Severe acute respiratory syndrome (SARS), by its very name,indicates a disease of the respiratory tract. But SARS can alsoinfiltrate brain tissue, causing significant central nervous systemproblems, according to an article in the Oct. 15 issue of ClinicalInfectious Diseases, now available online.
SARS, a potentiallyfatal illness caused by a coronavirus, was first reported in Asia inFebruary of 2003. The disease is usually transmitted by contact withcoronavirus-laden droplets sprayed into the air by an infected person’scoughing. Other symptoms can include high fever, headache, body aches,and pneumonia. However, some patients also exhibit central nervoussystem ailments. In a new study, the researchers report the case of a39-year-old doctor who treated SARS patients in China during the 2003outbreak and became infected himself.
He showed the usualsymptoms of SARS--fever, chills, headache, muscle pain--but afterhospitalization, he developed vision problems, then progressively worsecentral nervous system symptoms, like restlessness and delirium. Acomputed tomography scan indicated brain damage. He died about a monthafter being hospitalized, and his brain tissue was examined and foundto contain the SARS coronavirus. The researchers also discovered a highlevel of Mig, a type of immune system regulator called a chemokine, inthe man’s bloodstream and brain, which may have resulted from thecentral nervous system infection. The researchers speculated that Migcould also have contributed to his brain damage by attractingimmunological cells to the site of the viral infection in the brain,where their inflammatory effects may have done more harm than good.
Thereare a few possibilities for curbing Mig’s possible role in causingbrain damage in SARS patients with central nervous system infection,according to lead author Jun Xu, PhD, of the Guangzhou Institute ofRespiratory Diseases and senior author Yong Jiang, PhD, of the KeyLaboratory of Functional Proteomics of Guangdong Province. “There mightbe some ways of controlling the release of Mig, such as specificinhibitors that interfere [with] the signaling pathways involved,” Dr.Jiang said. “Other approaches, such as neutralizing antibodies [and]specific binding peptides, could be tried to block brain damage inducedby Mig.”
Four to five percent of SARS patients treated at theGuangzhou Institute of Respiratory Diseases experienced central nervoussystem symptoms, said Dr. Xu; therefore, physicians need to be aware ofthe potential for brain infection when evaluating patients with thedisease. Immunosuppressive drugs should be administered carefully andon an individual basis, as they may allow amplification of the SARScoronavirus in the brain. “Superinfection” with other pathogens couldalso contribute to SARS’ harmful effects on the brain. “Physiciansshould pay more attention to the prevention of brain damage if [SARSpatients] are superinfected with other conditional pathogens,”according to Dr. Xu and Dr. Jiang.
Founded in 1979,Clinical Infectious Diseases publishes clinical articles twice monthlyin a variety of areas of infectious disease, and is one of the mosthighly regarded journals in this specialty. It is published under theauspices of the Infectious Diseases Society of America (IDSA). Based inAlexandria, Virginia, IDSA is a professional society representing about8,000 physicians and scientists who specialize in infectious diseases.For more information, visit www.idsociety.org.
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