key: cord-1043893-qwk0jkqm authors: Delmage, D. A.; Kelly, D. F. title: Auricular chondritis in a cat date: 2008-06-28 journal: J Small Anim Pract DOI: 10.1111/j.1748-5827.2001.tb02457.x sha: eff71bd40689c4abaa18423d563e1962a91d2758 doc_id: 1043893 cord_uid: qwk0jkqm A four‐year‐old male neutered domestic shorthaired cat developed bilateral thickening of the pinnae, with slight curling, intense erythema and pain. No ear canal disease was present. The cat was negative for feline immunodeficiency virus, feline leukaemia virus and feline coronavirus. Biopsy of the ear lesion revealed auricular chondritis. In humans, histologically similar lesions may involve the pinnae, nose, trachea, joints, eyes and heart, and the disease is termed relapsing polychondritis. The cat reported had a history of corneal damage, resulting in corneal vascularisation and opacity, eyelid distortion, necessitating an entropion operation, and radiological evidence of mild cardiac enlargement. The ear disease responded rapidly to treatment with prednisolone and, apart from slight thickening and curling of the pinnae, the cat remained normal and pain‐free. After two years, the prednisolone was withdrawn, and there was no recurrence of the condition in a follow‐up period of 14 months. Relapsing polychondritis is very rare in the cat, and is diagnosed by characteristic pinna! lesions (Scott 1987 , Bunge and others 1992 , Gauguere and others 1992 , involving thickening, distortion, pain and intense erythema. To the authors' knowledge, only three cases have been reported in the literature. The present report describes a cat with a lesion histologically similar to the previously reported cases. Ocular disease was also present, and mild cardiomegaly was found on routine radiography. The latter signs were also described in the case by Bunge and others (1992) , but not in the other two cases. A four-year-old male neutered domestic shorthaired cat was presented with thickening and intense erythema of the inner surfaces of both pinnae; the ear flap edges were thickened, slightly curled, distorted and painful (Fig 1) . The condition had developed on both pinnae simultaneously, and the cat twitched and flicked the ear flaps frequently. The outer (haired) surfaces were unaffected, and no external ear canal disease was evident. The cat had exhibited an altered demeanour for about three months before presentation, manifested as hiding away, cowering, resentment of handling by the owner, and aggression towards the other cat in the household. Increased skin scaling was evident on the lumbodorsal area, and was non-pruritic, with no parasites found on coat brushings and scrapings. This was presumed to be due to reduced self-groo ming. No other skin disease was found, and there was no previous history of skin or ear disease. N ine months previo~s l y, the cat had been seen by another veterinary surgeo n for corneal vascularisation of the right eye. The condition was fluorescein-negative, and was diag nosed as an o ld wound; probably a resolvi ng corneal ulcer. One month late r, the cat had conjunctivitis in both eyes, in addition to blepharos pasm and slight entropion of the lower lid of the right eye. Steroid/antibiotic drops we re administered for these conditions. Two months later, the entropion had worsened, and a surgical correction was performed. Both eyes continued to show intermittent conjunctivitis, at times fairly severe, for several months. Corneal opacity, extensive vascularisation and a weakly positive uptake of fluorescein stain were noted during this time, but no further inves tigations we re performed. At the time of prese ntation for rhe ear problem, rh e ocular lesions had largel y resolved, leaving a slight corneal opacity in the right eye. Both eyes were now fluorescein-negative, and a Schirmer tear rest showed a slight reduction in tear producti o n in rhe ri ght eye (13 mm; normal range 500 15 to 25 mm), wirh normal rear production in the left eye (18 mm). The cat was anaes rherised ro obtain biopsy sam ples; rh e left pinna was biopsied, wirh a V-sec ri on taken from the edge, and a circular punch biopsy from the centre (including ca rtilage). Blood samples were taken for hae matological and serum biochemical analyses. Res ults we re unremarkable, except for hypoalbuminaemia (2 1 g/lirre; normal range 26 to 4 0 g!l itre) of undetermin ed cause. The blood sa mple was negati ve for feline leukaemia virus (FeLV) (ELISA), feline immunodeficiency virus (F IV) (ELISA) and felin e coronav irus (immunofluorescence test). An antinuclear antibody tesr was also negative. A direct Coombs' res r was negative at 30°C, but positive at a dilution of 1 :2 at 4°C. T horacic radiograp hs showed mild to moderate globular cardiomegaly on borh lateral and dorsoventral views. The ve rtebral heart score was approximately 8-5 (no rmal ran ge 6-9 to 8-1 ). T he hea rt rate was 128 beats/m inute and there was no radi ological or clinical evidence of co ngestive heart failure. It was fel t that the heart changes were sugges ti ve o f ca rdi o myopat hy, either dilared , hypertro phic o r intermediate. H owever, since no echocardiography o r ECG was performed, a diagnosis of ca rdi omyo pathy co uld no r be confirmed. The cat was euthyroi d ar this time (rota! thyroxine 34 nmolllitre; normal range 19 ro 65 nmol/litre). Biopsy of the pinn a showed a curling distortion of the rip of the auricular ca rtilage, with ex tensive intense fibropl as ia , ca pillary proliferati o n and infiltration by neutrophilic leucocytes (Fig 2) . Inflam matory cells exte nded into eroded superfi cial ca rtil age, where there was extensive linea r loss of matrix metac hrom as ia (Fig 3) . T here was intense mastocytosis o f auri cular dermis, but no histo logical evidence of its cause. Focal areas of dermal mi xed lymphocyte, plas ma cell and mast cell acc umulati