3. small Anim. Pract. Vol. 9, 1968, pp. 117 to 121. Pergamon Press Ltd. Printed in Great Britain

Difficulties in the Diagnosis of Distemper in Mink* BRENDAN FOX? Royal (Dick) School o f Veterinary Studies, Summerhall, Edinburgh

A “DISTEMPER” was the term historically applied to any infectious, febrile condition of man or animal but nowadays the use of the term is confined to describe a specific, highly infectious and contagious disease affecting members of the families Cunidae and Mustelidae. It is the disease perhaps most dreaded by the mink farmer, and an early, accurate diagnosis is essential in minimising losses and preventing further spread of the disease.

Principle among the difficulties met in the diagnosis of distemper are the limited experience of the disease in this country and the wide variation in clinical picture which may be presented, and therefore the possibility of distemper should always be borne in mind, even where losses are insidious and the more obvious catarrhal symptoms absent.

Any systematic investigation of a suspected outbreak of distemper should include a study of the following-the. epidemiology of the disease, the clinical signs, autopsy findings-including the results of any histological or neuropathological investigation, and finally the result of any serological studies undertaken, animal innoculation experiments etc. Thus, in reaching a diagnosis, several lines of approach may be followed but these should be regarded as complementary to each other. Each line of approach adopted will contribute a certain amount of informa- tion but only when all methods of investigation have been completed, and the results pooled, can a definite diagnosis be established. Short cuts may occasionally be justified, but are fraught with danger.

The epidemiology of the disease should first be considered. Information regar- ding the incidence and spread in the country as a whole, and in particular district under consideration is essential. There may be local outbreaks of distemper amongst dogs, or outbreaks on other mink farms and in this respect, the voluntary notification scheme promises to be of great value. Related to the epidemiology is a study of the possible methods of transmission of the disease such as direct or indirect contact

*Prize winning entry in 1966/67 Fur Breeders’ Association of the U.K. Essay Competition for Veterinary Students.

?Present Address : The Cooper Research Station, Berkhamstead, Herts.

117

118 BRENDAN FOX

with a sick animal, or any of its discharges or contaminated gloves, equipment or food etc. At this point it is worthy of note that an accurate and detailed history is essential in the diagnosis of this, or indeed of any disease. I t is in this respect that the mink farmer can be of great help by supplying a detailed history of feeding, manage- ment, vaccination programmes, movement of stock and disease history-past and present. In previous years, difficulties in the diagnosis of distemper have been caused due to a lack of information regarding the epidemiology of the disease amongst mink in this country and a failure to appreciate the great value of an accurate history to the veterinarian especially accompanying post-mortem specimens.

Having established an accurate history of the disease the next step is to examine the stock thoroughly to ascertain what clinical evidence of disease is displayed. At this point considerable difficulties may again be met. The clinical picture presented by this disease is subject to considerable variation and the clinician may therefore expect to meet a variety of disease symptoms. The classical disease picture is that of a catarrhal inflammation of mucous membranes especially those of the respiratory and digestive tracts, complicated by central nervous system involvement. In the acute disease the signs develop some 8-10 days after infection. The eyes have a slightly squinted appearance and a watery ocular discharge may be present. Later the eyelids become swollen, the discharge becomes purulent and the eyelids, after crusting, eventually shut. There is also a nasal discharge, watery at first later becoming purulent, and a swelling of the nose may cause a “Roman-nosed” appear- ance.

Pustules may develop on the lips and the feet swell and redden, the pads being encrusted with a light-brown granular material. Cracks in the pads and bleeding may develop. Pustular eruptions may appear on the skin particularly in the ab- dominal region where the skin may be reddened and a typical “musty” odour may be noticeable. Diarrhoea may occur, the faeces usually becoming loose and tarry. Appetite varies-kits usually losing theirs fairly quickly whereas adults may con- tinue eating until a day or two before death.

