Genetic Welfare Problems of Companion Animals

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West Highland White Terrier West Highland White Terrier

Demodicosis

Related terms: red mane, demodectic mange, demodectic acariosis, follicular mange

Outline: Demodicosis is a skin disease caused by the parasitic mite, Demodex. It causes itching, discomfort and pain which can be severe depending on the extent and seriousness of the skin disease. It can involve extensive areas of skin and severe secondary bacterial infections, which may lead to systemic illness and which can be fatal. Even successfully treated episodes can be prolonged (months) and may recur. West Highland White terriers are particularly susceptible to demodicosis and it is thought that this may be due to a genetic abnormality of the immune system.


Summary of Information

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1. Brief description

Demodicosis is a skin disease caused by the parasitic mite, Demodex. It causes itching, discomfort and pain which can be severe depending on the extent and seriousness of the skin disease. It can involve extensive areas of skin and severe secondary bacterial infections, which may lead to systemic illness and which can be fatal. Even successfully treated episodes can be prolonged (months) and may recur. West Highland White terriers are particularly susceptible to demodicosis and it is thought that this may be due to a genetic abnormality of the immune system.

The presence of large numbers of mites in the hair follicles and sebaceous glands of the skin causes inflammation and an immune system response (Caswell et al 1997; Day 1997). Demodicosis may be localized, and involve only a small area of skin, or it may be more widespread, affecting multiple areas, or even the whole body. In the latter, it is called generalized demodicosis (Nuttall et al 2009). There is a form that just affects the feet (pododermatitis) and this is usually considered to be a distinct condition. Demodicosis may occur in juvenile animals or may first develop only later in life (Nuttall et al 2009). Juvenile demodicosis affects puppies less than 10 months old; it often spontaneous resolves as the animal gets older and responds well to treatment.

Demodicosis may cause areas of baldness, scale, ulcers, pustules and crusts. There are certain variations that are said to be distinctive in the WHWT including one that is highly itchy and has a tendency to affect the midline of the back (Guaguere and Beugnet 2008; Nuttall et al 2009).

Dogs with severe, generalized demodicosis often become ill through the widespread secondary bacterial infection of the skin (deep pyoderma) commonly associated with the condition and sometimes from secondary septicaemia (blood poisoning). Anorexia, fever and shock sometimes occur and affected dogs may also develop kidney failure (Guaguere and Beugnet 2008). The disease can lead to death (Duclos et al 1994; Lewis 1998).

2. Intensity of welfare impact

Demodicosis can cause itching, discomfort and pain and the effects vary depending on the amount of skin affected and the degree of secondary infection and skin damage. Severe pain and illness are seen in some dogs with generalized demodicosis (Guaguere and Beugnet 2008). Treatment often involves the use of drugs that can have adverse welfare effects: nausea, vomiting and undesirable neurological signs are all quite common (Guaguere and Beugnet 2008; Nuttall et al 2009). Demodicosis can lead to the death of the affected individual; either from the disease itself and its secondary complications (Duclos et al 1994; Lewis 1998) or because affected dogs are euthanased to prevent further suffering (Guaguere and Beugnet 2008).

3. Duration of welfare impact

The duration of welfare impact depends on the type of demodocosis. Juvenile-onset, localised demodicosis usually resolves by itself in a few weeks, but adult-onset disease and generalized forms or pododermatitis (the type that affects the foot) usually require a considerable length of treatment. These affect welfare for months and the disease tends to recur in a significant proportion of cases (Guaguere and Beugnet 2008).

4. Number of animals affected

Demodicosis is a common disease of dogs (Guaguere and Beugnet 2008) and the West Highland White terrier is predisposed to it (Guaguere and Beugnet 2008; Nuttall et al 2009). However, we are unaware of any specific data on the proportion of these dogs that are affected. From data on estimates of total dog population in the UK and on the percentage of all micro-chip registered dogs that are West Highland white terriers (Lucy Asher, 2011, personal communication), we estimate that the UK population size of this breed may be around 250,000.

