WEST PEMBROKESHIRE HIT WITH MYXA AGAIN

[ratmogit 16]

WENT OUT LAMPING NIGHT BEFORE LAST ,HARDLY ANYTHING ABOUT . THERES ONLY THREE PLACES THATS GOT RABBITS ON AFTER THE LAST RAGE OF MIXXEY THREE YEARS AGO . IN ONE NIGHT YOU WOULD BE GRATEFUL FOR TEN RUNS . THESE PLACES WE KEPT TO BRING ON DOGS BEFORE THEY WENT ON TO BIGGER QUARRY . I WISH WE'D HAMMERED THESE AREAS NOW AS THEY'LL SOON BE ROTTING ON THE GROUND. WHO ON EARTH RELEASES THIS DISEASE , THERE WASN'T ENOUGH RABBITS IN ANY OF THE PLACES TO DO ANY DAMAGE ! ANYONE KNOW OF A BRED RABBIT THATS MIXXEY PROOF????? THEY COULD LET IT GO AS MUCH AS THEY LIKED!!!!!!!!!!!!

[Ian292 0]

I've had myxi up here on all my shoots since last spring and has had a big effect.

I'm led to believe that if a rabbit can survive the virus it will become immune and pass that immunity on to its offspring.

The virus is carried by rabbit fleas or mosquitos and can live for several month in these hosts blood and is then passed to the rabbit when the flea or mossy bites.

 

Regards,

Ian.

[sniffer 167]

Last year was a b*****d for mixy the year before i never caught many with but last year was realy bad i put it down to the wet weather they spent more time in the bury's keeping dry there for spreading more hope it clears up a bit for this year.

[Guest tawny]

I've had myxi up here on all my shoots since last spring and has had a big effect.

I'm led to believe that if a rabbit can survive the virus it will become immune and pass that immunity on to its offspring.

The virus is carried by rabbit fleas or mosquitos and can live for several month in these hosts blood and is then passed to the rabbit when the flea or mossy bites.

 

Regards,

Ian.

some rabbits get over it but immunity does'ent get passed on it kills them or it dont as simple as that

[stormrider8 59]

I've had myxi up here on all my shoots since last spring and has had a big effect.

I'm led to believe that if a rabbit can survive the virus it will become immune and pass that immunity on to its offspring.

The virus is carried by rabbit fleas or mosquitos and can live for several month in these hosts blood and is then passed to the rabbit when the flea or mossy bites.

 

Regards,

Ian.

some rabbits get over it but immunity does'ent get passed on it kills them or it dont as simple as that

 

Na mate, pretty sure your not right there. I read that immunity is past on, more so for around the first year of the youngs life. Maybe wrong.. google it

[Guest john2007oliver]

I've had myxi up here on all my shoots since last spring and has had a big effect.

I'm led to believe that if a rabbit can survive the virus it will become immune and pass that immunity on to its offspring.

The virus is carried by rabbit fleas or mosquitos and can live for several month in these hosts blood and is then passed to the rabbit when the flea or mossy bites.

 

Regards,

Ian.

some rabbits get over it but immunity does'ent get passed on it kills them or it dont as simple as that

 

Na mate, pretty sure your not right there. I read that immunity is past on, more so for around the first year of the youngs life. Maybe wrong.. google it

 

 

When they first relseased it it killed 99.9% of rabbits now its kills about 40-50% suggesting immunity.

 

^^ read that somewhere

[ratmogit 16]

I've had myxi up here on all my shoots since last spring and has had a big effect.

I'm led to believe that if a rabbit can survive the virus it will become immune and pass that immunity on to its offspring.

The virus is carried by rabbit fleas or mosquitos and can live for several month in these hosts blood and is then passed to the rabbit when the flea or mossy bites.

 

Regards,

Ian.

some rabbits get over it but immunity does'ent get passed on it kills them or it dont as simple as that

 

Na mate, pretty sure your not right there. I read that immunity is past on, more so for around the first year of the youngs life. Maybe wrong.. google it

 

 

When they first relseased it it killed 99.9% of rabbits now its kills about 40-50% suggesting immunity.

