FM 3-11.9 POTENTIAL MILITARY CHEMICAL/BIOLOGICAL AGENTS AND COMPOUNDS (JANUARY 2005) - page 4

 

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FM 3-11.9 POTENTIAL MILITARY CHEMICAL/BIOLOGICAL AGENTS AND COMPOUNDS (JANUARY 2005) - page 4

 

 

in chloroform (CNS). However, CS proved more effective and less toxic than any of the CN
series and largely has replaced them.
CAUTION
Benzene is a known carcinogen; carbon tetrachloride and chloroform
are suspected carcinogens.10
c.
Bromobenzylcyanide (CA). CA was the last irritating agent introduced by the
Allies in World War I (WWI), and it was the most potent. It corrodes iron and steel, is not
chemically stable in storage, and is sensitive to heat—all the characteristics that made it
unsuitable for storage and use in artillery shells. CA irritates the eyes and causes
lacrimation.3 CA is too toxic for use as an RCA and is considered obsolete.11
5.
Smokes, Obscurants, and Incendiaries
Smokes, obscurants, and incendiaries are combat multipliers. Their use provides
tactical advantages for offensive and defensive operations. For example, smoke has long
been employed as a means of concealing battlefield targets. Fire damage causes casualties
and material damage and can impact psychologically.12 This section contains the physical
and chemical properties of selected smokes, obscurants, and incendiaries.
a.
Smokes and Obscurants. Smoke is an aerosol that owes its ability to conceal or
obscure to its composition of many small particles suspended in the air. These particles
scatter or absorb the light, thus reducing visibility. When the density or amount of smoke
material between the observer and the object to be screened exceeds a certain minimum
threshold value, the object cannot be seen.12 Many types and combinations of smokes are
used, but the three basic types of screening smokes are hexachloroethane (HC) smoke,
phosphorous smoke, and fog oil smoke.6 White phosphorous (WP) and HC are hygroscopic;
they absorb water vapor from the atmosphere. This increases their diameters and makes
them more efficient at reflecting light rays. Fog oils are nonhygroscopic and depend upon
vaporization techniques to produce extremely small diameter droplets to scatter light
rays.12 Most smokes are not hazardous in concentrations that are useful for obscuring
purposes. However, any smoke can be hazardous to health if the concentration is sufficient
or if the exposure is long enough. The protective mask gives the respiratory tract and the
eyes adequate protection against all smokes.4
CAUTION
The protective mask must be worn when operating in or
around smoke material.
(1)
Hexachloroethane (HC). HC is a pyrotechnic containing an equal amount
of hexachloroethane and zinc oxide, with approximately 7 percent grained aluminum. On
combustion, the reaction products are zinc chloride and 10 percent phosgene, carbon
tetrachloride, ethyl tetrachloride, hexachloroethane, hexachlorobenzene, hydrogen chloride,
chlorine, and carbon monoxide. The toxicity of this chemical compound is generally
attributed to zinc chloride (ZnCl2) (see Table III-17). The ZnCl2 reacts with the moisture in
the air to form a grayish white smoke. The more humid the air, the more dense the HC
smoke.13 Immediately after exposure, symptoms include tightness in the chest, sore throat
or hoarseness, and cough.4 Exposures to very high doses of HC smoke commonly result in
sudden, early collapse and death.13
III-16
CAUTION
Hexachloroethane is a suspected carcinogen.10
Table III-17. ZnCl2
Chemical name: Zinc Dichloride
Synonyms: Zinc Dichloride Flume 1
CAS Registry No.: 7646-85-7 1
RTECS Number.: ZH1400000 1
Physical and Chemical Properties
Structural Formula:
Cl — Zn — Cl
Molecular Formula: ZnCl2 1
Molecular Weight: 136.3 1
Physical state
Hygroscopic white solid 2
Odor
Data not available
Boiling point
732°C (1350°F) 1
FP/MP
290°C (554°F) (MP) 1
Liquid density (g/mL)
Data not available
Vapor density (relative to air)
4.7 (calculated)
Vapor pressure (torr)
Approximately 0 @ 20°C (68°F) 1
Volatility (mg/m3)
Data not available
Specific gravity (water = 1 @ 4°C)
2.91 @ 25°C 1
Flash point
Data not available
Decomposition temperature
Data not available
Solubility
In water, 432 g/100 mL at 25°C 2
Stability in storage
Decomposes upon heating, producing toxic fumes of hydrogen chloride and zinc
oxide 2
Action on metals or other materials
The solution in water is a medium-strong acid. 2
Other Data
Skin and eye toxicity
Corrosive to the eyes and the skin 2
Inhalation toxicity
Irritant; inhalation of fumes may cause lung edema 2
Protection required
Try to remain out of smoke/obscurant clouds, and wear protective mask when
making smoke. Personnel can reduce exposure to smoke by rolling down their
sleeves and showering after exposure. 3
Decontamination
Remove contaminated clothing and shoes. Launder clothing following exposure. 3
Use
See FM 3-50, Smoke Operations
NOTES
¹NIOSH Pocket Guide to Chemical Hazards, “Zinc Chloride fume,” CAS 7646-85-7.
²ICSC 1064, “Zinc Chloride.”
³FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11, Treatment of Chemical Agent Casualties and Conventional
Military Chemical Injuries, 22 December 1995.
(2)
Phosphorous. Phosphorous occurs in three allotropic forms: white, red,
and black. The military uses white and red phosphorous.
CAUTION
Phosphorous smoke produces phosphoric acid. Soldiers must wear
respiratory protection.14
(a) White Phosphorous (WP) (see Table III-18 [page III-18]). WP
produces a hot, dense, white smoke composed of particles of phosphorous pentoxide, which
are converted by moist air into phosphoric acid.4 WP is a very active chemical that will
III-17
readily combine with oxygen in the air, even at room temperature. As oxidation occurs, WP
becomes luminous and bursts into flames within minutes. Complete submersion in water is
the only way to extinguish the flames.13 It is used primarily as a smoke agent and can also
function as an antipersonnel flame compound capable of causing serious burns.
Table III-18. WP
Chemical name: Phosphorus
Synonyms: Bonide-Blue-Death-Rat-Killer, Exolit-LPKN; Exolit VPK-n 361, Forforo-Bianco (Italian), Gelber-Phosphor
(German), Phosphore-Blanc (French), 1
elemental phosphorus, white phosphorus, 2 yellow phosphorus, WP, WP/F, Willie
Peter3
CAS Registry No.: 7723-14-0
Physical and Chemical Properties
Chemical formula
P4 2
Molecular weight
124.0 2
Physical state
White to yellow; soft waxy solid 2
Odor
Garlic-like 1
Boiling point
280°C (536°F) 2
FP/MP
44°C (111°F) (MP) 2
Density (g/mL)
1.83 4
Vapor density
4.28 (calculated)
Vapor pressure (torr)
0.03 at 20°C 2
Volatility (relative to air)
Data not available
Specific Gravity (water = 1 @ 4°C)
1.82 @ 20°C 2
Flash point (mg/m3)
20°C 4
Decomposition temperature
Data not available
Solubility
Insoluble in water; soluble in carbon disulfide 1
Rate of hydrolysis
Data not available
Hydrolysis products
Data not available
Stability in storage
Darkens on exposure to light. This substance spontaneously ignites on contact
with air producing toxic fumes. 4
Action on metals or other materials
Incompatible with sulfur, iodine, oil of turpentine, and potassium chlorate 1
Other Data
Skin and eye toxicity
Burns on skin are usually multiple, deep and variable in size. Particles on skin
continue to burn unless deprived of atmospheric oxygen. Smoke causes irritation
to the eyes, nose, and throat. 5
Inhalation toxicity
At room temperature may produce a toxic inhalational injury 6
Protection required
Protective mask. 7 Do not handle the charred wedges on the ground without
protective covering. 5
Decontamination
Flush skin with water. If burning WP strikes the skin, smother the flame with
water, a wet cloth, or mud. Keep the WP covered with the wet material to exclude
air until the particles can be removed. 5
Use
See FM 3-50, Smoke Operations
NOTES
¹Spectrum Chemical Fact Sheet, “Phosphorus,” CAS 7723-14-0.
²NIOSH Pocket Guide to Chemical Hazards, “Phosphorus (yellow),” CAS 7723-14-0.
3USA Corps of Engineers, Construction Engineering Research Laboratory, Methods for Field Studies of the Effects of
Military Smokes, Obscurants, and Riot-control Agents on Threatened and Endangered Species, Vol. 4: Chemical Analytical
Methods, USACERL Technical Report 99/56, July 1999.
4ISCS 0628, “Phosphorus (Yellow).”
5FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11, Treatment of Chemical Agent Casualties and Conventional
Military Chemical Injuries, 22 December 1995.
6BG Russ Zajtchuk, et al. (eds), Textbook of Military Medicine: Medical Aspects of Chemical and Biological Warfare, Office
of the Surgeon General, 1997, Chapter 9, “Toxic Inhalational Injury.”
7FM 3-50, Smoke Operations, 4 December 1990.
III-18
(b) Red Phosphorous (RP). RP smoke is deployed explosively from
grenades and mortar shells. The grenades consist of a 95:5 mixture of RP and butyl
rubber.15 RP is produced by heating WP to 270 to 300 degrees C in the absence of air. RP
is more dense, has a higher melting point, is much less reactive, is essentially nontoxic, and
is easier and safer to handle than WP. When RP is heated, WP molecules sublime from the
solid.16 RP will not ignite spontaneously and, therefore, requires ignition to burn and make
smoke.14
(3)
Titanium Tetrachloride (FM Smoke). FM smoke is a corrosive substance
typically dispersed by spray or explosive munitions. It is extremely irritating and corrosive
in both liquid and smoke formulations. Exposure to liquid may create burns similar to
those of mineral acids on conjunctiva or skin. A dense, white smoke results from the
decomposition of FM smoke into hydrochloric acid, titanium oxychloride, and titanium
dioxide (TiO2) (see Table III-19).13 TiO2 is the major component of training smoke grenade
XM82 and is also used in conjunction with HC in the production of white screening smoke.6
Table III-19. TiO2
Chemical name: Titanium Dioxide1
Synonyms: Titanium (IV) Oxide,1 Titanium Oxide, Titania, Titanium White, Brookite2
CAS Number: 13463-67-71
Physical and Chemical Properties
1
Molecular formula
TiO2
Molecular weight
79.871
Physical state
White Powder1
Odor
Odorless1
Boiling point
2500 - 3000°C (4532 - 5432°F) 1
FP/MP
1855°C (3371°F) (MP) 1
Solid density (g/mL)
4.17 2
Vapor density (relative to air)
2.75 (calculated)
Vapor pressure (torr)
Data not available
Volatility (mg/m3)
Data not available
Specific gravity (H2O = 1)
4.261
Flashpoint
Data not available
Decomposition temperature
Data not available
Solubility
Insoluble in water.1 Insoluble in hydrochloric acid, nitric acid, and alcohol. It is
soluble in hot concentrated sulfuric acid, hydrogen fluoride, and alkali. 3
Rate of Hydrolysis
Data not available
Hydrolysis Products
Data not available
Stability in storage
Stable under ordinary conditions of use and storage1
Action on metals or other materials
Violent reaction with lithium occurs around 200°C with a flash of light; the
temperature can reach 900°C. Violent or incandescent reaction may also occur
with other metals such as aluminum, calcium, magnesium, potassium, sodium, and
zinc. 1
Other Data
Skin and eye toxicity
May cause mild irritation and redness 1
Inhalation toxicity
May cause mild irritation 1
Protection required
Protective mask 4
Decontamination
Flush with water 4
Use
See FM 3-50, Smoke Operations
III-19
Table III-19. TiO2 (Continued)
NOTES
1Mallinckroct Baker, Inc., MSDS Number T3627, “Titanium Dioxide,” effective date: 15 February 1998.
2USA Corps of Engineers, Construction Engineering Research Laboratory, Methods for Field Studies of the Effects of
Military Smokes, Obscurants, and Riot-control Agents on Threatened and Endangered Species, Vol. 4: Chemical Analytical
Methods, USACERL Technical Report 99/56, July 1999.
