Genetic Welfare Problems of Companion Animals

An information resource for prospective pet owners

German Shepherd Dog (Alsatian)

German Shepherd Dog (Alsatian)

Anal Furunculosis

Related terms: Perianal fistula

Outline: German Shepherd dogs are predisposed to anal furunculosis, a condition in which there is inflammation and ulceration of the skin under the tail and around the anus, which can become severe with deep infection of underlying tissues. It is a chronic condition which is difficult to treat and which can cause moderate to severe irritation and pain, especially at defaecation. The cause is unclear but there is some evidence that it may be due to an underlying abnormality of the immune system and/or the abnormal tail conformation and carriage of this breed.


Summary of Information

(for more information click on the links below)

1. Brief description

Dogs with anal furunculosis have a long-term progressive inflammatory disease of the skin and underlying tissues which causes inflammation, skin ulceration, deep cavities and channels through the skin around the anus. The surface of the skin and the ulcers in the area around the anus are often covered by pus and faecal material (Nuttall et al 2009). Defaecation becomes difficult due to the pain felt by the dog while trying to pass faeces.

Conformational defects have been implicated as contributing factors to anal furunculosis in German Shepherd dogs (GSD). The densely furred tails of GSDs and the way in which they carry their tails may contribute to the disease, along with the presence of large numbers of sweat glands in the skin around the anus. However; there is stronger evidence that altered immune system function is important in the development of anal furunculosis in GSDs.

2. Intensity of welfare impact   

Ulceration and infection of the skin and underlying tissues causes irritation and pain, which can be moderate or severe, especially at defaecation. 

3. Duration of welfare impact

Once affected, animals often experience ongoing or recurrent episodes of discomfort and pain associated with the disease throughout their life. Additionally, the treatment of anal furunculosis may itself be a cause of discomfort.

4. Number of animals affected

Anal furunculosis is seen in dogs of other breeds but 84% of cases are in the GSD (Elkins 2004). From data on estimates of total dog population in the UK and on the percentage of all micro-chip registered dogs that are German Shepherd Dogs (Alsatians) (Lucy Asher, 2011, personal communication), we estimate that the UK population size of this breed may be around 400,000.

5. Diagnosis

The diagnosis is based on physical examination.

6. Genetics

There is a strong breed predisposition to this disease in the GSD (Elkins 2004, Nuttall et al 2009). The genetics underlying this are unknown although it is unlikely that it is attributable to a single genetic defect. It is more likely to be a complex genetic disorder with significant environmental factors (House et al 2001).

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

There is no way to identify which dogs will become affected.

8. Methods and prospects for elimination of the problem

There are currently no breeding schemes aimed at reducing the incidence of this problem in the German Shepherd dog. The best advice may be to avoid breeding from individuals affected by the disease or from those with affected relatives. Alteration of the breed standard may be necessary to eliminate the condition if tail conformation is proved to be an important casual factor in the disease.


For further details about this condition, please click on the following:
(these link to items down this page)


1. Clinical and pathological effects

Dogs with anal furunculosis have a progressive inflammatory disease of the skin and underlying tissues around their anus. It is a long-term (chronic) disease which causes skin inflammation, skin ulceration and deeper, long-lasting cavities called fistulas or fistulous tracts. The surface of the skin and ulcers in the area around the anus are often covered by pus and faecal material (Nuttall et al 2009). Defaecation becomes uncomfortable for the affected dog due to pain on passing faeces. Damage to the anal sacs (small sac-like structures next to the anus) and scarring of the tissue just inside the anus can occur and seem to be secondary to the underlying disease processes of anal furunculosis (Elkins 2004). The disease process which causes the disease to progress is poorly understood.

The condition is seen most often in entire, male, middle-aged GSDs (Elkins 2004, Shell 2008).

Two main factors have been blamed for anal furunculosis: defects of immunity and anatomical, conformational defects.

Affected animals usually have a thick, long-haired tail, the base of which is held tightly against the anal area; in effect creating a poorly aerated pocket of skin. Evidence suggests that dogs affected by anal furunculosis may also have more sweat glands in the perianal skin than non-affected animals. Together, these factors seem to result in raised levels of moisture on the skin around the anus which increase the likelihood of surface microbial infection (Budsberg et al 1985). The importance of these factors has been questioned (Shell 2008) as other breeds have similar tail carriage defects and do not seem to be affected with anal furunculosis (Elkins 2004). Nonetheless, the reported 80% success rate of tail amputation for treating anal furunculosis in GSDs suggests that the tail confirmation defect of GSDs is involved to some extent (Elkins 2004).

