A Major Outbreak of Severe Acute Respiratory Syndrome in Hong Kong
Nelson Lee, M.D., David Hui, M.D., Alan Wu, M.D., Paul Chan, M.D., Peter Cameron, M.D., Gavin M. Joynt, M.D., Anil Ahuja, M.D., Man Yee Yung, B.Sc., C.B. Leung, M.D., K.F. To, M.D., S.F. Lui, M.D., C.C. Szeto, M.D., Sydney Chung, M.D., and Joseph J.Y. Sung, M.D.
Background There has been an outbreak of the severe acute respiratorysyndrome (SARS) worldwide. We report the clinical, laboratory,and radiologic features of 138 cases of suspected SARS duringa hospital outbreak in Hong Kong.
Methods From March 11 to 25, 2003, all patients with suspectedSARS after exposure to an index patient or ward were admittedto the isolation wards of the Prince of Wales Hospital. Theirdemographic, clinical, laboratory, and radiologic characteristicswere analyzed. Clinical end points included the need for intensivecare and death. Univariate and multivariate analyses were performed.
Results There were 66 male patients and 72 female patients inthis cohort, 69 of whom were health care workers. The most commonsymptoms included fever (in 100 percent of the patients); chills,rigors, or both (73.2 percent); and myalgia (60.9 percent).Cough and headache were also reported in more than 50 percentof the patients. Other common findings were lymphopenia (in69.6 percent), thrombocytopenia (44.8 percent), and elevatedlactate dehydrogenase and creatine kinase levels (71.0 percentand 32.1 percent, respectively). Peripheral air-space consolidationwas commonly observed on thoracic computed tomographic scanning.A total of 32 patients (23.2 percent) were admitted to the intensivecare unit; 5 patients died, all of whom had coexisting conditions.In a multivariate analysis, the independent predictors of anadverse outcome were advanced age (odds ratio per decade oflife, 1.80; 95 percent confidence interval, 1.16 to 2.81; P=0.009),a high peak lactate dehydrogenase level (odds ratio per 100U per liter, 2.09; 95 percent confidence interval, 1.28 to 3.42;P=0.003), and an absolute neutrophil count that exceeded theupper limit of the normal range on presentation (odds ratio,1.60; 95 percent confidence interval, 1.03 to 2.50; P=0.04).
Conclusions SARS is a serious respiratory illness that led tosignificant morbidity and mortality in our cohort.
In March 2003, there was an outbreak of atypical pneumonia inHong Kong. As of March 27, there were 367 reported cases inHong Kong and more than 1400 cases worldwide.1 The disease mayprogress rapidly and often results in the acute respiratorydistress syndrome (ARDS). As of this writing, there have been10 deaths in Hong Kong related to the illness, which the WorldHealth Organization (WHO) has named the severe acute respiratorysyndrome (SARS). Globally, there have been at least 53 deathsrelated to SARS.1 Schools have been closed in Hong Kong, andmore than 1000 people who had a history of contact with a patientwith SARS were quarantined.
We describe the clinical, laboratory, and radiologic featuresof patients with SARS who were seen at the Prince of Wales Hospital,Hong Kong. These patients were either health care workers ina medical ward of the hospital or persons who had a historyof contact with an index patient or exposure to the same medicalward. We also included patients who had contracted the diseasethrough direct contact with these cases.
Methods
On March 10, 18 health care workers in a medical ward of thePrince of Wales Hospital reported that they were ill. Throughtelephone contact, more than 50 of the hospital's health careworkers were identified as having had a febrile illness overthe previous few days. On March 11, 23 of them were admittedto an isolation ward in the hospital. A team of "atypical pneumoniaphysicians" was formed to take responsibility for screeningof suspected cases and subsequent management. The team includedphysicians from the Department of Medicine and Therapeutics(infectious disease, respiratory medicine, and general medicine),the Department of Emergency Medicine, and the intensive careunit (ICU). Clinical findings and laboratory data were documentedprospectively.
Since the etiologic agent was not known at the onset of theoutbreak, the diagnosis was based on clinical symptoms and theruling out of common bacterial and viral pathogens that causepneumonia. On the basis of the criteria for SARS that have beenestablished by the Centers for Disease Control and Prevention(CDC),2 our case definition was a fever (temperature, >38°C),a chest radiograph (a plain radiograph, a computed tomographic[CT] image of the thorax, or both) showing evidence of consolidationwith or without respiratory symptoms (e.g., cough and shortnessof breath), and a history of exposure to an index patient suspectedto have SARS or direct contact with a person who became illafter exposure to an index patient.
All patients were initially admitted to medical wards with isolationfacilities. Initial investigations included a complete bloodcount (with a differential count), clotting profile (prothrombintime, activated partial-thromboplastin time, international normalizedratio, and D-dimer) and serum biochemical measurements (includingelectrolytes, renal-function and liver-function values, creatinekinase, and lactate dehydrogenase). These studies and chestradiography were performed daily until the fever had subsidedfor three days. Nasopharyngeal-aspirate samples obtained fromall study patients were screened for common viruses, includinginfluenzaviruses A and B, respiratory syncytial virus, adenovirus,and parainfluenzavirus types 1, 2, and 3, with the use of commercialimmunofluorescence assays. In addition, virus culture was performedwith the use of various cell lines (LLC-MK2, MDCK, Hep2, humanembryonic lung fibroblast, Buffalo green-monkey kidney, andVero cells). In addition, multiplex reverse-transcriptase–polymerase-chain-reaction(RT-PCR) assays for influenzavirus A, influenzavirus B, andrespiratory syncytial virus were performed in 65 randomly selectedpatients. Electron microscopy was used to study nasopharyngealaspirates in selected cases. Sputum cultures and blood cultureswere performed in all cases to complete the microbiologic workup.PCR assays for mycoplasma and Chlamydia pneumoniae were performedin 65 randomly selected patients. A legionella urinary antigenassay was performed in the first 25 patients.
Initial treatment included cefotaxime and clarithromycin (orlevofloxacin) to target common pathogens causing community-acquiredpneumonia, according to current recommendations.3,4 Oseltamivir(Tamiflu) was also given initially to treat possible influenzainfection. If fever persisted for more than 48 hours and theblood count showed leukopenia, thrombocytopenia, or both, oralribavirin (1.2 g three times a day) and corticosteroid therapy(prednisolone at a dose of 1 mg per kilogram of body weightper day) was given as a combined regimen. Patients with persistentfever and worsening lung opacities were given intravenous ribavirin(400 mg every eight hours) and corticosteroid therapy (an additionaltwo to three pulses of 0.5 g of methylprednisolone daily). Patientsin whom hypoxemia developed were given oxygen through a nasalcannula. Patients were admitted to the ICU if respiratory failuredeveloped, as evidenced by an arterial oxygen saturation ofless than 90 percent while the patient was receiving 50 percentsupplemental oxygen, a respiratory rate that exceeded 35 breathsper minute, or both.
An epidemiologic study was conducted shortly after the outbreak.We identified our index patient, whose exposure history hasbeen described elsewhere.5 He was a 26-year-old ethnic Chineseman who was admitted to the Prince of Wales Hospital on March4, 2003, with a high temperature, myalgia, and cough. His chestradiograph showed an ill-defined air-space opacity in the peripheryof the right upper lobe. He was treated with amoxicillin–clavulanateand clarithromycin. All bacteriologic and virologic tests wereunrevealing. The right lung opacity progressed to bilateralconsolidation. After seven days of antibiotic therapy, his fevergradually diminished, and the lung opacities started to resolve.During this period, he was treated with albuterol (0.5 mg througha jet nebulizer, delivered by oxygen at a flow rate of 6 litersper minute, four times daily for a total of seven days).
