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Anthrax infection can occur in three forms: cutaneous (skin), inhalation, and gastrointestinal. The three forms of anthrax differ only in the route by which the bacteria enter the system. Bacillus anthracis spores can live in the soil for many years, and humans can become infected with anthrax by handling products from infected animals or by inhaling anthrax spores from contaminated animal products. Anthrax can also be spread by eating undercooked meat from infected animals.
Method of Attack Terrorists are most likely to attack by dispersing anthrax spores on clear days when there is no wind, because buildings, wind, humidity, and rain provide considerable protection. Dispersing anthrax over a wide area would not be a trivial undertaking because commercial delivery platforms are not designed to spread substances over a wide area.
Additional difficulties for the terrorist are presented by the need to `weaponize' the spores. Weaponizing is a process which involves changing the spores in a certain way to ensure viability and to ensure efficient alveolar retention. The Japanese Aum Shinrikyo terrorists failed to produce casualties not because of any inability to create spores but because they chose the Sterne strain, a harmless "vaccine strain" of anthrax by mistake. Vaccine strains are special cultivated natural variant forms of anthrax that lack one of the two DNA plasmids that code for the lethal and edema factors in pathogenic anthrax, due to the absence of the polysaccharide capsule on these variant bacteria.
Because a one-micron spore is only a few wavelengths of light in diameter, a terrorist would need advanced and expensive equipment such as an electron microscope to create a powder with a narrow particle distribution. The more difficult steps of "weaponizing" can be omitted entirely if the terrorists are willing to tolerate low spore viability and poor long-term stability. However, since the primary difficulty for the terrorist is lack of information, even this obstacle could be overcome with assistance in the form of recipe-like procedures from a hostile country.
The most deadly form of anthrax is pulmonary anthrax, caused by inhaling spores. However, anthrax could also be ingested, which would cause gastrointestinal anthrax. This form of anthrax is a painful intestinal food poisoning, and causes death unless antibiotics are given. Ciprofloxacin and related fluoroquinolones are is the antibiotics of choice, although penicillin, doxycycline, and many other antibiotics also work. B anthracis is resistant to sulfamethoxazole, trimethoprim, cefuroxime, cefotaxime, aztreonam, and ceftazidime. Doxycycline is not recommended for children or pregnant women because it retards skeletal growth. Penicillin is poorly absorbed from the intestine and should be taken on an empty stomach, or preferably injected. The antibiotics must be taken daily for at least two months. You should never take antibiotics prophylactically, since this will kill intestinal bacteria which can result in colonization of the intestine by anaerobic Clostridia, causing botulism poisoning. The Soviet Union developed strains of Bacillus anthracis that are resistant to penicillin and tetracycline. Thus, ciprofloxaxin should be used if available.
Symptoms Symptoms of disease vary depending on how the disease was contracted, but symptoms usually occur within 7 days.
Cutaneous: Most (about 95%) anthrax infections occur when the bacterium enters a cut or abrasion on the skin, such as when handling contaminated wool, hides, leather or hair products (especially goat hair) of infected animals. Skin infection begins as a raised itchy bump that resembles an insect bite but within 1-2 days develops into a vesicle and then a painless ulcer, usually 1-3 cm in diameter, with a characteristic black necrotic (dying) area in the center. Lymph glands in the adjacent area may swell. About 20% of untreated cases of cutaneous anthrax will result in death. Deaths are rare with appropriate antimicrobial therapy.
Inhalation: Inhalational or pulmonary anthrax is a result of the deposition of spore-bearing particles into the alveolar spaces of the lung. Macrophages, which act as a host defense mechanism, lyse and destroy some of the spores. The surviving spores are transported to the mediastinal and peribronchial lymph nodes. Germination may occur in the mediastinal lymph nodes up to 60 days after infection. Disease immediately follows germination. Anthrax bacilli replicate in the lymph nodes. Hemorrhage, edema, and necrosis are the results of bacterial toxins released during replication.
Symptoms of pulmonary anthrax are those of a lung infection like influenza, and are easily distinguished from the runny nose and sneezing of upper respiratory diseases such as common cold.