There is evidence that GSDs with anal furunculosis often have concurrent chronic intestinal disease (Harkin et al 1996). There is also a clear link between perianal fistulas and chronic intestinal disease (Crohn’s disease) in humans; where around 1/3 of human Crohn’s disease patients have rectal or perianal disease (Lewis and Maron 2010).

Evidence from three different sources indicates that altered immune system function is important in anal furunculosis in GSDs too. Firstly, studies have shown that GSDs often have basic immunological defects, such as lowered numbers of T-lymphocytes (white blood cells involved in immune defences) in the skin (Day 1994) and blood (Chabanne 1995). They also have higher levels of certain proteins associated with inflammation and immunity (House et al 2003), and they have abnormal IgA metabolism (Whitbread et al 1984, Day and Penhale 1988). IgA is a class of antibodies active on body surfaces (antibodies are proteins produced by the body which are an important part of the immune defence). Additionally, GSDs are predisposed to many other syndrome associated with immune system disease such as: GSD pyoderma syndrome, adverse cutaneous and gastrointestinal reactions to foods, metatarsal fistulation of the GSD and inflammatory bowel disease, small intestinal bacterial overgrowth, disseminated aspergillosis, systemic lupus erythematosus, discoid lupus erythematosus, pemphigus erythematosus, multiple myeloma and progressive myelopathy (Waxman and others 1980, Batt and others 1983, Scott and others 1983, Day and others 1986, Matus and others 1986, Scott and others 1987a, Scott and others 1987b, Tams 2003, Nuttall et al 2009). However, the case for the role of an immunological defect in GSDs is not straightforward, as under the microscope the tissue damage and responses seen in anal furunculosis in GSD is very similar to that seen in other breeds with the condition (Day 1993, Day and Weaver 1997).

Recently, direct evidence for the association of genetic abnormalities of the immune system and anal furunculosis in the GSD has been reported by Kennedy et al (2008) and House et al (2008). House et al (2003) identified altered function of certain immune system cells (cells from the monocyte/macrophage series). So there is mounting evidence in GSDs with anal furunculosis having abnormalities of the immune system but further work is needed to confirm and clarify the role of these factors in the disease.

The second strand of evidence is that the most successful treatment for GSD furunculosis, which is now the standard treatment when it can be afforded, is long-term use of the T-lymphocyte inhibitor ciclosporin (cyclosporin). This drug has been used to treat other immune mediated diseases such as atopy, pannus and sebaceous adenitis and is widely used as an immunosuppressant in human transplant recipients (Mathews and Sukhiani 1997, Nuttall et al 2009). Tacrolimus, another immunosuppressive drug, has also been successfully used in treating anal furunculosis (Misseghers et al 2008, Nuttall et al 2009, Stanley and Hauptman 2009).

That drugs which are known to work by influencing the immune system, improve GSD anal furunculosis is evidence that disease of the immune system is involved, and Tivers et al (2008) found a reduction in products of the immune system in the skin after treatment with ciclosporin (Tivers et al 2008).

A third strand of evidence relating to the cause of anal furunculosis in GSDs is that, in humans, anal furunculosis can be associated with Crohn’s disease. Multiple genetic factors have been found to be involved in this human disease and the genes affected are involved with immune system function (Barrett et al 2008). However, particular genetic abnormalities associated with the immune system abnormalities of Crohn’s disease and inflammatory bowel disease in human beings (Hugot et al 2001, Franchimont et al 2004) were not found in  GSDswith furunculosis (House et al, 2009) (although these authors did find evidence of inbreeding which may have an effect on immunity).

In the past, many different treatments have been used for anal furunculosis including long-term or life-long medication with corticosteroids and antibiotics, removal of affected tissue using surgery, lasersand cryotherapy (freezing), or tail amputation (Shell 2008, Nuttall et al 2009).

Return to top

2. Intensity of welfare impact

Ulceration and infection of the skin and underlying tissues causes irritation and pain, which can be moderate or severe, especially during defaecation. Currently recommended therapies for anal furunculosis are based on medical treatment with powerful immunosuppressant drugs, the side effects of which can cause malaise and discomfort.

Return to top

3. Duration of welfare impact

Once affected with anal furunculosis, GSDs often have lifelong disease and ongoing or recurrent episodes of discomfort and pain associated with the disease and to treatments for the problem.

