Infection control of pandemic (H1N1) 2009 influenza in hospitals — a logistic challenge

Abstract

Clinical record On 1 June 2009, a 79-year-old man presented to the emergency department of a tertiary hospital in Melbourne with a 1-week history of dyspnoea and a productive cough. He had underlying chronic obstructive airways disease (COAD) and type 2 diabetes mellitus. He reported no history of fever and no recent travel or contact with people with influenza-like illness (ILI). On examination, his temperature was 37.0°C, oxygen saturation was 97% in room air, and he had an expiratory wheeze. No abnormalities were seen on chest x-ray. Full blood examination showed a peripheral white cell count within the reference range (RR), and a raised C-reactive protein level (27 mg/L; RR, < 5 mg/L). The patient was admitted to a four-bed hospital ward and treated with oral doxycycline, corticosteroids and nebulised salbutamol. A nasal swab was sent to the state reference laboratory for polymerase chain reaction (PCR) testing for respiratory viruses to identify any potential viral precipitant for the apparent exacerbation of COAD. Results received 2 days later were positive for influenza A virus, which was confirmed to be the pandemic (H1 N1 ) 2009 strain. Treatment was then begun with oseltamivir, and the patient was placed in a single room with droplet precautions. The patient's contacts within the hospital were traced through review of his bed movements and all staff rosters (medical, nursing, allied health, patient support services and clerical staff of the emergency department and wards). All health care workers who had come into contact with the patient were telephoned, and the extent of their contact and individual risk factors were assessed. High-risk contact was defined as having spent more than 15 minutes within 1 m of the patient without wearing appropriate personal protective equipment. Twenty-one people with high-risk contact were identified, comprising nine medical staff, six nurses, three allied health staff and three patients. All were given oseltamivir prophylaxis. By this time (2 days after the patient's admission), three of the medical staff who had high-risk contact with the patient (eg, taking a history or examining the patient while he was receiving nebulised therapy) reported the new onset of an ILI. They were therefore given treatment doses of oseltamivir. Furthermore, one of these medical staff reported having had significant contact, while symptomatic, with nine medical registrars during a 1-hour radiology tutorial in a confined space. At that stage of the pandemic, the reference laboratory was testing a high volume of specimens for H1 N1 2009 influenza, and the average time for results of specific tests to be returned was, in our experience, 2 working days. Consequently, we decided to assume that the three medical staff with ILI had pandemic 2009 influenza and to initiate a second round of contact tracing. This included contacting all patients and health care workers who had come into contact with any of these staff. We identified a further 17 medical staff and seven patients and offered them oseltamivir prophylaxis. All accepted this prophylaxis. Symptomatic staff were asked to stay home from work, but it was considered impractical to redeploy asymptomatic health care workers receiving prophylaxis to areas with less patient contact. The evaluation of exposed health care workers and dispensing of medication were conducted by infection control practitioners, infectious diseases staff and microbiology staff, in addition to their normal duties. The extra workload was estimated to be almost 2 full days for at least two staff members. Four days later, the swab results from the three symptomatic medical staff showed they were negative for influenza A, and prophylaxis for their contacts was ceased. None of the other 18 people who had significant contact with the index patient developed ILI.