So on to IPNV...
Viruses are one of the simple forms of life and in evolutionary terms fall well behind highly organised cells such as those found in animals and plants, so called eukaryotic cells. Next to bacterial cells, the prokaryotic cells, are finally the viruses and only slightly more advanced than crystals. Unlike the majority of bacteria, viruses can only grown in live cells whereas bacteria can be cultured on a variety of artificial media.
Viruses contain only one type of nucleic acid within their structure either DNA or RNA and IPNV is a double stranded RNA virus - a birnavirus. At least 9 different types of the IPN virus exist. The main types in Europe are Sp and Ab and VR299 in the USA.
IPNV disease was first described in salmonid fingerlings in a Canadian hatchery back in 1940 causing a very severe infection of the gut and the condition was referred to as a catarrhal enteritis. However the actual virus was not isolated until 1960 by Ken Wolf a virologist working in the USA. The virus has a worldwide distribution and has been shown to infect a wide range of salmonid species in fresh and in seawater. Seawater species including halibut, eels, mollusc and crustaceans have been shown to be infected by the virus.
2 different stages of virus infection are known to exist where in one stage fish may simply carry the virus with no apparent problems- referred to as asymptomatic or carrier stage. However the other form causes full-blown disease affecting a range of tissues. Clinical IPNV infection can afflict fish at any stage in freshwater but typically will affect early first-feeding fry with catastrophic effects.
In freshwater affected fry will often show corkscrew swimming behaviour with popeye of both eyes, a swollen belly and trailing casts. Internally, the liver is often almost transparent and is often a key feature to look out for when diagnosing IPNV infections. In seawater similar external signs are seen plus often the vent is protruding and when examined internally there are often blood spots over the pancreas. Extremely high blood chlorides are another feature of clinical disease in seawater fish whereas abnormally low blood chloride levels are seen in salmon afflicted with IPNV in freshwater.
Examination of diseased tissues under the microscope reveals severe necrosis of the pancreas and gut tissues. Extensive necrosis of the liver is a consistent finding in salmon fry in freshwater giving the liver a very characteristic, pale transparent appearance. Severe liver damage is not always so prevalent or extensive in salmon in seawater and is often restricted to a diffuse spread of solitary necrotic liver cells along with other more general changes indicative of osmoregulatory problems.
Interestingly in some cases recently, I have seen a significant change in the pathology seen under the microscope. Whilst demonstrating the very characteristic severe, acute necrosis of pancreas and liver, the gut tissue appears relatively less affected so maybe catarrhal enteritis is not a pertinent description for this disease in some instances.
Another virus, Salmon Pancreas Disease virus (SPDV) causes a similar disease with minimal gut damage but it is different as it also causes significant damage, sometimes irreparable, to skeletal and heart muscle. However using immunohistochemistry, all these cases have shown detectable IPNV associated with the liver and pancreatic lesions so it is unlikely that these fish were actually suffering from Salmon Pancreas Disease virus.
Gross signs and even microscopical examination of affected fish tissues although providing a strong presumptive diagnosis of clinical IPNV infection, for conclusive proof further specific tests are required. A wide variety of tests are available including a simple latex agglutination test as developed by the Norwegian Veterinary Institute, cell culture for actual isolation and identification of the virus, to specific antibody tests using various dyes and enzymes even the highly sophisticated polymerase chain reaction test (PCR) can be used.
With the upsurge in IPNV infections in recent years especially involving recently transferred smolts, a number of investigations have been carried out in an attempt to recognise significant risk factors associated with the development of disease. Major contributing factors identified include method of smolt transfer with wellboats carrying the greatest risk, seawater readiness, stock type and whether mixed year classes are present on sites and finally the incidence of IPNV infections afflicting previous year classes on a site. The latter may indicate a gradual increase in virus loading in the environment and make no mistake that IPNV is a resilient survivor. Experiments feeding cows IPNV-infected silage have shown good virus survival at the end of the long journey through the cows gut before finally ending up (no pun intended) on pasture.
