A Cluster of Cases of Severe Acute Respiratory Syndrome in Hong Kong
Kenneth W. Tsang, M.D., Pak L. Ho, M.D., Gaik C. Ooi, M.D., Wilson K. Yee, M.D., Teresa Wang, M.D., Moira Chan-Yeung, M.D., Wah K. Lam, M.D., Wing H. Seto, M.D., Loretta Y. Yam, M.D., Thomas M. Cheung, M.D., Poon C. Wong, M.D., Bing Lam, M.D., Mary S. Ip, M.D., Jane Chan, M.D., Kwok Y. Yuen, M.D., and Kar N. Lai, M.D., D.Sc.
Background Information on the clinical features of the severeacute respiratory syndrome (SARS) will be of value to physicianscaring for patients suspected of having this disorder.
Methods We abstracted data on the clinical presentation andcourse of disease in 10 epidemiologically linked Chinese patients(5 men and 5 women 38 to 72 years old) in whom SARS was diagnosedbetween February 22, 2003, and March 22, 2003, at our hospitalsin Hong Kong, China.
Results Exposure between the source patient and subsequent patientsranged from minimal to that between patient and health careprovider. The incubation period ranged from 2 to 11 days. Allpatients presented with fever (temperature, >38°C forover 24 hours), and most presented with rigor, dry cough, dyspnea,malaise, headache, and hypoxemia. Physical examination of thechest revealed crackles and percussion dullness. Lymphopeniawas observed in nine patients, and most patients had mildlyelevated aminotransferase levels but normal serum creatininelevels. Serial chest radiographs showed progressive air-spacedisease. Two patients died of progressive respiratory failure;histologic analysis of their lungs showed diffuse alveolar damage.There was no evidence of infection by Mycoplasma pneumoniae,Chlamydia pneumoniae, or Legionella pneumophila. All patientsreceived corticosteroid and ribavirin therapy a mean (±SD)of 9.6±5.42 days after the onset of symptoms, and eightwere treated earlier with a combination of beta-lactams andmacrolide for 4±1.9 days, with no clinical or radiologicefficacy.
Conclusions SARS appears to be infectious in origin. Fever followedby rapidly progressive respiratory compromise is the key complexof signs and symptoms from which the syndrome derives its name.The microbiologic origins of SARS remain unclear.
In the fall of 2002, there were reports from Guangdong Provincein southern China of 305 cases of highly contagious and verysevere atypical pneumonia of unknown cause. The condition appearedto be particularly prevalent among health care workers and theirhousehold members; many cases were rapidly fatal.1 On March13, 2003, as the condition began to spread from China, the WorldHealth Organization (WHO) issued a global alert about the outbreakand instituted worldwide surveillance. In March the U.S. Centersfor Disease Control and Prevention (CDC) termed this conditionthe severe acute respiratory syndrome (SARS) and provided aclinical case definition.2 Herein we report the clinical, radiologic,and laboratory features of 10 of our patients with SARS whosecases were epidemiologically linked. Since the microbiologyof these cases remains unresolved, we provide the clinical andepidemiologic information for use in case recognition and management.
Methods
Patients
Between February 22 and March 22, 2003, we identified 10 epidemiologicallylinked patients (all southern Chinese) whose disease met theCDC case definition of March 17, 2003, of SARS at our hospitalcluster (Queen Mary Hospital, Kwong Wah Hospital, and PamelaYoude Nethersole Eastern Hospital) in Hong Kong (Table 1).2Patients were interviewed to ascertain their possible contactswith each other, as noted in Figure 1.
Figure 1. Contact History (Panel A) and Temporal Relation between Contact and the Onset of Symptoms (Panel B) in the 10 Patients with SARS.
Radiologic Assessment
The chest radiographs of 10 patients were evaluated withoutreference to clinical details. Volumetric contrast-enhancedcomputed tomography (CT) with high-resolution CT scanning ofthe thorax was available in three patients (Patients 3, 4, and10), and these were also reviewed. The pattern of opacificationwas categorized as air space (ground-glass opacification, focalconsolidation, lobar consolidation, or patchy consolidation),interstitial (reticular), or diffuse (affecting all lung zones).The presence of pleural effusions was also noted.
