Toxins
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Toxins

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Animal Toxins

Batrachotoxin

On a weight basis the batrachotoxins are among the most toxic natural substances known, being 250-times more toxic than strychnine. Batrachotoxin comes from the Greek words “batrachos” meaning frog, and “toxine” meaning poison.  The lethal dose of this alkaloid in humans is estimated at 1 or 2 µg/kg. Thus, the lethal dose for a 68 kg (150 pound) person would be approximately 100 micrograms, or equivalent to the weight of two grains of ordinary table salt (NaCl).  Batrachotoxin is thus around fifteen times more potent than curare (another arrow poison used by South American Indians and derived from plants of the genera Strychnos and Curarea), and about ten times more potent than Tetrodotoxin contained in the puffer fish.  The toxin is a neurotoxin so it primarily affects the nervous system, although it also has significant effects on the heart muscle

Phyllobates terribilis

Batrachotoxin is found naturally in several higher organisms such as from the feathers and skin of birds belonging to genus Pitohui, endemic to New Guinea. Batrachotoxin was also later found in New Guinean birds of the genus Ifrita.  It is probable the birds contain such toxins to provide some protection against natural enemies, such as parasites and predators.  The most famous higher organism containing this toxin is undoubtedly Phyllobates terribilis the Golden Dart Frog, which is endemic to the Pacific coast of Colombia. Alkaloid Batrachotoxins toxins do not readily deteriorate, even when transferred to another surface, in fact dogs have died just from contact with an area on which a frog had previously sat.

Interestingly neither genus Ifrita nor P. terribilis has the genes to produce it and therefore the origin of the toxin remained unknown.  This resulted in Batrachotoxin being considered a low threat for use as a biological warfare agent.  However, it was recently discovered that the dart frog obtains this poison from the prey it consumes, a small beetle called Melyridae Choresine.  The poison dart frog is somehow immune or tolerant to the poisonous prey that it feeds upon while utilizing its prey’s toxin as a weapon of self defense.  The genes responsible for the toxin production in these beetles are being mapped and sequenced.  This is indeed an extremely frightening prospect especially as it is a toxin for which there is no antidote.

Tetrodotoxin TTX

Tetrodotoxin, known commonly as TTX is one of the deadliest toxins found on earth for which there is no antidote.  TTX is thousands of times more deadly than cyanide! Not only deadly but terrifying as the symptoms include total paralysis of the victim; although the brain is still fully conscious and aware of what is happening.  TTX is found in the livers of Puffer fish, certain newts, Blue ringed octopus, Gobie fish, Star fish, Parrot fish, Sea squirts, and Angel fish.

 

The fact that this toxin is found in so many different organisms led scientists to believe that it was not actually produced by them, but rather obtained from a common prey.  As with the batrachotoxin situation and the Poison dart fish most animals feeding on organisms containing TTX would die; however, a few built up a resistance to this organism and survived.  Recently a symbiotic Vibrio TTX producing bacterium (Tr-X) has been found living in TTX containing organisms.  Sequencing work for Vibrio Tr-X bacteria is underway and the gene or genes responsible for the production of Tr-X will soon be available though the public domain. Some readers may feel this is no big deal as the toxin is already available in the liver of the Japanese Puffer fish that is removed before consumption of the Japanese delicacy Fugi.  However to extract just 100 milligrams of TTX you would need approximately 100 kilograms of puffer fish liver!  On the other hand if the genes for its production are excised and then inserted into other faster growing organisms the amount of TTX that could be produced with ease is alarming to say the least.

Conotoxins

Conotoxins are one of a group of neurotoxic peptides isolated from the venom of the marine cone snail. Cone snails are marine organisms that prey on fish and other marine animals using a venom filled harpoon to paralyze their prey.  Some varieties are so deadly that one drop of its venom can kill more than 20 humans.

Symptoms of some cone snail stings can result in intense pain, muscle paralysis, vision changes and breathing failure.  There is no anti-venom for any cone snail toxin to date. 

Interestingly the venom of some cone snails is showing great promise as future medicinal drugs.  For example the venom of the Magician cone snail Conus Magus is a potential pain control drug perhaps many hundreds if not thousands of times more powerful than Morphine. Other cone snail derived toxins are showing promising signs for the treatments of Alzheimer’s disease, Parkinson’s disease, and epilepsy.  However, this research is providing an ever greater source of information that can be utilized by terrorists. There are many thousands of varieties of Cone snail each with their own unique toxin so that finding antidotes to all may prove an impossible task. 

Brazilian Wandering Spider venom

The Brazilian wandering spider appears in the Guinness Book of records as the world’s most venomous spider; this venom is a neurotoxin which causes loss of muscle control and breathing problems, resulting in paralysis and extreme pain.  Additionally this venom can cause painful penile erections many hours long which in some cases leads to impotence.  Drug companies are now investigating it, for use in erectile dysfunction treatments.  The sequencing of the gene (s) for its production is already being carried out which will result in “dark biology” having yet another deadly venom for the toxin larder. 

Readers may wonder that if the spider’s venom is really so deadly then why haven’t there been more human fatalities from wandering spider bites. This is a good question and one that is easily answered.  The relatively low fatality rate is not due to any failing on the part of the venom which is extremely deadly, but actually related to physiological factors of the spider’s mouth parts.  These evolved to kill and envenomate very small prey: not being well-adapted to attacking large mammals such as humans.  In addition the spider only injects a very small quantity of venom when biting, or often none at all when giving warning or defensive bites to larger mammals. 

 

Poisonous Plants an introduction

Atropa Belladonna the deadly nightshade plant

Ricin Communis

Poisonous Food Plants (poisons found in ever day food plants)

The dark biology complete poisonous plants guide

 

Poisonous plants an introduction.

 

Plants cannot move to escape their predators, so they must have other means of protecting themselves from herbivorous animals. Some plants have physical defenses such as thorns, but by far the most common protection is chemical.  Over millennia, natural selection has produced a complicated and vast array of chemical compounds that deter herbivores. Tannin is a compound that emerged relatively early in the evolutionary history of plants, while more complex molecules such as polyacetylenes are found in younger groups of plants such as the Asterales. Many of the plant defense compounds arose to defend against consumption by insects, although when livestock or humans consume such plants, they may also experience negative effects, ranging from mild discomfort to death.

Many of these poisonous compounds also have important medicinal benefits.

Below is an extensive, if incomplete, list of plants containing poisonous parts that pose a serious risk of illness, injury, ordeath to humans or animals.   If you wish to grow any of these plants do so responsibly and check to make sure they are legal.  Some of the plants listed below as poisonous may surprise you.  I find the list very interesting and enjoy to study and discover more about many in the list.  On this website I have also included individual pages on plants I find particularly interesting and those ones are usually associated with my northern European culture such as Henbane, Belladonna or the Datura.  Anyway enjoy the list I am learning all the time about mother nature's toxic and magical garden.

The more Infamous poison plants

 

Atropa belladonna

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deadly nightshade berriesdeadly nightshade flowers

Atropa belladonna or Atropa bella-donna, commonly known as Belladonna or Deadly Nightshade, is a perennial herbaceous plant in the family Solanaceae, native to Europe, North Africa, and Western Asia. The foliage and berries are extremely toxic, containing tropane alkaloids. These toxins include scopolamine and hyoscyamine which cause a bizarre delirium and hallucinations, and are also used as pharmaceutical anticholinergics. The drug atropine is derived from the plant.
It has a long history of use as a medicine, cosmetic, and poison. Before the Middle Ages, it was used as an anesthetic for surgery; the ancient Romans used it as a poison (the wife of Emperor Augustus and the wife of Claudius both were rumored to have used it to murder contemporaries); and predating this, it was used to make poison-tipped arrows. The genus name "atropa" comes from Atropos, one of the three Fates in Greek mythology, and the name "bella donna" is derived from Italian and means "beautiful woman" because the herb was used in eye-drops by women to dilate the pupils of the eyes to make them appear seductive.

The plant is a branching herbaceous perennial, often growing as a as a shrub, from a fleshy rootstock. Plants grow to 1.5 meters (4.9 ft) tall with 18 centimeters (7.1 in) long ovate leaves. The bell-shaped flowers are purple with green tinges and faintly scented. The fruits are berries, which are green ripening to a shiny black, and approximately 1 centimeter (0.39 in) in diameter. The berries are sweet and are consumed by animals  that disperse the seeds in their droppings, even though the seeds contain toxic alkaloids. There is a pale yellow flowering form called Atropa belladonna var. lutea with pale yellow fruit.
 It is naturalized in parts of North America, where it is often found in shady, moist locations with limestone-rich soils. It is considered a weed species in parts of the world, where it colonizes areas with disturbed soils. Germination of the small seeds is often difficult, due to hard seed coats that cause seed dormancy. Germination takes several weeks under alternating temperature conditions, but can be sped up with the use of gibberellic acid. The seedlings need sterile soil to prevent damping off and resent root disturbance during transplanting. This plant is a sign of water near by.[

The name Atropa belladonna was published by Linnaeus in Species Plantarum in 1753. It is in the nightshade family (Solanaceae), which it shares with potatoes, tomatoes, eggplants, jimsonweed, tobacco, wolfberry, and chili peppers. The common names for this species include belladonna, deadly nightshade, divale, dwale, banewort, devil's berries, naughty man's cherries, death cherries, beautiful death, devil's herb, great morel, and dwayberry.
The name Atropa is thought to be derived from that of the Greek goddess Atropos, one of the three Greek fates or destinies who would determine the course of a man's life by the weaving of threads that symbolized his birth, the events in his life and finally his death; with Atropos cutting these threads to mark the last of these. The name "belladonna" comes from the Italian language, meaning "beautiful lady"; originating either from its usage as cosmetic for the face, or, more probably, from its usage to increase the pupil size in women.

Flowers of belladonna
Belladonna is one of the most toxic plants found in the Eastern Hemisphere. All parts of the plant contain tropane alkaloids. The berries pose the greatest danger to children because they look attractive and have a somewhat sweet taste. The consumption of two to five berries by a human adult is probably lethal. The root of the plant is generally the most toxic part, though this can vary from one specimen to another. Ingestion of a single leaf of the plant can be fatal to an adult.


The active agents in belladonna, atropine, hyoscine (scopolamine), and hyoscyamine, have anticholinergic properties. The symptoms of belladonna poisoning include dilated pupils, sensitivity to light, blurred vision, tachycardia, loss of balance, staggering, headache, rash, flushing, severely dry mouth and throat, slurred speech, urinary retention, constipation, confusion, hallucinations, delirium, and convulsions.


Atropa belladonna is also toxic to many domestic animals, causing narcosis and paralysis. However, cattle and rabbits eat the plant seemingly without suffering harmful effects. In humans, its anticholinergic properties will cause the disruption of cognitive capacities, such as memory and learning.


Cosmetics


The common name belladonna originates from its historic use by women - Bella Donna is Italian for beautiful lady. Drops prepared from the belladonna plant were used to dilate women's pupils, an effect considered attractive. Belladonna drops act as an antimuscarinic, blocking receptors in the muscles of the eye that constrict pupil size. Belladonna is currently rarely used cosmetically, as it carries the adverse effects of causing minor visual distortions, inability to focus on near objects, and increased heart rate. Prolonged usage was reputed to cause blindness.


Medicinal uses
Belladonna has been used in herbal medicine for centuries as a pain reliever, muscle relaxer, and anti-inflammatory, and to treat menstrual problems, peptic ulcer disease, histaminic reaction, and motion sickness. At least one 19th-century eclectic medicine journal explained how to prepare a belladonna tincture for direct administration to patients.


Belladonna tinctures, decoctions, and powders, as well as alkaloid salt mixtures, are still produced for pharmaceutical use, and these are often standardized at 1037 partshyoscyamine to 194 parts atropine and 65 parts scopolamine. The alkaloids are compounded with phenobarbital and/or kaolin and pectin for use in various functional gastrointestinal disorders. The tincture, used for identical purposes, remains in most pharmacopoeias, with a similar tincture of Datura stramonium having been in the US Pharmacopoeia at least until the late 1930s. The combination of belladonna and opium, in powder, tincture, or alkaloid form, is particularly useful by mouth or as a suppository for diarrhea and some forms of visceral pain; it can be made by a compounding pharmacist, and may be available as a manufactured fixed combination product in some countries (e.g., B&O Supprettes). A banana-flavoured liquid (most common trade name: Donnagel PG) was available until 31 December 1992 in the United States.


Scopolamine is used as the hydrobromide salt for GI complaints, motion sickness, and to potentiate the analgesic and anxiolytic effects of opioid analgesics. It was formerly used in a painkiller called "twilight sleep" in childbirth.


Atropine sulphate is used as a mydriatic and cycloplegic for eye examinations. It is also used as an antidote to organophosphate and carbamate poisoning, and is loaded in an autoinjector for use in case of a nerve gas attack. Atropinisation (administration of a sufficient dose to block nerve gas effects) results in 100 per cent blockade of the muscarinic acetylcholine receptors and atropine sulphate is the benchmark for measuring the power of anticholinergic drugs.
Hyoscyamine is used as the sulphate or hydrobromide for GI problems and Parkinson's disease. Its side effect profile is intermediate to those of atropine and scopolamine, and can also be used to combat the toxic effects of organophosphates.


Scientific evidence to recommend the use of A. belladonna in its natural form for any condition is insufficient, although some of its components, in particular l-atropine which was purified from belladonna in the 1830s, have accepted medical uses. Donnatal is a prescription pharmaceutical, approved in the United States by the FDA, that combines natural belladonna alkaloids in a specific, fixed ratio with phenobarbital to provide peripheral anticholinergic/antispasmodic action and mild sedation. According to its labeling, it is possibly effective for use as adjunctive therapy in the treatment of irritable bowel syndrome (irritable colon, spastic colon, mucous colitis) and acute enterocolitis.
 

 
Berries of belladonna
Alternative-medicinal
Belladonna preparations are used in homeopathy as treatments for various conditions, although no scientific evidence supports their efficacy. Clinically and in research trials, the most common preparation is diluted to the 30C level in homeopathic notation. This level of dilution does not contain any of the original plant, although preparations with lesser dilutions which statistically contain trace amounts of the plant are advertised for sale.


Recreational drug


Atropa belladonna and related plants, such as jimson weed (Datura stramonium), have occasionally been used as recreational drugs because of the vivid hallucinations and delirium they produce. However, these hallucinations are most commonly described as very unpleasant, and recreational use is considered extremely dangerous because of the high risk of unintentional fatal overdose. In addition, the central nervous system effects of atropine include memory disruption, which may lead to severe confusion.


Poison
The tropane alkaloids of A. belladonna were used as poisons, and early humans made poisonous arrows from the plant. In Ancient Rome, it was used as a poison by Agrippina the Younger, wife of Emperor Claudius on advice of Locusta, a lady specialized in poisons, and Livia, who is rumored to have used it to kill her husband Emperor Augustus.
Macbeth of Scotland, when he was still one of the lieutenants of King Duncan I of Scotland, used it during a truce to poison the troops of the invading Harold Harefoot, King of England, to the point that the English troops were unable to stand their ground and had to retreat to their ships.[13]
Folklore  source

 European witchcraft and shamanism
 
Leaves of belladonna
In the past, witches were believed to have used a mixture of belladonna, opium poppy, and other plants, typically poisonous (such asmonkshood and poison hemlock) in flying ointment, which they applied to help them fly to gatherings with other witches. Carlo Ginzburgand others have argued that flying ointments were preparations meant to encourage hallucinatory dreaming; a possible explanation for the inclusion of belladonna and opium poppy in flying ointments concerns the known antagonism between tropane alkaloids of belladonna (specifically scopolamine) and opiate alkaloids in the opium poppy, Papaver somniferum (specifically morphine), which produces a dream-like waking state. This antagonism was known in folk medicine, discussed in eclectic (botanical) medicine formularies, and posited as the explanation of how flying ointments might have actually worked in contemporary writing on witchcraft. The antagonism between opiates and tropanes is the original basis of the Twilight Sleep that was provided to Queen Victoria to deaden pain as well as consciousness during childbirth, and which was later modified so isolated alkaloids were used instead of plant materials. The belladonna herb was also notable for its unpredictable effects from toxicity.

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Ricin Comnunis

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Ricin Manufacture

 

Ricin

Ricin (pron.: /ˈraɪsɪn/), from the castor oil plant Ricinus communis, is a highly toxic, naturally occurring protein. A dose the size of a few grains of table salt can kill an adult human. The median lethal dose (LD50) of ricin is around 22 micrograms per kilogram (1.78 mg for an average adult, around 1⁄228 of a standard aspirin tablet/0.4 g gross) in humans if exposure is from injection or inhalation. Oral exposure to ricin is far less toxic and a lethal dose can be up to 20–30 milligrams per kilogram.

Ricin is poisonous if inhaled, injected, or ingested, acting as a toxin by the inhibition of protein synthesis. That is,

It prevents the cell from assembling various amino acids into protein according to the messages it receives from RNA. This process, conducted by the cell's ribosome – literally a protein-making machine – is the most basic level of cell metabolism, essential to all living cells and thus to life itself. Ricin is resistant, but not impervious, to digestion by peptidases. By ingestion, the pathology of ricin is largely restricted to the gastrointestinal tract where it may cause mucosal injuries; with appropriate treatment, most patients will make a full recovery. Because the symptoms are caused by failure to make protein, they emerge only after a variable delay from a few hours to a full day after exposure. An antidote has been developed by the UK military, although it has not yet been tested on humans. Another antidote developed by the U.S. military has been shown to be safe and effective in lab mice injected with antibody-rich blood mixed with ricin, and has had some human testing. Symptomatic and supportive treatment are available.

Long term organ damage is likely in survivors. Ricin causes severe diarrhea and victims can die of shock. Death typically occurs within 3–5 days of the initial exposure. The ingestion of Ricinus communis cake used as fertilizer has been responsible for fatal ricin poisoning in animals. Deaths from ingesting castor plant seeds are rare, partly because of their indigestible capsule, and because the body can, only with difficulty, digest ricin.  The pulp from eight beans is considered dangerous to an adult. Rauber and Heard have written that close examination of early 20th century case reports indicates that public and professional perceptions of ricin toxicity "do not accurately reflect the capabilities of modern medical management".

Overdose

This section requires expansion. (April 2013) Most acute poisoning episodes in humans are the result of oral ingestion of castor beans, 5–20 of which could prove fatal to an adult. Victims often manifest nausea, diarrhea, tachycardia, hypotension and seizures persisting for up to a week.[10] Blood, plasma, or urine ricin concentrations may be measured to confirm diagnosis

Manufacture

Ricin is easily purified from castor oil manufacturing waste. The aqueous phase left over from the oil extraction process is called waste mash. It would contain about 5–10% ricin by weight, but heating during the oil extraction process denatures the protein, making the resultant seed cake safe for use as animal feed. Ricin can be isolated from fresh seed by chromatographic techniques similar to those routinely used for purification of many other plant proteins. Patented extraction process A process for extracting ricin has been described in a patent. The described extraction method is very similar to that used for the preparation of soy protein isolates. The patent was removed from the United States Patent and Trademark Office (USPTO) database sometime in 2004. Modern theories of protein chemistry cast doubt on the effectiveness of the methods disclosed in the patent.

Potential military and terrorist use

The United States investigated ricin for its military potential during World War I. At that time it was being considered for use either as a toxic dust or as a coating for bullets and shrapnel. The dust cloud concept could not be adequately developed, and the coated bullet/shrapnel concept would violate the Hague Convention of 1899 (adopted in U.S. law at 32 Stat. 1903), specifically Annex §2, Ch.1, Article 23, stating "... it is especially prohibited ... [to employ poison or poisoned arms". World War I ended before the United States weaponised ricin. During World War II the United States and Canada undertook studying ricin in cluster bombs. Though there were plans for mass production and several field trials with different bomblet concepts, the end conclusion was that it was no more economical than using phosgene. This conclusion was based on comparison of the final weapons, rather than Ricin's toxicity (LCt50 ~40 mg·min/m3). Ricin was given the military symbol W or later WA. Interest in it continued for a short period after World War II, but soon subsided when the U.S. Army Chemical Corps began a program to weaponise sarin. The Soviet Union also possessed weaponised ricin. There were speculations that the KGB used it outside the Soviet bloc; however, this was never proven. In 1978, the Bulgarian dissident Georgi Markov was assassinated by Bulgarian secret police who surreptitiously "shot" him on a London street with a modified umbrella using compressed gas to fire a tiny pellet contaminated with ricin into his leg.He died in a hospital a few days later; his body was passed to a special poison branch of the British Ministry of Defense (MOD) that discovered the pellet during an autopsy. The prime suspects were the Bulgarian secret police: Georgi Markov had defected from Bulgaria some years previously and had subsequently written books and made radio broadcasts which were highly critical of the Bulgarian communist regime. However, it was believed at the time that Bulgaria would not have been able to produce the pellet, and it was also believed that the KGB had supplied it.

