Abstract Background/Aims Nocardiosis is a rare infectious disease caused by the aerobic bacteria genus Nocardia and can cause severe suppurative disease affecting virtually any organ. It tends to affect the immunocompromised, making rheumatology patients a particular risk group for this infection. It is not normal human flora and is found in soil, decaying vegetable matter and aquatic environments. It can become airborne and the most common means of entry is thought to be dust inhalation. Methods Our patient is a 75-year-old woman with giant cell arteritis (GCA) treated with prednisolone, SC methotrexate and tocilizumab (started 4 months before her acute illness). Symptoms began with a fall in the garden sustaining a nasty laceration to her leg and an injury to her back worsening some chronic lower back pain (X-rays did not show any fracture). Over the next 5 weeks due to a productive cough and sweats she was prescribed oral antibiotics with no improvement. She was then admitted to hospital due to an acute increase in the severity of her lower back pain alongside a change in character to a burning pain. Her presenting CRP was 32, likely due to having held tocilizumab due to a presumed chest infection. MRI showed a collection in the right erector spinae muscle extending from C7 to the iliac crest and another large collection in the right thigh. A mass in the left sub-mammary area led to a chest CT that showed a chest wall abscess alongside a spiculated lesion in the lung, and further nodular changes. Peripheral blood cultures were negative and eventually draining of the erector spinae abscess led to culture of Nocardiosis nova. Imipenam and Septrin were given as per sensitivities. Unfortunately, our patient has had a difficult clinical course. During her hospital stay she has had possible DRESS syndrome/Septrin-induced liver injury alongside drug induced neutropaenia and lymphopaenia and a possible stroke (this was thought less likely to represent CNS Nocardiosis). Results Her rheumatology management initially involved stopping her DMARDs however due to flares in symptoms her doses of prednisolone have been up and down. It has been difficult to separate symptoms that may be due to cervical spine collections and a possible CNS lesion from GCA symptoms. Conclusion This case demonstrates the need to thoroughly investigate immunosuppressed patients when they are not responding as expected to antibiotics or present with atypical symptoms. It also demonstrates the importance of obtaining a microbiological diagnosis. Cellular immunity is generally thought to be key in preventing Nocardia dissemination however in our patient’s case she was only taking 2.5mg prednisolone when admitted. This is one of only a few case reports of patients developing Nocardia infection whilst on tocilizumab. Disclosure R.J. Crowder: None. H. Mills: None. O. Savanovic-Abel: None. J. King: None. O. Moore: None. M. Perry: None. S. Hewagamage: None. M. Gunathilaka: None.
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