5. Diagnosis

Demodicosis is usually diagnosed by observation of large numbers of Dermodex mites on examination of a skin scraping or on hairs plucked from an affected area of skin.

6. Genetics

It appears to be widely accepted that as a breed, the West Highland White terrier, has a predisposition to developing the disease (Guaguere and Beugnet 2008; Nuttall et al 2009) but as far as we are aware there is no information about  the mode of inheritance or the heritability.

7. How do you know if an animal is a carrier or likely to become affected?

There are no methods for detecting which puppies may go on to develop the disease and it is not known whether animals pass on a predisposition to the disease without being affected themselves.

8. Methods and prospects for elimination of the problem

The best advice for conditions where the genetic basis of a condition is strongly suspected but unknown, is not to breed from affected individuals (or at least from those that have been severely affected) and, generally, to avoid breeding from animals that have affected relatives (Bell 2010). Breeding West Highland White terriers with dogs of other breeds in which the prevalence of demodicosis is low might help reduce prevalence of the disease.


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1. Clinical and pathological effects

Demodicosis is a skin disease caused by a mite of the genus Demodex. All mammals have one or more species of Demodex that live on their skin, usually inside the hair follicles. There are three species of Demodex that can cause disease in dogs. Transmission is thought to occur only within a 72 hour period immediately after birth (Greve and Gaafar 1966). Small numbers of mites probably live on the skin of many healthy individuals with no skin disease, although they are usually not possible to detect (Scott et al 2001). Disease arises where there is a defect in the immune system that allows the mites to increase in number. Demodicosis is not considered to be a contagious disease (except between neonates in some circumstances (Kwochka 1983)).

As noted above, it is generally assumed that demodicosis only occurs where the immune system is compromised, although the evidence for this is inconclusive (Scott et al 1974, 1976; Hirsch 1975; Lemarie and Horohov 1996, Singh et al 2010). Indeed, Demodex mites themselves may produce substances that depress immunity (Hirsch 1975). Dogs with demodicosis usually have secondary bacterial infections and the immunosuppression caused by this can be difficult to distinguish from an underlying primary immune system dysfunction (Barta et al 1983; Barriga et al 1992). Demodicosis can also occur secondary to other conditions that cause immune deficiency such as: hyperadrenocorticism, hypothyroidism, diabetes mellitus and systemic neoplasia (Duclos et al 1994; Lemarie et al 1996). It can also occur following administration of drugs that depress immunity such as corticosteroids and chemotherapeutic agents (Kwotchka 1983, Lemarie et al 1996). Some such immune-suppressing factors have been identified in around 75% of dogs with adult-onset demodicosis (Scott et al 1976).

In individuals with non-compromised immune systems, the presence of large numbers of mites in the hair follicles and sebaceous glands causes inflammation and an immune system response (Caswell et al 1997; Day 1997). This immunological response is probably responsible for the spontaneous recovery that can be seen in dogs with the milder forms of the disease (see below).

The disease may be localized to a relatively small area of skin or it may be more widespread, affecting multiple areas, or even the whole body. In the latter case it is called generalized demodicosis (Nuttall et al 2009). There is a form that just affects the feet (pododermatitis) and this is particularly seen in the West Highland White terrier (WHWT) (Guaguere and Beugnet 2008).The disease can occur in juveniles or may occur only later in life (Nuttall et al 2009). Juvenile demodicosis affects puppies less than 10 months old; it often spontaneous resolves as the animal gets older and responds well to treatment. Adult-onset demodicosis has been found to be less likely to respond to treatment (Lemarie et al 1996).

In individuals affected with demodicosis there may be areas of alopecia (baldness), scale (dandruff), ulcers (loss of the surface of the skin), pustules (whiteheads) and crusts (scabs). A particularly itchy form of the disease has been recognised in West Highland White terriers (Guaguere and Beugnet 2008; Nuttall et al 2009).

Dogs with severe, generalized demodicosis often become ill through the widespread secondarybacterial infection of the skin (deep pyoderma) commonly associated with the condition and sometimes from secondary septicaemia (blood poisoning). Anorexia, fever and shock sometimes occur and affected dogs may also develop kidney failure (Guaguere and Beugnet 2008). The disease can lead to death (Duclos et al 1994; Lewis 1998).

