This article aims to provide our members with a summary of the available information about the Koi Herpes Virus in plain English. If you were not at our May General Meeting, the members voted in favour of the Club supporting the release of the Koi Herpes Virus (subject to the Government adequately funding the clean-up of waterways of dead and dying Carp, habitat restoration and restocking of native fish). This article will hopefully reassure members about any concerns they may have about the safety of the Koi Herpes virus.
Releasing a foreign virus into our waterways is not something that should be done lightly. In addition, there are only three occasions where the use of a virus to control a pest species was successful. Two involved the release of the Myxoma Virus and later the Calicivirus to control rabbits in Australia while the third was the release of feline panleukopaenia virus on the sub-Antarctic Marion Island to eradicate feral cats.
However, we all know what happened in 1935 when the Bureau of Sugar Experiment Stations (now Sugar Research Australia) introduced Cane Toads in an attempt to control Cane Beetles. As one of the key stakeholders who stand to benefit from the release of the Koi Herpes Virus, we in the recreational fishing community have a responsibility to educate ourselves about the virus and make sure we do not unwittingly become complicit in the next environmental disaster to hit Australia. This includes checking out the facts for ourselves rather than simply accepting the assurances provided in the public awareness campaign about the virus.
Assuming the virus is successful in controlling Carp in Australia without endangering our native fish species, a lack of public awareness about the virus can still be counter-productive. A number of successful government initiatives and scientific advances (such as immunisation and water fluoridation) suffer from myths spread within sections of the community, either due to a lack of knowledge or by misinformation spread by special interest groups.
At this early stage, it is difficult to predict what these might be although one that easily comes to mind is that some sections of the community might blame the Koi Herpes Virus for any future fish kills. Having a greater understanding of the Koi Herpes Virus will ensure the recreational fishing community do not unwittingly spread urban myths and unsubstantiated rumours about the virus.
The approach I took to researching and writing this article is similar to a literature review.
First, I did a google search on topics related to Carp control and the Koi Herpes Virus and downloaded over 30 academic journal articles, fact sheets and webpages from government and non‑government organisation websites, a few web pages from aquarium websites, and some online media articles. Twenty-two of those articles and web pages (which I loosely refer to as ‘the literature’) ended up being used for this article. The remainder were not directly relevant for this article but may get used for a future article on the topic of Carp control.
Second, I extracted the contents of the literature and reorganised them according to the questions posed in this article. Where the content of the literature was consistent in response to a particular question, I simply summarised the information with little or no qualification. Where the literature was not consistent on a particular question, then I highlighted the different views expressed in the literature.
Unlike a proper literature review, I have only looked at what the weight of the literature says on particular topics about the Koi Herpes Virus. A proper literature review will also assess the quality of the literature by evaluating and the critiquing its contents. This second step is beyond my level of scientific literacy. In addition, I only accessed material that was available on the internet. A proper literature review would require a visit to the local university library to look up academic journals not available on the internet.
I have attempted to reduce the amount of scientific jargon as much as possible. For example, the Koi Herpes Virus is a double stranded DNA virus but I only mentioned in the article that it is a DNA virus. The fact that the virus was a DNA virus is relevant to answering questions about whether the virus could mutate and some further information about DNA and RNA was needed to answer that question. However, where the scientific information was not relevant, this was not included. For example, I did not mention that the virus was a double stranded virus as it appeared to have no direct relevance to the questions in this article.
Finally, this article is not meant to be an academic dissertation so there will not be any footnotes and there will only be a few references provided. However, the hyperlinks to the literature used for this article can be found at the end. Any junior anglers wanting to use this article for a school assignment are encouraged to check the hyperlinks instead. I also have a comprehensive set of notes with references which I am willing to share with Club members on request.
The Koi Herpes Virus is also known as Cyprinid herpesvirus 3 or CyHV3. CyHV3 belongs to the family Alloherpesviridae (which includes fish herpesviruses). CyHV3 is closely related to Carp Pox Virus (Cyprinid herpesvirus 1; CyHV1) and Goldfish Hematopoietic Necrosis Virus (Cyprinid herpesvirus 2; CyHV2). For the purposes of this article, the virus will be referred to as CyHV3 and the disease caused by the virus will be referred to as Koi Herpes.
