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We read with interest the paper by Lim et al.1 The authors interestingly showed the importance of tonometer head wiping in reducing corneal epithelial cell count and the significance of damaged prism surfaces in trapping debris. They hypothesised the possible risk of variant Creutzfeld-Jakob disease (vCJD) transmission from cornea epithelial cells present on the tonometer surface. The question is really one of what constitutes the infectious dose of vCJD for this mode of transmission, and this is currently unknown.
There has been one definite, one probable, and two possible cases of CJD through corneal transplantation but one can hardly compare the prion load in a full thickness corneal graft with a mean epithelial cell count of 9/10 (after wiping or wipe/Milton). Two of the four cases of transmission had had multiple graft procedures.
The evidence from animal studies on CJD infected corneal transmission is also variable. Herzberg transplanted CJD infected corneas onto two Capuchin monkeys; both remained disease free for up to 4 years.2 Manuelidis et al showed transmission of CJD when infected corneas were placed directly into the anterior chamber of uninfected guinea pigs3 but did not show transmission of CJD after penetrating keratoplasty. Tateishi injected emulsified CJD infected cornea into the brains of six mice and only one developed characteristic changes after 2.8 years.4
These studies certainly suggest that an intraocular/intracerebral delivery must be needed for transmission but even then, the inocula that produced disease after intracerebral inoculation only irregularly transmit disease after peripheral (intraocular) inoculation.5 In addition, host genetic factors (homozygosity at codon 129) will also determine the risk of susceptibility.6 There is also convincing evidence that the agent strain and host genotype will determine whether ocular involvement even occurs in experimental rodent models of scrapie.7
More recently, western blot analysis on eyes of patients that had been infected with sporadic CJD and vCJD8 confirmed earlier results (also in human eyes) that PrPSc could only be detected in the retina and not in cornea or sclera. From the evidence, the risk of transmission from tonometry would suggest this to be more theoretical than practical, and may be reduced further—as the authors suggest—by adequate wiping or regular replacement of tonometer prisms. The question of risk can only be truly resolved by transmission studies using primary human diseased eye tissue.
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