Section II, 12 Exposure to Biological Warfare Agents



Download 40.15 Kb.
Date conversion29.04.2016
Size40.15 Kb.
2.12 Exposure to Biological Agents:

Types of biological warfare agents

Effects of exposure

Evaluation and management of exposure

Prevention and countermeasures
SECTION II, 2.12 Exposure to Biological Warfare Agents
Toxins are, by definition, biological agents produced by living organisms such as animals, bacteria or plants. There is a significant difference in toxins and other replicating agents, such as viruses and bacteria as well as chemical agents.
The physical characteristics and mechanisms of action will dictate how it may be used and, in turn, how it may be defended against. The replicating agents (bacteria/viruses) are generally accepted as biological warfare agents. Their route of exposure is primarily by inhalation or ingestion, such as through a food or water supply. The inhaled toxin is generally more severe than ingested toxins or those “injected”, such as animal bites or stings, and the clinical presentation may vary considerably depending on the route of exposure.
Mass Casualty Biological or Toxic Weapon (MCBW) is that which is capable of causing disease and/or death on a wide scale causing potentially significant destruction on a military and/or civilian population.

In spite of historical information available for the past centuries, biological warfare or terrorism defense is quite new to most military as well as civilian healthcare providers today. With Operation Desert Shield/Storm, the possibility of biological warfare has became more real. Not only the military, but also the civilian population is becoming more aware of the threats of domestic terrorists, brought literally “home” with the 9/11 attack on the World Trade Center, Pentagon and the failed attempt in Pennsylvania.


It is estimated that at least 10 countries around the world have offensive and usable biological weapons. The rationale for using biological weapons is many fold. They have the ability to wreak havoc even in relatively small amounts. A terrorist focused on destruction could, in fact, use enough of a super toxic agent such as botulinum, and with appropriate disbursement deliver this, undetected, to a significant civilian population. The terrorist could be long gone by the time the effect of the agent is felt due to the oft-delayed symptomatology.
Though there are other warfare agents used such as Staphylococcal Enterotoxin B (and related pyrogenic toxins), trichoethecene mycotoxins, and various viral encephalitides and hemorrhagic fevers such as Hanta virus, only the more common agents will be discussed below.
There are several types of biological agents with which this section will cover. They are:

  • Anthrax

  • 2. Botulism

  • 3. Brucellosis

  • 4. Plague

  • 5. Q fever

  • 6. Smallpox

  • 7. Tularemia


ANTHRAX
Anthrax is a zoonotic disease caused by Bacillus anthracis occurring in domesticated and wild animals. Humans usually become infected by contact with a diseased animal or diseased animal products. The main route of exposure is via the cutaneous route but, on rare occasion, could be from respiratory or gastrointestinal routes.
CLINICAL DISEASE

Cutaneous: (95%) After inoculation with a 1-5 day incubation, itching occurs at the inoculated skin site noted with the first (2-3 hours) followed by a usually painless lesion (papular then vesiculated) with varying degrees of edema. Systemic manifestations include fever, headache (particularly severe if edema is extensive), and often localized lymphadenitis. The mildest form of cutaneous anthrax forms a necrotic eschar (36 hours) that falls off without scarring. A black eschar follows (2-3 weeks) the initial ulcer which may leave scarring. (Surgical intervention for the skin lesions is not recommended). There is a less than 1% mortality rate and septicemia is rare.

Inhalation: After a 1-6 day incubation, malaise, fatigue, myalgia and fever. It often presents similar to mild URI and may be associated with a nonproductive cough and mild chest discomfort. Though there may be some improvement in 2-3 days in some cases, a more severe course can ensue characterized by pulmonary edema with increasing respiratory distress, dyspnea, stridor, cyanosis, chest pain and diaphoresis. Chest X-ray may show mediastinal widening and quite often, pleural effusions. Rapid shock and death can occur within 24-36 hours. Mortality has been essentially 100% in spite of appropriate therapy.

