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Letter
Severe Acute Respiratory Syndrome:
Relapse? Hospital Infection?
Owen Tak-Yin Tsang,* Tai-Nin Chau,* Kin-Wing Choi,* Eugene Yuk-Keung
Tso,* Wilina Lim,† Ming-Chi Chiu,* Wing-Lok Tong,* Po-Oi Lee,* Bosco Hoi
Shiu Lam,* Tak-Keung Ng,* Jak-Yiu Lai,* Wai-Cho Yu,* and Sik-To Lai*
*Princess Margaret Hospital, Hong Kong; and †Public Health Laboratory
Centre, Hong Kong
Suggested citation for this article: Tsang OT-Y,
Chau T-N, Choi K-W, Tso EY-K, Lim W, Chiu M-C, et al. Severe acute respiratory
syndrome: relapse? Hospital infection? Emerg Infect Dis [serial online]
2003 Sep [date cited]. Available from: URL: http://www.cdc.gov/ncidod/EID/vol9no9/03-0395.htm
To the Editor: Severe acute respiratory syndrome (SARS) is an
emerging infectious disease worldwide, and relapsing SARS is a major concern.
We encountered a 60-year-old woman who was admitted to the Princess Margaret
Hospital in Hong Kong on March 29, 2003, with a fever of 39°C, chills,
cough, malaise, and sore throat for 2 days before admission. She had no
history of travel within 2 weeks of admission. She also had no close contact
with patients who had a diagnosis of suspected or confirmed SARS. Chest
radiograph on admission indicated consolidation over the right middle
zone. In accordance with the diagnostic criteria proposed by the World
Health Organization (WHO), this patient’s condition was diagnosed as SARS
in view of her symptoms, temperature, and chest radiograph findings (1).
Standard microbiologic investigations to exclude common respiratory virus
and bacterium for community-acquired pneumonia, including Mycobacterium
tuberculosis, were negative in our patient. Reverse transcriptase–polymerase
chain reaction (RT-PCR) of nasopharyngeal aspirate samples was negative
for coronavirus twice. The coronavirus antibody titer was less than 1/25.
The patient was initially treated with oral clarithromycin (500 mg twice
a day) and intravenous amoxycillin-clavulanate combination (1.2 g three
times a day). Despite the negative evidence for coronavirus infection,
she was treated with intravenous ribavirin (24 mg/kg once a day) and hydrocortisone
(10 mg/kg once a day) after 48 hours of antibiotics therapy (2).
The patient’s symptoms were relieved, and she remained afebrile 3 days
after admission. Tolerance for medication was good except for a moderate
degree of hemolytic anemia (her hemoglobin level dropped to 9.1 g/dL)
and hypokalemia that developed during treatment. On day 15, the chest
radiography was clear. The patient was discharged after 3 weeks of hospital
stay.
The patient attended outpatient clinic on day 35, complaining of exertional
dyspnea, low-grade fever, and malaise since her discharge. Her chest radiography
showed extensive shadowing. Computer tomographic scan of the thorax indicated
widespread ground-glass shadowing in both lung fields, which was especially
prominent at left lower and lingular lobes. Her hemoglobin level had dropped
further to 8.4 g/dL. Sputum culture yielded substantial growth of methicillin-sensitive
Staphylococcus aureus and Pseudomonas aeruginosa. RT-PCR
results of throat and nasal swabs were positive twice for coronavirus,
but coronavirus cultures from these areas were negative. One month after
onset, her coronavirus antibody titer was 200. In view of possible relapse
of SARS, she was treated with oral ribavirin (1,200 mg/day) and lopinavir
(133.3 mg/day)/ritonavir (33.3 mg) combination (3 capsules twice a day)
in addition to intravenous piperacillin/tazobactam combination. The patient
was afebrile, and symptoms improved 3 days after admission. Serial chest
radiograph showed gradual resolution of shadowing. Subsequent RT-PCR and
sputum culture were negative.
This case illustrates several important issues regarding problems of
infection control, diagnosis, and management of SARS. As the definition
of SARS is nonspecific, patients with upper respiratory infection or community-acquired
pneumonia could be mislabeled as having SARS. Accommodating confirmed
SARS patients and patients mislabeled as having SARS in the same facility
may be disastrous. Unfortunately, isolating every single case is impossible,
particularly when a large number of patients are admitted. Our patient
may have acquired the disease after admission since she was placed in
the same ward with other patients confirmed to have SARS. For this reason,
special cohorting of SARS patients with closely related signs and symptoms
should be strictly implemented at admission. Since fever is the most common
feature of SARS, isolating febrile cases with respiratory or gastrointestinal
symptoms may be appropriate. Even patients with fever alone should be
quarantined since the other symptoms of SARS may not be clinically obvious.
Secondly, the sensitivity of diagnosing a coronavirus infection on admission
is only 32% to 50% by nasopharyngeal RT-PCR test (3,4).
Many infected cases will be missed as a result. Our patient may have had
a relapse of disease during her second admission, although she had positive
RT-PCR and antibody surge only 1 month after onset. However, we could
not conclude whether the first RT-PCR on admission was a false negative
or whether the patient acquired coronavirus infection in the hospital.
Our study showed that sensitivity for diagnosing coronavirus infection
could be increased by performing RT-PCR on samples from different parts
of the body (4). Unfortunately, these samples were not
taken from our patient. Furthermore, the chest infection with organisms
recovered from her sputum could be the sole reason for her second admission,
especially when her immune system was weakened by the administration of
a high-dose steroid. The presence of genetic material for coronavirus
from her nasal cavity and throat might not suggest that the virus is active.
The absence of coronavirus growth in this patient might indicate that
the virus is no longer viable, although the culture technique itself might
not be sensitive enough to justify this claim. Therefore, further refinement
of the diagnostic techniques for SARS is essential, especially for diagnosis
during early onset. Thirdly, giving treatment to a patient without a legitimate
diagnosis may be inappropriate, especially when the treatment carries
substantial adverse effects, as illustrated in our patient, and a universally
accepted therapy has not been available. Whether lopinavir/ritonavir combination
is the key to a cure remains to be clarified, despite the satisfactory
response that we observed, since the clinical and radiologic improvement
in our patient might be the natural course of the disease.
References
- World Health Organization. Case definitions for surveillance
of severe acute respiratory syndrome (SARS). [Accessed May 1, 2003].
Available from: URL: http://www.who.int/csr/sars/casedefinition/en/
- Hospital authority information on management of SARS. [Accessed April
10, 2003]. Available from: URL: http://www.ha.org.hk/hesd/nsapi/?MIval=ha_view_content&c_id=122711&lang=E
- Peiris JSM, Lai ST, Poon LLM, Guan Y, Yam LYC, Lim W, et al. Coronavirus
as a possible cause of severe acute respiratory syndrome. Lancet
2003;361:1319–25.
- Peiris JSM, Chu CM, Cheng VCC, Chan KS, Hung IFN, Poon LLM, et al.
Clinical
progression and viral load in a community outbreak of coronavirus-associated
SARS pneumonia: a prospective study. Lancet 2003;361:1767–72.
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