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.