3NRC, Toxicity of Military Smokes and Obscurants, Vol. 2, National Academy Press, 1999.
4FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11, Treatment of Chemical Agent Casualties and Conventional
Military Chemical Injuries, 22 December 1995.
(4)
Tantalum (Ta). Ta is a clear, colorless, odorless liquid. It is a mixture of
tantalum pentachloride, hydrogen fluoride, and water. It is stable at 68 degrees F when
stored and used under proper conditions. On heating to decomposition, it could yield toxic
fumes of fluorides. It attacks glass and other silicon-containing compounds. It reacts with
silica to produce silicon tetrafluoride, a hazardous, colorless gas. It is incompatible with
arsenic trioxide, phosphorus pentoxide, ammonia, calcium oxide, sodium hydroxide, sulfuric
acid, vinyl acetate, ethylenediamine, acetic anhydride, alkalis, organic materials, most
common metals, rubber, leather, water, strong bases, carbonates, sulfides, cyanides, oxides
of silicon, and especially glass, concrete, silica, and fluorine. It is a corrosive poison. It is
extremely hazardous in liquid and vapor form. It can cause severe burns that may not be
immediately painful or visible. It can be fatal if swallowed or inhaled. Liquid and vapor
can burn skin, eyes, and the respiratory tract. It can also cause bone damage.17
(5)
Synthetic Graphite (see Table III-20). Graphite is used as an obscurant to
screen electromagnetic tracking and targeting systems. Graphite flakes perform well in
obscuring mid- and far-infrared (IR) bands as well as a combination of visible, near-, mid-,
and far-IR bands. Graphite exists naturally and synthetically and is chemically inert.6 It
consists primarily of carbon, with trace impurities totaling less than one percent of the total
weight.18 Inhalation of dust can cause nose and/or throat irritation and shortness of
breath.19
CAUTION
Graphite is electrically conductive; exercise caution when
handling graphite in areas where contact with electrical
circuitry is possible. Handle and transfer in a manner that
avoids excessive dusting.19
Table III-20. Synthetic Graphite
Chemical name: Synthetic Graphite1
Synonyms: Crystalline carbon1
CAS Number: N/A2
Physical and Chemical Properties
Molecular formula
Carbon
Molecular weight
12
Physical state
Grey to Black1
Odor
Odorless1
Boiling point
3337.7°C2
FP/MP
N/A1
Density (g/mL)
2.25 g/mL2
Vapor density (relative to air)
N/A1
Vapor pressure (torr)
N/A1
Volatility (mg/m3)
Data not available
Specific gravity (H2O = 1)
2.20
- 2.261
III-20
Table III-20. Synthetic Graphite (Continued)
Flashpoint
Data not available
Decomposition temperature
Data not available
Solubility
Insoluble in water1
Rate of hydrolysis
Data not available
Hydrolysis products
Data not available
Stability in storage
This material is stable and will not polymerize. Incompatible with oxidizing agents.1
Action on metals or other materials
Data not available
Other Data
Skin and eye toxicity
Minor 1
Inhalation toxicity
Cases of pulmonary fibrosis, emphysema, and corpulmonale may result from
prolonged inhalation of dust1
Protection required
Protective mask 1
Decontamination
Move to fresh air; rinse skin with soap and water; rinse eyes with water1
Use
See FM 3-50, Smoke Operations
NOTES
1Asbury Graphite Mils, Inc., MSDS, “Synthetic Graphite,” CAS No. 7782-42-5, January 2003.
2Graphite obscurant materials are purchased from manufacturers in accordance with a specification that have specific purity
and performance requirements. These specifications do not contain CAS number requirements. The CAS numbers may
vary from contract to contract.
(6)
Brass. Brass in flake or powder form is one of the components of screening
smoke grenade M76. Smoke munitions containing metal flakes or powders are used to
screen against range finders, thermal surveillance systems, and laser target designators as
well as to provide protection for armored vehicles. Smoke screens containing brass
performed the best against far-IR bands but did poorly on visible light bands. Brass is a
metal alloy composed mostly of copper (70 percent) and zinc (30 percent) with
approximately 1 percent contamination of trace metals.6
(7)
Fog Oil (SGF-2). Fog oil is a low-viscosity petroleum oil used to generate
screening smokes. The fog is generated by evaporating the hydrocarbons in the oil. Fog oil
is composed of many different types of chemicals, but the predominant class of chemicals is
aliphatic hydrocarbons with very low levels of noncarcinogenic aromatic hydrocarbons.6
Fog oil is the overhead fraction of petroleum. It contains no additives and is not refined.20
Fog oil is commonly called smoke generator fuel number 2 (SGF-2) (see Table III-21).
Table III-21. SGF-2
Chemical name: Mineral Oil 1
Synonyms: SGF-2, Fog Oil 1
CAS Number: N/A 2
Physical and Chemical Properties
Molecular formula
N/A
Molecular weight
N/A
Physical state
Lube Oil 1
Odor
Hydrocarbon odor 1
Boiling point
600°F (316°C) 1
FP/MP
Data not available
Liquid density (g/mL)
Data not available
Vapor density (relative to air)
> 11
Vapor pressure (torr)
< 11
Volatility (mg/m3)
Data not available
Specific gravity (H2O = 1)
0.9
Flashpoint
Data not available
III-21
Table III-21. SGF-2 (Continued)
Decomposition temperature
Data not available
Solubility
In water, negligible1
Rate of hydrolysis
Data not available
Hydrolysis products
Data not available
Stability in storage
Avoid extreme heat and strong oxidants. No hazardous polymerization. 1
Action on metals or other materials
Data not available
Other Data
Skin and eye toxicity
Skin: Prolonged/repeated contact may cause dryness, defatting. Eyes: May
cause irritation. 1
Inhalation toxicity
May cause irritation1
Protection required
Protective mask 1
Decontamination
Move to fresh air 1
Use
See FM 3-50, Smoke Operations
NOTES
1Defense General Supply Center, MSDS MIL-F-12070C, “SGF-2 Type; Fog Oil.”
2Fog oil obscurant materials are purchased from manufacturers in accordance with a specification that has specific purity
and performance requirements. These specifications do not contain CAS number requirements. The CAS numbers may
vary from contract to contract.
(8)
No. 1 Diesel Fuel (DF-1). DF-1 is clear or straw-colored liquid when undyed
and low-sulfur diesel is red. Symptoms of overexposure include eye and skin irritation,
dermatitis, upper respiratory tract irritation, nausea, vomiting, diarrhea, lung damage,
weakness, headache, confusion, blurred vision, drowsiness, dizziness, slurred speech,
flushed face, aortic plaques, heart beat irregularities, convulsions, unconsciousness, and
death.21
(9)
Diesel Fuel No. 2 (DF-2). Symptoms of overexposure include redness,
drying to burns or blistering of skin. Overexposure by inhalation can produce symptoms of
intoxication such as headache, dizziness, nausea, vomiting, and loss of coordination.22
(10) Jet Fuel Grade (JP-8). High vapor concentrations can be irritating to the
eyes and respiratory tract, causing headaches, dizziness, anesthesia, drowsiness,
unconsciousness, and CNS effects. Chronic exposure of the skin can cause drying,
defatting, and dermatitis.23
(11) Signaling Smokes. These smokes are produced by explosive dissemination
of dyes. There are no reports of ill effects produced by exposure to these smokes.4
b.
Incendiaries. The purpose of incendiaries is to cause maximum fire damage on
flammable materials and objects and to illuminate. The initial action of the incendiary
munition may destroy these materials, or the spreading and continuing of fires started by
the incendiary may destroy them.12
(1)
Magnesium Incendiaries. Magnesium is a soft metal, which when raised to
its ignition temperature, spontaneously ignites on contact with air or moisture, producing
irritating or toxic fumes.24 Magnesium (Mg) burns at approximately 2000 degrees C with a
scattering effect. Its particles produce deep burns. Healing is slow unless these particles
are removed quickly. When explosive charges have been added, fragments may be
embedded deep in the tissues, causing the localized formation of hydrogen gas and tissue
necrosis.4
(2)
Thermite and Thermate Incendiaries. A thermite reaction occurs when
powdered aluminum metal and iron oxide mix. It is an exothermic reaction in which the
III-22
temperature rises to about 3000 degrees C, causing the aluminum and iron to become a
liquid.16 Explosive charges are frequently added. Particles of iron that lodge in the skin
produce multiple small, deep burns. The particles should be cooled immediately with water
and removed.4
(3)
Oil and Metal Incendiary Mixtures. Lung damage from heat and irritating
gases may be complications added to the injuries from incendiaries, especially in confined
spaces.4
NOTES
1USACHPPM TG 204, Glossary of Terms for Nuclear, Biological, and Chemical Agents and
Defense Equipment, December 2001.
2FM 3-11.11/MCRP 3-3.7.2, Flame, Riot Control Agents and Herbicide Operations, 19
August 1996 (Renumbered from FM 3-11).
3BG Russ Zajtchuk et al (eds), Textbook of Military Medicine: Medical Aspects of Chemical
and Biological Warfare, Office of the Surgeon General, 1997, Chap. 12, “Riot Control
Agents.”
4FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11, Treatment of Chemical Agent
Casualties and Conventional Military Chemical Injuries, 22 December 1995.
5Sharon Reutter, et al., Review and Recommendations for Human Toxicity Estimates for FM
3-11.9, ECBC-TR-349, September 2003.
6USA Corps of Engineers, Construction Engineering Research Laboratory, Methods for
Field Studies of the Effects of Military Smokes, Obscurants, and Riot-control Agents on
Threatened and Endangered Species, Vol. 4: Chemical Analytical Methods, USACERL
Technical Report 99/56, July 1999.
7ICSC 0126, “Chlorine (Cl2).
8A.K. Steumpfle, et al., Final Report of International Task Force-25: Hazard From Toxic
Industrial Chemicals, March 18, 1996.
9ICSC 0128, “2-Chloroacetophenone.”
10US HHS, Public Health Service, National Toxicology Program, 10th Report on
Carcinogens, December 2002.
11FM 8-9/NAVMED P-5059/AFJMAN 44-151, NATO Handbook on the Medical Aspects of NBC
Defense Operations AMEDP-6(B), 1 February 1996.
12FM 3-6/FMFM 7-11-H/AFM 105-7, Field Behavior of NBC Agents (Including Smoke and
Incendiaries), 3 November 1986.
13BG Russ Zajtchuk, et al. (eds), Textbook of Military Medicine: Medical Aspects of
Chemical and Biological Warfare, Office of the Surgeon General, 1997, Chap. 9, “Toxic
Inhalational Injury.”
14FM 3-50, Smoke Operations, 4 December 1990.
15NRC, Toxicity of Military Smokes and Obscurants, Vol. 1, National Academy Press, 1997.
16Henry F. Holtzclaw, Jr., et al., General Chemistry with Qualitative Analysis, 9th ed., D.C.
Heath and Company, Lexington, MA, 1991.
III-23
17Mallinckrodt Baker, Inc., MSDS Number T0080, “Tantalum, 1,000 µg/mL or 10,000
µg/mL,” effective date 29 October 2001.
18NRC, Toxicity of Military Smokes and Obscurants, Vol. 2, National Academy Press, 1999.
19Asbury Graphite Mills, Inc., MSDS, “Synthetic Graphite,” CAS No. 7782-42-5, January
2003.
20Defense General Supply Center, MSDS MIL-F-12070C, “SGF-2 Type; Fog Oil.”
21Conoco International, Inc., MSDS, “No. 1 Diesel Fuel, No. 1 Fuel Oil.”
22Costal Corporation, MSDS, “Diesel fuel 2.”
23Exxon Company, MSDS, “Jet Fuel Grade JP-8, 27020-00079.”
24ICSC 0701, “Magnesium (Pellets).”
III-24
Chapter IV
BIOLOGICAL AGENTS AND THEIR PROPERTIES
1.
