Weapions of mass destruction (full doc) (348 hits)
Category: GeneralRating: -2 on 9 reviews (Rate this item) (V)
Submitted by <evil-science.at.spamex.com> (View user info) at 2009-01-20 03:28:43 EST
Beginners guide to the manufacture of weapons of mass destruction
Compiled by Mike-H a.k.a. (Michael Webber)
The purpose of this guide is as a starting of point for anyone interested in research into the construction of weapons of mass destruction chemical biological or nuclear .I am not going to get into the ethics of such research or encourage the use of such weapons what you choose to do with this information is entirely up to you.
Some of the information contained in this guide is stolen from other sources I make no apology for this. Where possible I will give credit to the original source of my information and provide a list of web links useful for further research at the end.
Part 1 chemical weapons
Chemical warfare (CW) copied from wikipedia http://en.wikipedia.org/wiki/Chemical_weapons
(QUOTE) CW involves using the toxic properties of chemical substances as chemical weapons to kill, injure, or incapacitate an enemy.
Chemical warfare is different from the use of conventional weapons or nuclear weapons because the destructive effects of chemical weapons are not primarily due to any explosive force. The offensive use of living organisms (such as anthrax) is considered biological warfare rather than chemical warfare; however, the use of non living toxic products produced by living organisms (e.g. toxins such as botulism toxin, Rican, and saxitoxin) is considered chemical warfare under the provisions of the Chemical Weapons Convention. Under this Convention, any toxic chemical, regardless of its origin, is considered a chemical weapon unless it is used for purposes that are not prohibited (an important legal definition known as the General Purpose Criterion).[1]
About 70 different chemicals have been used or stockpiled as chemical warfare agents during the 20th century. Chemical weapons are classified as weapons of mass destruction by the United Nations, and their production and stockpiling was outlawed by the Chemical Weapons Convention of 1993. Under the Convention, chemicals that are toxic enough to be used as chemical weapons, or that may be used to manufacture such chemicals, are divided into three groups according to their purpose and treatment:
* Schedule 1 - Have few, if any, legitimate uses. These may only be produced or used for research, medical, pharmaceutical or protective purposes (i.e. testing of chemical weapons sensors and protective clothing). Examples include nerve agents, Rican, lewisite and mustard gas. Any production over 100 g must be notified to the OPCW and a country can have a stockpile of no more than one tone of these chemicals.
* Schedule 2 - Have no large-scale industrial uses, but may have legitimate small-scale uses. Examples include dimethyl methylphosphonate, a precursor to saran but which is also used as a flame regardant and Thiodiglycol which is a precursor chemical used in the manufacture of mustard gas but is also widely used as a solvent in inks.
* Schedule 3 - Have legitimate large-scale industrial uses. Examples include phosgene and chloropicrin. Both have been used as chemical weapons but phosgene is an important precursor in the manufacture of plastics and chloropicrin is used as a fumigant. Any plant producing more than 30 tones per year must be notified to, and can be inspected by, the OPCW. (END QUOTE)
Organic Toxins
Plant based
Copied from
Http://webecoist.com/2008/09/16/16-most-unassuming-yet-lethal-killer-plants/
See original source for photos.
(QUOTE) Most plants contain some level of toxins (like alkaloids) for defense. After all, they're plants. They can't go anywhere. Through millennia of trial and error, both animals and human beings have figured out which plants are safe, which are lethal, and which are somewhere in between. For example, did you know that many grain-bearing plants contain a toxin known as lectins? And that the African staple, cassava, must be thoroughly boiled and soaked to separate it from its poisonous compound, cyanide? Even the humble lima bean has been bred to contain less cyanide. Cherries, potatoes, peaches and apple seeds are all toxic - eat enough of the latter, in fact, and it will prove fatal. Fortunately, artificial selection and cooking methods have all but eliminated the threat of toxins in everyday foods. But you may be surprised to find out the incredibly lethal plants often hanging around the neighborhood park - or gracing your tabletop in the form of a centerpiece.
Castor Bean
Castor oil - for anyone unlucky enough to have been force spoon-fed this healthy yet disgusting fluid as a child, you may be surprised to learn that an ingredient in the castor bean just happens to be the deadliest plant poison on earth. Literally. Just one tiny castor bean is enough to kill an adult within a few minutes. Castor oil is made safe (but not palatable) with the removable of the lethal compound known as Rican. Amazingly, castor bean plants are grown for decorative purpose all over the place, particularly in California.
Rosary Pea
As if a deadly legume weren't bad enough, the pulses aren't so benign, either. The rosary pea may sound sweet and downright pious, but it's actually one of the most dangerous plants on earth. Its seeds contain a particular lectin known as abrin; if chewed and swallowed, death will follow shortly. The seeds are easily identified with their distinctive bright red jacket and single black dot (almost like a reverse Black Widow spider). Abrin, which does its damage by inactivating ribosome's, is one of the most fatal toxins on earth. After the vomiting, fever, nausea, drooling and G.I. dysfunction but before the bizarre hyper excitability, edema and fatally convulsive seizures, renal tubular degeneration, bladder and retinal hemorrhage and widespread internal lesions typically develop.
Monkshood
Another unassuming plant - until you learn that the nickname for monkshood is actually "wolfsbane". That's owing to its once common use by farmers as a very effective wolf extermination tool. (Not to be left out, fowl are also fatally affected by the related hensbane.) The monkshood has the distinction of evidently being the bane of many creatures: its nicknames include womensbane and leopard's bane, though it is also known as blue rocket and devil's helmet. It is technically part of the aconitum genus, of which there are more than 250 species. The wolfsbane used to be a popular werewolf detection tool, by the way. (Status was determined by holding the flower near the alleged's chin; a yellow-tinged shadow on the skin was thought to be confirmation.)
Busman's poison
The aptly-named Bushman's poison has famously been used by the Khoisan of South Africa to poison the tips of their arrows. Though the plant produces pleasantly scented flowers and a tasty plum-like berry, the milky sap can be fatal. The leaves, however, have medicinal properties. Bushman's poison is also known as the wintersweet.
Angel's trumpet
What could be sweeter than the sound of an angel's trumpet? Perhaps the moaning agony of a trip that won't end. Related to petunias, tomatoes and potatoes, the angel's trumpet (datura stramonium) is a highly effective hallucinogen, but should not be consumed for recreational purposes as it can also be lethal. According to wikipedia: "The active ingredients are atropine, hyoscyamine and scopolamine which are classified as deliriants, or anticholinergics. Due to the elevated risk of overdose in uninformed users, many hospitalizations, and some deaths, are reported from recreational use." This common plant also goes by many other names, including jimson weed, stink weed, loco weed, and devil's snare. One 18-year-old who was house-sitting alone for his uncle recounts how he decided to prepare some angel's trumpet tea in curiosity and almost died (a friend burst in on him convulsing on the bathroom floor and the authorities assumed he was on an acid trip).
Water hemlock
The poison hemlock famously drunk by Socrates is deadly, but the water hemlock is just as fatal. According to the USDA, water hemlock or poison parsnip is "the most violently toxic plant in North America". The flowers and stems are safe, but the stalky roots contain chambers that are full of a deadly sap containing the convulsant cicutoxin. Grand mal seizures are followed by a quick death if even a tiny amount is consumed.
English Yew
The English Yew, or taxus baccata ("taxus" meaning toxin), is one of the deadliest trees on the planet. The evergreen has a majestic and lush appearance and is fairly common in forests of Europe. The yew is considered by scientists to be an odd and primitive conifer along with the monkey puzzle tree of Chile and Gingko biloba tree of Asia. The yew has a rather sad history. All parts - save for the flesh of the berries - are extremely poisonous. Because the toxin causes convulsions and paralysis, it was once used as an abortifacient. Apothecaries would dry and powder the leaves and stems and give desperate women minute amounts in the days before birth control was available. Unfortunately, death would often result. The yew has been quite popular throughout history for a number of medicinal purposes at extremely dilute levels, but it is deemed too dangerous in modern medical practice to be of use. The yew's primary toxin is taxine, a cardiac depressant. The yew acts rapidly and there is no antidote.
