Blood transfusion poses CJD risk
Two studies in this week’s issue of THE LANCET highlight the public-health implications of blood transfusion as a possible route for infection by the prion protein responsible for variant Creutzfeldt-Jakob disease (vCJD).
The death from vCJD of an individual in the UK who had previously received a blood transfusion from a donor who went on to have vCJD was announced on December 17, 2003. Robert Will from the National CJD Surveillance Unit, Edinburgh, UK and colleagues outline the process which links individuals from the UK CJD register with data from the national blood-donor database to identify the number of blood donors who went on to develop vCJD and to compare vCJD incidence between donors and recipients. 48 individuals were identified as having received a blood component from 15 donors who later became vCJD cases. One of these recipients (the case whose death was reported last December) developed symptoms of vCJD 6.5 years after receiving a transfusion of red cells donated by an individual 3.5 years before the donor developed symptoms of vCJD.
Robert Will comments: “Our findings raise the possibility that this infection was transfusion transmitted. Infection in the recipient could have been due to past dietary exposure to the BSE agent. However, the age of the patient was well beyond that of most vCJD cases, and the chance of observing a case of vCJD in a recipient in the absence of transfusion transmitted infection is about 1 in 15 000 to 1 in 30 000.”
A second study in this week’s issue compared the degree of tissue infectivity (using the misfolded prion protein as a marker) among macaques (monkeys native to south and southeast Asia) who were given tissue containing the BSE agent orally or intravenously. Corinne Lasmézas and colleagues from the Department of Medical Research of the French Atomic Energy Commission found that the degree of organ infectivity was similar regardless of the route of entry of the prion protein. Tonsil tissue was the most strongly infected; the authors conclude that ‘in view of the high efficiency of transmission of the BSE agent to primates by the intravenous route, the latter should be regarded as a likely route of contamination for vCJD patients with a medical history involving a transfusion during the period at risk. To avoid further contamination to human beings from peripheral tissues, the same precautionary measures taken for primary vCJD cases should apply to possible transfusion cases of the disease.’
In an accompanying Commentary (p 411) Adriano Aguzzi and Markus Glatzel from the University Hospital of Zurich, Switzerland, state: “Shocking as it may be, the finding that vCJD can be transmitted via blood transfusion is not surprising. Stringent studies in sheep show that prion diseases can be transmitted via blood, even if blood is collected in preclinical stages of prion disease. By December, 2003, 153 cases of vCJD were reported worldwide. Although the epidemic may have peaked in the UK, the probable existence of subclinical vCJD carriers raises concerns of an iatrogenic human-to-human wave of vCJD transmission.”
They conclude: “Public-health authorities are faced with considerable insecurity about the prevalence of subclinical prion carriers, and any human-to-human transmission will complicate estimation of the size of the vCJD epidemic. Although cross-sectional studies to assess the prevalence of prion carriers pose organisational and ethical problems, there is no alternative for assessing the future of the vCJD epidemic.”
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