Background
The military application of biological agents concerns those microorganisms that may
be deliberately employed in weapon systems to cause disease or death to man, animals, or
plants. Biological agents consist of microorganisms such as pathogens (which include
disease-causing bacteria, rickettsiae, and viruses) and toxins.
NOTES:
1. See Table IV-1 (page IV-2) for the list of potential biological agents.
2. See Table IV-2 (page IV-3) for the list of animal and plant pathogens with
potential biological agent applications.
3. See Appendix I for the properties of selected biological agents.
4. See Appendix J for more detailed information on animal pathogens.
5. See Appendix K for more detailed information on plant pathogens.
6. See Appendix L for information on the dissemination of biological agents
IV-1
Table IV-1. List of Potential BW Agents26
Viruses
Bacteria
Chikungunya virus
Bacillus anthracis (Anthrax)
Crimean-Congo hemorrhagic fever virus
Brucella abortus (Brucellosis)
Dengue fever virus
Brucella melitensis (Brucellosis)
Eastern equine encephalitis virus
Brucella suis (Brucellosis)
Ebola virus
Chlamydia psittaci (Psittacosis)
Hantaan virus
Clostridium botulinum (Botulism)
Junin virus
Francisella tularensis (Tularemia)
Lassa virus
Burkholderia mallei, formerly Pseudomonas mallei
(Glanders)
Lymphocytic choriomeningitis virus
Burkholderia pseudomallei, formerly Pseudomonas
pseudomallei (Melioidosis)
Machupo virus
Salmonella typhi (Typhoid Fever)
Marburg virus
Shigella dysenteriae (Shigellosis)
Monkeypox
Vibrio cholerae (Cholera and other Vibrioses)
Rift Valley Fever virus
Yersinia pestis (Plague)
Tick-borne encephalitis virus
(Russian Spring-Summer encephalitis virus)
Toxins
Variola virus
Botulinum toxins
Venezuelan equine encephalitis virus
Clostidium perfringens toxins
Western equine encephalitis virus
Conotoxin
Yellow fever virus
Ricin
Japanese encephalitis virus
Saxitoxin
Shiga toxin
Staphylococcus aureus toxins
Rickettsia
Tetrodotoxin
Coxiella burnetii (Q Fever)
Verotoxin
Bart quintana, formerly Rochalimaea quintana or
Microcystin
Rickettsia quintana (Trench Fever)
Trichothecene mycotoxin (see Note)
Rickettsia prowasecki (Typhus Fever)
Rickettsia rickettsii (Rocky Mountain Spotted Fever)
NOTE: Trichothecene mycotoxin is not on the list of BW agents listed in the reference; however, mycotoxins
were alleged to have been used in Southwest Asia in the mid-1980s.
IV-2
Table IV-2. Animal and Plant Pathogens with Potential BW Applications26
Animal Pathogens for Export Control
Plant Pathogens for Export Control
Viruses
Bacteria
African swine fever virus
Xanthomonas albilineans
Highly pathogenic Avian influenza virus
Xanthomonas campestris pv. citri
(synonym: fowl plague)
Bluetongue virus
Fungi
Foot and mouth disease virus
Colletorichum coffeanum var
Goat pox virus
Cochiliobolus miyabeans
Herpes virus (Aujeszky’s disease)
(Helminthosporium oryzae)
Hog cholera virus
Microcylus ulei (syn. Dothidella ulei)
(synonym: Swine fever virus)
Puccinia graminis
Lyssa virus
(syn. Puccinia graminis fsp. Tritici)
Newcastle disease virus
Puccinia striformis (syn. Puccinia glumarium)
Peste des petits ruminants virus
Pyricularia grisea/Pyricularia oryzae
Porcine enterovirus type-9
(synonym: Swine vesicular disease virus)
Virus
Rinderpest virus (synonym: Cattle plague
Barley Yellow Dwarf Virus
Sheep pox virus
Teschen disease virus
Items for Inclusions in Awareness-Raising Guidelines
Vesicular stomatitis virus
Bacteria
Bacteria
Xanthomonas campestris pv. oryzae
Mycoplasma mycoides
Xylella fastidiosa
Other Animal Diseases/Pathogens of Concern
Fungi
Contagious bovine pleuropneumonia
Deutrrerophoma tracheiphila
Contagious Equine Metritis
(syn. Phoma Tracjeo[jo;a)
Heartwater (Cowdria)
Monlia rorei (syn. Moniliophtora rorei)
Screwworm Myiasis (synonym: Blowfly
Cochliomyia hominivorax)
Virus
Swine vesicular disease
Banana bunchy top virus
a.
The information presented in this chapter provides descriptions of selected
bacteria, rickettsiae, viruses, and toxins.
b.
The biological agents addressed in this chapter are presented in a standard
format that includes the following information:
(1)
Infectious Agent. Identifies the specific pathogen that causes the disease,
classifies the pathogen, and may indicate any of its important characteristics.
(2)
Occurrence. Provides information on where the disease is known to be
prevalent and/or in what population groups it is most likely to occur.
(3)
Reservoir. Indicates the ultimate and/or intermediate human, animal,
arthropod, plant, soil, or substance (or a combination of these) in which an infectious agent
normally lives and multiplies, on which it depends primarily for survival, and where it
reproduces itself in such a manner that it can be transmitted to a susceptible host.
IV-3
(4)
Transmission.1 Describes the mechanisms by which an infectious agent is
spread to humans. Such mechanisms include direct, indirect, and airborne.
(a) Direct transmission can be by direct contact (such as touching or
biting), or by the direct projection (droplet spread) of droplet spray onto the conjunctiva or
onto the mucous membranes of the eye, nose, or mouth during sneezing, coughing, spitting,
singing, or talking (usually limited to a distance of about 1 meter or less).
(b) Indirect transmission can be vehicle- or vector-borne. Vehicle-borne
transmission is when contaminated inanimate materials or objects (e.g., soiled clothes,
cooking or eating utensils, water, or food) serve as an intermediate means by which an
infectious agent is transported and introduced into a susceptible host through a suitable
portal of entry. Vector-borne transmission can be mechanical or biological. Mechanical
includes simple mechanical carriage by a crawling or flying insect through soiling of its feet
or proboscis, or by passage of organisms through its GI tract. This does not require
multiplication or development of the organism. Biological means that the propagation
(multiplication), cyclic development, or a combination of these is required before the
arthropod can transmit the infective form of the agent to humans. An incubation period is
required following infection before the arthropod becomes infective.
(c)
Airborne transmission is the dissemination of microbial aerosols to a
suitable portal of entry—usually the respiratory tract. Microbial aerosols are suspensions
of particles in the air consisting partially or wholly of microorganisms. They may remain
suspended in the air for long periods of time.
(5)
Symptoms. Describes the symptoms of the disease.
(6)
Incubation period. Identifies the interval (in hours, days, or weeks)
between initial, effective exposure to an infectious organism and the first appearance of
symptoms of the infection.
(7)
Communicability. Describes the time (days, weeks, or months) during
which an infectious agent may be transmitted, directly or indirectly, from an infected
person to another person or from an infected animal to humans.
(8)
Prevention. Describes prophylaxis measures.
(9)
Delivery. Describes the most likely means to disseminate the agent.
2.
Bacterial Agents of Potential Concern
Bacteria are single-celled, microscopic organisms. These unicellular forms outnumber
all other forms of microorganisms. However, few bacteria are of military significance. Of
several thousand identified species, only about 100 are known to be pathogenic.2 Some
bacteria that infect man are selective human parasites, but many are zoonotic,
transmittable from animals to humans. Zoonotic organisms include anthrax, tularemia,
and brucellosis. Bacteria have primary military potential as antipersonnel agents.
a.
Anthrax.
(1)
Infectious Agent. Bacillus anthracis. This organism forms a protective
spore under adverse environmental conditions or upon exposure to air. When conditions
improve, the spores germinate to produce vegetative bacteria. The spores are extremely
hardy and can survive extremes of temperature, dryness, and flooding.3
(2)
Occurrence. Worldwide.3
IV-4
(3)
Reservoir. The soil and domestic and wild animals (primarily herbivores,
including goats, sheep, cattle, horses, and swine) serve as reservoirs.4
(4)
Transmission. Humans can contract anthrax from the inhalation of
aerosolized spores, contact with infected animals (their hides, wool, or other products), or
ingestion of contaminated meat. Usually, humans do not contract anthrax directly from
the soil.3
(5)
Symptoms. Symptoms of anthrax depend upon the method of transmission.
(a) Cutaneous anthrax features a painless, necrotic ulcer with a black
scab and local swelling.3 Untreated cutaneous anthrax has a case-fatality rate between 5
and 20 percent.1
(b) Ingestion causes oropharyngeal and GI anthrax. Initial symptoms of
oropharyngeal anthrax are fever, sore throat, and difficulty swallowing. Acute symptoms
include ulcer or scab involving the hard palate or tonsils, swelling of neck tissues, and
abnormal enlargement of the lymph nodes. Initial symptoms of GI anthrax include fever,
loss of appetite, nausea, and vomiting. Abdominal pain, bloody vomiting, bloody diarrhea,
and possibly massive abdominal swelling may follow. In both cases, septic shock and death
may follow.3
(c)
Initial symptoms of inhalation anthrax are mild and nonspecific and
may include fever, malaise, fatigue, and mild cough or chest discomfort; acute symptoms of
respiratory distress, fever, and shock follow, with death occurring shortly thereafter.1
(6)
Incubation period. Hours to 7 days; although most cases occur within 48
hours post-exposure.2 Incubation periods up to 60 days are possible.1
(7)
Communicability. Transmission from person to person is very rare.
Articles and soil contaminated with spores may remain infective for decades.1
(8)
Prevention. Anthrax vaccine is available.2
(9)
Delivery. Missiles, bomblets, artillery fires, point release, or airborne line
release may deliver aerosolized spores. Contamination of food and water could also be
used.3
b.
Brucellosis.
(1)
Infectious Agent. Brucella abortus, cattle; Brucella melitensis, sheep, goats,
camels; Brucella suis, swine, Brucella canis, dogs and coyotes.3
(2)
Occurrence. Worldwide.1
(3)
Reservoir. Cattle, swine, goats, and sheep serve as reservoirs. Infection
may occur in bison, elk, caribou, and some species of deer.1 Dogs and coyotes have been
found to be infected.
(4)
Transmission. The disease is transmitted by the inhalation of aerosols or
dusts that contain organisms, ingestion of unpasteurized dairy products and contaminated
meat, or inoculation of abraded skin or mucosal surfaces.3
(5)
Symptoms. A bacterial disease with sudden or insidious onset,
characterized by continued, intermittent, or irregular fever of variable duration; headache;
weakness; profuse sweating; chills; severe pain in a joint, especially one not inflammatory
in character; depression; weight loss; and generalized aching. The disease may last for
IV-5
several days, months, or occasionally a year or more if not adequately treated. The
untreated case-fatality rate is 2 percent or less. Some of the original syndrome may
reappear as relapses.1
(6)
Incubation period. Varies from 5 days to 8 weeks, usually 2 to 8 weeks.3
(7)
Communicability. This disease is not communicable from person to
person.3
(8)
Prevention. Vaccines are not currently available for human use. Personnel
must avoid consuming unpasteurized dairy products or uncooked foods containing the dairy
products and avoid contact with suspect infected animals.3
(9)
Delivery. The primary threat is by aerosol release. A food-borne
brucellosis attack is unlikely, but could be executed.3
c.
Cholera and other Vibrioses.
(1)
Infectious Agent. Vibrio cholerae1
(2)
Occurrence. Worldwide.1
(3)
Reservoir. Humans and some strains of bacteria found in aquatic
environments, particularly brackish waters.1
(4)
Transmission. Through ingestion of food or water contaminated directly or
indirectly with feces or vomit of infected persons. Ingestion of raw or undercooked seafood
from polluted waters has caused outbreaks.1
(5)
Symptoms. Symptoms include profuse painless, watery stools; nausea and
vomiting; and (in untreated cases) rapid dehydration, acidosis, and circulatory collapse. In
severe untreated cases death may occur within a few hours and the case-fatality rate may
exceed 50 percent.1
(6)
Incubation period. From a few hours to 5 days, usually 2 to 3 days.1
(7)
Communicability. Transmission is negligible from person to person.6
Occasionally the carrier state may persist for several months, but usually only a few days
after recovery.1
(8)
Prevention. Following proper field sanitation and personal hygiene are
useful preventive measures. Do not eat raw seafood. A vaccine is available.1
(9)
Delivery. The primary threat is from contamination of food and water
supplies and secondly by aerosol spray.5
d.