Initial symptoms may resemble a very mild influenza including a dry, nonproductive cough, a low grade fever, myalgia (aching muscles), dyspnea (difficulty breathing), headache, vomiting, chills, abdominal pain, and chest pain. Occasionally there is a sensation of retrosternal pressure. These symptoms last for 2-3 days, then begin to recede. Antibiotics must be given during this first phase to be effective. A few days later, symptoms return with much greater severity, including sudden mild fever, dyspnea, and diaphoresis (heavy perspiration). Enlarged mediastinal lymph nodes scattered throughout the front part of the upper chest area may cause stridor (a harsh sound heard on inhalation) by partially occluding the trachea. Auscultation of the lungs is remarkable for crackles and signs of pleural effusions. These symptoms progress to severe breathing problems, cyanosis, hypotension and shock. As shock develops, the fever changes to hypothermia. In this second stage, antibiotics are useless. The characteristic sign, detected on a chest X-ray, is a widened mediastinum (the space in the thoracic cavity behind the sternum, between the two pleural sacs containing the lungs) consistent with lymphadenopathy. Up to half of victims develop hemorrhagic meningitis with concomitant meningismus (pain), delirium, and obtundation. Other symptoms include pleural effusions, hemorrhagic mediastinitis, respiratory distress, septic shock, cyanosis, elevated WBC, edema, myalgia, cough, chest pain, dyspnea, nausea. Death results 2-3 days after the onset of symptoms. Once the second stage is reached, antibiotics are usually ineffective. Death occurs in 99% of patients reaching the second stage.
Intestinal: The intestinal disease form of anthrax may follow the consumption of contaminated meat and is characterized by an acute inflammation of the intestinal tract. Initial signs of nausea, loss of appetite, vomiting, fever are followed by abdominal pain, vomiting of blood, and severe bloody diarrhea. Intestinal anthrax results in death in 25% to 60% of cases.
Protection Because the attack is usually undetected, a gas mask is impractical. The spores are too small to be visible, and only 8000 spores, approximately 0.08 micrograms, are enough to cause infection. A HEPA filter mask, if worn properly, will block the spores from entering your lungs and would protect you in the aftermath of an attack. For instance, if you ventured outdoors several days after an attack, a gust of wind theoretically could blow a sufficient number of spores off a tree or up from the ground to kill you. However, data from the Sverdlovsk incident suggest that this mode of infection is unlikely. Staying indoors and keeping windows shut would reduce exposure by 2/3 during an attack. If the building or vehicle is tightly sealed, or under positive air pressure, and if the air is filtered through HEPA filters, the inhabitants are relatively safe.
There are 3 classes of filter masks (respirators): N95, N99, and N100. These block 95%, 99% and 99.97%, respectively, of airborne particulates 0.1 micron or larger. This size cutoff is adequate to block spores, which are typically 1 micron in diameter. The rod-shaped vegetative bacterium is larger, rod-shaped, 1 x 8 microns in size, large for bacteria. P95, P99, and P100 masks are similar, but designed to block oil as well as dust in industrial settings. A common type of mask found in hardware stores is the "nuisance" mask, which is useless against anthrax. N95 and P95 filters are also not sufficient to provide safety. Masks and respirators range from $2 to $35 each. Some masks have an exhale valve that makes breathing easier. After an attack in one city is recognized, residents of other cities will undoubtedly want to wear filter masks continuously. There is a good argument for obtaining a mask in advance of an attack, rather than waiting for the Government to issue you one several days afterwards. Every person who is concerned about the possibility of anthrax attack should have a N100 filter mask in their car, desk, and at home.
Unless you have special training and a biohazard suit, you should never attempt to decontaminate an area or touch an item suspected of containing a weaponized biological agent such as anthrax. Attempting to wrap the item in a biohazard bag, for instance, would only spread the agent, causing more casualties, and would hamper the investigation. It could also activate a booby trap such as a dispersing mechanism or explosive.
Anthrax spores can be killed by washing with hot chlorine bleach or by boiling at 120° C (250° F) for 1-2 hours, or dry heat at 159° C. Food that is thoroughly cooked is not necessarily free of spores unless it has been cooked at well over boiling temperature. However, thorough cooking would kill any vegetative (growing) bacteria.
An anthrax vaccine is manufactured and distributed by BioPort Corp., Lansing, Michigan. The vaccine, produced from a non-pathogenic strain of anthrax, is a cell-free filtrate, which means it contains no dead or live bacteria. Anthrax vaccines intended for animals should not be used in humans.
