Viral load and outcome in SARS infection: the role of personal protective equipment in the emergency department

Abstract

This study was conducted to evaluate the effectiveness of personal protective equipment (PPE) against severe acute respiratory syndrome (SARS). Sixteen patients in a SARS cluster, including 4 health care workers (HCWs) and 12 non-HCWs were studied. We compared the initial viral load by nasopharyngeal swabs, clinical progression, and outcome of this cluster. The HCWs had a lower viral load. The non-HCWs had a higher mean C-reactive protein, lower oxygen saturation, and a higher incidence of intubation and death. Secondary household transmission developed in three of the non-HCWs' families. One month after discharge, non-HCWs had more signs of fibrosis on high resolution computed tomography (HRCT) scan and an impaired pulmonary function test. Although most of the PPE do not confer absolute protection against SARS, it seems that they may lower exposure to the virus, leading to a lower risk of secondary transmission, and be associated with relatively mild disease and a better early outcome.

Figure 1

Transmission of 16 cases of definite SARS in a case cluster. A nosocomial outbreak occurred on May 4–5, 2003, in the Emergency Department (ED) of Mackay Memorial Hospital, Taipei, Taiwan. Patient 1, who was not part of the ED cluster, had had dinner with the index patient on May 1, 2003, and developed a fever on May 10. His wife, patient 2, became febrile on May 20. Patient 3 was seen in the ED on May 4 with acute gastroenteritis and was accompanied by her mother, patient 4. Both subsequently developed fevers on May 10 and May 9, respectively, and were found to have SARS. Patient 5 was seen in the ED on May 4 for a renal stone, accompanied by his wife, patient 6. He developed a fever on May 9, his wife on May 12, and their daughter, patient 7, on May 15. Patient 8 was in the ED on May 4 accompanying an ill family member and developed fever on May 10. Patient 9 was in the ED with a leg wound on May 4 and developed a fever May 8. Patients 10, 11, 12, and 13 were ED staff (one doctor and three nurses) who took care of or were working near the index patient May 4 and early May 5. Patient 10 (an ED doctor) did not know he’d been exposed to SARS and developed a fever on May 9 while traveling in Japan. Patients 12 and 13 assisted during the intubation of the index patient early on May 5. Their fevers began May 9 and May 10. Patient 14 was seen in the ED on May 4 for pelvic inflammatory disease and developed a fever on May 12. Her husband, patient 15, became febrile May 23. Patient 16 was seen in the ED with upper gastrointestinal symptoms May 4 and became febrile May 9. Health care workers (HCWs) wore personal protective equipment, including N-95 masks, while working. Non-HCWs infected in the ED had been wearing only surgical or cloth masks. Three of the non-HCWs transmitted the infection to secondary household contacts. Four of the non-HCWs had respiratory failure, 3 of whom died. AGE = acute gastroenteritis; CHD = coronary heart disease; COPD = chronic obstructive pulmonary disease; CRI = chronic renal insufficiency; PID = pelvic inflammatory disease.

Figure 2

Typical HRCT scans through the middle lungs zones of SARS patients at 1 month after discharge. (A) No evidence of residual interstitial disease in Patient 11 (score = 0). (B) Mild disease (score = 1) in Patient 9. Note subtle ground-glass opacification at both superior segments of lower lobes. (C) Moderate disease (score = 2) in Patient 6. Note diffuse ground-glass opacification, thickening of interlobular septa, and mild traction bronchiectasis. (D) Severe disease (score = 3) in Patient 3. Note diffuse ground-glass opacification with coarse reticulation and consolidation, peribronchovascular thickening, and traction bronchiectasis with slight architectural distortion.

Figure 3

N-95 mask and personal protective equipment. During the SARS epidemic, the HCWs had been required to, and were wearing PPE, including an N-95 mask, gloves, gown, and head covering when working in the ED.

Figure 4

The un-normalized viral load of HCW and non-HCW by quantitative PCR showing HCW with an average of 24.36 ± 15.84 copies of RNA/mL and non-HCW with 4346 ± 3284 copies of RNA/mL (p < 0.0001).

Figure 5

The extent of mucosal shedding was significantly greater in non-HCWs (p < 0.001) as indicated by the greater amount of 18s-rRNA in the nasopharyngeal swabs.

Figure 6

Column statistics of HCW and non-HCW with normalized quantitative PCR showing HCW with an average of 463.8 ± 450.2 copies of RNA/mL and non-HCW with 9349 ± 7687 copies of RNA/mL.