Snakeroot
Snakeroot is most dangerous for livestock such as cattle and sheep. When cows consume the attractive fluffy white blooms and stems of the snakeroot, their milk and bones become saturated with the toxin tremetol and humans who consume these contaminated animal products will develop milk sickness (tremetol poisoning). In fact, milk sickness is what killed Abraham Lincoln's mother, Nancy Hanks.
Strychnine tree
Queen Cleopatra famously forced servants to commit suicide by means of a strychnine tree's fruit seeds, which contain lethal levels of strychnine and brucine, in order to determine if it would be the best means for her own suicide. Upon seeing their agony (which included painful vomiting, facial contortions and convulsions) she opted for the apparently less horrific choice of the asp. (The asp was actually an ancient term for any number of poisonous snakes, but experts think it was probably the cobra that Cleopatra chose to end her life.)
Moonseed
A otherworldly name and a plant with often fatal effects. The seeds of this Eastern North American drupe (stone fruit) are extremely toxic to humans, although birds can eat them. Moonseeds first cause paralysis but are fatal in larger doses and/or if treatment is not sought immediately.
Daphne
This plant, also called the spurge laurel, is a favorite ornamental shrub in Europe. This drupe-producing evergreen with waxy, attractive foliage and gorgeously fragrant blooms is also highly toxic. Consumption of the leaves or red or yellow fruits will first cause nausea and violent vomiting, followed by internal bleeding, coma and death. The daphne plant is rich in the toxin mezerein.
Narcissus
Narcissists are toxic enough when they come in human form, but the plant for which they are named, also called the daffodil, is highly poisonous. Poet's narcissus is more toxic than daffodil, but in both cases it is the bulbs, not the flower or stems, that cause illness. One famous fatal case in Toulouse in the early 1900s occurred when the bulbs were mistaken for onions and consumed. According to Botanical.com, "Socrates called this plant the 'Chaplet of the infernal Gods,' because of its narcotic effects. An extract of the bulbs, when applied to open wounds, has produced staggering, numbness of the whole nervous system and paralysis of the heart." Yet, there are medicinal properties, and some cultures even believe they can cure baldness and serve as a potent aphrodisiac. (Do not try at home.)
Oleander
The oleander is the most deadly plant in the world. It is also tremendously popular as a decorative shrub. Just one leaf can kill an adult, and fatal poisonings have resulted from minimal exposure to the twigs, blooms and berries. The plant contains numerous toxins, including nerioside, oleandroside, saponins, and cardiac glycosides. Though native to parts of the Mediterranean and Asia, it is now widely cultivated throughout the world. Fatalities among horses and other livestock are common. Once ingested, oleander goes to work simultaneously on the nervous system, the cardiovascular system, and the digestive tract.
Rhododendron
The toxic rhododendron, a stalky tree-like evergreen shrub with large, brilliant blooms, is famously seen throughout much of the Pacific Northwest and is the state flower of Washington. Its relative, the popular garden shrub azalea, is also poisonous. Both plants contain andromedatoxin, which can cause severe pain, lethargy, depression, vomiting and nausea, progressive paralysis, coma and eventual death. All parts are deadly.
Choke cherry
Chokecherry, or wild cherry, is a North American plant that is known for its large sprays of tiny white flowers. The cherries are small and not eaten. The plant's woody stalks and leaves are full of hydrocyanic acid, which is fatal if consumed. The poison affects the respiratory system, and rapid breathing, choking and asphyxiation result.
Nightshade
Also known as the devil's cherry, black cherry, great morel and belladonna, the nightshade is toxic from tip to top. Containing atropine, a deadly alkaloid, those who ingest even a small amount of the plant will soon notice they have lost their voice. Respiratory trouble and convulsions follow. The plant is problematic because its cherries are so sweet and children are frequently attracted to the wild fruit. Strangely, horses, birds, sheep, goats and pigs seem to be immune to the effects of nightshade. Nightshade poisoning is treatable with an emetic if treatment is sought swiftly. Plutarch spoke of armies being wiped out by nightshade, and legend has it that Macbeth's soldiers poisoned the invading Danes with wine made from the sweet fruit.
There are many, many more toxic plants, but these plants were chosen for inclusion in this post due to their incredible characteristics.
Sources: whmentors.org, Live Science, How Stuff Works, Wikipedia ( END QUOTE)
Most of these plants have a very unpleasant and often bitter taste making it unlikely they will be consumed unknowingly in the quantity's necessary to cause death how ever the alkalis can be extracted using the following method
EXTRACTION:
The method I use is a general one - I copied it from one
used by some scientists to extract mescaline from peyote, but I
have since seen close variations used on many plants.
This procedure is followed, whenever a plant is studied for its
alkaloids.
A few ingredients and bits of equipment are necessary.
I am a chemist, and have my own chemistry set. I have considered manufacture,
but I find that there are enough interesting things to do just
extracting natural compounds, which is much easier, indeed, possible
in the home.
You will need:
A few flasks, glass containers, etc. of suitable sizes, depending on how
large a volume you are playing with.
A separating funnel is almost essential - this could be tricky to get without
a little effort. If you don't know, it is an inverted conical flask with a
hole at the top to pour stuff in , and a tap at the bottom to let the stuff
out accurately . It is used for separating immiscible layers.
A vacuum filtration apparatus would be very useful; I did have a bodgy one
rigged up myself, but it was always difficult to use. Some kind of still,
though, is pretty important to have, although conceivably for a once off
you could get by without it, if you don't mind breathing in a lot of solvent.
As far as still goes it is to recover solvent, and leave goodness as a
residue at the bottom. I use a bit of quickfit I nicked: a round bottom
flask, short column, thermometer on top, and a small condenser... takes
for ever, but don't expect to follow this procedure in anything under a
day.
Other bits and pieces:
A filter of some sort is a necessity; preferably a good one, with a vacuum
pump if you are filtering gluggy stuff (cactus is the worst, sticky goo,
e.g., other things like seeds and bark are better). People have been
known to use such devices as coffee filters, T-shirts, tins with holes
in the bottom (as a filter press) and so on. Whatever you can scrounge.
A lab buchner funnel, sidearm flask, and venturi pump are ideal.
All this stuff is standard in any chemical lab, regardless of discipline.
Chemicals necessary:
The paydirt (obviously)
Some solvents: methanol (lots), and a non polar solvent. Some people use
ether - this is dangerous and doesn't dissolve everything. Your best bet
is probably something chlorinated - I use dichloromethane, although
chloroform will do (don't breath too much - it is fun at first, but ends
up making you feel ill). Dry-cleaning fluid... petrol.... I don't know
what you have access to.
Dichloromethane is good because it is nontoxic, volatile, and a good
solvent. It has a major drawback: separation is often very difficult
once you have placed your gluggy plant muck in there. The shot is to
use large quantities of everything, and be patient.
You will also need an acid (Hydrogen chloride is good)
and a base/alkali (Sodium hydroxide is good - that way, if you stuff up,
you end up synthesizing salt instead of something nasty.)
Also useful: acid/base indicator paper, boiling chips (porcelain grains)
and activated charcoal - see local chemist.
The idea is this:
Most fun compounds (the only exception is maybe THC, and alcohol if you count
that) are basic - they contain nitrogen.
So: in general, if you react them with hydrochloric acid, the form a water
soluble chloride. If you react them with dilute base in the aqueous phase,
they go back to being a base, which is insoluble in water, but soluble in
organic non-polar solvents (like CH2Cl2). So, the theory is, that only
a base will go from water to solvent and back to water etc. when changed
from acidic to basic and back to acidic. This gives you a way of removing
all the other crap which is not alkaloid from a sample. That is the theory.