Mild local reactions occur in 30% of vaccine recipients and consist of slight tenderness and redness at the injection site. Severe local reactions are infrequent and consist of extensive swelling of the forearm in addition to the local reaction. Systemic reactions occur in fewer than 0.2% of recipients.
Probability Many countries have samples of pathogenic anthrax. The Florida cases (October 2001) resulted from the penicillin-sensitive Ames strain. A state-sponsored terrorist group would be more likely to use a penicillin-resistant strain.
The Ames strain of anthrax that was used by the terrorists differs genetically from the Vollum 1B strain formerly used by the U.S. and from the strain used by the Soviet Union. According to the U.S. military, the Ames strain is "one of, if not the most, lethal strain[s]" and is resistant to the MDPH (Michigan) anthrax vaccine which has been used to protect American soldiers. Although this vaccine is partially effective against primates, in guinea pig tests, only 20 to 26% of vaccinated animals survived a challenge of Ames strain aerosol spores.
Microbiology of anthrax
Clinical tests and
medical treatment for anthrax

Gram-positive Bacillus anthracis
Nerve agents are toxic in the range of 10-20 micrograms/kg. This means a small drop of 1 microliter, about the size of the head of a pin, is sufficient to kill a person. VX is more dangerous because its lower volatility allows it to remain on the skin longer. In fact, most nerve agents have boiling points above 300° C, and are more like oils than volatile liquids. This means that the main risk is from skin contact, not inhalation.
Modern nerve `gases' are often binary agents, which contain two relatively benign chemicals that react to become lethal only when mixed together. An example is Novichok ("newcomer") agent, which is a particular threat because it can be synthesized from ordinary agricultural and industrial chemicals, and is 5-10 times more toxic than VX. The U.S. produced binary versions of standard nerve agents, which were designated by appending "2" to the name (e.g., GB-2, GD-2 and VX-2 were the binary forms of GB, GD and VX). VX is formed when QL and a harmless powder are mixed.
The first effect of mild exposure to organophosphate vapor is involuntary blushing. One's face feels hot and turns red as if embarrassed. Runny nose, miosis ("constriction" of the pupils of the eye to a small dot), salivation and chest tightness also occur. The next symptom, which may occur several hours later, is extreme mental excitement, i.e. uncontrolled racing thoughts caused by excess neuronal activity in the brain. It is essential for the victim to remain calm and try to slow their brain as much as possible. Nightmares occur if the victim tries to sleep. Overstimulation of the brain by organophosphates can cause neuronal cell death, resulting in permanent brain damage.
Skin contact of nerve agent causes fasciculations or twitching of the muscles near the point of exposure.
Stronger exposure must be treated immediately with atropine to prevent death. Researchers who use organophosphates in the laboratory are required to have a medical doctor in the same room holding two AtroPen syringes filled with atropine. These are pen-shaped single-use syringes (autoinjectors) which automatically inject the antidote when jammed against the victim's thigh through the clothing. They are designed to avoid the necessity of uncapping a needle or fumbling with the plunger of a syringe. If an accident occurs, the physician first injects him/herself with one syringe, then if still alive, the physician injects the researcher with the other one. Atropine blocks acetylcholine receptors, counteracting the effect of excess ACh. In the past, tiny amounts of atropine were used as the active ingredient in Contac cold medicine. The amount of atropine in these syringes (1-2 mg) would act as a potent sedative, but a single injection of atropine would probably not be fatal to an unexposed healthy adult person. In the event of an exposure to nerve agent, larger doses of up to 20-40 mg atropine may be necessary. These doses are much lower than the doses used to treat poisoning from organophosphorus insecticides. Pyridostigmine bromide and other reversible cholinergic antagonists can be used as protective agents against soman and tabun but are ineffective against sarin and VX.
The hazards of atropine autoinjectors were shown in the Gulf War. Despite the fact that no nerve gas was released by the Scud missiles, 230 Israelis were hospitalized from overdoses caused by inappropriate administration of atropine, and 8 deaths were caused by suffocation in gas masks.
In contrast to the way nerve gas situations depicted in the movies, you are not supposed to inject atropine directly into your heart. Also, unlike in the movies, nerve gas does not dissolve your flesh or cause you to scream in agony. And it's not green in color.
