**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

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-   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:]{.underline} (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:]{.underline} 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:]{.underline} 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]{.underline}: 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!]{.underline}** 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]{.underline} 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]{.underline} 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]{.underline}* 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]{.underline} 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]{.underline}, 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]{.underline}
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.