When I do this, if I can get down to some brown or green sludge that I can
throw down or smoke, I am happy with a good days work. Ideally, you should
end up with lovely white crystals, but I think that would require a lot
of time and effort, and indeed a considerable loss of product in the process.
Procedure:
Get your stuff.
Dry it as much as possible - this makes life easier later on. You will never
get all the water out, but too bad.
Chop it up as fine as possible: a blender comes in handy.
You may wish to chop then dry. A word of caution : try to avoid exposing
your stuff to excessive heat. I dry in low heat oven. Heat and air destroy
good compounds from upwards of 100 degs C. All this bit will depend on
exactly what you are extracting.
Once it is finely divided - powdered if possible, put it in a big container,
and cover it with methanol.
Alternatives to methanol here are ethanol (not as good) and acetone (good
solvent - rips the crap out of anything, but is more reactive - can react
with your actives).
Now, depending on what your stuff is, you have to let the methanol have time
to remove it all. This is best done by leaving in a quiet warm place for
a few days, even up to a week, and shaking it occasionally so it is mixed.
Some papers recommend solvent extraction (soxhlet apparatus) and refluxing
at the boiling point of the methanol (80 degs or so - I can't remember).
I usually just rely on time to get the good stuff out.
When you are ready (early in the morning), filter the muck, to give you
methanol+dissolved brown gunk, and a residue soaked with methanol.
The residue still contains a lot of good stuff, so soak again for an hour,
and repeat, and do a third time if you are feeling generous (3 is the
magic number in extraction work).
When you are done, there is another thing you can do finally, if desired:
depending on what your stuff is, mix it up with dilute hydrochloric acid,
1M is appropriate. let stand for an hour, then filter (this may be very
difficult) That will get the last of the alkaloids out of the substrate.
You now have a methanol-plant stuff mixture, and a dilute HCL-plant stuff
mixture, if you bothered to do that part.
Evaporate the methanol, to leave a small amount of goo. This will contain
water, a bit of methanol, and all kinds of resins and muck, and if you
are lucky, the alkaloids.
If a very quick and crude extraction was all that was desired, then after
stripping the last of the methanol with vacuum if possible, this residue
could be smoked eaten or what have you. I leave that to your discretion.
However, if a cleaner product is desired, the double layer extraction
will need to be performed.
Combine the evaporated methanol gunge with the hydrochloric acid filtrate
if you have any. If you don't then mix the methanol stuff with an excess
of dilute (1M) HCl. Feel free to filter again at this point. Anything of
marginal solubility here is no good to you. Get the stuff as clean as
possible. Boiling with activated charcoal is another useful trick for
removing gunge. Just boil it up, and filter off the charcoal for a
cleaner brew.
You should now have an acid aqueous solution of alkaloids and water
soluble from the plant.
Take your acidic solution, and bassify. This is done by mixing in dilute
sodium hydroxide (I use up to 5M to save on total volume. Be careful with
cone NaOH - apart from eating skin, it eats alkaloids) As you mix in the
NaOH, you will see swirls of white precipitate form and redissolve.
Continue until the white swirls stay, and until the solution is quite
cloudy. Indicator paper is necessary to see that the solution is basic.
If you can't get indicator paper, you can make an indicator by boiling
up some purple flowers. The dyes in most flowers go bright red in acid,
and green in strong alkali. Just a drop of dye and a drop of mixture
should tell you what is acid or base.
The white precipitate is the alkaloids. The more the better.
Next, add equal volume of non-polar solvent (dichloromethane) to the mix.
Place in separating funnel, and shake. Separate. This may be very difficult
or slow. Adding more solvent, more basic water, etc. may help. Adding lots
of salt to the water layer will help break an emulsion. Ideally you want it
do this step 3 times - to extract as much as possible from the water layer
into the organic. I find this part very difficult, and you have to accept
that you will lose quite a lot of material here. It is, however probably
easier with some plants that others: cactus is very difficult, barks and
seeds would be easier. Use plenty of salt, and agitate to separate.
When you have finished extraction, chuck the basic water layer.
The solvent layer is kept, and can be back washed with salty water for a
cleaner mixture.
The solvent can now be dried, (using salt or some dry powder, the filtered)
(I don't usually bother with this - the old hairdryer at the end can
remove some last solvent and water) then strip the solvent in a vacuum
to get your final product - some kind of syrup could be expected.
This is super concentrated, but may only be half the strength of the
original. e.g. put in enough for 10 doses of morning glory seeds, get
back 5 doses or more of concentrated alkaloids.
If it is desired to take the process still further, you can do the obvious
thing - mix your solvent layer with dilute acid again and extract back into
water. Acid layer could be evaporated under vacuum to give salts of
alkaloids. Alternatively, if the organic layer were scrupulously dry,
bases could be salted out with some organic acid - a tartrate, oxalate
could be formed. I have never bothered with such things - you would need
a lot of pure extract to be bothered.
The acid-base extraction process can be continued as many times as is
desired.
If a truly pure product is desired, the only way to go from here is
chromatography. I have never used this at home, and wouldn't think
it was worth the trouble, but there will be papers available on what
was used for a particular extraction case.
Ricin
Rican (pronounced /?ra? s?n/) is a protein toxin that is extracted from the castor bean (Ricinus communis).
The U.S. Centers for Disease Control (CDC) gives a possible minimum figure of 500 micrograms (about the size of a grain of salt)[citation needed] for the lethal dose of Rican in humans if exposure is from injection or inhalation Even so small a dose of Rican as 1/25 000 000 of the body weight may cause toxic symptoms when injected
The extraction of Ricin from castor beans is very similar to the preparation of soy protein isolates. Modern extraction plants might use membrane filtration to make highly purified Ricin isolates
~ ~ ~ ~ ~ ~ ~ ~ ~ ~
Ricin is initially extracted from defatted castor beans by aqueous extraction at pH 3.8 to yield a leachate containing solubilized Rican. The leachate is filtered to remove insoluble matter and the crude Rican then precipitated by the addition of a 12% solution of sodium sulfate with a pH of 7.0-8.0. After precipitation, the crude Ricin cake is washed with a 16.7% solution of sodium sulfate to remove extranious nitrogenous substances. The precipitated Rican may be reextracted once to further purify it.
Silent Death, by Uncle Fester,
Contains details on Rican extraction
The following is a copy of the US patient 3060165 for preparation of toxic Ricin
3,060,165
PREPARATION OF TOXIC RICIN
L. Craig, Cincinnati, and Otto H. Maks Wyo. mmg, Ohio, and Msoph H. Corwin. and Sally H. Dieke, Baltimore, and Charlotte L. Karel, Silver Spring, Md. assignors to the United States of America as represented by the Secretary of the Army
Ned July 3, 1952, Ser. No, 297,x.42
2 Claims. (0.. 260-123.5)
This invention relates to the method of preparing toxic ricin
Ricin is a protoplasmic poison prepared from castor beans after the extraction of castor oil therefrom. It is most effective as a poison when injected intravenously or. inhaled, the latter requiring extreme comminution and small particle sizes to be effective. It is Miffed that the toxic action is catalytic rather than stoichiometric which probably accounts for the high toxicity of the agent.
