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Clinical and epidemiological predictors of transmission in Severe Acute Respiratory Syndrome (SARS)

DOI: 10.1186/1471-2334-6-151

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We used epidemiological and clinical data on probable SARS patients admitted to Tan Tock Seng Hospital. Using a case-control approach, index patients who had probable SARS who subsequently transmitted the disease to at least one other patient were analysed as "cases" against patients with no transmission as "controls", using multivariate logistic regression analysis.98 index patients were available for analysis (22 with transmission, 76 with no transmission). Covariates positively associated with transmission in univariate analysis at p < 0.05 included delay to isolation (Day 7 of illness or later), admission to a non-isolation facility, pre-existing chronic respiratory disease and immunosuppressive disease, need for oxygen, shortness of breath, vomiting, and higher lactate dehydrogenase levels and higher neutrophil counts. In the multivariate analysis, only three factors were significant: delay to isolation, admission to a non-isolation facility and higher lactate dehydrogenase levels of >650 IU/L (OR 6.4, 23.8 and 4.7 respectively).Clinical and epidemiological factors can help us to explain why transmission was observed in some instances but not in others.Severe Acute Respiratory Syndrome (SARS) was the first emerging infectious disease of the new century with epidemic potential. First recognized on 26 Feb 2003, SARS spread rapidly and resulted in 8098 reported cases and 774 deaths in close to 30 countries [1]. While there was no endemic transmission in the majority of these countries, explosive outbreaks were observed in China, Hong Kong, Taiwan, Canada, Vietnam and Singapore. Ongoing research points to an existing animal reservoir for the virus [2,3], and future epidemics may hence sporadically emerge from this source [4].A key feature in the epidemiology of SARS is the widespread variation in the number of secondary infections caused by each potentially infectious case. While multiple secondary infections were traced to single individuals in several super-sprea


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