No abstract

The full spectrum of skin diseases related to travel in tropical areas is unknown. We prospectively studied 269 consecutive patients with travel-associated dermatosis who presented to our tropical disease unit in Paris during a 2-year period. The median age of these patients was 30 years; 137 patients were male; 76% of the patients were tourists; 38% had visited sub-Saharan Africa; and 85% had been appropriately vaccinated against tetanus. Cutaneous lesions appeared while the patient was still abroad in 61% of cases and after the patient's return to France in 39%. The diagnosis was definite in 260 cases; 137 of these cases (53%) involved an imported tropical disease. The most common diagnoses were cutaneous larva migrans (25%); pyodermas (18%); pruritic arthropod-reactive dermatitis (10%); myiasis (9%); tungiasis (6%); urticaria (5%); fever and rash (4%); and cutaneous leishmaniasis (3%). Hospitalization was necessary in 27 cases (10%), with a median duration of 5 days (range, 2-21 days). Travelers should be advised on how to avoid exposure to the agents and vectors of infectious dermatoses. Travel first-aid kits should include insect repellents and antibiotics effective against bacterial skin infections.

Key Points After being killed by artesunate, malaria parasites are expelled from red cells and then these pitted red cells reenter the circulation. When many pitted red cells are produced during therapy, their delayed clearance a few weeks later triggers hemolytic episodes.

During Plasmodium falciparum infection leading to cerebral malaria, cytokine production and cytoadherence of parasitized erythrocytes (PRBCs) to postcapillary venules are involved. We demonstrate that PRBC adhesion induces apoptosis in human endothelial cells (HLECs). PRBC adhesion modulated HLEC gene expression in tumor necrosis factor-alpha superfamily genes (Fas, Fas L, and DR-6) and apoptosis-related genes (Bad, Bax, caspase-3,SARP 2, DFF45/ICAD, IFN-gamma receptor 2, Bcl-w, Bik, and iNOS). Apoptosis was confirmed by (1) morphological modifications by electron microscopy, (2) annexin V binding, (3) DNA degradation, by measuring intracytoplasmic nucleosomes, and (4) caspase activity. The apoptotic stimulus was physical contact between HLECs and PRBCs and not parasite-secreted molecules. In addition, it was found that cytoplasmic (caspase 8) and mitochondrial (caspase 9) pathways were involved in this process. These data not only describe the direct apoptotic effect of PRBC adhesion on endothelial cells but also provide new useful tools that allow an evaluation of potential pharmaceuticals.