Glanders.
(1)
Infectious Agent. Burkholderia mallei (formerly Pseudomonas mallei).3
(2)
Occurrence. The disease is not widespread. The cases have been among
workers with jobs that involve horses, donkeys, or mules and laboratory workers.3 Cases
continue to occur in Asia, Africa, the Middle East, and Central and South America.6
(3)
Reservoir. Horses, mules, and donkeys serve as reservoirs.3
(4)
Transmission. The organism is transmitted from animals to humans by
invading the nasal, oral, and mucous membranes around the eyes; by inhaling into the
lungs; and by invading abraded or lacerated skin.3
IV-6
(5)
Symptoms. Symptoms include fever, rigors, sweating, muscle pain,
headache, pleuritis, chest pain, and generalized papular/pustular eruptions.3 Mortality
rate is over 50 percent despite antibiotic treatment.7
(6)
Incubation period. 10 to 14 days after inhalation.3
(7)
Communicability. Cases of person-to-person transmission have been
reported.6
(8)
Prevention. No vaccine is available.3
(9)
Delivery. The primary threat is aerosol release.3
e.
Melioidosis.
(1)
Infectious Agent. Burkholderia pseudomallei (formerly Pseudomonas
pseudomallei).3
(2)
Occurrence. In countries between 20 degrees north and south latitudes.3
(3)
Reservoir. Soil and water are the reservoirs. Several animals including
sheep, goats, horses, swine, monkeys, and rodents, can become infected. There is no
evidence that animals are important reservoirs except that they spread the agent to new
soil and water.3
(4)
Transmission. Contact with contaminated soil or water through gross or
unapparent skin lesions, aspiration or ingestion of contaminated water, or inhalation of
contaminated dust.3
(5)
Symptoms. Melioidosis will most likely present as an acute pulmonary
infection ranging from mild bronchitis to severe pneumonia. Other symptoms may include
fever (over 102 degrees F), headache, loss of appetite, and pain in one or more muscles.
Acute pulmonary disease can progress into a rapidly fatal septicemic disease. The case-
fatality rate for acute septicemic disease exceeds 90 percent.3
(6)
Incubation period. 10 to 14 days following inhalation.3
(7)
Communicability. Person-to-person transmission has not been proven.
Laboratory acquired infections are uncommon, but do occur, especially if procedures
produce aerosols.3
(8)
Prevention. No vaccines are available.3
(9)
Delivery. The primary threat is aerosol release.3
f.
Plague.
(1)
Infectious Agent. Yersinia pestis.1
(2)
Occurrence. Worldwide.8 Plague continues to be a threat because of vast
areas of persistent wild rodent infection.1
(3)
Reservoir. The primary reservoir is wild rodents (especially ground
squirrels). Domestic cats, wild carnivores, rabbits, and hares can also transmit plague to
humans.1
(4)
Transmission. The disease is transmitted from infected fleas—either from
rodents to humans, from dogs or cats to humans, or from person to person—and by
handling tissues of infected animals.1 In the most likely BW scenario, plague would be
IV-7
spread via aerosol. A rapidly person-to-person spread of fulminant pneumonia would
occur.8 Cat bites or scratches may also transmit plague.1
(5)
Symptoms. Initial signs and symptoms may be nonspecific with fever,
chills, malaise, muscular pain, nausea, exhaustion, sore throat, and headache. This is
bubonic plague, and it occurs more often in lymph nodes. The involved nodes become
swollen, inflamed, and tender and may form or discharge pus. Fever is usually present.
Untreated bubonic plague has a case-fatality rate of about 50 to 60 percent. Untreated
primary septicemic plague and pneumonic plague are invariably fatal. Modern therapy
markedly reduces fatality from bubonic plague; pneumonic and septicemic plagues also
respond if recognized and treated early. However, patients who do not receive adequate
therapy for primary pneumonic plague within 18 hours after onset of respiratory symptoms
are not likely to survive.1
(6)
Incubation period. From 1 to 7 days, maybe a few days longer for an
immunized individual. For primary plague pneumonia, 1 to 4 days, usually short.1
(7)
Communicability. Fleas may remain infective for months under suitable
conditions of temperature and humidity. Bubonic plague is not usually transmitted directly
from person to person unless there is contact with pus from suppurating buboes.
Pneumonic plague may be highly communicable under appropriate climatic conditions;
overcrowding facilitates transmission.1 Fleas flourish at humidity just above 65 percent
and temperatures between 20 to 26 degrees C, and can survive 6 months without a
feeding.8
(8)
Prevention. Use of insect repellents, approved for human use, will provide
a level of protection from bites by infected fleas. A vaccine is available to prevent bubonic
plague.3
(9)
Delivery. The primary threat is by aerosol release or by contamination of
food and water.3
g.
Psittacosis.
(1)
Infectious Agent. Chlamydia psittaci (c. psittaci).1
(2)
Occurrence. Worldwide.1
(3)
Reservoir. Parakeets, parrots, pigeons, turkeys, ducks, and other birds
serve as reservoirs. Apparently healthy birds can be carriers and occasionally shed the
infectious agent, particularly when subjected to the stresses of crowding and shipping.1
(4)
Transmission. Infection is acquired by inhaling dried droppings, secretions,
and dust from infected feathers of birds. Household birds, usually psittacine birds, are the
most frequent source of exposure, followed by turkey, squab, and duck farms and in poultry
processing plants.1
(5)
Symptoms. In humans, fever, headache, rash, muscle pain, chills, and
upper or lower respiratory tract disease are common. Respiratory symptoms are mild when
compared with the extensive pneumonia confirmed by X-ray.1 Before antimicrobial agents
were available, 15 to 20 percent of persons with C. psittaci infection were reported to have
died.9
(6)
Incubation period. From 1 to 4 weeks.1
IV-8
(7)
Communicability. Rare person-to-person transmission has been reported.
Diseased as well as seemingly healthy birds may shed the agent intermittently, and
sometimes continuously, for weeks or months.1
(8)
Prevention. No vaccine is available.5
(9)
Delivery. The primary threat is from aerosol release.5
h. Shigellosis (Bacillary dysentery).
(1)
Infectious Agent. The genus Shigella (S.) is comprised of four species:
Group A, S. dysenteriae; Group B, S. flexneri, Group C, S. boydii, and Group D, S. sonnei.1
(2)
Occurrence. Worldwide.1
(3)
Reservoir. Man; however, some outbreaks have occurred in primate
colonies.1
(4)
Transmission. Transmission is mainly by direct or indirect fecal-oral
transmission from a patient or carrier. Infection may occur after the ingestion of very few
(10 to 100) organisms. Individuals primarily responsible for transmission are those who
fail to clean hands and under fingernails thoroughly after defecation. They may then
spread infection to others directly by physical contact or indirectly by contaminating food.
Water and milk transmission may occur as the result of direct fecal contamination; flies can
transfer organisms from latrines to uncovered food items.1
(5)
Symptoms. Symptoms involve the large and distal small intestine,
characterized by diarrhea accompanied by fever, nausea, and sometimes toxemia, vomiting,
cramps, and tenesmus. In typical cases, the stools contain blood, and mucus (dysentery);
however, many cases present with a watery diarrhea. S. dysenteriae 1 is often associated
with serious disease. Case-fatality rates have been as high as 20 percent among
hospitalized cases even in recent years.1
(6)
Incubation period. From 12 to 96 hours (usually 1 to 3 days) up to 1 week
for S. Dysenteriae 1.1
(7)
Communicability. During acute infection and until the infectious agent is
no longer present in the feces, usually within 4 weeks after illness.1
(8)
Prevention. Follow proper personal hygiene and field sanitation
procedures.1
(9)
Delivery. The primary threat would be contamination of food and water
supplies.
i.
Tularemia.
(1)
Infectious Agent. Francisella tularensis (F. tularensis).3 There are two
biovars: Jellison type A (F. tularensis biovar tularensis) and type B (F. tularensis biovar
palaerctica).1 The type A strain is highly virulent. Ten virulent organisms injected
subcutaneously and 10 to 50 organisms given by aerosol can cause infection in humans.10
(2)
Occurrence. Tularemia occurs throughout North America and in many
parts of continental Europe, the former Soviet Union, China, and Japan.1
IV-9
(3)
Reservoir. This organism is maintained in numerous and diverse
mammalian (rabbits, hares, and rodents) and tick reservoirs.3 In addition, a rodent-
mosquito cycle has been described.1
(4)
Transmission. Transmission is through the bite of arthropods (ticks and
deerflies, also mosquitoes in Sweden, Finland, and Russia), direct contact with infected
animals, aerosols generated by skinning/processing infected animals, and ingestion of
contaminated food or water.3
(5)
Symptoms. This bacterial disease has a variety of clinical manifestations
related to the route of introduction and the virulence of the disease agent. Most often it
presents itself as an ulcer at the site of introduction of the organism, together with swelling
of the regional lymph nodes. There may be no apparent primary ulcer, but only one or more
enlarged and painful lymph nodes. Ingestion of organisms in contaminated food or water
may produce painful pharyngitis, abdominal pain, diarrhea, and vomiting. Inhalation of
infectious material may be followed by pneumonic involvement with a 30 to 60 percent
case-fatality rate if untreated. Type A has a 5 to 15 percent untreated case-fatality rate,
and type B produces few fatalities even without treatment.1
(6)
Incubation period. Related to virulence of infecting strain and to size of
inoculum; the range is 1 to 14 days (usually 3 to 5 days).1
(7)
Communicability. Not directly transmitted from person to person. Unless
treated, the infectious agent may be found in the blood during the first 2 weeks of disease
and in lesions for a month, sometimes longer. Flies can be infective for 14 days and ticks
throughout their lifetime (about 2 years). Rabbit meat frozen at -15 degrees C (5 degrees
F) has remained infective longer than 3 years.1
(8)
Prevention. The protective mask provides protection of the respiratory
tract from exposure to aerosol organisms. All food must be thoroughly cooked to kill any
organisms before consumption. Water must be thoroughly disinfected before consumption.
A live attenuated vaccine is available.3
(9)
Delivery. The primary threat is by aerosol release or by contamination of
food or water supplies.3
j.
Typhoid Fever.
(1)
Infectious Agent. Salmonella typhi.1
(2)
Occurrence. Worldwide. The annual incidence of typhoid fever is estimated
at about 17 million cases with approximately 600 thousand deaths.1
(3)
Reservoir. Man.1
(4)
Transmission. Transmission is by food and water contaminated by feces
and urine of patients and carriers. Important vehicles in some parts of the world include
shellfish taken from sewage-contaminated beds (particularly oysters), raw fruits, vegetables
fertilized by human excrement and eaten raw, and contaminated milk and milk products.
Flies may infect foods where the organisms then multiply and achieve an infective dose.1
(5)
Symptoms. Systemic bacterial diseases characterized by insidious onset of
sustained fever, severe headache, malaise, loss of appetite, a relative bradycardia,
enlargement of the spleen, rose spots on the trunk, nonproductive cough, and constipation.
Prior to antibiotics the case-fatality rate was 10 to 20 percent.1
IV-10
(6)
Incubation period. The incubation period depends on the size of the
infecting dose; range is from 3 days to 1 month and usually between 8 to 14 days.1
(7)
Communicability. Person-to-person transmission is possible. The period of
communicability is as long as the bacilli appear in excreta, usually from the first week
throughout convalescence; variable thereafter. About 10 percent of untreated typhoid fever
patients will discharge bacilli for 3 months after the onset of symptoms, and 2 to 5 percent
become permanent carriers.1
(8)
Prevention. Following proper field sanitation and personal hygiene are
useful preventive measures. A vaccine is available.1
(9)
Delivery. The primary threat is from the sabotage of food and water
supplies and, secondly, by aerosol.5
3.