It should be emphasised here that not all the clinical signs described above will be encountered in any one animal or in any one outbreak. They represent a com- posite of the signs which may be identified when many animals are examined at different stages of the disease in a number of outbreaks. Indeed, if all outbreaks of distemper in mink followed a similar pattern to that described above, diagnosis on clinical grounds alone would not present too many difficulties, however, there is evidence that this is not the disease picture commonly met in practice. A variety of factors may influence the type of clinical signs which appear-further complicating diagnosis. One such factor may be the strain of mink affected. Research in Denmark suggests that pastel mink are more susceptible to distemper than other strains of mink and may be more difficult to immunise against the disease by means of vaccina- tion. Breakdowns of vaccination would appear to be more common in this strain when subject to a severe challenge by the disease. This seems to indicate a genetic factor in resistance/susceptibility to the disease, which may have to be taken into account in the diagnosis.

The immune status of the individual animal will also cause a variation in the disease picture obtained. Certain animals may have an acquired immunity as a result of previous vaccination. Young kits may have a passive immunity due to

D I F F I C U L T I E S I N T H E D I A G N O S I S O F D I S T E M P E R I N MINK 119

protection by maternal antibodies*. However, it should be stressed that vaccination is a biological process and therefore the immunity provided is never 100 per cent. If, therefore, a severe “weight” of challenge is coupled with some other stress factor, then breakdowns in immunity must be expected. Similarly an animal suffering from distemper will be extremely susceptible to any other infection and so inter- current and secondary infections may cause considerable difficulties in diagnosis. Especially important in this respect are Salmonella infections. The nutrition of an animal also influences its resistance to disease. A well-balanced diet, adequate in both quality and quantity is essential in maintaining the health and vigour of the animal and a poorly fed mink will be more prone to other infections as well as distemper, and there may well be conditions of a purely dietary origin to further confuse the the clinical disease picture, e.g. vitamin B deficiency. However, even when all these possible influences have been taken into consideration there remains perhaps the most important single factor affecting the disease picture which will be obtained-the “strain”t of virus involved.

The causal organism of canine distemper was first described as a virus by Professor Carrt in 1905. Later, Laidlaw and Dunkin in 1926 described the classical catarrhal symptoms of canine distemper, Green adapted the virus to ferrets and the Wellcome “Hard Pad strain” was isolated. The strain (or type) of virus which appears to be prevalent amongst mink in the United Kingdom does not cause a “typical” catarrhal disease. Most commonly the onset of clinical signs occurs some 2-4 weeks after infection. The classical eye, nose and pad signs are not pronounced and may well be missed among the earlier cases.

As the disease progresses and the virus is passaged through a number of sus- ceptible hosts these signs may become more evident. Most animals appear to recover and probably many remain unaffected. However, nervous signs usually develop in a proportion of cases. These may include chorea, paralysis, or paraplegia but usually take the form of screaming fits. These gradually increase in frequency over the course of two or three days and the animal eventually dies in one.

This atypical distemper resembles that produced by a virus type isolated in Glasgow which, when inoculated into ferrets, gave rise to screaming fits, after an incubation period of 2-6 weeks, without showing any prior signs of disease. Repeated passage of the virus through several generations of ferrets reduced the incubation period and produced more typical catarrhal signs. Mansi, in 1952, compared the “classical” Laidlaw-Dunkin virus, the Wellcome Hard Pad virus, the Green’s virus

“This question has caused some interest with regard to interference with active immunisation by maternal antibodies. The time taken for the maternal antibodies to disappear depends on the level of antibodies in the dam at birth. In a dam which has been vaccinated in the period immediately preceding (2 weeks) parturition, it may take up to 12 weeks for the maternal antibodies to disappear sufficiently to allow successful active immunisation. As the kits are usually weaned a t 5&6 weeks the protection may persist for some weeks after this. Garham et al. (Vet. Med. (1962) 57,896) recommended that vaccination would give best results at 12 weeks. There are obvious parallels with the position in the dog.

