http://www.freerepublic.com/forum/a380199044cff.htm Not for commercial use. Solely to be used for the educational purposes of research and open discussion.
The U.S. forces stationed in Korea has begun to set up germ detection equipment in major military bases like Pyongtaek, for instance, in preprations for possible bacteriological and chemical attacks from North Korea. The USFK has been installing anti-germ warfare facilities called potal shield' beginning this May against possible North Korean offensives using bio-weapons,'' said Rep. Kim Deok of the opposition Grand National Party (GNP).
During an National Assembly inspection of the Joint Chiefs of Staff, Kim, former head of the Agency for National Security Planning, the predecessor of the National Intelligence Service, said the U.S. Army has been conducting smallpox vaccinations of the U.S. soldiers serving here in preparation for the biological warfare.
Antibodies have been found in the blood of North Korean soldiers who recently defected here, a fact that shows they got the preventive inoculation against smallpox and the reclusive North has been prepared to use the extremely harmful germ in case of war with the South,'' he claimed. But the nation's military has suspended the smallpox vaccination since 1979 and a survey conducted in June this year revealed that a majority of the soldiers are seriously concerned over the North's potential bacteriological and chemical offensives,'' the lawmaker said.
Leading U.S. organizations like the Central Intelligence Agency (CIA) and Centers for Disease Control and Prevention (CDC) have begun to warn against the North's possible dependence upon the germ and chemical warfare, putting the smallpox germ on the priority watch list, Kim said.
What matters is the fact that smallpox use has a lethality ratio of more than 50 percent, a fact that shows the majority of South Korean youths who lack immunity will suffer fatal damage, he said.
Starting from next year and the year after, most of the soldiers of the nation's armed forces will consist of those without having immunity from smallpox, according to the opposition lawmaker.
Touching upon the danger of the anthrax germ, Kim quoted a report from the World Health Organization (WHO) showing that the air dissemination of only 50kg of such material from 25km over a city with a population of 500,000 will take the lives of about 220,000 people.
Kim confirmed that the North is possessing 13 kinds of biological weapons and can produce one ton of anthrax per year through its 10 research and production facilities.
He went on to claim that North Korea is capable of manufacturing 4,500 tons and 12,000 tons of chemical weapons in peace and war periods, respectively, and many of them have been targeted mainly at Seoul and its vicinity areas.
In Seoul and its metropolitan region alone, the North's possible attack with bio-chemical weapons may result in harming more than 150,000 people, said Kim.
Despite the North's brisk move to utilize the chemical weapons, the nation has not been able to operate them at all since 1973 when it entered the Chemical Weapons Convention (CWC).
I found this in the archives and felt it needed to be brought up again, now that we are threatened by North Korea.
Interesting. Since NorKor is a totalitarian state, it is entirely possible that they have been pursuing biologic weapons procurement without UN oversight.
Since NorKor has really ignored UN oversight for nuclear programs, there seems to be widespread ignorance in our government regarding the perils of biological weapons.
I think I'm going to start a new thread where I discuss biological weapons and how they can be used to kill thousands.
in response to your prior freepmail message Jim, I'm doing a little homework on various nations and possible BT threat conditions for each.
This thread's data provided an opportunity to examine NorKor's biological capabilities.
Korean Hemorrhagic Fever is caused by something called hantavirus. Hantavirus appears to be a rather ubiquitous virus and appears to be transmitted from rodents to humans via rat urine.
(Mom always said rats were "icky". Now, you know why the RATS must go.)
Hemorrhagic Fever With Renal Failure Syndrome
http://www.emedicine.com/ped/topic968.htm
Author: Vellore K Sairam, MBBS, Fellow, Department of Pediatrics, Section of Pediatric Nephrology, University of Texas Medical Branch and Children's Hospital
Coauthor(s): Luther Travis, MD, William W Glauser Professor of Pediatrics and Pediatric Nephrology, Department of Pediatrics, Divisions of Nephrology and Diabetes, University of Texas Medical Branch and Children's Hospital
Editor(s): Deogracias Pena, MD, Medical Director of Dialysis, Cook Children's Medical Center; Clinical Associate Professor, Department of Pediatrics, Texas Tech University School of Medicine; Robert Konop, PharmD, Clinical Assistant Professor, Department of Pharmacy, Section of Clinical Pharmacology, University of Minnesota; Frederick J Kaskel, MD, PhD, Professor, Department of Pediatrics, Division of Pediatric Nephrology, Montefiore Medical Center and Albert Einstein School of Medicine; Howard Trachtman, MD, Program Director, Pediatrics Research, Schneider Children's Hospital, Professor, Department of Pediatrics, Division of Nephrology, Albert Einstein College of Medicine; and Craig B Langman, MD, Head, Division of Pediatric Nephrology, Children's Memorial Hospital of Chicago; Professor, Department of Pediatrics, Northwestern University School of Medicine
Background: Hemorrhagic fever with renal failure syndrome (HFRS) occurs mainly in Europe and Asia and is characterized by fever and renal failure associated with hemorrhagic manifestations. HFRS is caused by an airborne contact with secretions from rodent hosts infected with the group of viruses belonging to the genus Hantavirus of the family Bunyaviridae.