Viruses are infectious agents that can only replicate inside living cells of other organisms. Viruses fall into two broad categories – DNA viruses and RNA viruses. CyHV3 and other Herpes Viruses are DNA viruses, meaning it uses DNA as its genetic material to replicate itself. In contrast RNA viruses use RNA instead.
There are two known strains of CyHV3, referred to as the European strain and the Asian strain. There are seven different variants of the European strain but only two variants of the Asian strain. The European strain is found in Europe, Israel and North America. The A1 variant of the Asian strain is found in all Asian countries where CyHV3 is present, while the A2 variant is only found in Taiwan and Indonesia.
It is thought that the presence of seven variants in the European strain of CyHV3 compared with only two variants of the Asian strain indicates the virus has been present in Europe longer than in Asia.
The analysis of the European and Asian strains of CyHV3 show that both strains evolved independently of each other from an earlier virus, suggesting the CyHV3 was not introduced into Europe from Asia and vice versa. Identifying the earlier virus will help us understand the origins of CyHV3 and help predict the probability of the virus mutating in the future.
The first Koi Herpes outbreak was noticed in cultured common Carp in Israel and the USA in 1998. CyHV3 was also detected in preserved tissue samples taken from a mass Carp mortality in the UK in 1996. The virus has since spread to over 30 countries in Europe, Africa, Asia and North America. CyHV3 appears to spread by the transfer of ornamental Carp which, which then spreads to both domestic and wild populations of Common Carp in those countries.
Once the virus enters a country, it can spread rapidly. For example, CyHV3 was first detected in Japan in May 2003 and spread to 24 of its 47 prefectures by May 2004. One month later, it spread to a further 14 prefectures.
Mode of transmission
CyHV3 spreads via "horizontal" transmission or from an infected fish to an uninfected fish. This can lead to a rapid spread of the virus when Carp are crowded or spawning. The virus can also spread by "vectorial" transmission or by contact with virus in the water or mud, fishing gear and other items contaminated with the virus. However, there appears to be no evidence of "vertical" transmission or via an infected mother Carp to her eggs.
The virus enters the Carp via its body surfaces and gills although some of the earlier literature suggests it may also enter via the Carp's guts. The virus replicates in the Carp's gills, and is shed from the Carp via its body mucous, gills, faeces and urine. Depending on the water temperature, the virus can survive up to four hours in the water until it finds its next host.
All the literature on CyHV3 is in agreement that water temperature is a key factor in determining the severity of a Koi Herpes outbreak. Most of the literature is also in agreement that water temperature is a bigger factor than the concentration of virus in the water. Studies have shown low concentrations of the virus at the optimum temperature range will trigger severe outbreaks of the disease, resulting in high mortality. However, there is variation in the literature over what that optimum temperature range is. The various ranges contained in the literature falls somewhere between 13°C and 30°C and studies show Carp will survive infections outside that range. Studies also show that the virus can survive up to four hours outside a host fish in water temperatures of 23°C to 25°C.
Colder temperature and timing of infection
The literature agrees that timing of infection is also important. Firstly, some studies show that the virus becomes dormant under colder temperatures. Fish infected under cooler temperatures for up to 60 days will survive but can still infect other fish. However, shifting fish to higher temperatures within 30 days will trigger illness and death as the Carp's immune system, which has been suppressed by the colder temperatures in Winter, cannot reactivate in time to keep up with the virus' ability to replicate itself.
Secondly, while the literature agrees that outbreaks are most common in Spring and Autumn, some literature also suggests Carp are more vulnerable to infection in Spring. This is because their immune system is suppressed by the lower temperatures in Winter and stays suppressed as spawning commences.
- Damage to gills with red or white patches
- Damage to skin such as lesions, discolouration, sores or loss of skin.
- Sunken eyes
- Notch on the nose of the fish
- Excess mucous at early stages of the disease
- Loss of mucous at late stages of the disease (a couple of articles describe the skin as feeling, "rough'', "dry" or "like sandpaper"
- Internally, organs may be damaged, enlarged or discoloured
Sick fish also display abnormal swimming (slow or lethargic swimming at the surface, erratic or uncoordinated swimming) and may be seen gasping for air. One article notes that while this may appear like Carp basking at the surface, "... sick fish won’t spook away as vigorously as a healthy fish or at all."
