To the Editor: We read with interest the case report by Wong et al. (
). Three similar cases of serologically confirmed severe acute respiratory syndrome
(SARS) were treated in our hospital; all of the patients recovered uneventfully without
specific treatment. They had either negative results on polymerase chain reaction
(PCR) tests for SARS-associated coronavirus (SAR-CoV), or they were admitted when
such rapid diagnostic tests were not yet available; hence, SARS-specific treatment
was not prescribed.
The first patient was a 35-year-old, previously healthy female tourist from Guangzhou,
China, who was admitted to our hospital in late February 2003. She had visited several
family members who had atypical pneumonia; some eventually died from the disease.
The patient had fever, chills, and dry cough approximately l week after exposure but
experienced no mylagia, diarrhea, or shortness of breath. On physical examination,
scanty crepitations were heard in her right lower chest, and chest radiographs showed
right lower zone consolidation. Blood tests showed a slightly low platelet count of
119 x 109/L and mildly elevated alanine transaminase at 59 U/L (normal <55 U/L), but
total and differential leukocyte counts were normal. Tests for etiologic agents included
blood and sputum bacterial cultures; sputum for acid-fast bacilli; and nasopharyngeal
aspirates for influenza, parainfluenza, adenovirus, and respiratory syncytical virus.
Serologic titers for Mycoplasma, Chlamydia psittaci, and Legionella were negative.
Reverse transcription (RT)-PCR tests for SARS-CoV were not available at that time.
Oral clarithromycin and intravenous amoxillin-clavulanate (subsequntly switched to
levofloxacin) were prescribed. Her high fever (temperature 39.5°C) lasted for 4 days
and then gradually subsided; the radiologic abnormality also improved progressively
after the first week. Oxygen supplementation of 2 L/min was necessary for the first
2 days. The diagnosis of SARS was made when the patient's convalescent-phase serum
sample, collected 33 days after discharge (day 45 of illness), showed an elevated
anti-SARS immunoglobulin (Ig) G titer of 1:800 by immunofluorescence.
The second patient was a 34-year-old, previously healthy man; his father had shared
a hospital cubicle with a patient who was subsequently diagnosed with SARS. Fever
(temperature 39°C), chills, and rigors developed in patient 2 on December 3, 2003,
approximately 4 days after his first hospital visit to his father; he had no cough
or gastrointestinal symptoms. Chest radiographs showed right lower zone consolidation.
Blood tests showed low platelet count of 91 x 109/L, elevated creatinine kinase (370
U/L), and elevated lactate dehydrogenase levels (1,060 U/L). Total and differential
leukocyte counts were normal. Tests for etiologic agents of pneumonia had negative
results. His fever (the highest temperature was 39.5°C) subsided after day 2 of admission,
with a transient spike on day 11 that coincided with a slight increase in right lower
zone consolidation. Both abnormalities subsequently resolved promptly, and no oxygen
supplement was necessary. RT-PCR test for SARS-CoV was not available in our hospital
when he was admitted. However, SARS was diagnosed when his convalescent-phase serum,
collected on day 21 of illness, demonstrated a SARS-CoV IgG titer (by immunofluorescence)
of 1:3,200, from an initial baseline of <1:25, taken on day 12 of his illness. No
treatment was given, since the patient had already fully recovered when the results
The last patient was a 74-year-old, previously healthy man, who had visited a sick
relative; the relative was later diagnosed with SARS. Fever, chills, and cough developed
in our patient 4 days later. Chest radiograph showed left lower and middle zone consolidations.
Intravenous ceftriaxone and oral clarithromycin were started. Blood tests showed elevated
alkaline phosphatase of 226 U/L and alanine transaminase of 126 U/L. His initial leukocyte
count was 18.8 x 109/L with neutrophilia (16 x 109/L, 85.2%) and a normal lymphocyte
count of 1.2 x 109/L; platelet count was normal. No causative agent was identified,
including by RT-PCR test for SARS-CoV. His fever had subsided upon admission, and
serial chest radiographs, liver function, and leukocyte counts showed progressive
improvement without specific treatment. The diagnosis of SARS was made from two elevated
SARS-CoV IgG levels of both 1:3,200 (by immunofluorescence), taken at days 5 and 24
after his admission (days 19 and 38 of illness).
Although SARS was diagnosed in these three patients retrospectively, and they were
not treated with antiviral agents, they were managed in isolation wards. Patients
reported adhering to droplet precautions after discharge (mainly, wearing surgical
face masks when in close contact with others), and none was believed to have transmitted
the virus to others.
SARS can be associated with a substantial death rate (
). Ribavirin and systemic corticosteroids were used in our hospital during the SARS
epidemic. However, the efficacy of this regimen has not been proven, and concerns
exist about side effects of both drugs (
). Some retrospective analyses suggested using lopinavir/ritonavir and integrative
Chinese and Western medicine were associated with improved outcomes (
). In vitro (
) and animal (
) studies have suggested that interferon and monoclonal antibodies might have some
effects on the disease. However, data from randomized controlled trials are lacking.
All of our patients had been previously healthy, with no coexisting conditions identified
as poor prognostic risk factors (
). These three cases, together with the case of Wong et al. (
), suggested that at least a subset of SARS adult patients can have a relatively benign
clinical course and uneventful recovery, without any specific treatment other than