Ebola Virus Essays (717 words) - Ebola, Biological Weapons

Ebola Virus The Ebola virus, also know as Ebola hemorrhagic fever is a disease caused by viruses from four different families of viruses: 1)filoviruses, 2)arenavirus, 3)flavavirus, 4)bunyaviruses. The usual host for most of these viruses are rodents or anthropoids (such as ticks and mosquitoes). In some cases, such as the Ebola virus, the natural host for the virus is unknown. All forms of viral hemorrhagic fever begin with a fever and muscle aches. Depending on the particular virus, the disease can progress until the patient becomes very ill with repiratory problems, severe bleeding internally and externally, kidney problems and shock. The severity of viral hemorrhagic fever can range from relatively mild illness to death. The Ebola virus is one of the deadliest diseases known to man. When magnified several thousand times by an electron microscope, these viruses have the appearance of long filaments or threads. Ebola virus was discovered in 1976 and was named for a river in Zaire, Africa where it was first detected. The first case appeared from nowhere, it killed 340 people. The disease is spread to health care workers in contact with body fluids, and also from patient to the person who cares for him or her in the home .The disease is also spread among those who prepare the corpses for burial. The disease is not as yet to be thought airborne .The only way to contract this disease is from a vector or contact with infected body fluids. Illness occurs 2 - 21 days after infection but generally within 7 - 14 days, beginning with much the same symptoms of that of the common cold or flu. . The virus causes an unusual combination of clots and hemorrhages. The clots lodge throughout the body, King 2 filling capillaries and shutting off blood to parts of the internal organs, especially to the brain, liver, and spleen. This causes the affected organs to begin to decay. Blood begins to leak through the capillaries and into the tissues, but by this point the blood will not clot. The connective tissues lose their elasticity and become mushy. The body's internal cavities fill with blood, and blood leaks from all orifices and through the skin, which becomes easily ripped. As the disease progresses, both humans and monkeys develop a fixed and expressionless face, probably as a result of hemorrhages within the brain. Usually during this stage there is rectal bleeding and the patient finally goes into convulsions and dies. As of yet, no treatment exists outside of supportive care. Mortality ranges from 50% to 90%. Upon necropsy (examination of the dead body to find cause of death), the internal organs of the dead are barely recognizable. the internal organs are liquefied and it looks like a big thick red milkshake. This unstoppable virus is a member of RNA viruses known as filoviruses. . Filoviruses form bricklike structures in animal cells. These structures, called inclusion bodies, will often fill the cell completely. The inclusion bodies then come apart as they move toward the cell's outer membrane. The virus threads grow through the cell walls, bud off, and travel to neighboring cells or to other sites throughout the host organism's body, where the cycle is repeated. Filoviruses seem to overwhelm the body's immune system, either by reproducing too rapidly for the body to react or perhaps by creating substances that suppress the normal immune response. The most recent outbreak was that of the one that was reported in Gabon Africa this particular Epidemic claimed the lives of 45 people out of the 60 cases that were King 3 reported. This outbreak was declared official in November of 1997 and declared official over in early 1997. While I find no recent reports of any outbreaks I have found much information on the research for the cure of this horrible disease. There has been much success with a plant which seems to stop the Ebola virus dead in its tracks. Scientists have yet to locate the resivior of this disease and therefore making it harder to track down the source or exact cause of the virus. So the discovery that the same forest that this disease thrives in also holds the potential cure is quite exciting for all those involved in this study. They have found that a compound from the Garcinia kola plant a plant which is commonly eaten in West Africa has stopped the virus in its tracks in laboratory tests. If this anti-Ebola compound proves successful in animal and human tests it will be the first medicine to successfully

