Aleutian Disease - Information
ALEUTIAN DISEASE (AD) IN THE FERRET
A review for members of the Wessex Ferret Club
Michael Oxenham B Vet Med MRCVS
January 1991, revised and updated May 1993
Revised and updated Graham Campbell B Vet Med MRCVS March 1998.
This disease takes its name from the Aleutian strain of mink in which it was first discovered in 1956 in the USA. Spontaneous cases have been recorded in ferrets in the USA (1967), Canada (1978), New Zealand (1984) and in the UK early 1990.
The Cause
AD is caused by a parvovirus. The characteristics of this virus have been investigated in great detail in the USA over the last 30 years. There are at least 4 strains of the virus which affect mink – Utah 1, Ontario, Montana and Pullman. There is also probably a ferret strain. The severity of the illness in both mink and ferrets largely depends on the strain of virus present but the genetic make-up of the infected animal is also a factor. Attempts have been made at the Central Veterinary Laboratory to isolate and culture the virus from the Hampshire ferret cases, but unfortunately without success, although the virus has been seen under the electron microscope.
Species affected by AD
Mink, both ranch and feral, is the species most severely affected by AD. The ferret, which is closely related to the mink and can even interbreed with it, is affected to a lesser extent. Experimentally, in the USA, AD virus has been inoculated into other members of the mustelid family such as the skunk, marten weasel and raccoon etc. They have developed antibodies but not developed the disease. In the UK, in 1986, an otter died in Norfolk of symptoms consistent with AD. It was suggested by the veterinary pathologists involved that the infection might have come from the feral mink. It is probable that the AD virus was introduced into the UK from the USA with the large importation's of ranch mink about 30 years ago. Since that time mink have escaped from ranches and have become established in the wild in this country, and have a preference to be near rivers and lakes. In all probability the AD virus is endemic in these mink. At the present time no connection has been established between AD infection in the feral mink and the domestic ferret AD cases in Hampshire, but the suspicion remains that these mink may be the source of infection for the ferret.
Effects on the body of the AD virus (pathogenesis)
When considering this aspect of a disease, comparisons with diseases of other animals are often mentioned. Other diseases which follow a similar course to AD are, in fact, quite rare – the examples being equine infectious anaemia, African swine fever and lymphocytic choriomeningitis of mice.
The normal response of an animal to invasion by a virus is to produce specific antibodies, which bind to that virus and neutralise its effects. If these antibodies do not overcome the virus, then the disease progresses. This usually involves the destruction of specific areas of tissue within the body – such as the brain in the case of distemper or rabies, liver in virus hepatitis, surface tissues in foot and mouth disease and so on.
What make AD an unusual type of disease, is that the mink and ferret produce massive amounts of immune substances or complexes as a response to the virus, which are then deposited in various internal organs, hence the term immune-mediated disease. It is these deposits which cause the symptoms of AD. Most mink die from kidney dysfunction, whilst the symptoms in the ferret are much more variable and in some instances, mild or none at all. In the Hampshire cases, the most frequent symptom has been hindquarter paralysis in varying degrees of severity. At autopsy the pathologists have also found significant and characteristic changes in the kidneys, lungs and liver. Although antibodies are produced by the mink and ferret, for some reason which is still unknown, they do not neutralise the AD virus. This is the reason for the persistent nature of the infection. Another feature of AD is that the virus causes some degree of immuno-depression, which means that the ferret is unable to mount a defence against other types of infection.
Diagnosis
Because of the variety of the symptoms of AD – hindquarter weakness, unthrifty condition, respiratory symptoms, sudden death or stress etc., it is difficult to diagnose by signs alone. The only commercially available specific test in the live animal is done on a blood sample by the counter-current immuno-electropheresis method (CIEP or CEP). A specific antigen has been developed from the Utah 1 strain, which cross reacts with all identified strains of AD and is the one used in the CEP test. This test identifies the ferrets, which have developed AD antibodies, indicating exposure to the virus. Because of the persistent nature of the infection it has to be assumed, particularly for control purposes, that they may be carrying the virus. If a full and detailed postmortem is done on affected animals, characteristic microscopical changes are seen in various organs, which will confirm the diagnosis.
