ARCHIVE FILE
This article was published in 1978
See the original document
Some Problems With Bees and Trout
M. Hornitzky, B.Sc., (Microbiology) Veterinary Research Station, Glenfield
You are all familiar with cases of serious economic loss caused by diseases, viz livestock. The purpose of this talk is to briefly discuss similar situations which occur with bees and trout. Glenfield carries out the diagnostic work and sometimes research work, due to the lack of specialised laboratories which would handle such cases where severe economic loss is concerned as a result of disease in apiaries or trout farming enterprises.
The first case to be discussed is European Foulbrood.
EFB is a disease of honey bee larvae caused by the bacterium Streptococcus pluton. Its presence in Australia has been suspected for many years, especially in Victoria where sporadic outbreaks of a disease indistinguishable from the current outbreaks of EFB have occurred for the past 28 years. However, it was not until March, 1977 that this germ was isolated from Australian diseased bee larvae.
Its significance to the Australian honey industry and to other areas where it is known to occur, such as Europe, North America, South America and Africa, is that the causative agent Streptococcus pluton is present in hundreds of thousands of hives and it may persist in these hives for many years with little or no obvious sign of disease.
It appears that a balance can exist in an infected colony between the production and spread of the organism and its elimination. It is when this balance is upset, such as occurred in Australia as a result of the recent drought which inhibited the growth of bee colonies and thus reduced their capability of effectively eliminating diseased larvae which allowed the spread of infection, that mass deaths of larvae and serious losses of honey production occur, which has been roughly estimated at $7 million.
Currently, there are about 33 apiaries in South Australia affected, involving 13,000 hives and 22 apiaries in N.S.W. were found to be infected, involving 5,000 hives. No figures are available for Victoria, but it is known to occur in that State.
The significance of the condition can best be summed up in a couple of lines taken from an article in January's 'Australian Beekeeper', written by Bob Win:
'If left uncontrolled, EFB would make commercial apiculture an uneconomic industry.'
SYMPTOMS
The disease is characterised by:
1. The death of 4 or 5 day old larvae.
2. The change of colour of normal larvae from glistening white to a faint yellow.
3. The larvae lose their plump appearance and appear undernourished.
4. The diseased larvae sometimes appear to collapse from their upright state in the brood comb.
5. In serious cases a pepper box pattern of capped and uncapped cells develop in the brood comb.
THE ORGANISM
The causative agent Streptococcus pluton is a lemon shaped bacterium. These bacteria are swallowed with the feed and grow in the mid gut of the larvae. The bacteria compete with the larvae for food and kill it by starving it to death or make it prone to further infection by other bacteria.
The sick larvae excrete the organism and are an excellent form of infection and reinfection of other larvae.
It is also considered that H20 tanks used to supply bees in. drought situations are also a source of infection.
DIAGNOSIS
is based on two criteria:
a. The recognition of symptoms previously mentioned.
b. The demonstration of S. pluton in the larvae. In the field situation, apiary inspectors merely macerate a larvae that looks infected and place it on a microscope slide and send it to the laboratory for staining and examination.
If the lemon shaped bacteria appear on the slide, a positive diagnosis is made.
It may seem a little unusual for a disease which is relatively easy to diagnose and which has more than likely been here since the late 1800's should take until 1977 to be positively diagnosed. The answer to this lies in:
i. the unusual nature of the disease organism. It was not until the 1950's that this organism was definitely shown to be the causative agent of this condition.
ii. other bacteria which are associated with S. pluton have previously been isolated from cases which were EFB and therefore a condition known as False European Foulbrood was coined to describe the disease in Australia.
iii. the disease was not an economic problem nor posed the threat of American Foulbrood, hence no cultural work was done here.
iv. Streptococcus pluton (difficult to grow) has on many occasions been confused with other Streptococci which are not pathogenic for bees. (Therefore never the right treatment or control).
CONTROL
Now that it has been diagnosed in three States, various measures for control have been instituted:
1. A Quarantine Line was instituted which effectively trapped most infected colonies. Then a buffer zone was introduced which prevents any bee keeper placing bees 30 kilometres north of the quarantine line.
2. The second form of control seems to be due to purely geographical distribution. There is little doubt that infected colonies have been taken much further north in N.S.W but there have never been any reports of disease in these areas.
The disease seems to localise itself in epidemic proportions in certain areas. In the U.K.; the southern counties; the U.S.A; the Rocky Mountains area especially Colorado and probably going into the Dakotas and Minnesota; Europe, in northern Denmark, Switzerland, Austria and Poland and in Australia, north Victoria Southern New South Wales and South Australia (along the Murray River).
Outside these epidemic areas the incidence becomes markedly reduced. Often it has to be searched out with a 'fine toothed comb' but it is usually there. This has yet to be confirmed in Australia.