Meningitis: This can occur in as much as 50% of cases and often begins with the onset of the respiratory distress. The meningitis is often hemorrhagic and invariably fatal. This form of meningitis is often very hard to differentiate from meningitis due to other causes.
Oropharyngeal/Intestinal: Following a 2-5 day incubation, often resulting from ingestingundercooked contaminated meat, a severe sore throat or a local oral or tonsillar swelling occurs with fever and cervical/ submandibular lymphadenitis and edema. Gastrointestinal signs may begin with nausea, vomiting, fever and severe abdominal pain which may mimic an acute abdomen. Rapidly developing and massive ascites, and cholera-like diarrhea with fever and signs of septicemia can also occur.

TREATMENT
Penicillin is the drug of choice for anthrax. Oral is adequate for the cutaneous form if there is no toxicity or systemic symptoms, while the more severe spreading or systemic infection requires IV penicillin (2 million units Q6h) until a clinical response is obtained. Though the edema and systemic symptoms will usually abate, the skin lesions will not be affected by the antibiotic therapy, treatment should be continued for at least 7-10 days.
PROPHYLAXIS: If given within one day after exposure to a lethal aerosol exposure of anthrax spores, ciprofloxacin, penicillin and doxycycline were effective, particularly when coupled with active immunization.
BOTULISM:
The clostridial neurotoxins are the most toxic substances known to science! Clostridium tetani is encountered by humans as a result of wounds but rarely occurs today due to the mass immunizations given to civilized populations worldwide for many decades. Because of the extreme toxicity of C botulinum, it is a logical agent for biological warfare.

C botulinum and C tetani are spore-forming anaerobic bacteria found worldwide in soil. Whereas, C tetani present with rigid tetanic paralysis, the victims of C. botlinum present with peripheral, flaccid paralysis. Tetanus invades the body and multiplies there producing toxins, whereas botulism, in contrast, rarely occurs with (historically) wound contamination, but rather occurs as a neurotoxin in an anaerobic environment primarily associated with ingestion of home canned foods. Though not the subject of this piece, infant botulism is another form which occurs in the first year of life, due to the infant’s immature, developing intestinal flora. Documented cases in humans of intestinal infection have not occurred.


