At the end of 2010, an estimated 34 million people were living with HIV worldwide. In North America, Western Europe and Central Europe, the total number of people living with HIV reached an estimated 2.2 million and the HIV incidence has changed little since 2004 [1]. Similar to AIDS, the cause of Lyme disease was discovered in the early 1980s [2,3]. Lyme disease, an infection caused by the spirochete Borrelia burgdorferi, is the most frequent ixodid tick-borne human disease in the world, with an incidence of approximately 85 500 patients annually in Europe [4] and 16 500 in North America [5]. Remarkably, despite these high numbers, the incidence of Lyme disease in HIV-positive patients is not well known. Especially for neuroborreliosis in HIV-positive patients, very few cases have been described. Here, we report on an HIV-positive patient with neuroborreliosis whose diagnosis was complicated by a diagnostic pitfall, induced by an excess of positive findings both in blood and in liquor. An antiretroviral therapy naive 47-year-old man with asymptomatic HIV-1 infection and a CD4+ T-cell count of 471 cells/μl 2 months before was admitted to our ward with fever of 39°C and progressive detoriation. He had a 2-month history of progressively frequent headache, vomiting, fatigue and abrupt temporary pareses of his right leg occurring up to three times a week. Family members noticed he was more forgetful than usual and his speech was slower. They further described ‘absences’ where the patient was unresponsive with amnesia afterwards. In the past, three tick bites were documented in this patient by his general practitioner 10 years, 2 years and 5 months prior, respectively. Erythema migrans had not been observed at any time. At physical examination, the patient was bradyphrenic and showed difficulty in understanding complex tasks. Apart from this, there were no other neurological abnormalities. Biochemistry and haematology showed only an elevated C-reactive protein of 45 mg/l; his CD4+ T-cell count was 322 cells/μl. An MRI of the brain showed enhancement of the basal meninges compatible with meningitis. Analysis of the cerebrospinal fluid (CSF) revealed 0 erythrocytes and 340 leucocytes/μl, no bacteria in Gram and Ziehl Neelsen stain, a reduced glucose concentration of 1.6 mmol/l and an elevated protein concentration of 3.05 g/l. Empiric treatment for neuroborreliosis, meningitis tuberculosa and meningitis herpetica was started with ceftriaxon, tuberculostatics with dexamethason and acyclovir, respectively. Evolving results made a lymphoma, tuberculosis and herpes infection unlikely and the respective drugs were discontinued after 4 days. Other serological and molecular assays provided us with more information than expected, however. As illustrated in Table 1, there was a multiplicity of positive results in serology and western blot analysis. As many agents had negative PCRs in CSF, the increased CSF/serum ratios of IgG (herpes simplex virus, varicella zoster virus, cytomegalovirus) were considered to be caused by increased vascular permeability in the brain, an epiphenomenon in the context of inflammation. In contrast, the PCRs of HIV-1, Epstein–Barr virus (EBV) and B. burgdorferi were all positive, a surprising combination. Remarkably, HIV-1 viral load was higher in the CSF than in foregoing plasma samples. Similarly, B. burgdorferi DNA and EBV DNA were clearly positive in CSF but undetectable in blood plasma. Initially, the single diagnosis of Lyme neuroborreliosis was made and the tuberculostatics, as well as the aciclovir, was stopped (after 4 days of treatment). The patient received 2 g of ceftriaxone intravenously once daily for 4 weeks. Within 1 week, his symptoms began regressing and, at 6 months follow-up, he was symptom free. Diagnostics were repeated 9 months after presentation and these confirmed remission of the neuroborreliosis, as well as the EBV.Table 1: Time table of positive and negative results for HIV-1, Borrelia burgdorferi and Epstein–Barr virus in blood and in cerebrospinal fluid.To our knowledge, the combination of HIV-1, EBV and B. burgdorferi in the liquor of one patient – as demonstrated by PCR and with higher viral loads in liquor than in plasma – is unique. Our major concern is that in the eventuality of stepwise diagnostic procedures, a first positive result in liquor, for example for EBV and/or HIV, may lead to the withdrawal of supplementary diagnostic tests in liquor, resulting in a missed diagnosis. In conclusion, we describe the successful antibiotic treatment of neuroborreliosis in an HIV patient with simultaneous presence of B. burgdorferi, HIV-1 and EBV genomes in the CSF. Acknowledgements Conflicts of interest There are no conflicts of interest. Written informed consent for publication of clinical details was obtained from the patient.
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Open Access
Jan 1, 2014
Yoonjung Kim + 3