The KGB denied any involvement although high-profile KGB defectors Oleg Kalugin and Oleg Gordievsky have since confirmed the KGB's involvement. Earlier, Soviet dissident Aleksandr Solzhenitsyn also suffered (but survived) ricin-like symptoms after an encounter in 1971 with KGB agents.Given ricin's extreme toxicity and utility as an agent of chemical/biological warfare, it is noteworthy that the production of the toxin is rather difficult to limit. The castor bean plant from which ricin is derived is a common ornamental and can be grown at home without any special care, and the major reason ricin is a public health threat is that it is easy to obtain. Under both the 1972 Biological Weapons Convention and the 1997 Chemical Weapons Convention, ricin is listed as a schedule 1 controlled substance. Despite this, more than 1 million tonnes of castor beans are processed each year, and approximately 5% of the total is rendered into a waste containing negligible concentrations of undenatured ricin toxin. Ricin is several orders of magnitude less toxic than botulinum or tetanus toxin, but the latter are harder to come by. Compared to botulinum or anthrax as biological weapons or chemical weapons, the quantity of ricin required to achieve LD50 over a large geographic area is significantly more than an agent such as anthrax (tons of ricin vs. only kilogram quantities of anthrax). Ricin is easy to produce, but is not as practical nor likely to cause as many casualties as other agents. Ricin is inactivated (the protein changes structure and becomes less dangerous) much more readily than anthrax spores, which may remain lethal for decades. Jan van Aken, a Dutch expert on biological weapons, explained in a report for The Sunshine Project that Al Qaeda's experiments with ricin suggest their inability to produce botulinum or anthrax.[49] A biopharmaceutical company called Soligenix, Inc. has developed a vaccine called RiVax™ that is currently in trials. Incidents involving ricin Main article: Incidents involving ricin Ricin has been involved in a number of incidents, including the high-profile assassination of Georgi Markov in 1978 using a weapon disguised as an umbrella. Several terrorists and terrorist groups have experimented with ricin, and several incidents of the poison being mailed to U.S. politicians have occurred in the 21st century.

Poisonous food plants 

Many food plants possess toxic parts, are toxic unless processed, or are toxic at certain stages of their life. Notable examples include:

*          Apple (Malus domestica). Seeds are mildly poisonous, containing a small amount of amygdalin, a cyanogenic glycoside. The quantity contained is usually not enough to be dangerous to humans, but it is possible to ingest enough seeds to provide a fatal dose.

*          Cassava (Manihot esculenta) Roots and leaves contain two cyanogenic glucosides, linamarin and lotaustralin. These are decomposed by linamarase, a naturally occurring enzyme in cassava, liberating hydrogen cyanide .  Cassava varieties are often categorized as either sweet or bitter, respectively signifying the absence or presence of toxic levels of cyanogenic glucosides. The 'sweet' cultivars can produce as little as 20 milligrams of cyanide per kilogram of fresh roots, whereas bitter ones may produce more than 50 times as much (1 g/kg). Cassavas grown during drought are especially high in these toxins.[ A dose of 40 mg of pure cassava cyanogenic glucoside is sufficient to kill a cow. It can also cause severe calcific pancreatitis in humans, leading to chronic pancreatitis. Processing (soaking, cooking, fermentation, etc.) of cassava root is necessary to remove the toxins and avoid getting sick. "Chronic, low-level cyanide exposure is associated with the development of goiter and with tropical ataxic neuropathy, a nerve-damaging disorder that renders a person unsteady and uncoordinated. Severe cyanide poisoning, particularly during famines, is associated with outbreaks of a debilitating, irreversible paralytic disorder called konzo and, in some cases, death. The incidence of konzo and tropical ataxic neuropathy can be as high as 3 percent in some areas." For some smaller-rooted sweet varieties, cooking is sufficient to eliminate all toxicity. The cyanide is carried away in the processing water and the amounts produced in domestic consumption are too small to have environmental impact.The larger-rooted, bitter varieties used for production of flour or starch must be processed to remove the cyanogenic glucosides. Industrial production of cassava flour, even at the cottage level, may generate enough cyanide and cyanogenic glycosides in the effluents to have a severe environmental impact.

*          Cherry (Prunus cerasus), as well as other Prunus species such as peach (Prunus persica), plum (Prunus domestica), almond (Prunus dulcis), and apricot (Prunus armeniaca). Leaves and seeds contain cyanogenic glycosides.

*          Indian pea (Lathyrus sativus). A legume grown in Asia and East Africa as an insurance crop for use during famines. Like other grain legumes, L. sativus produces a high-protein seed. The seeds contain variable amounts of β-N-Oxalyl-L-α,β-diaminopropionic acid or ODAP, a neurotoxic amino acid.[ODAP causes wasting and paralysis if eaten over a long period, and is considered as the cause of the disease neurolathyrism, a neurodegenerative disease that causes paralysis of the lower body and emaciation of gluteal muscle (buttocks). The disease has been seen to occur after famines in Europe (France, Spain, Germany), North Africa and South Asia, and is still prevalent in Eritrea, Ethiopiaand parts of Afghanistan when Lathyrus seed is the exclusive or main source of nutrients for extended periods.

*          Kidney bean or common bean (Phaseolus vulgaris). The toxic compound phytohaemagglutinin, a lectin, is present in many varieties of common bean but is especially concentrated in red kidney beans. The lectin has a number of effects on cell metabolism; it induces mitosis, and affects the cell membrane in regard to transport and permeability to proteins. It agglutinates most mammalian red blood cell types. The primary symptoms of phytohaemagglutinin poisoning are nausea, vomiting, and diarrhea. Onset is from 1 to 3 hours after consumption of improperly prepared beans, and symptoms typically resolve within a few hours.  Consumption of as few as four or five raw kidney beans may be sufficient to trigger symptoms. Phytohaemagglutinin can be deactivated by cooking beans at 100 °C (212 °F) for ten minutes. However, for dry beans the U.S. Food and Drug Administration (FDA) also recommends an initial soak of at least 5 hours in water; the soaking water should be discarded.  The ten minutes at 100 °C(212 °F) is required to degrade the toxin, and is much shorter than the hours required to fully cook the beans themselves. However, lower cooking temperatures may have the paradoxical effect of potentiating the toxic effect of haemagglutinin. Beans cooked at 80 °C (176 °F) are reported to be up five times as toxic as raw beans.  Outbreaks of poisoning have been associated with the use of slow cookers, the low cooking temperatures of which may be unable to degrade the toxin.

*          Nutmeg (Myristica fragrans). Contains myristicin. Myristicin is a naturally occurring insecticide and acaricide with possible neurotoxic effects on neuroblastoma cells.  It has psychoactive properties at doses much higher than used in cooking. Raw nutmeg produces anticholinergic-like symptoms, attributed to myristicin and elemicin.   The intoxicating effects of myristicin can lead to a physical state somewhere between waking and dreaming; euphoria is reported and nausea is often experienced. Users also report bloodshot eyes and memory disturbances. Myristicin is also known to induce hallucinogenic effects, such as visual distortions. Nutmeg intoxication has an extremely long time before peak is reached, sometimes taking up to seven hours, and effects can be felt for 24 hours, with lingering effects lasting up to 72 hours.

*          Lima bean or butter bean (Phaseolus lunatus). Raw beans contain dangerous amounts of linamarin, a cyanogenic glucoside.

*          Lupin. Some varieties have edible seeds. Sweet Lupins have less, and Bitter Lupins have more of the toxic alkaloids lupinine and sparteine.

*          Onions and garlic. Onions and garlic (genus Allium) contain thiosulphate, which in high doses is toxic to dogs, cats and some other livestock.

*          Potato (Solanum tuberosum). Potatoes contain toxic compounds known as glycoalkaloids, of which the most prevalent are solanine and chaconine. Solanine is also found in other members of the Solanaceae plant family, which includes Atropa belladonna ("deadly nightshade") and Hyoscyamus niger ("henbane") . The concentration of glycoalkaloid in wild potatoes suffices to produce toxic effects in humans. The toxin affects the nervous system, causing headaches, diarrhea and intense digestive disturbances, cramps, weakness and confusion, and in severe cases coma and death. Poisoning from cultivated potatoes occurs very rarely however, as the toxic compounds in the potato plant are, in general, concentrated in the green portions of the plant and in the fruits,  and cultivated potato varieties contain lower toxin levels.  Cooking at high temperatures (over 170 °C or 340 °F) also partly destroys the toxin. However, exposure to light, physical damage, and age increase glycoalkaloid content within the tuber,  the highest concentrations occurring just underneath the skin. Tubers which are exposed to light turn green from chlorophyll synthesis, thus giving a visual clue as to areas of the tuber that may have become more toxic; however, this does not provide a definitive guide, as greening and glycoalkaloid accumulation can occur independently of each other. Some varieties of potato contain greater glycoalkaloid concentrations than others; breeders developing new varieties test for this, and sometimes have to discard an otherwise promising cultivar. Breeders try to keep solanine levels below 200 mg/kg (200 ppmw). However, when these commercial varieties turn green, even they can approach concentrations of solanine of 1000 mg/kg (1000 ppmw). The U.S. National Toxicology Program suggests that the average American consume at most 12.5 mg/day of solanine from potatoes (the toxic dose is actually several times this, depending on body weight). Douglas L. Holt, the State Extension Specialist for Food Safety at the University of Missouri, notes that no reported cases of potato-source solanine poisoning have occurred in the U.S. in the last 50 years, and most cases involved eating green potatoes or drinking potato-leaf tea

*          Rhubarb (Rheum rhaponticum). The leaf stalks (petioles) are edible, but the leaves themselves contain notable quantities of oxalic acid, which is a nephrotoxic and corrosiveacid that is present in many plants. Symptoms of poisoning include kidney disorders, convulsions and coma. Rarely fatal. The LD50 (median lethal dose) for pure oxalic acid in rats is about 375 mg/kg body weight, or about 25 grams for a 65 kg (~140 lb) human. While the oxalic acid content of rhubarb leaves can vary, a typical value is about 0.5%, so a rather unlikely 5 kg of the extremely sour leaves would have to be consumed to reach an LD50 of oxalic acid. Cooking the leaves with soda can make them more poisonous by producing soluble oxalates.

*           However, the leaves are believed to also contain an additional, unidentified toxin, which might be an anthraquinone glycoside(also known as senna glycosides)  In the edible leaf stalks (petioles), the amount of oxalic acid is much lower, only about 2-2.5% of the total acidity which is dominated bymalic acid.  This means that even the raw stalks may not be hazardous (though they are generally thought to be in the US). However the tart taste of raw stalks is so strong as to be unpalatable to many.

*          Tomato (Solanum lycopersicum). Like many other nightshades, tomato leaves and stems contain solanine that is toxic if ingested, causing digestive upset and nervous excitement. Use of tomato leaves as a tea (tisane) has been responsible for at least one death.[Leaves, stems, and green unripe fruit of the tomato plant also contain small amounts of the poisonous alkaloid tomatine, although levels are generally too small to be dangerous. Ripe tomatoes do not contain any detectable tomatine.Tomato plants can be toxic to dogs if they eat large amounts of the fruit, or chew plant material.

The poisonous plants guide

*          Abrus precatorius (known commonly as jequiritycrab's eyerosary pea, 'John Crow' beadprecatory beanIndian licoriceakar sagagiddee giddeejumbiebeadruti, and weather plant). The attractive seeds (usually about the size of a ladybug, glossy red with one black dot) contain abrin, which is related to ricin, and very potent. Symptoms of poisoning include nausea, vomiting, convulsions, liver failure, and death, usually after several days. Ingesting a single seed can kill an adult human. The seeds have been used as beads in jewelry, which is dangerous; inhaled dust is toxic and pinpricks can be fatal. The seeds are unfortunately attractive to children.

*          Aconitum (Several species, commonly called aconitewolfsbane and monkshood) All parts are poisonous. The poison is an alkaloid called aconitine, which disables nerves, lowers blood pressure, and can stop the heart. Even casual skin contact should be avoided; symptoms include numbness, tingling, and cardiac irregularity. It has been used as poison for bullets (by Germany in WWII), as a bait and arrow poison (ancient Greece), and to poison water supplies (reports from ancient Asia). If ingested, it usually causes burning, tingling, and numbness in the mouth, followed by vomiting and nervous excitement. It is usually a quick-acting poison. Used in the past for killing wolves (hence one of the common names).

*          Actaea pachypoda (also known as doll's eyes or white baneberry). All parts are poisonous, but especially the berries, the consumption of which has a sedative effect on cardiac muscle tissue and can cause cardiac arrest.

*          Adam and Eve – see Arum maculatum.

*          Adenium obesum (also known as sabi starkudu or desert-rose). Exudes a highly toxic sap which is used by the Meridian High and Hadza in Tanzania to coat arrow-tips for hunting.

*          Aesculus hippocastanum (commonly known as horse-chestnut). All parts of the plant are poisonous, causing nausea, muscle twitches, and sometimes paralysis.

*          African sumac – see Rhus lancia.

*          Agave. The juice of a number of species causes acute contact dermatitis, with blistering lasting several weeks and recurring itching for several years thereafter.

*          Ageratina altissima (commonly known as white snakeroot). All parts are poisonous, causing nausea and vomiting. Often fatal. Milk from cattle that have eaten white snakeroot can sicken, or kill, humans (milk sickness).

*          Agrostemma githago (commonly known as corn cockle). Contains the saponins githagin and agrostemmic acid. All parts of the plant are reported to be poisonous and may produce chronic or acute, potentially fatal poisoning, although it has been used in folk medicine to treat a range of ills, from parasites to cancer . There are no known recent clinical studies of corn cockle which provide a basis for dosage recommendations, however doses higher than 3 g [of seeds] are considered toxic.

*          Akar saga – see Abrus precatorius.

*          Amianthium – see Deathcamas.

*          Angel's Trumpet – see Brugmansia.

*          Angel Wings – see Caladium.

*          Anticlea – see Deathcamas.

*          Aquilegia (also known as columbine). Several species. Seeds and roots contain cardiogenic toxins which cause both severe gastroenteritis and heart palpitations if consumed. The flowers of various species were consumed in moderation by Native Americans as a condiment with other fresh greens, and are reported to be very sweet, and safe if consumed in small quantities. Native Americans also used very small amounts of the root as an effective treatment for ulcers. However, the medical use of this plant is difficult due to its high toxicity; columbine poisonings are easily fatal.

*          Areca catechu (commonly known as betel nut palm and pinyang). The nut contains an alkaloid related to nicotine which is addictive. It produces a mild high, some stimulation, and lots of red saliva, which cannot be swallowed as it causes nausea. Withdrawal causes headache and sweats. Use is correlated with mouth cancer, and to a lesser extent asthma and heart disease.

*          Arum maculatum (commonly known as cuckoo-pintlords and ladiesjack in the pulpitwake robinwild arumdevils and angelscows and bullsAdam and Eve, bobbins and starch-root). All parts of the plant can produce allergic reactions. The bright red berries contain oxalates of saponins and can cause skin, mouth and throat irritation, resulting in swelling, burning pain, breathing difficulties and stomach upset. One of the most common causes of plant poisoning.

*          Asparagus. The berries are poisonous.

*          Atropa belladonna (commonly known as deadly nightshadebelladonnadevil's cherry and dwale, an Anglo-Saxon term meaning stupifying drink). One of the most toxic plants found in the Western hemisphere. All parts of the plant contain tropane alkaloids.[ The active agents are atropine, hyoscine (scopolamine), and hyoscyamine, which have anticholinergic properties. The symptoms of poisoning include dilated pupils, sensitivity to light, blurred vision, tachycardia, loss of balance, staggering, headache, rash, flushing, dry mouth and throat, slurred speech, urinary retention, constipation, confusion, hallucinations, delirium, and convulsion.  The root of the plant is generally the most toxic part, though this can vary from one specimen to another. Ingestion of a single leaf of the plant can be fatal to an adult. Casual contact with the leaves can cause skin pustules. The berries pose the greatest danger to children because they look attractive and have a somewhat sweet taste. The consumption of two to five berries by children and ten to twenty berries by adults can be lethal. In 2009 a case of A. belladonna being mistaken for blueberries, with six berries ingested by an adult woman, was documented to result in severe anticholinergic syndrome.[The plant's deadly symptoms are caused by atropine's disruption of the parasympathetic nervous system's ability to regulate involuntary activities such as sweating, breathing, and heart rate. The antidote for atropine poisoning is physostigmine or pilocarpine.[A. belladonna is also toxic to many domestic animals, causing narcosis and paralysis.However, cattle and rabbits eat the plant seemingly without suffering harmful effects.[36]In humans its anticholinergic properties will cause the disruption of cognitive capacities like memory and learning.

*          Autumn crocus – see Colchicum autumnale.

*          Azalea – see Rhododendron.

*          Bittersweet nightshade – see Solanum dulcamara.

*          Black hellebore – see Helleborus niger.

*          Black locust – see Robinia pseudoacacia and see Robinia.

*          Black nightshade – see Solanum nigrum.

*          Bleeding heart – see Dicentra cucullaria.

*          Blind-your-eye mangrove – see Excoecaria agallocha.

*          Blister Bush – see Peucedanum galbanum.

*          Bloodroot – see Sanguinaria canadensis.

*          Blue-green algae – see Cyanobacteria.

*          Bobbins – see Arum maculatum.

*          Bracken – see Pteridium aquilinum.

*          Broom – see Cytisus scoparius.

*          Brugmansia (commonly known as angel's trumpet). All parts of the plant contain the tropane alkaloids scopolamine and atropine. Often fatal.

*          Calabar Bean – see Physostigma venenosum.

*          Caladium (commonly known as angel wingselephant ear and heart of Jesus). All parts of the plant are poisonous. Symptoms are generally irritation, pain, and swelling of tissues. If the mouth or tongue swell, breathing may be fatally blocked.

*          Castor oil plant – see Ricinus communis.

*          Cerbera odollam (commonly known as the suicide tree). The seeds contain cerberin, a potent toxin related to digoxin. The poison blocks the calcium ion channels in heart muscle, causing disruption of the heart beat. This is typically fatal and can result from ingesting a single seed. Cerberin is difficult to detect in autopsies and its taste can be masked with strong spices, such as a curry. It is often used in homicide and suicide in India; Kerala's suicide rate is about three times the Indian average. In 2004, a team led by Yvan Gaillard of the Laboratory of Analytical Toxicology in La Voulte-sur-Rhône, France, documented more than 500 cases of fatal Cerbera poisoning between 1989 and 1999 in Kerala. They said "To the best of our knowledge, no plant in the world is responsible for as many deaths by suicide as the odollam tree.' A related species is Cerbera tanghin the seeds of which are known as tanghin poison nut and have been used as an 'ordeal poison'.

*          Chelidonium majus (also known as greater celandine). The whole plant is toxic in moderate doses as it contains a range of isoquinoline alkaloids, but there are claimed to be therapeutic uses when used at the correct dosage. The main alkaloid present in the herb and root is coptisine, with berberine, chelidonine, sanguinarine and chelerythrinealso present. Sanguinarine is particularly toxic with an LD50 of only 18 mg per kg body weight.The effect of the fresh herb is analgesic, cholagogic, antimicrobial andoncostatic,with action as a central nervous system sedative. In animal tests, Chelidonium majus is shown to be cytostatic. Early studies showed that the latex causescontact dermatitis and eye irritation. Stains on skin of the fingers are sometimes reported to cause eye irritation after rubbing the eyes or handling contact lenses. The characteristic latex also contains proteolytic enzymes and the phytocystatin chelidostatin, a cysteine protease inhibitor.

*          Christmas rose – see Helleborus niger.

*          Cicuta (several species) (commonly known as water hemlockcowbanewild carrotsnakeweedpoison parsnipfalse parsleychildren's bane and death-of-man). The root, when freshly pulled out of the ground, is extremely poisonous and contains the toxin cicutoxin, a central nervous system stimulant, resulting in seizures. When dried, the poisonous effect is reduced. The most common species is C. maculata; one of the species found in the Western USA, C. douglasii, often found in pastures and swamps, has especially thick stems and very large and sturdy flowers which are sometimes harvested for flower displays. This is inadvisable as the sap is also toxic.

*          Cocklebur – see Xanthium.

*          Colchicum autumnale (commonly known as autumn crocus and meadow saffron). The bulbs contain colchicine. Colchicine poisoning has been compared to arsenic poisoning; symptoms start 2 to 5 hours after the toxic dose has been ingested and include burning in the mouth and throat, fever, vomiting, diarrhea, abdominal pain and kidney failure. These symptoms may set in as many as 24 hours after the exposure. Onset of multiple-system organ failure may occur within 24 to 72 hours. This includes hypovolemic shock due to extreme vascular damage and fluid loss through the GI tract, which may result in death. Additionally, sufferers may experience kidney damage resulting in low urine output and bloody urine; low white blood cell counts (persisting for several days); anemia; muscular weakness; and respiratory failure. Recovery may begin within 6 to 8 days. There is no specific antidote for colchicine, although various treatments do exist.Despite dosing issues concerning its toxicity, colchicine is prescribed in the treatment of gout, familial Mediterranean fever, pericarditis and Behçet's disease. It is also being investigated for its use as an anti-cancer drug.

*          Columbine – see Aquilegia.

*          Conium maculatum (commonly known as hemlockpoison hemlockspotted parsleyspotted cowbanebad-man's oatmealpoison snakeweed and beaver poison). All parts of the plant contain the alkaloid coniine which causes stomach pains, vomiting, and progressive paralysis of the central nervous system. Can be fatal; it is the poison that killed Socrates. Not to be confused with hemlock trees (Tsuga spp), which, while not edible, are not nearly as toxic as the herbaceous plant Conium.

*          Consolida (commonly known as larkspur).Young plants and seeds are poisonous, causing nausea, muscle twitches, paralysis. Often fatal.

*          Convallaria majalis (commonly known as lily of the valley). Contains 38 different cardiac glycosides.

*          Coriaria myrtifolia (commonly known as redoul). A Mediterranean plant containing the toxin coriamyrtin, ingestion of which produces digestive, neurological and respiratory problems. The poisonous fruits superficially resemble blackberries and may mistakenly be eaten as such. Can be fatal in children.

