Viral Gill Disease


Many folks will remember the funzies we had last year with a potent bug variously called:
Bacterial Gill Disease (BGD)
Viral Gill Disease (VGD)
Fulminate Gill Rot (FGR)
Necrotic Gill WhatChaMaCallIt (NGWCMCI)
Where this bug hit, it always caused staggering losses. Entire ponds were wiped clean in a matter of days. Whole collections were lost. Some very "advanced" ponders who generally would laugh at most of the common bugs suffered staggering losses. Having played with this bug myself and having been buried in piles of dead fish for more than 4 months, I can tell you its a real mover. A few folks deny that it exists at all, but I'm here to tell you otherwise. Fortunately we're seeing only a few scattered cases emerge this year, but it's far from certain this bug is really gone. We might be seeing the tail end of this disease process... or we might be seeing the build-up of a massive epidemic. All speculation and political posturing aside, nobody knows for sure. All we can do is wait, load our guns, and pray we never have to use them.

In the meantime, a few folks have been tracking this disease and working on treatment options. In the past this disease was considered completely untreatable. We think we've made substantial progress in this area, but understand our work has been "meatball" to put it mildly. Due to the fast-moving nature of the disease, just getting infected samples for culture often involves jumping through hoops and all sorts of monkey-motion. Many times these "infected" fish turn-out to have nothing more than a bad case of flukes, ick, or other common pathogen. But in other cases we've seen a complete lack of traditional bugs and still witness massive morts. These are the cases we've lived for.
Where actual cases of VGD were found to exist, we had a better than 70% recovery rate if the treatment was applied immediately upon onset. It must be stressed that the purpose of this paper is to bring to light the problem, relate its symptoms, and disclose certain treatment protocols we've developed to combat it. This paper is not to be taken as a call to panic. It is my personal opinion that 99% of all the ponders in the world will never have need of this information and can view this paper as a technical curiosity. But for those who are visited by this bug, knowledge is indeed power. We have demonstrated again and again that this disease can be stopped if caught early, treated aggressively, and the procedures herein followed carefully. To those folks who believe they have this bug: It must be stressed that 95% of the "Viral Gill Disease" cases we have seen turned-out to be something else after careful analysis. Anyone who looks at a pond full of sick fish and pronounces "Yep! They've got VGD!!" is completely and utterly milking without a bucket. As of this writing, VGD is still rare. It is only when all other avenues of explanation for epidemic losses have been exhausted that the thought of VGD should be seriously entertained. If you think you have VGD, contact any of the individuals at the end of this document. Finally, a cautionary note on the treatment protocols described herein: Because of the nature of this disease and due to the lack of any successful "scientific" effort within the koi community, we have resorted to the piscine equivalent of "battlefield medicine". The treatments we propose herein, effective as they are, are most definitely of a last-ditch nature. These treatments can kill fish. The dosing is absolutely critical. The difference between killing the bug and killing the fish is often only a 5% or 10% difference in dosing. These protocols are not for the chemically-disinclined or feeble-minded.
Do not begin these protocols until all other possibilities have been systematically exhausted and you are left with no choice. This is clearly a case where the cure can be as hard on the fish as the actual disease.
I would like to extend my personal gratitude to the author of this document, Spike Cover, for his continuing efforts to effect a cure as well as to Doc Conrad and Duncan Griffiths for their support, testing, and refining of the therapies.