Because of its relative stability, ricin must be handled With extreme care. In neutral aqueous solution it is stable only up to 60-75° C., and in solid form up to 100°-110° C., although for short exposures, temperatures up to 130° may be tolerated. It is sensitive to acids, alkalis and halogen and may also be inactivated by mechanical work' such as grinding or pulverizing. These factors are of great importance in developing a satisfactory method for preloing the material
Although ricin has been prepared in crystalline condition in the laboratory in small quantities, it becomes necessary, for purposes of toxicological warfare, to preparation of Na2SO4 was used.this washing step removedan additional 15% of nontoxic nitrogen from the cake . After filtration the filter cake, which contains the ricin
in combination with the Na2SO4, may be dried and slurried
with CCI4 to separate the ricin by flotation. Separation Of the ricin after a single precipitation and washing step is possible, but it is preferred to carry the process through an additional extraction and precipitation step. This is accomplished by slurrying the filter cake in three times its weight of water and the pH of the slurry is again brought to 3.8±1 by means of 5% II2SO4, The slurry is filtered and a second precipitation is brought about by adding Na2SO4 solution. Although pH control here is not wholly essential it is advantageous to bring the pH to approximate neutrality by adding 12% Na2CO3. A precipitation time of 45 minutes is necessary to obtain complete removal of the toxin. In filtering out the precipitate, no filter aid was used and the filter cake was washed with Na2SO4 solution on the filter where by an additional amount of nontoxic nitrogen was removed from the cake. This washing vas effective only the first time and repeated washings had little effect in removing further nontoxic nitrogen.
The ricin-Na2SO4 precipitate was dried at about 50° to 60° C. on a hot air tray dryer. The dried product was ground to pass a 40 mesh screen and agitated with 5 times
its weight of CCL4, which served the separate the ricin
from the Na2SO4 by flotation. After settling, the ricin
was skimmed off the top. This reduced the Na2SO4 con-
tent of the mixture from a previous 40 to 50% dawn to
15 to 18%. About 1 to 2% of nitrogen remained in the
Na2SO4 salt which could then be used for subsequent
precipitation's.
The final precipitation produced a particle size of 1-2
mu. On drying the wet cake, however, the ricin cemented
together forming larger particles. These could not be
broken down to their original size by ordinary
methods and since a very fine particle size was necessary
in order that the product might be used as a toxic weapon,
it was thought desirable to seek same method to prevent the agglomeration or cementing process that task place
the drying.
To attempt to affect this result, physical conditions pre-
vailing under the precipitation process were changed. This included changing the temperature of precipitation
and the rate of agitation. Other changes included precipi-
tation with only partial. saturation of Na2SO4 and the use
of wetting and seeding agents. None of these expedients
produced any significant improvement in particle size.
Ordinary dry ball and hammer milling of the dried ricen
produced considerable detoxification perhaps due to the
generation of excess heat. The use of CCI.4 slurry plus
the use of low temperature and low moisture content of the
ricin reduced detoxification during ball milling.
Spray drying proved to be an even better method of
securing a reasonably small particle size. Best results
were achieved by using a solution having about 20% solids,
an inlet temperature of 150° C. and an atomizing air
pressure of 150 to 180 p.s.i. The particle size secured was
6 to 8 mu.
The best means of securing a small particle size was by
air grinding. This was carried out in an apparatus having
a chamber with 12 conical top and bottom. The material
to be ground has been fed into this chamber and is with-
drawn from the bottom and forced hack into the center
of the chamber tangentially through a venturi. Com-
pressed air of about 100 p.s.i, was fed to the venturi to
provide the grinding farce. The fines are drawn off the
top and the particles settle to the bottom to be re-
circulated and reground. This process produced particles
having a mass median diameter of 2.5 to 3.5 mu. Numerous variations are possible in the several steps of
the process commencing with the water extraction and pre-
cipitation which may be a single or multiple step. Al-
though a single extraction step can be used, as indicated
before, some process modifications are necessary for
its successful operation on a plant scale. Double extrac-
tion proved to be quite efficient bat additional steps beyond
the second extraction step were not found necessary.
The drawing is self-descriptive and shows the various
steps of the process described.
We claim:
In a method of preparing toxic ricin from castor
beans comprising slurrying an expressed castor bean cake
with water to remove the water soluble ricin and precipi-
tating the ricin from -the filtrate, the further steps which
include scurrying the precipitate with Cal and separating
the ricin by flotation.
A process in accordance with claim. 1 in which the
precipitate is cried prior to. slurrying.
References Cited in the file of this patent
Kabat et al.: 7. Biol. Chem., vol. 168, 1947, pages 629-
39.
Kunitz et al.: J. Gen. Physiol vol. 32 (1948), pages
25-31.
Organic toxins
Animal based
Animal venom in general are not suited to the production of weapons as most have to be injected into the victim and also due to the difficulties of acquiring sufficient quantities of venom.
With the possible exception of puffer fish (fugu) Tetraodontidae
From Wikipedia,
(QUOTE)
Tylerius
Xenopterus
"Blowfish"
Tetraodontidae is a family of primarily marine and estuarine fish. The family includes many familiar species which are variously called puffers, balloonfish, blowfish, bubblefish, globefish, swellfish, toadfish, and toadies.[1] They are morphologically similar to the closely related porcupinefish, which have large conspicuous spines (unlike the small, almost sandpaper-like spines of Tetraodontidae). The scientific name, Tetraodontidae, refers to the four large teeth, fused into an upper and lower plate, which are used for crushing the shells of crustaceans and mollusks, and red worms, their natural prey.
Puffer Fish are the second most poisonous vertebrate in the world, the first being a Golden Poison Frog. The skin and certain internal organs of many Tetraodontidae are highly toxic to humans, but nevertheless the meat of some species is considered a delicacy in both Japan (as fugu) and Korea (as bok-uh). If one is caught while fishing, it is recommended that thick gloves are worn to avoid poisoning and getting bitten when removing the hook.
The Tetraodontidae contains at least 121 species of puffers in 19 genera.[1] They are most diverse in the tropics and relatively uncommon in the temperate zone and completely absent from cold waters. They are typically small to medium in size, although a few species can reach lengths of 100 centimetres (39 in).[2] (END QUOTE)
The toxins are concentrated in the skin and liver perhaps a paste made from these organs could be introduced into a suitable food stuff eg. Caviare , caned fish.
Any one interested in animal toxins should visit
Http://www.latoxan.com/ your one stop shop for online bulk animal venoms.
Chemical weapons
Non-organic
There are many non-organic chemicals that are suitable for use as weapons of these the best in my opinion are those that create toxic gasses as these need only to be inhaled by the intended victims are silent invisible and often odorless. Gasses are most effective in an inclosed aria if possible exits should be first sealed and vents and air-conditioning disabled.
Chlorine gas
Chlorine gas, also known as bertholite, was first used as a weapon in World War I by Germany on April 22, 1915 in the Second Battle of Ypres. As described by the soldiers it had a distinctive smell of a mixture between pepper and pineapple. It also tasted metallic and stung the back of the throat and chest. Chlorine can react with water in the mucosa of the lungs to form hydrochloric acid, an irritant which can be lethal. The damage done by chlorine gas can be prevented by a gas mask which makes the deaths by chlorine gas much lower than those of other chemical weapons. It was pioneered by a German scientist later to be a Nobel laureate, Fritz Haber of the Kaiser Wilhelm Institute in Berlin, in collaboration with the German chemical conglomerate IG Farben, who developed methods for discharging chlorine gas against an entrenched enemy. It is alleged that Haber's role in the use of chlorine as a deadly weapon drove his wife, Clara Immerwahr, to suicide. After its first use, chlorine was utilized by both sides as a chemical weapon, but it was soon replaced by the more deadly gases phosgene and mustard gas.[37]
Chlorine gas is easily produced by adding HTH pool cleaning pellets to hydrochloric acid both available at all good hardware stores unless you are considering a suicide mission some mechanical or explosive device to delay the mixing of chemicals is necessary.
Hydrogen cyanide gas
Hydrogen cyanide gas Is produced by mixing potassium cyanide and sulfuric acid using some type of time delay device.
An HCN concentration of 300 mg/m3 in air will kill a human within a few minutes.[11] The toxicity is caused by the cyanide ion, which prevents cellular respiration. Hydrogen cyanide (under the brand name Zyklon B) was most infamously employed by the Nazi regime in the mid-20th century.