CLINICAL DISEASE
Symptoms usually develop 12-36 hours after the toxin’s ingestion, but may occur as late as 14 days afterward. Initial symptoms are ptosis, blurred or double vision, constipation, dysphagia, dysarthria, descending paralysis, muscle weakness and decreased deep tendon reflexes. A dry sore throat as well as strabismus, nystagmus, and dilated pupils and even respiratory failure can also be seen. Inhalation botulism, most likely seen in the battlefield, is rare.
TREATMENT
The clinician is largely limited to supportive and symptomatic treatments.
BRUCELLOSIS
Brucellosis is a human zoonotic infection of domestic and wild animals caused by the organism Brucella. Infection is introduced through ingestion of contaminated food products, handling infected animals, or inhalation of infectious aerosols.
CLINICAL MANIFESTATIONS
Brucellosis can enter the human via cuts, skins abrasions, the conjuntiva, and the gastrointestinal and/or respiratory tract. Patients may present with an acute systemic febrile illness, an insidious chronic infection or localized inflammation. Incubation may be 3 days to several weeks. Fever, sweats, fatigue, anorexia, and muscle or joint aches may occur. Focal infections may cause bone, joint or GU pain. Pleuritic and chest pain, cough, and dyspepsia can also occur. Weight loss is a characteristic feature in many cases of chronc infection. Symptoms can last from 3-6 months or up to a year. Urinary tract infections such as pyelonephritis, cystitis and epididymitis may occur, mimicking tuberculosis and , like tuberculosis, may exhibit “sterile” pyuria on routine culture. Chest X-rays are usually normal, though diffuse infiltrates, pleural effusion, abcess and granuloma may be seen. Serology tests can be used to confirm the diagnosis.
TREATMENT
Brucellae are sensitive to a number of antibiotics and aminoglycosides but the use of a single drug has a high relapse rate. Therefore, a regimen consisting of a six week course of 20mg of daily oral doxycycline, combined with daily intramuscular injections of one Gram of streptomycen for the first 2-3 weeks, is recommended. Patients with spondylitis may require longer treatment (6 weeks) using rifampin 900mg/d combined with doxycycline. For endocarditis a combination of rifampin, streptomycin and doxycycline for 6 weeks is recommended. CNS infection may require prolonged therapy with rifampin and trimethoprim/sulfamethoxazole which is also appropriate in pediatric patients under 8 years of age. Rifampin is the recommended drug of choice for pregnant women, according to the World Health Organization. Weaponized biological agents may be resistant to first line antibiotics so tissue and environmental samples should be sought to adjust therapy accordingly.
PROPYLAXIS
In the event of a biological attack, the standard military gas mask should be adequate protection from airborne brucellae. Once evacuated, personnel must have clothing, skin, and other surfaces decontaminated with standard disinfectants to minimize risk of accidental ingestion or conjunctival inoculation.
PLAGUE
Plague is a zoonotic infection caused by Yersinia pestis, a gram negative bacillus which, historically, has had devastating effects since the 6th century A.D. The disease is transmitterd by rodents and is characterized by a sudden onset of high fever, painful lymphadenopathy draining at the exposure site (i.e. bubos) with a confluent mass of nodes, usually in the groin, which if untreated, may suppurate and drain. Septicemia and pulmonary plague can ensue from untreated plague; The pulmonary form is severe and frequently fatal.
It is an axiom of warfare that the actual battle casualties from battle are less than disease and non-disease injuries.
CLINICAL MANIFESTATIONS
Most patients with human plague present themselves almost 90% of the time with the bubonic form of plague. Approximately 10% present with the septicemic form, and about 1% present with the pneumonic form. If Y pestis is used as a warfare agent, the clinical manifestations could vary depending on the route of exposure. If aerosolized bacteria were used, epidemic pneumonia would be the clinical manifestation, as opposed to bubonic or septicemic plague if fleas were used as the vector.
Incubation period is 1-8 days with, as noted above, sudden fever, chills, headache followed within hours by nausea and vomiting. Altered mentation occurs in about 1/3 of cases, with apathy, confusion, fright and anxiety predominating. In addition, severe malaise, cough, chest and abdominal pain may also be seen. Severe pain develops within 6-8 hours after the onset of symptoms, usually in the femoral nodes (90%), but with inguinal, axillary and cervical adenopathy occurring as well. These buboes are usually visible within 24 hours and are excrutiatingly painful. Other manifestations include bladder distention, oliguria and anuria. Tachycardia, hypotension and leukocytosis are frequently seen and, if untreated, a septicemia will usually develop in 2-6 days.
Five to fifteen percent of those with bubonic plague will develop secondary plague pneumonia, thus causing a human to human hazard. Septicemic plague may occur primarily or secondarily as a complication of hematogenous dissemination. Primary septicemia’s signs and symptoms include fever, chills, nausea, vomiting and diarrhea. Later, purpura, disseminated intravascular coagulation (DIC)and acral cyanosis and necrosis may be seen.
As noted above, pneumonic plague may occur from inhalation or hematogenous dissemination. A productive cough with blood tinged sputum may occur within the first day after the onset of symptoms. On Chest X-ray, there are variable findings, but bilateral alveolar infiltrates bilaterally are the most common finding.
Plague meningitis is seen in 6-7% of cases, most often in the pediatric age group 9-14 days after ineffective therapy. Symptoms and signs are similar to other forms of meningitis.
Pharyngreal plague has been reported in contacts of plague patients. And rarely, pharyngitis, resembling tonsillitis with cervical lymphadenopathy has been reported