*          Corn cockle – see Agrostemma githago.

*          Corn lily – see Veratrum.

*          Cowbane – see Cicuta.

*          Cows and bulls – see Arum maculatum.

*          Crab's eye – see Abrus precatorius.

*          Cuckoo-pint – see Arum maculatum.

*          Cyanobacteria A phylum of bacteria, commonly known as blue-green algae. Many different species, including Anacystis cynea and Anabaena circinalis. Produce several different toxins known collectively as cyanotoxins. These can include neurotoxins, hepatotoxins, endotoxins and cytotoxins. Potentially hazardous particularly to marine animals, but also to humans.

*          Cytisus scoparius (commonly known as broom or common broom). Contains toxic alkaloids that depress the heart and nervous system.[49] The alkaloid sparteine is a class 1a antiarrhythmic agent; a sodium channel blocker. It is not FDA approved for human use as an antiarrhythmic agent, and it is not included in the Vaughn Williams classification of antiarrhythmic drugs.

*          Daffodil – see Narcissus.

*          Daphne. The berries (either red or yellow) are poisonous, causing burns to mouth and digestive tract, followed by coma. Often fatal.

*          Darnel – see Lolium temulentum.

*          Datura Contains the alkaloids scopolamine and atropine. Datura has been used as a hallucinogenic drug by the native peoples of the Americas and others. Incorrect dosage can lead to death.

*          Datura stramonium (commonly known as jimson weedthorn applestinkweed and Jamestown weed). All parts of the plant are poisonous, causing abnormal thirst, vision distortions, delirium, incoherence, coma. Often fatal. A significant grazing livestock poison in North America.

*          Deadly nightshade – see Atropa belladonna.

*          Deathcamas – various genera in the Melanthieae have species whose common name includes "deathcamas", including AmianthiumAnticleaStenanthium,Toxicoscordion and Zigadenus. All parts of the plants are toxic, due to the presence of alkaloids. Grazing animals, such as sheep and cattle, may be affected and human fatalities have occurred.

*          Delphinium (also known as larkspur). Contains the alkaloid delsoline. Young plants and seeds are poisonous, causing nausea, muscle twitches, paralysis, often fatal.

*          Dendrocnide moroides (also known as stinging tree and gympie gympie). Capable of inflicting a painful sting when touched. The stinging may last for several days and is exacerbated by touching, rubbing, and cold. Can be fatal.

*          Devils and angels – see Arum maculatum.

*          Dicentra cucullaria (also known as bleeding heart and Dutchman's breeches). Leaves and roots are poisonous and cause convulsions and other nervous symptoms.

*          Dichapetalum cymosum (also known as gifblaar). Well known as a livestock poison in South Africa; this plant contains the metabolic poison fluoroacetic acid.

*          Dieffenbachia (commonly known as dumbcane'). All parts are poisonous, causing intense burning, irritation, and immobility of the tongue, mouth, and throat. Swelling can be severe enough to block breathing, leading to death.

*          Digitalis purpurea (commonly known as foxglove). The leaves, seeds, and flowers are poisonous, containing cardiac or other steroid glycosides. These cause irregular heartbeat, general digestive upset, and confusion. Can be fatal.

*          Doll's eyes – see Actaea pachypoda.

*          Dumbcane – see Dieffenbachia.

*          Dutchman's breeches – see Dicentra cucullaria.

*          Elder/Elderberry – see Sambucus.

*          Euonymus europaeus (commonly known as spindleEuropean spindle or spindle tree). The fruit is poisonous, containing amongst other substances, the alkaloids the obromine and caffeine, as well as an extremely bitter terpene. Poisonings are more common in young children, who are enticed by the brightly coloured fruits. Ingestion can result in liver and kidney damage and even death. There are many other species of Euonymus, many of which are also poisonous.

*          Excoecaria agallocha (commonly known as milky mangroveblind-your-eye mangrove and river poison tree). Contact with latex can cause skin irritation and blistering; eye contact can cause temporary blindness.

*          False acacia – see Robinia pseudoacacia and see Robinia.

*          False hellebore – see Veratrum.

*          Foxglove – see Digitalis purpurea.

*          Frangipani – see Plumeria.

*          Gelsemium sempervirens (commonly known as yellow jessamine). All parts are poisonous, causing nausea and vomiting. Often fatal. It is possible to become ill from ingesting honey made from jessamine nectar.

*          Giant hogweed – see Heracleum mantegazzianum.

*          Giddee giddee – see Abrus precatorius.

*          Gifblaar – see Dichapetalum cymosum.

*          Greater celandine – see Chelidonium majus.

*          Gympie gympie – see Dendrocnide moroides.

*          Heart of Jesus – see Caladium.

*          Hedera helix (or common ivy) The leaves and berries are poisonous, causing stomach pains, labored breathing, possible coma.

*          Helleborus niger (also known as Christmas rose) Contains protoanemonin,or ranunculin,which has an acrid taste and can cause burning of the eyes, mouth and throat, oral ulceration, gastroenteritis and hematemesis.

*          Hemlock – see Conium maculatum

*          Hemlock water-dropwort – see Oenanthe crocata.

*          Henbane – see Hyoscyamus niger.

*          Heracleum mantegazzianum (also known as giant hogweed). The sap is phototoxic, causing phytophotodermatitis (severe skin inflammations) when affected skin is exposed to sunlight or to UV-rays. Initially the skin colours red and starts itching. Then blisters form as reaction continues over 48 hours. They form black or purplish scars, which can last several years. Hospitalization may become necessary. Presence of minute amounts of sap in the eyes can lead to temporary or even permanent blindness.

*          Hippomane mancinella (commonly known as manchineel). All parts of this tree, including the fruit, contain toxic phorbol esters typical of the Euphorbiaceae plant family. Specifically the tree contains 12-deoxy-5-hydroxyphorbol-6gamma, 7alpha-oxide, hippomanins, mancinellin, sapogenin, phloracetophenone-2, 4-dimethylether is present in the leaves, while the fruits possess physostigmine.[55] Contact with the milky white latex produces strong allergic dermatitis.[56] Standing beneath the tree during rain will cause blistering of the skin from even slight contact with this liquid (even a small drop of rain with the milky substance in it will cause the skin to blister). Burning tree parts may causeblindness if the smoke reaches the eyes. The fruit can also be fatal if eaten. Many trees carry a warning sign, while others have been marked with a red "X" on the trunk to indicate danger. In the French Antilles the trees are often marked with a painted red band a few feet above the ground.[57] The Caribs used the latex of this tree to poison their arrows and would tie captives to the trunk of the tree, ensuring a slow and painful death. A poultice of arrowroot (Maranta arundinacea) was used by the Arawaks and Taíno as an antidote against such arrow poisons.[58] The Caribs were also known to poison the water supply of their enemies with the leaves.   Spanish explorer Juan Ponce de León was struck by an arrow that had been poisoned with manchineel sap during battle with the Calusa in Florida, dying shortly thereafter.

*          Horse chestnut – see Aesculus hippocastanum.

*          Holly (European) – see Ilex aquifolium.

*          Hyacinth – see Hyacinthus orientalis.

*          Hyacinthus orientalis (commonly known as hyacinth). The bulbs are poisonous, causing nausea, vomiting, gasping, convulsions, and possibly death. Even handling the bulbs can cause skin irritation.

*          Hyoscyamus niger (commonly known as henbane). Seeds and foliage contain hyoscyamine, scopolamine and other tropane alkaloids. Can produce dilated pupils, hallucinations, increased heart rate, convulsions, vomiting, hypertension and ataxia.

*          Ilex aquifolium (commonly known as European holly). The berries cause gastroenteritis, resulting in nausea, vomiting and diarrhea.

*          Indian licorice – see Abrus precatorius.

*          Ivy (Common) – see Hedera helix.

*          Jack in the pulpit – see Arum maculatum.

*          Jacobaea vulgaris (commonly known as ragwort). Contains many different alkaloids, including jacobine, jaconine, jacozine, otosenine, retrorsine, seneciphylline, senecionine, and senkirkine. Poisonous to livestock and hence of concern to people who keep horses and cattle. Horses do not normally eat fresh ragwort due to its bitter taste, however it loses this taste when dried, and become dangerous in hay. The result, if sufficient quantity is consumed, can be irreversible cirrhosis of the liver. Signs that a horse has been poisoned include yellow mucus membranes, depression, and lack of coordination. The danger is that the toxin can have a cumulative effect; the alkaloid does not actually accumulate in the liver but a breakdown product can damage DNA and progressively kills cells. Jacobaea vulgaris is also theoretically poisonous to humans, although poisoning is unlikely as it is distasteful and not used as a food. However some sensitive individuals can suffer from an allergic skin reaction after handling the plant because, like many members of the compositae family, it contains sesquiterpine lactones (which are different from the pyrrolizidine alkaloids which are responsible for the toxic effects), which can cause compositae dermatitis.

*          Jamestown weed – see Datura stramonium and Datura.

*          Jequirity – see Abrus precatorius.

*          Jerusalem cherry – see Solanum pseudocapsicum.

*          Jimson weed – see Datura stramonium and Datura.

*          'John Crow' Bead – see Abrus precatorius.

*          Jumbie bead – see Abrus precatorius.

*          Kalanchoe delagoensis (commonly known as mother of millions) Contains bufadienolide cardiac glycosides[61] which can cause cardiac poisoning, particularly in grazing animals.During 1997, 125 head of cattle died after eating mother-of-millions on a travelling stock reserve near Moree, NSW.

*          Kalmia latifolia (commonly known as mountain laurel). Contains andromedotoxin and arbutin. The green parts of the plant, flowers, twigs, and pollen are all toxic, and symptoms of toxicity begin to appear about 6 hours following ingestion. Poisoning produces anorexia, repeated swallowing, profuse salivation, depression, uncoordination, vomiting, frequent defecation, watering of the eyes, irregular or difficulty breathing, weakness, cardiac distress, convulsions, coma, and eventually death. Autopsy will show gastrointestinal irritation and hemorrhage.

*          Laburnum. All parts of the plant and especially the seeds are poisonous and can be lethal if consumed in excess. The main toxin is cytisine, a nicotinic receptor agonist. Symptoms of poisoning may include intense sleepiness, vomiting, excitement, staggering, convulsive movements, slight frothing at the mouth, unequally dilated pupils, coma and death. In some cases, diarrhea is very severe and at times the convulsions are markedly tetanic.

*          Larkspur – see Consolida and Delphinium.

*          Ligustrum (several species, commonly known as privet). Berries and leaves are poisonous. Berries contain syringin, which causes digestive disturbances, nervous symptoms. Can be fatal. Privet is one of several plants which are poisonous to horses. Privet pollen is known to cause asthma and eczema in sufferers. It is banned from sale or cultivation in New Zealand due to the effects of its pollen on asthma sufferers.

*          Lilium (commonly known as lily). Most have an unknown water-soluble toxin found in all parts of the plant. Extremely poisonous, yet attractive, to cats, causing acute renal failure; 2 petals can kill.

*          Lily – see Lilium.

*          Lily of the valley – see Convallaria majalis.

*          Lolium temulentum (commonly called darnel or poison ryegrass). The seeds and seed heads of this common garden weed may contain the alkaloids temuline and loliine. Some experts also point to the fungus ergot or fungi of the genus endoconidium, both of which grow on the seed heads of rye grasses, as an additional source of toxicity.

*          Lords and ladies – see Arum maculatum.

*          Madiera winter cherry – see Solanum pseudocapsicum.

*          Manchineel tree – see Hippomane mancinella.

*          Mango tree – Mango peel and sap contains urushiol, the chemical in poison ivy and poison sumac that can cause urushiol-induced contact dermatitis in susceptible people. Cross-reactions between mango contact allergens and urushiol have been observed. Those with a history of poison ivy or poison oak contact dermatitis may be most at risk for such an allergic reaction. Urushiol is also present in mango leaves and stems. During mango's primary ripening season, it is the most common source of plant dermatitis in Hawaii.

*          Mayapple – see Podophyllum peltatum.

*          Meadow saffron – see Colchicum autumnale.

*          Menispermum (commonly known as moonseed). The fruits and seeds are poisonous, causing nausea and vomiting. Often fatal.

*          Milky mangrove – see Excoecaria agallocha.

*          Monkshood – see Aconitum.

*          Moonseed – see Menispermum.

*          Mother of millions – see Kalanchoe delagoensis.

*          Mountain laurel – see Kalmia latifolia.

*          Narcissus (commonly known as daffodil). Various species and garden cultivars. The bulbs are poisonous and cause nausea, vomiting, and diarrhea. Can be fatal. Stems also cause headaches, vomiting, and blurred vision. Nerium oleander (commonly known as oleander). All parts are toxic, but especially the leaves and woody stems. Contains nerioside, oleandroside, saponins and cardiac glycosides. Causes severe digestive upset, heart trouble and contact dermatitis. The smoke of burning oleander can cause reactions in the lungs, and can be fatal.

*          Oak – see Quercus.

*          Oenanthe crocata (commonly known as hemlock water dropwort). Contains oenanthotoxin. The leaves may be eaten safely bylivestock, but the stems and especially the carbohydrate-rich roots are much more poisonous. Animals familiar with eating the leaves may eat the roots when these are exposed during ditch clearance – one root is sufficient to kill a cow, and human fatalities are also known in these circumstances. Scientists at the University of Eastern Piedmont in Italy claimed to have identified this as the plant responsible for producing the sardonic grin,[and it is the most-likely candidate for the "sardonic herb," which was a neuro toxic plant used for the ritual killing of elderly people in Phoenician Sardinia. When these people were unable to support themselves, they were intoxicated with this herb and then dropped from a high rock or beaten to death. Criminals were also executed in this way.

*          Oleander – see Nerium oleander.

*          Ongaonga – see Urtica ferox.

*          Passiflora caerulea (also known as the blue passion flower or the common passion flower). The leaves contain cyanogenic glycoside, which breaks down into cyanide.

*          Passion flower (blue or common) – see Passiflora caerulea.

*          Peucedanum galbanum (commonly known as blister bush). All parts are poisonous, and contact causes painful blistering that is intensified with exposure to sunlight.

*          Physostigma venenosum (commonly known as calabar bean and also as ordeal beans due to their former use in trials by ordeal). The toxin in the seeds is the para sympathomimetic alkaloid physostigmine, a reversible cholinesterase inhibitor. Symptoms of poisoning include copious saliva, nausea, vomiting, diarrhea, anorexia, dizziness, headache, stomach pain, sweating, dyspepsia and seizures. and can lead to cholinergic syndrome or "SLUDGE syndrome". Medicinal uses of physostigmine include the treatment of myasthenia gravis, glaucoma, Alzheimer's disease and delayed gastric emptying.

*          Plumeria (commonly known as frangipani). Contact with the milky latex may irritate eyes and skin.

*          Phytolacca (commonly known as pokeweed). Leaves, berries and roots contain phytolaccatoxin and phytolaccigenin. Toxin in young leaves is reduced with repeated boiling and draining. Ingestion of poisonous parts of the plant may cause severe stomach cramping, persistent diarrhea, nausea, vomiting (sometimes bloody), slow and difficult breathing, weakness, spasms, hypertension, severe convulsions, and death.

*          Podophyllum peltatum (commonly known as Mayapple). Green portions of the plant, unripe fruit, and especially the rhizome contain the non-alkaloid toxin podophyllotoxin, which causes diarrhea, severe digestive upset.

*          Poison hemlock – see Conium maculatum.

*          Poison ivy – see Toxic Dendron.

*          Poison oak – see Toxicodendron.

*          Poison parsnip – see Cicuta.

*          Poison sumac – see Toxicodendron.

*          Poison ryegrass – see Lolium temulentum.

*          Pokeweed – see Phytolacca.

*          Precatory bean – see Abrus precatorius.

*          Privet – see Ligustrum.

*          Pteridium aquilinum (commonly known as bracken). Carcinogenic to humans and animals such as mice, rats, horses and cattle when ingested. The carcinogenic compound is ptaquiloside or PTQ, which can leach from the plant into the water supply, which may explain an increase in the incidence of gastric and oesophageal cancers in humans in bracken-rich areas.

*          Quercus (several species, commonly known as oak)). The leaves and acorns of oak species are poisonous in large amounts to humans and livestock, including cattle, horses, sheep and goats, but not pigs. Poisoning is caused by the toxin tannic acid, which causes gastroenteritis, heart trouble, contact dermatitis and kidney damage. Symptoms of poisoning include lack of appetite, depression, constipation, diarrhea (which may contain blood), blood in urine, and colic. Rarely fatal however, and in fact after proper processing acorns are consumed as a staple in many parts of the world.

*          Ragwort – see Jacobaea vulgaris.

*          Redoul – see Coriaria myrtifolia.

*          Rhododendron (certain species commonly known as Azaleas). All parts are poisonous and cause nausea, vomiting, depression, breathing difficulties, coma. Rarely fatal.

*          Rhus lancia (commonly known as African sumac). Closely related to poison ivy, all parts of this tree contain low levels of a highly irritating oil with urushiol. Skin reactions can include blisters and rashes. It spreads readily to clothes and back again, and has a very long life. Infections can follow scratching. As urushiol is not a poison but an allergen, it will not affect certain people. The smoke of burning Rhus lancia can cause reactions in the lungs, and can be fatal.

*          Ricinus communis (commonly known as castor oil plant or Palma Christi). The seeds contain ricin, an extremely toxic water-soluble protein. Also present are ricinine, an alkaloid, and an irritant oil. According to the 2007 edition of the Guinness Book of World Records, this plant is the most poisonous in the world. Castor oil, long used as a laxative, muscle rub, and in cosmetics, is made from the seeds, but the ricin is removed during processing. The lethal dose in adults is considered to be 4 to 8 seeds, but reports of actual poisoning are relatively rare. If ingested, symptoms may be delayed by up to 36 hours but commonly begin within 2–4 hours. These include a burning sensation in mouth and throat, abdominal pain, purging and bloody diarrhea. Within several days there is severe dehydration, a drop in blood pressure and a decrease in urine. Unless treated, death can be expected to occur within 3–5 days; if victims have not succumbed after this time, they often recover. In 1978, ricin was used to assassinate Georgi Markov, a Bulgarian dissident. He was stabbed with the point of an umbrella while waiting at a bus stop near Waterloo Station in London. After his death a perforated metallic pellet was found embedded in his leg; this had presumably contained the ricin toxin. Toxicity varies among animal species: 4 seeds will kill a rabbit, 5 a sheep, 6 an ox or horse, 7 a pig, and 11 a dog. Poisoning occurs when animals ingest broken seeds or break the seed by chewing; intact seeds may pass through the digestive tract without releasing the toxin. Ducks have shown substantial resistance to the seeds: it takes an average of 80 to kill them

*          River poison tree – see Excoecaria agallocha.

*          Robinia (also known as black locust and false acacia etc.). All species produce toxic lectins.The poison is a complex mix of lectins with the highest concentration in the fruit and seed, followed by the root bark and the flower. There is little poison in the leaf.[74] The lectins, generally called robin are less toxic than those of e.g. Abrus (abrin) or Ricinus (ricin), and in non-fatal cases the toxic effects tend to be temporary.

*          Rosary pea – see Abrus precatorius.

*          Sambucus (commonly known as elder or elderberry). The roots are considered poisonous and cause nausea and digestive upset.

*          Sanguinaria canadensis (commonly known as bloodroot). The rhizome contains morphine-like benzylisoquinoline alkaloids, primarily the toxin sanguinarine. Sanguinarine kills animal cells by blocking the action of Na+/K+-ATPase transmembrane proteins. As a result, applying S. canadensis to the skin may destroy tissue and lead to the formation of a large scab, called an eschar. Although applying escharotic agents, including S. canadensis, to the skin is sometimes suggested as a home treatment for skin cancer, these attempts can be severely disfiguring,as well as unsuccessful. Case reports have shown that in such instances tumor has recurred and/or metastasized]The United States Food and Drug Administration (FDA) has approved the inclusion of sanguinarine in toothpastes as an antibacterial or anti-plaque agent,[78][79][80][81] although it is believed that this use may cause leukoplakia, a premalignant oral lesion.[The safe level of sanguinarine in such products is subject to regulation and debate.[S. canadensis extracts have also been promoted by some supplement companies as a treatment or cure for cancer, but the FDA has listed some of these products among its "187 Fake Cancer 'Cures' Consumers Should Avoid".[85] Bloodroot is a popular red natural dye used by Native American artists, especially among southeastern river cane basket makers.[86] However in spite of supposed curative properties and historical use by Native Americans as an emetic, due to its toxicity internal use is not advisable (sanguinarine has an LD50 of only 18 mg per kg body weight).[43]

*          Solanum dulcamara (commonly known as bittersweet nightshade). All parts are poisonous, containing solanine and causing fatigue, paralysis, convulsions, and diarrhea. Rarely fatal.

*          Solanum nigrum (commonly known as black nightshade). All parts of the plant except the ripe fruit contain the toxic glycoalkaloid solanine. Solanine poisoning is primarily displayed by gastrointestinal and neurological disorders. Symptoms include nausea, diarrhea, vomiting, stomach cramps, burning of the throat, cardiac dysrhythmia, headache and dizziness. In more severe cases, hallucinations, loss of sensation, paralysis, fever, jaundice, dilated pupils and hypothermia can result. In large quantities, solanine poisoning can be fatal.