Microbiologic Evaluation
Respiratory secretions (sputum in all patients and trachealaspirate and bronchoalveolar-lavage fluid in Patients 1, 2,and 3) were analyzed for conventional bacteria (with blood,chocolate, and MacConkey agars), Legionella pneumophila (withBCYE medium), and mycobacteria (with LJ medium). Gram-stainedand auramine-rhodamine–stained smears were examined tosearch for bacterial or acid-fast morphotypes.
Single or, when available, paired serum samples were testedfor Mycoplasma pneumoniae (Serodia-Myco-II, Fujirebio) and Chlamydiapneumoniae and C. psittaci (MRL microimmunofluorescence kit).Urinary antigen detection (Binax Now test kits, Binax) was performedfor L. pneumophila and pneumococcus. Immunofluorescence techniqueswere used to detect antigens in nasopharyngeal aspirates (andbronchoalveolar-lavage fluid in Patient 1) with commerciallyavailable reagents from Dako Diagnostics and Chemicon International.
Results
Patients and Contact History
The mean (±SD) age of the 10 patients (5 men and 5 women)was 52.5±11.0 years (median, 49.5; range, 35 to 72).Except as noted below, all of the patients had unremarkablemedical histories. Patient 2 had stable hypertension and benignprostatic hypertrophy, Patient 4 had ischemic heart diseaseand non-insulin-dependent diabetes mellitus, and Patient 10had non-insulin-dependent diabetes and resected renal-cell carcinomaof the right kidney. Patient 2 was taking metoprolol and nifedipine;Patient 4 was taking aspirin, diltiazem, and metformin; andPatient 10 was taking gliclazide and metformin. Eight of the10 patients had never smoked, 1 was a current smoker (25 cigarettesper day), and 1 was a former smoker (20 cigarettes per day)who had stopped five years earlier.
The contact history among the patients in this cluster is shownin Figure 1A. Patient 1, who had the first known case of SARSin Hong Kong, was a nephrologist working in a hospital in southernChina who had traveled to Hong Kong on February 21, 2003, havingfirst had symptoms five days earlier. On arrival in Hong Konghe felt well enough to sightsee and shop with his brother-in-law,but the next day he sought urgent care and was directly admittedto the intensive care unit (ICU) of Hospital A with respiratoryfailure. Patient 2, a Hong Kong resident, was the brother-in-lawof Patient 1 and had had social contact with Patient 1 for 10hours while sightseeing and shopping. Patient 3 was a nursein the accident and emergency department of Hospital A who waspresent in the same resuscitation room but at least 1 m awayfrom Patient 1, who was being treated by another team of physiciansand nurses. Patient 3 had no direct contact with Patient 1 andwas wearing a surgical mask at the time. Patient 5 was a healthcare assistant who worked in the ICU of Hospital A and had unprotectedhospital contact (without a mask or gown) with Patient 2 forsix hours.
Patient 4 was a Chinese-Canadian businessman who had returnedto Hong Kong for a family reunion on February 13, 2003. He hadnot traveled outside Toronto for more than 12 months beforehis return to Hong Kong. His stay at Hotel X overlapped withthat of Patient 1 for one day. There was no known direct contactbetween Patient 1 and Patient 4. Patient 4 could not recollectwhether he had seen Patient 1 in the common areas of the hotel.Patients 6, 7, and 8 were nurses who worked at Hospital B, wherePatient 4 was admitted and remained for six days for treatmentof pneumonia before he was transferred to Hospital C. Duringthis period, the nurses spent five eight-hour shifts stationedon the general ward on which Patient 4 was hospitalized. Thethree nurses recalled a close encounter with Patient 4 duringwhich they cleaned him when he had fecal incontinence afteran episode of diarrhea on March 3, 2003. The nurses did notwear masks or gowns during their routine nursing care of anypatients on the ward. Patient 9 was the nephew of Patient 4and visited him once at Hotel X, once at Hospital B, and oncein the ICU of Hospital C, each time for 10 minutes. At the lastof these visits, Patient 4 was receiving noninvasive positive-pressureventilation. Patient 10 stayed in the same cubicle (with sixbeds) on the same ward of Hospital B as Patient 4 for a totalof five days while recovering uneventfully from a total nephrectomyfor a resectable right renal-cell carcinoma. Another bed separatedthem from one another. There was no social or other contactbetween the two patients, who were both largely bedridden. Apartfrom these contacts, and with the exception of Patient 1, noneof the patients had any known contacts with anyone with respiratoryillness or had traveled to southern China, Vietnam, or Singaporefor at least three months.