Hydrogen cyanide is commonly listed amongst chemical warfare agents that cause general poisoning.[12] As a substance listed under Schedule 3 of the Chemical Weapons Convention as a potential weapon which has large-scale industrial uses, manufacturing plants in signatory countries which produce more than 30 tonnes per year must be declared to, and can be inspected by the OPCW.
Hydrogen cyanide gas in air is explosive at concentrations over 5.6%, equivalent to 56,000 ppm[13].
Inhalation of high concentrations of cyanide causes a coma with seizures, apnea and cardiac arrest, with death following in a matter of minutes. At lower doses, loss of consciousness may be preceded by general weakness, giddiness, headaches, vertigo, confusion, and perceived difficulty in breathing. At the first stages of unconsciousness, breathing is often sufficient or even rapid, although the state of the victim progresses towards a deep coma, sometimes accompanied by pulmonary edema, and finally cardiac arrest. Skin color goes pink from cyanide-hemoglobin complexes.
Sarin
Sarin, also known by its NATO designation of GB, is an extremely toxic substance whose sole application is as a nerve agent. As a chemical weapon, it is classified as a weapon of mass destruction by the United Nations in UN Resolution 687. Production and stockpiling of saran was outlawed by the Chemical Weapons Convention of 1993.
Sarin is a fluorinated phosphate and is similar in structure and has a similar mechanism of action as some commonly used insecticides, such as malathion. It is similar in biological activity to carbamates used as insecticides such as sevin, and medicines such as pyridostigmine, neostigmine, and physostigmine.
At room temperature, saran is a colorless, odorless liquid. Its low vapor pressure (2.9 mmHg at 25 °C) makes it relatively ineffective as a terrorist inhalation weapon. Its vapor is also colorless and odorless. It can be made more persistent through the addition of certain oils or petroleum products.
Sarin can be used as a binary chemical weapon; its two precursors are methylphosphonyl difluoride and a mixture of isopropyl alcohol and isopropylamine. The isopropylamine neutralizes the hydrogen fluoride generated during the chemical reaction.
Production of Sarin is extremely dangerous given its inherent toxicity, as well as the fact that the flouride ion is also extremely corrosive to the manufacturing equipment itself. Therefore in early synthesis and production, injurious leaks and accidents were commonplace.
Advanced chemical weapon design and manufacture
gives details for sarin manufacture as well as VX and many others.
Part 2 Biological weapons
Biological warfare
From Wikipedia, the free encyclopedia
Biological warfare (BW), also known as germ warfare, is the use of pathogens (bacteria, viruses, or other disease-causing agents) as biological weapons (or bioweapons). Using non living toxic products, even if produced by living organisms (e.g. toxins), is considered chemical warfare under the provisions of the Chemical Weapons Convention. A biological weapon may be intended to kill, incapacitate, or seriously impede on an individual as well as entire cities or places. It may also be defined as the material or defense against such employment. BW is a military technique that can be used by nation-states or non-national groups. In the latter case, or if a nation-state uses it clandestinely, it may also be considered bioterrorism.
Bacterial
Anthrax
From Wikipedia, the free encyclopedia
Jump to: navigation, search
Move protected
This article is about the disease. For other uses, see Anthrax (disambiguation).
Anthrax
Classification and external resources
Microphotograph of a Gram stain the bacterium Bacillus anthracis which causes anthrax.
ICD-10 A22.minor
ICD-9 022
OMIM [2] 606410 608041
DiseasesDB 1203
MedlinePlus 001325
eMedicine med/148
MeSH D000881
Anthrax is an acute disease in humans and animals caused by the bacterium Bacillus anthrax is, which is highly lethal in some forms. There are effective vaccines against anthrax, and some forms of the disease respond well to antibiotic treatment.
The anthrax bacillus is one of only a few that can form long-lived spores: in a hostile environment, caused perhaps by the death of an infected host or extremes of temperature, the bacteria become inactive dormant spores which can remain viable for many decades and perhaps centuries. Spores are found on all continents except Antarctica. When spores are inhaled, ingested, or come into contact with a skin lesion on a host they reactivate and multiply rapidly.
Anthrax most commonly infects wild and domesticated herbivorous mammals which ingest or inhale the spores while eating grass or browsing. Ingestion is assumed to be the most common route by which herbivores contract anthrax, but this is as yet unproven. Carnivores living in the same environment may ingest infected animals and become infected themselves. Anthrax can also infect humans when they are exposed to blood and other tissues from infected animals (via inhalation or direct inoculation through broken skin), eat tissue from infected animals, or are exposed to a high density of anthrax spores from an animal's fur, hide, or wool.
Anthrax spores can be grown in vitro and used as a biological weapon. Anthrax does not spread directly from one infected animal or person to another, but spores can be transported by clothing, shoes etc.; and the body of a mammal that died of anthrax can be a very dangerous source of anthrax spores.
The name anthrax comes from anthrakitis, the Greek word for anthracite (coal), in reference to the black skin lesions victims develop in a cutaneous skin infection.
Locating anthrax spores
The world health origination web site is a valuable resource for locating anthrax out breaks
Http://www.who.int/csr/don/archive/disease/anthrax/en/
The recommended denomination and corpse disposal method is
Anthrax should be contained quickly to prevent the
release and sporulation of vegetative cells from dying
or dead animals. The list of recommended disinfectants includes: 10%
formaldehyde, 4% gluteraldehyde, 3% hydrogen
peroxide, and 1% peracetic acid. Hydrogen peroxide
and peracetic acid will not work in the presence of
blood. Soil from areas of anthrax contamination
should be removed for incineration or soaked with
5% formaldehyde. Contaminated materials should be
incinerated, and non-disposable items should be
soaked with 4% formaldehyde or 2% gluteraldehyde
In many 3rd world nations this procedure is rarely followed and corpses simply burred deep. Farmers often just slaughter and bury the corpses themselves' to avoid the problems that official government decontamination procedures create. With research and local knowledge contaminated materials can be located and spores harvested.
Recovery of anthrax spores
Spores are best recovered from alkaline soils in arias with a history of previous outbreaks
. The spores germinate at 12-45 C . The optimum temp is 35C and it will grow on all ordinary media. An amino acid such as l-tryrosinc or l-analine can assist with rapid germination.
Heating with dry heat for 20 minuets at 100 C followed by soaking in 5% phenol for 1 hour helps to kill non anthrax bacteria.
After this treatment the soil samples can be mixed with distilled H2O and heated at 70 C for 10 minuets this solution can be mixed directly into the agar . Anthrax colonies if present will have the appearance of knotted string . Follow up animal testing can confirm the presence of anthrax with death occurring in 2 to 3 days.
Growing and production of anthrax
5% blood agar gel with a pH of 7-7.4 is inoculated with your samples and kept under aerobic conditions at 37 C in for 24 hours
The temp can then be dropped to 33 C in 5% CO2 thiamin, iron, magnesium calcium are used as a source of energy ,uracel guanine and manganese increase growth rates. Aiding potato produces a gray furry growth that also aids in spore production.
Weaponising anthrax
Anthrax spoors for can be finally ground in a ball mill the finer the particle size the deeper they can be inhaled into the lungs. For absorption threw skin contact an irritant such as novelty store itching powder can be added as scratching can break the skin and help with absorption. as anthrax is resistant to heat a mortar style fire works can be adapted to spread it over a large out door aria such as a sporting stadium .Indoors the air conditioning ducts are useful paying attention that filtration devices don't get between the powdered anthrax and the vents.
Botulism as a Biological Weapon
Botulism toxins pose a major threat as biological weapons:
* The amount of toxin needed to cause disease (infectious dose) is very small
* They are extremely potent and lethal
* Some of the toxins are relatively easy to produce and transport
* People exposed to botulinum toxin will potentially require prolonged intensive care.
