured nitrate level is consistently low
or nonexistent? What does that mean? Well, it means just simply
what the test says, and that by itself implies nothing else
about the tank's water conditions. Countless compounds that
we cannot measure are constantly being produced in our aquariums
(Borneman, 2003.) Just because the water quality appears to
be in the proper ranges on standard aquarium test kits does
not necessarily mean that the water is in perfect condition
or that there are no foreign or deleterious dissolved compounds
in the water. To illustrate this point, consider a theoretical
tank that utilizes a deep sand bed (DSB), or other similar
means of denitrification, along with kalkwasser or another
balanced means of maintaining calcium, alkalinity and pH.
Is it not possible to maintain this theoretical tank indefinitely
without water changes, while also keeping all of the typically
measured parameters in their appropriate ranges? Does that
mean the water is perfect for marine aquarium keeping, or
that every organism added to this aquarium would live and
prosper? Of course not!
I don't mean to give the impression that aquarists should
not use standard test kits to monitor and track an aquarium's
water quality; it should be done, but the hobbyist needs to
be aware of the limitations of this methodology. Simply put,
one cannot measure all possible parameters. Monitoring nitrate
levels as well as pH, alkalinity, calcium and phosphate can
explain some of the things that are going on in a system;
it just doesn't reveal the entire picture. As an aside, please
don't use acceptable readings as an excuse to become lazy
with husbandry practices.
Remember also that saltwater fish drink nearly constantly
as a means of adaptation to a seawater environment. It is
entirely possible that the saying "You are what you eat,"
should be, "You are what you drink," when referring
to marine fish. Think of it this way: fish must eat in, drink,
breath through and simply be surrounded by and immersed in
whatever nasty compounds are in their ambient water. Hopefully,
we can see that proper water quality is particularly important,
regardless of whether or not it has a direct link to MHLLE.
An unusual 'flakey' appearance to a Blue regal tang (Paracanthurus
afflicted with MHLLE.
It has been suggested that activated
carbon might play a role in MHLLE (Frakes, 1988; Hemdal, 2003;
Hemdal, pers. comm. and Michael, 2003), although the exact
mechanism that these various authors suggest differs. Some
have theorized that the activated carbon in the aquarium's
filtration system could remove necessary trace elements that
the fish require. Others hypothesize that activated carbon
could leach something into the water that negatively affects
the fish. And still others speculate that carbon dust may
act as an irritant to the fish.
As additional "anecdotal support" for this theory,
Scott Michael noted that a local fish store he visited that
used activated carbon was experiencing MHLLE in almost every
fish under its care. And I must say, I too have witnessed
similar experiences at retail locations that use a lot of
activated carbon and then coincidentally experience massive
outbreaks of MHLLE. But this is anecdote, not proof. In these
situations there was simply no evidence of what might have
happed in the absence of activated carbon, all other things
remaining equal. It could just as easily be a dietary concern.
Or, perhaps the store was using activated carbon to make up
for a lack of water changes or other poor husbandry issues.
There are simply too many factors involved to point to a definitive
Additionally, activated carbon is used so frequently in the
ornamental fish industry and hobby that it is no surprise
some fish exposed to activated carbon develop MHLLE. Also,
since large numbers of fish routinely housed in systems utilizing
activated carbon don't develop MHLLE, and consequently
some fish develop MHLLE while not exposed to activated carbon,
additional factors must be playing a role in those cases in
which fish do exhibit symptoms of MHLLE.
Exposure to Copper:
Exposure to copper is another often-mentioned
theory (Blasiola, 1990; Frakes, 1988; Fry, 2003 and Hemdal,
2003). The beauty of this theory is that because so many fish
are treated with copper at various stages of the distributional
chain from the reef to retail markets, it is easy to show
that exposure to copper has some effect on the onset of MHLLE.