Cutaneous manifestations occur in 4-10% of patients with an ulcer or pustule at the inoculation site. Since a flea typically bites the lower extremity, femoral and inguinal nodes are most commonly affected. The buboes may spontaneously drain or may require incision and drainage due to pronounced necrosis. Petechiae and ecchymoses may occur during the hematogenous spread that may, in fact, appear to mimic severe meningococcemia. The secondary DIC is thought, most probably, be due to Y pestis endotoxin with purpura and acral gangrene, thus giving a poor prognosis when these signs are seen. In the terminal stages of pneumonic or septic plague, large ecchymoses occur on the back giving rise to what may have resulted in the historic medieval name “Black Death”. Included in the differential diagnosis would be tularemia, cat scratch fever, Lymphogranuloma venerium, chancroid, TBc, streptococcal adenitis and scrub typhus. With septicemic plague, meningococcemia, gram negative sepsis and ricketsiosis must be considered in the differential.
TREATMENT
All patients with plague should be isolated at least 48 hours after the initiation of therapy. Special care must be taken in handling blood and any purulent discharge from the buboes. With pneumonic plague, rigid respiratory isolation (i.e. gown, gloves and eye protection) is required. The isolation must be continued until at least 4 days of treatment has been carried out.
Since the late 1940’s, streptomycin has continued as the treatment of choice for bubonic, septicemic and pneumonic plague, in doses of 30mg/Kg divided in two doses per day. If meningitis is suspected, IV chloramphenical (50-75mg/Kg in 4 divided doses) should be added. Treatment should be continued for at least 10 days or 3-4 days after recovery. In pregnant women, streptomycin or gentamycin should be used unless chloramphenical is specifically indicated. Streptomycin can also be used in neonates with appropriate monitoring. If treated with antibiotics, buboes generally recede in 10-14 days and do not require incursion and drainage. As discussed, to survive primary pneumonic plague antibiotics must be started within 18 hours of the onset of symptoms. Mortality is 60% for untreated bubonic plague, 100% for untreated pneumonic and septicemic plague.
Q FEVER
Q fever is a zoonotic disease caused by Coxiella burnett, though not a true Rickettsiaceae, it is a ricketsial-like organism of low virulence but remarkable infectivity. This agent in its sporelike form is extremely hardy and can persist in the environment for weeks or months under harsh and rugged conditions. The primary mode of transmission is inhalation of infected aerosols, with acute infections often following even an indirect exposure to an infection source. The acute clinical disease associated with C burnetti is usually benign, although it can be temporarily incapacitating. Even without treatment, recovery is good. Chronic Q fever, albeit rare, can frequently be fatal. Humans are usually infected by contact or handling domestic livestock, particularly goats, cattle, and sheep.
CLINICAL MANIFESTATIONS
Man is the only host susceptible to infection resulting in illness. The incubation varies from 10-40 days with the duration inversely correlated with the magnitude of inoculum. As little as a single organism can be infective. There is no characteristic illness for acute Q fever. The onset may be acute or insidious, with fever, chills, and headache the most common symptoms. The headache is characteristically severe with throbbing in the frontal or retro-orbital regions. Diaphoresis, malaise, fatigue, and anorexia are common. Significant weight loss is often seen, especially when symptoms last more than 2 weeks. Though arthralgias are unusual, myalgia is common. Cough may appear later in the clinical course and may be accompanied by pleuritic chest pain or a vague substernal discomfort. Occasionally sore throat, gastrointestinal upset, and stiff neck severe enough that one might consider doing an LP are seen. In most patients with acute disease the febrile period can last up to two weeks, this may be somewhat longer in older patients. One may encounter neurological symptoms in about a fourth of acute cases. Encephalopathic symptoms, hallucinations (visual and auditory), expressive dysphasia, facial pain mimicking trigeminal neuralgia, diploplia, and dysarthria also occur. Later in the illness, one may see encephalitis, encephalomyelitis, optic neuritis or myopathy. On rales are probably the most common clinical sign, sometimes associated with pleural effusion and consolidation. About half of those infected will have an abnormal chest X-ray, even in the absence of pulmonary symptoms, exhibiting a unilateral homogenous infiltrate involving 1 or 2 lobes. Jaundice and hepatosplenomegaly are rare in the acute infection, though lab tests may give a picture of acute hepatitis including some elevation of the bilirubin. On a CBC, the WBC is usually normal, though 1/3 of patients will have an elevated ESR with mild anemia and/or thrombocytopenia.
Chronic Q fever is usually characterized by endocarditis, which is the most severe complication. In the chronic form of Q fever endocarditis, chills, headache, myalgias and weight loss are common, though fever was not as prominent in the chronic as the acute form of the disease. Serologic testing may confirm the diagnosis, the ELISA test being the test most utilized for this purpose.
TREATMENT
Tetracycline has been the mainstay of treatment since the 1950’s. When given during the first few days of the illness the therapy shortens the disease course. Macrolide antibiotics, such as erythromycin, are also effect. When endocarditis is present, treatment is more difficult resulting in a 24% mortality even with appropriate treatment; therefore a 2 year course of tetracycline combined with rifampin or a quinolone has been recommended for this complication.
SMALLPOX
Smallpox is a poxvirus (of the family Poxviridae) which are large, enveloped DNA viruses. The most notorious pox virus is variola, the causative agent of smallpox. The variola virus is quite stable and retains its infectivity for very long periods of time. In a natural exposure, the virus enters the respiratory tract, eventually infecting the regional lymph nodes, giving rise to a viremia and the subsequent rash. The incubation average is 12 days.
CLINICAL MANIFESTATIONS