 

^^ read that somewhere

Someone mentioned a strain of Brazillian rabbit that was immune.

[Guest tawny]

I've had myxi up here on all my shoots since last spring and has had a big effect.

I'm led to believe that if a rabbit can survive the virus it will become immune and pass that immunity on to its offspring.

The virus is carried by rabbit fleas or mosquitos and can live for several month in these hosts blood and is then passed to the rabbit when the flea or mossy bites.

 

Regards,

Ian.

some rabbits get over it but immunity does'ent get passed on it kills them or it dont as simple as that

 

Na mate, pretty sure your not right there. I read that immunity is past on, more so for around the first year of the youngs life. Maybe wrong.. google it

no mate you can google anything you want, but i tell you now immunity of mixi does not get passed on.

some live through it and if it does get passed on why do you still get the out breaks year after year ??????

there is no immunity only survivors

[poacher2225 2]

we only git it in them in the summer and it;s every year thay git it down hear

[stormrider8 59]

I've had myxi up here on all my shoots since last spring and has had a big effect.

I'm led to believe that if a rabbit can survive the virus it will become immune and pass that immunity on to its offspring.

The virus is carried by rabbit fleas or mosquitos and can live for several month in these hosts blood and is then passed to the rabbit when the flea or mossy bites.

 

Regards,

Ian.

some rabbits get over it but immunity does'ent get passed on it kills them or it dont as simple as that

 

Na mate, pretty sure your not right there. I read that immunity is past on, more so for around the first year of the youngs life. Maybe wrong.. google it

no mate you can google anything you want, but i tell you now immunity of mixi does not get passed on.

some live through it and if it does get passed on why do you still get the out breaks year after year ??????

there is no immunity only survivors

myxomatosis essay, then go to genetic resistance.. Does get passed on but only short term. If it didnt then surely we would have no rabbits.

[Danny123 1]

Bunnies seem to get hit by mixy around us every year, just as the weather starts to pick up like clockwork.

Pet rabbits can have a vaccine for mixy cant they?

Not saying we should try and vaccinated all the wild bunnies though .

Its sickening when you start seeing the mixy rabbits, what do people do with the mixy rabbits? I use to give them my ferrets but to be honest i havent given them a mixy rabbit for quite some time-the thought of it more than anything. :sick:

[Hywel 53]

As I've said before, all my permission has been truly hammered by myxi this season........

[hollands hope 1,024]

WENT OUT LAMPING NIGHT BEFORE LAST ,HARDLY ANYTHING ABOUT . THERES ONLY THREE PLACES THATS GOT RABBITS ON AFTER THE LAST RAGE OF MIXXEY THREE YEARS AGO . IN ONE NIGHT YOU WOULD BE GRATEFUL FOR TEN RUNS . THESE PLACES WE KEPT TO BRING ON DOGS BEFORE THEY WENT ON TO BIGGER QUARRY . I WISH WE'D HAMMERED THESE AREAS NOW AS THEY'LL SOON BE ROTTING ON THE GROUND. WHO ON EARTH RELEASES THIS DISEASE , THERE WASN'T ENOUGH RABBITS IN ANY OF THE PLACES TO DO ANY DAMAGE ! ANYONE KNOW OF A BRED RABBIT THATS MIXXEY PROOF????? THEY COULD LET IT GO AS MUCH AS THEY LIKED!!!!!!!!!!!!

yes there are mixy proof rabbits in fact, but not in england the french have them there south american cotton tails these rabbits resemble our rabbbits but in most casus they don,t dig holes but they will use them they were introduced after the native rabbit population tumbled down due to diseases (mixy) ,i think there around south eastern parts of france Edited February 6, 2008 by hollands hope

[VODAFONE 0]

see what you meen about mixy down west mate from cardiff down to the gower along the coast has been hit bad only seems to last for about 6/8 week . seen 1 or 2 young the last 2 or 3 week so any luck the rabbits will make a come back . all the best voda

[Wax jacket 0]

Here's the facts and the part your looking for is high lighted for those who can't be arsed to read it all.