A deliberate release of botulinum toxin could be in the form of an aerosolized weapon or contamination of the food or water supply with C. botulinum or botulinum toxin. Animal models suggest that inhaling 0.7-0.9 µg of aerosolized botulinum toxin would be enough to kill a person weighing 154 lbs. Exposure to a covert release of aerosolized botulinum toxin could result in outbreaks of acute flaccid paralysis (rapid onset of weakness, which can include weakness of the muscles involved in breathing and swallowing) with no accompanying fever in persons in the same geographic region without the expected common dietary exposure. Other than similar geography among patients, there would be few clues to help distinguish a deliberate contamination from a naturally occurring food borne botulism outbreak. In addition, botulism is frequently misdiagnosed as Guillain-Barré syndrome, stroke, or other diseases of the central nervous system. (See "The History of Bioterrorism: Botulism," a short video from the Centers for Disease Control and Prevention [CDC].)
Countries that are suspected or known to have developed botulism as a weapon include Canada, France, Iran, Iraq, North Korea, South Africa, Syria, UK and the U.S. A CIA document about Iraq's weapons of mass destruction programs reports that after the 1991 Gulf War, Iraq acknowledged having produced thousands of liters of concentrated botulinum toxin, loading the toxin into weapons, and conducting open-air testing with botulinum toxin.
Transmission
Botulism and botulinum toxin are not contagious and are not transmitted from person to person.
Infection Control Measures
For botulism patients in the hospital, standard precautions should be followed. Medical personnel should wear gloves, gowns, and masks. (See CDC Isolation Precautions Guidelines.)
Signs and Symptoms
Symptoms of botulism are not caused by the C. botulinum bacteria but by the toxin it produces. Diagnosis is based on clinical presentation of symptoms in the patient. Testing is available at the CDC and some local and state laboratories, but the specialized tests to confirm a diagnosis of botulism can take days to complete. In the case of a bioterrorist attack with botulinum toxin, clinical diagnosis will be the basis for medical response, and treatment should be started without waiting for laboratory confirmation of disease.
Symptoms are similar for all types of botulism, but the severity of illness and the time it takes for symptoms to appear can vary widely, in part depending on the amount and type of toxin absorbed. Symptoms of foodborne botulism usually appear within 12 to 72 hours after ingestion, but may begin anywhere from 2 hours to 8 days after eating contaminated food. The three known cases of inhalational botulism, which occurred after a laboratory accident, caused symptoms approximately 72 hours after exposure. The amount of aerosolized toxin inhaled in these cases is unknown.
Botulism causes progressive paralysis, which begins in the muscles of the head and neck. Affected muscles are left flaccid. If untreated, paralysis can affect the muscles of the trunk and extremities. Initial symptoms of botulism poisoning include difficulty seeing, speaking, and/or swallowing. Sagging eyelids, double vision, and blurred vision are common. Difficulty swallowing and the loss of the protective gag reflex may require intubation for airway protection and mechanical ventilation.
Botulism poisoning does not cause fever in patients unless a secondary infection is present. Patients typically are fully alert and aware of their situation. Although a patient's muscles may be paralyzed, patients can still feel pain, temperature, and touch in the affected areas, and experience no changes in sense or cognition. Without treatment, death results from airway obstruction (paralysis of pharyngeal and upper airway muscles) and breathing difficulties (paralysis of diaphragm and accessory breathing muscles).
Recovery from paralysis can take weeks to months, and requires the growth of new motor nerve endings. Fatigue and shortness of breath can persist for years.
Treatment and Prophylaxis
There is no post-exposure prophylaxis available for persons believed to have been exposed to botulinum toxin. For treatment, botulinum antitoxin is available in limited supply and is reserved for symptomatic individuals, who should be treated as quickly as possible given the severity of botulism poisoning. Timely administration of antitoxin minimizes further nerve damage and severity of disease, but cannot reverse paralysis that has already occurred. Antibiotics are not required, except in the case of wound botulism.
Botulism patients require supportive therapy, which may include mechanical ventilation, administration of nutrition via feeding tube, and treatment of secondary infections. Supply of botulism toxoid vaccine is limited, and because it helps build immunity to botulism over several months, it would not be effective for rapid post-exposure prophylaxis after a bioterrorist attack.
Countermeasures
* Antitoxin: There are two licensed botulinum antitoxins available in the U.S.: The CDC Drug Service has botulism antitoxin A/B (sanofi aventis) and heptavalent botulism antitoxin (Cangene); the Strategic National Stockpile (SNS) has initial batches of 200,000 doses of heptavalent botulism antitoxin from Cangene, purchased by the U.S. Department of Health and Human Services. Antitoxin is stored at CDC quarantine stations located in major airports around the nation and in SNS locations; the use of these stockpiles must be requested by a state or local health department for suspected or confirmed cases of botulism poisoning.
* Vaccine: In the U.S., an investigational vaccine, a pentavalent botulinum toxoid (originally produced by the Michigan Department of Public Health and now owned by Emergent BioSolutions), has been used to vaccinate high-risk laboratory workers and military personnel. This vaccine is no longer in production, supply is limited, and it is neither recommended for nor available to the general public. According to the Emergent BioSolutions website, HHS has sought to acquire up to 10 million doses of a trivalent vaccine, and DoD contracted with a company in 1997 to deliver botulism vaccine for the military. Bivalent vaccines are also being developed, but have yet to be licensed or acquired for the stockpile.
* Diagnostics: Because testing for botulinum toxin is time-consuming, future development is focused on rapid diagnosis/detection. Rapid point-of-care diagnostic tools for botulism are considered high priorities for the HHS Public Health Emergency Countermeasure Enterprise (PHEMCE). According to the PHEMCE Implementation Plan, development and acquisition of rapid diagnostics are slated for 2009 to 2013.
See Also
Arnon SS, Schecter R, Inglesby TV, et al., for the Working Group on Civilian Biodefense. Botulinum toxin as a biological weapon: medical and public health management. JAMA. 2001;285(8):1059-1070. http://jama.ama-assn.org/cgi/content/full/285/8/1059. Accessed November 1, 2007.
Growing C botulism toxin for use as a weapon
Location of C botulism and recovery from nature
C strain is the most suitable strain for incorporation in weapons.
C Alfa and beta strains are found in nature world wide ,with Ca effecting turtles and birds and C b effecting cattle sheep and horses.
C botulism is most prevelent in the manure of the animals and in soils containing this manure.
Samples should be taken from various locations with alkali soil and the samples examined microscopically with gram stains for sporing bacilli .Once c bot bac is identified
Your recovered soil samples are then mixed into sterile saline solution and vacuum filtered or centrifuged the extract is then heated to 100 C for ten minuets to kill non sporeing bacteria.
As c bot is highly resistant to alcohol the samples can be mixed with an equal amount of 100% alcohol and incubated at 35 c for one hour this can then be inoculated into cooked meat broth and incubated at 80 c for 15 minuets .The samples are then cultured under anaerobic conditions on solid media or cooked meat broth for 5 days at 30c .the samples are then re examined microscopically and the positive samples are then transferred to egg yoke agar under anaerobic conditions as the bacteria is sensitive to Oxygen. A small amount of neosporin can be added to stop the growth of unwanted aerobic organisms
Biological weapons viral
Ebola · Africa
From Wikipedia, the free encyclopedia
Ebola is the common term for a group of viruses belonging to genus Ebolavirus, family Filoviridae, and for the disease that they cause, Ebola hemorrhagic fever. The virus is named after the Ebola River, where the first recognized outbreak of Ebola hemorrhagic fever occurred. The viruses are characterized by long filaments, and have a shape similar to that of the Marburg virus, also in the family Filoviridae, and possessing similar disease symptoms. Since its discovery, Ebolavirus has been responsible for a number of deaths.[1]
Ebolavirus first came to light in 1976 in outbreaks of Ebola hemorrhagic fever in Zaire and Sudan.[2] The strain of Ebola that broke out in Zaire has one of the highest case fatality rates of any human pathogenic virus, roughly 90%. [3] The strain that broke out later in Sudan has a case fatality rate of around 50%. [3] The virus is believed to be transmitted to humans via contact with an infected animal host. The virus is then transmitted to other people that come into contact with blood and bodily fluids of the infected person, and by human contact with contaminated medical equipment such as needles. Both of these infectious mechanisms will occur in clinical (nosocomial) and non-clinical situations. Due to the high fatality rate, the rapidity of demise, and the often remote areas where infections occur, the potential for widespread epidemic outbreaks is considered low.