Figure 1B shows the temporal relation between contact and theonset of symptoms in the 10 patients. The incubation period,calculated as the number of days between likely exposure andthe onset of symptoms,3 could be precisely determined only forPatients 2, 3, 4, and 5 (two, two, six, and two days, respectively),since the other patients had multiple contacts with the sourcepatients. The ranges of possible incubation periods were 1 to6, 5 to 11, 5 to 11, 1 to 5, and 2 to 7 days for Patients 6,7, 8, 9, and 10, respectively.
Clinical and Other Features
All 10 patients presented with fever (temperature, >38°Cfor more than 24 hours), and all but 1 also had rigor (Table 1).There was a median interval of five days (range, three toseven) from the onset of fever to the occurrence of dyspnea.All patients remained febrile until the initiation of empiricaltreatment with corticosteroids and ribavirin. Over half thepatients also reported a nonproductive cough, dyspnea, malaise,and headache on presentation. On physical examination of thechest, crackles and dullness on percussion were detected inmost patients. The results of cardiovascular, abdominal, andneurologic examination were normal in all patients given theirknown preexisting conditions. Mild leukocytosis and leukopeniawere each observed in two patients at initial presentation.Lymphopenia (less than 1500 cells per cubic millimeter) wasobserved in nine patients; clinically significant thrombocytopenia(less than 50,000 platelets per cubic millimeter) was not observed.The aspartate aminotransferase level, alanine aminotransferaselevel, or both were elevated slightly (to less than four timesthe upper limit of the reference range in seven patients); serumcreatinine levels were normal in eight patients. Five patientspresented with hypoxemia, and three (Patients 4, 6, and 8) hadinfrequent diarrhea in the first three days after the onsetof fever. The onset of diarrhea could not be attributed to antibiotictherapy in Patients 6 and 8, since they had not received suchtreatment before its onset.
Microbiologic Assessment
The sputum culture yielded only commensal species (Table 2).Acid-fast staining of all respiratory secretions was negativein each patient. Examination of nasopharyngeal aspirates forrapid viral antigen detection of influenzavirus A and B, parainfluenzavirus1, 2, and 3, respiratory syncytial virus, and adenovirus wasnegative. The serologic titers of C. pneumoniae, C. psittaci,and M. pneumoniae showed no significant increase over a periodof 7 to 10 days in the entire cohort. Urinary antigen detectionfor L. pneumophila and pneumococcus was negative in all cases.At this time, the microbiologic origin of SARS was unknown.
Table 2. Results of Microbiologic Assessment in 10 Patients with SARS.
Radiologic Assessment
All patients except Patient 2 had abnormal chest radiographson presentation. The primary abnormality on the initial chestradiograph was air-space shadowing: ground-glass opacities (inPatients 4, 5, and 10), focal consolidation (in Patients 3 and9), or patchy consolidation (Patients 6, 7, and 8) (Figure 2A).No interstitial pattern was found on the chest radiographs.Opacities were predominantly in the lower lung zones in eightpatients (Patients 2, 3, 5, 6, 7, 8, 9, and 10) and in upperzones in one (Patient 4). None of the patients had pleural effusions.
Figure 2. Chest Radiographs of Patient 6 (Panel A), Showing Patchy Consolidation in the Right Lower Zone (Arrows), and Patient 2 (Panel B), Showing Diffuse Involvement of All Lung Zones in Both Lungs, and a High-Resolution CT Scan of Patient 4 (Panel C), Showing Subpleural Areas of Consolidation and Ground-Glass Opacification with Air Bronchogram (Arrow) Affecting the Posterior Aspects of the Lungs, Particularly the Lower Lobes.
The air-space opacities increased in size, extent, and severityin seven patients (Patients 3, 4, 5, 6, 7, 9, and 10) withinthe first 10 days after admission. The chest radiograph of Patient1 did not show clinically significant changes from presentationto death; a diffuse miliary nodulation was noted throughout.In Patient 2, the chest radiograph remained unremarkable formore than a week, after which diffuse opacification appeared(Figure 2B); a similar course was observed in Patient 5. Amongthe survivors, six patients (Patients 3, 4, 6, 8, 9, and 10)had some improvement of the air-space opacities, with variableresidual reticular opacities, within two weeks after presentation.