*          Solanum pseudocapsicum (commonly known as Jerusalem cherryMadiera winter cherry and winter cherry). All parts, especially the berries, are poisonous, causing nausea and vomiting. It is occasionally fatal, especially to children.

*          Sosnowsky's Hogweed. Plant has toxic sap and causes skin inflammation on contact.

*          Spindle tree or spindle – see Euonymus europaeus.

*          Starch-root – see Arum maculatum.

*          Stenanthium – see Deathcamas.

*          Stinging tree – see Dendrocnide moroides.

*          Stinkweed – see Datura stramonium and Datura.

*          Strychnine tree – see Strychnos nux-vomica.

*          Strychnos nux-vomica (commonly known as the strychnine tree). The seeds usually contain about 1.5% strychnine, an extremely bitter and deadly alkaloid. This substance throws a human into intense muscle convulsions and usually kills within three hours. The bark of the tree may also contain brucine, another dangerous chemical.

*          Suicide tree – see Cerbera odollam.

*          Taxus baccata (commonly known as English yew', common yew and graveyard tree). Nearly all parts contain toxic taxanes (except the red, fleshy, and slightly sweet aril surrounding the toxic seeds).The seeds themselves are particularly toxic if chewed.[Several people have committed suicide by ingesting leaves and seeds,including Catuvolcus, king of a tribe in what is now Belgium.

*          Thorn apple – see Datura stramonium and Datura.

*          Toxicodendron Several species, including Toxicodendron radicans (commonly known as poison ivy), Toxicodendron diversilobum (commonly known as poison-oak), and Toxicodendron vernix (commonly known as poison sumac). All parts of these plants contain a highly irritating oil with urushiol. Skin reactions can include blisters and rashes. It spreads readily to clothes and back again, and has a very long life. Infections can follow scratching. Despite the common names, urushiol is actually not a poison but an allergen, and because of this it will not affect certain people. The smoke of burning poison ivy can cause reactions in the lungs, and can be fatal.

*          Toxicoscordion – see Deathcamas.

*          Urtica ferox (commonly known as ongaonga). Even the lightest touch can result in a painful sting that lasts several days.

*          Veratrum (commonly known as false hellebore and corn lily). Several species, containing highly toxic steroidal alkaloids (e.g. veratridine) that activate sodium ion channels and cause rapid cardiac failure and death if ingested.[All parts of the plant are poisonous, with the root and rhizomes being the most toxic.[Symptoms typically occur between 30 minutes and 4 hours after ingestion and include nausea and vomiting, abdominal pain, numbness, headache, sweating, muscle weakness, bradycardia, hypotension, cardiac arrhythmia, and seizures.[Treatment for poisoning includes gastrointestinal decontamination with activated charcoal followed by supportive care including fluid replacement, antiemetics for persistent nausea and vomiting, atropine for treatment of bradycardia, and vasopressors for the treatment of hypotension.[Native Americans used the juice pressed from the roots to poison arrows before combat. The dried powdered root of this plant was also used as an insecticide.[The plants' teratogenic properties and ability to induce severe birth defects were well known to Native Americans,[although they also used minute amounts of the winter-harvested root (combined with Salvia dorii to potentiate its effects and reduce the toxicity of the herb) to treat cancerous tumors. The toxic steroidal alkaloids are produced only when the plants are in active growth, so herbalists and Native Americans who used this plant for medicinal purposes harvested the roots during the winter months when the levels of toxic constituents were at their lowest. The roots of V. nigrum and V. schindleri have been used in Chinese herbalism (where plants of this genus are known as "li lu" (藜蘆). Li lu is used internally as a powerful emetic of last resort, and topically to kill external parasites, treat tinea and scabies, and stop itching.[However some herbalists refuse to prescribe li lu internally, citing the extreme difficulty in preparing a safe and effective dosage, and that death has occurred at a dosage of 0.6 grams.[During the 1930sVeratrum extracts were investigated in the treatment of high blood pressure in humans. However patients often suffered side effects due to the narrow therapeutic index of these products. Due to its toxicity, the use of Veratrum as a treatment for high blood pressure in humans was discontinued.

*          Wake robin – see Arum maculatum.

*          Water hemlock – see Cicuta.

*          White baneberry – see Actaea pachypoda.

*          White snakeroot – see Ageratina altissima.

*          Wild arum – see Arum maculatum.

*          Winter cherry – see Solanum pseudocapsicum.

*          Wolfsbane – see Aconitum.

*          Xanthium (commonly known as cocklebur). Several species. The Common Cocklebur (X. strumarium), a native of North America, can be poisonous to livestock, including horses, cattle, and sheep. Some domestic animals will avoid consuming the plant if other forage is present, but less discriminating animals, such as pigs, will consume the plants and then sicken and die. The seedlings and seeds are the most toxic parts of the plants. Symptoms usually occur within a few hours, producing unsteadiness and weakness, depression, nausea and vomiting, twisting of the neck muscles, rapid and weak pulse, difficulty breathing, and eventually death. Xanthium has also been used for its medicinal properties and for making yellow dye, as indicated by its name (Greek xanthos = 'yellow').

*          Yellow jessamine – see Gelsemium sempervirens.

*          Yew – see Taxus baccata.

*          Zantedeschia (several species, also known as Lily of the Nile and Calla lily). Contain calcium oxalate. All parts of the plant are toxic, producing irritation and swelling of the mouth and throat, acute vomiting and diarrhea.[96] Can be fatal.

*          Zigadenus – see Deathcamas

 

 

 

 

 

 

 

 

 Plague and the black death

 

Plague in Biological warfare.    

Epidemiologist of plague following use as a biological weapon.       

Present day incidents of suspected attempted attacks using plague       

Larry Wayne Harris and Levitt American white supremacist  bio terrorists?       

 Al-Quaida 

General on Bubonic Plague & the Black Death.   

Signs and symptoms of Bubonic Plague.     

Pathophysiology of Bubonic Plague.    Treatment of Bubonic plague       Laboratory Testing for Bubonic Plague

Pneumonic plague       

 Pathology and transmission      

Symptoms       

Prognosis and treatment    

 Present Day

 Occurrences of Pneumonic Plague.      

The plague doctor

 

Bubonic plague 

Bubonic plague  is a zoonotic disease, circulating mainly among small rodents and their fleas, and is one of three types of infections caused by Yersinia pestis (formerly known as Pasteurella pestis), which belongs to the family Enterobacteriaceae. Without treatment, the bubonic plague kills about two out of three infected humans within 4 days.

The term bubonic plague is derived from the Greek word bubo, meaning "swollen gland." Swollen lymph nodes (buboes) especially occur in the armpit and groin in persons suffering from bubonic plague. Bubonic plague was often used synonymously for plague, but it does in fact refer specifically to an infection that enters through the skin and travels through the lymphatics, as is often seen in flea-borne infections.  The first recorded epidemic ravaged the Byzantine Empire during the sixth century, and was named the Plague of Justinian after emperor Justitinian.

Bubonic plague — along with the septicemic plague and the pneumonic plague is generally believed to be the cause of the Black Death that swept through Europe in the 14th century and killed an estimated 75 million people, or 30-60% of the European population. Because the plague killed so many of the working population, wages rose and some historians have seen this as a turning point in European economic development. Justinian I, who was infected but survived through extensive treatment.  The Black Death originated in or near China and spread by way of the Silk Road or by ship. Carried by the fleas on rats, it spread along trade routes and reached the Crimea in 1347.

 Signs and symptoms

The most famous symptom of bubonic plague is painful, swollen lymph glands, called buboes. These are commonly found in the armpits, groin or neck. Due to its bite-based form of infection, the bubonic plague is often the first step of a progressive series of illnesses. Bubonic plague symptoms appear suddenly, usually 2–5 days after exposure to the bacteria. Symptoms include:

Chills

General ill feeling (malaise)

High fever (39 °Celsius; 102 °Fahrenheit)

Muscle Cramps

Seizures

Smooth, painful lymph gland swelling called a bubo, commonly found in the groin, but may occur in the armpits or neck, most often at the site of the initial infection (bite or scratch)

Pain may occur in the area before the swelling appears

Skin color changes to a pink hue in some extreme cases

Bleeding out of the cochlea will begin after 12 hours of infection.

Other symptoms include heavy breathing, continuous blood vomiting, aching limbs, coughing, and extreme pain. The pain is usually caused by the decay or decomposure of the skin while the person is still alive. Additional symptoms include extreme fatigue, gastrointestinal problems, lenticulae (black dots scattered throughout the body), delirium and coma.

Two other types of Y. pestis plague are pneumonic and septicemic. Pneumonic plague, unlike the bubonic or septicemic, induces coughing and is very infectious, allowing to it be spread person-to-person.

Pathophysiology

Bubonic plague is an infection of the lymphatic system, usually resulting from the bite of an infected flea, Xenopsylla cheopis (the rat flea). The fleas are often found on rodents such as rats and mice, and seek out other prey when their rodent hosts die. The bacteria form aggregates in the gut of infected fleas and this results in the flea regurgitating ingested blood, which is now infected, into the bite site of a rodent or human host. Once established, bacteria rapidly spread to the lymph nodes and multiply. Y. pestis bacilli can resist phagocytosis and even reproduce inside phagocytes and kill them. As the disease progresses, the lymph nodes can hemorrhage and become swollen and necrotic. Bubonic plague can progress to lethal septicemic plague in some cases. The plague is also known to spread to the lungs and become the disease known as the pneumonic plague. This form of the disease is highly communicable as the bacteria can be transmitted in droplets emitted when coughing or sneezing, as well as physical contact with victims of the plague or flea-bearing rodents that carry the plague.

Treatment

Several classes of antibiotics are effective in treating bubonic plague. These include aminoglycosides such as streptomycin and gentamicin, tetracyclines (especially doxycycline), and the fluoroquinolone ciprofloxacin. Mortality associated with treated cases of bubonic plague is about 1-15%, compared to a mortality rate of 50-90% in untreated cases.

People potentially infected with the plague need immediate treatment and should be given antibiotics within 24 hours of the first symptoms to prevent death. Other treatments include oxygen, intravenous fluids, and respiratory support. People who have had contact with anyone infected by pneumonic plague are given prophylactic antibiotics.

Laboratory testing

Laboratory testing is required, in order to diagnose and confirm plague. Ideally, confirmation is through the identification of Y. pestis culture from a patient sample. Confirmation of infection can be done by examining serum taken during the early and late stages of infection. To quickly screen for the Y. pestis antigen in patients, rapid dipstick tests have been developed for field use.

Pneumonic plague

Pneumonic plague, a severe type of lung infection, is one of three main forms of plague, all of which are caused by the bacterium Yersinia pestis. It is more virulent and rare than bubonic plague. The difference between the versions of plague is simply the location of the infection in the body; the bubonic plague is an infection of the lymphatic system, the pneumonic plague is an infection of the respiratory system, and the septicemic plague is an infection in the blood stream.

Typically, pneumonic form is due to a secondary spread from advanced infection of an initial bubonic form. Primary pneumonic plague results from inhalation of fine infective droplets and can be transmitted from human to human without involvement of fleas or animals. Untreated pneumonic plague has a very high fatality rate.

 

Since 2002, the World Health Organization (WHO) has reported six plague outbreaks, though some may go unreported because they often happen in remote areas. Between 1998 and 2009, nearly 24,000 cases have been reported, including about 2,000 deaths, in Africa, Asia, the Americas and Eastern Europe. 98% of the world's cases occur in Africa.

 Pathology and transmission

Pneumonic plague can be caused in two ways: primary, which results from the inhalation of aerosolised plague bacteria, or secondary, when septicemic plague spreads into lung tissue from the bloodstream. Pneumonic plague is not exclusively vector-borne like bubonic plague; instead it can be spread from person to person. There have been cases of pneumonic plague resulting from the dissection or handling of contaminated animal tissue. This is one type of the formerly known Black Death. It could kill 90%–95% of a population if the victims coughed and passed on the bacteria.

 Symptoms

The most apparent symptom of pneumonic plague is coughing, often with hemoptysis (coughing up blood). With pneumonic plague, the first signs of illness are fever, headache, weakness, and rapidly developing pneumonia with shortness of breath, chest pain, cough, and sometimes bloody or watery sputum. The pneumonia progresses for two to four days and may cause respiratory failure and shock. Patients will die without early treatment, some within 36 hours.

Initial pneumonic plague symptoms can often include:

Fever

Weakness

Headache

Nausea

Rapidly developing pneumonia with:

Shortness of breath

Chest pain

Cough

Bloody or watery sputum (saliva and discharge from respiratory passages).

Prognosis and treatment

Pneumonic plague is a very aggressive infection requiring early treatment. Antibiotics must be given within 24 hours of first symptoms to reduce the risk of death,. Streptomycin, gentamicin, tetracyclines, and chloramphenicol are all effective against pneumonic plague.

Antibiotic treatment for 7 days will protect people who have had direct, close contact with infected patients. Wearing a close-fitting surgical mask also protects against infection.

The mortality rate from untreated pneumonic plague approaches 100%.

Present Day Occurrences  of Pneumonic Plague.

China

The People's Republic of China has eradicated the pneumonic plague from most parts of the country, but still reports occasional cases in remote Western areas where the disease is carried by rats and the marmots that live across the Himalayan plateau. Outbreaks can be caused when a person eats an infected marmot or comes into contact with fleas carried by rats. A 2006 WHO report from an international meeting on plague cited a Chinese government disease expert as saying that most cases of the plague in China's northwest occur when hunters are contaminated while skinning infected animals. The expert said at the time that due to the region's remoteness, the disease killed more than half the infected people. The report also said that since the 1990s, there was a rise in plague cases in humans—from fewer than 10 in the 1980s to nearly 100 cases in 1996 and 254 in 2000. Official statistics posted on the Chinese Health Ministry's Web site showed no cases of plague in 2007 and 2008.n September 2008, two persons in east Tibet died of pneumonic plague.

A recent outbreak of the disease in China began in August 2009 in Ziketan Town located in Qinghai Province. The town was sealed off and several people died as a result of the disease. According to spokesperson Vivian Tan of the WHO office in Beijing, "In cases like this [in August 2009], we encourage the authorities to identify cases, to investigate any suspicious symptoms among close contacts, and to treat confirmed cases as soon as possible. So far, they have done exactly that. There have been sporadic cases reported around the country in the last few years so the authorities do have the experience to deal with this."

In September 2010, there were 5 reported cases of pneumonic plague in Tibet.

Peru

Peru's health minister says an outbreak of plague has killed a 14-year-old boy and infected at least 31 people in a northern coastal province.

Health Minister Oscar Ugarte says authorities are screening sugar and fish meal exports from Ascope province, located about 325 miles (520 km) northwest of Lima. Popular Chicama beach isn't far away.

Ugarte says the boy, who had Down syndrome, died of bubonic plague July 26, 2010.

He said August 1 that most of the infections are bubonic plague, with four cases of pneumonic plague. The former is transmitted by flea bites, the latter by airborne contagion. The disease is curable if treated early with antibiotics.

The first recorded plague outbreak in Peru was in 1903. The last, in 1994, killed 35 people.

 Recent notable cases

On November 2, 2007, wildlife biologist Eric York died of pneumonic plague in Grand Canyon National Park. York was exposed to the bacteria while conducting a necropsy on a mountain lion carcass.

Plague in Biological warfare.

Some of the earliest instances of biological warfare were said to have been product of the plague, as armies of the 14th century were recorded catapulting diseased corpses over the walls of towns and villages in order to spread the pestilence.

Later, plague was used during the Second Sino-Japanese War as a bacteriological weapon by the Imperial Japanese Army. These weapons were provided by Shirō Ishii's units and used in experiments on humans before being used on the field. For example, in 1940, the Imperial Japanese Army Air Service bombed Ningbo with fleas carrying the bubonic plague. During the Khabarovsk War Crime Trials, the accused, such as Major General Kiyashi Kawashima, testified that, in 1941, some 40 members of Unit 731 air-dropped plague-contaminated fleas on Changde. These operations caused epidemic plague outbreaks.

Epidemiology of plague following use as a biological weapon.

 that plague had been artificially disseminated would be the occurrence of cases in locations not known to have enzootic infection, in peThe Epidemiology of plague following its use as a biological weapon would differ substantially from that of naturally occurring infection. Intentional dissemination of plague would most probably occur via an aerosol of Y pestis, a mechanism that has been shown to produce disease in nonhuman primates. A pneumonic plague outbreak would result with symptoms initially resembling those of other severe respiratory illnesses. The size of the outbreak would depend on factors including the quantity of biological agent used, characteristics of the strain, environmental conditions, and methods of aerosolization. Symptoms would begin to occur 1 to 6 days following exposure, and people would die quickly following onset of symptoms. Indicationsrsons without known risk factors, and in the absence of prior rodent deaths.

Present day incidents of suspected attempted attacks using .

Al-Quaida 

It was reported in 2006 that an al-Quaida cell killed by the Black Death may have been developing biological weapons when it was infected and all the operatives succumbed to the infection. It was initially believed that they could have caught the disease through fleas on rats attracted by poor living conditions in their forest hideout. But there are now claims the cell was developing the disease as a weapon to use against western cities. Some experts said that the group was developing chemical and biological weapons.  Dr Igor Khrupinov, a biological weapons expert at Georgia University, told The Sun: "Al-Quaida is known to experiment with biological weapons. And this group has direct communication with other cells around the world."Contagious diseases, like Ebola and anthrax, occur in northern Africa. It makes sense that people are trying to use them against Western governments."  Dr Khrupinov, who was once a weapons adviser to the Soviet president Mikhail Gorbachev, added: "Instead of using bombs, people with infectious diseases could be walking through cities."

Post graduate terrorists.

It was reported last year that up to 100 potential terrorists had attempted to become postgraduate students in Britain in an attempt to use laboratories. Ian Kearns, from the Institute for Public Policy Research, told the newspaper: "The biological weapons threat is not going away. We're not ready for it."

Larry Wayne Harris and William Job Leavitt American white supremacist  Bio Terrorists?

The FBI arrested two men in 1998, including a self-professed white separatist, on charges of developing and stockpiling a biological agent -- suspected of being deadly anthrax -- and conspiring to use it as a weapon.

The FBI announced the arrests of Larry Wayne Harris and William Job Leavitt Jr. at a news conference Thursday. The men were taken into custody Wednesday evening and were being held at the Clark County Detention Center in Las Vegas.

"These individuals posed a potential chemical and biological threat to our community," said FBI Special Agent Bobby Siller. "It was suspected that these individuals were in possession of a dangerous biological chemical, anthrax." However, Leavitt's lawyer, Lamond Mills, said that what the FBI actually seized was a substance the two men hoped to test and market as an anthrax vaccine.

Tip off

The FBI was tipped off to Harris' alleged activities by a man in Las Vegas who said Harris had told him of his ability to make biological agents, a top law enforcement source told CNN. The man apparently went with Harris to a medical office outside Las Vegas to observe Harris' makeshift laboratory, an official said. Agents responding to the tip seized unknown materials and Petri dishes and "locked them up," the source said. "We're not sure what the hell they got."

Harris on probation for buying bubonic plague

Harris, 46, a native of West Virginia who now lives in Lancaster, Ohio, has a microbiology degree from Ohio State University. He has written extensively on the dangers of biological warfare and how people can protect themselves with massive doses of antibiotics. Harris has described himself as a white separatist. He once held the rank of lieutenant colonel in the far-right white separatist group Aryan Nations, and he has also told reporters that he is a follower of the Christian Identity movement. During the 1980s, Harris was questioned about his involvement with the Aryan Nations by the Secret Service in advance of a visit to Ohio State by then-President George Bush. In 1995, he was arrested after purchasing three vials of bubonic plague by mail from a Maryland laboratory. That was not in and of itself a crime, but Harris was convicted on two counts of mail fraud and one count of wire fraud for misrepresenting the purpose of the purchase, a federal offense. At the time, Harris told prosecutors in Lancaster he was worried about the effects of "super germ-carrying rats" coming from Iraq. Though still on probation for his 1995 conviction, he has permission to travel and gives speeches at gun shows about biological warfare.

Leavitt

A behavior science expert who looked at Harris for the FBI after his previous arrest advised agents "to take him seriously because he had this stuff before," a source said. Less is known about Leavitt, 47. The FBI affidavit says he is also a microbiologist who owns clinics in Logandale, Nevada, where he lives, and Frankfurt, Germany.

"My son is the most caring person you would ever find," said his mother, Betty Leavitt. Describing her son as a very religious Mormon, she said he "prays every time" there is danger of a world conflict and is "extremely concerned about germ warfare."

Separatist allegedly described New York attack

According to an affidavit filed with his arrest warrant, Harris told a group last summer of a 1995 plan to "place a 'globe' of bubonic plague toxins in a New York City subway station, where it would be broken by a passing subway train, causing hundreds of thousands of deaths."

He told the group, according to the affidavit, that "the Iraqis would be blamed for that event."

However, Siller said that there is as of yet no indication as to "what the target might have been or even if there was a target at this point."

The Plague Doctors.

Fourteenth century plague doctors who wore a bird-like mask were referred to as "beak doctors". Straps held the beak in front of the doctor's nose.  The mask had glass openings for the eyes and a curved beak was shaped like a bird's. The mask had two small nose holes and was a type of respirator. The mask they wore had a protruded beak which contained aromatic items. .  The beak could hold dried flowers (including roses and carnations), herbs (including mint), spices, camphor or a vinegar sponge.  The purpose of the mask was to keep away bad smells, which were thought to be the principal cause of the disease in the miasma theory of infection, before it was disproved by germ theory. Doctors believed the herbs would counter the "evil" smells of the plague and prevent them from becoming infected.