Rickettsiae of Potential Concern
The rickettsiae are intracellular, parasitic microorganisms that are considered
intermediate in size between the bacteria and viruses. They resemble the bacteria in their
shape and resemble the viruses in their strict growth requirements for living host cells.
Most rickettsiae are parasites, primarily of lower animals and arthropods. Rickettsiae are
transmitted to man and animals by vectors such as ticks, lice, fleas, and mites. The
rickettsiae have a selective affinity for specific types of cells of the human and animal
bodies. As they require living tissue for reproduction, they are considered parasites.2
Usually, they are easily killed by heat, dehydration, or disinfectants.
a.
Query (Q) Fever.
(1)
Infectious Agent. Coxiella burnetii (C. burnetii). Despite the fact that C.
burnetii is unable to grow or replicate outside host cells, there is a sporelike form of the
organism that is extremely resistant to heat, pressure, desiccation, and many standard
antiseptic compounds; this allows the organism to persist in the environment for long
periods (weeks or months) under harsh conditions.11
(2)
Occurrence. Worldwide.3
(3)
Reservoir. Sheep, goats, cattle, dogs, cats, some wild mammals, birds, and
ticks serve as reservoirs. Infected animals usually do not develop the disease, but shed
large numbers of organism in placental tissues and body fluids.1
(4)
Transmission. The organism is highly communicable by aerosol. A single
viable organism is enough to cause infection in humans.3 It is commonly transmitted by
airborne dissemination of coxiellae in dust from premises contaminated by placental
tissues, birth fluids, and excreta of infected animals; in establishments processing infected
animals or their byproducts; and in necropsy rooms. Airborne particles containing
organisms may be carried downwind for a considerable distance (one-half mile or more);
also by direct contact with infected animals and other contaminated materials such as wool,
straw, fertilizer, and laundry. Raw milk from infected cows contains organisms and may be
responsible for some cases, but this has not been proven. Direct transmission by blood or
marrow transfusion has been reported.1
(5)
Symptoms. Symptoms include fever, fatigue, chills, sweats, muscular pain,
and severe headache in 75 percent of cases.3 The case-fatality rate in untreated acute cases
is usually less than 1 percent, but has been reported as high as 2.4 percent.1
IV-11
(6)
Incubation period. Varies from 10 to 40 days and depends on the size of the
infecting dose.11
(7)
Communicability. Direct transmission from person to person occurs rarely,
if ever. However, contaminated clothing may be a source of infection.1 Coxiella organisms
may persist in the environment and produce infection for weeks or months.11
(8)
Prevention. The military protective mask provides protection from
aerosols. Consume only pasteurized dairy products, and heat all foods sufficiently to
destroy the organisms (see TB MED 530 for food preparation guidelines). An
investigational vaccine is being tested.11
(9)
Delivery. The primary threat is by aerosol or through contamination of
food.3
b.
Rocky Mountain Spotted Fever.
(1)
Infectious Agent. Rickettsia rickettsii.1
(2)
Occurrence. Infection has been documented throughout the US, in Canada,
western and central Mexico, Panama, Costa Rica, Colombia, Argentina, and Brazil.1
(3)
Reservoir. Maintained in nature in ticks. The rickettsiae can be
transmitted to dogs, various rodents, and other animals. Disease in rodents and dogs have
been observed.1
(4)
Transmission. Transmission is ordinarily from the bite of an infected tick.
At least 4 to 6 hours of attachment and feeding on blood by the tick are required before the
rickettsiae become reactivated and infectious for people. Contamination of breaks in the
skin or mucous membranes with crushed tissues or feces of the tick may also lead to
infection.1
(5)
Symptoms. This disease is characterized by sudden onset of moderate to
high fever (which ordinarily persists 2 to 3 weeks in untreated cases), significant malaise,
deep muscle pain, severe headache, and chills. A rash generally appears on the extremities
on about the third to fifth day; this soon includes the palms and soles and spreads rapidly
to much of the body. The fatality rate ranges between 13 to 25 percent in the absence of
specific therapy.1
(6)
Incubation period. From 3 to about 14 days.1
(7)
Communicability. Not directly transmitted from person to person. The tick
remains infective for life, commonly as long as 18 months.1
(8)
Prevention. Measures that can be taken to reduce the opportunity for
exposure include good field sanitation and use of insect repellents. No vaccine is available.1
(9)
Delivery. The primary threat would be from aerosol or from infected
vectors.5
c.
Trench Fever.
(1)
Infectious Agent. Bartonella quintana (formerly Rochalimaea Quintana).1
(2)
Occurrence. The organism probably can be found wherever the human
body louse exists. Epidemics occurred in Europe during World Wars I and II among troops
and prisoners of war living in crowded, unhygienic conditions.1
IV-12
(3)
Reservoir. Humans serve as reservoirs; the intermediate host and vector is
the body louse, Pediculus humanus corporis. The organism multiplies extracellularly in the
gut lumen for the duration of the insect’s life, which is approximately 5 weeks after
hatching.1
(4)
Transmission. The body louse is infected by feeding on the blood of an
infected patient. The infected louse excrete rickettsiae in their feces and usually defecate at
the time of feeding; people are infected by rubbing feces or crushed lice into the bite or into
superficial abrasions.1
(5)
Symptoms. Trench Fever is typically a nonfatal, bacterial disease varying
in manifestations and severity. It is characterized by headache, malaise, and pain and
tenderness—especially on the shins. Onset is either sudden or slow, with a fever that may
be relapsing, typhoid-like, or limited to a single episode lasting for several days.1
(6)
Incubation period. Generally 7 to 30 days.1
(7)
Communicability. Not directly transmitted from person to person.
Organisms may circulate in the blood (by which lice are infected) for weeks, months, or
years and may recur with or without symptoms.1
(8)
Prevention. Delousing procedures will destroy the vector and prevent
transmission to man. Dust clothing and body with an effective insecticide.1 Washing
sheets and clothing in hot water will eliminate the louse. Good hygiene will help prevent
this condition.
(9)
Delivery. The primary threat would be by aerosol release or infected vector.
d.
Typhus Fever (Epidemic Louse-Borne Typhus Fever).
(1)
Infectious Agent. Rickettsia prowazekii.1
(2)
Occurrence. In colder areas where people may live under unhygienic
conditions and are louse-infested; enormous and explosive epidemics may occur during war
and famine.1
(3)
Reservoir. Humans are the reservoirs and are responsible for maintaining
the infection between epidemic periods.1
(4)
Transmission. The body louse, Pediculus humanus corporis, is infected by
feeding on the blood of a patient with acute typhus fever. Infected lice excrete rickettsiae in
their feces and usually defecate at the time of feeding. People are infected by rubbing feces
or crushed lice into the bite or into superficial abrasions. Inhalation of infective louse feces
in dust may account for some infections.1
(5)
Symptoms. Symptoms have variable onsets, often are sudden, and are
marked by headache, chills, exhaustion, fever, and general pains. A macular eruption
appears on the fifth to sixth day, initially on the upper trunk, followed by spreading to the
entire body (but usually not to the face, palms, or soles). The case-fatality rate increases
with age and varies from 10 to 40 percent in the absence of specific therapy.1
(6)
Incubation period. From 1 to 2 weeks, commonly 12 days.1
(7)
Communicability. No direct person-to-person transmission. Patients are
infective for lice during the febrile illness and possibly for 2 to 3 days after the temperature
returns to normal. Infected lice pass rickettsiae in their feces within 2 to 6 days after the
IV-13
blood meal; it is infective earlier if crushed. The louse invariably dies within 2 weeks after
infection; rickettsiae may remain viable in the dead louse for weeks.1
(8)
Prevention. Dust clothing and body with an effective insecticide.1 No
vaccine is available.5 Washing sheets and clothing in hot water will eliminate the louse.
Good hygiene will help prevent this condition.
(9)
Delivery. The primary threat would be by aerosol release or infected
vectors.5
4.
Viral Agents of Potential Concern
The groups of microorganisms called viruses are all parasites that live in the cells of
their selected hosts. Viruses cause about 60 percent of all infectious diseases. Once a virus
enters a living cell, it is capable of replicating itself by taking over the metabolic processes
of the invaded cell. Cells infected with viruses show one of the following responses:
degeneration and death, transformation to a nonfunctioning state, or survival without
transformation but with the evidence of the presence of one or more viral components.
Diseases of viral origin do not respond to treatment with antibiotics.2 Viruses have primary
military potential as antipersonnel agents.
a.
Chikungunya Virus Disease.
(1)
Infectious Agent. Chikungunya Virus (alphavirus).1
(2)
Occurrence. This virus is found in Africa, India, southeast Asia, and the
Philippine Islands.1
(3)
Reservoir. The reservoir is unknown for most viruses. An insect (mosquito)
reservoir is a possibility.1
(4)
Transmission. Mosquitoes transmit the virus.1
(5)
Symptoms. The usual onset of symptoms is characterized by arthalgia
(severe pain in a joint, especially one not inflammatory) or arthritis, primarily in the wrist,
knee, ankle, and small joints of the extremities, which lasts from days to months. Rashes
are common. Polyarthritis is a characteristic feature. Minor hemorrhages have been
attributed to this virus.1
(6)
Incubation period: From 3 to 11 days.1
(7)
Communicability. No direct person-to-person transmission.1
(8)
Prevention. Insecticides and proper field sanitation are examples of
preventive measures.1 An experimental vaccine is being tested.5
(9)
Delivery. The likely method of dissemination is aerosol.5
b.
Crimean-Congo Hemorrhagic Fever Virus (HFV).
(1)
Infectious Agent. Crimean-Congo HFV, genus Nairovirus.1
(2)
Occurrence. Observed in regions of Russia as well as in Albania and
Bosnia-Herzogovina, Bulgaria, Iraq, the Arabian Peninsula, Pakistan, western China,
tropical Africa, and South Africa.1
(3)
Reservoir. In nature, hares, birds and ticks in Eurasia and South Africa
are believed to be reservoirs; reservoir hosts remain undefined in tropical Africa, but ticks,
IV-14
insectivores, and rodents may be involved. Domestic animals (sheep, goats, and cattle) may
act as amplifying hosts.1
(4)
Transmission. Transmission is by a bite of infective adult ticks. Immature
ticks are believed to acquire infection from the animal hosts and by transovarian
transmission. Transmission from patients to medical workers after exposure to blood and
secretions has been important in recent outbreaks. Infection is also associated with
butchering infected animals.1
(5)
Symptoms. This is a disease with sudden onset of fever, malaise,
weakness, irritability, headache, severe pain in limbs and loins, and marked anorexia.
Vomiting, abdominal pain, and diarrhea occur occasionally. Flush on face and chest
develops early. There may be some bleeding from gums, nose, lungs, uterus, and intestine,
but in large amounts only in serious or fatal cases. Fever is constantly elevated for 5 to 12
days. The reported case fatality rate ranges from 2 to 50 percent.1
(6)
Incubation period. Range is from 1 to 12 days, usually 1 to 3 days.1
(7)
Communicability. Moderate person-to-person transmission.5
(8)
Prevention. Insecticides and proper field sanitation are examples of
preventive measures.1 An experimental vaccine is available.5
(9)
Delivery. Aerosol is the likely method of dissemination.5
c.
Dengue Fever.
(1)
Infectious Agent. Dengue-1, Dengue-2, Dengue-3, and Dengue-4. They are
all flaviviruses.1
(2)
Occurrence. Most countries in the tropics, Africa, Saudi Arabia, and the
Americas.1
(3)
Reservoir. The viruses are maintained in a human mosquito cycle in
tropical urban centers; a monkey mosquito cycle serves as a reservoir in southest Asia and
west Africa.1
(4)
Transmission. By the bite of infective mosquitoes.1
(5)
Symptoms. An acute febrile viral disease that is characterized by sudden
onset, fever for 3 to 5 days, intense headache, myalgia, arthralgia, retro-orbital pain,
anorexia, GI disturbances, and rash. Minor bleeding may occur. Epidemics are explosive,
but fatalities in the absence of dengue hemorrhagic fever are rare.1
(6)
Incubation period. From 3 to 14 days, commonly 4 to 7 days.1
(7)
Communicability. Not directly transmitted from person to person.