 

Happy Hunting

 

Myxomatosis

 

Eradication of a Species?

 

 

 

Myxomatosis

 

Caught in the centre of a soundless field

While hot inexplicable hours go by

What trap is this? Where were its teeth concealed?

You seem to ask.

I make a sharp reply,

 

Then clean my stick. I'm glad I can't explain

Just in what jaws you were to suppurate

You may have thought things would come right again

If you could only keep quite still and wait.

 

Philip Larkin

 

1. INTRODUCTION

 

In 1898 Loeffler and Frosch demonstrated that foot-and-mouth disease infecting cattle was transmitted between animals by a particle smaller than any bacteria, for which the name 'ultramicroscopic filterable viruses', shortened to viruses, was coined. Since the discovery of their existence and the invention of the electron microscope enabling the structure to be seen for the first time in 1959, more and more diseases have been shown to be caused by viruses, and their beneficial effects, unlike bacteria which have some use as gut flora, have been seen to be negligible. Indeed because viruses use the reproductive machinery of the cells they infect there is at present no 'wonder drug' equivalent of penicillin.

 

Since the arrival of techniques allowing gene manipulation, virologists and geneticists have conceived of using the infectious nature of viruses to transmit inoculation, repair gene damage and familial genetic abnormalities. However there has been much press about the ethics of such gene and virus manipulation, demonstrated by the popular myth that HIV is a man-made virus that was originally intended to strengthen the immune system, instead of which it destroys it.

 

Viruses have already been used to 'beneficial' effect, but not in the area of medicine rather in the area of pest control. It is strange that in a world with countless species dying out it would be necessary to use a disease and its infectious nature to attempt to eliminate a species, however this is the case with rabbits and myxomatosis.

 

2. MYXOMATOSIS

 

Myxomatosis is a highly lethal disease affecting rabbits, caused by the myxoma virus, a member of the large Poxvirus group about 280nm in length. The disease was uncovered in South America in 1896 where it had devastating effect on the rabbit population there. It was found that it was mainly the European rabbit (Oryctolagus cuniculus), imported early that century, that contracted the disease. Later examination showed that the myxoma virus was endemic to the local wild rabbit population (Sylvilagus brasiliensis) which was mostly resistant to the disease and acted at the natural reservoir.

 

 

 

Figure 1- The myxoma virus as seen using the electron microscope.

 

The disease was originally seen to be highly lethal with observed mortality rates of greater than 99%.

 

2.1 PATHOGENESIS

 

In Sylvilagus myxoma viruses produce localised benign fibromas which provide a source of infection for transmission of the virus by arthropod vectors. Following inoculation of Oryctolagus cuniculus with virulent myxoma virus there is a well-defined sequence of appearance of the virus in different organs. It is only found in the inoculation site on the first day, by the second day it is also found in lymph nodes, by the third day in the blood, spleen and liver. On the fourth day the virus can be seen in all tissues. Up until this point the only physical sign of infection is a lump in the skin at the inoculation point, however on the fifth day conjunctival swelling is apparent. Signs of infection are generalised on the sixth day by swellings on the skin and muco-cutaneous junctions, the eyelids, nose and anogenital region. Symptomatology reaches a peak on the eight and ninth days and death usually occurs on the tenth.

 

The cause of death is obscure because although the virus multiples to reach high concentrations in skin there is little involvement with the adrenals, kidneys, spleen, liver, lung and brain. The swellings cannot really be called tumours as they are due to a large extent to an accumulation of mucinous material as well as some degree of cellular proliferation in the dermis. There is also a proliferation of endothelial cells of the small capillaries and venules, and there is some thought that this may be a causative factor in the death of the host.

