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This Page will merely touch on other Wars; it is not meant to be all encompassing. For further information on other sources, please see the "Vet Links" Gallery in the "Veterans Organizations and Support Groups" main section of the "VVHP" at: vetlinks.htm
Using the new records, the VA now hopes to assist many veterans whose claims had previously been denied because no record was available to confirm medical disabilities that occurred during military service. Veterans and survivors unsure whether their disability compensation claims are affected should contact the VA Regional Office and Insurance Center in Philadelphia at 1-800-822-3920.
The National Archives and Records Administration on June 15 advised the VA that it is obtaining a collection of computer tape containing some 10 million Army medical treatment records that partially fill a gap created when a 1973 fire destroyed millions of military files at a federal record center in St. Louis. The newly found records cover the years from 1942 to 1945 and from 1950 to 1954.
For certain veterans whose claims for disability compensation were denied since the fire, the VA may now be able to establish documentary evidence to support their claims.
1997
It's about a Korean POW survivor, Johnnie Johnson, with the 24th Infantry, who had kept a list (risking his own survival if caught), of those that died while there...he felt it was important that a record be kept for the families.
That list, called the "Tiger Survivors List," has now been made public and Reader's Digest has made it available at its WebSite:
Also, for those families with questions or information regarding missing servicemen, you can write:
Defense POW/MIA OFFICE
2400 Defense Pentagon
Washington, D.C. 20301-2400
By Nancy Benac, Associated Press
WASHINGTON (AP) After 55 years, the men of World War II's forgotten fleet finally are getting their due.
"Out-numbered, out-gunned, out-everything, we fought like hell," recalls 75-year-old Charles Ankerberg, part of the Asiatic Fleet thrust to the front lines of World War II after the bombing of Pearl Harbor. "We've been waiting 55 years for recognition."
Based at Manila Bay in the Philippines when America joined the war, the fleet of aging ships with obsolete equipment and inadequate supplies battled the Japanese in the western Pacific for three months, outnumbered 10 to 1, in a combined force with Australian, Dutch, and British allies.
The cost to the Americans: 22 ships, 1,826 men killed, and 519 taken prisoner, many of whom did not survive Japanese forced labor camps.
On Friday, the survivors, many slowed by advancing years, gathered on the sunny plaza of the U.S. Navy Memorial to remember fallen comrades and celebrate the opening of an "Asiatic Fleet" room in the adjacent Navy Heritage Center.
"Nobody ever knew about these ships," said 85-year-old John Bracken of Philadelphia, who served as signal officer on one of the fleet's cruisers. Bracken, a retired Navy captain, donated $25,000 to create the memorial.
"We felt it was about time," he said.
Admiral Harold Gehman, Vice Chief of Naval Operations, told the veterans that "the tally sheet, while it records very few wins for our side or our allies in the six months (after) Dec. 7, 1941, it does record the courage and the fortitude shown by those men of the Asiatic Fleet.
"Due to the heroism of the allied Asiatic Fleet, final Japanese victory in the Western Pacific was destined to delay, and delay was the one thing the Japanese could not tolerate. Delay proved fatal."
Clarence Wills, 76, of Chicago, echoed the thoughts of many in speculating that the fleet's plight was overlooked at the time because President Roosevelt didn't think the American people could handle news of more devastating losses so soon after the bombing of Pearl Harbor.
"We were a forgotten fleet," he said.
"We gave 'em everything we had," said Al Haas, 75, of Virginia Beach, VA. He spent 3 1/2 years in forced labor for the Japanese after his destroyer was disabled in the Java Sea. "Everybody I ask, they never heard of us."
Diagnosis: Should be suspected if an aerosol attack occurs in the form of "yellow rain" with droplets of yellow fluid contaminating clothes and the environment. Confirmation requires testing of the blood, tissue and environmental samples.
Treatment: There is no specific antidote. Superactivated charcoal should be given orally if swallowed.
Prophylaxis: The only defense is to wear a mask and clothes during attack. No specific immunotherapy or chemotherapy is available for use in the field.
Decontamination: The outer uniform should be removed and exposed skin be deconed with soap and water. Eye exposure should be treated with copius saline irrigation. Once decon is completed, isolation is not required.
The trichothecene mycotoxins are low molecular weight(250-500daltons) nonvolatile compounds produced by filamentous fungi(molds) of the genera Fusarium, Myrotecium, Trichoderma, Stachybotrys and others. The structures of approximately 150 trichothecene derivatives have been described in the literature.
These substances are relatively insoluble in water but highly soluble in ethanol, methanol and propylene glycol. The trichothecenes are extremely stable to heat and ultraviolet light inactivation. Heating to 500*F for 30 minutes is required for inactivition, while brief exposure to NaCl destroys toxic activity.
