B-cell leukemia/lymphoma and neuroborreliosis: Diagnostic and therapeutic challenges.

a spirochaete of the genus Borrelia and transmitted by tick-bites of the genus Ixodes; is the most frequently reported vector-borne disease in the Northern Hemisphere1. Borreliosis is a multisystemic disease that can affect skin, joints, heart and central nervous system (CNS). Infection of the CNS by Borrelia, called neuroborreliosis (NB) produces multiple manifestations that includes: Encephalitis, myelitis, intracranial hypertension, aseptic meningitis, meningoencephalitis, meningoradiculitis, vasculitis and cranial or spinal nerve neuropathies2–3. The CNS involvement occurs in 15% of cases during early disseminated disease and is manifested predominantly as cranial neuropathies (8 to 10% cases); it is usually unilateral and mainly affects cranial nerve VII (80%). The other common manifestations include motor or sensitive radiculopathy present in 3% of cases and less frequently—Lymphocytic meningitis, mononeuritis multiplex, cerebellar ataxia and myelitis. The classic triad named Bannwarth syndrome, including meningitis, cranial neuropathy and radiculopathy is rare4. Late manifestations usually appear one year after infection, although the average time period is variable. The different symptoms have been explained by persistence of the spirochaete in untreated cases and also have been related to autoimmune phenomena in patients that do not improve after appropriate therapy5–6. The first challenge when facing this disease is to have a high degree of clinical suspicion for correct diagnosis and beginning antimicrobial therapy. The second is to decide the duration of therapy in patients with NB and immunosuppression, a point where there is controversy among clinicians. In the present report, a case of patient diagnosed with lymphoblastic leukemia/lymphoma is discussed while she was on a trip in Belgium. On her return to Mexico (Hometown), during the second chemotherapy cycle she developed ascending weakness associated with subcortical microangiopathic lesions, diagnosed in magnetic resonance imaging (MRI) that led to the suspicion of NB; the diagnosis was confirmed by western blot (WB) and polymerase chain reaction (PCR) of serum and cerebrospinal fluid (CSF).