Patients are infective for mosquitoes from shortly before to the end of the febrile period,
usually a period of 3 to 5 days. The mosquito becomes infective 8 to 12 days after the
viremic blood meal and remains so for life.1
(8)
Prevention. Use screening, protective clothing, and repellents and try to
eliminate breeding grounds.1 An experimental vaccine is available.5
(9)
Delivery. The primary threat is delivery by aerosol release.5
d.
Eastern and Western Equine Encephalitis (EEE and WEE), Japanese
Encephalitis (JE).
IV-15
(1)
Infectious Agent. A specific virus causes each disease; EEE and WEE are
caused by alphaviruses and JE by a flavivirus.1
(2)
Occurrence. The EEE is recognized in eastern and north central US,
Canada, Central and South America, and the Caribbean islands; WEE occurs in western
and central US, Canada, and parts of South America. The JE occurs in western Pacific
islands from Japan to the Philippines.1
(3)
Reservoir. The true reservoir or means of winter carryover for these
viruses is unknown—possibly birds, rodents, bats, reptiles, and/or amphibians; or it
survives in mosquito eggs or adult mosquitoes, with the mechanisms probably differing in
each virus.1
(4)
Transmission. Transmission is from the bite of infective mosquitoes.1
(5)
Symptoms. Symptoms of these diseases are similar, but vary in severity
and rate of progress. A large percentage of patients with vector-borne infections are either
asymptomatic or present with a nonspecific febrile illness or aseptic meningitis.12 Severe
infections are usually marked by acute onset, headache, high fever, stupor, disorientation,
coma, tremors, occasional convulsions, and spastic (but rarely flaccid) paralysis. Case-
fatality rates range from 0.3 to 60 percent (JE and EEE among the highest).1
(6)
Incubation period. Usually 5 to 15 days.1
(7)
Communicability. Not directly transmitted from person to person. Virus is
not usually demonstrable in the blood of humans after onset of the disease. Mosquitoes
remain infective for life. Viremia in birds usually lasts 2 to 5 days, but may be prolonged in
bats, reptiles, and amphibians, particularly if interrupted by hibernation. Humans and
horses are uncommon sources of mosquito infection.1
(8)
Prevention. Use screening, protective clothing, and repellents, and try to
eliminate breeding grounds. Vaccines are available.1
(9)
Delivery. The primary threat would be delivery from aerosol release.6
e.
Ebola Viral Hemorrhagic Fever (VHF) and Marburg Viral Disease.
(1)
Infectious Agent. The Ebola virus and the Marburg virus are in the
Filoviridea group.1
(2)
Occurrence. Confirmed cases of Ebola VHF have been reported in the
Democratic Republic of the Congo, Gabon, Sudan, the Ivory Coast, Uganda, and the
Republic of the Congo.13 Marburg disease was found in Germany and Yugoslavia after
exposure to green monkeys from Uganda, Zimbabwe, Kenya, and the Democratic Republic
of the Congo.1
(3)
Reservoir. Unknown despite extensive studies.1
(4)
Transmission. Person-to-person transmission occurs by direct contact with
infected blood, secretions, organs, or semen.1
(5)
Symptoms. These diseases are usually characterized by sudden onset with
malaise, fever, myalgia, headache, and pharyngitis, followed by vomiting, diarrhea, rash,
and hemorrhagic diathesis. Approximately 25 percent of reported primary cases of
Marburg virus infection have been fatal; case-fatality rates of Ebola infections have ranged
from 50 to nearly 90 percent.1
IV-16
(6)
Incubation period. Ebola—2 to 21 days; Marburg—3 to 9 days.1
(7)
Communicability. Person-to-person transmission is possible as long as
blood and secretions contain the virus.1
(8)
Prevention. No vaccines are available.5
(9)
Delivery. The primary threat would be delivery from aerosol release.5
f.
Far Eastern Tick-Borne Encephalitis (Russian Spring-Summer Encephalitis).
(1)
Infectious Agent. A complex within the flaviviruses.1
(2)
Occurrence. The disease is distributed spottily over much of the former
Soviet Union, other parts of eastern and central Europe, Scandinavia, and the United
Kingdom (UK). Areas of highest incidence are those where humans have intimate
association with large numbers of infected ticks, generally in rural or forested areas, but
also in some urban populations.1
(3)
Reservoir. Ticks, or ticks and mammals in combination, appear to be the
true reservoir. Rodents, other mammals, or birds serve as sources of tick infections.1
(4)
Transmission. By the bite of infective ticks or by consumption of milk from
certain infected animals.1
(5)
Symptoms. This is a viral disease clinically resembling the mosquito-borne
encephalitides (EEE, WEE, and JE). Symptoms also include focal epilepsy and flaccid
paralysis (particularly of the shoulder girdle).1
(6)
Incubation period. Usually 7 to 14 days.1
(7)
Communicability. No direct person-to-person transmission. A tick infected
at any stage remains infective for life. Viremia in a variety of vertebrates may last for
several days; in humans, up to 7 to 10 days.1
(8)
Prevention. Preventive measures can include effective personal hygiene,
field sanitation, and insect control.1 A vaccine is available.6
(9)
Delivery. The likely method of dissemination is aerosol or through milk.5
g.
Hantaviral Disease (Korean Hemorrhagic Fever [KHF]).
(1)
Infectious Agent. Hantaviruses, a genus of the Bunyaviridae family.1 The
prototype virus from this group, Hantaan, is the cause of the KHF.14
(2)
Occurrence. Worldwide.1
(3)
Reservoir. Field rodents; man is an accidental host.1
(4)
Transmission. Aerosol transmission from rodent excreta is presumed
(aerosol infectivity has been demonstrated experimentally). Virus is present in urine, feces,
and saliva of persistently infected rodents; highest virus concentration is found in the
lungs.1
(5)
Symptoms. An acute viral disease characterized by an abrupt onset of
fever, lower back pain, varying degrees of hemorrhagic manifestations, and renal
involvement. The case fatality rate is variable, but generally ranges from 5 to 15 percent.1
IV-17
(6)
Incubation period. As short as a few days, as long as nearly 2 months, but
usually 2 to 4 weeks.1
(7)
Communicability. Not well-defined. Person-to-person transmission is
rare.1
(8)
Prevention. Follow rodent control procedures. Experimental vaccine is
available.5
(9)
Delivery. The primary threat would be delivery from aerosol release.5
h. Junin Hemorrhagic Fever (Argentine Disease) and Machupo Hemorrhagic Fever
(Bolivian Disease).
(1)
Infectious Agent. Junin virus for the Argentine disease and closely related
Machupo virus for the Bolivian disease.1
(2)
Occurrence. Junin virus in Argentina and Machupo virus in northeastern
Bolivia.1
(3)
Reservoir. Rodents.1
(4)
Transmission. Airborne transmission may occur via dust contaminated
with infected rodent excreta; both saliva and excreta of infected rodents contain the virus.
Abraded skin may also be a portal of entry for infection.1
(5)
Symptoms. Acute febrile viral illnesses. The onset is gradual with malaise,
headache, retro-orbital pain, sustained fever, and sweats, followed by prostration. Case
fatality rates range from 15 to 30 percent or more.1
(6)
Incubation period: Usually 7 to 16 days.1
(7)
Communicability. Not often directly transmitted from person to person.1
(8)
Prevention. Follow rodent control procedures. A live-attenuated vaccine is
currently in field trials (unlicensed in the US).1
(9)
Delivery. The primary threat would be delivery from an aerosol release.
i.
Lassa Fever.
(1)
Infectious Agent. Lassa virus.1
(2)
Occurrence. Africa.1
(3)
Reservoir. Wild rodents.1
(4)
Transmission. Primarily through aerosol or direct contact with excreta of
infected rodents deposited on surfaces such as floors, beds, or in food and water. Person-to-
person and laboratory infections occur by direct contact with blood, pharyngeal secretions,
or urine, or by sexual contact.1
(5)
Symptoms. Lassa fever is an acute viral illness of 1 to 4 weeks duration.
Onset is gradual with malaise, fever, headache, sore throat, cough, nausea, vomiting,
diarrhea, myalgia, and chest and abdominal pain. Fever is persistent or intermittently
spiking. In severe cases, hemorrhage, seizures, and edema of the face and neck are
frequent. The Case-fatality rate is about 15 percent among hospitalized cases.1
(6)
Incubation period. Commonly 6 to 21 days.1
IV-18
(7)
Communicability. Person-to-person transmission spread may occur during
the acute febrile phase when the virus is present in the throat. The virus may be excreted
in the urine of patients for 3 to 9 weeks from onset of illness.1
(8)
Prevention. Follow specific rodent control procedures.1 No vaccine is
available.5
(9)
Delivery. The primary threat would be delivery from aerosol release.5
j.
Lymphocytic Choriomeningitis.
(1)
Infectious Agent. Lymphocytic choriomeningitis virus, an arenavirus.1
(2)
Occurrence. Not uncommon in Europe and the Americas.1
(3)
Reservoir. The infected house mouse is the natural reservoir.1
(4)
Transmission. Virus is excreted in urine, saliva, and feces of infected
animals—usually mice. Transmission to humans is probably through oral or respiratory
contact with virus-contaminated excreta, food, or dust or by contamination of skin lesions or
cuts.1
(5)
Symptoms. This disease is a viral infection of animals, especially mice,
transmissible to humans, with a marked diversity of clinical manifestations. At times,
there may be influenza-like symptoms, with myalgia and headache. The acute course is
usually short, very rarely fatal.1
(6)
Incubation period. Probably 8 to 13 days, 15 to 21 days until meningeal
symptoms appear.1
(7)
Communicability. Transmission from person to person has not been
demonstrated and is unlikely. Infected female mice transmit infection to the offspring,
which become asymptomatic persistent viral shedders.1
(8)
Prevention. Field hygiene and personal hygiene are effective individual
measures.1
(9)
Delivery. The primary threat would be delivery from an aerosol release.
k.
Monkeypox.
(1)
Infectious Agent. Monkeypox virus; it belongs to the genus orthopoxvirus,
which includes the smallpox virus (variola), the virus used in the smallpox vaccine
(vaccinia), and the cowpox virus.15
(2)
Occurrence. The rain forest countries of central and western Africa and the
US.16
(3)
Reservoir. Studies suggest several species of squirrels and Gambian rats in
Africa16 and pet prairie dogs in the US may be animal reservoirs.15 Other animals may be
possible reservoirs.16 Rats, mice, and rabbits can get monkeypox.13
(4)
Transmission. Limited data on the transmission of monkeypox virus are
available from studies conducted in Africa. Person-to-person transmission is believed to
occur primarily through direct contact and also by respiratory droplet spread. Airborne
transmission cannot be excluded, especially in patients presenting with cough.17
IV-19
(5)
Symptoms. In humans, the symptoms are similar to those of smallpox, but
usually milder. The illness begins with fever, headache, muscle aches, backache, swollen
lymph nodes, a general feeling of discomfort, and exhaustion. A papular rash develops,
often first on the face. The lesions usually develop through several stages before crusting
and falling off. In Africa, the reported case-fatality rate is 10 percent.15
(6)
Incubation period. About 12 days.15
(7)
Communicability. The Centers for Disease Control and Prevention (CDC)
suggests there is a relatively low risk of person-to-person transmission.17
(8)
Prevention. Because the monkeypox virus is related to the virus that
causes smallpox, the smallpox vaccine can protect people from getting monkeypox as well
as smallpox.18
(9)
Delivery. The likely method of dissemination is an aerosol release.
l.
Rift Valley Fever (RVF).
