Progressive multifocal leukoencephalopathy in a 44-year old male with idiopathic CD4+ T-lymphocytopenia treated with mirtazapine and mefloquine.

Progressive multifocal leukoencephalopathy (PML) is an opportunistic viral infection of the central nervous system caused by the reactivation of John Cunningham virus (JCV) in immunocompromised patients, most commonly in human immunodeficiency virus (HIV) infection, and less commonly in those receiving various immunosuppressive regimens. Prognosis of untreated PML is grave and the mainstay of treatment is the reversal of immunosuppression, usually by institution of antiretroviral drugs in HIV patients and cessation of immunosuppressive therapies in others. PML is increasingly being reported in those with minimal or occult immunosuppression. A small fraction of these patients meet the criteria for idiopathic CD4+ T-lymphocytopenia (ICL) after exclusion of all secondary causes of lymphocytopenia, including HIV. A 44-year-old previously healthy male presented with clinical and radiological features suggestive of PML. Cerebrospinal fluid samples were repeatedly negative for JCV. Immunohistochemistry on brain biopsy eventually confirmed PML. Despite extensive work-up, the only abnormality detected was an unexplained and persistently low absolute CD4+ T-lymphocyte count. Based on the limited available literature on the treatment of non-HIV PML, he was treated with a combination of mirtazapine and mefloquine with clinical improvement. Non-HIV PML remains relatively uncommon, and PML as a presenting feature of ICL is rare. It is important to document and follow these patients to be able to assess the relative risks associated with various causes and formulate effective therapeutic strategies.

Antihypertensive, Amlodipine Besilate Inhibits Growth and Biofilm of Human Fungal Pathogen Candida.

Candida albicans and Candida glabrata are two important human pathogens associated with high mortality. The anti-Candida potential of an antihypertensive drug, amlodipine besilate (AB), was studied against 10 strains of Candida, including 8 clinical isolates. AB is an inhibitor of voltage-gated Ca2+ channel (VGCC) of mammals. CCH1 expresses in a part of Ca2+ channel of Candida, which is a homologue of α subunit of mammalian VGCC. In plate assays, all strains of Candida showed sensitivity to AB on agar media at 256 µg/mL concentration, AB caused lethality at concentrations of 16 and 64 µg/mL in clinical isolates of C. glabrata and all strains of C. albicans, respectively. Minimum fungicidal concentration (MFC) values of AB varied for different strains. The clinical isolates of C. glabrata turned out to be more susceptible to AB than those of C. albicans. At 16 µg/mL, AB showed reduction of biofilm in the range of 41.51%-79.66% for C. glabrata strains and 32.00%-54.06% for C. albicans strains. AB has shown potential antifungal properties against the laboratory strains and clinical isolates of C. glabrata and C. albicans. In conclusion, AB exhibited potential antifungal properties against planktonic form and biofilm of C. glabrata and C. albicans. It was more effective against C. glabrata than against C. albicans in vitro.