Credonia
11-01-2004, 20:11
Credonian News Network *1/11/2004 2:02 pm CST*
Today, Credonian War Headquarters announced that it has been researching possible biological and chemical agents for use in combat for both offensive and defensive attacks. The missile system used to deliver the warheads is the L6-120B Freedom ICBM, a variant of the L6-120A ICBM which delivers 20 separate 100 kiloton warheads on each missile. The 'B' variant can only carry 10 warheads on each missile, but the warheads are interchangeable, therefore, being able to deliver more than one type of agent on each missile. At this time, Credonia possesses 300 of these ICBM's. Production of may come in the future but there is no guarantee. Please note that these weapons have been created for CREDONIA's USE ONLY and will not be sold at all to anyt nation. All requests to by, whether made "over the table" or "under the table" will be denied. The specifications of the missiles and the facts on the agents picked to use in combat are as follows:
L6-120B Freedom ICBM
Specifications
'L' Designates Silo Launched
'B' Designates 1st Missile Design in Series
Primary Function: Tactical Assault
Contractor: Credonian Arms Inc.
Powerplant: First 3 stages- Solid propellant; Fourth stage- storable liquid (LOX and LH2)
Warheads: 10
Biological/Chemical Agents: Ebola Haemorrhagic Fever Virus Biological Agent, Phosgene Oxime Chemical Agent, phosgene Coughing Chemical Agent, VX Nerve Gas Chemical Agent
Load: C-1 re-entry vehicles
Guidance system: Inertial
Thrust: First stage, 1 million pounds
Length: 142 ft (46.3 meters)
Weight: 390,000 pounds (176,901 kg) including re-entry vehicles
Diameter: 15 ft. 6 inches
Range: greater than 6,000 miles (5,217 nautical miles)
Speed: Approximately 15,000 mph at burnout (mach 20 at sea level) (24,140 km/hr)
Information On Agents Used In Warheads
Ebola Haemorrhagic Fever Virus
Ebola Haemorrhagic Fever is one of the most virulent viral disease known to humankind, causing death in 50-90% of all clinically-ill cases. Consequently, it has figured prominently in popular discussions of biological warfare, although its practical appli cations as an biological warfare agent remain speculative. The disease has its origins in the jungles of Africa and Asia and several different forms of Ebola virus have been identified and may be associated with other clinical expressions, on which furthe r research is required.
The Ebola virus is transmitted by direct contact with the blood, secretions, organs or semen of infected persons. Transmission through semen may occur up to 7 weeks after clinical recovery, as with Marburg haemorrhagic fever. Health care workers have f requently been infected while attending patients. In the 1976 epidemic in Zaire, every Ebola case caused by contaminated syringes and needles died.
After an incubation period of 2 to 21 days, Ebola is often characterised by the sudden onset of fever, weakness, muscle pain, headache and sore throat. This is followed by vomiting, diarrhoea, rash, limited kidney and liver functions, and both internal and external bleeding. Specialized laboratory tests on blood specimens (which are not commercially available) detect specific antigens or antibodies and/or isolate the virus. These tests present an extreme biohazard and are only conducted under maximum c ontainment conditions.
No specific treatment or vaccine exists for Ebola haemorrhagic fever. Severe cases require intensive supportive care, as patients are frequently dehydrated and in need of intravenous fluids. Experimental studies involving the use of hyperimmune sera on animals demonstrated no long-term protection against the disease after interruption of therapy.
Suspected cases should be isolated from other patients and strict barrier nursing techniques practised. All hospital personnel should be briefed on the nature of the disease and its routes of transmission. Particular emphasis should be placed on ensuri ng that high-risk procedures such as the placing of intravenous lines and the handling of blood, secretions, catheters and suction devices are done under barrier nursing conditions. Hospital staff should have individual gowns, gloves and masks. Gloves and masks must not be reused unless disinfected. Patients who die from the disease should be promptly buried or cremated.