 

2.2 TRANSMISSION

 

The mechanisms of transmission of myxomatosis are of extreme importance since they demonstrate why it is epidemic or endemic in some countries and has localised outbreaks in others. The reasons for differences is due to the effects of environment on transmission, particularly on the availability of vectors for the disease.

 

2.2.1 Contact Infection

 

Myxomatosis is accompanied by a profuse ocular discharge as well as a discharge from the skin lesions, both of which are rich in virus. These discharges allow transmission of the virus by direct contact with scratches on the skin or superficial mucous membranes as occurs during social or sexual interaction.

 

Transmission via the respiratory tract is also possible if rare. Infection does not occur by feeding and therefore there no faeco-oral transmission.

 

This method of infection is of primary importance in the warren environment of O. cuniculus where there are many rabbits in a small area.

 

2.2.2 Arthropod Vectors

 

Insect vectors form a very important method of transmission. A wide number of mosquitoes, fleas, ticks, mites and lice have been shown to be vectors. The insects can feed on the blood of the infected rabbit or more easily on the exposed area of skin lesions. Further more, unlike infected rabbits which die after about ten days after which the possibility of contact infection is reduced, it has been shown that mosquitoes can carry a virus capable of re-infecting rabbits for up to 6 weeks. Rabbit fleas, particularly Spilopsyllus cuniculi, can act a reservoir of infection for several months after rabbits have deserted a burrow.

 

Taking into account the range of mosquitoes this allows transmission of the myxoma virus over greater areas than are usually travelled by the rabbits alone. This allows the spread of the virus to take place between colonies of rabbits, and in the case of the fleas, allows rabbits from a different colony to become infected be entering a warren where all the occupants have been killed by myxomatosis some months previously.

 

2.3 CHANGES IN VIRULENCE

 

The virus exists in two serologically slightly different forms, the South American form and the Californian form. Both forms have for their animal reservoirs the local indigenous wild rabbit, S. brasiliensis and S. bachmani respectively, and the relevant myxomatosis was only uncovered when susceptible O. cuniculus was imported to both countries. The two forms also result in an almost identical pathogenesis.

 

The virus was originally found to result in 99% mortality, its high virulence due to the ease of transmission by arthropod vectors. However in areas where the availability of such vectors was scarce this highly virulent form acted to stop its own transmission by killing its host before it came in contact with any other possible hosts. This stringent selection provided an environment favouring a less lethal disease which would enable its host to survive for weeks instead of days, an attenuated strain of the virus. Generally such a virus is more likely to succeed since it less likely to kill its host so quickly, resulting in an increased likelihood of recovery. The naturally occurring strains of virus in Australia and Great Britain demonstrate that natural selection produces a virus less rapidly lethal that results in adequate susceptible population and that can survive through periods of low vector density i.e. overwinter.

 

However it is important to note that localised highly lethal outbreaks do still occur either due to mutant forms of the myxoma virus or to genetic resistance of the rabbit, which also is not conductive to successful overwintering.

 

2.4 GENETIC RESISTANCE

 

The majority of rabbits which recover from myxomatosis are immune to re-infection for the rest of their lives. At it is known that immune mothers pass passive immunity of short duration to their young. However due to the short lifetimes of rabbits, often little more than a year in the wild, this has little effect in practice. Of more importance was the in-built genetic immunity of certain rabbits in the population. Survival of these rabbits combined with their high reproduction rate and the death of the competition meant that a population of genetically more resistant rabbits was quickly built up. When combined with viral attenuation and the appearance of strains causing the survival of 10% or more of the genetically more resistant rabbits, this explains the rapid rise of a decimated rabbit population. [/color][/color]

3. RABBITS AS PESTS

 

Up until recently rabbits have been extensively hunted for both their fur and their meat. This activity as well as the presence of other predators such as foxes and feral cats has acted in the past to keep the down the population of rabbits, and man is still the main predator in South American countries. However in other countries the man has had a less and less important role as a predator and has in fact helped to reduce the population of the rabbitÕs natural predators through habitat destruction, urbanisation and cultivation. In counteraction to these effects rabbit habitats have also been destroyed as have rabbit colonies, which interfere with farming activities. These changes have resulted in a precarious balance of the rabbit population in many areas where any factors enhancing rabbit survival can result in a huge population boom.

