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.