As the primary mode of person-to-person transmission is contact with contaminated blood, secretion or body fluids, any person who has had close physical contact with patients should be kept under strict surveillance, i.e. body temperature checks twice a day, with immediate hospitalization and strict isolation recommended in case of temperatures above 38.3 C (101 F). Casual contacts should be placed on alert and asked to report any fever. Surveillance of suspected cases should continue for three weeks a fter the date of their last contact. Hospital personnel who come into close contact with patients or contaminated materials without barrier nursing attire must be considered exposed and put under close supervised surveillance.
The Ebola virus was first identified in a western equatorial province of Sudan and in a nearby region of Zaire in 1976 after significant epidemics in Yamkubu, northern Zaire, and Nzara, southern Sudan. Between June and November 1976 the Ebola virus inf ected 284 people in Sudan, with 117 deaths. In Zaire there were 318 cases and 280 deaths in September and October. An isolated case occurred in Zaire in 1977, a second outbreak in Sudan in 1979. In 1989 and 1990, a filovirus, named Ebola-Reston, was isola ted in monkeys being held in quarantine in a laboratory in Reston (Virginia), Alice (Texas) and Pennsylvania. In the Philippines, Ebola-Reston infections occurred in the quarantine area for monkeys intended for exportation, near Manila. A large epidemic o ccurred in Kikwit, Zaire in 1995 with 315 cases, 244 with fatal outcomes. One human case of Ebola haemorrhagic fever and several cases in chimpanzees were confirmed in Côte d'Ivoire in 1994-95. In Gabon, Ebola haemorrhagic fever was first documented in 19 94 and recent outbreaks occurred in February 1996 and July 1996. In all, nearly 1,100 cases with 793 deaths have been documented since the virus was discovered. The natural reservoir of the Ebola virus seems to reside in the rain forests of Africa and Asi a but has not yet been identified.
Different hypotheses have been developed to try to uncover the cycle of Ebola. Initially, rodents were suspected, as is the case with Lassa Fever whose reservoir is a wild rodent (Mastomys). Another hypothesis is that a plant virus may have caused the infection of vertebrates. Laboratory observation has shown that bats experimentally infected with Ebola do not die and this has raised speculation that these mammals may play a role in maintaining the virus in the tropical forest.
Phosgene Oxime
Phosgene oxime [CX] is a white crystalline powder. It melts between 39-40° C, and boils at 129° C.By the addition of certain compounds it is possible to liquify phosgene oxime at room temperature. It is fairly soluble in water and in organic solvents. In aqueous solution phosgene oxime is hydrolyses fairly rapidly, especially in the presence of alkali. It has a high vapour pressure, its odour is very unpleasant and irritating. Even as a dry solid, phosgene oxime decomposes spontaneously and has to be stored at low temperatures.
In low concentrations, phosgene oxime severely irritates the eyes and respiratory organs. In high concentrations, it also attacks the skin. A few milligrams applied to the skin cause severe irritation, intense pain, and subsequently a necrotising wound. Very few compounds are as painful and destructive to the tissues.
Phosgene oxime also affects the eyes, causing corneal lesions and blindness and may affect the respiratory tract causing pulmonary oedema. The action on the skin is immediate: phosgene oxime provokes irritation resembling that caused by a stinging nettle. A few milligrams cause intense pain which radiates from the point of application, within a minute the affected area turns white and is surrounded by a zone of erythema (skin reddening) which resembles a wagon wheel in appearance. In 1 hour the area becomes swollen and within 24 hours the lesion turns yellow and blisters appear. Recovery takes 1 to 3 months.
Phosgene
The toxic action of phosgene is typical of a certain group of lung damaging agents. Phosgene is the most dangerous member of this group and the only one considered likely to be used in the future. Phosgene was used for the first time in 1915, and it accounted for 80% of all chemical fatalities during World War I.
Phosgene is a colorless gas under ordinary conditions of temperature and pressure. Its boiling point is 8.2°C, making it an extremely volatile and non-persistent agent. Its vapour density is 3.4 times that of air. It may therefore remain for long periods of time in trenches and other low lying areas. In low concentrations it has a smell resembling new mown hay.
The outstanding feature of phosgene poisoning is massive pulmonary oedema. With exposure to very high concentrations death may occur within several hours; in most fatal cases pulmonary oedema reaches a maximum in 12 hours followed by death in 24-48 hours. If the casualty survives, resolution commences within 48 hours and, in the absence of complicating infection, there may be little or no residual damage.
