Ulceration of the footpads with plasma cell pododermatitis is an uncommon disease of cats. Clinically affected animals have large soft pads with the metacarpal and metatarsal pads being most noticeably affected.1.2.3 Owners usually notice the cat licking the affected paws or a trail of bloody foot prints. Affected cats are not always lame. This report provides details of two cases presented at a suburban veterinary practice in Sydney, Australia.
A 3 1/2 year old castrated male domestic short hair (cat 1) was presented with hemorrhage of the left fore metacarpal and right hind metatarsal pads. The owner reported that the cat had been intermittently lame and was seen licking its pads. The cat belonged to a multi cat household and was fed a range of commercial canned and dry foods. Clinical examination revealed a cat of average bodily condition. All pads were flaccid and spongy with an approximately one centimetre ulcerated area on each of two pads. The cat had halitosis with a generalised periodontitis consistent with being fed a processed food diet.4.5.6
A presumptive diagnosis of plasma cell pododermatitis was made. The owner was informed as to the uncertain aetiopathogenesis of the condition and that treatment modalities were unreliable. 7 At the time a number of degenerative diseases of cats e.g. Feline Lower Urinary Tract Disease, Miliary Dermatitis, Eosinophilic Granuloma and Inflammatory Bowel Disease were being treated at our practice with an experimental modality of radical dentistry, minimal drug therapy and dietary change. The owner agreed to this approach being adopted.
Under general anaesthesia the two upper canine teeth were found to be badly affected by periodontal disease and were removed. Remaining teeth were manually scaled. Punch biopsies of the ulcerated lesions were taken for confirmation of diagnosis. The ulcerated feet were bandaged. Penicillin was administered (Procaine Penicillin G 150 mg and Benzathine Penicillin G 112.5mg i.m.) and a six day course of Amoxycillin instituted (12.5 mg/kg, po, q 12h). The diet was to be changed to raw chicken wings, quail, rabbit, whole raw fish or similar with water to drink.
The histopathology report was: 'a large ulcerated area covered by a necrotic serocellular crust and separated from the underlying dermis by a fibrotic zone containing karyorrhectic debris and mixed inflammatory cells. There were dense infiltrates of plasma cells including many containing Russel bodies, and lymphocytes throughout the dermis. This lesion would fit with plasma cell pododermatitis.'
One week post surgery the bandages were removed. Within three weeks the lesions had healed. Five months after surgery the cat was re-examined and found to have soft but otherwise healed pads. Calculus was beginning to re-accumulate on the molar teeth. The owners were encouraged to be more fastidious with the natural diet. Four years later telephone communication with the client revealed that no further foot pad problems had arisen and that the cat had recently been euthanased for non medical reasons.
A seven year old castrated male domestic short hair cat (cat 2) was presented suffering from bilateral hemorrhage of the metacarpal pads. The cat had been fed various commercial cat foods as were the other cats in the household. Halitosis was evident as was severe periodontitis consistent with being maintained on an unnatural diet. The owners were unwilling for biopsy to be performed but agreed to dietary change and dental therapy. At checkup in seven days the feet and mouth were improved. Resolution occurred within three weeks. Three months later the pads were still soft but without ulceration. Calculus was beginning to build up. Accordingly the owners were encouraged to feed more raw meaty bones. Three years later telephone contact established that no further problem had arisen. The diet, whilst not as recommended, consisted of 1/3 raw meat, raw chicken wings twice weekly and whole raw fish on other days.
Footpad disease in cats needs to be differentiated from a list including: trauma, contact irritant hypersensitivity, thermal necrosis, granulomata (eosinophilic, foreign body, bacterial, mycotic, sterile idiopathic), viral disease (feline calici virus, rhinotracheitis virus, leukaemia virus, pox), neoplasia (squamous cell carcinoma, mastocytoma, eccrine sweat gland tumour, lymphoma, liposarcoma), autoimmune disease (pemphigus foliaceus).7 Although ulcerative plasma cell pododermatitis has a characteristic appearance a biopsy represents the best means of confirming the diagnosis.
Age, gender and breed predilections are not known.3.7 Two cats were found to be affected by concurrent plasma cell stomatitis. 3 Various studies have indicated that the condition may be immune mediated, or perhaps allergic. No consistent findings have been reported. 8 The condition may be asymptomatic or regress spontaneously in which case no treatment is required.1 In other instances corticosteroids and gold(crysotherapy) have provided benefit but the long term side effects are undesirable. It has been recommended that painful, hemorrhagic pads which do not respond to medical therapy should be surgically excised.7
Methodological problems loom large when seeking to elucidate the aetiopathogenesis of conditions which are rare, sporadic in occurrence or subject to spontaneous remission. As a starting point it would be reasonable to examine common features. Most authors do not report the dietary management but it would be a reasonable assumption that commercial food formed the basis of the diet. The two cases reported by Taylor and Schmeitzel were fed commercial food8 as were the two cases in the current study. Periodontal disease is prevalent in the modern pet population. In a review, commissioned by the Australian Veterinary Association, Watson reported that many clinicians consider periodontal disease affects more than 80% of domestic cats and dogs.
