Volume 6 • Issue 4 • 1000194 J Neuroinfect Dis ISSN: 2314-7326 JNID an open access journal Case Report Open Access Neuroinfectious Diseases J o u r n a l o f N e u r o i n f e c ti o u s D i s e a s e s ISSN: 2314-7326 f s Hamid et al., J Neuroinfect Dis 2015, 6;4 http://dx.doi.org/10.4172/2314-7326.1000194 *Corresponding author: Mohamed Faisal Abdul Hamid, Respiratory Unit, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur, Malaysia, Tel: +60391455555; Fax: +60391456679; E-mail: arabinose@hotmail.com Received March 17, 2015; Accepted November 15, 2015; Published November 20, 2015 Citation: Hamid MFA, Ian SC, Yu-Lin AB, Said MSM, Manap RA, (2015)Rifampicin- Resistance Tuberculous Meningitis in a Patient with Cerebral Lupus Diagnosed Using Cerebrospinal Xpert Mtb/Rif Test. J Neuroinfect Dis 6: 194. doi:10.4172/2314- 7326.1000194 Copyright: © 2015 Hamid MFA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Rifampicin-Resistance Tuberculous Meningitis in a Patient with Cerebral Lupus Diagnosed Using Cerebrospinal Xpert Mtb/Rif Test Mohamed Faisal Abdul Hamid 1 *, Soo Chun Ian 1 , Andrea Ban Yu-Lin 1 , Mohd Shahrir Mohamed Said 2 and Roslina Abdul Manap 1 1 Respiratory Unit, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur, Malaysia 2 Rheumatology Unit, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur, Malaysia Abstract Tuberculous (TB) meningitis or tubercular meningitis is a Mycobacterium tuberculosis infection of the meninges—the system of membranes which envelop the central nervous system. Molecular tests like the automated rapid molecular assay Xpert® MTB/RIF greatly expedites the detection of M. tuberculosis complex and rifampicin resistance. We report a 22-year old man with cerebral lupus and concurrent rifampicin resistance tuberculous meningitis which was detected by Xpert® MTB/RIF test in the cerebrospinal fuid. The rifampicin resistance in this patient was due to poor compliance. The patient took one tablet of akurit-4 throughout the intensive phase of treatment. This report highlights the usefulness of molecular testing which allowed a faster diagnosis than a bacteriologic confrmation of drug resistant tuberculosis. This is important as early diagnosis and treatment leads to better outcome in TBM. Keywords: Rifampicin-resistance (RR) tuberculosis; Cerebral lupus; Xpert® MTB/RIF; Meningitis Introduction Multidrug-resistant tuberculosis (MDR-TB) is caused by organ- isms that are resistant to at least isoniazid and rifampicin, the back- bone of current frst-line treatment regime [1]. Rifampicin-resistant TB (RR-TB) is caused by organisms that are resistant to rifampicin with or without resistance to other drugs [1]. MDR-TB and XDR-TB are both forms of RR-TB. Drug-resistant TB commonly occurs in pul- monary tuberculosis; extra-pulmonary involvement particularly tu- berculous meningitis (TBM) is rare and is associated with high mortal- ity. We would like to report the successful treatment of a patient with underlying central nervous system lupus with co-existing MDR-TBM which was diagnosed by a positive cerebrospinal fuid (CSF) Xpert® MTB/RIF assay. He showed marked improvement following com- mencement of second line anti-TB therapy. Case Report A 22-year-old man presented with prolonged fever, photosen- sitivity rash and multiple joint pains for 1 month duration. Clini- cal examination revealed malar rash, oral ulcers and alopecia. Full blood count showed bicytopenia (Hb 13.1 g/dL, white cells 1.3 X 10^9 /L, platelets 103 X 10^9/L). Renal profile and liver function test were both normal. ESR was 66 mm/hr, and CRP was 6 mg/ dL. There was evidence of mild pericardial effusion on transtho- racic echocardiogram. His chest radiograph (CXR) during that ad- mission was normal (Figure 1a). No mantoux test was performed. A clinical diagnosis of active SLE was made. Further blood tests confirmed this diagnosis. ANA 1: 640 (speckled) Anti-dsDNA was negative, and low complement levels. (C3 55.2 mg /dL, C4 15.9 mg/ dL.) He developed altered sensorium leading to aggressive behav- iour. We did not get consent for a lumbar puncture. On the basis of the investigations available, SLE with hematological, serositis, mus- culoskeletal and cerebral involvement was made. He was treated with methylprednisolone, followed by cyclosphomide, and rituximab, and discharged with oral prednisolone 30 mg twice a day. A month later, he presented again with fever, cough and whit- ish sputum for 3 days. His CXR (Figure 1b) showed features of mili- ary tuberculosis and sputum for acid-fast bacilli (AFB) was positive. Anti-TB using fxed-dose combination, Akurit-4 (3 tablets daily) was started. A scheduled second dose of rituximab was withheld in view of evidence of active tuberculosis. He was maintained with oral predniso- lone for SLE and subsequently discharged. He was subsequently lost to our follow-up. Four months later, he presented with generalised tonic-clonic sei- zures. We were worried of treatment interruption but he claimed he had continued anti-TB treatment at a clinic near his home. At that point of presentation he was on the maintenance phase of anti-TB (isoniazid + rifampicin). A lumbar puncture revealed an increased protein level (3029 g/dL) and an MRI brain showed multiple enhanc- ing lesions at the basal ganglia and grey-white matter junction sugges- tive of tuberculoma (Figure 2a and 2b). Further questioning revealed non-compliance to medications with a history of taking only 1 tablet of Akurit-4 throughout the intensive phase of treatment. Treatment was restarted with the addition of dexamethasone and streptomycin. He showed improvement clinically and was discharged well. A B Figure 1: a) Normal CXR in the frst presentation and one month later; b) showing generalized multiple reticula-nodular opacities consistent with miliary tuberculosis.