SARS: A tale of two epidemics
2003; Pulsus Group; Volume: 14; Issue: 3 Linguagem: Inglês
10.1155/2003/912170
ISSN1918-1493
Autores Tópico(s)Influenza Virus Research Studies
Resumo1Departments of Pathology and Laboratory Medicine, Medicine, and Microbiology and Infectious Diseases, University of Calgary, Calgary, Alberta; 2Queen Elizabeth II Health Sciences Centre and Dalhousie University, Halifax, Nova Scotia Correspondence: Dr John Conly, Departments of Pathology and Laboratory Medicine, Medicine, and Microbiology and Infectious Diseases, Room 930, 9th Floor, North Tower, 1403 29th Street Northwest, Calgary, Alberta T2N 2T9. Telephone 403-944-8222, fax 403-944-1095, e-mail jconly@ucalgary.ca and Dr Lynn Johnston, Department of Medicine, Room 5014 ACC, Queen Elizabeth II Health Sciences Centre, 1278 Tower Road, Halifax, Nova Scotia B3H 2Y9. Telephone 902-473-5553, fax 902-473-7394, e-mail ljohnsto@dal.ca In November 2002, cases of a life-threatening respiratory disease of unknown cause were reported from Guangdong Province, China, followed in early 2003 by reports from Vietnam and Hong Kong. The illness was designated as severe acute respiratory syndrome (SARS) in late February 2003 (1-3). In Vietnam the outbreak began with a single initial patient who was hospitalized for treatment of a severe, acute respiratory syndrome of unknown origin (4). The patient felt unwell during his journey and fell ill shortly after arriving in Hanoi from Shanghai and Hong Kong. By March 10, 2003, following the patient’s admission to a Hanoi hospital, approximately 22 hospital staff became ill with similar symptoms. By March 12, 2003 similar outbreaks had been reported among health care workers in Hong Kong. Recognizing the transmission of the illness to health care workers, the World Health Organization (WHO) issued a rare global health alert on March 12, 2003 (4). On March 14, 2003 the WHO received notification from Health Canada of four cases of a severe atypical pneumonia with an associated death in a single family in Toronto. Reports of probable SARS cases followed in Singapore, the Amoy Gardens apartment complex in Hong Kong, Taiwan, the United States and several European countries. As of April 28, 2003 a cumulative total of 5050 probable SARS cases with 321 deaths have been reported to the WHO from 26 countries (5). During this time the WHO has coordinated an international response unprecedented in modern times. The response has been aided significantly by the use of real-time communication and information exchange, much of it over the Internet using email and secure websites (6). The emergence of SARS in Canada has presented significant challenges, related not only to the epidemic of the disease itself but also to the epidemic of misconceptions and fear, which can present an even greater challenge. Given the recent unfolding of the SARS epidemic in Canada, it is considered timely to address the salient features of the disease and its potential repercussions. Are there lessons to be learned to better prepare us for the next new epidemic and pandemic influenza? Several papers from investigators in Hong Kong and Canada have described the clinical, laboratory and radiological features of the disease (7-9). In the outbreak described by Lee et al (9), there were 138 cases of SARS, of which 69 were health care workers. The most common symptoms were fever of more than 38°C (displayed in 100% of patients), chills, rigors, or both (73.2% of patients), myalgia (60.9% of patients), cough (57.3% of patients) headache (55.8% of patients) and dizziness (42.8% of patients). Other symptoms that occurred less commonly included sore throat, coryza, nausea and vomiting, dyspnea, sputum production and diarrhea. Major examination findings included fever and crepitations at the lung bases. Leukopenia was present in about one-third of patients but absolute lymphopenia and thrombocytopenia were present in over two thirds and almost half of all patients, respectively. Other laboratory abnormalities included elevation of lactate dehydrogenase in 71% of patients, creatine kinase in 32%, and serum alanine aminotransferase in 23% . Electrolyte abnormalities were noted in some patients. Radiological abnormalities were present in 80% to 100% of the patients at presentation (8,9), with initial findings of peripheral air space consolidation of a focal or multifocal nature that progressed after a week. In patients who deteriorated, progressive bilateral infiltrates were noted. Univariate analysis in one study (8) revealed that advanced age, presence of underlying illness, impaired liver function tests and late initiation of treatment were significantly associated with severe disease requiring intensive care and ventilatory support. Multivariate analysis in another study (9) with a larger number of patients revealed that advanced age (odds ratio of 1.8 for every 10 years), high lactate dehydrogenase and elevated absolute neutrophil count on presentation were associated with an adverse outcome. Another study (10) has suggested that chronic hepatitis B virus infection is also associated with a poor outcome. Major comorbidities were present in the majority of patients who have died (7-9). It is noteworthy that few reports of severe disease in children have emerged, despite significant exposure on a worldwide basis. One study (7) detailed exposure of three children (aged five months, nine years and 17 years) to an index case, all of whom had fever and/or respiratory symptoms but no evidence of pulmonary infiltrates on radiological examination. None of the children were reported as being hospitalized. The epidemiological features of the disease suggest that it is transmissible from person-to-person through direct contact, large droplet contact, and through indirect contact from fomites and unwashed hands. The mean and median incubation periods are five and six days, respectively (8,9). The maximum incubation period appears to be 10 days (11). The virus is present in the respiratory secretions of infected patients and has also been found in the urine and feces (7-9). Recent unpublished data (12) has demonstrated that the virus is stable in feces and urine at room temperature for at least one to two days. The virus is also more stable (up to four days) in stool from diarrhea patients (which has a higher pH) than in normal stool, where it could only be found for up to six hours. These findings have raised the possibility of fecal-oral spread in some situations, a hypothesis yet to be confirmed. In the search for an etiological agent, specimens from clinical cases of SARS were tested for a broad range of bacterial, viral, chlamydial and rickettsial agents. Initial laboratory testing focused
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