During and immediately after exposure, there is likely to be coughing, choking, a feeling of tightness in the chest, nausea, and occasionally vomiting, headache and lachrymation. The presence or absence of these symptoms is of little value in immediate prognosis. Some patients with severe coughs fail to develop serious lung injury, while others with little sign of early respiratory tract irritation develop fatal pulmonary oedema. A period follows during which abnormal chest signs are absent and the patient may be symptom-free. This interval commonly lasts 2 to 24 hours but may be shorter. It is terminated by the signs and symptoms of pulmonary oedema. These begin with cough (occasionally substernally painful), dyspnoea, rapid shallow breathing and cyanosis. Nausea and vomiting may appear. As the oedema progresses, discomfort, apprehension and dyspnoea increase and frothy sputum develops. The patient may develop shock-like symptoms, with pale, clammy skin, low blood pressure and feeble, rapid heartbeat. During the acute phase, casualties may have minimal signs and symptoms and the prognosis should be guarded. Casualties may very rapidly develop severe pulmonary oedema. If casualties survive more than 48 hours they usually recover.
VX Nerve Gas
VX is a relatively non-volatile liquid and therefore persistent. It is regarded as presenting little vapour hazard to people exposed to it. In the pure state nerve agents are colorless and mobile liquids. In an impure state nerve agents may be encountered as yellowish to brown liquids. Some nerve agents have a faint fruity odour.
VX doses which are potentially life-threatening may be only slightly larger than those producing least effects. Death usually occurs within 15 minutes after absorption of a fatal VX dosage.
Although only about half as toxic as GB by inhalation, GA in low concentrations is more irritating to the eyes than GB. Symptoms appear much more slowly from a skin dosage than from a respiratory dosage. Although skin absorption great enough to cause death may occur in 1 to 2 minutes, death may be delayed for 1 to 2 hours. Respiratory lethal dosages kill in 1 to 10 minutes, and liquid in the eye kills almost as rapidly.
Today, Credonian War Headquarters announced that it has been researching possible biological and chemical agents for use in combat for both offensive and defensive attacks. The missile system used to deliver the warheads is the L6-120B Freedom ICBM, a variant of the L6-120A ICBM which delivers 20 separate 100 kiloton warheads on each missile. The 'B' variant can only carry 10 warheads on each missile, but the warheads are interchangeable, therefore, being able to deliver more than one type of agent on each missile. At this time, Credonia possesses 300 of these ICBM's. Production of may come in the future but there is no guarantee. Please note that these weapons have been created for CREDONIA's USE ONLY and will not be sold at all to anyt nation. All requests to by, whether made "over the table" or "under the table" will be denied. The specifications of the missiles and the facts on the agents picked to use in combat are as follows:
L6-120B Freedom ICBM
Specifications
'L' Designates Silo Launched
'B' Designates 1st Missile Design in Series
Primary Function: Tactical Assault
Contractor: Credonian Arms Inc.
Powerplant: First 3 stages- Solid propellant; Fourth stage- storable liquid (LOX and LH2)
Warheads: 10
Biological/Chemical Agents: Ebola Haemorrhagic Fever Virus Biological Agent, Phosgene Oxime Chemical Agent, phosgene Coughing Chemical Agent, VX Nerve Gas Chemical Agent
Load: C-1 re-entry vehicles
Guidance system: Inertial
Thrust: First stage, 1 million pounds
Length: 142 ft (46.3 meters)
Weight: 390,000 pounds (176,901 kg) including re-entry vehicles
Diameter: 15 ft. 6 inches
Range: greater than 6,000 miles (5,217 nautical miles)
Speed: Approximately 15,000 mph at burnout (mach 20 at sea level) (24,140 km/hr)
Information On Agents Used In Warheads
Ebola Haemorrhagic Fever Virus
Ebola Haemorrhagic Fever is one of the most virulent viral disease known to humankind, causing death in 50-90% of all clinically-ill cases. Consequently, it has figured prominently in popular discussions of biological warfare, although its practical appli cations as an biological warfare agent remain speculative. The disease has its origins in the jungles of Africa and Asia and several different forms of Ebola virus have been identified and may be associated with other clinical expressions, on which furthe r research is required.
