Approximately 21 months have passed since the World Health Organization officially confirmed the severe acute respiratory syndrome (SARS) outbreak. Originating in the southern Chinese province of Guandong, from a putative animal source, the transmission of SARS from an infected physician to other guests at the Hotel Metropol in Hong Kong led to global spread. Eight thousand ninety-six individuals were infected and 774 died.1 Characterizations of the etiologic agent2 along with initial clinical descriptions of the syndrome3,4 were followed by reports of outcomes of affected patients.5 As the outbreak progressed, it became clear that this was largely a healthcare facility–based outbreak, with healthcare workers, patients, and visitors being at risk. The bulk of the evidence, namely the descriptive epidemiology and related observational studies, suggests that droplet spread is the most common form of transmission.6,7 Although airborne transmission has been proposed as a mode of spread, the extent to which this occurred remains controversial.8 Why did SARS not become more widespread in the community? The answer lies in both the characteristics of the SARS coronavirus and the efforts made in the hospital to reduce spread. The SARS coronavirus is not highly transmissible. The relatively low reproductive number (the number of secondary cases generated by an infectious case) contributed to the lack of community-wide spread.9 The fact that the viral load was low initially then increased (rather than being high initially then decreasing, like other respiratory viruses) may have played a role.10 Because the transmissibility of the virus was highest after 5 days of symptoms, isolation of new cases acquired in the hospital was possible with diminished spread. There is empiric evidence to substantiate this, an increase in secondary cases of SARS when time to isolation with respect to onset of symptoms lasts beyond 5 days.1 Nosocomial spread was also characterized by superspreading events. Although devastating to individuals in hospitals, superspreading where there is high variance in the number of secondary cases that arise, somewhat counterintuitively, is not an efficient strategy for viral epidemic spread.9 Efforts to reduce spread in the hospital undoubtedly prevented transmission and saved lives. It has been estimated that delaying the institution of control measures by 1 week would have nearly tripled the size of the epidemic and would have increased the expected duration of the epidemic by 4 weeks.11 In contrast, the role of mass quarantine in the community has been more controversial, particularly given that it is likely that the numbers quarantined in many jurisdictions were excessive.12 However, at the time of the outbreak, decisions made necessarily needed to be conservative given the incomplete knowledge about aspects of the transmission of SARS, such as the role played by asymptomatically infected individuals. A hard lesson learned from SARS was our lack of preparedness for emerging infectious diseases. In Canada, this was evident through failure to achieve a coordinated response at municipal, provincial, and national levels. This led to the creation of a new national public health agency. Given that hospital transmission was such a key characteristic of the spread of SARS, an important lesson for hospital infection control has been the artificial division between “public health” and “infection control”—infection control is “hospital public health.” In this issue of Infection Control and Hospital Epidemiology, preparedness, management, and the impact of SARS are addressed in three articles. In the first of the three articles, Srinivasan et al.
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