General conditions, Fortunately this disease has not become wide spread this year (as of June 2000). However sporadic cases have been reported this Spring in both Britain and the US. Two variations of the disease have been observed. One seems to activate at a temperature in the mid-70s F, the other about 10F cooler. The warm water variation seems to run its course in about two weeks, i.e., most of fish that are going to die, do so within about two weeks of the first death. Deaths are slower but steady and ongoing in the cold-water variation, lasting over a month or so. The disease has almost always occurred as the pond water is moving into a particular temperature range, i.e., 65F to 78F. Both variations are more prevalent as the temperature is on an upward trend. Fish exposed to the disease become symptomatic about 2 weeks after first exposure if the temperature is in the susceptibility range of 65F to 78F. Injectable antibiotics of any type seem to have no effect on the progress of the disease (which suggests the pathogen is viral in nature).
The disease frequently occurs within a few weeks of the introduction of new fish.
Also frequently (but not always), the new introductions are the first to die.
Symptoms include:
The affected fish exhibit a general listlessness (much more so than usual). Some fish, the ones that are affected the worst, begin hanging in the water; usually head down and not swimming much. This is also a symptom of gill flukes and other parasites that affect the gills. Microscopic examination should be employed to eliminate parasites as the cause of the gill function impairment.
Affected fish collect near a source of water that's well oxygenated.
Some fish having a blotchy appearance on their skin (usually a reddening)
Some fish having patches on the body that are rough to the touch like sandpaper and like the mucous layer is gone in that area.
Some fish may have patches of what appears to be skin/scales sloughing off - particularly on the head.
Some fish may exude a heavy gray mucus that is unevenly distributed about the body.
On inspection, the gills of most fish appear necrotic (dead tissue usually appearing whitish or tan in streaks or patches). However, a small percentage die w/o obviously necrotic gill tissue or other external lesions.
The eyes become very sunken in the advanced stages of the disease.
As disease advances, 5% to 10% of the fish die each day - less in the cold-water version.
The disease usually hits the larger fish hardest and first. They lay on the bottom with their pectoral fins spread (other fins clamped) as if to keep from rolling over.
Not all fish moralities are alike in the initial stages. A small number die with no signs of gill damage and no external lesions. However, as the disease gathers momentum, gill degeneration becomes rampant.
Pathology reports on diseased fish suggest that the gill damage is secondary to the viral infection with the virus weakening the subject to such a degree that it additionally falls pray to opportunistic pathogenic bacteria in the environment.
It should also be noted that while small numbers of ecto parasites may be present upon microscopic mucus examinations, they are typically deemed to be not significant contributors to the onset of the disease. In some cases, there may be no ectoparasites present.

Treatments: Chloramine-T ("C-T") (Developed by Roark and Dr. Erik Johnson in 1999 and revised through additional testing by Roark 1999-2000.
This is the most completely tested and successful of the treatments. Roark recovers 70%-80% of affected fish using this treatment if caught early.) Theory of the chemical treatments (C-T and PP): The virus weakens the immune system and its ability to combat the opportunistic bacteria that invade the fish in its weakened condition. The bacterial infections are likely secondary to the viral infection. The chemical treatments kill most of the bacterial on the fish and in the water. Additionally, Roark theorizes that C-T reaction products enter the fish's system thru the gills (one of the most affected organs) and passes out of the fish via the kidneys and the liver (two other organs typically affected by the disease). Further, if the secondary bacterial infection has infected the liver and/or the kidneys, the C-T may help kill the bacterial invaders in those organs. Day 1 - Take the fish off their food. This disease affects the kidneys and liver and they'll need these organs untaxed by wastes just to survive. Treat the pond (including all the fish in it) with potassium permanganate ("PP") sufficient to keep the water pink/purple for 6 hours (1 to 3 ppm depending on the strength of the fish) then immediately move all fish to a quarantine tank if possible and treat with about 25 ppm equal; to 9.2 gm per 100 US gal. of C-T for 4 hours (see the following Note).
Then do an immediate massive water change (80% or more). Note: that the therapeutic dose is only slightly less than the lethal dose, and these doses are very greatly influenced by pH and the water hardness. Note also that the above dose is perfectly acceptable with a pH of 8.0 to 8.5. The dosing table at
Note: J. Spangenberg's article on flukes and C-T. See Table 1 below which can be used as a rough guide but Roark found it was too conservative in dosing levels for this disease. He recommends that the level be raised to where the fish begin to tox-out, then do a 15-20% water change to dilute the dose a bit. If you did your guessing right, they'll still be slightly toxed for the duration of the treatment, but they'll make it. Again, this treatment is not for the meek.

Table 1: Doses of Chloramine-T with respect to water pH and hardness

Soft Water Dose (mg/L)
Hard Water Dose (mg/L)

From the above chart, it becomes obvious that treating at a pH of 8.0 or above is desirable as the hardness of the water becomes insignificant. Note: adding baking soda to water tends to buffer the pH to 8.4.

