Sickness in Australia

From ANIMAL PEOPLE, November 1996:

ducing a pest to control a pest, against
much scientific and humane advice,
Australian agriculture and wildlife authorities
in mid-October released millions of calicivirus-carrying
Spanish rabbit fleas at 280
sites, expecting to kill up to 120 million of
the nation’s estimated 170 million rabbits.
The rabbits are accused of outcompeting
endangered native marsupial species
for habitat––though they also draw predation
by feral foxes and cats away from marsupials––and
of costing farmers $23 million
to $60 million a year, chiefly by eating fodder
that would otherwise go to sheep.
Calicivirus induces internal hemorrhage,
killing about 90% of the rabbits
who contract it within 30 to 40 hours. It
spreads at about 25 miles per day.

The deliberate releases were actually
the second introduction of calicivirus to
Australia, following an accidental release
from a quarantined testing site on Wardang
Island in September 1995 that spread
through four states, killing millions of rabbits
and providing experience with the aftermath
of the biological attack.
The first rabbit victims were barely
spitting blood when on October 18
Member of Parliament Richard Evans
demanded the development and release of a
disease to kill cats.
“I am calling for the total eradication
of cats in Australia,” Evans stipulated,
blaming the 18 million Australian cats––one
per person–– for causing the extinction of
nine native species. Only about two million
of the cats are owned; the rest are feral,
hunting for their livings. Rabbits are among
their primary prey; if rabbits become inaccessible,
the cats may compensate by
attacking more birds and more marsupials.
Evans’ demand for a cat purge was
promptly and predictably endorsed by
Adelaide conservationist John Wamsley,
who accuses cats of wiping out 23 native
species, wears a catskin hat, and says he
plans to start selling cat meat soon in the
restaurants at his several centers for the captive
breeding of endangered marsupials.
Anticipating a surge in the grey
kangaroos, the native species best able to take over former rabbit
habitat, outback ranchers were at deadline preparing to kill them
en masse too. Of Australia’s estimated 30 million kangaroos, of
55 species, about 19 million are greys, of whom ranchers shoot
about three million a year to reduce competition for sheep forage.
Australia has been down this road before, introducing
the flea-borne disease myxomiatosis in 1950 to cut the rabbit population––and
the cane toad, native to Hawaii, in 1935 to control
sugar cane grubs. Myxomiatosis, reintroduced several times subsequently,
is officially considered a success, since it killed off an
estimated 99.9% of the rabbits before they developed resistance
and reconquered the habitat. The cane toad, on the other hand,
never did eat many grubs, but became one of the more common
non-native nuisances in Queensland, and is accused––like cats,
who came with Captain James Cook in 1788, and rabbits, also
brought in 1788 but only introduced into the wild in 1859––of contributing
to the loss of native species.
Calicivirus compared to BSE
Sheep, also brought to Australia in 1788, are more
numerous than any other introduced species, if not quite as abundant
as in 1988, when at the height of exports of live sheep to the
Middle East at Ramadan, the population rose to 160 million. It
has since been reduced to just over 100 million by drought and
declining global demand for wool and mutton.
Though a case can be made that sheep do more ecological
harm to Australia than all other introduced species combined,
extirpating sheep by disease is not on anyone’s public agenda.
The sheep ailment scrapie is, however, on the world
agenda, as the apparent source of the cattle disease bovine spongiform
encephalopathy, called BSE or “mad cow disease” for short,
which has attacked cattle in Britain and occasionally elsewhere
since 1986. It hasn’t yet appeared in Australia; if it does, the
sheer size of the Australian sheep population could form an almost
inexhaustible reservoir for infection.
On March 20 of this year, British health minister
Stephen Dorrell told the British Parliament that scrapie-becomeBSE
appears to have evolved further into Creutzfeldt-Jakob
Disease, a brain-destroying malady of humans, formerly believed
to be a condition of age, which only recently began appearing in
younger people––even teenagers.
The death toll of all suspected BSE-related CJDcases is
still roughly comparable to the toll from a bad bus crash. Britain is
in the midst of purging all cattle who might have been exposed to
BSE, at the rate of about 35,000 a week, with as many as 300,000
leftt to kill, to prevent any further transmission.
Yet since CJD apparently has a long incubation time,
estimated by some authorities as up to 30 years, many cases
already contracted may not be detected until well into the next century.
Whether or not almost a year of intense concern about CJD
worldwide was a panic or was warranted preparation for a possible
epidemic of invaribly fatal brain-rot won’t be known for at least
another decade.
BSE/CJD has nothing and everything to do with calicivirus.
The diseases are not related in any way. No means of
immunization against BSE has been discovered, nor do investigators
expect to find one; a vaccination against calicivirus, on the
other hand, has reportedly been deployed to protect rabbits raised
as livestock in as many as 40 nations where natural outbreaks have
occurred. But again, Victoria state chief veterinarian Andrew
Turner acknowledges that not all rabbits respond to the vaccination,
and it isn’t yet known whether it would be effective if needed
to deal with a leap into either humans or other species.
BSE/CJD and calicivirus have in common that for a
decade preceding March 20, the British government insisted that
though BSE had hit thousands of cattle in
hundreds of herds, bringing the destruction
of more than 160,000 cattle to contain the
outbreaks, it couldn’t jump into
humans––much as Australia now insists
calicivirus can’t and won’t.
Demanding a gesture of good
faith as well as glib reassurance, Animal
Liberation spokesperson Frankie Seymour
on October 21 dared the cabinet ministers
responsible for the calicivirus introduction