Some journals and articles also report that the disease leads to secondary bacterial or parasitic infections.
There is a bit of variance in the literature as to how long it takes for death to occur. It ranges from ‘24 to 48 hours after onset of symptoms’ to ‘within 25 days of initial infection’. It appears that water temperature is a key factor in determining how quickly the Carp will succumb to the virus after infection.
A number of journals and articles report mortality rates of 70% to 100% of Carp in overseas outbreaks (both in wild and domestic populations of Carp) and in laboratory studies. A number of articles also state that CyHV3 affects Carp of all ages and sizes and that Australian Carp are highly susceptible.
The literature shows that mortality rates will depend on the concentration of the virus, water temperature, and the size/age of the Carp. The presence of other viruses and Carp-Goldfish hybrids is also relevant but this will be addressed later.
Laboratory tests done at different temperatures between 13°C and 30°C are said to have resulted in high mortalities or even 100%, even at low concentrations of the virus. Tests showed no mortality outside that range.
However, it might be useful to look more closely at how those tests were carried out as other studies have shown that older or larger Carp have lower mortality rates. For example, overseas tests on Carp of 2.5 grams to 6 grams (or 1-3 months old) resulted in 90% mortality while tests on 230 gram Carp (or 1 year old) only resulted in 56% mortality. Other tests showed that fish under one cm were not susceptible to the virus.
Tests carried out on Australian Carp (reported in McColl KA and Crane MStJ (2013), Cyprinid herpesvirus 3, CyHV3: its potential as a biological control agent for carp in Australia, PestSmart Toolkit publication, Invasive Animal Cooperative Research Centre, Canberra, Australia.) resulted in lower than expected mortalities: 64% for bath infected Carp and 67% for Carp injected with the virus. In addition, only 40% of mature Carp infected with CyHV3 died. Some of the Carp that survived infection were Carp Goldfish hybrids, which will be discussed later.
It is difficult to reconcile the results of tests carried out overseas on Carp of different ages and the tests reported in McColl & Crane (2013) with claims of 70% to 100% mortality rates, let alone claims of ‘Carpageddon’ when CyHV3 is released into Australia. However, the public awareness campaign promoting the release of CyHV3 in Australia is unambiguous in predicting high mortality rates when the virus is released. And presumably, a well briefed Deputy Prime Minister would not use colourful language such as ‘Carpageddon without sound evidence when announcing the proposal to release CyHV3. Hopefully, that evidence includes conclusive tests done on Carp weighing between 1 kg and 10 kg.
The literature appears very unambiguous that CyHV3 is specific to European Carp and Koi. That does not mean other fish cannot be infected by CyHV3 but tests carried out on over 20 non-Carp species indicate only Carp and Koi will become sick and die as a result. Carp-Goldfish hybrids can also become sick and die from the virus but at a much lower rate.
Those tests generally involve placing fish in water contaminated with CyHV3 ("bath" infection) or injecting the virus into the fish ("intraperitoneal" infection or IP infection) and then observing the fish for signs of illness and later testing tissue samples for the presence of the virus. Some experiments also place infected fish with Carp to see if they transmit the virus to Carp.
Some tests have found the presence of CyHV3 in the tissue of some species (including Goldfish, Sturgeon, Tench, Crucian Carp, Grass Carp, shrimp and swan mussels) exposed to the virus but the literature is divided over whether the virus was replicating in the tissue of those species. The literature also appears divided over whether some non-Carp species such as Goldfish can transmit the virus to Carp.
It appears that Goldfish are unaffected when exposed to CyHV3 but there is debate whether it can transmit the virus to Carp. The literature is inconclusive on whether the virus will replicate in the tissue of Goldfish.