From our contact tracing, we found that the first patients beganto have symptoms two days after the index patient's admission.Moreover, all doctors and nurses who participated in the careof the patient, all medical students who had examined him, andthe patients around him were the ones who first reported febrileillness, on March 10. We therefore defined all cases that developedin persons who had had direct contact with the index patientor who had been exposed to him in the medical ward as secondarycases. Cases in patients who contracted the disease from thesepatients (e.g., family members of health care workers or ofpatients who had stayed in this medical ward) were defined astertiary cases.
Study Population and Data Analysis
Our study cohort included all secondary and tertiary cases.Their demographic, clinical, laboratory, and radiologic characteristicswere reported and analyzed. The clinical composite end pointwas the need for care in the ICU, death, or both. Univariateand multivariate analyses of clinical and laboratory data wereperformed to identify prognostic variables. Statistical analysiswas performed with SYSTAT software (version 7.0, SPSS, Chicago).Data are reported as means ±SD unless otherwise specified.Univariate analysis was performed to compare patients who reachedthe end point and those who did not, with the use of an unpairedStudent's t-test or chi-square test, as appropriate. Multivariatelogistic-regression analysis was then performed, with backwardstepwise analysis, to identify independent predictors of theend point. All comparisons of clinical variables with a P valueof less than 0.20 by univariate analysis were entered into themodel. A P value of less than 0.05 was considered to indicatestatistical significance. All probabilities are two-tailed.
Results
Between March 11 and March 25, 2003, a total of 156 patientswere hospitalized with SARS, of whom 138 were identified ashaving either secondary or tertiary cases as a result of exposureto our index patient. There were 112 patients with secondarycases and 26 with tertiary cases in this cohort, including 69health care workers (20 doctors, 34 nurses, and 15 allied healthworkers) and 16 medical students who had worked in the indexward, plus 53 patients who were either in the same medical wardor had visited their relatives there. There were 66 male patientsand 72 female patients; their mean age was 39.3±16.8years. A total of 19 patients had coexisting conditions: cardiovasculardisease in 4, the myelodysplastic syndrome in 2, chronic liverdisease in 3, diabetes mellitus in 5, chronic renal failurein 2, and chronic pulmonary disease in 3. Most of the healthcare workers were previously healthy. All patients were ethnicChinese.
In our cohort of 138 patients, there were five positive sputumcultures; three were positive for Haemophilus influenzae, onefor Streptococcus pneumoniae, and one for Klebsiella pneumoniae.None of the blood cultures were positive. Other bacteriologicinvestigations were unrevealing. Of all the nasopharyngeal aspiratescollected, one was positive for influenzavirus A, one was positivefor influenzavirus B, and two were positive for respiratorysyncytial virus. Microscopical examination of nasopharyngealaspirates from five patients showed paramyxovirus-like viralparticles in one and coronavirus-like viral particles in another.The aspirates from the other three patients were negative. Furthervirologic studies are in progress.
Figure 1. Frontal Chest Radiograph in a 25-Year-Old Woman Showing Ill-Defined Air-Space Shadowing (Arrows).
There is no associated pleural effusion or hilar or mediastinal adenopathy.
The initial radiographic changes were indistinguishable fromthose associated with other causes of bronchopneumonia. Interestingly,peripheral-zone involvement was predominant. Pleural effusion,cavitation, and hilar lymphadenopathy were absent in our cohort.Among patients with clinical deterioration, serial chest radiographsshowed progression of pulmonary infiltrates approximately 7to 10 days after admission. Lung opacities enlarged, and multipleareas of involvement were often seen (Figure 2A and Figure 2B).A successful response to therapy could be demonstrated by serialchest radiographs showing the resolution of lung opacities (Figure 2C).In cases in which typical lung opacities could not be foundon the initial plain chest radiograph, conventional and high-resolutionCT images of the thorax proved to be useful. The typical findingon thoracic CT images, as shown in 25 cases, was ill-defined,ground-glass opacification in the periphery of the affectedlung parenchyma, usually in a subpleural location (Figure 3).The characteristic peripheral alveolar opacities were very similarto those found in bronchiolitis obliterans with organizing pneumonia.6,7There was no obvious bronchial dilatation.
Figure 2. Frontal Chest Radiographs in a 46-Year-Old Man.
Panel A shows an obvious area of air-space shadowing (arrows) on the left side. A follow-up chest radiograph showed progression of the disease, with multiple, bilateral areas of involvement (Panel B). A subsequent chest radiograph shows improvement of bilateral lung opacities after therapy (Panel C).
Figure 3. A High-Resolution CT Scan Showing the Characteristic Ground-Glass Abnormality in a Subpleural Location.
There is no cavitation. A conventional CT scan did not show pleural effusion or lymphadenopathy.
Clinical Outcomes
Of the 138 patients, 32 (23.2 percent) were admitted to theICU, all because of respiratory failure. Mechanical ventilatorysupport with positive end-expiratory pressure was required in19 patients (13.8 percent). Among the 32 patients in the ICU,dramatic increases in lung opacity, shortness of breath, andhypoxemia occurred at a median of 6.5 days (range, 3 to 12)and led to their ICU admission. By day 21 of the outbreak, fivepatients had died (crude mortality rate, 3.6 percent). All fivehad originally been admitted because of major medical conditions.Two patients had the myelodysplastic syndrome, one had congestiveheart failure, one had alcoholic liver cirrhosis, and one hada reactivation of hepatitis B. None of the health care workersor medical students died. At this writing, a total of 76 patients(55.1 percent) have been discharged, of whom 44 (31.9 percent)were health care workers. Fitness for discharge was based ondefervescence for at least 96 hours, with radiographic evidenceof improvement in lung consolidation.
Factors Predictive of ICU Admission and Death
Univariate analysis showed that advanced age, male sex, a highpeak creatine kinase value, a high lactate dehydrogenase levelon presentation and a high peak value, a high initial absoluteneutrophil count, and a low serum sodium level were significantpredictive factors for ICU admission and death (Table 2). Thepresence of coexisting conditions (in 19 patients) did not appearto be associated with a worse clinical outcome (P=0.14). Onmultivariate analysis, the only factors that were predictiveof an adverse outcome were advanced age (odds ratio for every10 years of age, 1.80; 95 percent confidence interval, 1.16to 2.81; P=0.009), a high peak lactate dehydrogenase level (oddsratio for every 100 U per liter, 2.09; 95 percent confidenceinterval, 1.28 to 3.42; P=0.003), and an absolute neutrophilcount that exceeded the upper limit of the normal range on presentation(odds ratio, 1.60; 95 percent confidence interval, 1.03 to 2.50;P=0.04).
Table 2. Univariate Analyses of Clinical and Laboratory Variables Associated with the Combined Outcome of ICU Care or Death.
