Perch Disease

Bacterial infections - a possible cause

Scientists from the FBA and government (MAFF as it was then) worked together to research this disease studying fish from a range of locations. The diseased fish usually had what they referred to as ‘ulcerative lesions’ on the body, what we might call obvious ‘sores’. The scientists set about testing both infected and non-infected perch from Windermere and other locations. They quickly isolated a number of Aeromanous species of bacteria from infected fish, but also apparently healthy fish as well. The media quickly picked this up and started to name this common freshwater microbe (Aeromanous hydrophilia) as the culprit and indeed you can still see this bacteria quoted today as a source of the disease. But this is not what the scientists said. They thought the Aeromanous infection was ‘secondary’ not primary cause of death. They could not find the primary cause of the disease. We feel this result is interesting in itself. We think that if a body parasite had been responsible they would have quickly found it. They found fungi associated with the sores (Saprolegnia spp) but again these were secondary infections. The most interesting bacterial found we believe was not the often quoted Aeromanous hydrophilia but the salmon-specific strain Aeromanous samonicida found in many perch. Indeed the scientists described this as ‘interesting’. We will return to this find later as we might wish to consider that they may not have been in a position to identify all the available Aeromanous species. They tested for viruses using tissue culture and electron microscopy and did not find any in their studies – this again is key and we will return again to this lack of viral evidence.

Aeromonas salmonicida is an obligate parasite, i.e., it is unable to survive outside its host for any significant length of time. This means that spread via non-fish carriers is unlikely. It is worth noting that scientists at Oregon State University found a particularly virulent strain of Aeromonas salmonicida that produced a leucocytolytic factor. This destroys white blood cells that play a critical role in fighting infections.

Significant numbers of perch raised on a pilot fish farm in Switzerland presented focal skin lesions on the lateral sides and fin rot. These symptoms are characteristic of those noted during the perch disease. Mortality rates reached levels of up to 1% of the total fish on the farm per day, somewhat lower than the 98-99% mortality observed on Lake Windermere in 1976! Virtually pure cultures of Aeromonas sobria were isolated from the liver, kidney, spleen and skin lesions of affected fish. Experimental infection of naive perch with a single colony isolate of Aeromonas sobria from an affected farm fish resulted in the development of clinical signs identical to those seen on the farm. The scientists conclude that the results indicate that Aeromonas sobria can act as a primary pathogen of perch. However, it seems obvious that Aeromonas sobria is not the sole cause of the perch disease. There are a number of different bacteria causing these farmed fish attacks but the two that keep cropping up are Aeromanous sobria and the even more interesting Aeromanous veronii. This (called by Belgium scientists – ‘Unexpected Mortality Disease) was more recently isolated. However, there is not at present extensive information about these new Aeromanous strains. Both of these were not discussed at the time of the Windemere work.

Flavobacterium psychrophilum has been reported to be associated with mortality of farmed perch. However, there is no research indicating this bacterium the sole cause of the perch disease.

Before delving into viral perch infections, let’s take another look at some of the information we have so far. The initial spread of the disease was found primarily on large reservoirs. Perch live everywhere so why were reservoirs mainly affected? The answer may lie with bird movements and in particular, those of gulls. Ducks and other wildfowl have migrated to the reservoirs and Thames waters for many years. Gulls on the other hand were really building up inland in the early sixties. Clearly there was great potential for these birds to act as vectors (carriers) for a disease agent be it bacterial, viral or other. The gull’s daily habitat of human waste material could be seen as a rich collection point for such diverse organisms. Cormorants could also fit this pattern of change but their inland increase in numbers was much later (early 1980’s) than that of the gulls and is not therefore relevant to the disease. One clearly has to be very careful about honing in on this kind of coincidental evidence and coming up with a correlation. To make this link more plausible, hard evidence is needed to make the causal connection between gulls and the disease. It is tempting to point towards one of man’s negative interventions as above, but it could equally be some form on natural change or transformation that is at work.

A historical review

The origin of the perch disease was not known in the 1970s and, from the research The Perchfishers have done, a clear and unambiguous cause remains unidentified, although as with all mysteries theories abound. Early investigations conducted overseas suggested a bacterial infection. Viruses have also been blamed. Below we take a look at some of the infections associated with the perch disease and how this fits in with perch population changes.

The first big ‘hit’ of the disease seemed to occur in the Outer London reservoirs of the Thames Valley in 1966, and later that year in nearby Essex reservoirs. These were reported to be major kills with ‘lorry loads of dead perch’ being removed and it was noted in London that bream and roach were unaffected. The next major deaths occurred in Huntingdon and Northants reservoirs (Pitsford, Hollowell, etc). At Grafham Water records show 25 tons of perch were removed over a couple of months. Lower level infections were cited in Lincolnshire and Yorkshire waters between 1972 and 1975 and in Windermere in 1976 where major mortality was recorded in detail. This major geographic spread looked like moving across the country at a rate of 30-40 miles per year, although the pattern becomes more sporadic. Beyond this major regional spread of the disease, outbreaks occurred in Kent and elsewhere until the early 80’s. From these accounts it seems likely that we had a major epidemic and not part of the cyclic population trends.