A second drug used in the treatment of nerve gas poisoning is pralidoxime chloride (2-PAM Cl), also known as Protopam. It is used to reactivate the acetylcholinesterase that is bound by the nerve agent. PAM is an oxime compound that inactivates the organophosphorus-esterase complex. As this complex ages over time due to dealkylation, it loses its susceptibility to PAM. Because the soman (GD) complex ages very rapidly, PAM is not effective against Soman (GD) poisoning. The dosage for PAM is normally 600 mg per injection; multiple injections may be required. PAM may also be given as 1 gram intravenously over an eight hour period. PAM does not cross the blood-brain barrier and cannot reverse the CNS effects of nerve agents.
Diazepam or other tranquilizers are frequently also used to reduce CNS overstimulation and seizures.
Some of the symptoms commonly associated with acute exposure to chemical nerve agents include miosis, frontal headaches, eye pain on focusing, slight dimness of vision, occasional nausea and vomiting, runny nose, tightness in chest, sometimes with prolonged wheezing, expiration suggestive of bronchoconstriction or increased secretion and coughing. Following systemic absorption, typical symptoms are: tightness in chest, wheezing, anorexia, nausea, vomiting, abdominal cramps, epigastric and substernal tightness, heartburn, diarrhea, involuntary defecation, increased sweating, increased salivation, increased tearing, slight bradycardia, miosis, blurring vision, urinary urgency and frequency, fatigue, mild weakness, muscular twitching, cramps, generalized weakness, including muscles of respiration, with dyspnea and cyanosis, pallor and occasional elevation of blood pressure; giddiness, tension, anxiety, jitteriness, restlessness, emotional lability, excessive dreaming, insomnia, nightmares, headaches, tremors, withdrawal and depression; bursts of slow waves of elevated voltage in EEG (especially on over ventilation), drowsiness, difficulty concentrating, slowness on recall, confusion, slurred speech, ataxia, coma (with absence of reflexes), Cheyne-Stokes respirations, convulsions, depression of the respiratory and circulatory centers, with dyspnea, cyanosis and fall in blood pressure.
Protection Nerve gas is a liquid that would be dispersed as a vapor or aerosol. Gas masks would provide some protection to individuals who need to cross contaminated areas or floors to escape, but would be of less value in a subway car because the victim would only have a few seconds to deduce that an attack is underway.
Depending on the agent and mode of dispersal, cutaneous absorption might also make the gas mask irrelevant. Nerve gas both in liquid and vapor form is easily absorbed through the skin, and will readily penetrate latex gloves. Persons in contaminated areas should avoid touching any object or surface, and never touch or move any suspected victim of a chemical attack, even with gloves. All twelve persons that died in the Tokyo subway attack came into contact with the liquid. Sarin, the most volatile nerve agent, is odorless; tabun has a sweetish or fruity smell. VX intoxication has a slower onset than other organophosphates, but is more toxic, and is less soluble in water. VX has a low volatility (it is 2200 times less volatile than sarin) and is thus more difficult for terrorists to use because it must be delivered as an aerosol. Its proposed military use was to deny physical access to territory.
Protection Sealed biohazard suits are the only protection. If an attack is imminent, go to a sealed room where all air is filtered through a filter containing sodium hydroxide or DS2 (2% sodium hydroxide, 70% diethylene triamine, and 28% ethylene glycol monomethyl ether). Basic solutions such as washing soda and lye dissolved in water react with the nerve gas, inactivating it.
Symptoms Three to 9 days after infection, onset of symptoms is sudden, with fever, myalgia (aching muscles), dizziness, neck pain and stiffness, backache, extreme headache, sore eyes and photophobia (sensitivity to light). There may be nausea, vomiting and sore throat early on, which may be accompanied by diarrhea and generalized abdominal pain. Over the next few days, the patient may experience sharp mood swings, and may become confused and aggressive. After two to four days, the agitation may be replaced by sleepiness, depression and lassitude, and the abdominal pain may localize to the right upper quadrant, with detectable hepatomegaly (liver enlargement).