Postmortem Findings
Postmortem examination in two cases showed gross consolidationof the lungs. Histologic features varied from region to region.The early phase and organizing phase of diffuse alveolar damagewere seen in different parts of the lung. The early phase wascharacterized by pulmonary edema with hyaline membrane formationsuggestive of the early phase of ARDS (Figure 4). Cellular fibromyxoidorganizing exudates in air spaces indicated the organizing phaseof alveolar damage. There was a scanty lymphocytic inflammatoryinfiltrate in the interstitium. Vacuolated and multinucleatedpneumocytes were also identified. Viral inclusions were notdetected. There was no evidence of the involvement of otherorgans.
Figure 4. Lung-Biopsy Specimen Obtained at Autopsy.
Panel A shows diffuse alveolar damage with pulmonary congestion, edema, and formation of hyaline membrane (hematoxylin and eosin, x100). Panel B shows the organizing phase of diffuse alveolar damage, with scanty interstitial inflammatory-cell infiltrates (hematoxylin and eosin, x200). Panels C and D show vacuolated and multinucleated pneumocytes (hematoxylin and eosin, x400).
Discussion
We report an outbreak in our hospital of a deadly pneumonia,which caused rapid deterioration of pulmonary function requiringICU admission in 23.2 percent of cases and mechanical ventilationin 13.8 percent. Within a period of less than two months, SARShas become a global health problem, prompting the WHO to issuea global alert for the first time in more than a decade.1
The clinical presentation and radiologic features of SARS bearsome resemblance to the syndrome commonly referred to as "atypicalpneumonia"; mycoplasma, chlamydia, and legionella are the usualpathogens implicated in this syndrome. Fever, chills, headache,myalgia, and dry cough are the common features in patients presentingwith the syndrome. However, the clinical and radiographic characteristicsof atypical pneumonia are not useful in differentiating thesepathogens from usual bacterial pathogens such as S. pneumoniaeand H. influenzae. The exclusion of common extracellular pathogensand a response to empirical therapy with macrolides or quinolonesare the usual strategy of management. In our cohort, most ofthe common bacterial pathogens were ruled out, in addition toviral diseases such as influenza and respiratory syncytial virusinfection. Moreover, lack of a response to the initial antimicrobialtreatment we provided led to the suspicion that we were dealingwith a novel virus that causes lower respiratory tract infection.So far, there have been only preliminary data reported on thecausative agent of SARS, and metapneumovirus and coronavirushave been implicated.5 The relevance of histologic featuressuch as vacuolated and multinucleated pneumocytes in the pathogenesisof SARS remains to be determined. As of this writing, no reliablediagnostic test is available. In the first 138 cases, we haveidentified several cardinal symptoms of SARS. Besides fever,chills, and rigor, which were present in more than 70 percentof cases, cough was present in more than 50 percent and dizzinessin more than 40 percent of cases. Rigor may represent the viremicphase of the disease, which subsided gradually as the illnessprogressed. In addition, moderate lymphopenia and its subsequentprogression, thrombocytopenia, a prolonged activated partial-thromboplastintime, elevated lactate dehydrogenase and creatine kinase levels,and elevated alanine aminotransferase levels were prevalentin the early phase of the illness in our cohort; all these findingsare quite different from those associated with pneumonia causedby usual bacterial pathogens. Although these symptoms and laboratoryfindings are nonspecific, the constellation of these featuresshould alert medical practitioners to the possibility of SARS.9
We have also found that the chest radiograph offers an importantdiagnostic clue to this condition. Typically, our patients presentedwith unilateral, predominantly peripheral areas of consolidation.After approximately one week, it progressed rapidly to bilateralpatchy consolidation, and the extent of the lung opacities wascorrelated with the deterioration in respiratory function. Incases in which plain chest radiographs appeared normal in thepresence of a high spiking fever and lymphopenia, CT of thethorax was a sensitive imaging approach for the diagnosis. Thecharacteristic finding on CT was bilateral peripheral air-spaceground-glass consolidation mimicking that in bronchiolitis obliteranswith organizing pneumonia. In fact, the similarity of this radiographicpicture to that of bronchiolitis obliterans with organizingpneumonia and the similarity of the histologic features to thoseof early ARDS in postmortem studies have prompted us to usecorticosteroids in combination with ribavirin for the treatmentof SARS. In ARDS and particularly in bronchiolitis obliteranswith organizing pneumonia, corticosteroid therapy has been usedwith some success.7 The majority of our cohort appeared to havea response to corticosteroid therapy, in addition to ribavirin,with resolution of fever and lung opacities within two weeks.
In this study, we were able to identify some clinical and laboratoryfeatures on presentation that were associated with the adverseclinical outcome of respiratory failure requiring care in theICU or death. Univariate analyses showed that advanced age,male sex, a high neutrophil count, a high peak creatine kinaselevel, high initial and peak lactate dehydrogenase levels, anda low serum sodium level were associated with an adverse outcome.Only advanced age, a high neutrophil count, and a high peaklactate dehydrogenase level were independent predictors. Sincehigh lactate dehydrogenase levels are often seen in associationwith tissue damage, we propose that this finding indicates moreextensive lung injury. The significant association between ahigh neutrophil count and an adverse outcome remains to be explained.All five patients who died had major coexisting disorders; however,in our analyses, coexisting illness was not correlated witha poor outcome, probably because of the small number of suchpatients.
SARS has already become a global health hazard, and its highinfectivity is alarming. The discovery of the infective agentand studies of its behavior are crucial to an understandingof this new disease. A reliable, rapid diagnostic test, basedon blood samples or nasopharyngeal aspirates, is of great importancein the future management of this disease. Until such a diagnostictest is available, a clear picture of its clinical presentationwill help physicians be on the alert for this condition. Earlyrecognition, prompt isolation, and appropriate therapy are thekeys in combating this deadly infection.
We wish to dedicate this report to the patients we have described,many of whom are our colleagues and their family members, togetherwith medical students from the Faculty of Medicine, ChineseUniversity of Hong Kong. We are also indebted to the many membersof the frontline medical and nursing staff who demonstratedselfless and heroic devotion to duty in the face of this outbreak,despite the potential threat to their own lives and those oftheir families.
Source Information
From the Departments of Medicine and Therapeutics (N.L., D.H., A.W., C.B.L., S.F.L., C.C.S., J.J.Y.S.), Microbiology (P. Chan), Emergency Medicine (P. Cameron), Anesthesia and Intensive Care (G.M.J.), Diagnostic Radiology and Organ Imaging (A.A.), Surgery (M.Y.Y., S.C.), and Anatomical and Cellular Pathology (K.F.T.), Chinese University of Hong Kong, Hong Kong, China. This article was published at www.nejm.org on April 7, 2003.
Address reprint requests to Dr. Sung at the Department of Medicine and Therapeutics, Prince of Wales Hospital, Shatin, New Territories, Hong Kong, China, or at joesung{at}cuhk.edu.hk.
References
World Health Organization. Cumulative number of reported cases (SARS) from 1 February to 27 March 2003. (Accessed April 22, 2003, at http://www.who.int/csr/sarscountry/2003_03_27.)
Centers for Disease Control and Prevention. Severe acute respiratory syndrome (SARS) updated interim case definition. (Accessed April 22, 2003, at http://www.cdc.gov/ncidod/sars/casedefinition.htm.)