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2. Intensity of welfare impact

Nuttall et al (2009 p 276) described demodicosis as: “Possibly the most serious non-neoplastic (ie non-cancerous) dermatological disease.” It can cause itching, discomfort and pain and its effects vary depending on the area of skin affected and the degree of associated secondary infection and skin damage. When there is only a small area of mildly affected skin the welfare consequences are minor, but when large areas of skin are severely affected there is great discomfort and pain. Severe pain and illness are seen in some dogs with generalized demodicosis (Guaguere and Beugnet 2008).

Treatment of generalised demodicosis and pododermatitis (where only the foot is affected) caused by Demodex is not straightforward. Medication often has to be prolonged, lasting for months, until the lesions have resolved and mites are no longer seen on skin scrapings (Mueller 2004). Some animals are never cured but require life-long treatment to control the number of mites. About 15% of treated animals relapse within a year (Guaguere and Beugnet 2008). The drugs used in treatment of demodicosis can themselves have adverse welfare effects, quite commonly causing nausea and vomiting (and undesirable neurological signs (Guaguere and Beugnet 2008; Nuttall et al 2009)). Frequent shampooing is often required and this process may cause distress to some dogs.

Demodicosis can lead to the death of the affected individual; either from the effects of the disease itself or its secondary complications (Duclos et al 1994; Lewis 1998). Severely affected dogs may be euthanased for welfare reasons, to prevent further suffering (Guaguere 1995; Guaguere and Beugnet 2008).

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3. Duration of welfare impact

The duration of welfare impact depends on the type of disease that occurs. Juvenile-onset, localised demodicosis usually resolves by itself in a few weeks, but adult-onset disease and generalized forms or pododermatitis (the type that affects the foot) usually require a considerable length of treatment. These are likely to affect welfare for months and the disease tends to recur in a significant proportion of cases (Guaguere and Beugnet 2008).

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4. Number of animals affected

Demodicosis is a common disease of dogs (Guaguere and Beugnet 2008) and the West Highland White terrier is predisposed to it (Guaguere and Beugnet 2008; Nuttall et al 2009). However, we are unaware of any specific data on the proportion of these dogs that are affected. From data on estimates of total dog population in the UK and on the percentage of all micro-chip registered dogs that are West Highland white terriers (Lucy Asher, 2011, personal communication), we estimate that the UK population size of this breed may be around 250,000.

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5. Diagnosis

The appearance of demodicosis is highly variable so virtually any skin lesion could be a sign of the disease (Kwotchka 1983). The allergic skin disease atopy (Nuttall et al 2009), to which West Highland Whites are also predisposed, can appear similar so care is needed to avoid a misdiagnosis. Demodicosis is usually diagnosed by observation of large numbers of Dermodex mites on examination of skin scrapings or on hairs plucked from an affected area of skin. Further diagnostic tests may be required to rule out non-genetic causes of the immune insufficiency that underlies demodicosis.

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6. Genetics

It appears to be widely accepted that as a breed, the West Highland White terrier, has a predisposition to developing the disease (Guaguere and Beugnet 2008; Nuttall et al 2009) but as far as we are aware there is no information about the mode of inheritance or the heritability.

It has recently been suggested that the canine leukocyte antigen system may play a role in the pathogenesis of demodicosis, and this is a target for future genetic research (Barrientos et al 2010).

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7. How do you know if an animal is a carrier or likely to become affected?

There are no methods for detecting which puppies may go on to develop the disease and it is not known whether animals pass on a predisposition to the disease without being affected themselves.

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8. Methods and prospects for elimination of the problem

The best advice for conditions where the genetic basis of a condition is strongly suspected, but unknown, is not to breed from affected individuals (or at least from those that have been severely affected) and, generally, to avoid breeding from animals that have affected relatives (Bell 2010). Breeding West Highland White terriers with dogs of other breeds in which the prevalence of demodicosis is low might help reduce prevalence of the disease.

