Minimal Cerebrospinal Fluid Concentration of Miltefosine despite Therapeutic Plasma Levels during the Treatment of Amebic Encephalitis.

Miltefosine is an alkylphosphocholine compound that is used primarily for treatment of leishmaniasis and demonstrates in vitro and in vivo antiamebic activity against Acanthamoeba species. Recommendations for treatment of amebic encephalitis generally include miltefosine therapy. Data indicate that treatment with an amebicidal concentration of at least 16 µg/ml of miltefosine is required for most Acanthamoeba species. Although there is a high level of mortality associated with amebic encephalitis, a paucity of data regarding miltefosine levels in plasma and cerebrospinal fluid in vivo exists in the literature. We found that despite aggressive dosing (oral miltefosine 50 mg every 6 h) and therapeutic plasma levels, the miltefosine concentration in cerebrospinal fluid was negligible in a patient with AIDS and Acanthamoeba encephalitis.

Utility of C-reactive protein and serum amyloid A in the diagnosis of equine protozoal myeloencephalitis.

BACKGROUND: Accurate antemortem EPM diagnosis requires evidence of intrathecal antibody production. Some advocate the use of acute phase proteins in addition to serology, which alone results in substantial false positives. HYPOTHESIS/OBJECTIVES: The purpose of this study was to determine if serum C-reactive protein (CRP) or serum amyloid A (SAA) concentrations were elevated in cases of equine protozoal myeloencephalitis (EPM) compared to other neurological diseases. ANIMALS: 25 clinical cases of equine neurological disease: EPM (10), cervical vertebral stenotic myelopathy (CVSM) (10), neuroborreliosis (2), equine motor neuron disease (1), degenerative myelopathy (1), and leukoencephalomalacia (1). METHODS: Serum and CSF CRP and SAA were measured. Selection criteria included neurologic disease, antemortem diagnosis of EPM or CVSM, or postmortem diagnosis of EPM, CVSM, or other neurologic disease, and availability of serological results and archived samples for testing. RESULTS: Serum SAA and serum CRP levels were generally undetectable or low in horses with EPM (median CRP ≤0.1 mg/L, ≤0.1-14.4 mg/L; median SAA ≤0.1 mg/L, ≤0.1-6.11 mg/L) and CVSM (median CRP ≤0.1, ≤0.1-2.41 mg/L; median SAA ≤0.1mg/L, ≤0.1-13.88 mg/L). CSF CRP and SAA for horses with EPM (median CRP 3.35 mg/l, 0.19-13.43 mg/l; median SAA ≤0.1 mg/L, ≤0.1-2.4 mg/L) and CVSM (median CRP 4.015 mg/L, 0.16-9.62 mg/L; median SAA 0.62 mg/L, ≤0.1-2.91 mg/L) were also undetectable or low. Kruskal-Wallis test showed no statistically significant differences between serum CRP (P = .14), serum SAA (P = .79), spinal fluid CRP (P = .65), or spinal fluid SAA between horses with EPM and CVSM (P = .52). CONCLUSION: Neither SAA nor CRP in serum or CSF aid diagnosis of EPM.

Increased CXCL-13 levels in human African trypanosomiasis meningo-encephalitis.

OBJECTIVES: To determine the role of the B-cell attracting chemokine CXCL-13, which may initiate B-cell trafficking and IgM production in diagnosing HAT meningo-encephalitis. METHODS: We determined CXCL-13 levels by ELISA on paired sera and CSF of 26 patients from Angola and of 16 controls (six endemic and ten non-endemic). Results were compared to standard stage determination markers and IgM intrathecal synthesis. RESULTS: CXCL-13 levels in patients' sera had a median value of 386.6 pg/ml and increased levels were associated with presence of trypanosomes in the CSF but not with other stage markers. CXCL-13 levels in patients' CSF had a median value of 80.9 pg/ml and increased levels were associated with all standard stage determination markers and IgM intrathecal synthesis. CONCLUSION: CXCL-13 levels in CSF increased significantly during the course of HAT. Hence the value of CXCL-13 for diagnosis, follow-up or as a marker of disease severity should be tested in a well-defined cohort study.