Barlett JG, Dowell SF, Mandell LA, File TM Jr, Musher DM, Fine MJ. Practice guidelines for the management of community-acquired pneumonia in adults. Clin Infect Dis 2000;31:347-382. [CrossRef][Medline]
Guidelines for the management of adults with community-acquired pneumonia: diagnosis, assessment of severity, antimicrobial therapy, and prevention. Am J Respir Crit Care Med 2001;163:1730-1754. [Free Full Text]
Update: outbreak of severe acute respiratory syndrome -- worldwide, 2003. MMWR Morb Mortal Wkly Rep 2003;52:241-248. [Medline]
Muller NL, Staples CA, Miller RR. Bronchiolitis obliterans organizing pneumonia: CT features in 14 patients. AJR Am J Roentgenol 1990;154:983-987. [Free Full Text]
Epler GR. Bronchiolitis obliterans organizing pneumonia. Arch Intern Med 2001;161:158-164. [Free Full Text]
Centers for Disease Control and Prevention. Updated interim domestic infection control guidance in the health care and community setting for patients with suspected SARS. (Accessed April 22, 2003, at http://www.cdc.gov/ncidod/sars/infectioncontrol.htm.)
Preliminary clinical description of severe acute respiratory syndrome. MMWR Morb Mortal Wkly Rep 2003;52:255-256. [Medline]
Nichols, W. G., Peck Campbell, A. J., Boeckh, M.
(2008). Respiratory Viruses Other than Influenza Virus: Impact and Therapeutic Advances. Clin. Microbiol. Rev.
21: 274-290
[Abstract][Full Text]
Cheng, V. C. C., Lau, S. K. P., Woo, P. C. Y., Yuen, K. Y.
(2007). Severe Acute Respiratory Syndrome Coronavirus as an Agent of Emerging and Reemerging Infection. Clin. Microbiol. Rev.
20: 660-694
[Abstract][Full Text]
Li, Y., Ching, W.H., Qian, H., Yuen, P.L., Seto, W.H., Kwan, J.K., Leung, J.K.C., Leung, M., Yu, S.C.T.
(2007). An Evaluation of the Ventilation Performance of New SARS Isolation Wards in Nine Hospitals in Hong Kong. Indoor and Built Environment
16: 400-410
[Abstract]
Frieman, M., Yount, B., Heise, M., Kopecky-Bromberg, S. A., Palese, P., Baric, R. S.
(2007). Severe Acute Respiratory Syndrome Coronavirus ORF6 Antagonizes STAT1 Function by Sequestering Nuclear Import Factors on the Rough Endoplasmic Reticulum/Golgi Membrane. J. Virol.
81: 9812-9824
[Abstract][Full Text]
Ko, F. W S, Tam, W., Wong, T. W., Chan, D. P S, Tung, A. H, Lai, C. K W, Hui, D. S C
(2007). Temporal relationship between air pollutants and hospital admissions for chronic obstructive pulmonary disease in Hong Kong. Thorax
62: 780-785
[Abstract][Full Text]
Hui, D. S., Hall, S. D., Chan, M. T.V., Chow, B. K., Ng, S. S., Gin, T., Sung, J. J.Y.
(2007). Exhaled Air Dispersion During Oxygen Delivery Via a Simple Oxygen Mask. Chest
132: 540-546
[Abstract][Full Text]
Tansey, C. M., Louie, M., Loeb, M., Gold, W. L., Muller, M. P., de Jager, J., Cameron, J. I., Tomlinson, G., Mazzulli, T., Walmsley, S. L., Rachlis, A. R., Mederski, B. D., Silverman, M., Shainhouse, Z., Ephtimios, I. E., Avendano, M., Downey, J., Styra, R., Yamamura, D., Gerson, M., Stanbrook, M. B., Marras, T. K., Phillips, E. J., Zamel, N., Richardson, S. E., Slutsky, A. S., Herridge, M. S.
(2007). One-Year Outcomes and Health Care Utilization in Survivors of Severe Acute Respiratory Syndrome. Arch Intern Med
167: 1312-1320
[Abstract][Full Text]
Hsu, C.-H., Hwang, K.-C., Chao, C.-L., Chang, S. G. N., Ho, M.-S., Lin, J.-G., Chang, H.-H., Kao, S.-T., Chen, Y.-M., Chou, P.
(2007). An Evaluation of the Additive Effect of Natural Herbal Medicine on SARS or SARS-like Infectious Diseases in 2003: a Randomized, Double-blind, and Controlled Pilot Study. Evid Based Complement Alternat Med
0: nem035v1-8
[Abstract][Full Text]
Nagata, N., Iwata, N., Hasegawa, H., Fukushi, S., Yokoyama, M., Harashima, A., Sato, Y., Saijo, M., Morikawa, S., Sata, T.
(2007). Participation of both Host and Virus Factors in Induction of Severe Acute Respiratory Syndrome (SARS) in F344 Rats Infected with SARS Coronavirus. J. Virol.
81: 1848-1857
[Abstract][Full Text]
Severson, W. E., Shindo, N., Sosa, M., Fletcher, T. III, White, E. L., Ananthan, S., Jonsson, C. B.
(2007). Development and Validation of a High-Throughput Screen for Inhibitors of SARS CoV and Its Application in Screening of a 100,000-Compound Library. J Biomol Screen
12: 33-40
[Abstract]
Louie, L., Simor, A. E., Chong, S., Luinstra, K., Petrich, A., Mahony, J., Smieja, M., Johnson, G., Gharabaghi, F., Tellier, R., Willey, B. M., Poutanen, S., Mazzulli, T., Broukhanski, G., Jamieson, F., Louie, M., Richardson, S., Ontario Laboratory Working Group for the Rapid Dia,
(2006). Detection of Severe Acute Respiratory Syndrome Coronavirus in Stool Specimens by Commercially Available Real-Time Reverse Transcriptase PCR Assays. J. Clin. Microbiol.
44: 4193-4196
[Abstract][Full Text]
Hui, D. S., Hall, S. D., Chan, M. T.V., Chow, B. K., Tsou, J. Y., Joynt, G. M., Sullivan, C. E., Sung, J. J.Y.
(2006). Noninvasive positive-pressure ventilation: an experimental model to assess air and particle dispersion.. Chest
130: 730-740
[Abstract][Full Text]
Zhou, M., Xu, D., Li, X., Li, H., Shan, M., Tang, J., Wang, M., Wang, F.-S., Zhu, X., Tao, H., He, W., Tien, P., Gao, G. F.
(2006). Screening and Identification of Severe Acute Respiratory Syndrome-Associated Coronavirus-Specific CTL Epitopes. J. Immunol.
177: 2138-2145
[Abstract][Full Text]
Cowling, B. J., Muller, M. P., Wong, I. O. L., Ho, L.-M., Lo, S.-V., Tsang, T., Lam, T. H., Louie, M., Leung, G. M.
(2006). Clinical prognostic rules for severe acute respiratory syndrome in low- and high-resource settings.. Arch Intern Med
166: 1505-1511
[Abstract][Full Text]
Chen, R.-c., Tang, X.-p., Tan, S.-y., Liang, B.-l., Wan, Z.-y., Fang, J.-q., Zhong, N.
(2006). Treatment of Severe Acute Respiratory Syndrome With Glucosteroids: The Guangzhou Experience. Chest
129: 1441-1452
[Abstract][Full Text]
Li, W., Wong, S.-K., Li, F., Kuhn, J. H., Huang, I-C., Choe, H., Farzan, M.
