Severe acute respiratory syndrome (SARS) is a respiratory disease in humans which is caused by the SARS coronavirus (SARS-CoV).[1] There has been one near pandemic to date, between November 2002 and July 2003, with 8,096 known infected cases and 774 deaths (a case-fatality rate of 9.6%) worldwide being listed in the World Health Organization's (WHO) 21 April 2004 concluding report.[2] Within a matter of weeks in early 2003, SARS spread from the Guangdong province of China to rapidly infect individuals in some 37 countries around the world[3]


Initial symptoms are flu like and may include: fever, myalgia, lethargy, gastrointestinal symptoms, cough, sore throat and other non-specific symptoms. The only symptom that is common to all patients appears to be a fever above 38 °C (100.4 °F). Shortness of breath may occur later. Symptoms usually appear 2–10 days following exposure, but up to 13 days has been reported. In most cases symptoms appear within 2–3 days. About 10–20% of cases require mechanical ventilation.


SARS may be suspected in a patient who has: 1. Any of the symptoms including a fever of 38 °C (100.4 °F) or more AND 2. Either a history of: 1. Contact (sexual or casual) with someone with a diagnosis of SARS within the last 10 days OR 2. Travel to any of the regions identified by the WHO as areas with recent local transmission of SARS (affected regions as of 10 May 2003[5] were parts of China, Hong Kong, Singapore and the province of Ontario, Canada). A probable case of SARS has the above findings plus positive chest x-ray findings of atypical pneumonia or respiratory distress syndrome. With the advent of diagnostic tests for the coronavirus probably responsible for SARS, the WHO has added the category of "laboratory confirmed SARS" for patients who would otherwise fit the above "probable" category who do not (yet) have the chest x-ray changes but do have positive laboratory diagnosis of SARS based on one of the approved tests (ELISA, immunofluorescence or PCR).


Antibiotics are ineffective as SARS is a viral disease. Treatment of SARS so far has been largely supportive with antipyretics, supplemental oxygen and ventilatory support as needed. Suspected cases of SARS must be isolated, preferably in negative pressure rooms, with complete barrier nursing precautions taken for any necessary contact with these patients. There was initially anecdotal support for steroids and the antiviral drug ribavirin, but no published evidence has supported this therapy. Many clinicians now suspect that ribavirin is detrimental.[citation needed] Researchers are currently testing all known antiviral treatments for other diseases including AIDS, hepatitis, influenza and others on the SARS-causing coronavirus. There is some evidence that some of the more serious damage in SARS is due to the body's own immune system overreacting to the virus. There may be some benefit from using steroids and other immune modulating agents in the treatment of the more acute SARS patients. Research is continuing in this area. In December 2004 it was reported that Chinese researchers had produced a SARS vaccine. It has been tested on a group of 36 volunteers, 24 of whom developed antibodies against the virus.[11] A 2006 systematic review of all the studies done on the 2003 SARS epidemic found no evidence that antivirals, steroids or other therapies helped patients. A few suggested they caused harm.[12] The clinical treatment of SARS has been relatively ineffective with most high risk patients requiring artificial ventilation. Currently, corticosteroids and Ribavirin are the most common drugs used for treatment of SARS (Wu et al., 2004). In vitro studies of Ribavirin have yielded little results at clinical, nontoxic concentrations. Better combinations of drugs that have yielded a more positive clinical outcome (when administered early) have included the use of Kaletra, Ribavirin and corticosteroids. The administration of corticosteroids, marketed as Prednisone, during viral infections has been controversial. Lymphopenia can also be a side effect of corticosteroids even further decreasing the immune response and allowing a spike in the viral load; yet physicians must balance the need for the anti-inflammatory treatment of corticosteroids (Murphy 2008). Clinicians have also noticed positive results during the use of human interferon and Glycyrrhizin. No compounds have yielded inhibitory results of any significance. The HIV protease inhibitors Ritonavir and Saquinavir did not show any inhibitory affect at nontoxic levels. Iminocyclitol 7 has been found to have an inhibitory effect on SARS-CoV in that it disrupts the envelope glycoprotein processing. Iminocyclitol 7 specifically inhibits the production of human fucosidase and in vitro trials yielded promising results in the treatment of SARS, yet one problem exists. A deficiency of fucosidase can lead to a condition known as fucosidosis in which there is a decrease in neurological function.