?The use of the word “strain” in no way implies an antigenic difference since as far as is known these have not been demonstrated: However, and presumably by a combination of factors, the clinical picture can vary between outbreaks; this is also probably related to the invasiness of the virus under given circumstances.-Editor.

120 B R E N D A N FOX

strain and the Glasgow (“s 123”) strain and found significant differences in duration of illness and clinical signs. Following this, Larin ( 1954a and 1954b) described three types of distemper distinguished by their effects produced when innoculated into ferrets. Again the varying duration of illness and variations in clinical signs pro- duced were used as criteria.

Thus the virus type involved in any particular outbreak may markedly alter the clinical picture expected of distemper and although the more prevalent, neurotropic strain does appear to resemble the milder forms of distemper described in North America, it should be remembered that both Larin and Mansi considered that repeated ferret passage could alter the clinical appearance of the disease. Hence, in any one outbreak, early cases could resemble the Glasgow strain disease picture, while later cases could be more closely related to the Laidlaw-Dunkin type disease.

All the evidence goes to show that the wide variation in clinical signs possible in an outbreak must be borne in mind when a diagnosis of distemper is considered. This variation in disease picture presents the major problem in establishing a clinical diagnosis of distemper.

Confirmation of a clinical diagnosis of distemper requires post-mortem, histo- logical and virological examination of specimens. On post-mortem examination, a careful examination of visceral lesions should be carried out as these are often of great value in differential diagnosis. A histological search for inclusion bodies should be made as these are specific lesions and as such are essential in differential diagnosis. Zimmermann describes finding inclusion bodies in the epitheIium of the trachea and urinary bladder in about thirty per cent of affected animals. The usual signs of intercurrent and secondary infections will be present such as pneumonia and enteritis. The pathological changes produced will, however, be of little use in diagnosing distemper as they are of a non-specific nature. Bacteriological examina- tion may cause difficulties in diagnosis because of frequent findings of Salmonellae as a secondary phenomenon.

When facilities are available virological techniques offer an excellent method of establishing a conclusive diagnosis. Serological techniques, such as the serum neutralisation test should be possible in nearly all cases. However, when considering the results of such tests it is advisable to refer them to the course of events on the farm, this correlation of laboratory and clinical findings should eliminate possible mistakes in diagnosis, as might happen where the prolonged course of the disease might produce low levels of viral antigen in the tissues.

Biological methods of diagnosing distemper offer perhaps the most certain diagnosis of distemper possible. The results of transmission experiments to ferrets should be considered very important as they lead to findings which are almost 100 per cent accurate. But again difficulties may be encountered such as the provision of facilities, transport of material, necessity of keeping test animals disease- free and for the clinician, the disadvantage of having to wait a considerable length of time before a positive result is obtained. Incubation periods in the ferret vary from 10 days-6 weeks according to the isolate of virus involved.

The two most common differential diagnoses of distemper are avitaminosis B- which may require an examination of the diet, and salmonellosis-as a primary disease condition ; both may be intercurrent with distemper.

D I F F I C U L T I E S I N T H E DIAGN'OSIS O F D I S T E M P E R I N M I N K 121

To summarise, therefore, the diagnosis of distemper in mink presents a number of problems to the veterinarian. The inherent difficulties of establishing a conclusive diagnosis have been detailed and these are such as to make it essential that as much information as possible be made available to help the investigator, and the maximum use be made of this information. I t is, therefore, in the farmer's own interest to supply an accurate and detailed disease history and, where necessary, fresh post- mortem material so that an accurate diagnosis can be made as soon as possible. I t is only by a close co-operation between veterinarian and farmer, and a mutual understanding of the problems involved that the ravages of this and other diseases may be minimised and the health of the mink promoted for the benefit of the animal itself, the individual farmer and the mink farming community as a whole.

REFERENCES MANS W. (1952) State Vet. J . 7 , 22. LARIN N. M. (1954a) Vet. Rec. 66, 339. LARIN, N. M. (1954b) Nature 173, 174. ZIMMERMANN, H. (1964) Die Kleintierpraxis 9 Jahrg. s 43-6.