(2006). Animal Origins of the Severe Acute Respiratory Syndrome Coronavirus: Insight from ACE2-S-Protein Interactions. J. Virol.
80: 4211-4219
[Full Text]
Parker, M J, Goldman, R D
(2006). Paediatric emergency department staff perceptions of infection control measures against severe acute respiratory syndrome. Emerg. Med. J.
23: 349-353
[Abstract][Full Text]
Chow, S C S, Ho, C Y S, Tam, T T Y, Wu, C, Cheung, T, Chan, P K S, Ng, M H L, Hui, P K, Ng, H K, Au, D M Y, Lo, A W I
(2006). Specific epitopes of the structural and hypothetical proteins elicit variable humoral responses in SARS patients. J. Clin. Pathol.
59: 468-476
[Abstract][Full Text]
Chu, L.-H. M., Choy, W.-Y., Tsai, S.-N., Rao, Z., Ngai, S.-M.
(2006). Rapid peptide-based screening on the substrate specificity of severe acute respiratory syndrome (SARS) coronavirus 3C-like protease by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry.. Protein Sci.
15: 699-709
[Abstract][Full Text]
Yen, Y.-T., Liao, F., Hsiao, C.-H., Kao, C.-L., Chen, Y.-C., Wu-Hsieh, B. A.
(2006). Modeling the Early Events of Severe Acute Respiratory Syndrome Coronavirus Infection In Vitro. J. Virol.
80: 2684-2693
[Abstract][Full Text]
Khattari, Z., Brotons, G., Akkawi, M., Arbely, E., Arkin, I. T., Salditt, T.
(2006). SARS Coronavirus E Protein in Phospholipid Bilayers: An X-Ray Study. Biophys. J
90: 2038-2050
[Abstract][Full Text]
Wang, L-M, Chen, Y-C, Tung, S-P, Chen, C-Y, Chang, S-C, Chiang, S-C, Lee, C-H
(2006). The rationale of fever surveillance to identify patients with severe acute respiratory syndrome in Taiwan. Emerg. Med. J.
23: 202-205
[Abstract][Full Text]
Pang, R. T.K., Poon, T. C.W., Chan, K.C. A., Lee, N. L.S., Chiu, R. W.K., Tong, Y.-K., Wong, R. M.Y., Chim, S. S.C., Ngai, S. M., Sung, J. J.Y., Lo, Y.M. D.
(2006). Serum Proteomic Fingerprints of Adult Patients with Severe Acute Respiratory Syndrome. Clin. Chem.
52: 421-429
[Abstract][Full Text]
Lin, H., Chie, W., Lien, H.
(2006). Epidemiological Analysis of Factors Influencing an Episode of Exertional Rhabdomyolysis in High School Students. Am J Sports Med
34: 481-486
[Abstract][Full Text]
Caputo, K. M., Byrick, R., Chapman, M. G., Orser, B. J., Orser, B. A.
(2006). Intubation of SARS patients: infection and perspectives of healthcare workers: [L'intubation de patients atteints du SRAS: infection et perspectives des travailleurs de la sante]. Canadian J. Anesthesia
53: 122-129
[Abstract][Full Text]
Cai, Q.-C., Xu, Q.-F., Xu, J.-M., Guo, Q., Cheng, X., Zhao, G.-M., Sun, Q.-W., Lu, J., Jiang, Q.-W.
(2006). Refined Estimate of the Incubation Period of Severe Acute Respiratory Syndrome and Related Influencing Factors. Am J Epidemiol
163: 211-216
[Abstract][Full Text]
Yu, C-M, Wong, R S-M, Wu, E B, Kong, S-L, Wong, J, Yip, G W-K, Soo, Y O Y, Chiu, M L S, Chan, Y-S, Hui, D, Lee, N, Wu, A, Leung, C-B, Sung, J J-Y
(2006). Cardiovascular complications of severe acute respiratory syndrome. Postgrad. Med. J.
82: 140-144
[Abstract][Full Text]
Huang, C., Narayanan, K., Ito, N., Peters, C. J., Makino, S.
(2006). Severe Acute Respiratory Syndrome Coronavirus 3a Protein Is Released in Membranous Structures from 3a Protein-Expressing Cells and Infected Cells. J. Virol.
80: 210-217
[Abstract][Full Text]
Weiss, S. R., Navas-Martin, S.
(2005). Coronavirus Pathogenesis and the Emerging Pathogen Severe Acute Respiratory Syndrome Coronavirus. Microbiol. Mol. Biol. Rev.
69: 635-664
[Abstract][Full Text]
Deurenberg-Yap, M., Foo, L. L., Low, Y. Y., Chan, S. P., Vijaya, K., Lee, M.
(2005). The Singaporean response to the SARS outbreak: knowledge sufficiency versus public trust. HEALTH PROMOT INT
20: 320-326
[Abstract][Full Text]
Antonio, G. E., Ooi, C. G. C., Wong, K. T., Tsui, E. L. H., Wong, J. S. W., Sy, A. N. L., Hui, J. Y. H., Chan, C. Y., Huang, H. Y. H., Chan, Y. F., Wong, T. P., Leong, L. L. Y., Chan, J. C. K., Ahuja, A. T.
(2005). Radiographic-Clinical Correlation in Severe Acute Respiratory Syndrome: Study of 1373 Patients in Hong Kong. Radiology
237: 1081-1090
[Abstract][Full Text]
Tang, N. L.-S., Chan, P. K.-S., Wong, C.-K., To, K.-F., Wu, A. K.-L., Sung, Y.-M., Hui, D. S.-C., Sung, J. J.-Y., Lam, C. W.-K.
(2005). Early Enhanced Expression of Interferon-Inducible Protein-10 (CXCL-10) and Other Chemokines Predicts Adverse Outcome in Severe Acute Respiratory Syndrome. Clin. Chem.
51: 2333-2340
[Abstract][Full Text]
Hsieh, P.-K., Chang, S. C., Huang, C.-C., Lee, T.-T., Hsiao, C.-W., Kou, Y.-H., Chen, I-Y., Chang, C.-K., Huang, T.-H., Chang, M.-F.
(2005). Assembly of Severe Acute Respiratory Syndrome Coronavirus RNA Packaging Signal into Virus-Like Particles Is Nucleocapsid Dependent. J. Virol.
79: 13848-13855
[Abstract][Full Text]
Kong, W.-p., Xu, L., Stadler, K., Ulmer, J. B., Abrignani, S., Rappuoli, R., Nabel, G. J.
(2005). Modulation of the Immune Response to the Severe Acute Respiratory Syndrome Spike Glycoprotein by Gene-Based and Inactivated Virus Immunization. J. Virol.
79: 13915-13923
[Abstract][Full Text]
Yeh, K.-M., Chiueh, T.-S., Siu, L. K., Lin, J.-C., Chan, P. K. S., Peng, M.-Y., Wan, H.-L., Chen, J.-H., Hu, B.-S., Perng, C.-L., Lu, J.-J., Chang, F.-Y.
(2005). Experience of using convalescent plasma for severe acute respiratory syndrome among healthcare workers in a Taiwan hospital. J Antimicrob Chemother
56: 919-922
[Abstract][Full Text]
Chapman, W. W., Dowling, J. N., Wagner, M. M.
(2005). Generating a Reliable Reference Standard Set for Syndromic Case Classification. J. Am. Med. Inform. Assoc.