Periodontal disease is interpreted in different ways by different authors.5 The modern view is that periodontal disease includes gingivitis (inflammation confined to the gingival soft tissues) and periodontitis (the more severe form in which bone supporting the tooth is lost, with eventual loss of the tooth).9 It is generally well accepted that periodontal disease arises as a result of the bacterial plaque/host immune defence interaction.9.10 Authors agree that a departure from the normal diet, which requires vigorous chewing and tearing, is the reason for the build up of plaque on the teeth of carnivores.4.6.11
Aspects of both the dietary change and the dental treatment are thought to have influenced the rapid and lasting resolution of the presenting signs in the two cases of plasma cell pododermatitis. Artificial diets are almost invariably heat treated and contain chemical additives. Many formulations contain grains, milk byproducts and soya beans for which the carnivore biology is ill suited. Apart from the physiological and anatomical incompatibility for digestion of these products there remains the issue of bacterial fermentation and production of irritating chemical products.12 Wills and Harvey report that the pathogenesis of an adverse reaction to a food component involves the interaction of the component with a biological amplification system that leads to inflammation and the development of clinical signs. The amplification system may include immunological mechanisms, complement pathway, eicosanoid synthesis, chemotaxis of phagocytes, and production of inflammatory mediators, such as kinins, leukotrienes and histamine. On occasion, there may be direct toxicity from the ingested component, without amplification, such as reactions to pharmacologic substances.13 Chemically the administration of a more natural raw meaty bone diet would circumvent these potential problems.
The radical dental treatment of the two cats served to physically remove plaque, calculus and diseased teeth. Chewing once daily on raw meaty bones ensures that cats continue to abrade the teeth and gums thereby removing plaque deposits. Chemically this is highly significant for the microbes exert their direct destructive action in a number of ways including the production of exotoxins, endotoxins, proteases, fibroblastic cytotoxins, potent lymphocyte mitogens, chemotactic inhibitors and other damaging metabolites.10 In response the host immune system becomes activated producing cellular changes involving neutrophils and lymphocytes. Lysosomal enzymes are released by the damaged cells including elastase, hyaluronidase, collagenase, lymphokines and prostaglandins.10
From the potential vast array of biochemical interactions, patterns do emerge. In a series of periodontal disease affected cats and dogs systemic leucocyte counts were shown to be seriously reduced but were restored to mid range values after dentistry and diet change.14 The early histological feature of periodontal disease within the gingiva is a vasculitis with loss of perivascular collagen.9 Scott has remarked that in two of his series of five cats the concurrent plasma cell stomatitis was histopathologically and immunopathologically identical with the footpad lesion. 3 It may be contemplated that an immune and chemical response creating a vasculitis in the gingiva can also bring about similar changes in the vasculature generally. Footpads are subject to constant deformation. Even slight vascular and perivascular collagen disease within pads could be expected to become magnified in time. Such explanations are in keeping with HamlinÕs postulate that periodontal bacteria and immune responses can give rise to degenerative disease.15 Degeneration over time is a feature of many collagen and immune system dysfunctions, which it has been suggested, may form a necessary regulatory role in carnivore population dynamics.16
The two cases of plasma cell pododermatitis have remained in remission for more than three years. This suggests that the treatment regime has served a curative and preventative function. A natural raw meaty bone diet has had a proventative effect for kittens which have matured into adults remaining free of a range of degenerative diseases including plasma cell pododermatitis. 17 The current evidence gives veterinarians reason to believe that the adoption of natural food fed control groups of animals in veterinary research should assist in the understanding of many disease processes.15.18
1. Muller GH, Kirk RW, Scott DW. Small animal dermatology.4thed.Philadelphia: WB Saunders Co. 1989;547-549.
2. Gruffydd-Jones TO, Our CM, Locke VM. Foot pad swelling and ulceration in cats: a report of five cases. J Small Anim Pract 1980;21:381-389.
3. Scott DW. Feline dermatology 1979-1982: introspective retrospections. J Am Anim Hosp Assoc 1984;20:537-564.
4. Harvey CE. Optimising oral health: diet and periodontal disease. Vet Forum September 1993;52-53.
5. Watson ADJ. Diet and periodontal disease in dogs and cats. Australian Veterinary Journal 1994;7:313-318.
6. Page RC. Schroeder HE. Periodontitis in man and other animals. Basel: Karger. 1982;273
7. Curtis C. Feline plasma cell pododermatitis, Royal Vet College SAMS News 1993/1994;2(3):3.
8. Taylor JE, Schmeitzel LP. Plasma cell pododermatitis with chronic footpad hemorrhage in two cats. J Am Vet Med Assoc 1990;197:375-377
9. Harvey CE. Emily PP. Periodontal disease. Small Animal Dentistry St Louis: Mosby. 1993;89-144
10. Liebana J. Castillo A. Physiopathology of primary periodontitis associatedwith plaque. Microbial and host factors, A review. Parts 1 and 2. Australian Dental Journal 1994;39:228-232&310-315
11. Colyer F. Dental Disease in Animals. British Dental Journal 1947; 82:31-35
12. Zentek J. Meyer H. Normal handling of diets - are all dogs created equal? J Small Anim Pract 1995;36:354-359
13. Wills J. Harvey R. Diagnosis and management of food allergy and intolerance in dogs and cats. Australian Veterinary Journal 1994;71:322-326
14. Lonsdale T. Periodontitis and leucopaenia. J Small Anim Pract 1995;36:542-546
15. Hamlin RL. A theory for the genesis of certain chronic degenerative diseases of the aged dog. Veterinary Scope, International Edition Kalamazoo: The Upjohn Company 1991; 6-10
16. Lonsdale T. Cybernetic Hypothesis of Periodontal Disease in Mammalian Carnivores. J Vet Dent 1993;11:5-8
17. Lonsdale T. Putting FLUTD in context. J. Small Anim Pract 1993;34:592-593
18. Anon. Diet and disease link - final report. Australian Veterinary Association News. Sydney. Australian Veterinary Association. February 1994; 1-6
Publishing Editor: Arlo Guthrie
Clinical Editor: Alasdair Hotston Moore MA VetMB CertSAC CertVR CertSAS FRCVS
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