Other clinical signs which emerge include tachycardia (fast heart rate), lymphadenopathy (enlarged lymph nodes), and a petechial rash (a rash caused by bleeding into the skin), both on internal mucosal surfaces, such as in the mouth and throat, and on the skin. The petechiae may give way to ecchymoses (like a petechial rash, but covering larger areas) and other haemorrhagic phenomena such as melaena (bleeding from the upper bowel, passed as altered blood in the faeces), haematuria (blood in the urine), epistaxis (nosebleeds) and bleeding from the gums. There is usually evidence of hepatitis. The severely ill may develop hepatorenal (i.e., liver and kidney) and pulmonary failure after the fifth day of illness.
The mortality rate from CCHF is approximately 30%, with death occurring in the second week of illness. In those patients who recover, improvement generally begins on the ninth or tenth day after onset of illness.
Treatment Ribavirin has been effective in vitro against some Bunyaviridae. It is possible that prophylactic doses of Ribavirin may also be effective in preventing disease in people who have high-risk contact with patients.
Although an inactivated, mouse brain-derived vaccine against CCHF has been developed and used on a small scale in Eastern Europe, there is no safe and effective vaccine widely available for human use.
Probability Considerable technical skill is required to cultivate large quantities of any virus, including CCHF or dengue fever. CCHF is less contagious than smallpox.
Cancer patients are routinely administered 100 millicuries of radioactive materials, which stays in their bodies for several days, and produces only a 1% incidence of radiation-induced leukemia. This amount of radioactivity is enough to cause any Geiger counter to go crazy, yet 100 times this amount would be needed to cause radiation poisoning.
Small radiation detectors that can detect alpha, beta, and gamma radiation are available for as little as $250 and are highly recommended, if not as protection against terrorism, then as a way to become familiar with the many natural sources of radiation. If terrorists should sabotage a hospital or nuclear power plant, a radiation detector would enable a citizen to assess the true risk. Linux software is available that can interface with Radalert detectors to provide continuous monitoring of ambient radiation.
Small particles of insoluble radioactive material such as plutonium dust floating in the air pose a small but significant cancer risk because they can emit continuous exposure to a small area over a long period of time. The damaging effects of acute radiation exposure depend on the type of radiation, the amount (dose), duration of exposure, and rate of exposure. A single, rapid dose of radiation can be fatal, but the same total dose given over a period of weeks or months may have little measurable effect.
Acute radiation syndromes can affect many different organs.
The cerebral (brain) syndrome occurs when the total dose of radiation is extremely high (more than 3000 rem), and is always fatal. The first symptoms, nausea and vomiting, are followed by listlessness, drowsiness, and sometimes coma. Tremors, convulsions, inability to walk, and death occur within a few hours.
The gastrointestinal syndrome results from smaller exposures (400 rem or more). The symptoms are severe nausea, vomiting, and diarrhea, leading to severe dehydration. Initially, the syndrome is caused by the death of cells lining the gastrointestinal tract. Symptoms are perpetuated by the progressive wasting away of the tract's lining and by bacterial infections. Ultimately, the cells that absorb nutrients are completely destroyed, and blood, often in large amounts, leaks from the diseased area into the intestines. New cells may grow, usually 4 to 6 days after exposure to radiation. But even if they do, people who have this syndrome are likely to die of bone marrow failure, which usually occurs 2 or 3 weeks later.
The hematopoietic syndrome affects the bone marrow, spleen, and lymph nodes--the primary sites of blood cell production (hematopoiesis). It develops after exposure to 200 to 1000 rem of radiation and begins with loss of appetite (anorexia), apathy, nausea, and vomiting. These symptoms are most severe 6 to 12 hours after exposure and may subside completely by 24 to 36 hours after exposure. During this symptom-free period, the blood-producing cells in the lymph nodes, spleen, and bone marrow begin to waste away, leading to a severe shortage of red and white blood cells. A shortage of white blood cells, which fight infections, often leads to severe infections.
Occasionally, severe injuries to organs exposed to radiation develop long after the exposure has ended. Kidney function may decline following a delay (latent period) of 6 months to a year. Therapeutic radiation to lung tumors can cause lung inflammation (radiation pneumonitis) and severe scarring (fibrosis) of lung tissue, which can be fatal. Large accumulated doses of radiation to the spinal cord can cause paralysis. These are serious concerns for cancer radiotherapy.