 

Rabbits compete with livestock and native herbivores for food. They are highly selective grazers that concentrate on the most nutritious plants, including seedlings, and eat them to below ground level. This can change the species composition of pastures and reduce productivity. Indeed they act as competition for hares and other herbivores and grazing animals reducing the agricultural output of the land.

 

3.1 RABBIT LIFE-CYCLE AND REPRODUCTION

 

The potential life span of the rabbit is ten years, but in nature it is actually quite short, with the majority of rabbits living for only about a year. Rabbits have a long breeding season from autumn until the middle of the summer, during which a doe produces about 4 litters with an average litter size of 6 kittens resulting in a maximum of about 24 young per season. Since a new-born doe can reach sexual maturity and be ready to breed at six to ten months of age, if it is born early in the season it can have its first litter by the end. Male rabbits take longer to attain sexual maturity, about nine months.

 

This demonstrates the highly reproductive nature of the rabbit. Even with pre-adult death there can be expected to be an eight-fold increase in population in a year, indicating that it would take rabbits twelve months to recover from a disease causing % mortality.

 

Maximum population is limited by the food supply, if there is too little, firstly does produce fewer young, and secondly, there is a reduction in numbers due to starvation.

 

3.2 Why Oryctolagus cuniculus in particular

 

O. cuniculus has been spread round the world by man, mainly because of their value as a popular pet rabbit in the late nineteenth century, as well as for hunting purposes. The process of their domestication was started by the Romans in the first century BC when a writer suggested the idea of leporium or rabbit gardens, however it was found early this century that they can readily adapt to many different environments in the wild. This adaptation is enhanced by O. cuniculus being the only rabbit to build warrens, a habitat which provides much protection against extreme environments, as well as providing a safe location from predators and in which to breed.

 

The genetic variation of O. cuniculus from other species which enables the myxoma virus to have such an effect is unknown. However the general differences between it and other species are quite marked and the fact that the myxoma virus originated in these other species, combined with their genetic resistance, indicates much.

 

4. MXYOMATOSIS FOR PEST CONTROL

 

In the opening of the twentieth century tests confirmed that myxomatosis only infected the European rabbit, O. cuniculus in any number, the population of which had already reach levels indicating their existence as a major pest in many countries. This information combined with the 99% fatality of the South American strain of the myxoma virus lead to the suggestion of using the myxoma virus and its disease myxomatosis for control of the rabbit population in Australia by Dr H. Aragao in 1919.

 

It is important to realise that by no means was everybody in favour of releasing myxomatosis into the rabbit population. The main voices against such a move were those who believed it was cruel to the rabbits, those who depended on rabbit fur and meat for their livelihood, a number of people in the scientific community who thought the epidemic would get out of control, those who owned and breed domesticated rabbits in captivity, and those who thought that man might be able to develop myxomatosis.

 

4.1 AUSTRALIA

 

The European wild rabbit O. cuniculus was introduced into Australia by Thomas Austin of Barwon Park, Winchelsea, Victoria. In 1759 Austin imported 24 rabbits from England where it was also an exotic animal, having been introduced from Spain during the Norman conquests. He released the rabbits on his property for sport hunting.

 

The rabbit spread so rapidly that it reached Queensland - New South Wales border by 1886, giving it a rate of advance of about 110 kilometres each year. It now occurs over half of Australia. The northern limit of its spread is generally regarded as the Tropic of Capricorn but it may ebb and flow further north depending on seasonal conditions. Almost all of the rabbits in Australia are descendants of the 24 original rabbits and are genetically homogenous, this fact beyond all others might result in the spectacular effect the introduction of the virus had on the rabbit population as a whole.