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9. Acknowledgements

UFAW is grateful to Rosie Godfrey BVetMed MRCVS and David Godfrey BVetMed FRCVS for their work in compiling this section.

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10. References

Barrientos L, López Gappa J, Posik D, Díaz S, Golijow C and Giovambattista G (2010) Association of canine juvenile generalized demodicosis with the dog leukocyte antigen system. Tissue Antigens 76: 67–70

Barriga OO, Al-Khalidi NW, Martin S and Wyman M (1992) Evidence of immunosuppression by Demodex canis. Veterinary Immunology and Immunopathology 32: 37-46

Barta O, Waltman C, Oyekan PP, McGrath RK and Hribernik TN (1983) Lymphocyte transformation suppression caused by pyoderma—Failure to demonstrate it in uncomplicated demodectic mange. Comparative Immunology, Microbiology and Infectious Diseases 6: 9-18

Bell JS (2010) Genetic Testing and Genetic Counselling in Pet and Breeding Dogs. World Small Animal Veterinary Association World Congress Proceedings

Caswell JL, Yager JA, Parker WM and Moore PF (1997) Prospective study of the immunophenotype and temporal changes in the histologic lesions of canine demodicosis. Veterinary Pathology 34: 279-87

Day MJ (1997) An immunohistochemical study of the lesions of demodicosis in the dog. Journal of Comparative Pathology 116: 203-216

Duclos DD, Jeffers JG and Shanley KJ (1994) Prognosis for treatment of adult-onset demodicosis in dogs: 34 cases (1979-1990). Journal of the American Veterinary Medical Association 204: 616-9

Greve JH and Gaafar SM (1966) Natural transmission of Demodex canis in dogs. Journal of the American Veterinary Medical Association 148: 1043-9

Guaguere E (1995) La demodecie canine. Strategie therapeutique. Practique Medicale et Chirurgicale de l’Animal de Compagnie 30: 295-307

Guaguere E and Beugnet F (2008) Parasitic skin conditions. In: A Practical Guide to Canine Dermatology 194-203: Kalianxis Italy

Hirsch D (1975) Suppression of in vitro lymphocyte transformation by serum of dogs with generalized demodicosis in dogs. Veterinary Research 36: 1591-5

Kwochka KW (1983) Demodicosis. In: Griffin CE, Kwochka KW and MacDonald JM (eds) Current Veterinary Therapy pp 72-84. Mosby Year Book, St Louis USA

Lemarie SL and Horohov DW (1996) Evaluation of interleukin-2 production and interleukin-2 receptor expression in dogs with generalized demodicosis. Veterinary Dermatology 7: 213-7

Lemarie SL, Hosgood G and Foil CS (1996) A retrospective study of juvenile- and adult-onset generalized demodicosis in dogs (1986–91). Veterinary Dermatology 7: 3–10

Lewis DT (1998) Life-Threatening Dermatoses in Dogs. Compendium of Continuing Education for the Practicing Veterinarian 20: 271-283

Mueller RS (2004) Treatment protocols for demodicosis: an evidence-based review. Veterinary Dermatology 15: 75-89

Nuttall T, Harvey RG and McKeever PJ (2009) In: Skin diseases of the dog and cat pp 272. Manson Publishing: London

Scott DW, Farrow BRH and Scultz RD (1974) Studies on the therapeutic and immunologic aspects of generalized demodectic mange in the dog. Journal of the American Animal Hospital Association 10: 233-44

Scott D, Miller W and Griffin C (2001) Muller and Kirk’s Small Animal Dermatology. WB Saunders Company: Philadelphia, USA

Scott DW, Scultz RD and Baker E (1976) Further studies on the therapeutic and immunological aspects of generalized demodectic mange in the dog.  Journal of the American Animal Hospital Association 12: 203-13

Singh SK, Dimri U, Sharma MC, Sharma B and Saxena M (2010) Determination of CD4+ and CD8+ T cells in the peripheral blood of dogs with demodicosis. Parasitology 137: 1921-1924

© UFAW 2011


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