on were noted . T he ca t was give n I 0 mg of o ral predniso lo ne daily (3 mg/ kg bodywe ight dail y; Prednicare; Animalcare) and within I 0 days showed a marked improve ment. T he ea r fl aps were much less painful and eryt hemarous, and the ca t was playi ng with rh e o ther ca t in the ho use ho ld and showed improved demeanour. The dorsal sca ling had reso lved . There was no alrerari o n ro the righr co rn ea l opac ity, and no pulmo nary or ca rdi ac abn o rm alities were detected o n ausc ultati on. After rhree weeks, th e predniso lone was reduced ro 5 mg daily ( I ·5 mg/kg/day), and afte r six mo nths co 2-5 mg o n alternate days. Eighteen months later, the prednisolone was withdrawn completely. There was no subsequent recurrence in the ear condition during the 14 months follow-up period. Relapsing polychondritis in humans is a rare condition in which auricular distortion and discomfort are major signs. Cartilage in other sites may also be affected, and in a proportion of cases this results in saddle nose deformity (collapse of the nasal septa! cartilage), joint disease, laryngeal/tracheal disease (leading to collapse of the tracheal rings), ocular disease, cardiovascular disease and skin disease. Fever, hearing loss, vertigo and anaemia may also occur. Associated ocular diseases can include conjunctivitis, scleritis, keratitis and keratoconjunctivitis sicca. Cardiovascular changes include aortic insufficiency, pericarditis, arterial aneurysms and arteritis (White 1985, Michet and others 1986) . The disease in humans is believed to be a true autoimmune disorder in which autoantibodies (predominantly immunoglobulin [Ig]G) to native type II collagen are found in titres of up to 1 :320 (McKee 1996) . This contrasts with the situation in rheumatoid arthritis, in which autoantibodies to unfurled rype I, II and III collagen are found, suggesting that antibody production in this condition is an epiphenomenon rather than the cause of disease (Foidart and others 1978 , Ebringer and others 1981 , Meyer and others 1981 . In some strains of rats, idiopathic auricular chondritis is common, and is characterised by histological changes similar to those described in the present case (that is, auricular inflammation, invasion of conchal cartilage by inflammatory cells and chondrolysis) (McEwen and Barsoum 1990) . In the cat, relapsing polychondritis is very rare. To the authors' knowledge, only three confirmed cases have been reported in the literature. The case described here is interesting because it is similar to that described by Bunge and others (1992) ; both cats had evidence of ocular and cardiac changes in addition to the pinna! disease, as can occur in human cases. The other changes seen in humans have not yet been reported in cats. Gauguere and Declercq ( 1999) , calling the condition plasma cell chondritis, suggested a possible viral aetiology, since one reported case was FIV positive (Gauguere and others 1992) and one FeLV positive (Bunge and others 1992) ; the present case was negative for FIV, FeLV and feline coronavirus. The significance of the positive cold Coombs' test result in the present case is uncertain. A titre of 1 :2 is a low positive result; the cat was not anaemic, and did not have signs of cold agglutinin disease, such as punched-out necrosis of the earflap edges, or a vascular pattern of ulceration and necrosis. Also, the histopathological findings were not compatible with cold agglutinin disease. It is of interest that a weak positive Coombs' test result of 1 :4 was found in the case reported by Bunge and others (1992) . Although the disease in cats has been designated relapsing polychondritis, the authors prefer the description of auricular chondritis in their patient, since they have no evidence of involvement of other cartilaginous tissues, nor does the benign clinical course in this case warrant the use of the qualifier 'relapsing'. Clinical differentiation of auricular chondritis from aural haematoma and aural trauma is straightforward; haematoma and trauma are unlikely to be bilateral, nor to be as painful or intensely erythematous. Aural haematomas may exhibit cartilage degeneration and irregular erosion adjacent to the haematoma (Joyce and Day 1997) but do not show the severe, aggressive and extensive changes seen in the present case. Other differential diagnoses include scarring from irritation associated with ear mite infestation, actinic scarring and distortion in cats with unpigmented eartips, discoid and systemic lupus erythe-JOURNAL OF SMALL ANIMAL PRACTICE• VOL 42 •OCTOBER 2001 matosus, and vascular diseases, such as frost-bite damage, and immune-mediated vasculitis. Cases of floppy pinnae in cats (Pearson 1998 , Rest 1998 ) may have the same aetiology as reported here. It is clear that such cases justify as full an investigation as possible, including cardiac and ocular assessment, and detailed histopathological examination, in order to assist with diagnosis and understanding of this condition. Relapsing polychondritis in a cat Autoantibodies to cartilage and type II collagen in relapsing polychondritis and other rheumatic diseases Antibodies to type II collagen in relapsing polychondritis Guaguere and P. Prelaud. Veterinary Times/ Veterinary Business Development Polychondrite auriculaire atrophiante: a propos d'un cas chez un chat lmmunopathogenesis of canine aural haematoma Relapsing polychondritis Auricular chondritis in Wistar rats Relapsing polychondritis -pathogenic role of anti-native collagen type II antibodies: a case report Relapsing polychondritis: survival and predictive role of early disease manifestations Floppy pinnae in Siamese cats Floppy pinnae in Siamese cats Feline dermatology 1983-1985 -'The secret sits' Relapsing polychondritis The authors are very grateful to Dr S. P. Dunham for examining and commenting on the radiographs.