Historically, HFRS initially was recognized between 1913 and 1930 by Soviet scientists who described sporadic outbreaks of fever with renal failure in the eastern Soviet Union. The disease came to the attention of the western world in 1950 when the North American soldiers serving with the United Nations forces in Korea developed a febrile illness associated with shock, hemorrhage, and renal failure.
In 1993, in the southwestern United States, an outbreak of respiratory illness caused by the Sin Nombre virus belonging to the Hantavirus genus occurred and is described as the Hantavirus pulmonary syndrome (HPS).
Pathophysiology: The pathogenesis is largely unknown, but several studies have suggested that immune mechanisms play an important role. Following the infection, marked cytokine production, kallikrein-kinin activation, complement pathway activation, or an increase in circulating immune complexes occur. These components play a significant role during the febrile and hypotensive stages. Damage to the vascular endothelium, capillary dilatation, and leakage are significant features of the disease. There are reports of an increased nitric oxide production during the acute phase of the illness, with its levels correlating with the disease activity.
Frequency:
In the US: The rodent reservoir of Seoul virus (Rattus norvegicus) exist in many port cities of the eastern United States and were introduced from Europe by cargo ships. Enhanced surveillance for Hantavirus infection in humans eventually suggested the presence of HFRS caused by Seoul infection in few reported cases.
Internationally: The severe form of HFRS occurs in China, Japan, and Singapore. The milder form of HFRS (nephropathic epidemica) occurs in the Scandinavian countries of Sweden, Finland, Norway, and Denmark. The number of cases reported in China is approximately 100,000-250,000 per year. The disease is observed throughout the year, but prevalence depends on the population dynamics of the carrier rodents.
Mortality/Morbidity: The mortality and morbidity rates vary from 5%-15%, depending on the strain of the virus.
Race: No apparent racial predilection exists.
Sex: The increased incidence in males caused by their probable increased frequency of outdoor activities, which leads to contact with the infected rodents.
Age: HFRS commonly is reported in persons older than 15 years. In children younger than 15 years, the disease is mild.
History: The clinical features consist of a triad of fever, hemorrhage, and renal insufficiency. The disease severity may range from mild to severe. Subclinical infections are especially common in children. The average incubation period varies from 4-42 days. The disease is characterized by fever, capillary dilatation, and leakage of blood, causing hemorrhagic manifestations and, if severe, hypovolemic shock. The disease has 5 progressive stages (febrile, hypotensive, oliguric, diuretic, convalescent), and the physician should be aware of the variable presentations during each stage. Individual patients can skip stages completely.
Physical: The physical examination of the patient is based on the stage of the illness.
The febrile stage occurs in all patients and lasts about 4-6 days. An abrupt onset of fever occurs in the range of 40°C.
Patients may complain of headache, chills, abdominal pain, and malaise.
Flushing of the face, neck, and chest due to probable vascular dysregulation may be observed.
Petechia may occur in the axilla and soft palate.
Subconjunctival hemorrhage is noted in one third of the patients.
Absolute bradycardia may be noted during the febrile stage.
A normal or mildly elevated hematocrit level caused by hemoconcentration may be observed. Leucocytosis with atypical lymphocytes and thrombocytopenia usually occurs.
Onset of proteinuria may be observed.
The hypotensive stage lasts approximately a few hours to 2 days. It occurs in 11% of the patients and coincides with defervescence.
Patients may have tachycardia, which may indicate an impending shock.
Patients may have an acute abdomen caused by a paralytic ileus.
Patients may have convulsions or purposeless movements.
The coagulation profile may include prolonged bleeding time, elevated prothrombin time (PT), and activated partial thromboplastin time (aPTT).