Predominant abnormalities found on initial CT scans were subpleuralfocal consolidation with air bronchograms and ground-glass opacities.These occurred mostly, but not exclusively, in the posterioraspects of the lower lobes (Figure 2C). No pleural effusions,mediastinal nodes, or central pulmonary emboli were found.
Treatment and Outcome
All of the patients were treated empirically with corticosteroidsand ribavirin, as noted below. Before this combination was administered,all patients except Patients 7 and 8 received a combinationof a beta-lactam (Augmentin, Rocephin, or Maxipime) and a macrolide(clarithromycin or azithromycin) for a mean (and median) offour days (range, two to six), which had no effect on the overallclinical course, fever, or radiographically evident profusionof disease (Table 2 and Figure 2 and Figure 3). Empirical treatmentconsisted of a combination of intravenous ribavirin (8 mg perkilogram of body weight every eight hours) or oral ribavirin(1.2 g every eight hours, in Patient 4 only) and intravenouscorticosteroids (hydrocortisone at a dose of 4 mg per kilogramevery eight hours tapered to 200 mg every eight hours or methylprednisoloneat a dose of 240 to 320 mg daily) in all patients (Figure 3).There was a mean of 9.6±5.42 days (median, 12.5; range,3 to 22) between the onset of symptoms and treatment with thecombination of corticosteroids and ribavirin. Figure 3 showsthe response in temperature, heart rate, oxygen saturation,and total leukocyte, lymphocyte, and platelet counts after thebeginning of therapy. There was resolution of fever and improvementin heart rate within the first two days of starting treatment.There was also an increasing trend toward improved lymphocyteand platelet counts after eight days of treatment.
Figure 3. Response to Treatment with an Intravenous Corticosteroid and Ribavirin for the 10 Patients with SARS.
In Patients 1 and 2 there was a steady deterioration in gasexchange despite an increase in ventilatory support from noninvasivesupport to intubation and mechanical pressure-controlled ventilationwith high positive end-expiratory pressures and a fraction ofinspired oxygen of 1.0. Despite intensive physiological support,both patients died. Postmortem examination of the lungs of Patient1 revealed marked alveolar edema with foci of hemorrhage andhyaline membrane formation. There was desquamation of pneumocytes,but there were few free inflammatory cells, either polymorphonuclearor mononuclear cells in the alveolar spaces. There were scatteredfoci of alveolar myxoid fibroblastic tissue, a finding consistentwith the early organization phase of progressive pneumonia.Interalveolar septa were mildly thickened, with a mild mononuclearinfiltrate. There was no tissue necrosis, viral inclusions,fungi, or bacteria on the sections. These features were consideredto reflect severe diffuse alveolar damage. Patient 2 underwenta biopsy by video-assisted thoracoscopy on day 5 that showedonly mild diffuse alveolar damage.
From the onset of disease to the time of this writing, onlyPatient 3 has had a complete clinical recovery (no supplementaryoxygen as of day 12) and radiographic recovery (resolution ofright-lower-lobe consolidation on day 18), leading to her dischargeon day 20. This patient has continued to have nonspecific malaise,even on day 26. From the onset of symptoms, Patients 4 through10 have been unwell for 23.1±5.5 days (median, 25.5;range, 18 to 33) and have had a partial radiologic and clinicalrecovery. Only Patients 4, 7, and 9 are still oxygen-dependent;the mean oxygen saturation was 95.1±2.6 percent (median,96; range, 90 to 99) in the eight survivors. Patient 3 recoveredcompletely and had no exercise restriction, whereas Patients4, 7, and 9 were able to walk only three to five steps on thelevel, and Patients 5, 6, 8, and 10 were able to walk on thelevel without apparent restriction, within the confines of theisolation wards. Patients 4, 6, 7, 8, and 9 still reported drycough, which was considered subjectively to be milder than thatexperienced at the onset of disease. None of the surviving patientsreported any of the other symptoms listed in Table 2.
Discussion
Our experience with these 10 epidemiologically linked patientsconfirms that SARS is a contagious and rapidly progressive infectiousdisease that can affect otherwise healthy persons, sometimesafter even trivial contacts. It is not known why some persons(such as the wife of Patient 4, who stayed in the same hotelroom with him throughout) remain asymptomatic despite substantialexposure.