But again, the opposite argument must be examined: why don't
all fish exposed to copper develop MHLLE? There is no easy
answer to that one, but first let's look at how copper might
be involved. Copper is a known immunosuppressant
(Noga, 2000). Theoretically, copper treatment could simply
help allow an infectious agent which causes MHLLE to gain
a foothold on a fish. Additionally, copper is thought by some
hobbyists to harm beneficial intestinal infauna that fish
need to properly digest their food and thereby absorb the
necessary vitamins from it (Fenner, 2001). It may be possible
that copper may play an indirect role in the dietary deficiency
theory. And lastly, all heavy metals, including copper, are
poisons that can build up in the tissues (Shimek, pers. comm.).
This could help to explain why some fish develop MHLLE while
others do not; the number of exposures of varying concentrations
resulting in vastly different "body burdens" of
specific heavy metals could be playing a role.
Stray Voltage and Ground Probes:
Of all the theories regarding MHLLE,
this is the one that I have the most trouble believing, and,
after subsequent readings by David Kessner, it would appear
my gut impression turns out to be correct. The phenomenon
that we aquarists refer to as stray voltage is actually capacitive
coupling; the so-called cure of using a grounding probe actually
causes the effect to occur. The abbreviated description
of this occurrence is that any electrical device in an aquarium,
be that of a heater, pump, etc., acts as a resistor. These
are sealed in plastic, glass, or some other nonconductive
material, in electrical terms - an insulator. Once the aquarist
places a ground probe in the water, another resistor is created
by completing the circuit and turning the water into a second
resistor. Two resistors separated by an insulator is capacitive
coupling and this allows electrons to flow out of the tank
through the ground probe. The point being, without the ground
probe, the circuit is not completed and no charges flow. Hence,
the "cure" for stray voltage and its impact on MHLLE
by the use of a ground probe is what causes the stray voltage
in the first place. Without the ground probe, there is no
Now, I am neither an electrical engineer nor some Radio Shack
technology buff. I am a fish geek. I apologize if my laymen's
explanation bothers some. If you are interested in reading
more, please make use of my listed references and delve into
the discussion on capacitive coupling, resistors, insulators,
induction and other things that aren't particularly interesting
to me. Otherwise, if you are like me, feel free to skip to
the next topic with the knowledge that stray voltage is nothing
to worry about with regard to your fishes' well-being.
While I may be making light of stray voltage and grounding
probes, I do not mean to discourage their use in general.
I am specifically referring to them only in the confines of
a discussion on MHLLE. Ground probes and GFI outlets should
be used in all aquariums, but not for the health of the fish.
They are for the fishkeeper's protection. Electrocution is
a distinct possibility, and a ground probe along with a GFI
outlet could save your life one day, so use them.
Lack of Natural Sunlight:
Some hobbyists and scientists hypothesize
that exposure to sunlight can help reverse MHLLE. Tom Frakes
cited information in his 1993 article that tangs affected
with MHLLE at Disney's EPCOT facility were simply transferred
from indoor displays to outside holding tanks on the same
central system with the same water, and later were noted to
have recovered. Hence, the conclusion that sunlight can cure
or prevent MHLLE. This makes sense coupled with the complete
absence of MHLLE in all wild reef fishes (Blasiola, 1990),
which are constantly exposed to sunlight. But it is possible
that sunlight could have had only an indirect effect. Perhaps
in the outdoor tanks the sunlight encouraged a different,
more nutritious growth of algae that was not able to grow
under the light of the indoor displays; maybe consuming this
improved diet is what actually reversed the MHLLE. Another
possible explanation is that this alga (if it existed) removed
excess nutrients and dissolved organics from the water. Depending
on the flow into and out of these outdoor tanks, it is conceivable
that their overall water quality could have been better than
in the main indoor tanks, because of the extra algae and the
sunlight. Plus, this was not a controlled study. It is possible
that the staff and methodologies of caring for the indoor
tanks was different than the people/methodologies involved
in caring for the outdoor display. Unless great pains were
undertaken to eliminate other variables, there is no telling
what other changes could have occurred and affected the outcome.
Overall, not enough information is given in this brief account
to fairly evaluate whether or not sunlight played any direct
role in the fishes' recovery.