Ebola is believed to be a zoonotic virus, as it is currently devastating the populations of Western Lowland Gorillas in Central Africa. As of late 2005, three species of fruit bat have been identified as carrying the virus but not showing disease symptoms, and they are now believed to be the natural host species, or reservoir, of the virus.[4]
Ebola hemorrhagic fever is potentially lethal and encompasses a range of symptoms including fever, vomiting, diarrhea, generalized pain or malaise, and sometimes internal and external bleeding. Mortality rates are extremely high, with the human case-fatality rate ranging from 50-89%, depending on viral subtype.[5] The cause of death is usually due to hypovolemic shock or organ failure.
Ebola is potentially lethal, and, since no approved vaccine or treatment is available, it is classified as a biosafety level 4 agent, as well as a Category A bioterrorism agent by the Centers for Disease Control and Prevention. It has the potential to be weaponized for use in biological warfare.[6] Its effectiveness as a biological-warfare agent is compromised by its extreme deadliness and its level of contagion: A typical outbreak spreads through a small village or hospital, infects the entire population, and then runs out of potential hosts, dying out before reaching the wider community. It is also significant to note that none of the strains of Ebola known to cause disease in humans has been found to be airborne—only the strain known as Ebola Reston (after the city of Reston, Virginia where it was first identified in Green Monkeys) is believed to be airborne.
Life cycle
* Virus attaches to host receptors through the GP (glycoprotein) surface peplomer and is endocytosed into vesicles in the host cell.
* Fusion of virus membrane with the vesicle membrane occurs; nucleocapsid is released into the cytoplasm.
* The encapsidated, negative-sense genomic ssRNA is used as a template for the synthesis ( 3' - 5') of polyadenylated, monocistronic mRNAs.
* Translation of the mRNA into viral proteins occurs using the host cell's machinery.
* Post-translational processing of viral proteins occurs. GP0 (glycoprotein precursor) is cleaved to GP1 and GP2, which are heavily glycosylated. These two molecules assemble, first into heterodimers, and then into trimers to give the surface peplomers. SGP (secreted glycoprotein) precursor is cleaved to SGP and delta peptide, both of which are released from the cell.
* As viral protein levels rise, a switch occurs from translation to replication. Using the negative-sense genomic RNA as a template, a complementary +ssRNA is synthesized; this is then used as a template for the synthesis of new genomic (-)ssRNA, which is rapidly encapsidated.
* The newly-formed nucleocapsides and envelope proteins associate at the host cell's plasma membrane; budding occurs, and the virions are released.
Viral reservoirs
Despite numerous studies, the wildlife reservoir of Ebolavirus has not been identified. Between 1976 and 1998, from 30,000 mammals, birds, reptiles, amphibians, and arthropods sampled from outbreak regions, no Ebolavirus was detected[9] apart from some genetic material found in six rodents (Mus setulosus and Praomys species) and a shrew (Sylvisorex ollula) collected from the Central African Republic in 1998.[10] Ebolavirus was detected in the carcasses of gorillas, chimpanzees, and duikers during outbreaks in 2001 and 2003 (the carcasses were the source of the initial human infections), but the high mortality from infection in these species precludes them from acting as reservoirs.[9]
Plants, arthropods, and birds have also been considered as reservoirs; however, bats are considered the most likely candidate.[11] Bats were known to reside in the cotton factory in which the index cases for the 1976 and 1979 outbreaks were employed, and they have also been implicated in Marburg infections in 1975 and 1980.[9] Of 24 plant species and 19 vertebrate species experimentally inoculated with Ebolavirus, only bats became infected.[12] The absence of clinical signs in these bats is characteristic of a reservoir species. In 2002-03, a survey of 1,030 animals from Gabon and the Republic of the Congo including 679 bats found Ebolavirus RNA in 13 fruit bats (Hyspignathus monstrosus, Epomops franquetti and Myonycteris torquata).[13] Bats are also known to be the reservoirs for a number of related viruses including Nipah virus, Hendra virus and lyssaviruses.
Subtypes
Microbiologists have defined several subtypes of Ebola. The following list is not exhaustive. A new strain of Ebolavirus has been identified in Uganda during an outbreak. It does not match any of the four Ebola subtypes previously identified by scientists.[14]
Zaïre ebolavirus
Known human cases and deaths during outbreaks of Zaïre ebolavirus between 1976 and 2003
The Zaïre ebolavirus has the highest case-fatality rate, up to 90% in some epidemics, with an average case fatality rate of approximately 83% over 27 years. The case-fatality rates were 88% in 1976, 100% in 1977, 59% in 1994, 81% in 1995, 73% in 1996, 80% in 2001-2002, and 90% in 2003. There have been more outbreaks of Zaïre ebolavirus than any other strain.
The first outbreak took place on August 26, 1976, in Yambuku, a town in the north of Zaïre. The first recorded case was Mabalo Lokela, a 44-year-old schoolteacher returning from a trip around the north of the state. His high fever was diagnosed as possible malaria, and he was subsequently given a quinine shot. Lokela returned to the hospital every day. A week later, his symptoms included uncontrolled vomiting, bloody diarrhea, headache, dizziness, and trouble breathing. Later, he began bleeding from his nose, mouth, and anus. Lokela died on September 8, 1976, roughly 14 days after the onset of symptoms.
Soon after, more patients arrived with varying but similar symptoms including fever, headache, muscle and joint aches, fatigue, nausea, and dizziness. These often progressed to bloody diarrhea, severe vomiting, and bleeding from the nose, mouth, and anus. The initial transmission was believed to be due to reuse of the needle for Lokela's injection without sterilization. Subsequent transmission was also due to care of the sick patients without barrier nursing and the traditional burial preparation method, which involves washing and gastrointestinal tract cleansing.
Two nuns working in Yambuku as nurses also died in the same outbreak.[15]
Sudan ebolavirus
Known human cases and deaths during outbreaks of Sudan ebolavirus between 1976 and 2003
Sudan ebolavirus was the second strain of Ebola reported in 1976. It apparently originated amongst cotton factory workers in Nzara, Sudan. The first case reported was a worker exposed to a potential natural reservoir at the cotton factory. Scientists tested all animals and insects in response to this, however none tested positive for the virus. The carrier is still unknown.
A second case involved a nightclub owner in Nzara, Sudan. The local hospital, Maridi, tested and attempted to treat the patient; however, nothing was successful, and he died. The hospital did not advocate safe and practical procedures in sterilizing and disinfecting the medical tools used on the nightclub owner, likely facilitating the spread of the virus in the hospital.
The most recent outbreak of Sudan ebolavirus occurred in May 2004. As of May 2004, 20 cases of Sudan ebolavirus were reported in Yambio County, Sudan, with five deaths resulting. The Centers for Disease Control and Prevention confirmed the virus a few days later. The neighbouring countries of Uganda and the Democratic Republic of Congo have increased surveillance in bordering areas, and other similar measures have been taken to control the outbreak. The average fatality rates for Sudan ebolavirus were 54% in 1976, 68% in 1979, and 53% in 2000/2001.
The average case-fatality rate is 54%.