So, how much radioactivity is harmful? As a very rough estimate, for a 165-lb person (i.e., a typical American adult female), a lethal dose of 400 rem would be on the order of 1 x 10¹³ disintegrations per minute (DPM), or around 5 curies, over the entire body continuously for one day, or 10 million DPM per cm³ for one day. By comparison, background radiation levels are about 20-30 DPM/cm³. If ambient readings exceed 200 DPM, it is cause for alarm because it indicates a radiation source is nearby. The course of action to take depends on whether it is a point source or widespread contamination. Clearly, if citizens are armed with radiation monitors and a basic knowledge of radiation detection, they could make a rational decision about whether to wait for ambient levels to decay or to try to escape, while a citizen with no such knowledge would have to wait until told what to do.
Because patients are sometimes discharged from hospitals with small amounts of radioactive material still in their systems, a radioactive signal picked up by a hand-held detector should be interpreted with caution.
Method of Attack Unless a nuclear plant is hit, attacks with radioactive materials pose relatively small risk; the main risk is from fear and panic. A sensible precaution would be to maintain a large storage container full of water in a secure location.
Types of radioactive material Radioactive materials can be in any chemical form and physical state (solid, liquid, or gas). Radioactive isotopes vary widely in their danger. For example, tritium emits a beta particle that is easily blocked and is so low in energy that Geiger counters cannot detect it. Unless you ingested large amounts of tritium, it would not be harmful. On the other hand, cobalt 60 and cesium 137 emit high energy gamma rays that are difficult to block and are harmful from several meters away. Heavy atoms such as uranium and plutonium emit neutrons and alpha particles. Because alpha particles cannot penetrate the skin, alpha particles are only harmful if the plutonium is ingested. The neutrons from uranium, at the high levels found in nuclear plants, create other radioactive isotopes by inducing fission, and also can be absorbed by ordinary substances such as water, causing them to become radioactive. This does not occur to any appreciable extent outside of a nuclear reactor.
Protection All persons should use iodized salt and have iodide tablets available before an attack. This prevents radioactive iodine from being absorbed by the thyroid gland. The only effective protection against radiation after an attack is to move to a different location. If this is impossible, a basement or fallout shelter will provide some protection, but if the contamination is widespread, you will have to leave eventually.
Method of Attack Cyanide must be at relatively high concentration to kill a person, so the terrorist would probably release cyanide in an enclosed area such as a subway car, airplane, or the ventilation system of a building. Because the gas disperses very rapidly and is lighter than air, it would not be used outdoors. Terrorists would not put cyanide in the water supply, but might try to contaminate food.
Because HCN condenses below room temperature, there is considerable risk that cyanide that condenses on the ground at night will evaporate and once again become hazardous as temperatures rise the next morning. This also occurs with mustard gas, and was a frequent cause of exposure during World War I as soldiers removed their gas masks thinking the danger had passed.
Protection A gas mask will provide some protection, but in a closed compartment the user would have to recognize the attack and put on the mask within seconds. The effectiveness of a gas mask for cyanide can be greatly increased by cartridges containing special chemicals that react with cyanide. The best use for a gas mask would be in a building. If warning were received that one floor had been attacked using cyanide, occupants of other floors would be protected during their escape if they had gas masks. However, both inhaling and exhaling require strong effort when a gas mask is being worn. This means that most people cannot wear a gas mask for more than 1-2 hours without becoming exhausted, and running is extremely difficult, especially in a panic situation, because of the difficulty of pushing air through the mask. Ordinary filter masks or respirators without charcoal provide no protection.
Symptoms Cyanide blocks cellular respiration by binding to the iron in cytochrome oxidase, and interferes with neuronal transmission. The characteristic initial symptom is difficulty in catching one's breath, then dryness and burning of the throat. It causes tachycardia (rapid heartbeat), headache, drowsiness, hypotension, and convulsions, and has an extremely rapid onset. Cyanide is a relatively forgiving poison because the victim usually either fully recovers or is dead. This is in sharp contrast to nerve gas which often causes life-long disability. However, anoxia caused by sublethal cyanide poisoning can also cause long-term neurological problems.
Treatment Cyanide can kill in less than a minute. Give immediate emetics or lavage, amyl nitrite inhalation (0.2 ml, 30 sec each minute), 10 ml 3% sodium nitrite (2.5-5 ml/min IV) followed by 50 ml of 25% sodium thiosulfate (2.5-5 ml/min IV), and 100% oxygen. Nitrites oxidize the iron in hemoglobin to Fe3+. The oxidized methemoglobin binds cyanide avidly. A number of other chemicals have physiological effects similar to cyanide. Many of these substances can be absorbed through the skin as well as by inhalation.