12: 618-629
[Abstract][Full Text]
Li, A M, Ng, P C
(2005). Severe acute respiratory syndrome (SARS) in neonates and children. Arch. Dis. Child. Fetal Neonatal Ed.
90: F461-F465
[Abstract][Full Text]
Hui, D. S., Wong, K. T., Ko, F. W., Tam, L. S., Chan, D. P., Woo, J., Sung, J. J.Y.
(2005). The 1-Year Impact of Severe Acute Respiratory Syndrome on Pulmonary Function, Exercise Capacity, and Quality of Life in a Cohort of Survivors. Chest
128: 2247-2261
[Abstract][Full Text]
Naldini, A., Bernini, C., Pucci, A., Carraro, F.
(2005). Thrombin-mediated IL-10 up-regulation involves protease-activated receptor (PAR)-1 expression in human mononuclear leukocytes. J. Leukoc. Biol.
78: 736-744
[Abstract][Full Text]
Chang, Y.-C., Yu, C.-J., Chang, S.-C., Galvin, J. R., Liu, H.-M., Hsiao, C.-H., Kuo, P.-H., Chen, K.-Y., Franks, T. J., Huang, K.-M., Yang, P.-C.
(2005). Pulmonary Sequelae in Convalescent Patients after Severe Acute Respiratory Syndrome: Evaluation with Thin-Section CT. Radiology
236: 1067-1075
[Abstract][Full Text]
He, Y., Zhou, Y., Siddiqui, P., Niu, J., Jiang, S.
(2005). Identification of Immunodominant Epitopes on the Membrane Protein of the Severe Acute Respiratory Syndrome-Associated Coronavirus. J. Clin. Microbiol.
43: 3718-3726
[Abstract][Full Text]
Tseng, C.-T. K., Tseng, J., Perrone, L., Worthy, M., Popov, V., Peters, C. J.
(2005). Apical Entry and Release of Severe Acute Respiratory Syndrome-Associated Coronavirus in Polarized Calu-3 Lung Epithelial Cells. J. Virol.
79: 9470-9479
[Abstract][Full Text]
Tan, Y.-J., Tham, P.-Y., Chan, D. Z. L., Chou, C.-F., Shen, S., Fielding, B. C., Tan, T. H. P., Lim, S. G., Hong, W.
(2005). The Severe Acute Respiratory Syndrome Coronavirus 3a Protein Up-Regulates Expression of Fibrinogen in Lung Epithelial Cells. J. Virol.
79: 10083-10087
[Abstract][Full Text]
LU, S.-N., JIANG, D. D.-S., LIU, J.-W., LIN, M.-C., CHEN, C.-L., SU, I.-J., CHEN, S.-S.
(2005). OUTBREAK OF SEVERE ACUTE RESPIRATORY SYNDROME IN SOUTHERN TAIWAN, 2003. Am J Trop Med Hyg
73: 423-427
[Abstract][Full Text]
Gu, J., Gong, E., Zhang, B., Zheng, J., Gao, Z., Zhong, Y., Zou, W., Zhan, J., Wang, S., Xie, Z., Zhuang, H., Wu, B., Zhong, H., Shao, H., Fang, W., Gao, D., Pei, F., Li, X., He, Z., Xu, D., Shi, X., Anderson, V. M., Leong, A. S.-Y.
(2005). Multiple organ infection and the pathogenesis of SARS. J. Exp. Med.
202: 415-424
[Abstract][Full Text]
Yu, F., Le, M. Q., Inoue, S., Thai, H. T. C., Hasebe, F., del Carmen Parquet, M., Morita, K.
(2005). Evaluation of Inapparent Nosocomial Severe Acute Respiratory Syndrome Coronavirus Infection in Vietnam by Use of Highly Specific Recombinant Truncated Nucleocapsid Protein-Based Enzyme-Linked Immunosorbent Assay. CVI
12: 848-854
[Abstract][Full Text]
NISHIURA, H., KURATSUJI, T., QUY, T., PHI, N. C., VAN BAN, V., HA, L. D., LONG, H. T., YANAI, H., KEICHO, N., KIRIKAE, T., SASAZUKI, T., ANDERSON, R. M.
(2005). RAPID AWARENESS AND TRANSMISSION OF SEVERE ACUTE RESPIRATORY SYNDROME IN HANOI FRENCH HOSPITAL, VIETNAM. Am J Trop Med Hyg
73: 17-25
[Abstract][Full Text]
Leung, T. W., Wong, K. S., Hui, A. C., To, K. F., Lai, S. T., Ng, W. F., Ng, H. K.
(2005). Myopathic Changes Associated With Severe Acute Respiratory Syndrome: A Postmortem Case Series. Arch Neurol
62: 1113-1117
[Abstract][Full Text]
Chen, H., Hou, J., Jiang, X., Ma, S., Meng, M., Wang, B., Zhang, M., Zhang, M., Tang, X., Zhang, F., Wan, T., Li, N., Yu, Y., Hu, H., Yang, R., He, W., Wang, X., Cao, X.
(2005). Response of Memory CD8+ T Cells to Severe Acute Respiratory Syndrome (SARS) Coronavirus in Recovered SARS Patients and Healthy Individuals. J. Immunol.
175: 591-598
[Abstract][Full Text]
Cheng, F W T, Ng, P C, Chiu, W K, Chu, W C W, Li, A M, Lo, K L, Hon, E K L, Nelson, E A S, Leung, T F, Ng, W H, Wong, E, Ip, P, Fok, T F
(2005). A case-control study of SARS versus community acquired pneumonia. Arch. Dis. Child.
90: 747-749
[Abstract][Full Text]
Chen, L., Gui, C., Luo, X., Yang, Q., Gunther, S., Scandella, E., Drosten, C., Bai, D., He, X., Ludewig, B., Chen, J., Luo, H., Yang, Y., Yang, Y., Zou, J., Thiel, V., Chen, K., Shen, J., Shen, X., Jiang, H.
(2005). Cinanserin Is an Inhibitor of the 3C-Like Proteinase of Severe Acute Respiratory Syndrome Coronavirus and Strongly Reduces Virus Replication In Vitro. J. Virol.
79: 7095-7103
[Abstract][Full Text]
Xie, L., Liu, Y., Xiao, Y., Tian, Q., Fan, B., Zhao, H., Chen, W.
(2005). Follow-up Study on Pulmonary Function and Lung Radiographic Changes in Rehabilitating Severe Acute Respiratory Syndrome Patients After Discharge. Chest
127: 2119-2124
[Abstract][Full Text]
Ng, K H L, Wu, A K L, Cheng, V C C, Tang, B S F, Chan, C Y, Yung, C Y, Luk, S H, Lee, T W, Chow, L, Yuen, K Y
(2005). Pulmonary artery thrombosis in a patient with severe acute respiratory syndrome. Postgrad. Med. J.
81: e3-e3
[Abstract][Full Text]
Roberts, A., Paddock, C., Vogel, L., Butler, E., Zaki, S., Subbarao, K.
(2005). Aged BALB/c Mice as a Model for Increased Severity of Severe Acute Respiratory Syndrome in Elderly Humans. J. Virol.