The beak doctor costume worn by the plague doctors had a wide brimmed leather hood to indicate their profession. They used wooden canes to point out areas needing attention and to examine the patients without touching them. The canes were also used to keep people away, to remove clothing from plague victims without having to touch them, and to take a patient's pulse

 

 

Bubonic plague 

Bubonic plague  is a zoonotic disease, circulating mainly among small rodents and their fleas, and is one of three types of infections caused by Yersinia pestis (formerly known as Pasteurella pestis), which belongs to the family Enterobacteriaceae. Without treatment, the bubonic plague kills about two out of three infected humans within 4 days.

The term bubonic plague is derived from the Greek word bubo, meaning "swollen gland." Swollen lymph nodes (buboes) especially occur in the armpit and groin in persons suffering from bubonic plague. Bubonic plague was often used synonymously for plague, but it does in fact refer specifically to an infection that enters through the skin and travels through the lymphatics, as is often seen in flea-borne infections.  The first recorded epidemic ravaged the Byzantine Empire during the sixth century, and was named the Plague of Justinian after emperor Justitinian.

Bubonic plague — along with the septicemic plague and the pneumonic plague is generally believed to be the cause of the Black Death that swept through Europe in the 14th century and killed an estimated 75 million people, or 30-60% of the European population. Because the plague killed so many of the working population, wages rose and some historians have seen this as a turning point in European economic development. Justinian I, who was infected but survived through extensive treatment.  The Black Death originated in or near China and spread by way of the Silk Road or by ship. Carried by the fleas on rats, it spread along trade routes and reached the Crimea in 1347.

 Signs and symptoms

The most famous symptom of bubonic plague is painful, swollen lymph glands, called buboes. These are commonly found in the armpits, groin or neck. Due to its bite-based form of infection, the bubonic plague is often the first step of a progressive series of illnesses. Bubonic plague symptoms appear suddenly, usually 2–5 days after exposure to the bacteria. Symptoms include:

Chills

General ill feeling (malaise)

High fever (39 °Celsius; 102 °Fahrenheit)

Muscle Cramps

Seizures

Smooth, painful lymph gland swelling called a bubo, commonly found in the groin, but may occur in the armpits or neck, most often at the site of the initial infection (bite or scratch)

Pain may occur in the area before the swelling appears

Skin color changes to a pink hue in some extreme cases

Bleeding out of the cochlea will begin after 12 hours of infection.

Other symptoms include heavy breathing, continuous blood vomiting, aching limbs, coughing, and extreme pain. The pain is usually caused by the decay or decomposure of the skin while the person is still alive. Additional symptoms include extreme fatigue, gastrointestinal problems, lenticulae (black dots scattered throughout the body), delirium and coma.

Two other types of Y. pestis plague are pneumonic and septicemic. Pneumonic plague, unlike the bubonic or septicemic, induces coughing and is very infectious, allowing to it be spread person-to-person.

Pathophysiology

Bubonic plague is an infection of the lymphatic system, usually resulting from the bite of an infected flea, Xenopsylla cheopis (the rat flea). The fleas are often found on rodents such as rats and mice, and seek out other prey when their rodent hosts die. The bacteria form aggregates in the gut of infected fleas and this results in the flea regurgitating ingested blood, which is now infected, into the bite site of a rodent or human host. Once established, bacteria rapidly spread to the lymph nodes and multiply. Y. pestis bacilli can resist phagocytosis and even reproduce inside phagocytes and kill them. As the disease progresses, the lymph nodes can hemorrhage and become swollen and necrotic. Bubonic plague can progress to lethal septicemic plague in some cases. The plague is also known to spread to the lungs and become the disease known as the pneumonic plague. This form of the disease is highly communicable as the bacteria can be transmitted in droplets emitted when coughing or sneezing, as well as physical contact with victims of the plague or flea-bearing rodents that carry the plague.

Treatment

Several classes of antibiotics are effective in treating bubonic plague. These include aminoglycosides such as streptomycin and gentamicin, tetracyclines (especially doxycycline), and the fluoroquinolone ciprofloxacin. Mortality associated with treated cases of bubonic plague is about 1-15%, compared to a mortality rate of 50-90% in untreated cases.

People potentially infected with the plague need immediate treatment and should be given antibiotics within 24 hours of the first symptoms to prevent death. Other treatments include oxygen, intravenous fluids, and respiratory support. People who have had contact with anyone infected by pneumonic plague are given prophylactic antibiotics.

Laboratory testing

Laboratory testing is required, in order to diagnose and confirm plague. Ideally, confirmation is through the identification of Y. pestis culture from a patient sample. Confirmation of infection can be done by examining serum taken during the early and late stages of infection. To quickly screen for the Y. pestis antigen in patients, rapid dipstick tests have been developed for field use.

Pneumonic plague

Pneumonic plague, a severe type of lung infection, is one of three main forms of plague, all of which are caused by the bacterium Yersinia pestis. It is more virulent and rare than bubonic plague. The difference between the versions of plague is simply the location of the infection in the body; the bubonic plague is an infection of the lymphatic system, the pneumonic plague is an infection of the respiratory system, and the septicemic plague is an infection in the blood stream.

Typically, pneumonic form is due to a secondary spread from advanced infection of an initial bubonic form. Primary pneumonic plague results from inhalation of fine infective droplets and can be transmitted from human to human without involvement of fleas or animals. Untreated pneumonic plague has a very high fatality rate.

 

Since 2002, the World Health Organization (WHO) has reported six plague outbreaks, though some may go unreported because they often happen in remote areas. Between 1998 and 2009, nearly 24,000 cases have been reported, including about 2,000 deaths, in Africa, Asia, the Americas and Eastern Europe. 98% of the world's cases occur in Africa.

 Pathology and transmission

Pneumonic plague can be caused in two ways: primary, which results from the inhalation of aerosolised plague bacteria, or secondary, when septicemic plague spreads into lung tissue from the bloodstream. Pneumonic plague is not exclusively vector-borne like bubonic plague; instead it can be spread from person to person. There have been cases of pneumonic plague resulting from the dissection or handling of contaminated animal tissue. This is one type of the formerly known Black Death. It could kill 90%–95% of a population if the victims coughed and passed on the bacteria.

 Symptoms

The most apparent symptom of pneumonic plague is coughing, often with hemoptysis (coughing up blood). With pneumonic plague, the first signs of illness are fever, headache, weakness, and rapidly developing pneumonia with shortness of breath, chest pain, cough, and sometimes bloody or watery sputum. The pneumonia progresses for two to four days and may cause respiratory failure and shock. Patients will die without early treatment, some within 36 hours.

Initial pneumonic plague symptoms can often include:

Fever

Weakness

Headache

Nausea

Rapidly developing pneumonia with:

Shortness of breath

Chest pain

Cough

Bloody or watery sputum (saliva and discharge from respiratory passages).

Prognosis and treatment

Pneumonic plague is a very aggressive infection requiring early treatment. Antibiotics must be given within 24 hours of first symptoms to reduce the risk of death,. Streptomycin, gentamicin, tetracyclines, and chloramphenicol are all effective against pneumonic plague.

Antibiotic treatment for 7 days will protect people who have had direct, close contact with infected patients. Wearing a close-fitting surgical mask also protects against infection.

The mortality rate from untreated pneumonic plague approaches 100%.

Present Day Occurrences  of Pneumonic Plague.

China

The People's Republic of China has eradicated the pneumonic plague from most parts of the country, but still reports occasional cases in remote Western areas where the disease is carried by rats and the marmots that live across the Himalayan plateau. Outbreaks can be caused when a person eats an infected marmot or comes into contact with fleas carried by rats. A 2006 WHO report from an international meeting on plague cited a Chinese government disease expert as saying that most cases of the plague in China's northwest occur when hunters are contaminated while skinning infected animals. The expert said at the time that due to the region's remoteness, the disease killed more than half the infected people. The report also said that since the 1990s, there was a rise in plague cases in humans—from fewer than 10 in the 1980s to nearly 100 cases in 1996 and 254 in 2000. Official statistics posted on the Chinese Health Ministry's Web site showed no cases of plague in 2007 and 2008.n September 2008, two persons in east Tibet died of pneumonic plague.

A recent outbreak of the disease in China began in August 2009 in Ziketan Town located in Qinghai Province. The town was sealed off and several people died as a result of the disease. According to spokesperson Vivian Tan of the WHO office in Beijing, "In cases like this [in August 2009], we encourage the authorities to identify cases, to investigate any suspicious symptoms among close contacts, and to treat confirmed cases as soon as possible. So far, they have done exactly that. There have been sporadic cases reported around the country in the last few years so the authorities do have the experience to deal with this."

In September 2010, there were 5 reported cases of pneumonic plague in Tibet.

Peru

Peru's health minister says an outbreak of plague has killed a 14-year-old boy and infected at least 31 people in a northern coastal province.

Health Minister Oscar Ugarte says authorities are screening sugar and fish meal exports from Ascope province, located about 325 miles (520 km) northwest of Lima. Popular Chicama beach isn't far away.

Ugarte says the boy, who had Down syndrome, died of bubonic plague July 26, 2010.

He said August 1 that most of the infections are bubonic plague, with four cases of pneumonic plague. The former is transmitted by flea bites, the latter by airborne contagion. The disease is curable if treated early with antibiotics.

The first recorded plague outbreak in Peru was in 1903. The last, in 1994, killed 35 people.

 Recent notable cases

On November 2, 2007, wildlife biologist Eric York died of pneumonic plague in Grand Canyon National Park. York was exposed to the bacteria while conducting a necropsy on a mountain lion carcass.

Plague in Biological warfare.

Some of the earliest instances of biological warfare were said to have been product of the plague, as armies of the 14th century were recorded catapulting diseased corpses over the walls of towns and villages in order to spread the pestilence.

Later, plague was used during the Second Sino-Japanese War as a bacteriological weapon by the Imperial Japanese Army. These weapons were provided by Shirō Ishii's units and used in experiments on humans before being used on the field. For example, in 1940, the Imperial Japanese Army Air Service bombed Ningbo with fleas carrying the bubonic plague. During the Khabarovsk War Crime Trials, the accused, such as Major General Kiyashi Kawashima, testified that, in 1941, some 40 members of Unit 731 air-dropped plague-contaminated fleas on Changde. These operations caused epidemic plague outbreaks.

Epidemiology of plague following use as a biological weapon.

 that plague had been artificially disseminated would be the occurrence of cases in locations not known to have enzootic infection, in peThe Epidemiology of plague following its use as a biological weapon would differ substantially from that of naturally occurring infection. Intentional dissemination of plague would most probably occur via an aerosol of Y pestis, a mechanism that has been shown to produce disease in nonhuman primates. A pneumonic plague outbreak would result with symptoms initially resembling those of other severe respiratory illnesses. The size of the outbreak would depend on factors including the quantity of biological agent used, characteristics of the strain, environmental conditions, and methods of aerosolization. Symptoms would begin to occur 1 to 6 days following exposure, and people would die quickly following onset of symptoms. Indicationsrsons without known risk factors, and in the absence of prior rodent deaths.

Present day incidents of suspected attempted attacks using .

Al-Quaida 

It was reported in 2006 that an al-Quaida cell killed by the Black Death may have been developing biological weapons when it was infected and all the operatives succumbed to the infection. It was initially believed that they could have caught the disease through fleas on rats attracted by poor living conditions in their forest hideout. But there are now claims the cell was developing the disease as a weapon to use against western cities. Some experts said that the group was developing chemical and biological weapons.  Dr Igor Khrupinov, a biological weapons expert at Georgia University, told The Sun: "Al-Quaida is known to experiment with biological weapons. And this group has direct communication with other cells around the world."Contagious diseases, like Ebola and anthrax, occur in northern Africa. It makes sense that people are trying to use them against Western governments."  Dr Khrupinov, who was once a weapons adviser to the Soviet president Mikhail Gorbachev, added: "Instead of using bombs, people with infectious diseases could be walking through cities."

Post graduate terrorists.

It was reported last year that up to 100 potential terrorists had attempted to become postgraduate students in Britain in an attempt to use laboratories. Ian Kearns, from the Institute for Public Policy Research, told the newspaper: "The biological weapons threat is not going away. We're not ready for it."

Larry Wayne Harris and William Job Leavitt American white supremacist  Bio Terrorists?

The FBI arrested two men in 1998, including a self-professed white separatist, on charges of developing and stockpiling a biological agent -- suspected of being deadly anthrax -- and conspiring to use it as a weapon.

The FBI announced the arrests of Larry Wayne Harris and William Job Leavitt Jr. at a news conference Thursday. The men were taken into custody Wednesday evening and were being held at the Clark County Detention Center in Las Vegas.

"These individuals posed a potential chemical and biological threat to our community," said FBI Special Agent Bobby Siller. "It was suspected that these individuals were in possession of a dangerous biological chemical, anthrax." However, Leavitt's lawyer, Lamond Mills, said that what the FBI actually seized was a substance the two men hoped to test and market as an anthrax vaccine.

Tip off

The FBI was tipped off to Harris' alleged activities by a man in Las Vegas who said Harris had told him of his ability to make biological agents, a top law enforcement source told CNN. The man apparently went with Harris to a medical office outside Las Vegas to observe Harris' makeshift laboratory, an official said. Agents responding to the tip seized unknown materials and Petri dishes and "locked them up," the source said. "We're not sure what the hell they got."

Harris on probation for buying bubonic plague

Harris, 46, a native of West Virginia who now lives in Lancaster, Ohio, has a microbiology degree from Ohio State University. He has written extensively on the dangers of biological warfare and how people can protect themselves with massive doses of antibiotics. Harris has described himself as a white separatist. He once held the rank of lieutenant colonel in the far-right white separatist group Aryan Nations, and he has also told reporters that he is a follower of the Christian Identity movement. During the 1980s, Harris was questioned about his involvement with the Aryan Nations by the Secret Service in advance of a visit to Ohio State by then-President George Bush. In 1995, he was arrested after purchasing three vials of bubonic plague by mail from a Maryland laboratory. That was not in and of itself a crime, but Harris was convicted on two counts of mail fraud and one count of wire fraud for misrepresenting the purpose of the purchase, a federal offense. At the time, Harris told prosecutors in Lancaster he was worried about the effects of "super germ-carrying rats" coming from Iraq. Though still on probation for his 1995 conviction, he has permission to travel and gives speeches at gun shows about biological warfare.

Leavitt

A behavior science expert who looked at Harris for the FBI after his previous arrest advised agents "to take him seriously because he had this stuff before," a source said. Less is known about Leavitt, 47. The FBI affidavit says he is also a microbiologist who owns clinics in Logandale, Nevada, where he lives, and Frankfurt, Germany.

"My son is the most caring person you would ever find," said his mother, Betty Leavitt. Describing her son as a very religious Mormon, she said he "prays every time" there is danger of a world conflict and is "extremely concerned about germ warfare."

Separatist allegedly described New York attack

According to an affidavit filed with his arrest warrant, Harris told a group last summer of a 1995 plan to "place a 'globe' of bubonic plague toxins in a New York City subway station, where it would be broken by a passing subway train, causing hundreds of thousands of deaths."

He told the group, according to the affidavit, that "the Iraqis would be blamed for that event."

However, Siller said that there is as of yet no indication as to "what the target might have been or even if there was a target at this point."

The Plague Doctors.

Fourteenth century plague doctors who wore a bird-like mask were referred to as "beak doctors". Straps held the beak in front of the doctor's nose.  The mask had glass openings for the eyes and a curved beak was shaped like a bird's. The mask had two small nose holes and was a type of respirator. The mask they wore had a protruded beak which contained aromatic items. .  The beak could hold dried flowers (including roses and carnations), herbs (including mint), spices, camphor or a vinegar sponge.  The purpose of the mask was to keep away bad smells, which were thought to be the principal cause of the disease in the miasma theory of infection, before it was disproved by germ theory. Doctors believed the herbs would counter the "evil" smells of the plague and prevent them from becoming infected.

The beak doctor costume worn by the plague doctors had a wide brimmed leather hood to indicate their profession. They used wooden canes to point out areas needing attention and to examine the patients without touching them. The canes were also used to keep people away, to remove clothing from plague victims without having to touch them, and to take a patient's pulse

 

 

Bubonic plague 

Bubonic plague  is a zoonotic disease, circulating mainly among small rodents and their fleas, and is one of three types of infections caused by Yersinia pestis (formerly known as Pasteurella pestis), which belongs to the family Enterobacteriaceae. Without treatment, the bubonic plague kills about two out of three infected humans within 4 days.

The term bubonic plague is derived from the Greek word bubo, meaning "swollen gland." Swollen lymph nodes (buboes) especially occur in the armpit and groin in persons suffering from bubonic plague. Bubonic plague was often used synonymously for plague, but it does in fact refer specifically to an infection that enters through the skin and travels through the lymphatics, as is often seen in flea-borne infections.  The first recorded epidemic ravaged the Byzantine Empire during the sixth century, and was named the Plague of Justinian after emperor Justitinian.

Bubonic plague — along with the septicemic plague and the pneumonic plague is generally believed to be the cause of the Black Death that swept through Europe in the 14th century and killed an estimated 75 million people, or 30-60% of the European population. Because the plague killed so many of the working population, wages rose and some historians have seen this as a turning point in European economic development. Justinian I, who was infected but survived through extensive treatment.  The Black Death originated in or near China and spread by way of the Silk Road or by ship. Carried by the fleas on rats, it spread along trade routes and reached the Crimea in 1347.

 Signs and symptoms

The most famous symptom of bubonic plague is painful, swollen lymph glands, called buboes. These are commonly found in the armpits, groin or neck. Due to its bite-based form of infection, the bubonic plague is often the first step of a progressive series of illnesses. Bubonic plague symptoms appear suddenly, usually 2–5 days after exposure to the bacteria. Symptoms include:

Chills

General ill feeling (malaise)

High fever (39 °Celsius; 102 °Fahrenheit)

Muscle Cramps

Seizures

Smooth, painful lymph gland swelling called a bubo, commonly found in the groin, but may occur in the armpits or neck, most often at the site of the initial infection (bite or scratch)

Pain may occur in the area before the swelling appears

Skin color changes to a pink hue in some extreme cases

Bleeding out of the cochlea will begin after 12 hours of infection.

Other symptoms include heavy breathing, continuous blood vomiting, aching limbs, coughing, and extreme pain. The pain is usually caused by the decay or decomposure of the skin while the person is still alive. Additional symptoms include extreme fatigue, gastrointestinal problems, lenticulae (black dots scattered throughout the body), delirium and coma.

Two other types of Y. pestis plague are pneumonic and septicemic. Pneumonic plague, unlike the bubonic or septicemic, induces coughing and is very infectious, allowing to it be spread person-to-person.

Pathophysiology

Bubonic plague is an infection of the lymphatic system, usually resulting from the bite of an infected flea, Xenopsylla cheopis (the rat flea). The fleas are often found on rodents such as rats and mice, and seek out other prey when their rodent hosts die. The bacteria form aggregates in the gut of infected fleas and this results in the flea regurgitating ingested blood, which is now infected, into the bite site of a rodent or human host. Once established, bacteria rapidly spread to the lymph nodes and multiply. Y. pestis bacilli can resist phagocytosis and even reproduce inside phagocytes and kill them. As the disease progresses, the lymph nodes can hemorrhage and become swollen and necrotic. Bubonic plague can progress to lethal septicemic plague in some cases. The plague is also known to spread to the lungs and become the disease known as the pneumonic plague. This form of the disease is highly communicable as the bacteria can be transmitted in droplets emitted when coughing or sneezing, as well as physical contact with victims of the plague or flea-bearing rodents that carry the plague.

Treatment

Several classes of antibiotics are effective in treating bubonic plague. These include aminoglycosides such as streptomycin and gentamicin, tetracyclines (especially doxycycline), and the fluoroquinolone ciprofloxacin. Mortality associated with treated cases of bubonic plague is about 1-15%, compared to a mortality rate of 50-90% in untreated cases.

People potentially infected with the plague need immediate treatment and should be given antibiotics within 24 hours of the first symptoms to prevent death. Other treatments include oxygen, intravenous fluids, and respiratory support. People who have had contact with anyone infected by pneumonic plague are given prophylactic antibiotics.

Laboratory testing

Laboratory testing is required, in order to diagnose and confirm plague. Ideally, confirmation is through the identification of Y. pestis culture from a patient sample. Confirmation of infection can be done by examining serum taken during the early and late stages of infection. To quickly screen for the Y. pestis antigen in patients, rapid dipstick tests have been developed for field use.

Pneumonic plague

Pneumonic plague, a severe type of lung infection, is one of three main forms of plague, all of which are caused by the bacterium Yersinia pestis. It is more virulent and rare than bubonic plague. The difference between the versions of plague is simply the location of the infection in the body; the bubonic plague is an infection of the lymphatic system, the pneumonic plague is an infection of the respiratory system, and the septicemic plague is an infection in the blood stream.

Typically, pneumonic form is due to a secondary spread from advanced infection of an initial bubonic form. Primary pneumonic plague results from inhalation of fine infective droplets and can be transmitted from human to human without involvement of fleas or animals. Untreated pneumonic plague has a very high fatality rate.

 

Since 2002, the World Health Organization (WHO) has reported six plague outbreaks, though some may go unreported because they often happen in remote areas. Between 1998 and 2009, nearly 24,000 cases have been reported, including about 2,000 deaths, in Africa, Asia, the Americas and Eastern Europe. 98% of the world's cases occur in Africa.