The potential for use as a BW toxin was demonstrated to the Russian military shortly after World War II when flour contaminated with species of Fusarium was baked into bread that was ingested by civilians. Some developed a protracted lethal illness called: Ailmentary, Toxic, Aleukia(ATA) characterized by initial symptoms of abdominal pain, diarrhea, vomiting, prostration and within days, fever, chills, myalgias, and bone marrow depression with granulocytopenia and secondary sepsis.
Survival beyond this point allowed the developement of painful pharyngeal/laryngeal ulceration and diffuse bleeding into the skin(petechiae and ecchymoses), melena, bloody diarrhea, hematuria, hemalemesis, epistaxsis, and vaginal bleeding. Pancytoperia, and gastrointestinal ulceration and erosion were secondary to the ability of these toxins to profoundly arrest bone marrow and mucosal protein synthesis and cell cycle progression through DNA replication.
Mycotoxins allegedly have been used in aerosol form ("yellow rain") to produce lethal and nonlethal casualties in LAOS(1975-1981), KAMPUCHEA(1979-1981), and AFGHANISTAN(1979-1981). It has been estimated that there were more than 6,300 deaths in Laos; 1,000 in Kampuchea; and 3,042 in Afghanistan.
The alleged, unarmed victims were not protected with masks and chemical protective clothing and had little or no capability of destroying the attacking enemy aircraft. These attacks were alleged to have occurred in remote jungle areas which made confirmation of attacks and recovery of agent extremely difficult. Much controversy has centered about the veracity of eyewitnesses and victim accounts, but there is enough evidence to make agent use in these areas highly probable. (IRAN/IRAQ WAR suspected of delivery)
T2 and other mycotoxins may enter the body through the skin and aerodigestive epithelium. They are fast-acting, potent inhibitors of protein and nucleic acid synthesis.
Their main effects are on rapidly proliferating tissues such as the bone marrow, skin, mucosal epithelia and germ cells. In a successful Biologic War (BW) attack with trichothecene toxin(T2), the toxin(s) will adhere to and penetrate skin, be inhaled, and swallowed. Clothing will be contaminated and serve as a reservoir for further toxin exposure.
Early symptoms, beginning within minutes of exposure, include burning skin pain, redness, tenderness, blistering, and progression to skin necrosis with leathery blackening and sloughing of large areas of skin in lethal cases. Nasal contact is manifested by nasal itching and pain; sneezing; epistaxis and rhinorrhea; pulmonary/tracheobronchial toxicity by dyspnea, wheezing, and cough; and mouth and throat exposure by pain and blood tinged saliva and sputum.
Anorexia, nausea, vomiting, and watery or bloody diarrhea with abdominal crampy pain occurs with gastrointestinal toxicity. Eye pain, learing, redness, foreign body sensation, and blurred vision may follow entry of toxin into eyes. Skin symptoms occur in minutes to hours and eye symptoms in minutes.
Systemic toxicity is manifested by weakness, prostration, dizziness, ataxia, and loss of coordination. Tachycardia, hypothermia, and hypotension follow in fatal cases. Death may occur in minutes, hours or days. The commonest symptoms were vomiting, diarrhea, skin involvement with burning pain, redness and pruritus, rash or blisters, bleeding and dyspnea.
Rapid onset of symptoms in minutes to hours supports a diagnosis of a chemical or toxin attack. Mustard agent must be considered, but they have odor, are visible, and can be rapidly detected by a field available chemical test. Symptoms from mustard toxicity are also delayed for several hours after which mustard can cause skin, eye, and respiratory symptoms.
Staphylococcal enterotoxin B delivered by an aerosol attack can cause fever, cough, dyspnea and wheezing but does not involve the skin and eyes. Nausea, vomiting, and diarrhea may follow swallowing of inhaled toxin. Ricin inhalation can cause severe respiratory distress, cough, nausea and arthralgia. Swallowed agent can cause vomiting, diarrhea, and gastrointestinal bleeding; but it spares the skin, nose, and eyes.
Specific diagnosis of T-2 mycotoxins in the form of a rapid diagnostic test is not presently available in the field. Removal of blood, tissue from fatal cases, and environmental samples for testing using a gas liquid chromatography-mass spectrometry technique will confirm the toxic exposure. This system can detect as little as .1-1 ppb of T-2. This degree of sensitivity is capable of measuring T-2 levels in the plasma of toxin victims.
This is the latest information corresponding to the ailments incurred by Gulf War Veterans. They cover all symptoms, not just a few.
1997
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