(1)
Infectious Agent. RVF Virus (RVF is a phlebovirus).1
(2)
Occurrence. This virus is found in Africa.1
(3)
Reservoir. Unknown.1
(4)
Transmission. Mosquitoes transmit the virus. Many human infections of
RVF are associated with handling infective material of animal tissues during autopsy and
butchering. Mechanical transmission by flies and transmission by aerosols or contact with
highly infective blood may contribute to the explosive nature of RVF outbreaks.1
(5)
Symptoms. The usual onset is fever, headache, malaise, arthralgia,
myalgia, occasional nausea and vomiting, and generally some conjunctivitis and
photophobia. Encephalitis, hemorrhage, or retinitis may develop.1
(6)
Incubation period. Usually 3 to 12 days.1
(7)
Communicability. No direct person-to-person transmission. Infected
mosquitoes probably transmit the virus throughout life. Epidemics may involve thousands
of people.1
(8)
Prevention. Insecticides, field sanitation, and personal hygiene are
examples of preventive measures. Precautions in the care and handling of infected animals
and their products are important.1 A vaccine is available.5
(9)
Delivery. The likely method of dissemination is aerosol or through infected
vectors.5
m. Smallpox. In response to concerns that variola stocks may by needed for
counterterrorism research in the event that clandestine stocks held by other countries fall
into terrorist hands, the World Health Assembly (WHA), in May 1999, authorized that the
virus be held at laboratories in the US and Russia until no later than 2002. The World
Health Organization (WHO) reaffirmed that destruction of all the remaining virus stocks is
still the organization’s ultimate goal and will appoint a group of experts to consider what
research needs to be carried out before the virus can be destroyed. The WHO will also set
up an inspection schedule for the two laboratories where the official stocks are kept to make
sure that they are secure and that research can be carried out safely.1
IV-20
(1)
Infectious Agent. Variola virus, a species of Orthopoxvirus.1
(2)
Occurrence. Formerly, smallpox was a worldwide disease. The last
naturally acquired case of smallpox occurred in October 1977 in Somalia; global eradication
was certified two years later by the WHO and sanctioned by the WHA in May 1980.1
(3)
Reservoir. Humans were the only natural reservoir of variola. All known
variola virus stocks are held under security at the CDC, Atlanta, Georgia, or the State
Research Center (SRC) of Virology and Biotechnology, Koltsovo, Novosibirsk Region,
Russian Federation (RF).3
(4)
Transmission. Usually by respiratory droplet transmission, following close
face-to-face contact. Smallpox was also transmitted by direct contact with skin lesions or
drainage, or with contaminated objects. Although uncommon, airborne transmission (long-
distance) also occurred.3
(5)
Symptoms. Smallpox was a systemic viral disease that generally presented
with a characteristic skin eruption. Onset was sudden, with fever, malaise, headache,
prostration, severe backache, and occasional abdominal pain and vomiting—a clinical
picture that resembled influenza. After 2 to 4 days, the fever began to fall and a deep-
seated rash developed in which individual lesions containing infectious virus progressed
through successive stages of macules, papules, vesicles, pustules, and crusted scabs, which
fell off after 3 to 4 weeks. The lesions were first evident on the face and extremities and
subsequently on the trunk. Two epidemiologic types of smallpox were recognized during
the twentieth century: variola minor (alastrim), which had a case-fatality rate of less than
1 percent, and variola major (ordinary) with a fatality rate among unvaccinated populations
of 20 to 40 percent or more. Fatalities normally occurred in 5 to 7 days, occasionally as late
as the second week.1
(6)
Incubation period. From 7 to 19 days; commonly 10 to 14 days to onset of
illness and 2 to 4 days more to onset of rash.1
(7)
Communicability. Smallpox is very contagious from the time of
development of the earliest lesions to disappearance of all scabs—about 3 weeks. The
patient is most contagious during the pre-eruptive period by aerosol droplets from lesions.1
(8)
Prevention. There are no routine immunizations of US forces for smallpox.
When the threat indicates, senior leadership may direct vaccination of personnel with
vaccinia.3
(9)
Delivery. The primary threat is delivery by aerosol release.3
n. Venezuelan Equine Encephalitis.
(1)
Infectious Agent. VEE virus (alphavirus).3
(2)
Occurrence. Present in northern South America, Trinidad, and Central
America.1
(3)
Reservoir. During outbreaks, VEE virus is transmitted in a cycle involving
horses—which serve as the major source of the virus—to mosquitoes, which in turn infect
humans. Humans also serve as hosts in a human-to-mosquito-to-human transmission
cycle.1
(4)
Transmission. By the bite of an infected mosquito; laboratory infections by
aerosol are common.1
IV-21
(5)
Symptoms. Clinical manifestations of this viral infection are influenza-like,
with an abrupt onset of severe headache, chills, fever, myalgia, retro-orbital pain, nausea,
and vomiting. Most infections are relatively mild, with symptoms lasting from 3 to 5 days.
There may be CNS involvement ranging from somnolence to disorientation, convulsions,
paralysis, coma, and death.1
(6)
Incubation period. Usually 2 to 6 days, can be as short as 1 day.1
(7)
Communicability. Low risk of person-to-person transmission.5 Infected
humans and horses are infectious for mosquitoes for up to 72 hours; infected mosquitoes
probably transmit the virus throughout life.1
(8)
Prevention. Use general mosquito control procedures.1 Vaccine is
available.5
(9)
Delivery. The primary threat is by aerosol release or through infected
vectors.5
o.
Yellow Fever.
(1)
Infectious Agent. Yellow Fever Virus of the genus Flavivirus.1
(2)
Occurrence. Sylvatic type: tropical regions of Africa and Latin America.
Urban type: North, Central, and South America, and Trinidad.1
(3)
Reservoir. Sylvatic: vertebrates other than humans—mainly monkeys,
possibly marsupials, and mosquitoes. Urban: humans and mosquitoes.1
(4)
Transmission. Sylvatic: from infective monkey to mosquito to man. Urban:
from the bite of an infective mosquito.1
(5)
Symptoms. Typical attacks are characterized by a sudden onset of fever,
chills, headache, backache, generalized muscle pain, prostration, nausea, and vomiting.
Jaundice is moderate early in the disease and is intensified later.1
(6)
Incubation period. From 3 to 6 days.1
(7)
Communicability. No person-to-person transmission.5 Blood of patients is
infective for mosquitoes shortly before onset of fever and for the first 3 to 5 days of illness.
The disease is highly communicable where many susceptible people and abundant vector
mosquitoes co-exist. The incubation period in mosquitoes is commonly 9 to 12 days at the
usual tropical temperatures. Once infected, mosquitoes remain so for life.1
(8)
Prevention. A vaccine is available.5
(9)
Delivery. The likely method of dissemination is aerosol.5
5. Toxins of Potential Concern
Toxins are poisonous byproducts of living organisms. They are very stable and
produce severe illness when ingested, inhaled, or introduced into the body by any other
means. Some toxins are susceptible to heat, while others are heat-stable. Their effects on
the human body range from minor illness to death.3
a.
Botulinum Toxins.
(1)
Toxin Origin. Botulinum toxins are a group of seven toxins produced by
Clostridium (C.) botulinum. The spores are ubiquitous; they germinate to give rise to
IV-22
vegetative bacteria that produce toxins during anaerobic incubation. Industrial-scale
fermentation can produce large quantities of toxins for use as a BW agent. There are three
forms of naturally occurring botulism—food-borne, infantile, and wound. Botulinum toxin
is the most potent neurotoxin known.3
(2)
Occurrence. Worldwide.1
(3)
Reservoir. The reservoirs are soil, animals, and fish. The organisms can be
recovered from honey and other agriculture products. High-risk foods are primarily
improperly canned foods and dried meat or fish.3
(4)
Transmission. Transmission is from consumption of contaminated food or
contamination of a wound by ground-in soil or gravel.1
(5)
Symptoms. The autonomic features of botulism are typical anticholinergic
signs and symptoms: dry mouth, ileus, constipation, and urinary retention. Nausea and
vomiting can occur. Dilated pupils occur in approximately 50 percent of cases. The motor
complications of botulism feature a descending paralysis leading to blurred vision and,
eventually, respiratory failure may occur. Symptoms usually begin 12 to 36 hours following
intoxication; time can vary according to the amount of toxin absorbed and could be reduced
to hours following a BW attack.3 The case-fatality rate in the US for food-borne botulism is
5 to 10 percent.1
(6)
Incubation period. The incubation period for food-borne botulism is usually
24 to 36 hours; for wound botulism it is usually 3 or more days.3
(7)
Communicability. No person-to-person transmission.6
(8)
Prevention. The vaccine currently available is used under Investigational
New Drug (IND) status.19
(9)
Delivery. The primary threats are by sabotage of food and water supply
and by aerosol release.5
b.
Clostridium Perfringens (C. perfringens) Toxins.
(1)
Toxin Origin. C. perfringens is a common anaerobic bacillus that produces
at least 12 toxins.3
(2)
Occurrence. Worldwide.3
(3)
Reservoir. The reservoirs are soil and the GI tract of healthy people and
animals.3
(4)
Transmission. Transmission is by the ingestion of food that was
contaminated by soil or feces and then held under conditions that permit multiplication of
the organism. Almost all outbreaks are associated with inadequately heated or reheated
meats. Spores survive cooking and then germinate and multiply in storage at ambient
temperatures, slow cooling, or inadequate rewarming.1 Gas gangrene results from wound
contamination with soil containing spores.3
(5)
Symptoms. Gas gangrene features pathological death of skeletal muscles
and overlying soft tissue and constitutes a surgical emergency.3 Food poisoning is an
intestinal disorder characterized by sudden onset of colic followed by diarrhea; nausea is
common, but vomiting and fever are usually absent. Generally, it is a mild disease of short
duration, one day or less, and rarely fatal in healthy persons.1
IV-23
(6)
Incubation period. The incubation period is 1 to 6 hours.3
(7)
Communicability. No person-to-person transmission.5
(8)
Prevention. Educate food handlers.1 No vaccine is available.5
(9)
Delivery. The primary threat is delivery of C. perfringens alpha toxin as an
aerosol to the respiratory tract. This would result in pulmonary disease, vastly different
from the naturally occurring diseases associated with C. perfringens. The toxin may also be
delivered in combination with other toxins to produce a variety of effects.3
c.
Conotoxins.
(1)
Toxin Origin. Conotoxins are a neurotoxin from the mollusks of the genus
Conus, commonly known as cone snails. There are potentially over 50,000 different
conotoxins present in the venoms of species in the genus Conus.20
(2)
Occurrence. These cone snails live in intertidal regions of the Indian and
Pacific Oceans, east to Hawaii, north to Japan, and south to New Zealand and Australia.20
(3)
Reservoir. Cone snails.20
(4)
Transmission. Conotoxins are injected by the sting of a cone snail.17
(5)
Symptoms. The sting produces a small, deep, triangular puncture wound.
Pain results immediately, ranging from mild to severe, followed by numbness and swelling
at the point of envenomation. Nausea, vomiting, difficulty swallowing, malaise, and
weakness may occur. Paralysis of the respiratory muscles might cause the airway to
collapse. The heart may beat irregularly. Neurological effects may include impaired
coordination, decreased visual acuity, altered level of consciousness, diminished or absent
reflexes, and paralysis. The untreated case-fatality rate is 70 percent.20
(6)
Incubation period. Symptoms begin immediately.20
(7)
Communicability. No person-to-person transmission.
(8)
Prevention. No specific antivenom exists.20
(9)
Delivery. The likely dissemination is by respirable aerosols or
contamination of food or water supply.19
d.