There is a passing mention of a type
of tumor that can cause lesions similar to those seen in Blasiola's
1990 article. He states that some species of damselfish have
exhibited raised or eroded areas that resemble MHLLE on their
head, and that this was caused by a type of tumor that spread
from nerve fibers. Unfortunately, that is the extent of this
passage and no reference for further investigation is provided.
Along these same lines, I will add that I have seen some
wrasses, most notably the green bird wrasse (Gomphosus
varius) and lunar wrasse (Thalassoma lunare), develop
tumor-like lumps around their face after being in captivity
for extended periods of time. While wrasses are generally
thought to be resistant to MHLLE (Hemdal, 2003), I believe
it is possible that this is a different manifestation of MHLLE.
However, I will freely admit that this could be something
else entirely. At the very least, it is another abnormal,
mysterious aliment that seems to only afflict fish held in
captivity. As such, in my opinion, it warrants further investigation.
This is yet another instance of a
potential cause being mentioned briefly but not thoroughly
discussed. Fungal infections are mentioned in a list of factors
implicated in MHLLE in both Blasiola's 1990 and Frakes' 1988
articles, but without discussion as to why it was thought
that fungi may be the cause and without reference to this
possibility to follow-up on. Blasiola does state later in
the same article that he was unable to find "any evidence
of a fungal infection" in the fishes he had examined
that had the typical lesions associated with MHLLE, suggesting
that fungi do not likely cause MHLLE.
The Varner and Lewis paper (1991)
centered upon a viral infection as the possible cause of MHLLE.
They were able to isolate a reovirus-like agent from what
they describe as a moribund Koran angelfish (Pomacanthus
semicirculatus). For those readers who don't know what
moribund means (I had to look it up), it means dying, declining
in health or on its way out. To confirm their suspicions,
they exposed an otherwise healthy angelfish to this virus-like
agent and were able to elicit lesions similar to MHLLE. There
are two problems with this study. First, MHLLE is generally
not lethal (Michael, 2003), yet the fish from which they obtained
this virus was dying. Second, the study merely exposed healthy
fish to this virus, then later noted MHLLE, but did so without
a control group. Therefore, their conclusions are more than
a little suspect. They didn't, for example, keep a separate
but similar group of fish under the same conditions as those
in the test group, but without exposure to the virus, to ensure
that some other condition(s) that the fish were exposed to,
instead of the virus, didn't actually cause the MHLLE outbreak.
A control group is an extremely important part of the scientific
process, which they chose to omit for some reason that is
not clear to me. Because of this, it could be that the virus
is what killed the angelfish, but is not what initiated the
There are some who believe a parasite
in the genus Spironucleus causes this condition (Bassleer,
1996). Spironucleus is the correct name of this protozoan,
although many still use the name Hexamita when referring
to this condition in freshwater fish. So, it seems reasonable
that a similarly appearing condition could have a similar
causative agent. Additionally, Spironucleus has been
found in some marine fish (Blasiola, 1990), although no indication
is given that these same infected fish suffered from MHLLE.
According to this theory, the parasite infects the intestine
and interferes with its uptake of nutrients. This then is
alleged to cause stress and the resulting tissue loss characteristic
Also, in at least one other instance a marine tropical fish
was confirmed to be infected with another parasite that causes
digestive problems (Hoover et al, 1981). In this paper,
a Naso tang (Naso lituratus) was found to be infested
with Cryptosporidian parasites which caused the fish
to be emaciated from regurgitating its food and passing food
with its feces, which appeared to be completely undigested.
This fish did not exhibit the characteristic lesions associated
with MHLLE, although it did lose muscle tissue. The other
thing to note is that Naso tangs are generally thought to
not be susceptible to MHLLE (Hemdal, 2003). So it is difficult
to say whether or not this fish would have been able to develop
MHLLE lesions or if this emaciated appearance is simply another
form of this ailment similar to the atypical appearance of
Yellow tangs discussed previously.