It appears that Carp-Goldfish hybrids are susceptible to CyHV3 but are more resistant to the virus than Carp. Some studies suggest the mortality rate of Carp-Goldfish hybrids are similar to Carp mortality rates, while others suggest it is as low as 5%. The lower than expected mortality rates for Carp exposed to CyHV3 reported by McColl & Crane (2013) was blamed on the sample being contaminated with hybrids. It is estimated that Carp-Goldfish hybrids only make up 3% of the Carp population in the Murray Darling System. If this estimate is correct, then the presence of hybrids should not affect the release of CyHV3 in Australia to control Carp.
Native species and Rainbow Trout
The literature and public awareness campaign is unambiguous in claiming that CyHV3 will not affect Australian native species such as Murray Cod and Golden Perch. However, the results of only one of the tests carried out on native species appear online. Those results were reported by McColl & Crane (2013) and appear to confirm that the virus does not affect Murray Cod, Golden Perch, Silver Perch, Galaxias and Rainbow Trout. Those tests were carried out by bath infecting and IP infecting each species and comparing them with uninfected control group of those species. Carp were also bath and IP infected as part of the experiment so that the effect of the virus on Carp and non-Carp species could be compared.
However, whether you accept those results will depend on your levels of scepticism or cynicism. Those tests did not result in a tank full of Carp going belly-up and tanks full of native fish remaining alive and healthy at the end of the experiment. The results of the experiment on Carp and a selection of native species and Rainbow Trout were as follows:
- 64% of bath infected Carp and 67% of IP infected Carp died
- Dead or dying fish showed symptons of Koi Herpes and CyHV3 virus was detected in tissue samples
- 40% of mature Carp died
- 35% of bath infected fish and 55% of IP infected fish died
- No signs of Koi Herpes symptoms on dead or dying fish although a few fish had lesions which might have been due to Epitheliocystis (a Chlamydia like disease that affects both freshwater and saltwater fish)
- Very low levels of CyHV3 detected in the tissue of 22% of IP infected fish that had died and it is believed that those levels were residual traces of the virus left over when injected into the fish
- CyHV3 not detected in bath infected fish that died
- Problems in temperature control in experiments led to a number of Cod becoming sick and had to be euthanised
- 22% of bath infected Cod died
- A higher percentage of uninfected Cod in the control group also died
- No signs of Koi Herpes Virus symptoms
- CyHV3 was detected in very low level in only 2 out of the 15 dead and dying Cod and it is thought that this was due to contamination from the work area when conducting the experiments
- High mortality rates but the control group had higher mortality rates than infected fish
- No sign of Koi Herpes Virus symptoms
- CyHV3 was not detected in tissue samples taken from the dead fish
- Not clear what happened here but:
- 6 fish (27%) died 23 days after IP infection and it appears the rest (100%) died after 25 days
- No explanation for why 100% of Rainbow Trout died other than 'there was a severy episode of mortality on the last two days of the experiment'
- 40%-45% of bath infected Rainbow Trout died
- CyHV3 was not detected in tissue samples from dead bath infected Trout
- CyHV3 was only detected in one of the IP infected Trout - that fish died one day after infection which is too soon to be attributable to Koi Herpes and the virus detected was probably a residue from IP infection.
- No signs of Koi Herpes symptoms
- Appears that the experiment ran into difficulties keeping the Galaxias alive
- Galaxia mortalities in the control group were much higher than the Galaxias in the infected group
- CyHV3 was not detected in tissue samples taken from dead bath infected fish
- No signs of Koi Herpes symptoms
In a nutshell, the tests reported by McColl & Crane (2013) concluded that, despite the large numbers of dead native species and Trout, CyHV3 do not affect native species and Trout because those fish did not display symptoms of Koi Herpes nor was the CyHV3 virus detected in their tissue samples. The unstated assumption is that those fish died from other causes.
It would have been far more reassuring if the native fish remained alive and healthy. Very little explanation was offered on why such huge numbers of native fish died during the experiments. Such explanations would help sceptics accept the findings of the experiment.
It would be helpful for anglers if details of all experiments on native species and trout were available online. In addition, it would be useful to know experiments were conducted on other species including Australian Bass, Trout Cod, Mary River Cod, eels, other species of Perch (such as Spangled Perch), catfish, mullet, Rainbow Fish, Sunfish, Blue-Eyes, Gudgeons, Gobies, and Hardyheads.