to inject themselves with it. “Of course,”
she added, “if the ministers don’t get sick,
it won’t prove calicivirus is safe. It won’t
diminish the severe cruelty and disastrous
ecological consequences. But at least the
people of Australia will know their governments
are not consciously gambling with
human lives.”
Oregon State University veterinary
virologist Alvin Smith said calicivirus
is “virtually certain” to infect people, sooner
or later, citing the case of a Mexican
laboratory worker who developed antibodies
to calicivirus by eating infected rabbits
as part of an experiment.
The Perth-based Rabbit Information
service argued that four out of five
known strains of calicivirus already occur
in humans.
The Australian Conservation
Foundation said the release was “premature
and dangerous.”
Warning New Zealand to proceed
more cautiously than Australia with a
release scheduled for later this year, Bristol
University rabies and tuberculosis
researcher Stephen Harris called the calicivirus
release “one of the most significant
ecological experiments in living memory.”
New Zealand Veterinary
Association past president Catherine Smith
suggested that preliminary data shows some
rabbits are already developing resistance to
calicivirus. Apparently rabbits who contract
the disease between the age of five and
eight weeks survive through one breeding
cycle, and may be able to pass along their
acquired resistance to offspring.
Mad cow disease
Hypothesized for several years,
the likelihood of a causal link between eating
BSE-infected beef and contracting CJD
was reinforced with the October 24 publication
in Nature of the discovery by Imperial
College School of Medicine professor John
Collinge of a characteristic molecular “signature”
common to both BSE and the CJD
strain afflicting younger victims.
Officially, the U.S. doesn’t have
BSE yet, though at least one American is
believed to have died of the BSE-related
CJD strain after eating a tin of British beef
several years before. But there are similar
diseases in the U.S., afflicting ranched elk
and mink, and are other avenues by which
a case could be transmitted.
Centers for Disease Control and
Prevention director Richard J. Jackson on
October 19 warned at a symposium on neurotoxins
and fetal injury at the Society of
Environmental Journalists’ annual conference
that melatonin supplements, often
taken as a “natural” sleeping pill, are most
commonly made from the pineal glands of
cattle, and accordingly should be viewed as
a possible BSE/CJD transmission
vector––especially if the supplements originate
from a nation where BSE occurs.
Synthetic melatonin is available.
Jackson also pointed out that
“natural” calcium supplements are often
made from cattle bones, which may also be
a vector for BSE/CJD transmission, inasmuch
as bone meal cattle diet supplements
are believed to have been the avenue by
which the sheep disease scrapie became
BSE in the first place. A better documented
threat from cattle bone calcium supplements,
Jackson added, is that they may
contain dangerous levels of lead, absorbed
as cows eat grass contaminated by 50 years
of lead fallout from the exhaust pipes of
cars burning leaded gasoline. While leaded
gasoline is now off the market, resultant
ground-level lead pollution could persist
indefinitely––and the lead content of food
supplements, Jackson reminded, is not
federally regulated.
Animal tests
Laboratory animal data has been
conspicuously absent from most professional
discussion of the BSE/CJD relationship,
largely because investigators have been
able to study the disease in actual human
and livestock victims.
The first monkey known to have
contracted the apparent BSE-related form
of CJD was a zoo-dwelling rhesus, born in
Britain, who was sold to a facility in
Montpelier, France, until she was euthanized
at age nine in 1991 due to erratc and
aggressive behavior. The monkey had been
fed meat products. The case was treated by
scentific publications more as a curiosity
than as a possible source of valuable data.
The Central Veterinary
Laboratory in Weybridge, Surrey, studied
the health of 303 calves born to mothers
with BSE and 303 others born to healthy
cows, publishing the data on October 7.
Studying the calves’ brains after slaughter,
the team reported that while some calves of
infected mothers did contract BSE, maternal
transmission did not seem to occur.
They suggested that genetic susceptibility
to BSE might be a factor, however, since
not all calves exposed to suspected BSEtransmitting
agents actually got the disease.
In mid-October, Zurich
University professor Charles Weissman
told the European Union Commission study
group on BSE/CJD that, “In my personal
view, the evidence we so far have is sufficiently
suggestive of transmission from cattle
to man that we should act as though it
were true. Therefore we must make an
assessment of the risk of transmission,”
which he suggested should be done though
a major primate study. The subjects would
be given increasing amounts of BSE-infected
material until they showed a reaction.
The proposal was shredded by
fellow researchers as too costly, too timeconsuming,
and ethically dubious. When
J. Ralph Blanchfield of the International
Fund for Science and Technology defended
parts of Weissman’s argument on the
ProMED-AHEAD online zoonotic diseasebulletin
board, a project of the Federation
of American Scientists, moderator Martin
Hugh-Jones responded, “Just because
something would be useful to know, e.g.
the oral dose response curve for one species
of primate, is not of itself persuasive.”
Added Grace S. McLaughlin, of
the University of Florida College of
Veterinary Medicine in Gainesville,
Florida, “It seems like a waste of time and
monkeys. Just as HIV/AIDS has provided
a natural experiment [permitting longterm
clinical observation of human victims], so,
it seems, has BSE/CJD. The limited scope
of the latter [relative to HIV/AIDS, which
has tens of thousands of observable victims] and the long time necessary even to
detect infection does not, to me, justify the
use of nonhuman primates.”
Hugh-Jones ended the discussion
as redundant before anyone from the antivivisection
perspective even got involved.

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