Variant CJD and tonometry
http://www.100md.com
《英国眼科学杂志》
The Western Eye Hospital, London, UK
Correspondence to:
Dr J S Mehta
9 Sandringham Court, King & Queen Wharf, Rotherhithe Street, London SE16 5SQ, UK; jodmehta@hotmail.com
Accepted for publication 10 July 2003
Keywords: variant Creutzfeld-Jakob disease; tonometry
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.
References
Lim R, Dhillon B, Kurian KM, et al. Retention of corneal epithelial cells following Goldmann tonometry: implications for CJD risk. Br J Ophthalmol 2003;87:583–6.
Herzberg L. Creutzfeldt-Jakob disease and corneal grafts. Med J Aust 1979;1:248.
Manuelidis EE, Angelo JN, Gorgacz EJ, et al. Experimental Creutzfeldt-Jakob disease transmitted via the eye with infected cornea. N Engl J Med 1977;296:1334–6.
Tateishi J. Transmission of Creutzfeldt-Jakob disease from human blood and urine into mice. Lancet 1985;2:1074.
Brown P, Gibbs DJ, Rodgera-Johnson P, et al. Human spongiform encephalopathy: the National Institutes of Health series of 300 cases of experimental transmitted disease. Ann Neurol 1994;35:513–29.
Mehta JS, Franks WA. The sclera, the prion, and the ophthalmologist. Br J Ophthalmol 2002;86:587–92.
Foster JD, Fraser H, Bruce ME. Retinopathy in mice with experimental scrapie. Neuropathol Appl Neurobiol 1986;12:185–96.
Head MW, Northcott V, Rennison K, et al. Prion protein accumulation in eyes of patients with sporadic and variant CJD. Invest Ophthalmol Vis Sci 2003;44:342–6.(J S Mehta, R J Osborne an)
Correspondence to:
Dr J S Mehta
9 Sandringham Court, King & Queen Wharf, Rotherhithe Street, London SE16 5SQ, UK; jodmehta@hotmail.com
Accepted for publication 10 July 2003
Keywords: variant Creutzfeld-Jakob disease; tonometry
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.
References
Lim R, Dhillon B, Kurian KM, et al. Retention of corneal epithelial cells following Goldmann tonometry: implications for CJD risk. Br J Ophthalmol 2003;87:583–6.
Herzberg L. Creutzfeldt-Jakob disease and corneal grafts. Med J Aust 1979;1:248.
Manuelidis EE, Angelo JN, Gorgacz EJ, et al. Experimental Creutzfeldt-Jakob disease transmitted via the eye with infected cornea. N Engl J Med 1977;296:1334–6.
Tateishi J. Transmission of Creutzfeldt-Jakob disease from human blood and urine into mice. Lancet 1985;2:1074.
Brown P, Gibbs DJ, Rodgera-Johnson P, et al. Human spongiform encephalopathy: the National Institutes of Health series of 300 cases of experimental transmitted disease. Ann Neurol 1994;35:513–29.
Mehta JS, Franks WA. The sclera, the prion, and the ophthalmologist. Br J Ophthalmol 2002;86:587–92.
Foster JD, Fraser H, Bruce ME. Retinopathy in mice with experimental scrapie. Neuropathol Appl Neurobiol 1986;12:185–96.
Head MW, Northcott V, Rennison K, et al. Prion protein accumulation in eyes of patients with sporadic and variant CJD. Invest Ophthalmol Vis Sci 2003;44:342–6.(J S Mehta, R J Osborne an)