Typhoid fever as a cause of opportunistic infection: case report

BACKGROUND: Typhoid fever is a systemic infection caused by the bacterium Salmonella enterica subspecies enterica serotype typhi, which is acquired by ingestion of contaminated food and water. Each year the disease affects at least 16 million persons world-wide, most of whom reside in the developing countries of Southeast Asia and Africa. In Italy the disease is uncommon with a greater number of cases in Southern regions than in Northern ones. CASE PRESENTATION: We report on a 57-year-old Sri-Lankan male affected by typhoid fever, the onset of which was accompanied by oropharyngeal candidiasis. This clinical sign was due to a transient cell-mediated immunity depression (CD4+ cell count was 130 cells/mm(3)) probably caused by Salmonella typhi infection. Human immunodeficiency virus infection was ruled out. Diagnosis of typhoid fever was made by the isolation of Salmonella typhi from two consecutive blood cultures. The patient recovered after a ten days therapy with ciprofloxacin and his CD4+ cell count improved gradually until normalization within 3 weeks. CONCLUSION: Our patient is the first reported case of typhoid fever associated with oropharyngeal candidiasis. This finding suggests a close correlation between Salmonella typhi infection and transitory immunodepression

The trypanocidal effect of NO-releasing agents is not due to inhibition of the major cysteine proteinase in Trypanosoma brucei

The lysosomal cysteine proteinase activity of bloodstream forms of Trypanosoma brucei is a validated drug target. Previously, it was reported that nitric oxide (NO)-releasing agents inhibit the catalytic activity of cysteine proteinases of the protozoan parasites Leishmania infantum, Trypanosoma cruzi and Plasmodium falciparum. In this study, we investigated the effect of the NO-donors S-nitrosoglutathione, (+/-)-(E)-4-ethyl-2[(E)-hydroxyimino]-5-nitro-3-hexenamide, 3-morpholinosydnonimine (SIN-1) and S-nitroso-N-acetyl-DL-penicillamine on the activity of the cysteine proteinase of T. brucei. At a concentration of 1 mM, the NO donors inhibited the catalytic activity of purified T. brucei cysteine proteinase by 50-90%. With the exception of SIN-1, all NO donors displayed trypanocidal activities against bloodstream forms of T. brucei in vitro with 50% growth inhibition values of around 30 microM. However, the NO donors were ineffective in significantly inhibiting the cysteine proteinase activity within the parasites. This finding was confirmed by the ineffectiveness of the NO donors to block proteinolysis in the lysosome of the parasites. The results show that the trypanocidal activity of NO donors cannot be attributed to the inhibition of the major lysosomal cysteine proteinase in bloodstream forms of T. brucei