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By
John Trotti
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John
Trotti
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I want to
start by saying that my instincts tell me the threat
posed by the recent "Mad Cow" situation—bovine
spongiform encephalopathy (BSE) in Washington State—is
not as great as some experts have suggested, a suspicion
no doubt prompted in part by my undeniable hankerings
for meat. This, however, is not to say that I think
the issue itself isn't significant; quite the opposite
is true, in fact, especially for waste managers who
likely will be dealing with disease-toting organic wastes
of one kind or another from now until the cows come
home. But—and here's where my beef lies—when
the best minds are divided or at least unsure how to
deal with prions or the threat they pose to humans,
my hunger for a lot more clarity outweighs my belly's
cravings for steak.
In his article
"Chronic Wasting Disease and Waste Disposal: Making
an Informed Decision" in the September/October
2003 issue of MSW Management, C. Douglas Goldsmith
Jr. discusses at some length the disposal of chronic
wasting disease (CWD) in deer and elk. According to
Goldsmith, "Prions, although they have been on
the planet for quite some time, are a newly identified
form of infectious agent that are made of protein and
contain no DNA or RNA. They are resistant to most standard
disinfection techniques. Their mode of infection in
the ecosystem is undefined but assumed to be a result
of consumption of contaminated foodstuffs or animal-to-animal
contact." With this as background, let's look at
the situation.
The Life
and Times of Prions
The first
thing to recognize about a prion is that, unlike most
infectious diseases with which we're familiar, a prion
does not have a nucleic acid genome; that is, in simpler
terms, prions are protein-only infectious agents. Thus,
a generally accepted definition of a prion—one
that can be found on a number of Web sites, including
http://meat.tamu.edu/pdf/BSEresource.pdf—is
a "small proteinaceous infectious particle which
resists inactivation by procedures that modify nucleic
acids…. Prion diseases are often called spongiform
encephalopathies due to the post mortem histopathologic
appearance of the brain with large vacuoles (a spongy
look) in the cortex and cerebellum." Many of these
Web sites say most mammalian species probably
will develop these diseases, but if your thought process
is anything like mine, you no doubt picked up on the
word "probably" and consider it somewhat less
than reassuring coming from the mouths of experts.
Unfortunately
cattle are just part of the prion problem. Aside from
BSE, confirmed links include scrapie in sheep, transmissible
mink encephalopathy, and CWD in at least several forms
of deer and elk. Not even humans are immune since prions
are associated with Creutzfeldt-Jakob Disease (CJD),
which occurs most often in people in their 60s with
an incidence of one person per million per year, with
approximately one out of 10,000 people infected at the
time of death; Gerstmann-Straussler-Scheinker syndrome,
which typically occurs in people in their 40s and 50s
and has a slower progression than CJD; fatal familial
insomnia, which is characterized by severe selective
atrophy of the thalamus; and Alpers syndrome, which
is found in infants.
What singles
out prion diseases for particular attention is that
they are both infectious and hereditary. They also are
sporadic in the sense that there are cases in which
there is no known risk factor, although it seems likely
that infection was acquired through diet or by following
such medical procedures as surgery, growth hormone injections,
corneal transplants, or hereditary transmission where
the disease is not sex-linked but is a dominant trait.
Death,
Transfiguration, and the Fate of Prions
We all might
rest easier if there were a reliable way to recognize
infected animals in the early stages of disease, but
unfortunately there is no current test that can do this.
Worse still is the resistance of prions to sterilization
techniques. As Goldsmith points out, "Dry heat,
boiling, radiation (microwave, ultraviolet, ionizing),
chemicals (e.g., alcohol, ammonia, and acids) and gaseous
disinfectants (e.g., ethylene oxide and formaldehyde)
have all been cited as ineffective. Chlorine dioxide,
glutaraldehyde, iodophores, sodium dichloroisocyanate,
sodium meta-periodate, and autoclaving at 250†F for
15 minutes or boiling in 3% sodium dodecyl sulfate have
been listed as variable or partially effective disinfect
ion methods." The bottom line here is that no single
decontamination method has proved to be totally effective
against agents that cause transmissible spongiform encephalopathy
(TSE). If that weren't ominous enough, prion survivability
appears to increase in the presence of organic matter.
There seems
to be general agreement that confirmed TSE-positive
cases should be incinerated in the manner of medical
wastes, but what about those that have been exposed
but have yet to exhibit signs of infection? Here the
situation is murkier, but we can expect that landfills
will be asked to dispose of carcasses on the assumption
that nature will take care of the problem if one indeed
exists.
While my
guess is that this approach is probably sufficient,
two concerns persist: First, in the absence of generally
accepted science on how to deal with prions, "probably"
just doesn't seem to be a wise rack on which to hang
your hat. Second, regardless of the medical aspects,
this leaves public perception issues to flare up in
the face of any subsequent, unexplained, TSE-related
incident that takes place in the neighborhood.
The US Department
of Agriculture has the lead in TSE research and management,
and no doubt we will begin to see results of its studies
in the near future. But what do we do now?
None of us
wishes to see our regulatory bodies go off half-cocked
and take what amounts to draconian measures in the face
of an uncertain threat, but at the same time it makes
no sense where such uncertainty exists to err anywhere
but on the side of safety. Presently disposal procedures
place landfill operators in the untenable position of
having to make decisions based on insufficient knowledge.
The answer in the long run is, of course, better science—funded
federally and quickly. Plenty of animal specimens are
available for study in the deer and elk herds, but carefully
bear in mind that junk science would be even worse than
no science. In the meantime, the best we can do is follow
the example of those with experience in handling infected
humans and cremate the animals.
Send
John an Email
MSW
- March/April 2004
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