快猫短视频

INDIA without vultures. It鈥檚 hard to imagine. Since time immemorial they have
lurked everywhere, in cities and the countryside, waiting for food to scavenge.
Five thousand could live on one waste dump or around a single abattoir. A gang
of vultures could pick a water buffalo carcass clean in 20 minutes.

No more. In only a few years the once-ubiquitous griffon vulture has all but
disappeared from India. Other vulture species are not affected鈥攂ut none of
them is big enough or numerous enough to replace the griffons. The stench of
rotting cattle carcasses pervades villages. And with plenty of meat on offer,
packs of vicious, rabid dogs are multiplying.

鈥淎ll our reports and data show the vultures are dying of some viral disease,鈥�
says Asad Rahmani, director of the Bombay Natural History Society. One species
of the griffons, unique to India, even faces extinction. Why?

Griffon vultures are merely the latest in a long line of wild animals that
have fallen prey to 鈥渆merging diseases鈥�, caused by pathogens that may have been
harmless in their original setting, but turned nasty when released among
previously unexposed hosts.

Rinderpest, a virus brought to Kenya with imported cattle in 1887, killed
three-quarters of the native antelope, kudu, wildebeest and other ungulates in
southern Africa within ten years. When distemper virus was brought to the North
Sea in 1988 by hungry harp seals鈥攄riven from the Atlantic by
overfishing鈥攊t killed three-quarters of the local harbour seals. And when
West Nile virus arrived in New York from Israel last September, the news reports
focused on the seven people who died. But the virus also killed ten thousand
crows in New York City alone. Migrating birds might now have spread the virus
across North America
(快猫短视频, 8 July, p 4).

Catastrophic epidemics among wild creatures used to be considered rare,
one-off events. But animal pathogens are travelling the world with increasing
ease as the global trade in food, plants and animals spirals upwards, and humans
become increasingly mobile. All over the planet, lethal infections are killing
off populations of creatures ranging from abalone to kangaroos, from coral to
honeybees, and from pilchards to flamingoes. Yet ecologists, wildlife biologists
and governments alike are ignoring the threat that emerging diseases pose to
natural ecosystems, according to an international group of animal health
experts.

That complacency, they say, is based on the belief that pathogens and wild
populations invariably reach a happy equilibrium, even though a spate of recent
studies contradicts this assumption. The upshot is that virtually no precautions
are being taken to prevent pathogens that are dangerous to native fauna from
globetrotting.

鈥淯ntil the last three or four years, disease was scarcely on the radarscope
as a potential cause of endangerment,鈥� says Ross McPhee of the American Museum
of Natural History in New York City.

鈥淔orgetting disease was a big omission in our thinking about wild
populations,鈥� agrees Andy Dobson of Princeton University in New Jersey. That
omission has come about in part because there has been an apparently more
sinister culprit to shoulder any blame: chemical pollution.

Frog fungus

鈥淲hen there is a sudden die-off of wild animals, people usually suspect
pollution,鈥� says Peter Daszak, a wildlife disease specialist at the University
of Georgia at Athens, who helped to identify the fungal plague that is killing
off the world鈥檚 amphibians
(快猫短视频, 27 June 1998, p 4). 鈥淧eople
spent an enormous amount of time pursuing environmental explanations for the
amphibian deaths . . . but disease was the primary cause of the mass
尘辞谤迟补濒颈迟测.鈥�

Pollution undoubtedly harms wildlife. Ever since the 1960s when DDT wiped out
populations of eagles and other birds, inspiring Rachel Carson鈥檚 book Silent
Spring, generations of ecologists and environmentalists have been taught to
see chemical pollutants as biodiversity鈥檚 number one enemy.

Infectious diseases, on the other hand, are usually seen as part of the
natural order. Hence the widely held view that the damage is rarely permanent
when wild populations are invaded by a new infection. Extreme virulence is not
good for pathogens, it鈥檚 true. They need their hosts to live at least long
enough to pass the disease on. So most evolve a truce: the host develops
immunity, the pathogen becomes less virulent, and the disease settles down at a
tolerable level. The classic example is myxomatosis, introduced into western
Europe and Australia in the 1950s to control rabbits. After a huge initial
die-off, rabbits and virus adapted. They now coexist.