Usually the patient experiences malaise, fever, rigors, vomiting, headache, and backache. Fifteen percent will experience some delirium. About 10% of fair skinned individuals will exhibit an erythematous rash, followed 2-3 days later with an enanthem consisting of a discrete rash about the face, hands and forearms. Following subsequent eruptions on the lower extremities, the rash progresses centrally during the next week to the trunk evolving from macules to papules and, eventually, characteristic vesicles. The lesions are more abundant on the face and extremities; this centrifugal distribution is an important diagnostic feature. From 8-14 days after the onset, the pustules form scabs, which leave depressed depigmented scars on healing. Since the virus can easily be recovered from these scabs through the convalescent phase, patients must be isolated and considered infectious during this time until all scabs separate. Arthritis and osteomyelitis may develop late in the course of the disease occuring in 1-2 % of patients. Pneumonia is unusual. In some epidemics studies, there was a 3% fatality rate in those vaccinated, 30% in those unvaccinated. Keratitis and corneal ulcers were complications leading to blindness in less than 1% of the cases.


TREATMENT AND MEDICAL MANAGEMENT
All persons in direct contact with an infected patient should be strictly quarantined for 17 days, with respiratory isolation. This is particularly important for the unvaccinated individual. All persons working around infected patients must be vaccinated with a verified “take”, the local response whereby a vesicle forms with surrounding erythema and induration. The vaccine’s effective immunity would be expected to last about 3 years. There is no chemotherapy effective against smallpox. Because of the risk-benefit factors, the contraindications must be kept in mind for certain individuals. These contraindications are:
1. Immunosuppression, such as with those with agammaglobulinemia, leukemia, lymphoma, generalized malignancy or those receiving antimetabolite therapy.

2. HIV: Severe vaccinia infections have been reported in immunosupressed persons with HIV.

3. History or evidence of eczema or extensive skin lesions such as atopic dermatitis, psoriasis or burns.

4. Current household, sexual or close physical contact with a person or persons possessing the conditions in 1 through 3.



