Yellow fever is a mosquito-borne viral hemorrhagic fever endemic to sub-Saharan Africa and South America associated with significant morbidity and mortality. The use of a live attenuated vaccine can prevent yellow fever, but vaccine-associated neurologic disease has been reported and is a safety concern. We present the case of a previously healthy 35-year-old active-duty man who received the yellow fever vaccine prior to deployment and subsequently developed progressive neurologic dysfunction consistent with transverse myelitis. KEYWORDS Transverse myelitis; yellow fever; yellow fever vaccine-associated neurologic disease Y ellow fever (YF) is a mosquito-borne viral hemorrhagic fever endemic to sub-Saharan Africa and South America with significant morbidity and mortality. The World Health Organization estimates that 200,000 cases occur each year. 1,2 YF can result in severe illness with hepatic dysfunction, renal failure, coagulopathy, and shock. 3 Supportive care is the mainstay of therapy, because there is no specific treatment for YF. Primary prevention with the YF vaccine is pivotal in reducing its incidence. The Centers for Disease Control and Prevention recommends YF vaccination for travelers to and residents of endemic areas aged 9 months and older. The YF vaccine was developed in 1937, with over 600 million doses administered to date, and has been described as a safe vaccine with rare cases of serious adverse reactions. 4 YF vaccine-associated neurologic disease has been reported by the Yellow Fever Working Group. Encephalitis, meningoencephalitis, Guillain-Barre syndrome, and acute disseminated encephalomyelitis are among the most frequently described neurologic complications. These complications account for 0.4 to 0.8 cases per 100,000 doses, as reported to the Vaccine Adverse Event Reporting System. 5 We present the case of a 35-yearold active-duty man who received the YF vaccine prior to deployment and subsequently developed progressive neurologic dysfunction consistent with transverse myelitis.
Myocyte enhancer factor 2A (MEF-2A) is a calcium-regulated transcription factor that promotes cell survival during nervous system development. To define and further characterize the distribution pattern of MEF-2A in the adult mammalian brain, we used a specific polyclonal antiserum against human MEF-2A to identify nuclear-localized MEF-2A protein in hippocampal and frontal cortical regions. Western blot and immunocytochemical analyses showed that MEF-2A was expressed not only in laminar structures but also in blood vessels of rat and human brains. MEF-2A was colocalized with doublecortin (DCX), a microtubule-associated protein expressed by migrating neuroblasts, in CA1 and CA2 boundaries of the hippocampus. MEF-2A was expressed heterogeneously in additional structures of the rat brain, including the striatum, thalamus, and cerebellum. Furthermore, we found a strong nuclear and diffuse MEF-2A labeling pattern in spinal cord cells of rat and human material. Finally, the neurovasculature of adult rats and humans not only showed a strong expression of MEF-2A but also labeled positive for hyperpolarization-activated, cyclic nucleotide-regulated (HCN) channels. This study further characterizes the distribution pattern of MEF-2A in the mammalian nervous system, demonstrates that MEF-2A colocalizes with DCX in selected neurons, and finds MEF-2A and HCN1 proteins in the neurovasculature network.
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