The oliguric stage occurs in 65% of the patients and lasts about 3-6 days.
Oliguria, hypertension, bleeding tendency (caused by uremia), and edema are characteristic of this stage.
Patients may develop pulmonary edema.
Thrombocytopenia usually resolves in the oliguric stage.
The diuretic stage lasts 2-3 weeks.
Diuresis in the range of 3-6 L/d follows the disappearance of the symptoms from the previous stage.
Rapid signs of dehydration and severe shock can occur.
The convalescent stage may last for as long as 3-6 months.
Clinical recovery usually begins in the middle of the second week, with gradual resolution of symptoms and azotemia.
The convalescent stage may last for as long as 3-6 months, during which the glomerular filtration rate (GFR) normalizes.
The renal tubular concentrating capacity recovers over many months.
Causes: The viruses of the genus Hantavirus cause different forms of HFRS. The severity of the illness depends on the type of the infecting virus and on the geographic distribution.
Korean hemorrhagic fever, a severe type of HFRS observed in Asia, is caused by the Hantavirus and is transmitted by the infected Apodemus agrarius (striped field mouse).
Balkan hemorrhagic fever, a severe type of HFRS observed in Balkan countries, is caused by the Dobrava virus and is transmitted by the infected Apodemus flavicollis (yellow-necked field mouse).
A mild-to-moderate form of HFRS is caused by the Seoul virus and is transmitted by the infected Rattus rattus (black rat) or the Rattus novergicus (urban rat).
Nephropathia epidemica (NE), a mild form of HFRS observed in Europe, is caused by the Puumala virus and is transmitted by the infected Clethrionomys glariolus (European bank vole).
Other Problems to be Considered:
Spotted fevers
Murine typhus
Malaria
Non-A, non-B hepatitis
Colorado tick fever
Septicemia
Heat stroke
Disseminated intravascular coagulation (DIC)
leptospirosis
Scrub typhus
Hemolytic uremic syndrome
In high-risk geographic areas, HFRS should be included in the differential diagnosis of acute renal failure of uncertain cause associated with febrile illness, hemorrhagic phenomenon, or renal or hepatic dysfunction.
Lab Studies:
The diagnosis is suspected based on the geographic distribution of the disease, exposure to rodents, clinical symptoms and signs, and laboratory evaluations.
Enzyme-linked immunosorbent assay (ELISA) is useful to detect antihantaviral-specific immunoglobulin M (IgM) early in the course of the illness.
Antihantaviral immunoglobulin G (IgG) titers may be elevated for prolonged periods (as long as 10 y).
Blood work usually shows significant leukocytosis, elevated or normal hematocrit, and thrombocytopenia.
Elevated liver enzymes, blood urea nitrogen (BUN), and serum creatinine can be observed.
Hyponatremia, hyperphosphatemia, and hyperkalemia may occur during the oliguric phase.
Complement level (C3) may be decreased; therefore, HFRS should be included in the differential diagnosis of hypocomplementemic acute nephritic syndrome.
Coagulation profile can be altered with an elevated PT/aPTT or prolonged bleeding time. Fibrin degradation products also may be elevated.
Urinalysis consistently shows hematuria and proteinuria.
Imaging Studies:
No specific radiologic studies are indicated.
Other Tests:
Hantavirus antigen can be detected in various tissues, predominately in the microvasculature by immunohistochemical (IHC) methods.
Procedures:
Kidney biopsy is generally not essential for diagnosis. As discussed earlier, the diagnosis of HFRS is based on history of exposure to infected rodents, clinical symptoms and signs, and laboratory findings. However, if the diagnosis cannot be clearly made during the course of the illness, then a renal biopsy is indicated if the patient’s hemodynamic and coagulation status is stable.
Histologic Findings: The renal histological alterations in HFRS have the features of acute interstitial nephritis, including acute tubular necrosis with evidence of glomerular and endothelial damage. Hemorrhagic necrosis has been identified in the renal medulla. Hemorrhage is observed in different organs, especially the right atrium of the heart, anterior pituitary, pancreas, and the skin. Pulmonary infiltrates may be observed, and, occasionally, pulmonary edema is present. Infiltration of large atypical mononuclear cells in the spleen, lymph node, and hepatic portal triad has been reported.
Medical Care: The treatment depends on the stage of the disease process, status of hydration, and overall hemodynamic condition of the patient.