5. Pregnancy: though rare, fetal vaccinia can occur when primary vaccination is given to a pregnant woman.
There is some evidence that vaccinia-immune globulin may be of some value in post exposure prophylaxis of smallpox when it is given the first week after exposure, concurrent with vaccination. During the 1960’s, methisazone (no longer manufactured) was therapeutically ineffective for active smallpox though there was some indication that there might be some value in administering it prophylactically to susceptible contacts of patients with smallpox. Methisazone has caused considerable gastrointestinal intolerance and thus was a factor in lack of patient compliance. Other antiviral agents such as rifampin have activity against vaccinia and may be useful in the propylaxis or treatment of the disease.
TULAREMIA
Because of its very high infectivity after aerosolization, F. tularensis has been considered an important biological warfare agent. Tularemia is characterized by fever, localized skin or mucosal ulcerations, regional lymphadenopathy and, occasionally, pneumonia.
CLINICAL MANIFESTATIONS
Tularemia can be divided into the ulceroglandular (75% of patients) and typhoidal (25% of patients) based on clinical signs. Ulceroglandular tularemia is defined by lesions on the skin or mucous membranes (including conjunctiva), lymph nodes larger than 1cm, or both. Typhoidal tularemia presents with lymph nodes smaller than 1cm, and there are no skin or mucosal lesions. After an incubation of 3-6 days, ulceroglandular patients present with fever (85%), chills(52%), headache(45%), cough(38%), and myalgias (31%).These patients may also complain of chest pain, vomiting, arthralgia, sore throat, abdominal pain, diarrhea, dysuria, back pain and/or stiff neck. A characteristic cutaneous ulcer occurs in about 60% of patients and is the most common sign in tularemia. These lesions are almost invariably accompanied by regional lymphadenopathy, but enlarged lymph nodes may be the initial or the only sign of infection. Though occurring singly, the skin lesions may also appear in groups, becoming fluctuant and draining spontaneously, or they may persist for as long as 3 years. Pharyngitis is another key feature in this disease, with approximate incidence of 25%. Though the posterior pharynx may not be inflamed, there may be erythema, exudates, petechiae, hemorrhage or ulcers of the pharynx. Retropharyngeal abscess or suppuration of regional lymph nodes may occur. Pneumonia may accompany the pharyngitis with radiographic evidence of pneumonia seen in about half the cases of those experiencing lower respiratory signs and symptoms. Thirty percent of patients with ulceroglandular disease and 80% of those with typhoidal tularemia have pneumonia, accounting for the higher mortality in the typhoidal form. Pericarditis, appendicitis, peritonitis, erythema nodosum and meningitis may also occur. The WBC may be mildly elevated; microscopic pyuria may lead to an erroneous diagnosis of a UTI.
TREATMENT
Patients who do not receive antibiotics may have a prolonged illness characterized by malaise, weakness, and weight loss lasting for up to several months. Streptomycin is the drug of choice, with patients usually responding within 48 hours of starting therapy. Chloramphenicol and tetracycline have also been used. Relapses occur if antibiotics are not continued long enough.
UTILITY OF BIOLOGICAL/CHEMICAL WEAPONS
Historically, it is important to note that it has been 8 decades (World War I) since the U. S. military medical personnel have treated a battlefield chemical casualty. Thus far, the U. S. military has never treated a battlefield biological casualty; however, with enhanced biological and chemical weaponry and the development of more effective delivery systems, non-conventional warfare remains a real possibility. The relatively recent use of Anthrax in the U.S. as a terrorist weapon underscores this possibility.
Since we have not had the experience of using biological/chemical and/or treating injuries from the same, we must draw knowledge from the experiences of those who have. In the mid to late 1970’s and mid 1980’s, chemical/biological weapons were allegedly used in Laos, Kampuchea, and Afghanistan and it is confirmed that they were used in the 1980’s in the Iran-Iraq War. Later use on the Iraqi Kurds by the Iraqi government gave us valuable information on the subject.
We have also learned, though not in a warfare setting, from incidents such as the accidental discharge of a biological agent in 1979, from a biological weapons plant in Sverdlovsk, Russia, where 66 humans living downwind of the plant died of pulmonary anthrax. In June, 1994, in Matsumoto, Japan sarin was used by terrorists producing over 200 casualties and 7 deaths. One year later sarin use in a Tokyo subway well over 5000 people being taken to medical facilities, where twenty percent were hospitalized and 12 died.
Chemical and biological weapons differ in several significant ways:

Chemicals are made through industrial chemical processes, whereas biological agents are either replicating (bacteria or viruses) or non replicating materials (toxins, physiologically active proteins or peptides), which can be produced in living organisms or by way of chemical synthesis or recombinant expression methods.

