this is a VERY informative article on Marine Head and Lateral LIne Erosion by Mr. Steven Pro (used with permission of course). I would like to thank Mr. Pro for allowing it to be used on this forum, as i think it could seriously help people to know what to look for to diagnose thier fish better. As you all know i just aquired a Red Sea Sailfin Tang that i was told got "beat up", but it did in fact have Marine Head and Lateral LIne Erosion. This article is really what helped me to uproperly diagnose the fish ...

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 of MHLLE.

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 this article.

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.

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.

Susceptibility:

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.

THEORIZED POTENTIAL CAUSES

Dietary Deficiencies:

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.


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.

Activated Carbon:

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 cause.

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 stray voltage.

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.