The Ebola virus is transmitted by direct contact with the blood, secretions, organs or semen of infected persons. Transmission through semen may occur up to 7 weeks after clinical recovery, as with Marburg haemorrhagic fever. Health care workers have f requently been infected while attending patients. In the 1976 epidemic in Zaire, every Ebola case caused by contaminated syringes and needles died.
After an incubation period of 2 to 21 days, Ebola is often characterised by the sudden onset of fever, weakness, muscle pain, headache and sore throat. This is followed by vomiting, diarrhoea, rash, limited kidney and liver functions, and both internal and external bleeding. Specialized laboratory tests on blood specimens (which are not commercially available) detect specific antigens or antibodies and/or isolate the virus. These tests present an extreme biohazard and are only conducted under maximum c ontainment conditions.
No specific treatment or vaccine exists for Ebola haemorrhagic fever. Severe cases require intensive supportive care, as patients are frequently dehydrated and in need of intravenous fluids. Experimental studies involving the use of hyperimmune sera on animals demonstrated no long-term protection against the disease after interruption of therapy.
Suspected cases should be isolated from other patients and strict barrier nursing techniques practised. All hospital personnel should be briefed on the nature of the disease and its routes of transmission. Particular emphasis should be placed on ensuri ng that high-risk procedures such as the placing of intravenous lines and the handling of blood, secretions, catheters and suction devices are done under barrier nursing conditions. Hospital staff should have individual gowns, gloves and masks. Gloves and masks must not be reused unless disinfected. Patients who die from the disease should be promptly buried or cremated.
As the primary mode of person-to-person transmission is contact with contaminated blood, secretion or body fluids, any person who has had close physical contact with patients should be kept under strict surveillance, i.e. body temperature checks twice a day, with immediate hospitalization and strict isolation recommended in case of temperatures above 38.3 C (101 F). Casual contacts should be placed on alert and asked to report any fever. Surveillance of suspected cases should continue for three weeks a fter the date of their last contact. Hospital personnel who come into close contact with patients or contaminated materials without barrier nursing attire must be considered exposed and put under close supervised surveillance.
The Ebola virus was first identified in a western equatorial province of Sudan and in a nearby region of Zaire in 1976 after significant epidemics in Yamkubu, northern Zaire, and Nzara, southern Sudan. Between June and November 1976 the Ebola virus inf ected 284 people in Sudan, with 117 deaths. In Zaire there were 318 cases and 280 deaths in September and October. An isolated case occurred in Zaire in 1977, a second outbreak in Sudan in 1979. In 1989 and 1990, a filovirus, named Ebola-Reston, was isola ted in monkeys being held in quarantine in a laboratory in Reston (Virginia), Alice (Texas) and Pennsylvania. In the Philippines, Ebola-Reston infections occurred in the quarantine area for monkeys intended for exportation, near Manila. A large epidemic o ccurred in Kikwit, Zaire in 1995 with 315 cases, 244 with fatal outcomes. One human case of Ebola haemorrhagic fever and several cases in chimpanzees were confirmed in Côte d'Ivoire in 1994-95. In Gabon, Ebola haemorrhagic fever was first documented in 19 94 and recent outbreaks occurred in February 1996 and July 1996. In all, nearly 1,100 cases with 793 deaths have been documented since the virus was discovered. The natural reservoir of the Ebola virus seems to reside in the rain forests of Africa and Asi a but has not yet been identified.
Different hypotheses have been developed to try to uncover the cycle of Ebola. Initially, rodents were suspected, as is the case with Lassa Fever whose reservoir is a wild rodent (Mastomys). Another hypothesis is that a plant virus may have caused the infection of vertebrates. Laboratory observation has shown that bats experimentally infected with Ebola do not die and this has raised speculation that these mammals may play a role in maintaining the virus in the tropical forest.