Since writing this artice, I subsequently found this blog by Dr Ken McColl on the CSIRO website which states:
It has been shown to pose no danger to 13 native species such as Murray cod, various species of perch, eel and catfish, as well as a crustacean (yabbies) and a non-native fish species, the rainbow trout. Our work has shown that there are no clinical or pathological changes in these non-target animals, nor is there any evidence that the virus multiplies in these species.
Chickens, mice, frogs, turtles and water dragons have also been tested as representatives of a wider community of birds, mammals, amphibians and reptiles. Again the virus has shown no effect on them which also makes us confident that it won’t affect that other major group of mammals – humans.
Other overseas species
The literature reports that American Silver Perch, Nile Tilapia, Silver Carp, Giant Gourami, Indonesian Catfish, Siamese Catfish, Golden Shiners, and Flathead Minnows are not affected by CyHV3. The literature is divided on whether Grass Carp, Crucian Carp, Russian Sturgeon, Atlantic Sturgeon, and Tench can be asymptomatic carriers of CyHV3.
The probability is low. Given that CyHV3 presumably mutated from an earlier virus, this might appear to be a bold statement. Admittedly, it is difficult to say with certainty how low that probability is until more is known about the origins of CyHV3. However, there are a few reasons why it can be regarded to be as a low probability.
DNA viruses are more stable and less prone to mutation
CyHV3 and other Herpes Viruses are DNA viruses, which are more stable and less prone to mutations. In contrast, RNA viruses (such as influenza viruses and HIV) are highly unstable and frequently mutate. Explaining in plain English why this occurs is rather challenging and requires a little understanding of the nature of viruses.
Viruses are infectious agents that cannot replicate outside a host cell. To survive and replicate, a virus must penetrate a host cell, reproduce itself within the host cell and avoid the immune system of the host organism. DNA is an organic molecule containing genetic blue prints. DNA viruses use its own DNA to hijack the DNA of the host cell by rewriting the genetic blue print. RNA in the host cell reads the rewritten blue print, causing the host cell to replicate the virus. Because the host cell’s DNA has been rewritten, it will correct any mistakes in virus replication to prevent virus mutations. On the other hand, RNA viruses skips the rewiring of the DNA and instead hijacks the host cell’s RNA to reproduce itself. Without the backup of the genetic blue print rewritten in the host cell’s DNA, mutations in RNA viruses are very common.
No evidence of mutation occuring in CyHV3
While DNA viruses can mutate, there is no evidence of KyHV3 mutating and jumping to other species in any of the 30 countries it is found since it the virus first appeared in 1996.
No evidence that closely related Cyprinid Herpesvirus have mutated either
There is also no evidence that two closely related viruses, Carp Pox Virus (CyHV1) and Goldfish Hematopoietic Necrosis Virus (CyHV2), have jumped species either. Carp Pox Virus was first discovered about 400 years ago while Goldfish Hematopoietic Necrosis Virus was first observed in 1992.
...and what about those rabbits?
The Myxoma Virus was introduced in 1951 and the Calicivirus, which is an RNA virus more prone to mutations, was introduced in 1995 (albeit accidentally) to control rabbits. There is little evidence that the Myxoma Virus and the Calicivirus have mutated since they were introduced.
There was not a lot of information available on the internet on whether there is a cure for Koi Herpes. There appears to be no antiviral drugs available but a few aquarium sites claim that sick Koi can be cured by slowly increasing water temperature to 30°C. This is consistent with research that shows Carp will survive an infection by CyHV3 at 30°C or higher although it is unclear whether this treatment actually rids the fish of the virus.
One aquarium website claims that Koi and Carp that recover from Koi Herpes following heat treatment become virus free. Other journals and websites are of the view that such fish may remain infected for life but resistant to disease. It is also possible such fish pass on that resistance to their young through the yolk sac.
The Israelis use a similar method to make Carp resistant to the virus. They expose 3-month Carp and Koi to CyHV3 for 2-3 days at 23˚C and then transfer them (just before the fish develop Koi Herpes symptoms) to water heated at 30˚C for 30 days. The Israelis claim that this method can reduce mortality from a Koi Herpes outbreak from 80%-90% to 40%.
