Case History:
A 15-year-old Irish sport horse gelding used for show jumping and eventing was presented to the authors’ hospital 13 days after intra-articular medication of the left tarsocrural joint with triamcinolone acetonide, 25mg gentamicin sulfate and hyaluronic acid. The gelding received IA medication of the left tarsocrural joint (TCJ) due to mild, performance-limiting lameness localised to the region, effusion of the joint and an associated OCD lesion. Six days after medication, the gelding developed moderate left hind limb lameness (grade 2/5). The referring veterinary surgeon instigated medical management for lymphangitis/cellulitis; procaine penicillin (17.5mg/kg, I.M., BID), gentamicin sulfate (6.6mg/kg, I.V., SID) and phenylbutazone (4.4mg/kg, I.V. BID). On day 11 a more severe left tarsocrural joint effusion was noted and arthrocentesis revealed a synovial white cell count of 14 x109cells/L. Medical management was continued for a further 2 days before referral on day 13. On arrival at the author’s hospital, a marked left hindlimb lameness was evident (grade 3/5) at the walk with a moderate tarsocrural joint effusion and generalised, mild-moderate proximal third metatarsal swelling.
Four standard radiographic projections of the tarsus were taken (LM, DLPMO, DP, DMPLO) which revealed a medium-sized, displaced OCD DIRT lesion and a shallow subchondral bone defect on the medial trochlea ridge of the talus. Arthrocentesis yielded turbid synovial fluid with a total nucleated cell count (TNCC) of 49x109cells/L, total protein 40g/L and total neutrophil count of 62.8%. These findings were consistent with bacterial synovial sepsis (Morton 2005, Steel 2008). However, these findings were interpreted with caution given the previous intra-articular corticosteroid medication (Tulamo et al.1989, Morton 2005, Steel 2008). The synovial fluid was sent for aerobic culture and sensitivity.
Arthroscopic lavage of the tarsocrural joint was performed under general anaesthesia in dorsal recumbency. A 9x6x3mm OCD fragment that was mobile and free within the joint was removed. There was an obvious exposed subchondral bone “bed” from where this fragment had originated on the DIRT. There was moderate, generalised fibrillation of articular cartilage and moderate to severe fibrin depositions. The fibrinous material was removed from the dorsal and plantar pouches. All pouches of the joint were thoroughly lavaged with 20 litres of balanced isotonic solution following debridement. The debrided material was sent for culture and sensitivity.
Initial antimicrobial and anti-inflammatory therapy consisted of ceftiofur sodium (2.2mg/kg, IM, BID) and gentamicin sulfate (6.6mg/kg, IV, SID) with phenylbutazone (4.4mg/kg, IV, BID). At the end of the surgery, ceftriaxone (1000mg) was injected into the joint and repeated at 48-hour intervals.
The day after surgery the culture and sensitivity showed a marked, diffuse cream-coloured growth that was not sensitive to any of the antimicrobials tested on disc diffusion [IMAGE 1]. The blood agar plate was sent to the Irish Equine Centre for further identification. Six days after the initial surgery the growth was identified as Candida sp. The sample was sent to Public Health England’s mycology reference laboratory and was identified as Wickerhamomyces anomalus(formerly Candida pelliculosa ). Fungal sensitivity revealed sensitivity to amphotericin B and fluconazole with intermediate sensitivity to itraconazole and voriconazole. The sensitivity profile was only available from day 23 following further laboratory analysis.
The horse was initially sound at the walk post-surgery, there was a gradual deterioration in comfort levels and by day 9 a grade 2/5 lameness was present at the walk. Arthrocentesis on day 9 revealed a white blood cell count of 7.1x109cells/L with 86.6% neutrophils. Intra-articular voriconazole (100mg)(Sherman et al.2006, Cohen 2011) was administered on days 9, 10, 13, 18 and 21. On day 14, the horse was grade 3/5 lame at the walk and worsened with walking. The white cell count had mildly increased to 8.1 x109cells/L with 64% neutrophils; these values suggested the infection was being controlled. Further culture and sensitivity performed on a separate synovial fluid sample confirmed the continued presence of Wickerhamomyces anomalus. Injectable anti-microbials were ceased and oral enrofloxacin (7.5mg/kg, PO, SID) was started. On day 22, oral fluconazole was initiated at a loading dose of 14mg/kg (PO, SID) and then continued at 5mg/kg (Cohen et al.2008). Due to the poor response to treatment, a 2ndarthroscopic lavage was performed on day 23 with fluconazole (20mg) (Cohen et al. 2008) injected into the joint immediately at the end of surgery. The joint on arthroscopy at this time was severely inflamed with greater articular cartilage fibrillation noted. Intra-articular fluconazole (20mg) was administered at 48-hour intervals following surgery. On day 25, the horse was 2-3/5 lame at the walk, but on day 26 a toe-touching lameness (grade 5/5) was present. On day 28, repeat radiographs showed the presence of a subchondral lytic lesion with articular involvement associated with the distal tibia. From day 28 until day 39 fluconazole was administered IA once daily with a notable improvement in lameness at walk noted by day 40. On day 42, oral enrofloxacin was ceased following multiple negative bacterial cultures. A repeat synovial culture was performed on day 55 due to the persistence of a mild (grade 1/5) lameness at the walk. The joint was medicated with 20mg amphotericin-B and hyaluronic acid. This was repeated 7 and 10 days later and then again after 3 days. There was a transient, marked increase in lameness following IA amphotericin-B. The culture obtained from the synovial fluid on day 55 was the first negative result obtained. A mild-moderate (grade 2/5) left hind limb lameness persisted at a trot until day 107 when the horse became grade 2/5 lame at the walk and non-weight bearing lame at the trot with moderate to severe TCJ effusion. The culture of synovial fluid returned a positive result forWickerhamomyces anomalus . On day 126 progression of the subchondral lytic lesion on the distal tibia was evident with significant arthritic changes in the TCJ and distal tarsal joints [IMAGE 2]. A moderate-to-severe lameness was still present at the walk. The decision was made to humanely euthanise the horse.
A post-mortem examination was performed. On gross examination, the tarsocrural joint was noted to be distended with a markedly proliferative synovial membrane [IMAGE 3] almost occluding the joint space. Within the joint capsule, multiple 2-4mm white-cream friable nodules were evident. There was an irregular erosion on the distomedial trochlear ridge with superficial erosion of the articular cartilage on the medial aspect of the lateral tracheolar ridge. There was an erosion of the dorsal third in the intercondylar fossa. There was cartilage erosion of the articular surface of the distal tibia over the central ridge and in the fossa on either side [IMAGE 4]. These erosions extended into the subchondral bone.
Histopathological examination showed fibrosis, neovascularisation and haemosiderin deposition in the synovial membrane with chronic inflammatory foci. There was superficial necrosis of the synovial membrane and marked inflammatory infiltrates (macrophages, lymphocytes, plasma cells and some neutrophils). Fungal yeast-like organisms [IMAGE 5] were identified predominantly within the necrotic tissue. A heavy growth of yeast previously identified as Wickerhamomyces anomaluswas isolated from the joint.