ABSTRACT
Aims: This study’s primary purpose was to determine whether earlier findings suggesting an association between sporadic Creutzfeldt-Jakob disease (sCJD), a transmissible spongiform encephalopathy of humans and specific dietary components could be replicated. The a priori hypotheses were that consumption of (i) foods likely to contain organ tissue and (ii) raw/rare meat are associated with increased sCJD risk. Study Design: Population-based case-control study. Place and Duration of Study: Department of Neurology, School of Medicine, Loma Linda University, Loma Linda, CA, USA; 4 years. Methodology: An 11-state case-control study of pathologically confirmed, definite sCJD cases, matched controls, and a sample of control-surrogates was conducted. Ninety-six percent (106/110) of the case data was obtained in 1991-1993, prior to variant CJD publicity. Results: Using control self-responses, consumption of hot dogs, sausage, pepperoni, kielbasa, "other" canned meat, poultry liver, any stomach/intestine, beef stomach/intestine, any organ tissue, and beef organ tissue was individually associated with increased sCJD risk; odds ratios (OR) ranged from 2.4 to 7.2 (0.003 <p<0.025). Rare/raw meat consumption was associated with sCJD (OR=2.0; p<0.05). Greater consumption of hot dogs, bologna, salami, sausage, pepperoni and kielbasa was associated with significantly higher risk. The OR for gizzard consumption was 7.6, p<0.04. Bologna, salami, any liver, beef liver and pork stomach/intestine were marginally associated with sCJD: ORs ranged from 1.7 to 3.7; 0.05 <p< 0.10. Brain consumption was not associated with an elevated risk. Analyses using control-surrogate data indicate that use of the control self-responses did not bias the results away from the null hypothesis. Conclusions: The a priori hypotheses were supported. Consumption of various meat products may be one method of transmission of the infectious agent for sCJD.
ABSTRACT
Aims: To evaluate the hypothesis that sporadic Creutzfeldt-Jakob disease (sCJD) may be transmitted through ocular tonometry. Background: The infectious agent of sCJD may be present in the cornea prior to clinical symptoms. Cornea infectiousness has been documented by cornea transplants in guinea pigs and humans. sCJD is resistant to complete inactivity by conventional sterilization techniques. Thus contact tonometry equipment is not disinfected sufficiently to kill sCJD. We previously hypothesized that contact tonometry is a sCJD risk factor. Study Design: Population-based case-control study. Place and Duration of Study: Department of Neurology, School of Medicine, Loma Linda University, Loma Linda, CA, USA; 4 years. Methodology: An 11-state case-control study of pathologically confirmed definite sCJD cases, individually matched controls, and a sample of control surrogates was conducted. Ocular tonometry histories were obtained from case-surrogates, controls, and a sample of controlsurrogates. Results: The odds ratio (OR) for ever vs never having had an ocular tonometry test was statistically significant for matched and unmatched analyses for 15 through 3 years prior to disease onset, using both control self-responses and control surrogates: ORs were ∞ and 19.4 with 1-sided P-values <0.0001 and 0.003 and ORs=∞ and 11.1 with 1-sided P-values <0.003 and 0.02, respectively. ORs increased as the number of tonometry tests increased during this age period: trend test, 2-sided P-value < 0.0001. For ≥5 vs <5 tonometry tests, the OR was 5.8 (unmatched) and 3.7 (matched), 2-sided P-value<0.00005. Respondents generally could not specify the type of tonometry. There was no indication of increased tonometry testing among cases within 2 years of disease onset. Conclusions: The a priori hypothesis was supported. Contact tonometry, preferred by ophthalmologists, may be capable of transmitting sCJD. Consideration should be given to using disposable instrument covers after each use. The use the disposable covers or non-contact tonometry is preferable in the absence of effective disinfectant processes at this time.