Heat treatment of sick fish can be counterproductive as it can encourage opportunistic infections from other viruses and parasites.
The Israelis have developed a "live attenuated virus" vaccine. A live attenuated virus vaccine uses a live virus that has been altered to make it less harmful (for example the Measles Mumps & Rubella vaccine). However, this vaccine only provides short term protection (around eight months) and there are concerns that the attenuated virus can revert to its more harmful form.
Could Carp in Australia already have a natural immunity to CyHV3 due to the presence of other viruses in our waterways? Back to contents
The effectiveness of CyHV3 in controlling Carp in Australia might be reduced if Carp have built a natural immunity as a result of being exposed to other viruses. As stated earlier, there are two similar Cyprinid Herpes virus being Carp Pox Virus (Cyprinid herpesvirus 1; CyHV1) and Goldfish Hematopoietic Necrosis Virus (Cyprinid herpesvirus 2; CyHV2).
It appears that CyHV1 and CyHV2 may be present in Australia but it appears this has never been scientifically confirmed. McColl & Crane (2013) reported that tests on 849 Carp in Australia failed to detect the presence of CyHV1, CyHV2, CyHV3 and other possible unknown Cyprinid herpesviruses.
Only a handful of articles touched on this subject but all those articles stated unambiguously that CyHV3 is not an infectious animal disease that can be transmitted to humans (or "zoonosis"). According to one of those articles, there is no evidence of infection by humans who handled diseased fish.
In addition, the European Commission (European Commission, Health and Consumer Protection Directorate-General, Scientific Committee on Animal Health and Welfare, 2000. Assessment of zoonotic risk from Infectious Salmon Anaemia virus) has found no evidence for any fish virus causing disease in humans.
However, it is never wise for humans or pets to consume any sick or dying fish.
The following webpages, fact sheets, online articles, and academic journal articles were used to compile this article. The hyperlinks were correct as of 28 May 2016. In addition, I have since come across a blog on the CSIRO webpage that has a similar Q & A segment on CyHV3. I am hoping to get in contact with the author of that blog to see if I can get further information about tests on Carp and native species in Australia in the near future.
Hartman, K.H., Yanong, R.P.E., Pouder, D.B., Denise Petty, B., Francis-Floyd, R., Riggs, A.C., and Waltzek, T.B. (2013, April). Koi Herpesvirus Disease (KHVD), Fact Sheet VM-149. School of Forest Rescources and Conservation Program in Fisheries and Aquatic Sciences and the Department of Large Animal Clinical Sciences (College of Veterinary Medicine), Florida Cooperative Extension Service, Institute of Food and Agricultural Sciences, University of Florida.
McColl, K., Cook, B.D., Sunarto, A. (2014). Viral biocontrol of invasive vertebrates - Lessons from the past applied to cyprinid herpesvirus-3 and carp (Cyprinus carpio) control in Australia. Biological Control. 72: 109–117 (This article is highly recommended, although a fee is payable to download a copy of this article)
Kurita, J., Yuasa, K., Ito, T., Sano, M., Hedrick, R.P., Engelsma, M.Y., Haenen, O.L.M., Sunarto, A., Kholidin, E.B., Chou, H., Tung, M., de la Pena, L., Lio-Po, G., Tu, C., Way, K., and Iida, T. (2009). Molecular Epidemiology of Koi Herpesvirus. Fish Pathology. 44 (2): 59-66.
McColl KA (2013). Review of the literature on cyprinid herpesvirus 3 (CyHV-3) and its disease. PestSmart Toolkit publication, Invasive Animals Cooperative Research Centre, Canberra, Australia. (This article is highly recommended)
McColl KA and Crane MStJ (2013), Cyprinid herpesvirus 3, CyHV3: its potential as a biological control agent for carp in Australia, PestSmart Toolkit publication, Invasive Animal Cooperative Research Centre, Canberra, Australia. (This article is highly recommended)
McKoll, K. (2016, January 13). Using herpes virus to eradicate feral fish? Carp diem! CSIRO Blog. (This article is highly recommended)