A previously well 21-year-old Bangladesh-born man presented with a six-month history of night sweats, fever, and axillary lymphadenopathy and a four-week history of evolving neurological symptoms including vertigo, diplopia, ataxia, left sided weakness, and right facial droop. On examination there were multiple cranial nerve palsies, reduced power in the left upper and lower limbs, and enlarged left axillary lymph nodes. Multiple enhancing lesions in the pontomedullary junction, right cerebellum, and left frontal lobe were detected on magnetic resonance imaging (MRI) (see Figure 1(a)). A left axillary mass biopsy demonstrated granulomatous lymphadenitis, with negative Truant's stain and negative mycobacterial PCR. HIV testing was negative, and a CT of the chest, abdomen, and pelvis showed isolated left axillary lymphadenopathy.
Rifampicin, isoniazid, pyrazinamide, ethambutol (HREZ), and dexamethasone were commenced. He had partial neurological improvement in left sided weakness but approximately one month later developed nausea, vomiting, dysphagia, and headache, with further reduction in power and coordination on the left. Repeat MRI showed increased oedema and size of the pontomedullary and right cerebellar lesions with hydrocephalus (see Figure 1(b)). The dexamethasone dose was increased, HREZ continued, and he improved symptomatically. Mycobacterium tuberculosis was isolated from the lymph node biopsy and after seven weeks of therapy provisional rifampicin and probable isoniazid resistance was identified. Therapy was changed to rifabutin, isoniazid, pyrazinamide, ethambutol, amikacin, moxifloxacin, cycloserine, and prothionamide. Final susceptibility results demonstrated resistance to isoniazid, rifampicin, rifabutin, clofazimine, and streptomycin with sensitivity to ethambutol, pyrazinamide, amikacin, capreomycin, ciprofloxacin, cycloserine, and ethionamide. The regimen was continued without rifabutin. After two weeks of inpatient treatment, he was discharged on a weaning dose of dexamethasone, with mild left facial droop and paresthesia in the left arm.
Repeat MRI approximately two months after commencement of the MDR TB regimen showed a marked reduction in the size of the right-sided pontine and cerebellar lesions (see Figure 1(c)). Dexamethasone was ceased, precipitating an adrenal crisis and immune reaction in the right middle lobe of the lung. He was recommenced on steroids, improved, and was discharged on a weaning dose of cortisone. Amikacin was ceased after twelve months while other treatment was continued for a total of two years after repeat MRI showed almost complete resolution of the lesions. He was monitored for the next five years with repeat MRI scanning showing complete resolution of the right cerebellar lesion and continued improvement in the pontomedullary lesion (see Figure 1(d)). Complications during treatment included avascular necrosis of the hip, which was managed conservatively. After seven years of follow-up, his residual symptoms included minor difficulty with left upper limb fine motor tasks and hip pain.