Serological testing for syphilis in the differential diagnosis of cognitive decline and polyneuropathy in geriatric patients.

BACKGROUND: In the 19th century, neurosyphilis was the most frequent cause of dementia in Western Europe. Now dementia caused by syphilis has become rare in Germany. We studied whether routine testing of patients with cognitive abnormalities or neuropathy for antibodies against Treponema pallidum has therapeutic consequences in geriatric patients. METHODS: A Treponema pallidum electrochemiluminescence immunoassay (TP-ECLIA) is routinely performed in all in-patients treated at our institution with cognitve decline or neuropathy and no or insufficient previous diagnostic workup. Patients with a positive TP-ECLIA treated from October 2015 to January 2022 (76 months) were retrospectively evaluated. In cases of positive TP-ECLIA, further specific laboratory investigations were performed to assess whether antibiotic therapy was indicated. RESULTS: In 42 of 4116 patients (1.0%), TP-ECLIA detected antibodies directed against Treponema in serum. Specifity of these antibodies was ensured by immunoblot in 22 patients (11 × positiv, 11 × borderline values). Treponema-specific IgM was detectable in the serum of one patient, in 3 patients the Rapid Plasma Reagin (RPR) test, a modified Venereal Disease Research Laboratory test (VDRL), in serum was positiv. CSF analysis was performed in 10 patients. One patient had CSF pleocytosis. In 2 other patients, the Treponema-specific IgG antibody index was elevated. 5 patients received antibiotic therapy (4 × ceftriaxone 2 g/d i.v., 1 × doxycycline 300 mg/d p.o.). CONCLUSION: In approx. 1‰ of patients with previously undiagnosed or not sufficiently diagnosed cognitive decline or neuropathy, the diagnostic workup for active syphilis resulted in a course of antibiotic treatment.

Chronic Candida albicans meningitis misdiagnosed as polymyalgia rheumatica and successfully treated with voriconazole.

The outcome of chronic meningitis depends to a large degree on the causative pathogen and the interval between onset of symptoms and diagnosis. We present a patient with a delayed diagnosis and several complications, for whom adequate therapy resulted in a favorable outcome. In a 76-year-old male patient, Candida albicans meningitis was diagnosed 4 months after the onset of symptoms. CSF findings (protein >1000 mg/L, predominance of intrathecal immunoglobulin A synthesis, lactate concentrations of approx. 10 mmol/L, leukocyte counts around 1000/µl, variable differential leukocyte counts) resembled tuberculous meningitis. In spite of the long interval without treatment, voriconazole 200 mg every 12 h for 7 weeks followed by fluconazole 300 mg/day maintenance therapy for 7 months led to a recovery with only mild deficits. The case illustrates that 1. C. albicans can cause chronic meningitis in patients without severe immune defects, 2. patients can survive C. albicans meningitis with mild long-term sequelae even when diagnosis and adequate treatment are delayed, and 3. voriconazole as a sole agent may be suitable for treatment of C. albicans meningitis.

Modification of CSF findings in multiple sclerosis in the era of rapidly expanding treatment options.

BACKGROUND: The detection of cerebrospinal fluid (CSF)-specific oligoclonal bands (OCB) as well as an elevated antibody production directed against neurotrophic viruses remain hallmark findings in multiple sclerosis (MS). In general, individual patients show a unique pattern of OCB, which is believed to persist over time. Here, the authors revisited this assumption and investigated to what extent common anti-inflammatory MS medications can alter the level of immunoglobulins produced within the CSF. METHODS: The authors analyzed three patients and compared CSF findings longitudinally. Two of these patients received corticosteroids, either systemically or intrathecally, the third patient was treated continuously with natalizumab. RESULTS: In line with reports from other groups, the authors observed that continuous natalizumab treatment dampened the intrathecal immunoglobulin production in our patient. Exceeding this anticipated scenario, the authors detected that the continued administration of corticosteroids similarly reduced the production of CSF immunoglobulins, down to a level at which these parameters are considered normal. CONCLUSION: These observations suggest that inflammatory CSF findings are more accessible to immunomodulatory MS treatment than previously thought, and that accordingly, their significance may transition from a sole diagnostic finding to a valuable therapeutic biomarker which may help to assess effective targeting of CNS-established inflammation in MS.