 Pathology and transmission

Pneumonic plague can be caused in two ways: primary, which results from the inhalation of aerosolised plague bacteria, or secondary, when septicemic plague spreads into lung tissue from the bloodstream. Pneumonic plague is not exclusively vector-borne like bubonic plague; instead it can be spread from person to person. There have been cases of pneumonic plague resulting from the dissection or handling of contaminated animal tissue. This is one type of the formerly known Black Death. It could kill 90%–95% of a population if the victims coughed and passed on the bacteria.

 Symptoms

The most apparent symptom of pneumonic plague is coughing, often with hemoptysis (coughing up blood). With pneumonic plague, the first signs of illness are fever, headache, weakness, and rapidly developing pneumonia with shortness of breath, chest pain, cough, and sometimes bloody or watery sputum. The pneumonia progresses for two to four days and may cause respiratory failure and shock. Patients will die without early treatment, some within 36 hours.

Initial pneumonic plague symptoms can often include:

Fever

Weakness

Headache

Nausea

Rapidly developing pneumonia with:

Shortness of breath

Chest pain

Cough

Bloody or watery sputum (saliva and discharge from respiratory passages).

Prognosis and treatment

Pneumonic plague is a very aggressive infection requiring early treatment. Antibiotics must be given within 24 hours of first symptoms to reduce the risk of death,. Streptomycin, gentamicin, tetracyclines, and chloramphenicol are all effective against pneumonic plague.

Antibiotic treatment for 7 days will protect people who have had direct, close contact with infected patients. Wearing a close-fitting surgical mask also protects against infection.

The mortality rate from untreated pneumonic plague approaches 100%.

Present Day Occurrences  of Pneumonic Plague.

China

The People's Republic of China has eradicated the pneumonic plague from most parts of the country, but still reports occasional cases in remote Western areas where the disease is carried by rats and the marmots that live across the Himalayan plateau. Outbreaks can be caused when a person eats an infected marmot or comes into contact with fleas carried by rats. A 2006 WHO report from an international meeting on plague cited a Chinese government disease expert as saying that most cases of the plague in China's northwest occur when hunters are contaminated while skinning infected animals. The expert said at the time that due to the region's remoteness, the disease killed more than half the infected people. The report also said that since the 1990s, there was a rise in plague cases in humans—from fewer than 10 in the 1980s to nearly 100 cases in 1996 and 254 in 2000. Official statistics posted on the Chinese Health Ministry's Web site showed no cases of plague in 2007 and 2008.n September 2008, two persons in east Tibet died of pneumonic plague.

A recent outbreak of the disease in China began in August 2009 in Ziketan Town located in Qinghai Province. The town was sealed off and several people died as a result of the disease. According to spokesperson Vivian Tan of the WHO office in Beijing, "In cases like this [in August 2009], we encourage the authorities to identify cases, to investigate any suspicious symptoms among close contacts, and to treat confirmed cases as soon as possible. So far, they have done exactly that. There have been sporadic cases reported around the country in the last few years so the authorities do have the experience to deal with this."

In September 2010, there were 5 reported cases of pneumonic plague in Tibet.

Peru

Peru's health minister says an outbreak of plague has killed a 14-year-old boy and infected at least 31 people in a northern coastal province.

Health Minister Oscar Ugarte says authorities are screening sugar and fish meal exports from Ascope province, located about 325 miles (520 km) northwest of Lima. Popular Chicama beach isn't far away.

Ugarte says the boy, who had Down syndrome, died of bubonic plague July 26, 2010.

He said August 1 that most of the infections are bubonic plague, with four cases of pneumonic plague. The former is transmitted by flea bites, the latter by airborne contagion. The disease is curable if treated early with antibiotics.

The first recorded plague outbreak in Peru was in 1903. The last, in 1994, killed 35 people.

 Recent notable cases

On November 2, 2007, wildlife biologist Eric York died of pneumonic plague in Grand Canyon National Park. York was exposed to the bacteria while conducting a necropsy on a mountain lion carcass.

Plague in Biological warfare.

Some of the earliest instances of biological warfare were said to have been product of the plague, as armies of the 14th century were recorded catapulting diseased corpses over the walls of towns and villages in order to spread the pestilence.

Later, plague was used during the Second Sino-Japanese War as a bacteriological weapon by the Imperial Japanese Army. These weapons were provided by Shirō Ishii's units and used in experiments on humans before being used on the field. For example, in 1940, the Imperial Japanese Army Air Service bombed Ningbo with fleas carrying the bubonic plague. During the Khabarovsk War Crime Trials, the accused, such as Major General Kiyashi Kawashima, testified that, in 1941, some 40 members of Unit 731 air-dropped plague-contaminated fleas on Changde. These operations caused epidemic plague outbreaks.

Epidemiology of plague following use as a biological weapon.

 that plague had been artificially disseminated would be the occurrence of cases in locations not known to have enzootic infection, in peThe Epidemiology of plague following its use as a biological weapon would differ substantially from that of naturally occurring infection. Intentional dissemination of plague would most probably occur via an aerosol of Y pestis, a mechanism that has been shown to produce disease in nonhuman primates. A pneumonic plague outbreak would result with symptoms initially resembling those of other severe respiratory illnesses. The size of the outbreak would depend on factors including the quantity of biological agent used, characteristics of the strain, environmental conditions, and methods of aerosolization. Symptoms would begin to occur 1 to 6 days following exposure, and people would die quickly following onset of symptoms. Indicationsrsons without known risk factors, and in the absence of prior rodent deaths.

Present day incidents of suspected attempted attacks using .

Al-Quaida 

It was reported in 2006 that an al-Quaida cell killed by the Black Death may have been developing biological weapons when it was infected and all the operatives succumbed to the infection. It was initially believed that they could have caught the disease through fleas on rats attracted by poor living conditions in their forest hideout. But there are now claims the cell was developing the disease as a weapon to use against western cities. Some experts said that the group was developing chemical and biological weapons.  Dr Igor Khrupinov, a biological weapons expert at Georgia University, told The Sun: "Al-Quaida is known to experiment with biological weapons. And this group has direct communication with other cells around the world."Contagious diseases, like Ebola and anthrax, occur in northern Africa. It makes sense that people are trying to use them against Western governments."  Dr Khrupinov, who was once a weapons adviser to the Soviet president Mikhail Gorbachev, added: "Instead of using bombs, people with infectious diseases could be walking through cities."

Post graduate terrorists.

It was reported last year that up to 100 potential terrorists had attempted to become postgraduate students in Britain in an attempt to use laboratories. Ian Kearns, from the Institute for Public Policy Research, told the newspaper: "The biological weapons threat is not going away. We're not ready for it."

Larry Wayne Harris and William Job Leavitt American white supremacist  Bio Terrorists?

The FBI arrested two men in 1998, including a self-professed white separatist, on charges of developing and stockpiling a biological agent -- suspected of being deadly anthrax -- and conspiring to use it as a weapon.

The FBI announced the arrests of Larry Wayne Harris and William Job Leavitt Jr. at a news conference Thursday. The men were taken into custody Wednesday evening and were being held at the Clark County Detention Center in Las Vegas.

"These individuals posed a potential chemical and biological threat to our community," said FBI Special Agent Bobby Siller. "It was suspected that these individuals were in possession of a dangerous biological chemical, anthrax." However, Leavitt's lawyer, Lamond Mills, said that what the FBI actually seized was a substance the two men hoped to test and market as an anthrax vaccine.

Tip off

The FBI was tipped off to Harris' alleged activities by a man in Las Vegas who said Harris had told him of his ability to make biological agents, a top law enforcement source told CNN. The man apparently went with Harris to a medical office outside Las Vegas to observe Harris' makeshift laboratory, an official said. Agents responding to the tip seized unknown materials and Petri dishes and "locked them up," the source said. "We're not sure what the hell they got."

Harris on probation for buying bubonic plague

Harris, 46, a native of West Virginia who now lives in Lancaster, Ohio, has a microbiology degree from Ohio State University. He has written extensively on the dangers of biological warfare and how people can protect themselves with massive doses of antibiotics. Harris has described himself as a white separatist. He once held the rank of lieutenant colonel in the far-right white separatist group Aryan Nations, and he has also told reporters that he is a follower of the Christian Identity movement. During the 1980s, Harris was questioned about his involvement with the Aryan Nations by the Secret Service in advance of a visit to Ohio State by then-President George Bush. In 1995, he was arrested after purchasing three vials of bubonic plague by mail from a Maryland laboratory. That was not in and of itself a crime, but Harris was convicted on two counts of mail fraud and one count of wire fraud for misrepresenting the purpose of the purchase, a federal offense. At the time, Harris told prosecutors in Lancaster he was worried about the effects of "super germ-carrying rats" coming from Iraq. Though still on probation for his 1995 conviction, he has permission to travel and gives speeches at gun shows about biological warfare.

Leavitt

A behavior science expert who looked at Harris for the FBI after his previous arrest advised agents "to take him seriously because he had this stuff before," a source said. Less is known about Leavitt, 47. The FBI affidavit says he is also a microbiologist who owns clinics in Logandale, Nevada, where he lives, and Frankfurt, Germany.

"My son is the most caring person you would ever find," said his mother, Betty Leavitt. Describing her son as a very religious Mormon, she said he "prays every time" there is danger of a world conflict and is "extremely concerned about germ warfare."

Separatist allegedly described New York attack

According to an affidavit filed with his arrest warrant, Harris told a group last summer of a 1995 plan to "place a 'globe' of bubonic plague toxins in a New York City subway station, where it would be broken by a passing subway train, causing hundreds of thousands of deaths."

He told the group, according to the affidavit, that "the Iraqis would be blamed for that event."

However, Siller said that there is as of yet no indication as to "what the target might have been or even if there was a target at this point."

The Plague Doctors.

Fourteenth century plague doctors who wore a bird-like mask were referred to as "beak doctors". Straps held the beak in front of the doctor's nose.  The mask had glass openings for the eyes and a curved beak was shaped like a bird's. The mask had two small nose holes and was a type of respirator. The mask they wore had a protruded beak which contained aromatic items. .  The beak could hold dried flowers (including roses and carnations), herbs (including mint), spices, camphor or a vinegar sponge.  The purpose of the mask was to keep away bad smells, which were thought to be the principal cause of the disease in the miasma theory of infection, before it was disproved by germ theory. Doctors believed the herbs would counter the "evil" smells of the plague and prevent them from becoming infected.

The beak doctor costume worn by the plague doctors had a wide brimmed leather hood to indicate their profession. They used wooden canes to point out areas needing attention and to examine the patients without touching them. The canes were also used to keep people away, to remove clothing from plague victims without having to touch them, and to take a patient's pulse

 

 

Bubonic plague 

Bubonic plague  is a zoonotic disease, circulating mainly among small rodents and their fleas, and is one of three types of infections caused by Yersinia pestis (formerly known as Pasteurella pestis), which belongs to the family Enterobacteriaceae. Without treatment, the bubonic plague kills about two out of three infected humans within 4 days.

The term bubonic plague is derived from the Greek word bubo, meaning "swollen gland." Swollen lymph nodes (buboes) especially occur in the armpit and groin in persons suffering from bubonic plague. Bubonic plague was often used synonymously for plague, but it does in fact refer specifically to an infection that enters through the skin and travels through the lymphatics, as is often seen in flea-borne infections.  The first recorded epidemic ravaged the Byzantine Empire during the sixth century, and was named the Plague of Justinian after emperor Justitinian.

Bubonic plague — along with the septicemic plague and the pneumonic plague is generally believed to be the cause of the Black Death that swept through Europe in the 14th century and killed an estimated 75 million people, or 30-60% of the European population. Because the plague killed so many of the working population, wages rose and some historians have seen this as a turning point in European economic development. Justinian I, who was infected but survived through extensive treatment.  The Black Death originated in or near China and spread by way of the Silk Road or by ship. Carried by the fleas on rats, it spread along trade routes and reached the Crimea in 1347.

 Signs and symptoms

The most famous symptom of bubonic plague is painful, swollen lymph glands, called buboes. These are commonly found in the armpits, groin or neck. Due to its bite-based form of infection, the bubonic plague is often the first step of a progressive series of illnesses. Bubonic plague symptoms appear suddenly, usually 2–5 days after exposure to the bacteria. Symptoms include:

Chills

General ill feeling (malaise)

High fever (39 °Celsius; 102 °Fahrenheit)

Muscle Cramps

Seizures

Smooth, painful lymph gland swelling called a bubo, commonly found in the groin, but may occur in the armpits or neck, most often at the site of the initial infection (bite or scratch)

Pain may occur in the area before the swelling appears

Skin color changes to a pink hue in some extreme cases

Bleeding out of the cochlea will begin after 12 hours of infection.

Other symptoms include heavy breathing, continuous blood vomiting, aching limbs, coughing, and extreme pain. The pain is usually caused by the decay or decomposure of the skin while the person is still alive. Additional symptoms include extreme fatigue, gastrointestinal problems, lenticulae (black dots scattered throughout the body), delirium and coma.

Two other types of Y. pestis plague are pneumonic and septicemic. Pneumonic plague, unlike the bubonic or septicemic, induces coughing and is very infectious, allowing to it be spread person-to-person.

Pathophysiology

Bubonic plague is an infection of the lymphatic system, usually resulting from the bite of an infected flea, Xenopsylla cheopis (the rat flea). The fleas are often found on rodents such as rats and mice, and seek out other prey when their rodent hosts die. The bacteria form aggregates in the gut of infected fleas and this results in the flea regurgitating ingested blood, which is now infected, into the bite site of a rodent or human host. Once established, bacteria rapidly spread to the lymph nodes and multiply. Y. pestis bacilli can resist phagocytosis and even reproduce inside phagocytes and kill them. As the disease progresses, the lymph nodes can hemorrhage and become swollen and necrotic. Bubonic plague can progress to lethal septicemic plague in some cases. The plague is also known to spread to the lungs and become the disease known as the pneumonic plague. This form of the disease is highly communicable as the bacteria can be transmitted in droplets emitted when coughing or sneezing, as well as physical contact with victims of the plague or flea-bearing rodents that carry the plague.

Treatment

Several classes of antibiotics are effective in treating bubonic plague. These include aminoglycosides such as streptomycin and gentamicin, tetracyclines (especially doxycycline), and the fluoroquinolone ciprofloxacin. Mortality associated with treated cases of bubonic plague is about 1-15%, compared to a mortality rate of 50-90% in untreated cases.

People potentially infected with the plague need immediate treatment and should be given antibiotics within 24 hours of the first symptoms to prevent death. Other treatments include oxygen, intravenous fluids, and respiratory support. People who have had contact with anyone infected by pneumonic plague are given prophylactic antibiotics.

Laboratory testing

Laboratory testing is required, in order to diagnose and confirm plague. Ideally, confirmation is through the identification of Y. pestis culture from a patient sample. Confirmation of infection can be done by examining serum taken during the early and late stages of infection. To quickly screen for the Y. pestis antigen in patients, rapid dipstick tests have been developed for field use.

Pneumonic plague

Pneumonic plague, a severe type of lung infection, is one of three main forms of plague, all of which are caused by the bacterium Yersinia pestis. It is more virulent and rare than bubonic plague. The difference between the versions of plague is simply the location of the infection in the body; the bubonic plague is an infection of the lymphatic system, the pneumonic plague is an infection of the respiratory system, and the septicemic plague is an infection in the blood stream.

Typically, pneumonic form is due to a secondary spread from advanced infection of an initial bubonic form. Primary pneumonic plague results from inhalation of fine infective droplets and can be transmitted from human to human without involvement of fleas or animals. Untreated pneumonic plague has a very high fatality rate.

 

Since 2002, the World Health Organization (WHO) has reported six plague outbreaks, though some may go unreported because they often happen in remote areas. Between 1998 and 2009, nearly 24,000 cases have been reported, including about 2,000 deaths, in Africa, Asia, the Americas and Eastern Europe. 98% of the world's cases occur in Africa.

 Pathology and transmission

Pneumonic plague can be caused in two ways: primary, which results from the inhalation of aerosolised plague bacteria, or secondary, when septicemic plague spreads into lung tissue from the bloodstream. Pneumonic plague is not exclusively vector-borne like bubonic plague; instead it can be spread from person to person. There have been cases of pneumonic plague resulting from the dissection or handling of contaminated animal tissue. This is one type of the formerly known Black Death. It could kill 90%–95% of a population if the victims coughed and passed on the bacteria.

 Symptoms

The most apparent symptom of pneumonic plague is coughing, often with hemoptysis (coughing up blood). With pneumonic plague, the first signs of illness are fever, headache, weakness, and rapidly developing pneumonia with shortness of breath, chest pain, cough, and sometimes bloody or watery sputum. The pneumonia progresses for two to four days and may cause respiratory failure and shock. Patients will die without early treatment, some within 36 hours.

Initial pneumonic plague symptoms can often include:

Fever

Weakness

Headache

Nausea

Rapidly developing pneumonia with:

Shortness of breath

Chest pain

Cough

Bloody or watery sputum (saliva and discharge from respiratory passages).

Prognosis and treatment

Pneumonic plague is a very aggressive infection requiring early treatment. Antibiotics must be given within 24 hours of first symptoms to reduce the risk of death,. Streptomycin, gentamicin, tetracyclines, and chloramphenicol are all effective against pneumonic plague.

Antibiotic treatment for 7 days will protect people who have had direct, close contact with infected patients. Wearing a close-fitting surgical mask also protects against infection.

The mortality rate from untreated pneumonic plague approaches 100%.

Present Day Occurrences  of Pneumonic Plague.

China

The People's Republic of China has eradicated the pneumonic plague from most parts of the country, but still reports occasional cases in remote Western areas where the disease is carried by rats and the marmots that live across the Himalayan plateau. Outbreaks can be caused when a person eats an infected marmot or comes into contact with fleas carried by rats. A 2006 WHO report from an international meeting on plague cited a Chinese government disease expert as saying that most cases of the plague in China's northwest occur when hunters are contaminated while skinning infected animals. The expert said at the time that due to the region's remoteness, the disease killed more than half the infected people. The report also said that since the 1990s, there was a rise in plague cases in humans—from fewer than 10 in the 1980s to nearly 100 cases in 1996 and 254 in 2000. Official statistics posted on the Chinese Health Ministry's Web site showed no cases of plague in 2007 and 2008.n September 2008, two persons in east Tibet died of pneumonic plague.

A recent outbreak of the disease in China began in August 2009 in Ziketan Town located in Qinghai Province. The town was sealed off and several people died as a result of the disease. According to spokesperson Vivian Tan of the WHO office in Beijing, "In cases like this [in August 2009], we encourage the authorities to identify cases, to investigate any suspicious symptoms among close contacts, and to treat confirmed cases as soon as possible. So far, they have done exactly that. There have been sporadic cases reported around the country in the last few years so the authorities do have the experience to deal with this."

In September 2010, there were 5 reported cases of pneumonic plague in Tibet.

Peru

Peru's health minister says an outbreak of plague has killed a 14-year-old boy and infected at least 31 people in a northern coastal province.

Health Minister Oscar Ugarte says authorities are screening sugar and fish meal exports from Ascope province, located about 325 miles (520 km) northwest of Lima. Popular Chicama beach isn't far away.

Ugarte says the boy, who had Down syndrome, died of bubonic plague July 26, 2010.

He said August 1 that most of the infections are bubonic plague, with four cases of pneumonic plague. The former is transmitted by flea bites, the latter by airborne contagion. The disease is curable if treated early with antibiotics.

The first recorded plague outbreak in Peru was in 1903. The last, in 1994, killed 35 people.

 Recent notable cases

On November 2, 2007, wildlife biologist Eric York died of pneumonic plague in Grand Canyon National Park. York was exposed to the bacteria while conducting a necropsy on a mountain lion carcass.

Plague in Biological warfare.

Some of the earliest instances of biological warfare were said to have been product of the plague, as armies of the 14th century were recorded catapulting diseased corpses over the walls of towns and villages in order to spread the pestilence.

Later, plague was used during the Second Sino-Japanese War as a bacteriological weapon by the Imperial Japanese Army. These weapons were provided by Shirō Ishii's units and used in experiments on humans before being used on the field. For example, in 1940, the Imperial Japanese Army Air Service bombed Ningbo with fleas carrying the bubonic plague. During the Khabarovsk War Crime Trials, the accused, such as Major General Kiyashi Kawashima, testified that, in 1941, some 40 members of Unit 731 air-dropped plague-contaminated fleas on Changde. These operations caused epidemic plague outbreaks.

Epidemiology of plague following use as a biological weapon.

 that plague had been artificially disseminated would be the occurrence of cases in locations not known to have enzootic infection, in peThe Epidemiology of plague following its use as a biological weapon would differ substantially from that of naturally occurring infection. Intentional dissemination of plague would most probably occur via an aerosol of Y pestis, a mechanism that has been shown to produce disease in nonhuman primates. A pneumonic plague outbreak would result with symptoms initially resembling those of other severe respiratory illnesses. The size of the outbreak would depend on factors including the quantity of biological agent used, characteristics of the strain, environmental conditions, and methods of aerosolization. Symptoms would begin to occur 1 to 6 days following exposure, and people would die quickly following onset of symptoms. Indicationsrsons without known risk factors, and in the absence of prior rodent deaths.

Present day incidents of suspected attempted attacks using .

