Margaret G. Fritsma, MA MT (ASCP) SBB and I just returned from Tegucigalpa, Honduras. Milena Vanegas, MS (CLS) graduate of UAB’s Master of Science in Clinical Laboratory Science program, invited us there to speak at the VI Congreso Nacional de Microbiologica, which was hosted by the Colegia de Microbiologos y Quimicos Clinicos, Honduras. Dra. Vanegas directs the clinical rotations in the Medical Laboratory Science program at the Universidad Nacional Autonoma de Honduras in Tegucigalpa, and has temporarily released her fourth-year students to assist in managing a dengue fever epidemic that has infected numerous Honduran citizens and has caused several deaths. Dra. Vanegas reports the epidemic is also in Guatemala and Nicaragua.
Dengue fever is transmitted by the Aedes mosquito, which has adapted to high altitudes and urban environments. The usual symptoms are high fever, intense bone pain (break-bone fever), skin rash, nausea, headache, and general malaise lasting about seven days. There is no effective treatment, only supportive therapy. Patients must avoid aspirin as a small percentage of cases progress to hemorrhagic fever, wherein the platelet count drops precipitously to below 10,000/mcL and the patient develops petechiae. Hemorrhagic dengue is often fatal.
Hemorrhagic fever appears to be triggered by reinfection or simultaneous infections. There are four strains of dengue virus. Patients who have developed an immune response to one strain may be subsequently infected by a second strain. Reinfection seems to trigger an intense immune and inflammatory response with severe thrombocytopenia. Dra. Vanegas reports that vasodilation, a part of the inflammatory response, accounts for the sudden platelet loss.
I see nothing on the WHO web site about this current outbreak, and I’ve found relatively little in my dusty microbiology and pathology textbooks to unpack the pathophysiology of dengue hemorrhagic fever. Do you have more information on how dengue triggers hemorrhage? Geo.
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