Sep. 15, 2005
Severe acute respiratory syndrome (SARS), by its very name, indicates a disease of the respiratory tract. But SARS can also infiltrate brain tissue, causing significant central nervous system problems, according to an article in the Oct. 15 issue of Clinical Infectious Diseases, now available online.
SARS, a potentially fatal illness caused by a coronavirus, was first reported in Asia in February of 2003. The disease is usually transmitted by contact with coronavirus-laden droplets sprayed into the air by an infected person’s coughing. Other symptoms can include high fever, headache, body aches, and pneumonia. However, some patients also exhibit central nervous system ailments. In a new study, the researchers report the case of a 39-year-old doctor who treated SARS patients in China during the 2003 outbreak and became infected himself.
He showed the usual symptoms of SARS--fever, chills, headache, muscle pain--but after hospitalization, he developed vision problems, then progressively worse central nervous system symptoms, like restlessness and delirium. A computed tomography scan indicated brain damage. He died about a month after being hospitalized, and his brain tissue was examined and found to contain the SARS coronavirus. The researchers also discovered a high level of Mig, a type of immune system regulator called a chemokine, in the man’s bloodstream and brain, which may have resulted from the central nervous system infection. The researchers speculated that Mig could also have contributed to his brain damage by attracting immunological cells to the site of the viral infection in the brain, where their inflammatory effects may have done more harm than good.
There are a few possibilities for curbing Mig’s possible role in causing brain damage in SARS patients with central nervous system infection, according to lead author Jun Xu, PhD, of the Guangzhou Institute of Respiratory Diseases and senior author Yong Jiang, PhD, of the Key Laboratory of Functional Proteomics of Guangdong Province. “There might be some ways of controlling the release of Mig, such as specific inhibitors 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 induced by Mig.”
Four to five percent of SARS patients treated at the Guangzhou Institute of Respiratory Diseases experienced central nervous system symptoms, said Dr. Xu; therefore, physicians need to be aware of the potential for brain infection when evaluating patients with the disease. Immunosuppressive drugs should be administered carefully and on an individual basis, as they may allow amplification of the SARS coronavirus in the brain. “Superinfection” with other pathogens could also contribute to SARS’ harmful effects on the brain. “Physicians should pay more attention to the prevention of brain damage if [SARS patients] are superinfected with other conditional pathogens,” according to Dr. Xu and Dr. Jiang.
Founded in 1979, Clinical Infectious Diseases publishes clinical articles twice monthly in a variety of areas of infectious disease, and is one of the most highly regarded journals in this specialty. It is published under the auspices of the Infectious Diseases Society of America (IDSA). Based in Alexandria, Virginia, IDSA is a professional society representing about 8,000 physicians and scientists who specialize in infectious diseases. For more information, visit www.idsociety.org.
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