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Decontamination of Creutzfeldt-Jakob disease agent.

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Decontamination
of Creutzfeldt-Jakob
Disease Agent
David M. Taylor, PhD
Some comments are necessary about the January Health
Care Issues paper on handling materials from patients with
Creutzfeldt-Jakob disease (CJD). The United Kingdom Department of Health and Social Security standard for autoclaving such materials is 18 minutes at 134"C, based upon studies
in which brain macerates containing scrapie agents of differing thermal stability (139A and 22A) were inactivated within
4 minutes at 136°C [3]. The method of autoclaving proposed
for the United States (132°C for 1 hour), although unsupported by references, is not incompatible with these results,
but it is important to note that the UK standard applies to
surgical, porous-load sterilizers. These are more efficient
than gravity-displacement autoclaves but are not suitable for
fluids. Because 263K scrapie in hamsters has produced the
highest titers of infectivity in brain, it has been assumed that
this model is the best choice for inactivation studies. This is
untenable in terms of thermal inactivation; the UK study
confirmed that 22A scrapie is the most thermostable strain
known. Until CJD strains of equal or higher stability are
available, it is better to base decontamination standards for
human materials on 22A scrapie rather than o n CJD, chosen
arbitrarily from the few uncloned strains available, about
which relatively little is known.
The January publication excluded sodium hypochlorite as
a useful disinfectant, because undiluted domestic bleach (5%
sodium hypochlorite) had not been shown to be consistently
effective in inactivating infectivity in brain homogenates.
However, a major problem in interpreting and comparing
data from hypochlorite and other inactivation experiments is
the lack of standard methodology (e.g., considerable differences in the concentration of brain tissue). Because hypochlorite reacts not only with infectivity in tissue but also, to a
major extent, with the tissue itself, the ratio of hypochlorite
to tissue is crucial. The presence of residual hypochlorite
must, therefore, be confirmed to ensure that it has not been
unduly consumed by the tissue effect; such checks have been
rare, but are essential if experimental results are to be a basis
for recommended decontamination regimens in hospital
wards, operating rooms, autopsy rooms, and diagnostic and
research laboratories. The largest study on hypochlorite inactivation, using the 139A and 22A scrapie strains, demonstrated that infected 10% brain homogenates were inactivated when mixed with an equal volume of 2.75%
hypochlorite for 30 minutes and that at least 10,000 ppm of
chlorine was available at the end of the exposure period; the
original infectivity titers were
and
intracerebral
LD50 units per gram of brain tissue for 139A and 22A,
respectively [31.
Reference was made to inactivation by thiocyanate and
hydroxyl ions [4]; these data do not provide a realistic basis
for dealing with the practical aspects of decontamination of
materials from CJD patients because they were derived from
experiments on partially purified preparations; these are
known to be much easier to inactivate than clinical material.
Also, the estimates of residual infectivity were calculated
from incubation period assays, not end-point titration; the
serious errors of interpretation that can arise using this technique following chemical or physical treatments have been
described frequently (see [2, 51).
Finally, the conjecture that CJD does not appear to be
transmissible by intrauterine or perinatal routes is subject to
the major caveat that the onset of clinical disease is typically
beyond childbearing age. Cases have occurred in younger
females but have been too few to be certain that vertical
transmission may not occur. Although maternal transmission
is apparently absent in kuru, horizontal and vertical transmission appear to occur in scrapie of sheep and goats, though
not in mice El]. Since the period between infection and
onset of clinical symptoms is unknown for natural cases of
CJD, there could be an opportunity for vertical transmission
that is unrecognized, particularly if all of those with an incubating infection do not become clinical cases within their
lifetimes. Perhaps the increasing awareness of the Gerstmann-Straussler syndrome, a familial form of CJD, will shed
some light on this potential problem.
AFRC C MRC Neuropathogenesis Unit
West Mains Road
Edinburgh EH9 3JF, United Kingdom
References
1. Dickinson AG: Scrapie in sheep and goats. In Kimberlin RH
(ed): Slow Virus Diseases of Animals and Man. Amsterdam,
North Holland, 1976, pp 209-241
2. Dickinson AG, Fraser H: Modification of the pathogenesis of
scrapie in mice by treatment of the agent. Nature 222:892-893,
1969
3. Kimbertin RH,Walker CA, Millson GC, et al: Disinfection studies with two strains of mouse-passaged scrapie agent. J Neurol Sci
59:355-369, 1983
4 . Prusiner SB, Groth DF, McKinley MP, et al: Thiocyanate and
hydroxyl ions inactivate the scrapie agent. Proc Natl Acad Sci
USA 78:4606-4610, 1981
5. Somerville RA, Carp RI: Altered scrapie infectivity estimates by
titration and incubation period in the presence of detergents. J
Gen Virol64:2045-2050, 1983
Reply
Committee on Health Care Issues,
American Neurological Association'
Familial Creutzfeldt-Jakob disease (CJD) is a rare but recognized entity. Dr Austin is correct that at-risk persons must
not be tissue donors and their tissues and body fluids must
be considered as being infectious even in the pre-symptomatic period. We agree with him that familial CJD remains an
infectious disease produced by the same agent as in nonfamilial CJD. The basis for a genetic pattern of disease is presumably a susceptibility to the infectious agent, as Dr Austin
suggests.
We thank Dr Taylor for his comments but remain firm in
*Roger N. Rosenberg, MD, Charles L. White 111, MD, Paul Brown,
MD, D. Carleton Gajdusek, MD, Joseph J. Volpe, MD, Jerome
Posner, MD, and Peter James Dyck, M D (authors of original paper).
Annals of Neurology Vol 20 NO 6 December 1986
749
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