Introduction: Muscle-specific tyrosine kinase (MuSK) myasthenia gravis (MG) is a severe, subtype of MG with different pathogenesis, atypical clinical features, lack of symptom fluctuations, and acetylcholinesterase inhibitors failure making MuSK-MG diagnosis challenging. Such patients may suffer a worsening of symptoms upon exposure to a variety of medications such as fluoroquinolones. Fluoroquinolones of any generation may interfere with neuromuscular transmission and may lead to MG symptoms by simply unmasking a pre-existing mild case. This case report describes the development of myasthenic crisis and respiratory distress following the use of levofloxacin in a patient who was initially diagnosed as tuberculous meningitis with no previous diagnosis of MG. Case description: A 24-year-old woman presented with 1 month history of low-grade fever and headache without any raised intracranial pressure features or neck stiffness. All her routine laboratory investigations and brain imaging were normal. Cerebrospinal fluid analysis showed normal protein and sugar levels, zero cell count with mild cartridge-based nucleic acid amplification test (CB-NAAT) positivity for mycobacterium tuberculosis. She was started on routine anti-tubercular therapy (ATT) initially, later changed to modified ATT with levofloxacin, rifampicin, and ethambutol in view of deranged liver function tests. One month later, she returned with complaints of double vision, drooping of eyelids, unsteadiness while walking, dysphagia to solids and liquids, and shortness of breath. On examination, patient had bilateral ptosis and restricted extraocular movements in all directions. Curtain sign was present. Single breath count was eight. As the patient's clinical condition worsened despite adequate ATT regimen and in view of mild CB-NAAT positivity, evaluation for alternate diagnosis was considered. Ice pack test and neostigmine challenge test were done and both were positive. Repetitive nerve stimulation (RNS) showed more than 10% decremental response in facial and limb muscles. Acetylcholine receptor and MuSK antibody tests were sent. A working diagnosis of MG with myasthenic crisis was made and patient was started on intravenous immunoglobulin (IVIG) at a dose of 2 gm/kg for 5 days and oral pyridostigmine. Antibody testing came positive for anti-MuSK antibody. As the patient did not show any improvement to IVIG, she was given injection rituximab 1 gm and simultaneously started on mycophenolate mofetil. Even with rituximab, patient did not show adequate response, so she was taken up for plasma exchange with which her symptoms improved dramatically and was continued on mycophenolate mofetil. Conclusion: Muscle-specific tyrosine kinase-MG is a subtype of MG with atypical clinical presentations causing a delay in diagnosis. In such cases MuSK-Ab testing confirms the diagnosis. Fluoroquinolone exposure may result in potentially life-threatening myasthenia gravis in patients with underlying disease. Our case shows that levofloxacin can unmask MuSK-MG, which has not been much reported in the literature. Response to acetylcholinesterase inhibitors is often unsatisfactory from that expected in MG patients. Among all immunotherapies, plasma exchange can be considered as the cornerstone of treatment for MuSK-MG which was evident in our case where inadequate response was showed to IVIG and rituximab.