Day 2 thru 5 - Do nearly the same C-T/water-change treatment except reduce the C-T dosage by 10% to 15% of the rate determined on Day 1. If the fish show signs of overt toxicity, execute a small water change.

Day 6 thru 10 or 12 - Once the fish are on the mend, don't hesitate to run 1 ppm PP for 6 to 8 hour a day if you think you need to "clean-up" the water and keep it sterile.

Do not feed the fish to soon after the treatment as the kidney an liver will be working overtime clearing up the mess left from the virus/bacteria and do not need the extra load from feeding. Wean them back to food slowly and lightly after 10 days or so feeding high quality food (such as ShoKoi Impact) sparingly. After treatment, if you lose fish due to massive gill damage, there is an experimental protocol Roark has used which doses a 3% H2O2 solution at 0.2 ml per US gallon every 12 to 18 hours combined with a one-time "standard" dose of methylene blue ("M-B"). The H2O2 provides "chemical" oxygen support (1-2 ppm O2 gain) and also tends to kill some bugs at the same time, while the M-B provides an alternate means of getting O2 into these fish. M-B is used here as an oxygen transport mechanism. This is a poorly understood effect but it works and indeed is documented in some of the (non-koi) literature.
Use it only if you have clear signs of mortality due to impaired gill function. Do not use M-B in combination with the PP discussed above for days 6 thru 10 or 12. A water change to eliminate the M-B prior to treatment will be required.
AlsoNote that excessive use of H2O2 as an oxygen support mechanism is to be discouraged. H2O2 is a oxidizer which, if overused, will contribute to gill failure and necrosis. Note too that the use of salt is a good idea, but it is neither reasonable or necessary to exceed 0.3% salinity with this disease. This salt level is used to help relieve the osmotic pressure difference the fish must contend with between its body and the surrounding water, not for any real bug-killing effect. It is also useful to run a 5% to 10% (of total salt dose by weight) mixture of *potassium* chloride. This further unloads the fish and provides potassium (a secondary electrolyte) that may help with stress. Also note the above dosing rates are for US gallons. (Imperial gallon = approx 1.2 US gallons)

If the local tap water temperature is lower than 65F, it is suggested that a two-tank system be used so that the water in the holding tank and filter can be left intact and heated while treatment is under taken in the second tank. Extra O2 should be placed in the treatment tank during the treatment. After the 4 hour treatment is complete, the fish can simply be placed back in the untreated water of matched temperature. This effects a 100% water change. The treatment tank can then be emptied, filled and heated to the holding tank temperature in preparation for the next day's treatment. Warming the water to 70 to 75F is desirable because very little tissue regeneration takes place below about 65F.

Heat Theory of heat treatment:
Many viruses have temperature limits beyond which they are not active or will deconstruct. Many bacteria are also adversely affected by high temperature. When the temperature is raised above the upper threshold of the virus' preferred range, the koi's immune system is better able to cope with the virus and many of the pathogenic bacteria as well. Heat treatment would need to be done in the early stages of the disease since the oxygen saturation level of water is lower at higher temperatures making it more difficult for compromised gills to absorb adequate oxygen. It has been reported that placing the koi in water at a temperature of 30C (86F), will aid the fish in beating the disease (this bug does not like heat). This was reported on the KoiVet web board in December of 1999. This post claimed that the Israelis had intentionally infected their koi with the viral disease and then put them in 30C water where many recovered w/o any further treatment. Potassium Permanganate There have been several reports of fish being cured with potassium permanganate. The reports indicated that the treatments were at 1 gram/100 gallons for 4 hours for 5 consecutive days, then repeated again after 3 days
Contributors The following persons were instrumental in developing this document and treatment methodology:
Name EMail Contribution Area Roark Chlor-T, M-Blue / H2O2 protocol development
Griffiths.D Chlor-T, M-Blue / H2O2 protocol validation
Conrad, R. Chemistry Advisor
Cover, S. Disease history,
Document author Copyright 2000 by S.Cover, D.Griffiths, R.Conrad and Roark. All Rights Reserved. Email comments to: Page rev 1.10 of 28JUN2000