I found one reference suggesting that
a dinoflagellate in the genus Amyloodinium could be
responsible for an outbreak of MHLLE that occurred at the
Newport Aquarium in Kentucky (Fry, 2003). The basic premise
is that fishes in a large display at that aquarium were developing
MHLLE. In this same display, a sponge was found to harbor
a dinoflagellate tentatively identified as belonging to the
genus Amyloodinium. One of the aquarium's interns began
an experiment to establish whether this dinoflagellate caused
the MHLLE. Unfortunately, this experiment suffered a series
of setbacks, which brings into question whether any results
can be drawn from it. For one, most of the fish in the experiment
were lost to a Marine Ich (Cryptocaryon irritans) outbreak.
Also, one of the other fish died due to a heater malfunction
and subsequent electrocution. So, while some of the fish experimentally
exposed to the Amyloodinium did exhibit MHLLE, there
was no way to determine whether any of the control fish were
still alive to verify the dinoflagellate, and not some other
variable, as the cause of the MHLLE. As such, there is no
way to draw any conclusions from this study.
One report I found theorized that
a bacterial infection might be responsible for a MHLLE outbreak
(Hemdal, 1989). In this particular instance, a fish was in
quarantine and because of a bad test kit, was exposed to a
rather high level of copper, 0.4 ppm, greater than a ten-fold
overdose. The error was discovered and water changes and activated
carbon were employed to reduce the copper concentration. But
the fish was still doing poorly, so it was transferred to
a different system. Approximately two months after its exposure
to copper, the fish developed a bacterial infection. The fish
was treated with antibiotics and recovered, but relapsed shortly
thereafter, necessitating a second course of antibiotics.
Again, the fish recovered, but soon developed the classic
appearance of MHLLE. The characteristic lesions developed
rather quickly. It was said that in two weeks the fish showed
erosion comparable to other fish that had been suffering with
this ailment for six months or more. But, in an unexpected
turn of events, as quickly as the condition appeared, it also
vanished without any subsequent treatments, or dietary or
Since the release of this report, its author has made a few
additional commentaries. For one, he regrets not obtaining
a histopathology report to back up his assertion that bacteria
were responsible for the MHLLE lesions. Also, he wonders if
the activated carbon, used to remove the overdose of copper
medications from the quarantine tank, played some role in
this outbreak. His current area of interest involves studying
the irritant action of activated carbon dust and its possible
effects in triggering MHLLE (Hemdal, pers. comm.).
But I am not sure that I am willing to dismiss Jay's original
inference. For one, Fish Tuberculosis (Mycobacterium marinum,
has been known to cause similar external lesions (Blasiola,
1990). Additionally, Noga briefly mentions in his book "Fish
Disease: Diagnosis and Treatment" that he has documented
cases of an acid-fast bacterial infection associated with
MHLLE. He suggests that this may be evidence that the disease
is a symptom of chronic stress in the afflicted fish, which
leads me right into the next possible cause.
Chronic Stress and Autoimmune Disease:
This is probably one of this most
interesting and novel ideas offered with regard to the causes
of MHLLE. The basic premise is that fish held under certain
conditions can be subjected to chronic stress and that due
to this chronic stress, their immune system does not function
properly (Bartelme, 2003a, b, c). This malfunction causes
the body's own immune system to seek out and destroy healthy
cells that it should otherwise be protecting. The author suggests
a variety of ways this might occur, and I encourage all to
read his works for further information. It simply would not
be fair to try to sum up in a paragraph or two Mr. Bartelme's
thoughts on this topic from his entire three part series of
articles, so please follow up with my references (Bartelme,
2003a, b, c) below to read the complete and thorough explanation
What I found most interesting about this theory is that it
ties together most all of the other theories of MHLLE's causes
(Note: there are at least a dozen other theorized causes.
Just about anything and everything has been blamed at one
time for causing this affliction.), groups them under
the general category of stress, or as an opportunistic infection
that thrives under stressful conditions, and then addresses
what to do about this "disease complex." The practical
application of these articles is in the recommendations Terry
gives for combating this ailment. The first part of the treatment
would be to eliminate or reduce any and all stress. This is
broken down into four broad categories: extreme changes in
the physical environment, animal interactions (such as predation,
aggression and competition), poor water quality (low pH, high
nitrate, heavy metals or dissolved organics) and human interference
(such as overcrowding). The second step is to improve the
diet as well as to add vitamin supplements and highly unsaturated
fatty acids (HUFA's) to the fishes' food. Third, improve water
quality via water changes and protein skimming while also
limiting the use of activated carbon just in case it plays
a role. And finally, he recommends enhancing the fishes' immune
function by adding beta glucan and garlic extract to their
food as immunostimulants.