There are two types of smallpox: variola major and variola minor. The severe form, variola major, is 30-50% lethal, typically killing between the 5th and 7th day of illness. Variola minor is 1-2% lethal. About 3% of those with variola major also get the most severe form of smallpox known as purpura variolosa or hemorrhagic-type smallpox, in which a dark, purplish, blotchy flushing of the skin occurs during the initial stage of the illness (before the rash appears). This is caused by blood hemorrhaging into the skin and internal organs. These victims die before a rash appears. Another 5% of victims of variola major get the equally deadly "flat smallpox", in which the lesions are not raised above the surface of the skin.
Smallpox can be distinguished from chickenpox as follows:
Method of Attack The most likely starting point for smallpox would be a transportation center. The terrorist would travel to numerous cities to start a large number of simultaneous outbreaks in order to prevent containment of the epidemic. The disease could also be spread through the mail.
Probability It is not necessary for the terrorist to cultivate viruses in order to use smallpox as a weapon; thus, smallpox is a weapon that can be used by an unskilled person to kill hundreds of millions of people. However, if a terrorist released smallpox, it would eventually make its way back to the terrorist's host country and kill them as well. Moreover, because no natural cases of smallpox have occurred since 1977, the country of origin would be immediately flagged by small smallpox outbreaks occurring early in the epidemic. Terrorists might be deterred by the knowledge that more than harsh words would be used against a country that reintroduced smallpox to the world.
Protection There are no drugs approved for smallpox; however, recent research suggests that the experimental DNA polymerase inhibitor cidofovir may be effective against orthopoxviruses. Because viruses can integrate invisibly into the host's genomic DNA, antiviral agents generally cannot be directed against viruses themselves, but against their gene products. This approach has been most effective against retroviruses, with drugs directed against the viral enzyme reverse transcriptase, which is not found normally in humans.
Vaccination is the only effective way to prevent smallpox. Smallpox vaccination in most countries, including the US, was stopped in or around 1972. This means there is no resistance to smallpox in any segment of the population. Vaccination against smallpox is effective even when given 4 days after exposure to the virus.
Smallpox is extremely contagious: you can catch smallpox from a person sneezing many yards away. Among populations that have a resistance, it is fatal 30% of the time. Smallpox killed 300-500 million people during the 20th century and decimated the Native Indian populations of North and South America over a period of 300 years. Currently protection can only be carried out by public health officials who must have adequate supplies of vaccine on hand before the attack and who have authority to impose quarantine on large areas of a city.
Symptoms Patients with pneumonic plague exhibit extreme fever, exhaustion, chills, difficulty breathing, severe cough, and frothy, bloody sputum within 2 to 6 days after exposure. Headache, hemoptysis, and toxemia, progress rapidly to dyspnea, stridor, and cyanosis. Chest X-rays reveal a patchy or consolidated bronchopneumonia. Patients with bubonic plague have muscular pains, large, painful, very tender lymph glands, and reddened, oval, painful swellings near the lymph glands in the groin, armpits, and neck. Pneumonic plague is considered a public health emergency because a cough can quickly spread the disease to others. Untreated pneumonic plague is usually fatal.
Method of Attack Although historically plague was carried by fleas living on rats, terrorists would most likely spray plague bacteria as an aerosol cloud from a plane. In 1970 the World Health Organization concluded that dissemination of 50 kg of Y pestis over a city of 5 million could result in 150,000 cases of pneumonic plague and kill 36,000 people.
Protection A vaccine has been licensed for bubonic plague, but no adequate vaccine exists for pneumonic plague. The disease requires contact with bodily fluids or airborne droplets to spread from person to person. Surgical masks provide good protection. Mortality is reduced from 100% to 5% if treated within 24 hours with streptomycin, gentamycin, chloramphenicol, tetracycline, or fluoroquinolone antibiotics.
Probability Only the USA and Russia are believed to possess the technology to weaponize plague bacteria for pneumonic plague. Japan used flea-borne bubonic plague against China in WWII. Yersinia pestis is very sensitive to sunlight and does not survive long outside the host, making it very difficult to deploy as a weapon.