Al-Quaida 

It was reported in 2006 that an al-Quaida cell killed by the Black Death may have been developing biological weapons when it was infected and all the operatives succumbed to the infection. It was initially believed that they could have caught the disease through fleas on rats attracted by poor living conditions in their forest hideout. But there are now claims the cell was developing the disease as a weapon to use against western cities. Some experts said that the group was developing chemical and biological weapons.  Dr Igor Khrupinov, a biological weapons expert at Georgia University, told The Sun: "Al-Quaida is known to experiment with biological weapons. And this group has direct communication with other cells around the world."Contagious diseases, like Ebola and anthrax, occur in northern Africa. It makes sense that people are trying to use them against Western governments."  Dr Khrupinov, who was once a weapons adviser to the Soviet president Mikhail Gorbachev, added: "Instead of using bombs, people with infectious diseases could be walking through cities."

Post graduate terrorists.

It was reported last year that up to 100 potential terrorists had attempted to become postgraduate students in Britain in an attempt to use laboratories. Ian Kearns, from the Institute for Public Policy Research, told the newspaper: "The biological weapons threat is not going away. We're not ready for it."

Larry Wayne Harris and William Job Leavitt American white supremacist  Bio Terrorists?

The FBI arrested two men in 1998, including a self-professed white separatist, on charges of developing and stockpiling a biological agent -- suspected of being deadly anthrax -- and conspiring to use it as a weapon.

The FBI announced the arrests of Larry Wayne Harris and William Job Leavitt Jr. at a news conference Thursday. The men were taken into custody Wednesday evening and were being held at the Clark County Detention Center in Las Vegas.

"These individuals posed a potential chemical and biological threat to our community," said FBI Special Agent Bobby Siller. "It was suspected that these individuals were in possession of a dangerous biological chemical, anthrax." However, Leavitt's lawyer, Lamond Mills, said that what the FBI actually seized was a substance the two men hoped to test and market as an anthrax vaccine.

Tip off

The FBI was tipped off to Harris' alleged activities by a man in Las Vegas who said Harris had told him of his ability to make biological agents, a top law enforcement source told CNN. The man apparently went with Harris to a medical office outside Las Vegas to observe Harris' makeshift laboratory, an official said. Agents responding to the tip seized unknown materials and Petri dishes and "locked them up," the source said. "We're not sure what the hell they got."

Harris on probation for buying bubonic plague

Harris, 46, a native of West Virginia who now lives in Lancaster, Ohio, has a microbiology degree from Ohio State University. He has written extensively on the dangers of biological warfare and how people can protect themselves with massive doses of antibiotics. Harris has described himself as a white separatist. He once held the rank of lieutenant colonel in the far-right white separatist group Aryan Nations, and he has also told reporters that he is a follower of the Christian Identity movement. During the 1980s, Harris was questioned about his involvement with the Aryan Nations by the Secret Service in advance of a visit to Ohio State by then-President George Bush. In 1995, he was arrested after purchasing three vials of bubonic plague by mail from a Maryland laboratory. That was not in and of itself a crime, but Harris was convicted on two counts of mail fraud and one count of wire fraud for misrepresenting the purpose of the purchase, a federal offense. At the time, Harris told prosecutors in Lancaster he was worried about the effects of "super germ-carrying rats" coming from Iraq. Though still on probation for his 1995 conviction, he has permission to travel and gives speeches at gun shows about biological warfare.

Leavitt

A behavior science expert who looked at Harris for the FBI after his previous arrest advised agents "to take him seriously because he had this stuff before," a source said. Less is known about Leavitt, 47. The FBI affidavit says he is also a microbiologist who owns clinics in Logandale, Nevada, where he lives, and Frankfurt, Germany.

"My son is the most caring person you would ever find," said his mother, Betty Leavitt. Describing her son as a very religious Mormon, she said he "prays every time" there is danger of a world conflict and is "extremely concerned about germ warfare."

Separatist allegedly described New York attack

According to an affidavit filed with his arrest warrant, Harris told a group last summer of a 1995 plan to "place a 'globe' of bubonic plague toxins in a New York City subway station, where it would be broken by a passing subway train, causing hundreds of thousands of deaths."

He told the group, according to the affidavit, that "the Iraqis would be blamed for that event."

However, Siller said that there is as of yet no indication as to "what the target might have been or even if there was a target at this point."

The Plague Doctors.

Fourteenth century plague doctors who wore a bird-like mask were referred to as "beak doctors". Straps held the beak in front of the doctor's nose.  The mask had glass openings for the eyes and a curved beak was shaped like a bird's. The mask had two small nose holes and was a type of respirator. The mask they wore had a protruded beak which contained aromatic items. .  The beak could hold dried flowers (including roses and carnations), herbs (including mint), spices, camphor or a vinegar sponge.  The purpose of the mask was to keep away bad smells, which were thought to be the principal cause of the disease in the miasma theory of infection, before it was disproved by germ theory. Doctors believed the herbs would counter the "evil" smells of the plague and prevent them from becoming infected.

The beak doctor costume worn by the plague doctors had a wide brimmed leather hood to indicate their profession. They used wooden canes to point out areas needing attention and to examine the patients without touching them. The canes were also used to keep people away, to remove clothing from plague victims without having to touch them, and to take a patient's pulse

 

 

Bubonic plague 

Bubonic plague  is a zoonotic disease, circulating mainly among small rodents and their fleas, and is one of three types of infections caused by Yersinia pestis (formerly known as Pasteurella pestis), which belongs to the family Enterobacteriaceae. Without treatment, the bubonic plague kills about two out of three infected humans within 4 days.

The term bubonic plague is derived from the Greek word bubo, meaning "swollen gland." Swollen lymph nodes (buboes) especially occur in the armpit and groin in persons suffering from bubonic plague. Bubonic plague was often used synonymously for plague, but it does in fact refer specifically to an infection that enters through the skin and travels through the lymphatics, as is often seen in flea-borne infections.  The first recorded epidemic ravaged the Byzantine Empire during the sixth century, and was named the Plague of Justinian after emperor Justitinian.

Bubonic plague — along with the septicemic plague and the pneumonic plague is generally believed to be the cause of the Black Death that swept through Europe in the 14th century and killed an estimated 75 million people, or 30-60% of the European population. Because the plague killed so many of the working population, wages rose and some historians have seen this as a turning point in European economic development. Justinian I, who was infected but survived through extensive treatment.  The Black Death originated in or near China and spread by way of the Silk Road or by ship. Carried by the fleas on rats, it spread along trade routes and reached the Crimea in 1347.

 Signs and symptoms

The most famous symptom of bubonic plague is painful, swollen lymph glands, called buboes. These are commonly found in the armpits, groin or neck. Due to its bite-based form of infection, the bubonic plague is often the first step of a progressive series of illnesses. Bubonic plague symptoms appear suddenly, usually 2–5 days after exposure to the bacteria. Symptoms include:

Chills

General ill feeling (malaise)

High fever (39 °Celsius; 102 °Fahrenheit)

Muscle Cramps

Seizures

Smooth, painful lymph gland swelling called a bubo, commonly found in the groin, but may occur in the armpits or neck, most often at the site of the initial infection (bite or scratch)

Pain may occur in the area before the swelling appears

Skin color changes to a pink hue in some extreme cases

Bleeding out of the cochlea will begin after 12 hours of infection.

Other symptoms include heavy breathing, continuous blood vomiting, aching limbs, coughing, and extreme pain. The pain is usually caused by the decay or decomposure of the skin while the person is still alive. Additional symptoms include extreme fatigue, gastrointestinal problems, lenticulae (black dots scattered throughout the body), delirium and coma.

Two other types of Y. pestis plague are pneumonic and septicemic. Pneumonic plague, unlike the bubonic or septicemic, induces coughing and is very infectious, allowing to it be spread person-to-person.

Pathophysiology

Bubonic plague is an infection of the lymphatic system, usually resulting from the bite of an infected flea, Xenopsylla cheopis (the rat flea). The fleas are often found on rodents such as rats and mice, and seek out other prey when their rodent hosts die. The bacteria form aggregates in the gut of infected fleas and this results in the flea regurgitating ingested blood, which is now infected, into the bite site of a rodent or human host. Once established, bacteria rapidly spread to the lymph nodes and multiply. Y. pestis bacilli can resist phagocytosis and even reproduce inside phagocytes and kill them. As the disease progresses, the lymph nodes can hemorrhage and become swollen and necrotic. Bubonic plague can progress to lethal septicemic plague in some cases. The plague is also known to spread to the lungs and become the disease known as the pneumonic plague. This form of the disease is highly communicable as the bacteria can be transmitted in droplets emitted when coughing or sneezing, as well as physical contact with victims of the plague or flea-bearing rodents that carry the plague.

Treatment

Several classes of antibiotics are effective in treating bubonic plague. These include aminoglycosides such as streptomycin and gentamicin, tetracyclines (especially doxycycline), and the fluoroquinolone ciprofloxacin. Mortality associated with treated cases of bubonic plague is about 1-15%, compared to a mortality rate of 50-90% in untreated cases.

People potentially infected with the plague need immediate treatment and should be given antibiotics within 24 hours of the first symptoms to prevent death. Other treatments include oxygen, intravenous fluids, and respiratory support. People who have had contact with anyone infected by pneumonic plague are given prophylactic antibiotics.

Laboratory testing

Laboratory testing is required, in order to diagnose and confirm plague. Ideally, confirmation is through the identification of Y. pestis culture from a patient sample. Confirmation of infection can be done by examining serum taken during the early and late stages of infection. To quickly screen for the Y. pestis antigen in patients, rapid dipstick tests have been developed for field use.

Pneumonic plague

Pneumonic plague, a severe type of lung infection, is one of three main forms of plague, all of which are caused by the bacterium Yersinia pestis. It is more virulent and rare than bubonic plague. The difference between the versions of plague is simply the location of the infection in the body; the bubonic plague is an infection of the lymphatic system, the pneumonic plague is an infection of the respiratory system, and the septicemic plague is an infection in the blood stream.

Typically, pneumonic form is due to a secondary spread from advanced infection of an initial bubonic form. Primary pneumonic plague results from inhalation of fine infective droplets and can be transmitted from human to human without involvement of fleas or animals. Untreated pneumonic plague has a very high fatality rate.

 

Since 2002, the World Health Organization (WHO) has reported six plague outbreaks, though some may go unreported because they often happen in remote areas. Between 1998 and 2009, nearly 24,000 cases have been reported, including about 2,000 deaths, in Africa, Asia, the Americas and Eastern Europe. 98% of the world's cases occur in Africa.

 Pathology and transmission

Pneumonic plague can be caused in two ways: primary, which results from the inhalation of aerosolised plague bacteria, or secondary, when septicemic plague spreads into lung tissue from the bloodstream. Pneumonic plague is not exclusively vector-borne like bubonic plague; instead it can be spread from person to person. There have been cases of pneumonic plague resulting from the dissection or handling of contaminated animal tissue. This is one type of the formerly known Black Death. It could kill 90%–95% of a population if the victims coughed and passed on the bacteria.

 Symptoms

The most apparent symptom of pneumonic plague is coughing, often with hemoptysis (coughing up blood). With pneumonic plague, the first signs of illness are fever, headache, weakness, and rapidly developing pneumonia with shortness of breath, chest pain, cough, and sometimes bloody or watery sputum. The pneumonia progresses for two to four days and may cause respiratory failure and shock. Patients will die without early treatment, some within 36 hours.

Initial pneumonic plague symptoms can often include:

Fever

Weakness

Headache

Nausea

Rapidly developing pneumonia with:

Shortness of breath

Chest pain

Cough

Bloody or watery sputum (saliva and discharge from respiratory passages).

Prognosis and treatment

Pneumonic plague is a very aggressive infection requiring early treatment. Antibiotics must be given within 24 hours of first symptoms to reduce the risk of death,. Streptomycin, gentamicin, tetracyclines, and chloramphenicol are all effective against pneumonic plague.

Antibiotic treatment for 7 days will protect people who have had direct, close contact with infected patients. Wearing a close-fitting surgical mask also protects against infection.

The mortality rate from untreated pneumonic plague approaches 100%.

Present Day Occurrences  of Pneumonic Plague.

China

The People's Republic of China has eradicated the pneumonic plague from most parts of the country, but still reports occasional cases in remote Western areas where the disease is carried by rats and the marmots that live across the Himalayan plateau. Outbreaks can be caused when a person eats an infected marmot or comes into contact with fleas carried by rats. A 2006 WHO report from an international meeting on plague cited a Chinese government disease expert as saying that most cases of the plague in China's northwest occur when hunters are contaminated while skinning infected animals. The expert said at the time that due to the region's remoteness, the disease killed more than half the infected people. The report also said that since the 1990s, there was a rise in plague cases in humans—from fewer than 10 in the 1980s to nearly 100 cases in 1996 and 254 in 2000. Official statistics posted on the Chinese Health Ministry's Web site showed no cases of plague in 2007 and 2008.n September 2008, two persons in east Tibet died of pneumonic plague.

A recent outbreak of the disease in China began in August 2009 in Ziketan Town located in Qinghai Province. The town was sealed off and several people died as a result of the disease. According to spokesperson Vivian Tan of the WHO office in Beijing, "In cases like this [in August 2009], we encourage the authorities to identify cases, to investigate any suspicious symptoms among close contacts, and to treat confirmed cases as soon as possible. So far, they have done exactly that. There have been sporadic cases reported around the country in the last few years so the authorities do have the experience to deal with this."

In September 2010, there were 5 reported cases of pneumonic plague in Tibet.

Peru

Peru's health minister says an outbreak of plague has killed a 14-year-old boy and infected at least 31 people in a northern coastal province.

Health Minister Oscar Ugarte says authorities are screening sugar and fish meal exports from Ascope province, located about 325 miles (520 km) northwest of Lima. Popular Chicama beach isn't far away.

Ugarte says the boy, who had Down syndrome, died of bubonic plague July 26, 2010.

He said August 1 that most of the infections are bubonic plague, with four cases of pneumonic plague. The former is transmitted by flea bites, the latter by airborne contagion. The disease is curable if treated early with antibiotics.

The first recorded plague outbreak in Peru was in 1903. The last, in 1994, killed 35 people.

 Recent notable cases

On November 2, 2007, wildlife biologist Eric York died of pneumonic plague in Grand Canyon National Park. York was exposed to the bacteria while conducting a necropsy on a mountain lion carcass.

Plague in Biological warfare.

Some of the earliest instances of biological warfare were said to have been product of the plague, as armies of the 14th century were recorded catapulting diseased corpses over the walls of towns and villages in order to spread the pestilence.

Later, plague was used during the Second Sino-Japanese War as a bacteriological weapon by the Imperial Japanese Army. These weapons were provided by Shirō Ishii's units and used in experiments on humans before being used on the field. For example, in 1940, the Imperial Japanese Army Air Service bombed Ningbo with fleas carrying the bubonic plague. During the Khabarovsk War Crime Trials, the accused, such as Major General Kiyashi Kawashima, testified that, in 1941, some 40 members of Unit 731 air-dropped plague-contaminated fleas on Changde. These operations caused epidemic plague outbreaks.

Epidemiology of plague following use as a biological weapon.

 that plague had been artificially disseminated would be the occurrence of cases in locations not known to have enzootic infection, in peThe Epidemiology of plague following its use as a biological weapon would differ substantially from that of naturally occurring infection. Intentional dissemination of plague would most probably occur via an aerosol of Y pestis, a mechanism that has been shown to produce disease in nonhuman primates. A pneumonic plague outbreak would result with symptoms initially resembling those of other severe respiratory illnesses. The size of the outbreak would depend on factors including the quantity of biological agent used, characteristics of the strain, environmental conditions, and methods of aerosolization. Symptoms would begin to occur 1 to 6 days following exposure, and people would die quickly following onset of symptoms. Indicationsrsons without known risk factors, and in the absence of prior rodent deaths.

Present day incidents of suspected attempted attacks using .

Al-Quaida 

It was reported in 2006 that an al-Quaida cell killed by the Black Death may have been developing biological weapons when it was infected and all the operatives succumbed to the infection. It was initially believed that they could have caught the disease through fleas on rats attracted by poor living conditions in their forest hideout. But there are now claims the cell was developing the disease as a weapon to use against western cities. Some experts said that the group was developing chemical and biological weapons.  Dr Igor Khrupinov, a biological weapons expert at Georgia University, told The Sun: "Al-Quaida is known to experiment with biological weapons. And this group has direct communication with other cells around the world."Contagious diseases, like Ebola and anthrax, occur in northern Africa. It makes sense that people are trying to use them against Western governments."  Dr Khrupinov, who was once a weapons adviser to the Soviet president Mikhail Gorbachev, added: "Instead of using bombs, people with infectious diseases could be walking through cities."

Post graduate terrorists.

It was reported last year that up to 100 potential terrorists had attempted to become postgraduate students in Britain in an attempt to use laboratories. Ian Kearns, from the Institute for Public Policy Research, told the newspaper: "The biological weapons threat is not going away. We're not ready for it."

Larry Wayne Harris and William Job Leavitt American white supremacist  Bio Terrorists?

The FBI arrested two men in 1998, including a self-professed white separatist, on charges of developing and stockpiling a biological agent -- suspected of being deadly anthrax -- and conspiring to use it as a weapon.

The FBI announced the arrests of Larry Wayne Harris and William Job Leavitt Jr. at a news conference Thursday. The men were taken into custody Wednesday evening and were being held at the Clark County Detention Center in Las Vegas.

"These individuals posed a potential chemical and biological threat to our community," said FBI Special Agent Bobby Siller. "It was suspected that these individuals were in possession of a dangerous biological chemical, anthrax." However, Leavitt's lawyer, Lamond Mills, said that what the FBI actually seized was a substance the two men hoped to test and market as an anthrax vaccine.

Tip off

The FBI was tipped off to Harris' alleged activities by a man in Las Vegas who said Harris had told him of his ability to make biological agents, a top law enforcement source told CNN. The man apparently went with Harris to a medical office outside Las Vegas to observe Harris' makeshift laboratory, an official said. Agents responding to the tip seized unknown materials and Petri dishes and "locked them up," the source said. "We're not sure what the hell they got."

Harris on probation for buying bubonic plague

Harris, 46, a native of West Virginia who now lives in Lancaster, Ohio, has a microbiology degree from Ohio State University. He has written extensively on the dangers of biological warfare and how people can protect themselves with massive doses of antibiotics. Harris has described himself as a white separatist. He once held the rank of lieutenant colonel in the far-right white separatist group Aryan Nations, and he has also told reporters that he is a follower of the Christian Identity movement. During the 1980s, Harris was questioned about his involvement with the Aryan Nations by the Secret Service in advance of a visit to Ohio State by then-President George Bush. In 1995, he was arrested after purchasing three vials of bubonic plague by mail from a Maryland laboratory. That was not in and of itself a crime, but Harris was convicted on two counts of mail fraud and one count of wire fraud for misrepresenting the purpose of the purchase, a federal offense. At the time, Harris told prosecutors in Lancaster he was worried about the effects of "super germ-carrying rats" coming from Iraq. Though still on probation for his 1995 conviction, he has permission to travel and gives speeches at gun shows about biological warfare.

Leavitt

A behavior science expert who looked at Harris for the FBI after his previous arrest advised agents "to take him seriously because he had this stuff before," a source said. Less is known about Leavitt, 47. The FBI affidavit says he is also a microbiologist who owns clinics in Logandale, Nevada, where he lives, and Frankfurt, Germany.

"My son is the most caring person you would ever find," said his mother, Betty Leavitt. Describing her son as a very religious Mormon, she said he "prays every time" there is danger of a world conflict and is "extremely concerned about germ warfare."

Separatist allegedly described New York attack

According to an affidavit filed with his arrest warrant, Harris told a group last summer of a 1995 plan to "place a 'globe' of bubonic plague toxins in a New York City subway station, where it would be broken by a passing subway train, causing hundreds of thousands of deaths."

He told the group, according to the affidavit, that "the Iraqis would be blamed for that event."

However, Siller said that there is as of yet no indication as to "what the target might have been or even if there was a target at this point."

The Plague Doctors.

Fourteenth century plague doctors who wore a bird-like mask were referred to as "beak doctors". Straps held the beak in front of the doctor's nose.  The mask had glass openings for the eyes and a curved beak was shaped like a bird's. The mask had two small nose holes and was a type of respirator. The mask they wore had a protruded beak which contained aromatic items. .  The beak could hold dried flowers (including roses and carnations), herbs (including mint), spices, camphor or a vinegar sponge.  The purpose of the mask was to keep away bad smells, which were thought to be the principal cause of the disease in the miasma theory of infection, before it was disproved by germ theory. Doctors believed the herbs would counter the "evil" smells of the plague and prevent them from becoming infected.

The beak doctor costume worn by the plague doctors had a wide brimmed leather hood to indicate their profession. They used wooden canes to point out areas needing attention and to examine the patients without touching them. The canes were also used to keep people away, to remove clothing from plague victims without having to touch them, and to take a patient's pulse

  Plague Doctors Costumes www.darkbiology.com

(Top left, Paulus Furst’s 1656 engraving of Dr. Schnabel ("Beak") of Rome wearing protective clothing typical of the plague doctors of Rome at the time.  Top middle Plague Doctor costume 1720.  Top right, an 1841 version of the frontispiece to Jean-Jacques Manget’s Traité de la peste (1721),used to illustrate an article in the Saturday, June 5, 1841 issue of The Mirror of literature, amusement, and instruction on the 1637–37 plague in Nijmegen.  Bottom left, Plague Doctor (Medicus in Pestilentia) from Thomas Bartholin’s Historiae anatomicae of 1661. (Perhaps copied from Gerhart Altzenbach’s 1656 image.  Bottom Middle, Johann Melchior Füssli, engraving, c. 1721, of a plague doctor of Marseilles. His nose-case is filled with smoking material to keep off the plague.  Bottom right, a beaked Venetian carnival mask with the inscription Medico della Peste (‘Plague doctor’) beneath the right eye.)

