A 2-year-old female neutered domestic shorthair cat presented with a 6-month history of an intermittent bilateral forelimb lameness, an intermittent 'bunny-hopping' hindlimb gait, difficulty with use of stairs and jumping and occasional vocalisation suspected to be pain-related. The gait was worse following rest and improved with walking. Eighteen months prior to presentation, there had been a period of right hindlimb lameness followed by a period of left hindlimb lameness that later resolved. The cat had been in the owner's possession since the age of 12 weeks, had not left the UK, had outdoor access and was fed a complete commercial cat food. Meloxicam (0.05 mg/kg PO q24h [Metacam; Boehringer Ingelheim]) had been used intermittently for several months prior to presentation but with limited effect.
On initial presentation to the neurology department, there was a right forelimb lameness at rest, which improved with walking. A mild medial patellar luxation was palpable bilaterally. Neurological examination detected a normal gait with normal postural reactions, normal spinal reflexes, normal cranial nerve testing and no pain on spinal palpation. The cat was discharged with a further course of 0.05 mg/kg meloxicam PO q24h and restricted activity was advised.
On follow-up examination with the orthopaedic department 8 weeks later, the cat was markedly lame on all four limbs but particularly on the forelimbs. There was alternation between toe-walking on the forelimbs with a hunched posture and using the dorsal aspect of the carpi to walk on (Figure 1a,b). The cat would hiss repeatedly when walking and would lie down tentatively, appearing happier and less painful when lying down. When not lying down, the cat preferred to sit back on the hindlimbs and non-weightbear on the forelimbs (Figure 1c; so-called kangaroo stance). A source of pain could not be localised on the forelimbs, but there was a repeatable pain response to palpation around the calcaneus bone and insertion of the Achilles tendon bilaterally. Differential diagnoses included a diffuse neuromuscular disease, an autoimmune disease such as systemic lupus erythematosus or polyarthritis, or an infectious disease such as toxoplasmosis.
Haematology was unremarkable. Serum biochemistry revealed a mild elevation in creatine kinase (237 U/l; reference interval [RI] 50-150 U/l) but was otherwise unremarkable. Serology for feline leukaemia virus and feline immunodeficiency virus (FIV) was negative. Serology for antinuclear antibodies (ANA) and T gondii IgG and IgM were pending.
The cat was sedated with 5 microg/kg dexmedetomidine (Dexdomitor; Zoetis) intravenously (IV) and 0.02 mg/kg buprenorphine (Buprecare; Animalcare) IV with a top-up of propofol (Propoflo Plus; Zoetis) IV to effect. Radiographs of the elbows and antebrachii were unremarkable. Radiographs of the tarsi revealed a small spur of bone projecting distally from the plantar aspect of the flexor surface of the left calcaneus, slight undulation to the plantar surface of the proximal calcaneal tuberosity bilaterally, and mild soft tissue swelling over the point of the calcaneal tuberosity and distal calcaneus and Achilles tendon bilaterally. These changes were considered mild and non-specific. Arthrocentesis of the left stifle, left shoulder, left carpus and left tarsus was unremarkable. A sample of bursal fluid from the right Achilles tendon revealed neutrophilic inflammation with intracytoplasmic inclusions suspected to be lupus cells or Dohle bodies (Figure 2). Sedation was reversed with 50 microg/kg atipamezole (Antisedan; Zoetis) intramuscularly.
The cat was hospitalised prior to further investigations and received 0.02 mg/kg buprenorphine IV q6-8h and 0.05 mg/kg meloxicam PO q24h. There was no improvement with this treatment.
Anaesthesia was induced with propofol IV to effect, following a premedication of 0.2 mg/kg methadone (Methadyne; Jurox) IV and 5 microg/kg dexmedetomidine IV and was maintained with isoflurane (IsoFlo; Zoetis) and oxygen. Cefuroxime 20 mg/kg (Zinacef; GlaxoSmithKline) IV was provided perioperatively. Nerve conduction velocity (NCV) studies of the left tibial motor nerve, left ulnar motor nerve and left tibial sensory nerves were within normal limits. All F wave latencies were within normal limits. Sensory nerve studies were also normal. Electromyography (EMG) of the left flexor carpi ulnaris, left biceps, left supraspinatus, left gastrocnemius, left cranial tibial and left middle gluteal muscles showed increased insertional activity. The left extensor carpi radialis longus, left deltoid and the left triceps muscle showed increased spontaneous activity. The left supraspinatus muscle showed increased insertional activity and slightly increased spontaneous activity. The left palmar interossei, left semimembranosus, left biceps femoris and left quadriceps muscles showed no evidence of electrical instability.
NCV and EMG findings were consistent with a diffuse muscular disease, worse in the proximal thoracic limb and distal pelvic limb muscles. An axonopathy without secondary myelin disturbance was considered less likely. Results from the EMG are summarised in Table 1. A sample of fluid taken from the left Achilles tendon bursa was consistent with findings from the contralateral side: neutrophilic inflammation with intracytoplasmic inclusions suspected to be lupus cells or Dohle bodies. Biopsies were taken from the right infraspinatus, right triceps brachii, right extensor carpi radialis, right cranial tibialis and right gastrocnemius muscles and submitted for histopathology and T gondii PCR. The cat was discharged from hospital with 0.05 mg/kg meloxicam PO q24h while results were pending.
T gondii serology using an immunofluorescent antibody assay returned with a markedly elevated IgG titre of 1:1600 (RI <1:50) and borderline IgM titre of 1:25 (RI <1:25). ANA titre was negative. Clindamycin (Antirobe; Zoetis) was started at 19.2 mg/kg PO q12h and the course of 0.05 mg/kg meloxicam PO q24h continued. Histopathology of each muscle biopsy revealed a diffuse, chronic, moderate myopathy with some myofibre resorption. There was no evidence of T gondii DNA on PCR testing of the right triceps brachii muscle.
An improvement was seen within 3 days of starting the clindamycin. T gondii serology 2 weeks after starting the clindamycin revealed a markedly elevated IgG titre of 1:1600 and a mildly elevated IgM titre of 1:50.
The cat re-presented following a 6-week course of clindamycin. The owners reported an occasional forelimb lameness, but otherwise there had been significant improvement. The cat was more sociable, would play with the other in its home cat and had stopped vocalising. On examination, the cat was walking relatively normally. There was no toe-walking, no walking on the dorsal aspect of the carpi and no sitting back on the hindlimbs. There was mild enlargement of the Achilles tendon bursae, more so on the right, with some resentment on palpation. An ophthalmological examination detected a small chorioretinal scar that could be compatible with a toxoplasmosis lesion; there was no evidence of active lesions and no ophthalmic nerve pathology. The clindamycin was stopped, and meloxicam continued at the same dose for a further 3 weeks. T gondii serology repeated 13 weeks after finishing the clindamycin revealed a positive IgG titre of 1:400 and a normal IgM titre of 1:20.
The cat was presented for a follow-up examination 20 months after the cessation of treatment. The owners reported there was full resolution of clinical signs 3 months from the start of the clindamycin. The cat had not received any medication since that time and there had been no recurrence of clinical signs. On examination, the gait was normal with no signs of lameness (see video 1 in the supplementary material). The cat could jump up and down from a chair and consultation table normally (see video 2 in the supplementary material). There was mild irregularity on palpation of the point of the calcaneus bilaterally, but no swelling of the Achilles tendon bursae and no patellar luxation. The remainder of the physical examination was unremarkable.