79: 5833-5838
[Abstract][Full Text]
Chan, J C K
(2005). Recovery pathway of post-SARS patients. Thorax
60: 361-362
[Full Text]
Hui, D S, Joynt, G M, Wong, K T, Gomersall, C D, Li, T S, Antonio, G, Ko, F W, Chan, M C, Chan, D P, Tong, M W, Rainer, T H, Ahuja, A T, Cockram, C S, Sung, J J Y
(2005). Impact of severe acute respiratory syndrome (SARS) on pulmonary function, functional capacity and quality of life in a cohort of survivors. Thorax
60: 401-409
[Abstract][Full Text]
Yip, P. S. F., Lau, E. H. Y., Lam, K. F., Huggins, R. M.
(2005). A Chain Multinomial Model for Estimating the Real-Time Fatality Rate of a Disease, with an Application to Severe Acute Respiratory Syndrome. Am J Epidemiol
161: 700-706
[Abstract][Full Text]
Griffith, J. F., Antonio, G. E., Kumta, S. M., Hui, D. S. C., Wong, J. K. T., Joynt, G. M., Wu, A. K. L., Cheung, A. Y. K., Chiu, K. H., Chan, K. M., Leung, P. C., Ahuja, A. T.
(2005). Osteonecrosis of Hip and Knee in Patients with Severe Acute Respiratory Syndrome Treated with Steroids. Radiology
235: 168-175
[Abstract][Full Text]
Cheng, Y., Cheng, G., Chui, C. H., Lau, F. Y., Chan, P. K. S., Ng, M. H. L., Sung, J. J. Y., Wong, R. S. M.
(2005). ABO Blood Group and Susceptibility to Severe Acute Respiratory Syndrome. JAMA
293: 1450-1451
[Full Text]
Zhong, X., Yang, H., Guo, Z.-F., Sin, W.-Y. F., Chen, W., Xu, J., Fu, L., Wu, J., Mak, C.-K. G., Cheng, C.-S. S., Yang, Y., Cao, S., Wong, T.-Y., Lai, S.-T., Xie, Y., Guo, Z.
(2005). B-Cell Responses in Patients Who Have Recovered from Severe Acute Respiratory Syndrome Target a Dominant Site in the S2 Domain of the Surface Spike Glycoprotein. J. Virol.
79: 3401-3408
[Abstract][Full Text]
Ito, N., Mossel, E. C., Narayanan, K., Popov, V. L., Huang, C., Inoue, T., Peters, C. J., Makino, S.
(2005). Severe Acute Respiratory Syndrome Coronavirus 3a Protein Is a Viral Structural Protein. J. Virol.
79: 3182-3186
[Abstract][Full Text]
Antonio, G. E., Wong, K. T., Tsui, E. L. H., Chan, D. P. N., Hui, D. S. C., Ng, A. W. H., Shing, K. K., Yuen, E. H. Y., Chan, J. C. K., Ahuja, A. T.
(2005). Chest Radiograph Scores as Potential Prognostic Indicators in Severe Acute Respiratory Syndrome (SARS). Am. J. Roentgenol.
184: 734-741
[Abstract][Full Text]
Levy, M. M., Baylor, M. S., Bernard, G. R., Fowler, R., Franks, T. J., Hayden, F. G., Helfand, R., Lapinsky, S. E., Martin, T. R., Niederman, M. S., Rubenfeld, G. D., Slutsky, A. S., Stewart, T. E., Styrt, B. A., Thompson, B. T., Harabin, A. L.
(2005). Clinical Issues and Research in Respiratory Failure from Severe Acute Respiratory Syndrome. Am. J. Respir. Crit. Care Med.
171: 518-526
[Abstract][Full Text]
Wu, D., Tu, C., Xin, C., Xuan, H., Meng, Q., Liu, Y., Yu, Y., Guan, Y., Jiang, Y., Yin, X., Crameri, G., Wang, M., Li, C., Liu, S., Liao, M., Feng, L., Xiang, H., Sun, J., Chen, J., Sun, Y., Gu, S., Liu, N., Fu, D., Eaton, B. T., Wang, L.-F., Kong, X.
(2005). Civets Are Equally Susceptible to Experimental Infection by Two Different Severe Acute Respiratory Syndrome Coronavirus Isolates. J. Virol.
79: 2620-2625
[Abstract][Full Text]
de Groot-Mijnes, J. D. F., van Dun, J. M., van der Most, R. G., de Groot, R. J.
(2005). Natural History of a Recurrent Feline Coronavirus Infection and the Role of Cellular Immunity in Survival and Disease. J. Virol.
79: 1036-1044
[Abstract][Full Text]
Chen, C.-S., Wu, H.-Y., Yang, P., Yen, C.-F.
(2005). Psychological Distress of Nurses in Taiwan Who Worked During the Outbreak of SARS. Psychiatr. Serv.
56: 76-79
[Abstract][Full Text]
Lai, E. K. Y., Deif, H., LaMere, E. A., Pham, D. H., Wolff, B., Ward, S., Mederski, B., Loutfy, M. R.
(2005). Severe Acute Respiratory Syndrome: Quantitative Assessment from Chest Radiographs with Clinical and Prognostic Correlation. Am. J. Roentgenol.
184: 255-263
[Abstract][Full Text]
Chang, Y.-J., Liu, C. Y.-Y., Chiang, B.-L., Chao, Y.-C., Chen, C.-C.
(2004). Induction of IL-8 Release in Lung Cells via Activator Protein-1 by Recombinant Baculovirus Displaying Severe Acute Respiratory Syndrome-Coronavirus Spike Proteins: Identification of Two Functional Regions. J. Immunol.
173: 7602-7614
[Abstract][Full Text]
Lorber, B.
(2004). Update in Infectious Diseases. ANN INTERN MED
141: 875-881
[Full Text]
Tsang, K.W., Ooi, G.C., Ho, P.L.
(2004). Diagnosis and pharmacotherapy of severe acute respiratory syndrome: what have we learnt?. Eur Respir J
24: 1025-1032
[Abstract][Full Text]
Lau, J. T F, Yang, X., Tsui, H Y, Pang, E.
(2004). SARS related preventive and risk behaviours practised by Hong Kong-mainland China cross border travellers during the outbreak of the SARS epidemic in Hong Kong. J. Epidemiol. Community Health
58: 988-996
[Abstract][Full Text]
Wu, V.-C., Hsueh, P.-R., Lin, W.-C., Huang, J.-W., Tsai, H.-B., Chen, Y.-M., Wu, K.-D., The SARS Research Group of the National Taiwan Uni,
(2004). Acute renal failure in SARS patients: more than rhabdomyolysis. Nephrol Dial Transplant
19: 3180-3182
[Full Text]
Chu, C.-M., Poon, L. L.M., Cheng, V. C.C., Chan, K.-S., Hung, I. F.N., Wong, M. M.L., Chan, K.-H., Leung, W.-S., Tang, B. S.F., Chan, V. L., Ng, W.-L., Sim, T.-C., Ng, P.-W., Law, K.-I., Tse, D. M.W., Peiris, J. S.M., Yuen, K.-Y.
(2004). Initial viral load and the outcomes of SARS. CMAJ
171: 1349-1352
[Abstract][Full Text]
Boutis, K., Stephens, D., Lam, K., Ungar, W. J., Schuh, S.