Phosgene Oxime
Phosgene oxime [CX] is a white crystalline powder. It melts between 39-40° C, and boils at 129° C.By the addition of certain compounds it is possible to liquify phosgene oxime at room temperature. It is fairly soluble in water and in organic solvents. In aqueous solution phosgene oxime is hydrolyses fairly rapidly, especially in the presence of alkali. It has a high vapour pressure, its odour is very unpleasant and irritating. Even as a dry solid, phosgene oxime decomposes spontaneously and has to be stored at low temperatures.
In low concentrations, phosgene oxime severely irritates the eyes and respiratory organs. In high concentrations, it also attacks the skin. A few milligrams applied to the skin cause severe irritation, intense pain, and subsequently a necrotising wound. Very few compounds are as painful and destructive to the tissues.
Phosgene oxime also affects the eyes, causing corneal lesions and blindness and may affect the respiratory tract causing pulmonary oedema. The action on the skin is immediate: phosgene oxime provokes irritation resembling that caused by a stinging nettle. A few milligrams cause intense pain which radiates from the point of application, within a minute the affected area turns white and is surrounded by a zone of erythema (skin reddening) which resembles a wagon wheel in appearance. In 1 hour the area becomes swollen and within 24 hours the lesion turns yellow and blisters appear. Recovery takes 1 to 3 months.
Phosgene
The toxic action of phosgene is typical of a certain group of lung damaging agents. Phosgene is the most dangerous member of this group and the only one considered likely to be used in the future. Phosgene was used for the first time in 1915, and it accounted for 80% of all chemical fatalities during World War I.
Phosgene is a colorless gas under ordinary conditions of temperature and pressure. Its boiling point is 8.2°C, making it an extremely volatile and non-persistent agent. Its vapour density is 3.4 times that of air. It may therefore remain for long periods of time in trenches and other low lying areas. In low concentrations it has a smell resembling new mown hay.
The outstanding feature of phosgene poisoning is massive pulmonary oedema. With exposure to very high concentrations death may occur within several hours; in most fatal cases pulmonary oedema reaches a maximum in 12 hours followed by death in 24-48 hours. If the casualty survives, resolution commences within 48 hours and, in the absence of complicating infection, there may be little or no residual damage.
During and immediately after exposure, there is likely to be coughing, choking, a feeling of tightness in the chest, nausea, and occasionally vomiting, headache and lachrymation. The presence or absence of these symptoms is of little value in immediate prognosis. Some patients with severe coughs fail to develop serious lung injury, while others with little sign of early respiratory tract irritation develop fatal pulmonary oedema. A period follows during which abnormal chest signs are absent and the patient may be symptom-free. This interval commonly lasts 2 to 24 hours but may be shorter. It is terminated by the signs and symptoms of pulmonary oedema. These begin with cough (occasionally substernally painful), dyspnoea, rapid shallow breathing and cyanosis. Nausea and vomiting may appear. As the oedema progresses, discomfort, apprehension and dyspnoea increase and frothy sputum develops. The patient may develop shock-like symptoms, with pale, clammy skin, low blood pressure and feeble, rapid heartbeat. During the acute phase, casualties may have minimal signs and symptoms and the prognosis should be guarded. Casualties may very rapidly develop severe pulmonary oedema. If casualties survive more than 48 hours they usually recover.
VX Nerve Gas
VX is a relatively non-volatile liquid and therefore persistent. It is regarded as presenting little vapour hazard to people exposed to it. In the pure state nerve agents are colorless and mobile liquids. In an impure state nerve agents may be encountered as yellowish to brown liquids. Some nerve agents have a faint fruity odour.
VX doses which are potentially life-threatening may be only slightly larger than those producing least effects. Death usually occurs within 15 minutes after absorption of a fatal VX dosage.
Although only about half as toxic as GB by inhalation, GA in low concentrations is more irritating to the eyes than GB. Symptoms appear much more slowly from a skin dosage than from a respiratory dosage. Although skin absorption great enough to cause death may occur in 1 to 2 minutes, death may be delayed for 1 to 2 hours. Respiratory lethal dosages kill in 1 to 10 minutes, and liquid in the eye kills almost as rapidly.