Most of the biological agents are dermally inactive (with the rare exception of the mycotoxins) and none are volatile. Chemical agents are conversely dermally active and/or volatile.

Chemical agents can be disseminated as liquids or aerosols, however, biological agents must be dispersed as respiratory aerosols requiring a high-energy generating system to produce the small particle size. Both types of weapons often depend on appropriate weather conditions to assure the aerosol cloud stays near the ground and adequate infectivity or toxicity to assure the agent’s desired effects.


Military chemical agents are classified as “persistent” (e.g. vesicant, VX) or “nonpersistent” (e.g. phosgene, cyanide). The “persistent” agents have low volatility and evaporate slowly, but can remain on terrain, material or equipment for several months depending on the weather. The “nonpersistent” agents are volatile, thus evaporating quickly and do not persist for more than several hours.
Most of the chemical compounds generally described above have characteristics that make them uniquely suited to warfare. They are chemically similar to substances commonly used throughout the civilian community (such as the similarity of nerve agents to pesticides and insecticides). Therefor known diagnostic and therapeutic methods can be applied to these related “warfare” agents.
Biological weapons, on the other hand, contain either replicating organisms or chemicals similar to reproduced by them. Hundreds of these agents (bacteria, viruses, toxins and “designer compounds”) could be used by an aggressor; however, a finite number of these are actually useful as area weapons. The agents’ utility is limited by production factors, stability, infectivity and toxicity.
Many of the biological agents are found in nature, unlike chemical agents, and can cause the same or very similar diseases and syndromes.
In World War I, without many of the therapeutic and supportive measures or antidotes we have today, there was only a 3% death rate from exposure to chemical/biological weapons. Even in the Iran-Iraq War when highly toxic nerve agents were used against unprotected troops, the death rate was less than 5% for those who reached medical care. Obviously, with well trained, well protected troops (such as those we have today), those numbers would be considerably lower.
Detectors are available to test for chemical and biological weapons in the military and civilian settings. These detectors, however, are not responsive enough to allow for a timely warning to a troop or civilian population. Although adequate protection exists, such as masks and protective clothing, adequate warning of these agents in time to use protective measures, could pose a problem.
Meteorological conditions can significantly affect the time a population is at risk of exposure to these agents. Effective countermeasures such as vaccines, drugs and diagnostics are available today for many agents of greatest concern. So, if chemical or biological agents were used on civilian populations, the emergency response would be able to effectively treat most agent’s effects as well as the secondary psychological panic or anxiety. For an example, from January 18 to February 28, 1991, 39 Iraqi non-chemical, non-biological SCUD missiles reached Israel. Many others were off target or malfunctioned. Approximately 1000 people were treated as a result of the attacks with only 2 deaths. Anxiety, on the other hand, was listed as a reason for admitting 544 patients and 230 admissions were for atropine overdose. Though these SCUD’s caused significant population disruption in Tel Aviv, had these missiles contained chemical or biological agents, the “terror effect” would have been even greater.

In summary, it is important to consider that though biological, chemical and even radiation warfare agents can be devastating, there are many advantages that we, as civilian medical personnel, have as well. We have methods of detection, education, training and medical experience to deal with many of the chemical, biological and radiation threats that, up until now in this country, have been just that, threats. However, we must be constantly vigilant and avoid the complacency of “it can’t happen here” as we so abruptly learned on “9/11”.


SUMMARY

Though there are other agents which have not been discussed in this section, they deserve inclusion. Those are staphylococcal enterotoxin B and related pyrogenic toxins, trichothecene mycotoxins, viral encephalitides and viral hemorrhagic fevers including such agents as the hantavirus. The U. S. Army Medical Research Institute of Infectious Disease, Ft. Detrick, MD, is an excellent source of information on the subject of biological warfare agents and has been used for developing this section. In addition, the NIH’s National Library of Medicine (www.nlm.nih.gov) would be another excellent source of detailed information on the subject.


The database is protected by copyright ©essaydocs.org 2016
send message

    Main page