But populations do not always bounce back. When a new strain of vibrio
bacteria killed off starfish along the coastline of California in 1984, some
species recovered faster than others, and maintained their advantage. What used
to be the most common species is now rare.

And starfish are not alone in having their populations sculpted by disease.
Since 1993, a team led by evolutionary biologist Andre Dhondt of Cornell
University in Ithaca, New York, has followed the spread through songbird
populations of a new strain of bacterium, Mycoplasma gallisepticum,
that evolved in the crowded battery farms of the eastern US. Counts made by
birdwatchers each winter showed that whether house finch populations were large
or small before the infection arrived, they ended up at the same, low density
afterwards. At this density, the disease is passed on just often enough to kill
finches at the same rate at which the birds are reproducing (Proceedings of
the National Academy of Sciences, vol 97, p 5303). In other words, disease
determines numbers.

鈥淧eople thought large predators were the major control on numbers,鈥� says
Dobson. 鈥淥r it was the availability of food.鈥� But it now seems that even
ordinary pathogens鈥攏ever mind virulent newcomers such as the finch
infection鈥攃an dramatically alter wildlife populations. In 1998, Dobson
helped to show that the cycle of boom and bust typical of many temperate species
is, in British grouse, actually caused by cyclic variations in gut parasites.
The observation may be a turning point in ecologists鈥� thinking about
disease.

It makes sense that pathogens should play such an important role, says
Dobson. For instance, they have far more opportunities to kill off the
all-important breeding animals in a population than, say, wolves, which
typically take out the old. Pathogens are much more important controls on wild
populations than predators, he says, even when the pathogens are long
established. Novel pathogens, to which the victims typically have no immunity,
should have even more impact.

Still, according to biological theory, even a new disease shouldn鈥檛 be able
to wipe a species out on its own. Once the host gets too scarce, the pathogen is
no longer passed on frequently enough to keep in circulation. The disease will
always die out before the host does. Or will it?

Not according to a 1997 study by Mike Bonsall of Imperial College in Silwood
Park, near Windsor. Two species of moth can, individually, coexist indefinitely
in the lab with a wasp that lays her eggs in the moth鈥檚 caterpillars. The wasp
parasite, like any other infectious disease, needs a continual supply of fresh
hosts to propagate itself. Wasp numbers plummet when caterpillars become scarce,
so the two remain in balance.

Wasp waste

But if the wasp is allowed to attack both species at once, the moth that has
the least resistance to the parasite dies out, fast. The more tolerant moth
keeps wasp numbers up even when the other moths are too few to support the wasp
population. The less tolerant moth goes 鈥渆xtinct鈥�. Similarly, North American
grey squirrels have all but replaced native red squirrels in Europe, possibly
because reds are more susceptible to a parapox virus that strikes both.

But while some ecologists and wildlife biologists are coming around to the
idea that pathogens can cause extinctions when there is a reservoir to top up
the infection, few were prepared for just how many apparently innocuous forms a
reservoir can take.

Burgeoning livestock populations and even pet animals are creating a
multitude of artificial reservoirs. Domestic ducks harbour duck plague, a herpes
virus that causes massive die-offs in wild ducks. African village dogs spread
distemper and rabies to lions and wild canids
(快猫短视频, 19 April 1997, p 32).

Even captive breeding programmes, the last hope for many endangered species,
can be threatened by nearby artificial reservoirs for new diseases. A release of
field crickets bred at London Zoo was delayed last year, says Andrew Cunningham
of the Zoological Society of London, because the insects were infected with a
protozoan possibly picked up from African crickets kept close by. The zoo now
carries out pre-release screening for its captive-bred animals.

