Volume 4, Number 2—June 1998
Rabbit Hemorrhagic Disease
The RHD exposure categories of "low" and "high" used by Mead et al. and mentioned in the first column of page 18 (1) are not related to the categories of "low" and "high" given in the same paragraph at the top of the second column. The reader might easily assume that it was Mead et al. who considered that Jul—Dec 1995 was "a low exposure period." This is not so—such a classification is made by Smith et al.
Further, the reader might assume that it was the study by Mead et al. that concluded "that exposure to RHD virus remains a plausible explanation for increased disease incidence." Again this is an inference drawn by Smith et al. and is the opposite of the conclusion of Mead et al.
The basis of exposure in the study by Mead et al. is at an individual level—the respondents were chosen either because they had been handling rabbits or as controls in determining the level of disease. In contrast, Smith et al. consider exposure at a broad environmental level and disregard whether the respondents had been handling infected rabbits or not. Actually, more contact with rabbits occurred during the first half of the study than during the second.
Smith et al. do not mention the conclusions of Mead et al.: These neither showed any significant difference between levels or types of illness in those exposed and those not exposed to RHD virus nor demonstrated any association between the exposure to RHD and number of episodes of illness in the subsequent 1 to 2 months.
The results of the study by Mead et al. may be summarized by noting that the average number of episodes of illness over the 13-month reporting period was 2.6 for respondents who had not been exposed to RHD virus, 2.2 for those classified as having a low level of exposure, and 2.3 for those classified as having a high level.
The study by Mead et al. concluded that, on the basis of the health survey and the lack of any serologic reaction of the respondents, there was considerable support to the view that RHD virus is not associated with infection or disease in humans. The results of the study have been submitted for publication in a scientific journal.
Reference 31 should refer to the Bureau of Resource Sciences (not Studies).
- Smith AW, Skilling DE, Cherry N, Mead JH, Matson DO. Calicivirus emergence from ocean reservoirs: zoonotic and interspecies movements. Emerg Infect Dis. 1998;4:13–20.
- Mead C, Kaldor J, Canton M, Gamer G, Crerar S, Thomas S. Rabbit calicivirus and human health. Canberra, Australia: Department of Primary Industries and Energy, Australian Government (Released under the Official Information Act). Report of the Rabbit Calicivirus Human Health Study Group; 1996.