Return to top

4. Number of animals affected

Anal furunculosis is seen in dogs of other breeds also, but 84% of cases are in the GSD (Elkins 2004). The proportion of GSDs affected has not been reported. The condition is seen most often in entire, male, middle-aged GSDs (Elkins 2004, Shell 2008). From data on estimates of total dog population in the UK and on the percentage of all micro-chip registered dogs that are German Shepherd Dogs (Alsatians) (Lucy Asher, 2011, personal communication), we estimate that the UK population size of this breed may be around 400,000.

Return to top

5. Diagnosis

Diagnosis of the disease is based on physical examination of the skin around the anus. Tests to rule out possible underlying causes of inflammation and ulceration that require different treatments may be considered – such as a food trial to rule out that the skin disease is caused by allergic reaction to substances in the food.

Return to top

6. Genetics

There is a strong breed predisposition to anal furunculosis in the GSD (Elkins 2004, Nuttall et al 2009). The genetics underlying this are unknown. Rather than the result of a single genetic defect, it is likely to be a complex genetic disorder with significant environmental factors (House et al 2001). The anatomical and/or physiological defects that underlie this predisposition are unclear. The increased number of sweat glands in the perianal skin of GSDs and the breed’s characteristic tail conformation and carriage must be partly genetically determined. Given that the analogous human disease has a strong genetic component it seems likely that anal furunculosis in GSDs may be associated with immune system defects with a genetic basis. However, it is unlikely that the disease is due to a single genetic defect.

Return to top

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

There is no way to identify which dogs will become affected.

Return to top

8. Methods and prospects for elimination of the problem

As far as we are aware, there are currently no breeding schemes aimed at reducing the prevalence of this problem in the GSD. With complicated polygenetic conditions, which this is likely to be, the best advice may be to avoid breeding from affected individuals or their relatives.

Because the conformation of the tail may be important, efforts to select for improved tail conformation and carriage might prove effective.  Currently the GSD breed standard states that tails should be,

Bushy-haired, reaches at least to hock – ideal length reaching to middle of metatarsus. At rest tail hangs in slight sabre-like curve; when moving raise and curve increased, ideally never above level of back.

http://www.thekennelclub.org.uk/item/136)

Encouraging the breeding of dogs with normal tail conformation, carriage and movement can only be beneficial. Normal dogs can raise their tail above the level of their backs.

Return to top

9. Acknowledgements

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

Return to top

10. References

Barrett JC, Hansoul S, Nicolae DL et al (2008) Genome-wide association defines more than 30 distinct susceptibility loci for Crohn's disease. Nature Genetics 40 955–962

Batt RM, Needham JR and Carter MW (1983) Bacterial overgrowth associated with a naturally occurring enteropathy in the German shepherd dog. Research in Veterinary Science 35: 42-46

Budsberg SC, Spurgeon TL and Liggitt HD (1985) Anatomic predisposition to perianal fistulae formation in the German shepherd dog. American Journal of Veterinary Research 46: 1468-72

Chabanne L, Marchal T, Denerolle P, Magnol JP, Fournel C, Monier C and Rigal D (1995) Lymphocyte subset abnormalities in German shepherd dog pyoderma (GSP). Veterinary Immunology and Immunopathology49: 189-198

Day MJ, Pendale WE, Eger CE, Shaws SE, Kabay MJ, Robinson WF, Huxtable CRR, Mills JN and Wyburn RS (1986) Disseminated aspergillosis in dogs. Australian Veterinary Journal 63: 55-59

Day MJ (1993) Immunopathology of anal furunculosis in the dog. Journal of Small Animal Practice 34: 381-389

Day MJ (1994) An immunopathological study of deep pyoderma in the dog. Res Vet Sci. 56:18-23

Day MJ and Penhale WJ (1988) Serum immunoglobulin A concentrations in normal and diseased dogs. Research in Veterinary Science 45: 360-363

Day MJ and Weaver Q (1992) Pathology of surgically resected tissue from 305 cases of anal furunculosis in the dog. Journal of Small Animal Practice 33: 583-589

Elkins AD (2004) Perianal Fistulas, the Good, the Bad and the Ugly. Proceedings of the Western Veterinary Conference.