 

The lack of any herbivores capable of competing with the rabbit resulted in the decline of many species of native wildlife by competing with them for food or burrows. This applies particularly to the small ground-dwelling mammals of the arid lands. This situation was made worse by the lack of a large population of predators able to deal with this new prey.

 

However to the human population of Australia all of this was irrelevant next to the economical loss caused by rabbits grazing on pasture used by sheep and other herbivores reducing the number of sheep capable of grazing per acre and the loss of wool and revenue thus caused. After myxomatosis was released in Australia the wool clip reached a record figure in 1953 and it was estimated that a 24 million pound fraction of the gained revenue was due to the decreased rabbit population

 

4.1.1 Release of the myxoma virus

 

It was not until 1950 that myxomatosis was successfully released among Australian rabbits. This occurred after much debate, experimentation of what the effects of such a drastic move would be, and political wrangling.

 

After a slow start the initial results fulfilled all expectation with a mortality of over 90%. The virus spread most quickly during the summer when the mosquito population was at its maximum, resulting in very successful transmission of the virus between separate colonies, due to their high mobility. The exact number of rabbits killed is unknown but the rabbit population was decimated, environmental signs of the reduced population could be easily seen by visible signs of revegetation.

 

The initial epidemic continued after the next few years, spreading and remaining highly virulent spreading rapidly in the summer due to arthropod vectors. This was helped by the continued inoculation by farmers of the wild rabbit population every summer and spring. However the capacity for the virus to survive over the winter favoured a less lethal disease, and within four years these attenuated forms of the virus became the dominant strains allowing the rabbit population once more to increase, although the virus remained endemic. This combined with genetic resistance, as mentioned early, resulted in a much reduced mortality, even though sporadic outbreaks of the original virulent virus sometimes occurred.

 

Today myxomatosis in Australia kills only about 40% of infected rabbits, but rabbit numbers are much lower than they would be in the absence of this disease. However they still are a major pest in Australia and other methods for their eradication are being investigated.

 

4.2 EUROPE

 

The rabbit population had similar effects on the environment as in Australia, particularly causing much damage to the national forests of France by eating seedlings and damaging young saplings. In 1952 Dr P.F. Armand Delille inoculated two wild rabbits at Maillebois in northern France. From these two rabbits myxomatosis spread all round Europe, including Britain and Ireland, and as far a field as North Africa. Once more the main means of transmission of the virus was the mosquito as well as the rabbit flea. The disease had the same result as in Australia, the majority of the wild rabbit population of Europe was wiped out, including an estimated 90% of French and British rabbits, however about 40% of domestic rabbits produced for consumption in 1953 and 1954 were also killed.

 

Attenuation and genetic resistance has occurred in Europe, however unlike in Australia where the highly attenuated strains have replaced the virulent original, in Europe the two coexist. This is due to a different vector situation where the rabbit flea is believed to be the main vector, especially in Britain where the variation in number of cases of myxomatosis does not vary greatly throughout the year.

 

Myxomatosis is now an enzootic disease in the wild rabbits of Europe, with occasional summer epizootics, particularly in France.

 

5. A NEW SOLUTION REQUIRED

 

While the rabbit population in Australia, as well as in some other countries, has not returned to is pre-myxomatosis numbers, there are still large enough numbers to once again consider the rabbit to be a pest. At present the damage caused by rabbits, the cost of control, and production losses, is estimated at more than 115 million dollars per annum just to the Australian wool industry. This figure does not account for any of the serious, long-term environmental damage caused by rabbits.

 

Research continues into diseases that may be effective in reducing rabbit numbers, as well as being socially acceptable, in an age where animal welfare considerations are often as important as controlling environmental damage. Research is being undertaken into the possibility of altering the myxoma virus so that it produces infertility in infected rabbits but it is too early to know whether it might be effective. Such a virus would work by persuading the female to regard the male sperm as an antigen and to produce anitbodies to it.