Individual broodstock testing is probably the only way to ensure, as much as is practical, that IPNV-free fry are obtained. There is still some debate on whether the virus is transmitted from affected parents through into the egg ie vertical transmission. However there is a great deal of anecdotal evidence that the incidence of IPNV infection is higher in fry, even in those produced from IPNV tested negative parents, where the incidence in a particular stock has been shown to be high and eggs from positive parents has been destroyed.
So what can we do once a diagnosis of IPNV is given ?
All the commonsense that any good husbandry person would come up with including:
Reduce stress at all costs
Ensure that nets are clean ensuring that water flows through cage are optimal
If any predators are around make sure that everything is being done to prevent them getting access to fish eg bird top nets are complete and predator nets are in place
Some people have reported that starving works, I personally do not subscribe to this advice having diagnosed clinical IPNV infections in longterm non-feeding fish. However I would advise that fish are not over or underfed thus avoiding the stress that either scenario might induce.
Some benefits have been reported by feeding nucleotides, the so-called building blocks, for the immune system, and increased vitamin C levels for a few weeks
A number of experimental vaccines are being trialled at present and I await their results with baited breath as effective vaccination would be a significant step towards getting IPNV under control
So finally to return to possible reasons as to why I think that IPNV is becoming more of a problem.
With increasing episodes of virus infections it could be argued that the virus is more prevalent in the environment and more likely to infect fish. Additionally it is well known, experimentally at least, that the virulence of pathogens, the ability to cause disease, can be increased by repeatedly passing an infectious agent through susceptible animals. So maybe this is part of the reason why IPNV infections are more prevalent. A lot is said about the virulence of Shetland's IPNV but I have not seen any experimental evidence that proves that it is any more damaging than Scottish mainland strains of IPNV.
Thinking about what has changed since the 1980's when although IPNV could be found in fish the actual disease condition was very rare. Over the last 2 decades considerable advances have been made in feed and feeding strategies, photoperiod manipulation and light exposure per se for salmon fry have produced smolting fish at different times of the year and much faster (I hesitate to say better) growth. In land-based freshwater rearing systems with the introduction of oxygen injection the stocking density has increased significantly in a number of farms; along with baseline carbon dioxide levels. So it could be argued that salmon in the 21st century are more highly "stressed" than their counterpart from the 20th Century. A bit like finely tuned athletes walking a fine line between health and disease susceptibility. Elite human athletes often fall prey to opportunistic and exotic pathogens such as colds and Epstein-Barr virus, the cause of Infectious mononucleosis or alternatively known as the "Kissing bug".
Highly effective vaccines have been developed against that bete noir of the eighties- furunculosis. It's along this path of thought that I wander and wonder if this has anything to do with the increasing incidence of outbreaks. My simple (infallible) logic says that highly effective vaccines must generate significantly more immune energy than that previously required with the much less effective water-based vaccines around in the eighties. So what happens when all the immune energy is used up. IPNV is probably more of an opportunist rather than a primary pathogen. A salmon's normal immune is almost certainly more than capable of keeping IPNV at bay and preventing the development of clinical disease.
So maybe it is when the immune system is otherwise occupied or used up that IPNV can get going causing clinical disease. This thesis should be easy enough to prove or disprove by challenging recently vaccinate smolts and comparing with nave, non-vaccinated smolts. Further might be interesting to compare monovalent vaccines against multivalent vaccines in an IPNV challenge scenario.
There is some evidence from mammalian vaccination in support of this thesis that indicates that effective individual vaccines can lose their protectiveness when used in a multivalent vaccine format. The reason is thought to be that some vaccines are more immunogenic than others and sequester more of the available immune energy reserves than others thereby reducing immune protection of the less efficient vaccines. The upshot of this is that animals are no longer protected, or so well protected from disease. In fish vaccines there can be up to 5 different vaccines in one injectable vaccine plus oil adjuvant.
So there is a lot to think about, a lot to understand and a lot to do before we can get back to growing fish free from the threat of IPNV.
Source: Fish Vet Group - May 2002