But the most troubling development is the recent realisation that dead matter
might act as a reservoir for potentially devastating emerging diseases. Take the
catastrophic die-offs of the world鈥檚 amphibians. In the Americas and Australia,
the culprit turned out to be a fungus that consumes keratin, a major protein in
skin. Some species鈥攖he Central American golden toad and two species of
Australian frogs that brood their young in their stomachs鈥攈ave been driven
to extinction, even though there are no obvious reservoir species for the fungus
in their habitats.

The problem, says Daszak, is that keratin is widespread in the environment in
carcasses to shed skin. This means that the fungus might persist on dead tissue,
until its hosts were well and truly extinct.

Even so, Daszak and others are hopeful that there may be ways to limit the
numbers of pathogen-induced die-offs in the future. Of prime importance, they
say, is improving the ways animals are screened before they are transported
across borders. 鈥淚n Britain you have to declare any animal import that might be
carrying a pathogen that could affect livestock, or fish stocks,鈥� Cunningham
points out. 鈥淣o one checks for things that might threaten wildlife.鈥�

The same applies in North America. Rabies, for example, was spread out of the
southeastern US during the 1980s by hunters moving raccoons to boost their
populations elsewhere. 鈥淭hey were moving them in truckloads,鈥� says Daszak.

Some biologists are equally to blame. Conservationists often transport
animals to reserves or reintroduce them into the wild. The World Conservation
Union, based in Switzerland, recommends that such animals be checked for
infection, and that any deaths after such moves be investigated. But a 1993
survey of 700 鈥渢errestrial vertebrate translocations鈥� in North America,
Australia and New Zealand found that conservationists failed to screen for
diseases in one-quarter of moves, and to investigate whether deaths had occurred
in three-quarters.

But new rules and regulations won鈥檛 be enough without a better understanding
of how diseases are spread through wild populations, which ones exist there
naturally, and how environmental changes, such as crowding within dwindling
habitats, can speed contagion. 鈥淲e need to learn much more about wildlife
pathogens, where they have been moved in the past, and which pose the most
risk,鈥� says Daszak. Then, he hopes, it may be possible to prevent the accidental
introduction of pathogens that are most likely to have an adverse impact on
biodiversity. 鈥淲e may never be able to predict everything,鈥� adds Cunningham.
鈥淏ut just because a mountain is high is no reason not to start climbing it.鈥�

Gaining that understanding will also require more thorough investigations of
animal die-offs. In India, for example, scientists looked for signs of chemical
poisoning in the dead vultures, but until this year no one froze a carcass for
pathological examination.

It鈥檚 about time, say Cunningham and his colleagues, that emerging diseases in
wildlife got the same respect they do in humans. 鈥淓merging diseases, such as
AIDS and Ebola, have been recognised as a threat to humans for some time now,鈥�
says Daszak. 鈥淭he same conditions that apply to us also apply to wild
补苍颈尘补濒蝉.鈥�

The difference, of course, is that for the time being, at least, we are
unlikely to go extinct.

What could be more wholesome than feeding the birds in your garden? The
bird-loving British feed more than 15 000 tonnes of peanuts to wild birds every
year. Yet bird tables provide a mixing bowl for droppings and food, and
encourage birds to congregate in numbers, and a mix of species, that would never
occur in the wild.

Those picturesque bird tables may be behind the worsening epidemics of
Salmonella and E. coli that have killed thousands of songbirds, especially
finches, in Europe and North America in recent years, says James Kirkwood of the
Universities Federation for Animal Welfare in Potters Bar, Hertfordshire. In one
survey, Kirkwood found that people who put out more than half a litre of food a
day attracted significantly more birds and saw a far greater proportion die from
what appeared to be infectious diseases than people who put out less food.

But despite dramatic local die-offs, so far no bird species has been
threatened. However, there may be other reasons to be concerned. In Quebec, for
example, cats have caught Salmonella from sick birds, raising fears that it
could be passed on to pet owners.

The answer, says Kirkwood, is not to stop feeding the birds. 鈥淛ust do it in
moderation,鈥� he advises. And clean the feeder.