Continuing on with our series of vaccine-preventable disease, this week I was honoured to get an E-mail interview with Emeritus Professor Christopher Burrell. Chris has a CV longer than my arm: Officer of the Order of Australia, Head of the Infectious Disesase Laboratories at the IMVS, Professor of Virology at the University of Adelaide, co-founder and musical director of the Coriole Music Festival… the list goes on and on. As my own personal connection, he was the PhD supervisor of my PhD supervisor, Associate Professor Allison Jilbert.
He was also one of the members of the team that investigated the 1969-70 hepatitis outbreak in Edinburgh at the Royal Infirmary and Western General Hospital. The outbreak coincided with the opening of a new unit, the Maintenance Hemodialysis Unit. Forty-four people came down with illness during the outbreak. Seven health care workers and four patients died from liver failure. It later gained noteriety in the general press and public with much damning of the hospital staff.
The following is a transcript of my E-mail interview with Chris Burrell:
TT: I’d like to start off with how you got to be working in Edinburgh in the first place.
CB: I finished my PhD on Polio and Semliki Forest virus, and then took a job as lecturer at University of Edinburgh. They had just had a terrible outbreak of hepatitis B in the dialysis unit, and wanted another virologist to research hepatitis B, so I changed to this field when I started in Edinburgh.
TT: What was the clinic like when you were there before the outbreak? Was it a high-tech hospital? How did it compare to others of the time?
CB: They had recently opened a new unit and it was pretty high standard. However, hepatitis B virus had only just been recognised, tests were primitive and very insensitive. Little was known about its epidemiology and transmission – in fact, a lot about transmission in hospital, and how to prevent it, was worked out by studying the Edinburgh outbreak.
TT: How and when did you find out you had an outbreak in the unit?
CB: There were clusters of cases of acute hepatitis in patients and staff, that tested positive for the Australia antigen [Ed: Hepatitis B surface antigen, a marker for the presence of hepatitis B virus in the blood] which had only just been discovered. The true extent of carriage and subclinical infection was only worked out over the next two years using better tests. The mortality was 24% in patients and 31% in staff.
TT: What was the carriage rate in patients and staff? Was it much higher than other hospitals at the time?
CB: Around 40% of the patients had anti-HBs [Ed: The protective antibodies to hepatitis B virus] prior to the outbreak, possibly passive antibody from blood transfusions as well as prior infection. This did not appear to protect. 58% of the patients became infected with HBV during the outbreak. In general, US and European units had a worse problem and there was a feeling amongst them that nothing could be done about it. The management of the Edinburgh outbreak demonstrated that with proper segregation and infection control measures, the infection could be stopped.
TT: What was the feeling amongst the staff and patients at the time when the news of the outbreak was known?
CB: The unit was closed to new patients and there was quite a sense of fear amongst clinical and lab staff, especially after some of them died. Any blood samples “from the outbreak” were kept in secure bags and not opened except under primitive PC3 conditions (PC3 containment in labs had not been conceived of then). The newspapers in the city gave it a lot of publicity, criticism of the hospital and general scaremongering. There was one carrier patient whose blood probably caused 3-4 deaths, and her identity got out and people would not ride on the same bus with her. There is a book “The Houseman’s Tale” written by a doctor in the hospital at the time, with the backdrop of the outbreak and all the fear and gossip.
TT: You mentioned that we learnt about the transmission of hepatitis B during this outbreak. Did you find the cause behind this outbreak?
CB: It was probably introduced by unscreened blood (as happened often). Transmission by the blood route was not understood so all sorts of simple parenteral contact [Ed: transfer of bodily fluids through needles] would have happened. Many of these routes were worked out during this and other outbreaks; for example, a splash of blood in the eye, needlestick injury, blood-contaminated cards and lab equipment. There was a special route that contributed in Edinburgh via blood-contaminated venous monitors in the dialysis machines. Infection was endemic in probably nearly all units at the time. The Edinburgh one was studied intensively because of the high mortality.
TT: Finally, we don’t hear much about hepatitis B outbreaks now; what has changed in hospitals/dialysis units or society in general to stop them?
CB: The problem was greatly contained by use of screened blood, proper cross-infection policies, regular testing and segregation of infected and uninfected patients. Thus it was perfectly possible to keep a unit HBV-free if this was done properly. Then when the vaccine became available, it of course became easier as this provided extra backup.
Review of the outbreak available at:
Marmion BP, Burrell CJ, Tonkin RW, & Dickson J (1982). Dialysis-associated hepatitis in Edinburgh; 1969-1978. Reviews of infectious diseases, 4 (3), 619-37 PMID: 6812192