Some people promote this fishkeeping
methodology as an alleged cure of MHLLE (Hildreth
& Paletta webpages). As such, it is worth reviewing
the theory behind this allegation and comparing its reasoning
against the theorized causes of MHLLE to see if there is any
correlation. Unfortunately, the online articles don't have
much to say about why or exactly how the system works. They
merely state that fish held in EcoSystem filtered aquariums
don't contract MHLLE, and fish afflicted with the syndrome
get better when placed in an EcoSystem filtered tank. While
their testimonials are interesting, it is hard to draw much
information from them other than that we should all run out
and buy EcoSystem's Miracle Mud!
(Disclaimer: The author does use Miracle Mud in his home
reef display, but does not work for this company or actively
promote this product. Additionally, the author also utilizes
a DSB, protein skimming and low stocking levels, as well as
regular large water changes, as part of his overall aquarium
Joe Yaiullo of the Atlantis Aquarium
was kind enough to share some information he received on treating
MHLLE. Some individuals at the National Aquarium in Baltimore
did small-scale testing of a drug commonly used to treat non-healing
foot ulcers in human diabetes patients. The drug goes by the
trade name Regranex or by its active ingredient, becaplermin.
The aquarium staff was having a problem with an Atlantic Ocean
surgeonfish (Acanthurus bahianus) that developed MHLLE.
They did the standard things: scraping to determine if some
pathogen was the cause, changing from their own homemade salt
mix to a high-quality commercial blend, providing better full-spectrum
lighting on a 12-hour photoperiod and reviewing and improving
the diet, all to no avail. After all these changes, the most
they had accomplished was to simply stop the disease's progression,
with only a very slight improvement in appearance.
It was at this point that they began the drug treatment.
The Regranex was applied topically twice per week for four
months. By fourteen weeks, the treated area was almost completely
healed. The most interesting part of this little experiment
was the control. They applied the drug to only one side of
the fish and that was the only side that healed.
The downside to this treatment is two-fold. For one, it does
not address this ailment's underlying cause(s); it treats
only the signs. Second, it is expensive and unavailable to
most. At approximately $500 per tube, it would be cost prohibitive
to most aquarists. The only people likely to afford this treatment
are those aquarists able to justify spending $100 per polyp
on Acanthastrea, Dendrophyllia or whatever is
the new flavor of the month.
After all this, I guess I should go
out on a limb and give my opinion as to the cause of this
syndrome. Well, I am going to go a bit farther than that.
I am going to say conclusively, once and for all, what causes
this condition. Are you ready? Here goes
Yes, captivity causes MHLLE. I say that jokingly, but there
is also some truth in this statement. As I said previously,
MHLLE has not been seen on wild fish on the reefs (Blasiola,
1990). We therefore deduce that it is obviously something
we, collectively as hobbyists, are doing or not providing
for our aquatic pets that causes this ailment. What exactly
that is will require further scientific experimentation
to definitively prove. Until then, I agree with the broad
recommendations of Terry Bartelme: reduce stress, improve
nutritional regime, add vitamins and HUFA supplements to the
diet, enhance water quality and also try beta glucan and garlic.
Those same things have almost always worked for me when I
have had an occurrence of MHLLE in the fish I care for, and
hopefully they will work for you.
If you have any questions
about this article, please visit my author forum
on Reef Central.
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Bartelme, Terry. 2003b. "Hypothesis
of Head and Lateral Line Erosion in Fish: What Really Causes
HLLE?, Part Two" Freshwater and Marine Aquarium Magazine,
September 2003, pages 88-92.
Bartelme, Terry. 2003c. "Hypothesis
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in Enhancing Immune Function, Part Three" Freshwater
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