Charles de Lorme adopted in 1619 the idea of a full head-to-toe protective garment, modeled after a soldier's armour. This consisted of not only the bird-like mask, but of a long leather (Moroccan or Levantine)or waxed-canvas gown which was from the neck to the ankle. The over-clothing garment, as well as leggings, gloves, boots, and a hat, were made of waxed leather. The garment was impregnated with similar fragrant items as the beak mask.


This popular seventeenth century poem describes the plague doctor's costume.

As may be seen on picture here,

In Rome the doctors do appear,

When to their patients they are called,

In places by the plague appalled,

Their hats and cloaks, of fashion new,

Are made of oilcloth, dark of hue,

Their caps with glasses are designed,

Their bills with antidotes all lined,

That foulsome air may do no harm,

Nor cause the doctor man alarm,

The staff in hand must serve to show

Their noble trade where'er they go.

The Genevese physician Jean-Jacques Manget, in his 1721 work Treatise on the Plague written just after the Great Plague of Marseille, describes the costume worn by plague doctors at Nijmegen in 1636-1637. The costume forms the frontispiece of Manget's 1721 work. The plague doctors of Nijmegen also wore beaked masks. Their robes, leggings, hats, and gloves were made of morocco leather.

This costume was also worn by plague doctors during the Plague of 1656, which killed 145,000 people in Rome and 300,000 in Naples. The overcoat was sometimes made of levant morocco. The costume terrified people because it was a sign of imminent death. Plague doctors wore these protective costumes per their agreements when they attended their plague patients.

Traditional treatment

Medieval doctors thought the plague was created by air corrupted by humid weather, decaying unburied bodies, and fumes produced by poor sanitation. The recommended treatment of the plague was a good diet, rest, and relocating to a non-infected environment so the individual could get access to clean air. This did help, but not for the reasons the doctors of the time thought. In actuality, because they recommended moving away from unsanitary conditions, people were, in effect, getting away from the rodents that harbored the fleas carrying the infection.

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Anthrax

 

Exposure and mode of infection

Signs and symptoms.

Diagnosis

Anthrax Prevention

Anthrax treatment

Anthrax site clean up

Anthrax in biological warfare

Sverdlovsk anthrax leak

Anthrax in bio terrorism

 

Anthrax is an acute disease caused by the bacterium Bacillus anthracis. Most forms of the disease are lethal, and it affects both humans and other animals. Like many other members of the genus Bacillus, Bacillus anthracis can form dormant endospores (often referred to as "spores" for short, but not to be confused with fungal spores) that are able to survive in harsh conditions for decades or even centuries.  Such spores can be found on all continents, even Antarctica. When spores are inhaled, ingested, or come into contact with a skin lesion on a host they may reactivate and multiply rapidly.

Anthrax commonly infects wild and domesticated herbivorous mammals that ingest or inhale the spores while grazing. Ingestion is thought to be the most common route by which herbivores contract anthrax. Carnivores living in the same environment may become infected by consuming infected animals. Diseased animals can spread anthrax to humans, either by direct contact (e.g., inoculation of infected blood to broken skin) or by consumption of a diseased animal's flesh.

Anthrax spores can be produced in vitro (in the lab) and used as a biological weapon. Anthrax does not spread directly from one infected animal or person to another; it is spread by spores. These spores can be transported by clothing or shoes. The body of an animal that had active anthrax at the time of death can also be a source of anthrax spores.

 

Exposure and mode of infection.

Occupational exposure to infected animals or their products (such as skin, wool, and meat) is the usual pathway of exposure for humans. Workers who are exposed to dead animals and animal products are at the highest risk, especially in countries where anthrax is more common. Anthrax in livestock grazing on open range where they mix with wild animals still occasionally occurs in the United States and elsewhere. Many workers who deal with wool and animal hides are routinely exposed to low levels of anthrax spores but most exposures are not sufficient to develop anthrax infections. It is presumed that the body's natural defenses can destroy low levels of exposure. These people usually contract cutaneous anthrax if they catch anything. Throughout history, the most dangerous form of inhalational anthrax was called Woolsorters' disease because it was an occupational hazard for people who sorted wool. Today this form of infection is extremely rare, as almost no infected animals remain. The last fatal case of natural inhalational anthrax in the United States occurred in California in 1976, when a home weaver died after working with infected wool imported from Pakistan. The autopsy was done at UCLA hospital. To minimize the chance of spreading the disease, the deceased was transported to UCLA in a sealed plastic body bag within a sealed metal container.

In November 2008, a drum maker in the United Kingdom who worked with untreated animal skins died from anthrax. In December 2009 an outbreak of anthrax occurred amongst heroin addicts in Glasgow, Scotland, resulting in ten deaths. The source of the anthrax is believed to be dilution of the heroin with bone meal in Afghanistan.  Also during December 2009, The New Hampshire Department of Health and Human Services confirmed a case of gastrointestinal anthrax in an adult female. The CDC (Center for Disease Control) investigated the source and the pox

Anthrax can enter the human body through the intestines (ingestion), lungs (inhalation), or skin (cutaneous) and causes distinct clinical symptoms based on its site of entry. In general, an infected human will be quarantined. However, anthrax does not usually spread from an infected human to a non- infected human. But, if the disease is fatal to the person's body, its mass of anthrax bacilli becomes a potential source of infection to others and special precautions should be used to prevent further contamination. Inhalational anthrax, if left untreated until obvious symptoms occur, may be fatal.

Anthrax can be contracted in laboratory accidents or by handling infected animals or their wool or hides. It has also been used in biological warfare agents and by terrorists to intentionally infect as exemplified by the 2001 anthrax attacks.  

Signs and symptoms

Pulmonary (in other words airborne infection)

Respiratory infection in humans initially presents with cold or flu-like symptoms for several days, followed by severe (and often fatal) respiratory collapse. Historical mortality was 92%, but, when treated early (seen in the 2001 anthrax attacks), observed mortality was 45%.[Distinguishing pulmonary anthrax from more common causes of respiratory illness is essential to avoiding delays in diagnosis and thereby improving outcomes. An algorithm for this purpose has been developed. Illness progressing to the fulminant phase has a 97% mortality regardless of treatment.

A lethal infection is reported to result from inhalation of about 10,000–20,000 spores, though this dose varies among host species. As with all diseases, it is presumed that there is a wide variation to susceptibility with evidence that some people may die from much lower exposures; there is little documented evidence to verify the exact or average number of spores needed for infection. Inhalational anthrax is also known as Woolsorters' or Ragpickers' disease as these professions were more susceptible to the disease due to their exposure to infected animal products. Other practices associated with exposure include the slicing up of animal horns for the manufacture of buttons, the handling of hair bristles used for the manufacturing of brushes, and the handling of animal skins. Whether these animal skins came from animals that died of the disease or from animals that had simply laid on ground that had spores on it is unknown. This mode of infection is the type used  weaponization in biological warfare..

Gastrointestinal (needs to be ingested)

Gastrointestinal infection in humans is most often caused by eating anthrax-infected meat and is characterized by serious gastrointestinal difficulty, vomiting of blood, severe diarrhea, acute inflammation of the intestinal tract, and loss of appetite. Some lesions have been found in the intestines and in the mouth and throat. After the bacterium invades the bowel system, it spreads through the bloodstream throughout the body, making even more toxins on the way. Gastrointestinal infections can be treated but usually result in fatality rates of 25% to 60%, depending upon how soon treatment commences. This form of anthrax is the rarest form. In the United States, there is only one official case reported in 1942 by the CDC.  

Cutaneous (on the skin).

Anthrax lesion

Anthrax skin lesion

Cutaneous (on the skin) anthrax infection in humans shows up as a boil-like skin lesion that eventually forms an ulcer with a black center (lesion). The black lesion often shows up as a large, painless necrotic ulcer (beginning as an irritating and itchy skin lesion or blister that is dark and usually concentrated as a black dot, somewhat resembling bread mold) at the site of infection. In general, cutaneous infections form within the site of spore penetration between 2 and 5 days after exposure. Unlike bruises or most other lesions, cutaneous anthrax infections normally do not cause pain.

Cutaneous anthrax is typically caused when bacillus anthracis spores enter through cuts on the skin. This form of Anthrax is found most commonly when humans handle infected animals and/or animal products (e.g., the hide of an animal used to make drums).

Cutaneous anthrax is rarely fatal if treated, because the infection area is limited to the skin, preventing the Lethal Factor, Edema Factor, and Protective Antigen from entering and destroying a vital organ. Without treatment about 20% of cutaneous skin infection cases progress to toxemia and death.

Diagnosis

Other than Gram stain of specimens, there are no specific direct identification techniques for identification of Bacillus species in clinical material. These organisms are Gram-positive but with age can be Gram-variable to Gram-negative. A specific feature of Bacillus species that makes it unique from other aerobic microorganisms is its ability to produce spores. Although spores are not always evident on a Gram stain of this organism, the presence of spores confirms that the organism is of the genus Bacillus.

All Bacillus species grow well on 5% Sheep blood agar and other routine culture media. PLET (polymyxin-lysozyme-EDTA-thallous acetate) can be used to isolate B.anthracis from contaminated specimens, and bicarbonate agar is used as an identification method to induce capsule formation.   Bacillus sp. will usually grow within 24 hours of incubation at 35 degrees C, in ambient air (room temperature) or in 5% CO2. If bicarbonate agar is used for identification then the media must be incubated in 5% CO2. This ability to grow well makes it a great threat for the possible use as a biological warfare agent.

 Prevention

Vaccines

An anthrax vaccine (BioThrax or Anthrax Vaccine Adsorbed) licensed by the U.S. Food and Drug Administration (FDA) and produced from one non-virulent strain of the anthrax bacterium was formerly administered in a six-dose primary series at 0, 2, 4 weeks and 6, 12, 18 months, with annual boosters to maintain immunity. On December 11, 2008, the FDA approved omitting the week 2 dose, resulting in the currently recommended five-dose series. Unlike NATOcountries, the Soviets developed and used a live spore anthrax vaccine, known as the STI vaccine, produced in Tbilisi, Georgia. Its serious side-effects restrict use to healthy adults.

Treatment

Anthrax cannot be spread directly from person to person, but a peoples clothing and body may be contaminated with anthrax spores. Effective decontamination of people can be accomplished by a thorough wash-down withantimicrobial effective soap and water. Waste water should be treated with bleach or other anti-microbial agent. Effective decontamination of articles can be accomplished by boiling contaminated articles in water for 30 minutes or longer. Chlorine bleach is ineffective in destroying spores and vegetative cells on surfaces, though formaldehyde is effective. Burning clothing is very effective in destroying spores. After decontamination, there is no need to immunize, treat or isolate contacts of persons ill with anthrax unless they were also exposed to the same source of infection.

 Antibiotics

Early antibiotic treatment of anthrax is essential—delay significantly lessens chances for survival.

Treatment for anthrax infection and other bacterial infections includes large doses of intravenous and oral antibiotics, such as fluoroquinolones like ciprofloxacin, or doxycycline, erythromycin, vancomycin or penicillin. FDA-approved agents include ciprofloxacin, doxycycline and penicillin.

In possible cases of inhalation anthrax, early antibiotic prophylaxis treatment is crucial to prevent possible death.

In May 2009, Human Genome Sciences submitted a Biologic License Application (BLA, permission to market) for its new drug,raxibacumab (brand name ABthrax) intended for emergency treatment of inhaled anthrax.   If death occurs from anthrax the body should be isolated to prevent possible spread of anthrax germs. Burial does not kill anthrax spores.

In recent years there have been many attempts to develop new drugs against anthrax, but existing drugs are effective if treatment is started soon enough.

Anthrax in bioterrorism and biological warfare.

The virulent Ames strain, which was used in the 2001 anthrax attacks in the United States, has received the most news coverage of any anthrax outbreak. The Ames strain contains two virulence plasmids, which separately encode for a three-protein toxin, called anthrax toxin, and a poly-glutamic acid capsule. Nonetheless, the Vollum strain, developed but never used as a biological weapon during the Second World War, is much more dangerous. The Vollum (also incorrectly referred to as Vellum) strain was isolated in 1935 from a cow in Oxfordshire, UK. This is the same strain that was used during the Gruinard bioweapons trials. A variation of Vollum known as "Vollum 1B" was used during the 1960s in the US and UK bioweapon programs. Vollum 1B is widely believe to have been isolated from William A. Boyles, a 46-year-old scientist at the U.S. Army Biological Warfare Laboratories at Camp (later Fort) Detrick (precursor to USAMRIID) who died in 1951 after being accidentally infected with the Vollum strain. The Sterne strain, named after the Trieste-born immunologist Max Sterne, is an attenuated strain used as a vaccine, which contains only the anthrax toxin virulence plasmid and not the poly-glutamic acid capsule expressing plasmid.

 Site cleanup

Anthrax spores can survive for very long periods of time in the environment after release. Methods for cleaning anthrax-contaminated sites commonly use oxidizing agents such as peroxides, ethylene oxide, Sandia Foam, chlorine dioxide (used in the Hart Senate Office Building), and liquid bleach products containing sodium hypochlorite. These agents slowly destroy bacterial spores. A bleach solution for treating hard surfaces has been approved by the EPA.]Bleach and vinegar must not be combined together directly, as doing so could produce chlorine gas. Rather some water must first be added to the bleach (e.g., two cups water to one cup of bleach), then vinegar (e.g., one cup), and then the rest of the water (e.g., six cups). The pH of the solution should be tested with a paper test strip; and treated surfaces must remain in contact with the bleach solution for 60 minutes (repeated applications will be necessary to keep the surfaces wet).

Chlorine dioxide has emerged as the preferred biocide against anthrax-contaminated sites, having been employed in the treatment of numerous government buildings over the past decade. Its chief drawback is the need for in situ processes to have the reactant on demand.

To speed the process, trace amounts of a non-toxic catalyst composed of iron and tetro-amido macrocyclicligands are combined with sodium carbonate and bicarbonate and converted into a spray. The spray formula is applied to an infested area and is followed by another spray containing tert-Butyl hydroperoxide.

Using the catalyst method, a complete destruction of all anthrax spores can be achieved in under 30 minutes. A standard catalyst-free spray destroys fewer than half the spores in the same amount of time. They can be heated, exposed to the harshest chemicals, and they do not easily die.]

Cleanups at a Senate office building, several contaminated postal facilities and other U.S. government and private office buildings showed that decontamination is possible, but it is time-consuming and costly. Clearing the Senate office building of anthrax spores cost $27 million, according to the Government Accountability Office. Cleaning the Brentwood postal facility outside Washington cost $130 million and took 26 months. Since then newer and less costly methods have been developed.

Clean up of anthrax-contaminated areas on ranches and in the wild is much more problematic. Carcasses may be burned, though it often takes up to three days to burn a large carcass and this is not feasible in areas with little wood. Carcasses may also be buried, though the burying of large animals deeply enough to prevent resurfacing of spores requires much manpower and expensive tools. Carcasses have been soaked in formaldehyde to kill spores, though this has environmental contamination issues. Block burning of vegetation in large areas enclosing an anthrax outbreak has been tried; this, while environmentally destructive, causes healthy animals to move away from an area with carcasses in search of fresh graze and browse. Some wildlife workers have experimented with covering fresh anthrax carcasses with shade cloth and heavy objects. This prevents some scavengers from opening the carcasses, thus allowing the putrefactive bacteria within the carcass to kill the vegetative B. anthracis cells and preventing sporulation. This method also has drawbacks, as scavengers such as hyenas are capable of infiltrating almost any exclosure. The occurrence of previously dormant anthrax, stirred up from below the ground surface by wind movement in a drought-stricken region with depleted grazing and browsing, may be seen as a form of natural culling and a first step in rehabilitation of the area.

Biological warfare

Anthrax was first tested as a biological warfare agent by Unit 731 of the Japanese Kwantung Army in Manchuria during the 1930s; some of this testing involved intentional infection of prisoners of war, thousands of whom died. Anthrax, designated at the time as Agent N, was also investigated by the allies in the 1940s. Weaponised anthrax was part of the U.S. stockpile prior to 1972, when the United States signed the Biological Weapons Convention.

Anthrax spores can and have been used as a biological warfare weapon. Its first modern incidence occurred when Scandinavian freedom fighters ("the rebel groups") supplied by the German General Staff used anthrax with unknown results against the Imperial Russian Army in Finland in 1916.There is a long history of practical bioweapons research in this area. For example, in 1942 British bioweapons trials severely contaminated Gruinard Island in Scotland with anthrax spores of the Vollum-14578 strain, making it a no-go area until it was decontaminated in 1990.The Gruinard trials involved testing the effectiveness of a submunition of an "N-bomb"—a biological weapon. Additionally, five million "cattle cakes" impregnated with anthrax were prepared and stored at Porton Down for "Operation Vegetarian"—an anti-livestock weapon intended for attacks on Germany by the Royal Air Force. The infected cattle cakes were to be dropped on Germany in 1944. However neither the cakes nor the bomb was used; the cattle cakes were incinerated in late 1945.

More recently, the Rhodesian government used anthrax against cattle and humans in the period 1978–1979 during its war with black nationalists.

American military and British Army personnel are routinely vaccinated against anthrax prior to active service in places where biological attacks are considered a threat. The anthrax vaccine, produced by BioPort Corporation, contains non-living bacteria, and is approximately 93% effective in preventing infection.

Weaponised stocks of anthrax in the US were destroyed in 1971–72 after President Nixon ordered the dismantling of US biowarfare programs in 1969 and the destruction of all existing stockpiles of bioweapons.

The Soviet Union created and stored 100 to 200 tons of anthrax spores at Kantubek on Vozrozhdeniya Island. They were abandoned in 1992 and destroyed in 2002.

Sverdlovsk incident

2 April 1979

Sverdlovsk anthrax leak

Despite signing the 1972 agreement to end bioweapon production the government of the Soviet Union had an active bioweapons program that included the production of hundreds of tons of weapons-grade anthrax after this period. On 2 April 1979, some of the over one million people living in Sverdlovsk (now called Ekaterinburg, Russia), about 850 miles east of Moscow, were exposed to an accidental release of anthrax from a biological weapons complex located near there. At least 94 people were infected, of whom at least 68 died. One victim died four days after the release, ten over an eight-day period at the peak of the deaths, and the last six weeks later. Extensive cleanup, vaccinations and medical interventions managed to save about 30 of the victims. Extensive cover-ups and destruction of records by the KGB continued from 1979 until Russian President Boris Yeltsin admitted this anthrax accident in 1992. Jeanne Guillemin reported in 1999 that a combined Russian and United States team investigated the accident in 1992.

Nearly all of the night shift workers of a ceramics plant directly across the street from the biological facility (compound 19) became infected, and most died. Since most were men, there were suspicions by NATO governments that the Soviet Union had developed a sex-specific weapon. The government blamed the outbreak on the consumption of anthrax-tainted meat and ordered the confiscation of all uninspected meat that entered the city. They also ordered that all stray dogs be shot and that people not have contact with sick animals. There was also a voluntary evacuation and anthrax vaccination program established for people from 18–55.

To support the cover-up story Soviet medical and legal journals published articles about an outbreak in livestock that caused GI anthrax in people having consumed infected meat, and cutaneous anthrax in people having come into contact with the animals. All medical and public health records were confiscated by the KGB. In addition to the medical problems that the outbreak caused, it also prompted Western countries to be more suspicious of a covert Soviet Bioweapons program and to increase their surveillance of suspected sites. In 1986, the US government was allowed to investigate the incident, and concluded that the exposure was from aerosol anthrax from a military weapons facility. In 1992, President Yeltsin admitted that he was "absolutely certain" that "rumors" about the Soviet Union violating the 1972 Bioweapons Treaty were true. The Soviet Union, like the US and UK, had agreed to submit information to the UN about their bioweapons programs but omitted known facilities and never acknowledged their weapons program.

Anthrax bioterrorism

In theory, anthrax spores can be cultivated with minimal special equipment and a first-year collegiate microbiological education, but in practice the procedure is difficult and dangerous. To make large amounts of an aerosol form of anthrax suitable for biological warfare requires extensive practical knowledge, training, and highly advanced equipment.

Concentrated anthrax spores were used for bioterrorism in the 2001 anthrax attacks in the United States, delivered by mailing postal letters containing the spores. The letters were sent to several news media offices as well as to two Democratic senators: Tom Daschle of South Dakota and Patrick Leahy of Vermont. As a result, 22 were infected and five died.  Only a few grams of material were used in these attacks and in August 2008 the US Department of Justice announced they believed that Dr. Bruce Ivins, a senior biodefense researcher employed by the United States government, was responsible. These events also spawned many anthrax hoaxes.

Due to these events, the U.S. Postal Service installed biohazard detection systems at its major distribution centers to actively scan for anthrax being transported through the mail.

Decontaminating mail

In response to the postal anthrax attacks and hoaxes the US Postal Service sterilized some mail using a process of gamma irradiation and treatment with a proprietary enzyme formula supplied by Sipco Industries Ltd.

A scientific experiment performed by a high school student, later published in The Journal of Medical Toxicology, suggested that a domestic electric iron at its hottest setting (at least 400 °F (204 °C)) used for at least 5 minutes should destroy all anthrax spores in a common postal envelope.