Franchimont D, Vermeire S, El Housni H et al (2004) Deficient host-bacteria interactions in inflammatory bowel disease? The toll-like receptor (TLR)-4 Asp299gly polymorphism is associated with Crohn’s disease and ulcerative colitis. Gut 53: 987–92

Harkin KR, Walshaw R and Mullaney TP (1996) Association of perianal fistula and colitis in the German shepherd dog: response to high-dose prednisone and dietary therapy. Journal of the American Animal Hospital Association 32: 515-520

House A, Gregory SP and Catchpole B (2003) Expression of cytokine mRNA in canine anal furunculosis lesions. Veterinary Record 153: 354-358

House AK, Catchpole B and Gregory SP (2007) Matrix metalloproteinase mRNA expression in canine anal furunculosis lesions. Veterinary Immunology and Immunopathology 115: 68-75.

House AK, Gregory SP and Catchpole B (2008) Pattern-recognition receptor mRNA expression and function in canine monocyte/macrophages and relevance to canine anal furunuclosis. Veterinary Immunology and Immunopathology 124: 230–240

House AK, Binns MM, Gregory SP and Catchpole B (2009) Analysis of NOD1, NOD2, TLR1, TLR2, TLR4, TLR5, TLR6 and TLR9 genes in anal furunculosis of German shepherd dogs. Tissue Antigens 73: 250–254

Hugot JP, Chamaillard M, Zouali H et al (2001) Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn’s disease. Nature 411: 599–603

Kennedy LJ, O’Neill T, House A et al (2008) Risk of anal furunculosis in German shepherd dogs is associated with the major histocompatibility complex. Tissue Antigens 71: 51–516

Lewis RT and Maron DJ (2010) Anorectal Crohn's disease. Surgical Clinics of North America. 90 83-97

Mathews KA and Sukhiani HR (1997) Randomized controlled trial of cyclosporine for treatment of perianal fistulas in dogs. Journal of the American Veterinary Medical Association. 211: 1249-1253

Matus RE, Leifrer CE, Macewen EG and Hurvitz AI (1986) Prognostic factors for multiple myeloma in the dog. Journal of the American Veterinary Medical Association 188:1288-1292

Miller WH (1991) Deep pyoderma in two German shepherd dogs associated with a cell-mediated immunodeficiency. Journal of the American Animal Hospital Association 27: 513-517

Misseghers BS, Binnington AG and Mathews KA (2004) Clinical observations of the treatment of canine perianal fistulas with topical tacrolimus in 10 dogs. Canadian Veterinary Journal 41: 623-627

Nuttall T, Harvey RG and McKeever PJ (2009) Anal furinculosis. In: A Colour Handbook of Skin Diseases of the Dog and Cat. Manson Publishing. pp 174

Scott DW, Walton DK, Manning TO, Smith CA and Lewis RM (1983) Canine lupus erythematosus. Systemic lupus erythematosus. Journal of the American Animal Hospital Association 19: 461-479

Scott DW, Walton DK, Slater M, Smith CA and Lewis RM (1987a) Immune-mediated dermatoses in domestic animals: ten years after - Part I. Compendium of Continuing Education for the Practising Veterinarian 9: 424-435

Scott DW, Walton DK, Slater M, Smith CA and Lewis RM (1987b) Immune-mediated dermatoses in domestic animals: ten years after - part 11. Compendium of Continuing Education for the Practising Veterinarian 9: 539-551

Shell L (2008) Perianal fistula. Veterinary Information Network: Associate. http://www.vin.com/Members/Associate/Associate.plx?DiseaseId=1282andFindingList=374758,375366  accessed 6th October 2010.

Stanley BJ and Hauptman JG (2009) Long-term prospective evaluation of topically applied 0.1% tacrolimus ointment for treatment of perianal sinuses in dogs Journal of the American Veterinary Medical Association 235: 397-404

Tams TR (2003) Inflammatory Bowel Disease in Dogs; Intestinal Disease in Shar-Peis; German Shepherd Enteropathy; Pythiosis. Atlantic Coast Veterinary Conference 2003

Tivers MS, Catchpole B, Gregory SP and House AK (2008) Interleukin-2 and interferon-gamma mRNA expression in canine anal furunculosis lesions and the effect of ciclosporin. therapy. Veterinary Immunology and Immunopathology 125: 31-36

Waxman FJ, Clemmons RM, Johnson G, Everyman JN, Johnson MI, Roberts TSC and Hinrichs DJ (1980) Progressive myelopathy in older German shepherd dogs. Journal of Immunology 124: 1209-1215

Whitbread TJ, Batt RM and Garthwait GE (1984) Relative deficiency of serum IgA in the german shepherd dog: a breed abnormality. Research in Veterinary Science 37: 350-352 http://www.thekennelclub.org.uk/item/136 accessed 6th October 2010

© UFAW 2011