A 16-year-old adolescent was admitted to Princess Margaret Hospital, Hong Kong with high swinging fever up to 39.9 C for 5 days. He developed profuse diarrhoea with passage of greenish, watery, loose stools 1 day before admission. He also complained of dry cough, myalgia and general malaise. There was no running nose, chills, rigor, headache or shortness of breath. He resided in a housing estate (Amoy Garden) where a massive outbreak of SARS had occurred. There was no travel history or history of contact with SARS patients. General examination showed a febrile lethargic child with mild dehydration (ca. 5%). Examination of the abdomen showed mild epigastric tenderness but no organomegaly and bowel sounds were normal. There was no respiratory distress. Examination of the other systems was unremarkable. A chest X-ray film revealed right upper zone infiltrates (Fig. 1a). He was administered intravenous cefotaxime and oral clarithromycin to cover the usual organisms associated with community acquired pneumonia. Isolation in a negative pressure room was instituted in view of the epidemiological link to a SARS outbreak.
His fever persisted after admission and a maximum temperature of 40 C was recorded on day 6 from onset of illness. He refused oral intake as he vomited after every meal. A pulse-temperature deficit resembling that of typhoid fever was noted on the observation chart (Fig. 2). On day 6 from onset of fever, intravenous ceftriaxone, the empiric treatment of choice for typhoid fever in our locality, was administered in place of cefotaxime. Ribavirin was commenced for suspected SARS in view of the lack of clinical response to the initial antibiotic regimen. His general condition did not improve and he continued to run a high swinging fever with malaise, epigastric pain, and persistent vomiting and diarrhoea. On day 8, intravenous hydrocortisone was instituted because of radiographic progression of the right upper lobe consolidation (Fig. 1b).
Fever subsided 1 day after the initiation of hydrocortisone therapy and his general condition as well as the gastrointestinal symptoms improved rapidly. Radiological resolution was more gradual. Steroids were continued in the form of oral prednisolone after 4 days of intravenous hydrocortisone therapy and tailed off over 10 days. Ribavirin was given for a total of 10 days. Ceftriaxone and clarithromycin were discontinued after 7 days. He was kept under isolation and discharged on day 21 after onset of fever.
The initial total white cell count was 4.4x109/l (reference range 4.0-10.0x109/l) with absolute neutrophil and lymphocyte counts of 3.2x109/l (reference range 2.0-7.0x109/l) and 0.9x109/l (reference range 1.0-3.0x109/l) respectively. The lowest lymphocyte count was 0.6x109/l which occurred on day 13. The initial platelet count was 132x109/l (reference range 150-600x109/l). Reactive thrombocytosis up to 635x109/l was noted on day 21. Haemoglobin level and the clotting profile were normal. C-reactive protein, erythrocyte sedimentation rate, creatine kinase and lactate dehydrogenase levels were not elevated. Alanine aminotransferase level was elevated to 472 IU/l (reference range 1-40 IU/l) on day 13. Total bilirubin was elevated up to 37 micromol/l (reference range 4-20 micromol/l) on day 15.
No bacteria were recovered from stool and blood cultures. Widal serology was negative. Viral culture and reverse transcriptase polymerase chain reaction (RT-PCR) assay targeting severe acute respiratory syndrome-associated coronavirus (SARS-CoV) were performed on nasopharyngeal aspirates, stool and urine samples. RT-PCR was positive in nasopharyngeal aspirates collected on days 5 and 12. RT-PCR was also positive in stool samples collected on days 8, 15, 19, 21 and 22. Viral culture was negative. Cold agglutinin titre was not raised and anti-mycoplasma IgM was negative. Paired acute and convalescent serum samples showed a rise in SARS-CoV titre (<25 on day 2, 25 on day 32, and 400 on day 118). No increase in antibody titres to influenza A and B, parainfluenza virus types 1, 2 and 3, adenovirus, respiratory syncytial virus,  Mycoplasma pneumoniae and  Chlamydia pneumoniae were demonstrated in convalescent serum samples.