Battle of Kwajalein in World War II

Battle of Kwajalein in World War II The Battle of Kwajalein occurred January 31 to February 3, 1944 in the Pacific Theater of World War II (1939-1945). Moving forward from victories in the Solomons and Gilbert Islands in 1943, Allied forces sought to penetrate the next ring of Japanese defenses in the central Pacific. Attacking into the Marshall Islands, the Allies occupied Majuro and then commenced operations against Kwajalein. Striking at both ends of the atoll, they succeeded in eliminating the Japanese opposition after brief but fierce battles. The triumph opened the way for the subsequent capture of Eniwetok and a campaign against the Marianas.   Background In the wake of the American victories at Tarawa and Makin in November 1943, Allied forces continued their island-hopping campaign by moving against Japanese positions in Marshall Islands. Part of the Eastern Mandates, the Marshalls were originally a German possession and were awarded to Japan after World War I. Considered part of the outer ring of Japanese territory, planners in Tokyo decided after the loss of the Solomons and New Guinea that the islands were expendable. With this in mind, what troops were available were shifted to the area to make the islands capture as costly as possible. Japanese Preparations Led by Rear Admiral Monzo Akiyama, Japanese forces in the Marshalls consisted of the 6th Base Force which initially numbered approximately 8,100 men and 110 aircraft. While a sizable force, Akiyamas strength was diluted by the need to spread his command over the entirety of the Marshalls. In addition, many of Akiyamas troops were labor/construction details or naval forces with little ground combat training. As a result, Akiyama could only muster around 4,000 effectives. Believing the assault would strike one of the outlying islands first, he positioned the bulk of his men on Jaluit, Mili, Maloelap, and Wotje. In November 1943, American airstrikes began whittling down Akiyamas air power, destroying 71 aircraft. These were partially replaced over the next several weeks by reinforcements flown in from Truk. On the Allied side, Admiral Chester Nimitz originally planned a series of assaults on the outer islands of the Marshalls, but upon learning of Japanese troop dispositions through ULTRA radio intercepts altered his approach. Rather than strike where Akiyamas defenses were strongest, Nimitz directed his forces to move against Kwajalein Atoll in the central Marshalls. Armies Commanders Allies Rear Admiral Richmond K. TurnerMajor General Holland M. Smithapprox. 42,000 men (2 divisions) Japanese Rear Admiral Monzo Akiyamaapprox. 8,100 men Allied Plans Designated Operation Flintlock, the Allied plan called for Rear Admiral Richmond K. Turners 5th Amphibious Force to deliver Major General Holland M. Smiths V Amphibious Corps to the atoll where Major General Harry Schmidts 4th Marine Division would assault the linked islands of Roi-Namur while Major General Charles Corletts 7th Infantry Division attacked Kwajalein Island. To prepare for the operation, Allied aircraft repeatedly struck Japanese airbases in the Marshalls through December. This saw B-24 Liberators stage through Baker Island to bomb a variety of strategic targets including the airfield on Mili. Subsequent strikes saw A-24 Banshees and B-25 Mitchells mount several raids across the Marshalls. Moving into position, US carriers began a concerted air offensive against Kwajalein on January 29, 1944. Two days later, US troops captured the small island of Majuro, 220 miles to the southeast, without a fight. This operation was conducted by the V Amphibious Corps Marine Reconnaissance Company and 2nd Battalion, 106th Infantry.    Coming Ashore That same day, members of the 7th Infantry Division landed on small islands, dubbed Carlos, Carter, Cecil, and Carlson, near Kwajalein to establish artillery positions for the assault on the island. The next day, the artillery, with additional fire from US warships, including USS Tennessee (BB-43), opened fire on Kwajalein Island. Pummeling the island, the bombardment allowed the 7th Infantry to land and easily overcome the Japanese resistance. The attack was also aided by the weak nature of the Japanese defenses which could not be built in depth due to the islands narrowness.   Fighting continued for four day with the Japanese mounting nightly counterattacks. On February 3, Kwajalein Island was declared secure. Roi-Namur At the north end of the atoll, elements of the 4th Marines followed a similar strategy and established fire bases on islands dubbed Ivan, Jacob, Albert, Allen, and Abraham. Attacking Roi-Namur on February 1, they succeeded in securing the airfield on Roi that day and eliminated Japanese resistance on Namur the next day. The largest single loss of life in the battle occurred when a Marine threw a satchel charge into a bunker containing torpedo warheads. The resulting blast killed 20 Marines and wounded several others. Aftermath The victory at Kwajalein broke a hole through the Japanese outer defenses and was a key step in the Allies island-hopping campaign. Allied losses in the battle numbered 372 killed and 1,592 wounded. Japanese casualties are estimated at 7,870 killed/wounded and 105 captured. In assessing the outcome at Kwajalein, Allied planners were pleased to find that the tactical changes made after the bloody assault on Tarawa had bore fruit and plans were made to attack Eniwetok Atoll on February 17. For the Japanese, the battle demonstrated that beachline defenses were too vulnerable to attack and that defense in-depth was necessary if they hoped to stop Allied assaults.