3. In other countries such as England, the method of control is burning of the infected hives.
4. Chemotherapy is another form of control. Terramycin has been used successfully in many countries. The antibiotic is mixed with sugar syrup and poured over the combs. A trial was carried out in South Australia to determine the effectiveness of Streptomycin but the results were not encouraging.
A further trial is to commence in N.S.W. in the next few months to further test the use of antibiotics.
A return to the more usual chronic endemic infection might be anticipated when the effects of drought come to an end.
FISH
The second major problem to be discussed involves trout.
In recent months there have been two severe outbreaks of contagious fish diseases at commercial trout farms.
In December and January last year there were severe losses of rainbow trout at Berridale. On the 20th January, 10 recently dead diseased trout were received at Glenfield with an accompanying history, part of which I will quote to demonstrate the rapidity and seriousness of the outbreaks:—
'On the 12th December, 10,000 3½cm rainbow fry were obtained from Triton Trout, Tumut and 2,000 were lost in transit. A further 1,000 were lost up to 26th December and from then to 5th January the remaining 7,000 died. Also during the period 26th December to 5th January, 4,000 10 cm fish were also lost.
On the 13th January, the area experienced violent storms and high winds though little rain was recorded. Deaths in the larger fish from 13cm to 23cm in size occurred between 13th and 17th January when 8 or 10 died out of 1,500. Between 17th and 18th January, over 400 of these remaining fish died and it is estimated that the majority died over a period of no more than 3 hours on the 18th January.'
There are now 120 trout left out of about 15,400. This represents a loss of about $31,000.
All the trout received for examination were dissected out and examined. In each case the only visible abnormalities were the accumulation of a mucoid clear fluid in the gills and around the internal organs and an inflammation of the gastrointestinal tract.
Cultures were made from the internal organs which were shown to contain a profuse number of Aeromonas hydrophila - this bacteria is a common inhabitant of water.
When isolated from non-aquatic livestock this organism is usually considered as a very low grade pathogen. For aquatic animals it is also usually considered as a low grade pathogen and rarely, if ever, affects fish which are kept under optimal conditions. However, if fish are placed in stress situations such as the transportation from one farm to another or are kept in artificial situations which might cause stress and weakening of stock, Aeromonas hydrophila will invade the fish tissue and produce toxins causing death with few symptoms.
In this case the acquired stressed stock became infected and as a result excreted the organism in large amounts. They subsequently infected the fish already at the farm and all the fish became infected and all but 120 died.
It should be noted that this is the first case of this condition, haemorrhagic septicaemia caused by Aeromonas hydrophila, to be recorded in trout in New South Wales.
Treatment would have involved feeding Terramycin impregnated feed pellets. However, most of the fish were dead before a diagnosis was made.
The second case involved a trout hatchery which had recently purchased trout fingerlings for growing out and commercial sale. The caretakers noticed that fish in two tanks began to swim violently and erratically and great numbers began to die.
As 'White spot', a contagious disease of fish which is caused by the protozoan Ichthyopthirius multifilis, better known as: 'Ich', is characterised by these symptoms, live fish were taken for examination. Microscopic examination of gill material showed the presence of the protozoan. This protozoan is a round unicellular organism about 0.2mm to 1mm in diameter. Even though the correct treatment of a solution of malachite green which destroys one of the respiratory enzymes, Cytochrome C, in the parasite, was commenced within 24 hours, 10,000 fingerlings had died within 24 hours.
This parasite, which is endemic in most rivers and streams, penetrates the mucous coat and upper layers of the fishes' skin, The fish react by producing a white spot on the area of irritation. The parasite then grows and feeds on the fluids and red blood cells of the fish. It develops to maturity in the fish in about 4 weeks at 10°C and in about 3 to 4 days at 21-26°C, after which it perforates the skin to the exterior.
In this particular case the temperature of the water in the tank holding the fish had inadvertently been increased from 13°to 20° reducing the life cycle of the organism from 4 weeks to about 6 days, increasing the number of infective particles at an exponential rate. With the combination of increased infective particles, stressed situation and the confined space of the tanks, the incidence of re-infection and new infection reached a point where the fish became so infected with the parasite that mass deaths resulted. Over 60,000 fingerlings with a potential value of $120,000 perished over a five day period, even though the disease was recognised and treatment begun within 24 hours.
CONCLUSION
In all cases where trout are raised for commercial purposes in high numbers in artificial or restricted areas, all possible eventualities such as feed, crowding, temperature of water, plus the influx of new stock, should be monitored or examined as closely as possible to avoid stress situations or the presence of overt disease. Many of the potential pathogens are closely associated with these trout in their environment and if this environment is unwisely or accidentally altered, it may allow these organisms to produce a severe epidemic of disease.
Diseases as previously mentioned take their course very quickly, resulting in severe loss even though treatment may have been commenced as soon as symptoms appear.