 

5.1 VHD/RCD

 

The Australian government is at the moment sponsoring tests of the rabbit calicivirus, which causes rabbit calicivirus disease (RCD), or viral haemorrhagic disease (VHD) as it is also called, on Wardang Island as a method for rabbit control. It is a naturally occurring virus, prevalent in the northern hemisphere, that was first noted in China in 1984 and Europe in 1986. The virus only infects O. cuniculus and causes death in greater than % of the rabbits 30 to 40 hours after being infected.

 

According to the Australian government trials have been very successful so far. However uncontrolled spread from the island to the mainland, up until now thought highly improbable, occurred at the end of last year with a couple of localised, and controlled, outbreaks of RCD on the mainland. The transmitting vector was thought to be either a bird or insect, the exact mechanism of transmission is unknown. The continued infectiousness of RCD is thought be good with the rabbits generating little genetic resistance over a test period of ten years. However if the rabbit calicivirus is used in practice, one expects that the same attenuation of the highly virulent form of the virus will occur, as occurred with the myxoma virus, resulting in reduced mortality with time.

 

Whether or not RCD will actually be used to control the rabbit population is unknown. There are no definite conclusions and while scientific information indicates a high probability of success, the gauntlet of politics still needs to be run.

 

6. SUMMARY

 

While there has been some success with attempts at 'species eradication' in various countries using myxomatosis, the virus and host have eventually, through the negative selection of highly virulent forms, reach an equilibrium where mortality is not extremely high and the population of the host can rebuild itself.

 

With the advent of genetic engineering and the almost world-wide availability of the necessary equipment, the worry is that care will not be taken in using it. There are many ethical and safety factors to be considered before using this new technology especially in the area of genetic manipulation of viruses. Until the exact mechanism of mutation of viruses in known along with why viruses can sometimes suddenly infect across species barriers, it would be inadvisable to release such a virus into the environment. An example of a virus involved in cross species transmission resulting in a disease condition in both is a morbillivirus infection causing severe respiratory illness in both horses and humans uncovered at a stable in Queensland in September of 1994.

 

A further danger is the intended manipulation of human viruses to create more virulent forms as a biological weapon or to sterilise the population. As one doomsayer suggests:-

 

Because sterilisation is a far more humane form of genocide than gas chambers, some of the ecologists or green activists might have little objection to releasing engineered viruses to reduce human populations to their 'ideal' level. The humane nature of a sterility virus also makes it far more effective than traditional forms of genocide, which involve visible, violent death and thus stir the passions of people into resistance. A sterility virus not only blocks human reproduction, it also makes an end run around the genetically evolved emotions which motivate such reproduction. The only defence against such a virus is a rational assessment of its consequences, and the ability to motivate extreme, prolonged defence based on that emotionally neutral knowledge.

 

As for the eradication of a species, poisons are more effective, there will always been some animals infected who through luck or a correctly genetically adapted immune system will not die from the virus. However unlike rabbits humans do not increase their population eight fold a year, and humans take much longer to reach sexual maturity. The day a pandemic human myxomatosis appears the majority of a species may be eradicated.

 

 

7. REFERENCES

 

1. F. Fenner & F.M. Ratcliffe - Myxomatosis

Cambridge University Press (1965)

 

2. F. Fenner et al. - The Biology of Animal Viruses, 2nd Edition

Academic Press (1974)

 

3. Peter Radetsky

Invisible Invaders - viruses and the scientists who pursue them

Little, Brown & Company (1991)

 

4. Philip Larkin - Myxomatosis

 

5. Nick Szabo - Life in the Era of Humane Genocide (1993)

 

6. Keith Murray et al. - A Novel Morbillivirus Pneumonia of Horses and its Transmission to Humans

J. of Emerging Infectious Diseases; Vol. 1, No. 1 (Jan-Mar 1995)

 

7. E. Rolls - They all ran wild

Angus & Robertson, Sydney (1983)

 

8. G. Wilson et al.

Pest animals in Australia: a survey of introduced wild mammals Kangaroo Press (1992)

 

9. Various short texts by the CSIRO Australian Animal Health Laboratory on RCD

Edited March 13, 2008 by Wax jacket