However, we should take a closer look at the Windermere outbreak in 1976. Windermere in terms of perch is not just another large expanse of water. This lake is home of the Freshwater Biological Association (FBA) at Ambleside. Perch populations have been studied here since the 1930’s by some of the best-known fishery scientists in the world. Much of our scientific understanding of perch ecology comes from studies done here over the years. So we can study the accounts of scientists who saw this drama unfold and examine their findings. Unlike other waters perch were regularly scientifically sampled here and the ‘dramatic depletion’ (to use their words) of stocks can be seen using data from those years.


So what can we learn from this story?

Can we save perch from a future population crash? The answer is probably sadly not but the good news is that the perch can probably achieve this themselves. Today we have a large and thriving population of perch. The ancestors of these fish would have lived through the disease of the 60’s and 70’s, surviving and hopefully spreading their resistant genes into future generations. If the disease comes again in a new and virulent form we are sure, and would hope, a few perch would survive to re-colonise our waters. What saved the perch previously and should save it again from extinction is the level of genetic diversity in populations such that some individuals will have the right combination of genes and alleles to ‘overcome’ the next infection. Nature is good at maximising diversity by making sure that the eggs and milt in each spawning will contain a newly shuffled pack of genes in the fry.

Viral infections - a possible cause

Two viruses that might play a role in the perch disease. The first is Viral Haemorrhagic Septicaemia (VHS). Whilst VHS causes some of the symptoms of the perch disease, it has only been investigated in salmon and trout. No recent evidence has emerged to indicate this virus as the cause of the perch disease. Spring Viraemia of Carp (SVC) and Swim Bladder Inflammation (SBI) are diseases caused by Rhabdovirus carpio. Given the recent increase in the prevalence of SVC and the current abundance of perch, we think we can safely assume Rhabdovirus carpio does not play a role in the perch disease.

Epizootic haematopoietic necrosis (EHN) virus is an iridovirus that affects perch (and rainbow trout). It emerged in Australia in the 1980s and has not been discovered elsewhere. It causes a high level of mortality in perch resulting in steep population declines. The main possible routes of introduction of the virus to England and Wales are the importation of infected live fish or carcasses. The virus is hardy and low levels of challenge can infect perch. Although it seems clear that this virus did not cause the perch disease, mechanical transmission through the importation of non-susceptible fish species should be considered as a potential route of introduction and establishment in future times. Carp have been imported to the UK from Australia for release into still-water fisheries. However, a qualitative risk assessment concluded that the likelihood of EHN virus introduction and establishment in England and Wales with the importation of a consignment of carp was very low. The virus would only establish when the water temperature is greater than 12 degrees C. Analysis of 10 years of data from two rivers in south-west England indicated that establishment could occur over a period of at least 14 weeks a year in southern England (when average water temperature exceed 12 degrees C).

Scientists developed a challenge model for comparison of the virulence of EHN virus to European stocks of fish species including perch. They concluded that EHN virus does not pose a high risk for wild perch populations in Europe by natural exposure. Mortality appears to be primarily a function of environmental factors, with temperature playing an important role, and not just the presence of the virus in the fish. It seems clear that should the EHN virus reach the UK, it would not help perch in anyway. However, it was not the cause of our UK disease.

The viral solution to our problem is very tempting but FBA and MAFF scientists found no evidence at all for viral infection.

Other factors

Stress has often been stated as a contributory factor in the perch disease. Stress can be caused by a number of factors including exertion during spawning, trauma caused, for example, by angling pressure or attack from a predator, pollution or poor water quality caused by over-population or reduced oxygen levels and water temperature.

Temperature is probably the biggest ecological stressor to fish. Perch, like all fish, have a normal temperature range, optimal for their survival. A small change in temperature within the normal range will not have any impact on the health of a perch. However, a sudden change in temperature could cause stress. Additionally, higher temperatures can cause the rapid multiplication of microorganisms and an invasion of pathogens can occur.

Conclusions

A definitive cause of the perch disease has not been found. One can hypothesize that a combination of environmental factors cause the fish stress and result in a lower level of resistance to infection. This makes the fish more susceptible to infections of aeromonas or other as yet unidentified bacterial pathogens or viruses or combination. Perhaps, at times, the bacteria that infect perch develop a particularly high level of virulence or evolve in such a way that they are more damaging to perch. It may also be the case that there is not a single perch disease, but that there are different variants, with multiple causes, some the same and some different. However, the early ferocity of the disease with those ‘lorry loads of dead perch’ means we can also not rule out a single pathogen. We also have to consider that the original agent was missed, or misidentified This might at least explain the fact that a single cause has not been identified, although many theories still exist among interested parties.

Now we might remember the original scientists at the FBA in Windemere found the presence of Aeromanous samonicida interesting and unexpected. On the perch one has to wonder whether they would have found a new but very similar species (sobria or veronii) had it got into the system or could they have misclassified it as Aeromanous samonicida.