SARS presents predominantly with high fever (temperature, >38°Cfor more than 24 hours) and rigor, followed by dry cough, whichmay in some cases proceed rapidly to respiratory failure, accompaniedby radiographic evidence of air-space disease. The incubationperiod in our patients was between 1 and 11 days, and in mostof our clear-cut cases, the patients presented 2 days afterexposure. Our experience therefore singles out at-risk exposure(however trivial) to source patients and fever as the most importantpointers to the diagnosis of SARS. Indeed, the finding thatmany people whose condition meets the CDC case definition2 ofSARS do not have respiratory failure.4 Although there was noclinical response to combined therapy with a beta-lactam anda macrolide, empirical treatment with a combination of a high-dosecorticosteroid and ribavirin coincided with clinical improvement.Most patients appeared to have clinical and radiographic improvement,although the full time course of the illness is not known. Itis also of note that the two patients who died did not havemultiorgan failure, as is often the case with patients withthe acute respiratory distress syndrome.
The primary radiologic appearance of SARS is air-space shadowingdetermined on CT to be subpleural focal consolidation with airbronchograms and ground-glass opacities predominantly affectingthe lower lobes. The initial radiographic appearance, however,may be normal. Air-space opacification progresses within a fewdays of presentation, increasing in size, extent, and severity.In some cases, there is further progression to diffuse opacificationsuggestive of the acute respiratory distress syndrome. Resolutionof air-space shadowing occurs with features suggesting thatthe disease is entering a fibrotic phase. Radiographically,SARS may be indistinguishable from bacterial bronchopneumoniaor viral infections, and more important, it shares CT featureswith other conditions that result in subpleural air-space disease,such as bronchiolitis obliterans with organizing pneumonia andacute interstitial pneumonia.5,6,7 In the later stages, particularlywith diffuse involvement of the lungs, the radiographic appearanceis similar to that of the acute respiratory distress syndrome.
The clinical and radiographic features of the disease in ourpatients and, in particular, its highly contagious nature stronglypoint to a viral cause of SARS. Most patients with SARS hadthe onset of symptoms two to five days after exposure to therespective source patients. Such a short incubation period arguesagainst infection with M. pneumoniae or C. pneumoniae. For M.pneumoniae, the reported incubation period ranges from 6 to32 days, with a median of 14 days.3 The incubation period forC. pneumoniae is unclear but appears to be long, with estimatesranging from 10 to 30 days.8L. pneumophila is not known tobe transmitted from human to human and is thus most unlikelyto be the causative agent. Our microbiologic tests also showedno evidence of infection by these agents. Research to identifypotential viral infective agents in SARS is ongoing.
Given the information we present on case transmission, it isimportant to take appropriate isolation precautions with patientssuspected to have SARS. Information on current recommendationscan be found at http://www.who.int/csr/sars/guidelines and http://www.cdc.gov/ncidod/sars/ic.htm.Because the disease has appeared in many health care workers,they should have a high index of suspicion when fever and featuressuggestive of SARS develop in them or their family members.In such cases, we believe that health care workers should presentthemselves for evaluation, to avoid putting others at risk.When the microbiology of SARS is more fully understood, bettermethods of case identification should follow.
We are indebted to Ms. Christina Yan, June Sun, and ChristineSo for technical assistance and to all the medical and nursingstaff members who assisted in the care of these patients.
Source Information
From the University Departments of Medicine (K.W.T., M.C.-Y., W.K.L., P.C.W., B.L., M.S.I., J.C., K.N.L.), Clinical Microbiology (P.L.H., T.W., W.H.S., K.Y.Y.), and Diagnostic Radiology (G.C.O.), University of Hong Kong; the Department of Medicine, Kwong Wah Hospital (W.K.Y.); and the Department of Medicine, Pamela Youde Nethersole Eastern Hospital (L.Y.Y., T.M.C.) — all in Hong Kong, China. This article was published at www.nejm.org on March 31, 2003.
Address reprint requests to Dr. Lai at the University Department of Medicine, University of Hong Kong, Queen Mary Hospital, Pokfulam, Hong Kong, China.
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medium), and mycobacteria (with LJ medium). Gram-stained and auramine-rhodamine–stained smears were examined to search for bacterial or acid-fast morphotypes. 
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