(2004). The impact of SARS on a tertiary care pediatric emergency department. CMAJ
171: 1353-1358
[Abstract][Full Text]
Leung, G. M., Hedley, A. J., Ho, L.-M., Chau, P., Wong, I. O.L., Thach, T. Q., Ghani, A. C., Donnelly, C. A., Fraser, C., Riley, S., Ferguson, N. M., Anderson, R. M., Tsang, T., Leung, P.-Y., Wong, V., Chan, J. C.K., Tsui, E., Lo, S.-V., Lam, T.-H.
(2004). The Epidemiology of Severe Acute Respiratory Syndrome in the 2003 Hong Kong Epidemic: An Analysis of All 1755 Patients. ANN INTERN MED
141: 662-673
[Abstract][Full Text]
He, Y., Zhou, Y., Wu, H., Kou, Z., Liu, S., Jiang, S.
(2004). Mapping of Antigenic Sites on the Nucleocapsid Protein of the Severe Acute Respiratory Syndrome Coronavirus. J. Clin. Microbiol.
42: 5309-5314
[Abstract][Full Text]
Chang, L.-Y., Huang, F.-Y., Wu, Y.-C., Su, I.-J., Chiu, N.-C., Chen, K.-T., Wu, H.-S., Lin, T.-H., Peng, S.-F., Kao, C.-L., Lee, C.-Y., Huang, L.-M.
(2004). Childhood Severe Acute Respiratory Syndrome in Taiwan and How to Differentiate It From Childhood Influenza Infection. Arch Pediatr Adolesc Med
158: 1037-1042
[Abstract][Full Text]
Hui, D. S. C., Wong, K. T., Antonio, G. E., Lee, N., Wu, A., Wong, V., Lau, W., Wu, J. C., Tam, L. S., Yu, L. M., Joynt, G. M., Chung, S. S. C., Ahuja, A. T., Sung, J. J. Y.
(2004). Severe Acute Respiratory Syndrome: Correlation between Clinical Outcome and Radiologic Features. Radiology
233: 579-585
[Abstract][Full Text]
Li, Y., Yu, I. T. S., Xu, P., Lee, J. H. W., Wong, T. W., Ooi, P. L., Sleigh, A. C.
(2004). Predicting Super Spreading Events during the 2003 Severe Acute Respiratory Syndrome Epidemics in Hong Kong and Singapore. Am J Epidemiol
160: 719-728
[Abstract][Full Text]
Pang, H., Liu, Y., Han, X., Xu, Y., Jiang, F., Wu, D., Kong, X., Bartlam, M., Rao, Z.
(2004). Protective humoral responses to severe acute respiratory syndrome-associated coronavirus: implications for the design of an effective protein-based vaccine. J. Gen. Virol.
85: 3109-3113
[Abstract][Full Text]
Ko, S.-F., Lee, T.-Y., Huang, C.-C., Cheng, Y.-F., Ng, S.-H., Kuo, Y.-L., Lin, M.-C., Liu, J.-W., Yang, K. D., Chen, M.-C., Chen, C.-L.
(2004). Severe Acute Respiratory Syndrome: Prognostic Implications of Chest Radiographic Findings in 52 Patients. Radiology
233: 173-181
[Abstract][Full Text]
Leung, G. M., Rainer, T. H., Lau, F.-L., Wong, I. O.L., Tong, A., Wong, T.-W., Kong, J. H.B., Hedley, A. J., Lam, T.-H., for the Hospital Authority SARS Collaborative Grou,
(2004). A Clinical Prediction Rule for Diagnosing Severe Acute Respiratory Syndrome in the Emergency Department. ANN INTERN MED
141: 333-342
[Abstract][Full Text]
Hui, D. S.C., Sung, J. J.Y.
(2004). Treatment of Severe Acute Respiratory Syndrome. Chest
126: 670-674
[Full Text]
Cheung, T. M. T., Yam, L. Y. C., So, L. K. Y., Lau, A. C. W., Poon, E., Kong, B. M. H., Yung, R. W. H.
(2004). Effectiveness of Noninvasive Positive Pressure Ventilation in the Treatment of Acute Respiratory Failure in Severe Acute Respiratory Syndrome. Chest
126: 845-850
[Abstract][Full Text]
Chiu, R. W.K., Tang, N. L.S., Hui, D. S.C., Chung, G. T.Y., Chim, S. S.C., Chan, K.C. A., Sung, Y.-m., Chan, L. Y.S., Tong, Y.-k., Lee, W.-s., Chan, P. K.S., Lo, Y.M. D.
(2004). ACE2 Gene Polymorphisms Do Not Affect Outcome of Severe Acute Respiratory Syndrome. Clin. Chem.
50: 1683-1686
[Full Text]
Clark, A. M., Jamieson, R., Findlay, I. N., McKenna, M. T., Wingo, P., Gibson, J. J., Haidinger, G., Vutuc, C., Maier, M., Tu, J. V., Silver, F. L., Kapral, M. K.
(2004). Registries and Informed Consent. NEJM
351: 612-614
[Full Text]
Apostolakos, M. J.
(2004). SARS, Cough, and Fever--or Is It SARS, Fever, and Cough?. Chest
126: 333-335
[Full Text]
Liu, C.-L., Lu, Y.-T., Peng, M.-J., Chen, P.-J., Lin, R.-L., Wu, C.-L., Kuo, H.-T.
(2004). Clinical and Laboratory Features of Severe Acute Respiratory Syndrome Vis-A-Vis Onset of Fever. Chest
126: 509-517
[Abstract][Full Text]
WU, K.-L., LU, S.-N., CHANGCHIEN, C.-S., CHIU, K.-W., KUO, C.-H., CHUAH, S.-K., LIU, J.-W., LIN, M.-C., ENG, H.-L., CHEN, S.-S., LEE, C.-M., CHEN, C.-L.
(2004). SEQUENTIAL CHANGES OF SERUM AMINOTRANSFERASE LEVELS IN PATIENTS WITH SEVERE ACUTE RESPIRATORY SYNDROME. Am J Trop Med Hyg
71: 125-128
[Abstract][Full Text]
Yu, W C, Hui, D S C, Chan-Yeung, M
(2004). Antiviral agents and corticosteroids in the treatment of severe acute respiratory syndrome (SARS). Thorax
59: 643-645
[Full Text]
Parashar, U. D, Anderson, L. J
(2004). Severe acute respiratory syndrome: review and lessons of the 2003 outbreak. Int J Epidemiol
33: 628-634
[Full Text]
Wu, C.-Y., Jan, J.-T., Ma, S.-H., Kuo, C.-J., Juan, H.-F., Cheng, Y.-S. E., Hsu, H.-H., Huang, H.-C., Wu, D., Brik, A., Liang, F.-S., Liu, R.-S., Fang, J.-M., Chen, S.-T., Liang, P.-H., Wong, C.-H.
(2004). Small molecules targeting severe acute respiratory syndrome human coronavirus. Proc. Natl. Acad. Sci. USA
101: 10012-10017
[Abstract][Full Text]
Wu, C.-J., Jan, J.-T., Chen, C.-M., Hsieh, H.-P., Hwang, D.-R., Liu, H.-W., Liu, C.-Y., Huang, H.-W., Chen, S.-C., Hong, C.-F., Lin, R.-K., Chao, Y.-S., Hsu, J. T. A.
(2004). Inhibition of Severe Acute Respiratory Syndrome Coronavirus Replication by Niclosamide. Antimicrob. Agents Chemother.
48: 2693-2696
[Abstract][Full Text]
Previous