During the active illness, maintaining fluid and electrolyte balance is mandatory. Early and effective fluid therapy is the cornerstone in the management of renal failure. The indications for various medications are based on the specific requirements during the different stages of the disease process.
The use of vasoactive agents and albumin during the period of shock is extremely helpful. Excessive administration of fluids can lead to extravasation caused by vascular leak, especially during the febrile and hypotensive stages.
Consider diuretics, such as furosemide, when the patient has volume overload and is oliguric. Consider dialysis if no response is observed.
One prospective placebo-controlled trial suggests that intravenous ribavirin decreases the severity and mortality of HFRS in China. In contrast, 30 patients with HPS who received investigational open-label intravenous ribavirin tolerated it well; furthermore, treatment was accompanied by drug-induced anemia, which required transfusion, and no clear evidence of benefit was obtained. These contrasting responses cannot be explained by differences in dosing schedules, and the lack of response in the HPS patients may be caused by the rapidity of progression of the disease. Ribavirin is not licensed for intravenous use in the United States, pending further ongoing studies.
Antihypertensives are indicated in patients with hypertension, which is usually present during the oliguric phase of the illness.
Dialysis is indicated if the patient is oliguric for a prolonged time with no response to diuretics, and renal failure is rapid with worsening fluid and electrolyte abnormality.
Surgical Care:
If extravasation of plasma in the abdomen (suggestive of an acute abdomen and subsequent development of paralytic ileus) is the clinical presentation, the patient probably needs a surgical evaluation but occasionally may need exploratory laparotomy.
When conservative management fails, the renal rupture that rarely occurs requires operative procedure.
A pediatric nephrologist should perform a renal biopsy, if indicated.
Consultations: Consultation with a pediatric nephrologist, a pediatric infectious disease specialist, pediatric critical care personnel, and a pediatric surgeon are indicated as needed.
Diet: A low-sodium diet with restriction of fluid during the oliguric phase followed by liberal intake of fluid in the diuretic phase is recommended.
Activity: Bed rest during the acute phase of the illness is recommended.
Deterrence/Prevention:
Human habits have been shown to increase incidence of the disease; hence, basic preventive measures are required, including the following:
Proper storing of food and avoiding contamination by rats
Taking precautions during work or travel in farms contaminated with rodents
Avoiding camping in grain fields
Avoiding stocking straw stacks outside houses
Avoiding sleeping outside homes
Complications:
The complications that develop during the illness are rare.
Abdominal pain and back pain occurs because of retroperitoneal hemorrhage.
During the oliguric or early diuretic phase, renal rupture occurs, but it responds to conservative management and only occasionally requires surgical intervention.
Pulmonary edema and intraventricular hemorrhage occur.
Transient hypopituitarism occurs, causing abnormal anterior pituitary hormonal response, leading to delayed diuresis and late appearance of Sheehan syndrome.
HFRS is a self-limiting disease, and most patients recover without any sequelae; however, in few residual patients, neurological and renal tubular defects may persist. Defective sodium reabsorption is observed to occur in patients 1 year after the illness, thereby causing increased sodium excretion.
Some patients may develop hypercalciuria and hyperphosphaturia.
Although recovery from hantaviral disease is complete, chronic renal insufficiency and hypertensive renal disease have been reported.
Approximately 10% of adult patients with end-stage renal disease (ESRD) have shown to have hantaviral-specific antibodies.
The Dobrava virus causes severe form of HFRS in Balkan regions of eastern Europe. It is associated with an increased mortality rate, and the infected patients develop hepatomegaly, with dysfunction observed more commonly than hemorrhagic manifestations.
Patient Education:
The prevalence of the disease largely depends on human habits; therefore, patient health education is essential for the prevention of the disease. Educate patients regarding the following:
Living in barracks and not sleeping in open areas outside homes
Eradication of rodents
Effective storage techniques of food items
Early reporting of illness and obtaining medical expertise (Suspect HFRS when there is history of travel to an endemic area, and onset of symptoms occurs within 3 wk of return.)
No person-to-person transmission or nosocomial transmission
Suspicion of the disease if the patient has clinical symptoms and has returned from an endemic area (For any advice or questions regarding the disease, patients are advised to call the Centers for Disease Control [CDC] at 800-311-3435.)
Liberal intake of fluid during the diuretic phase of the illness to avoid dehydration and shock
Thanks for the ping bones. This is tremendously important information to have out there.