Treatment and prevention
There is no simple effective treatment or cure for AD. In some of the cases in ferrets in Hampshire, a response to antibiotics and steroids has been observed in those which had mild hindquarter weakness. But several animals relapsed at varying intervals. In the USA, immunosuppresive and chemotherapy drugs have been used experimentally with beneficial results. However, these treatment regimes cannot be regarded as practical or realistic from a cost point of view. There is no suitable vaccine for AD and it is unlikely that one will be produced for the simple reason that a "vaccine" would produce the same severe immune response as the natural disease.
Epidemiology (How the disease spreads)
Transmission of the virus occurs both "vertically" and "horizontally". Vertical transmission is from jill to kit through the placenta. Horizontal transmission is through body fluids – saliva, blood, urine, faeces and aerosol droplets through the lungs. The last of which can occur up to a metre in distance. An infected hob is obviously a risk at mating. The evidence we have collected since 1990 indicates that not all ferrets in contact with CEP positive animals, become infected themselves. This may be because not all CEP positive ferrets are actively shedding the virus.
Parvoviruses are quite resistant once they have left the body – unlike most other viruses, and only certain disinfectants are effective against them. A recommended and pleasant one to use is Parvocide (Duphar).
C control
A once yearly blood test is the basis of control. The following action should be taken in the case of negative and positive results:-
Negative – Only breed with other tested/negative stock. Obtain new stock from similar-tested animals. Keep out of direct or indirect contact with untested ferrets. It is most unlikely that infection will be contracted whilst out hunting.
Positive – This does present some difficult choices, particularly with CEP positive ferrets that look healthy. If an owner has one or two ferrets then he or she may decide to keep them for their natural life, but obviously no breeding should be done and they must be strictly isolated from other ferrets. Where an owner has a number of ferrets and only one or two are positive, then culling them has to be considered. From a practical point of view it would be very difficult to keep the positives totally isolated from the negatives on the same premises. If the positives are culled, then the negative contact ferrets should be retested once, not less than 4 weeks later, in order to establish that the group is CEP negative.
Summary up to January 1991
33 ferrets have been identified as CEP positive and most of these have been culled. The others have been kept in isolation, and some of these developed paralysis up to 9 months later. Positives are still being found, so it is important that testing is continued for the present. The fact that no positives have been identified in other areas such as Sussex, Essex, Berkshire and Devon gives one confidence that the problem may only be local to the Wessex area.
May 1993 update
Since 1991 there have been several isolated outbreaks of AD in areas other than central southern England. These have been in Berkshire, London, Oxfordshire and Lancashire. Comparatively little routine screening has been done around the country, but where it has been done, few positives have been found. However, routine screening has continued in this area and as the positives are still occurring, mainly in ferrets tested for the first time.
Summary
As can be seen, the figures show a steady reduction until 1992, but this year there has been an increase in the number of positives. The very low incidence in the previously tested ferrets shows the effectiveness of the control measures. These figures indicate that there is a continuing need for AD screening in the Wessex area. In spite of this number of positives, it is interesting to note that I have not seen any clinically affected ferrets since 1991, although clinical cases were seen elsewhere in 1992. Only seven mink have been tested of which three have been positive, although efforts in this respect are continuing. Information from this source might indicate if the mink are the reservoir of the virus.
Aleutian Disease in The Ferret.
April 1997
Aleutian Disease virus (ADV) is a parvovirus and is known to cause a persistent viraemia in ferrets.Some infected ferrets may develop signs of clinical illness such as degrees of ataxia or paralysis, weight loss, respiratory symptoms, melena and occasionally sudden death. The pathologicalchanges are of an immune~mediated nature. Transmission is both vertical (trans-placental) and horizontal (saliva, blood, urine and faeces). There is no known cure but steroids and antibiotics may give some help in mild cases. There is no vaccine for the disease.
Diagnosis is based on histopathology, garnmaglobulin estimation and serology using the counterimmunoelectrophoresis (CIEP or CEP) test. The CIEP test has been developed for screening the stock of mink farms and is suitable for use in the ferret.