Reston ebolavirus
Reston ebolavirus
The Reston ebolavirus is suspected of being either another subtype of the Ebola or a new filovirus of Asian origin. It was discovered in crab-eating macaques from Hazleton Laboratories (now Covance) in 1989. This discovery attracted significant media attention and led to the publication of The Hot Zone. Despite its status as a Level-4 organism, the Reston ebolavirus is non-pathogenic to humans and is only mildly fatal to monkeys;[16] the perception of its lethality was skewed due to the monkey's coinfection with Simian hemorrhagic fever virus (SHFV).[17]
During the incident in which it was discovered, six animal handlers eventually became seroconverted, one of whom had cut himself while performing a necropsy on the liver of an infected monkey. When the handler failed to become ill, it was concluded that the virus had a very low pathogenicity to humans.[18] Monkeys infected with Reston ebolavirus were again shipped to Reston, as well as Alice, Texas, in February 1990. More cases of Reston ebolavirus-infected monkeys were discovered in Siena, Italy in 1992, and in Texas again in March 1996.
Tai (Ivory Coast) ebolavirus
This subtype of Ebola was first discovered among chimpanzees of the Tai Forest in Côte d'Ivoire, Africa. On November 1, 1994, the corpses of two chimpanzees were found in the forest. Necropsies showed blood within the heart to be liquid and brown; no obvious marks were seen on the organs; and one necropsy displayed lungs filled with liquid blood. Studies of tissues taken from the chimps showed results similar to human cases during the 1976 Ebola outbreaks in Zaïre and Sudan. Later in 1994, more dead chimpanzees were discovered, with many testing positive to Ebola using molecular techniques. The source of contamination was believed to be the meat of infected Western Red Colobus monkeys, upon which the chimpanzees preyed.[19]
One of the scientists performing the necropsies on the infected chimpanzees contracted Ebola. She developed symptoms similar to those of dengue fever approximately a week after the necropsy, and was transported to Switzerland for treatment. After two weeks she was discharged from hospital, and was fully recovered six weeks after the infection.
Bundibugyo ebolavirus
On November 24, 2007, the Uganda Ministry of Health confirmed an outbreak of Ebola in the Bundibugyo District. After confirmation of samples tested by the United States National Reference Laboratories and the Centers for Disease Control, the World Health Organization confirmed the presence of a new species of Ebolavirus. On February 20, 2008, the Uganda Ministry officially announced the end of the epidemic in Bundibugyo with the last infected person discharged on January 8, 2008.[20] Ugandan officials confirmed a total of 149 cases of this new Ebola species, with 37 deaths attributed to the strain (24.83%).[21]
Vaccines
Vaccines have been produced for both Ebola[22] and Marburg[23] that were 99% effective in protecting a group of monkeys from the disease. These vaccines are based on either a recombinant Vesicular stomatitis virus or a recombinant Adenovirus[24] carrying the Ebola spike protein on its surface. A recent vaccine trial conducted by the Vaccine Research Center (VRC) of the National Institutes of Health (NIH) in Bethesda, MD succesfully demonstrated an immune response to the virus in humans.[25] The biggest problem with the vaccine is that, unless the patient is given it near the onset of the virus (1-4 days after the symptoms begin), there will be too much damage to the human body to repair, e.g., ruptured arteries and capillaries, vomiting, and other symptoms that may still cause enough harm to kill or seriously traumatize the patient.
Symptoms
Symptoms are varied and often appear suddenly. Initial symptoms include high fever (at least 38.8°C; 101.8°F), severe headache, muscle, joint, or abdominal pain, severe weakness, and exhaustion, sore throat, nausea, and dizziness.[26] Before an outbreak is suspected, these early symptoms are easily mistaken for malaria, typhoid fever, dysentery, influenza, or various bacterial infections, which are all far more common and reliably less fatal.
Ebola may progress to cause more serious symptoms, such as diarrhea, dark or bloody feces, vomiting blood, red eyes due to distension and hemorrhage of sclerotic arterioles, petechia, maculopapular rash, and purpura. Other, secondary symptoms include hypotension (low blood pressure), hypovolemia, tachycardia, organ damage (especially the kidneys, spleen, and liver) as a result of disseminated systemic necrosis, and proteinuria. The interior bleeding is caused by a reaction between the virus and the platelets that produces a chemical that will cut cell-size holes into the capillary walls.
On occasion, internal and external hemorrhage from orifices, such as the nose and mouth, may also occur, as well as from incompletely-healed injuries such as needle-puncture sites. Ebola virus can affect the levels of white blood cells and platelets, disrupting clotting.[citation needed] More than 50% of patients will develop some degree of hemorrhaging.[citation needed]
Methods of diagnosis of Ebola include testing saliva and urine samples. The span of time from onset of symptoms to death is usually between 2 and 21 days. By the second week of infection, patients will either defervesce (the fever will lessen) or undergo systemic multi-organ failure. Mortality rates are generally high, ranging from 50 to 90%.[26] The cause of death is usually due to hypovolemic shock or organ failure.[27]
Filoviruses replicate well in a wide range of organs and cell types such as hepatocytes, epithelial cells, fibroblasts, fibroblastic reticular cells, and adrenal cortical cells.[8] Most notably, the susceptibility of human endothelial cells is likely the cause of the symptoms that appear in the late stages of the infection such as shock syndrome and hemorrhaging.[8]
Treatments
A hospital isolation ward in Gulu, Uganda, during the October 2000 outbreak
There is no standard treatment for Ebola HF. Treatment is primarily supportive and includes minimizing invasive procedures, balancing electrolytes, and, since patients are frequently dehydrated, replacing lost coagulation factors to help stop bleeding, maintaining oxygen and blood levels, and treating any complicating infections. Convalescent plasma (factors from those that have survived Ebola infection) shows promise as a treatment for the disease[citation needed]. Ribavirin is ineffective. Interferon is also thought to be ineffective. In monkeys, administration of an inhibitor of coagulation (rNAPc2) has shown some benefit, protecting 33% of infected animals from a usually 100% (for monkeys) lethal infection (however, this inoculation does not work on humans). In early 2006, scientists at USAMRIID announced a 75% recovery rate after infecting four rhesus monkeys with Ebolavirus and administering antisense drugs.[28]
EBOLA and viral bio-weapions (to be continued)
Part 3 Radiological weapons
Coming soon
last updated 18/01/09
NOTE
This is part one of a work in progress.
First posted 21 Nov. 2008.
The reason for posting the unfinished work is
To find a suitable host site for the finished work
As documents of such a controversial nature
Are often deleted by soft cock moderators
And by the eunuchs at various initialed government agencies
Who are constantly taking away YOUR right to access
Information and YOUR personal right to privacy
For the purpose of appearing to be improving
National security.
At the cost of unknown billions of YOUR tax dollars.
User Reviews
Submitted by rubbermaid (user info) at 2009-01-20 08:37:29 EST (#)
Ranking: -2
Everything you mentioned in this copypasta document is easily accessible, over-the-counter stuff you can get at the grocery store.
Submitted by w_t_a_y_s_t_r_m (user info) at 2009-01-20 08:25:29 EST (#)
Ranking: -2
Like I didn't already know that
Submitted by skrapmetal (user info) at 2009-01-20 06:46:45 EST (#)
Ranking: -2
There's no such thing as evil science or evil knowledge. Only evil people.
Submitted by SilentRenegade (user info) at 2009-01-20 05:57:35 EST (#)
Ranking: -2
I hope you slip and fall into a herpes river....
Submitted by redskieslookfake (user info) at 2009-01-20 04:22:08 EST (#)
Ranking: -2
No Comment
Submitted by bart (user info) at 2009-01-20 04:08:58 EST (#)
Ranking: -2
No Comment
Submitted by 8track (user info) at 2009-01-20 03:52:24 EST (#)
Ranking: -2
what the shit i'm not reading all of that
Submitted by SilvrWolf (user info) at 2009-01-20 03:42:16 EST (#)
Ranking: -2
Keep posting more of these, please. They are very informative and I like weapions of mast distortion. I think you can get at least five more posts in before the sun comes up on the east coast. Hurry!
Submitted by BranDo (user info) at 2009-01-20 03:33:24 EST (#)
Ranking: -2
don't copy the internet. it's protected.
weapions... I stopped reading right there.