Diarrhea Caused by Enterohemorrhagic (EHEC) Strains (Shiga toxin-producing
E. coli [STEC], E. coli O157:H7, Verotoxin-producing E. coli [VTEC]).
(1)
Toxin Origin. The main EHEC serotype in North America is E. coli
O157:H7. This category of diarrheogenic E. coli produces cytotoxins. Previously, these
toxins were called Verotoxins 1 and 2 or Shiga-like toxins I and II.1
(2)
Occurrence. These infections are now recognized to be an important
problem in North America, Europe, South Africa, Japan, South America, and Australia.1
(3)
Reservoir. Cattle are the most important reservoir; however, humans may
also serve as a reservoir for person-to-person transmission. There is increasing evidence in
North America that deer may also serve as a reservoir.1
(4)
Transmission. Transmission occurs mainly by ingestion of contaminated
food. It is most often due to inadequately cooked beef (especially ground beef), raw milk,
IV-24
and fruit or vegetables contaminated with ruminant feces. Waterborne transmission has
been documented. Transmission also occurs directly from person to person.1
(5)
Symptoms. The diarrhea may range from mild and nonbloody to stools that
are virtually all blood but no fecal leukocytes. Approximately 2 to 7 percent of subjects
develop hemolytic uremic syndrome.1
(6)
Incubation period. Ranges from 2 to 8 days, with a median of 3 to 4 days.1
(7)
Communicability. Person-to-person transmission is possible. The duration
of excretion of the pathogen is typically a week or less in adults. Prolonged carriage is
uncommon.1
(8)
Prevention. Field sanitation and personal hygiene are useful tools to help
prevent exposure.1
(9)
Delivery. The likely method of dissemination is by respirable aerosols or
contamination of food or water supply.19
e.
Microcystin.
(1)
Toxin Origin. Common species of the blue-green algae that produce
microcystins include Anabaena, Nostoc, Oscillatoria, Hapalosiphon, and Microcystic. Their
structural class is cyanobacteria. Freshwater cyanobacteria accumulate in surface water
supplies and appear as blue-green “scums.”21 For microcystin, unlike most toxins, the
toxicity is the same, no matter what the route of exposure.22 Microcystin is extremely
stable and resistant to chemical hydrolysis or oxidation and remain potent even after
boiling.23
(2)
Occurrence. Worldwide.23
(3)
Reservoir. Blue-green algae.22
(4)
Transmission. Drinking or swimming in contaminated water. Very limited
available information suggests that inhalation in aerosols may be an equally important
route of exposure.23
(5)
Symptoms. Microcystin cause gastroenteritis.20 It is a membrane-
damaging toxin. Unless uptake of the toxin by the liver is blocked, irreversible damage to
the organ occurs within 15 to 60 minutes after exposure to a lethal dose. When this
happens, the tissue damage to the liver is so severe that therapy may have little or no
value.22
(6)
Incubation period. Data not available.
(7)
Communicability. In natural waters and in the dark, microcystins may
persist for months or years.23
(8)
Prevention. Data not available.
(9)
Delivery. The likely method of dissemination is by respirable aerosol or
contamination of food and water supply.
f.
Ricin.
(1)
Toxin Origin. Ricin is a potent cytotoxin derived from the beans of the
castor plant (Ricinus communis). Large quantities of ricin are easily and inexpensively
produced. Ricin toxins are potent inhibitors of DNA replication and protein synthesis.3
IV-25
(2)
Occurrence. N/A.
(3)
Reservoir. Castor beans.3
(4)
Transmission. Transmission has been by inhalation of organism during
industrial operations and ingestion of castor bean meal.3
(5)
Symptoms. The clinical signs, symptoms, and pathological manifestations
of ricin toxicity vary with the dose and the route of exposure. Inhalation results in
respiratory distress and airway and pulmonary lesions; ingestion causes GI signs and GI
hemorrhage with necrosis of liver, spleen, and kidneys; and intramuscular intoxication
causes severe localized pain, muscle and regional lymph node necrosis, and moderate
involvement of the visceral organs.24
(6)
Incubation period. From 18 to 24 hours.3
(7)
Communicability. No person-to-person transmission.3
(8)
Prevention. Candidate vaccines are under development.3
(9)
Delivery. The primary threat is delivery by aerosol release. A large
quantity is required to cover a significant area on a battlefield; however, it can be used for
small-scale operations. The agent may also be delivered through contamination of food and
water supplies.3
g.
Saxitoxin.3
(1)
Toxin Origin. Saxitoxin is the parent compound of a group of related
neurotoxins produced by marine dinoflagellates of the genus Gonyaulax.
(2)
Occurrence. N/A.
(3)
Reservoir. Shellfish.
(4)
Transmission. Saxitoxin is transmitted to humans by ingesting bivalve
mollusks, which accumulate dinoflagellates during filter feeding.
(5)
Symptoms. Paralytic shellfish poisoning (PSP) is a severe, life-threatening
neuromuscular condition. Saxitoxin is rapidly absorbed from the GI tract following
ingestion of contaminated shellfish. Symptoms begin as early as 10 minutes to several
hours after ingestion, depending on the ingested dose and host factors. Initial symptoms
include numbness and tingling of the lips, tongue, and fingertips followed by numbness of
the neck and extremities and motor incoordination. Other symptoms may include light-
headedness, dizziness, weakness, confusion, memory loss, and headache. Flaccid paralysis
and respiratory failure are life-threatening complications and occur within 2 to 12 hours
after ingestion. Supportive care is essential.
(6)
Incubation period. Minutes to hours.
(7)
Communicability. No person-to-person transmission.
(8)
Prevention. No vaccine is available.
(9)
Delivery. The primary threat is delivery by aerosol release. Saxitoxin may
also be delivered by projectiles or by contamination of food and water.
h. Staphylococcal Enterotoxin B.
IV-26
(1)
Toxin Origin. Staphylococcal enterotoxin B (SEB) is one of numerous
exotoxins produced by Staphylococcus (S.) aureus. The SEB toxin is heat-stable and is the
second most common source of outbreaks of food poisoning.3
(2)
Occurrence. Worldwide and relatively frequent.1
(3)
Reservoir. The reservoirs of S. aureus are humans and contaminated milk
and milk products. The SEB is usually produced in foods contaminated with S. aureus.3
(4)
Transmission. Ingestion of food, milk, or milk products containing
preformed toxin.3
(5)
Symptoms. Symptoms include the acute onset of fever, nausea, vomiting,
and diarrhea within hours of intoxication. Illness due to inhalation will result in
respiratory tract disease not encountered in the endemic disease. Symptoms may also
occur in the GI tract due to inadvertent swallowing of SEB delivered via aerosol and
deposited in the upper aero-digestive tract.3
(6)
Incubation period. Variable, 4 to 10 hours for GI illness.3
(7)
Communicability. No person-to-person transmission.3
(8)
Prevention. Follow strict food hygiene and sanitation controls.1 Protecting
food and water supplies from contamination and avoiding potentially contaminated food
and water will protect individuals from the effects of ingested toxins. No vaccine is
available.3
(9)
Delivery. The primary threat is SEB aerosol release. The SEB may also be
employed by sabotage contamination of food and/or water supplies.5
i.
Tetrodotoxin (Puffer Fish Poisoning).
(1)
Toxin Origin. The causative toxin is tetrodotoxin, a heat-stable, nonprotein
neurotoxin1 that even in small amounts can cause rapid and violent death in humans.17
(2)
Occurrence. Majority of cases occur in Japan where puffer fish is a
traditional delicacy.20
(3)
Reservoir. A variety of marine species—notably the puffer fish, California
newt,20 porcupine fish, ocean sunfish, and species of newts and salamanders.1
(4)
Transmission. Poisoning results from consuming tetrodotoxin.20
(5)
Symptoms. Puffer fish poisoning is characterized by onset of paresthesias,
dizziness, GI symptoms, and ataxia, which often progresses rapidly to paralysis and death
within several hours after eating. The case-fatality rate approaches 60 percent.1
(6)
Incubation period. Symptoms can appear 20 minutes to 3 hours after toxin
is introduced. Death can occur 4 to 6 hours after introduction.20
(7)
Communicability. No person-to-person transmission.20
(8)
Prevention. There is no specific antidote available.20 Avoid ingesting any
of the fish or amphibians that produce tetrodotoxin.1
(9)
Delivery. The likely method of dissemination is by respirable aerosols or
contamination of food or water supply.22
j.
Trichothecene Mycotoxins.
IV-27
(1)
Toxin Origin. Trichothecene (T-2) mycotoxins are a diverse group of over 40
compounds produced by molds of the genus Fusarium. These toxins inhibit protein and
DNA synthesis and mitochondrial respiration and alter cell membrane structure and
function.3
(2)
Occurrence. Worldwide. Naturally occurring mycotoxicosis occurs in
livestock following ingestion of grains contaminated with molds. When maintained as
either crystalline powders or liquid solutions, these compounds are stable when exposed to
air, light, or both. They are not inactivated by autoclaving but require heating at 900
degrees F for 10 minutes or 500 degrees F for 30 minutes for complete inactivation. A 3 to
5 percent solution of bleach is an effective inactivation agent for them.25
(3)
Reservoir. Moldy grain.3
(4)
Transmission. Ingestion of moldy grains.3
(5)
Symptoms. Mycotoxins are highly cytotoxic and have effects similar to
vesicants, especially mustard agents. Delivery to the skin may cause a burning skin pain,
redness, tenderness, blistering, and progression to skin necrosis with eschar formation and
sloughing. Respiratory exposure may result in nasal itching with pain, rhinorrhea,
sneezing, wheezing, and cough.3
(6)
Incubation period. The incubation period is minutes after exposure.3
(7)
Communicability. No person-to-person transmission.3
(8)
Prevention. As a pre-exposure prophylaxis, the use of topical antivesicant
cream or ointment may provide limited protection of skin surfaces. Food and water
contaminated with mycotoxins must not be consumed.3 Washing the exposed skin areas
with soap and water will decrease absorption through the skin.25
(9)
Delivery. The toxin may be delivered by aerosol release or through the
contamination of food and water supplies. These toxins are the agents allegedly delivered
via aerosol during the “Yellow Rain” attacks in Afghanistan and Southeast Asia during
1970s and 1980s. The T-2 mycotoxins are the only potential BW agents that can harm and
be absorbed through the intact skin.3
IV-28
NOTES
1James Chin (ed.), Control of Communicable Diseases Manual, 17th ed., United Book Press,
Inc., Baltimore, MD, 2000.
2TM 3-216/AFM 355-6, Technical Aspects of Biological Defense, 12 January 1971.
3FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C, Treatment of Biological
Warfare Agent Casualties, 17 July 2000.
4BG Russ Zajtchuk, et al. (eds), Textbook of Military Medicine: Medical Aspects of Chemical
and Biological Warfare, Office of the Surgeon General, 1997, Chap. 22, “Anthrax.”
5 FM 8-9/NAVMED P-5059/AFJMAN 44-151, NATO Handbook on the Medical Aspects of
NBC Defense Operations AMEDP-6(B), 1 February 1996.
6CDC, Division of Bacterial and Mycotic Diseases, “Disease Information: Glanders
(Technical Information), 7 March 2003,
7CDC, Division of Bacterial and Mycotic Diseases, “Disease Information: Glanders (General
29 August 2003.
8BG Russ Zajtchuk, et al. (eds), Textbook of Military Medicine: Medical Aspects of Chemical
and Biological Warfare, Office of the Surgeon General, 1997, Chap. 23, “Plague.”
9US HHS, CDC, “Compendium of Measures to Control Chlamydia psittaci Infection Among
Humans (Psittacosis) and Pet Birds (Avian Chlamydiosis), 1998,” Morbidity and Mortality
Weekly Report, Vol. 47, N0. RR-10, 10 July 1998.
10BG Russ Zajtchuk, et al. (eds), Textbook of Military Medicine: Medical Aspects of
Chemical and Biological Warfare, Office of the Surgeon General, 1997, Chapter 24,
“Tularemia.”
11BG Russ Zajtchuk, et al. (eds), Textbook of Military Medicine: Medical Aspects of
Chemical and Biological Warfare, Office of the Surgeon General, 1997, Chapter 26, “Q
Fever.”
12BG Russ Zajtchuk, et al. (eds), Textbook of Military Medicine: Medical Aspects of
Chemical and Biological Warfare, Office of the Surgeon General, 1997, Chapter 28, “Viral
Encephalitides.”
13CDC, Special Pathogens Branch, “Ebola Hemorrhagic Fever,” 6 August 2003,
14BG Russ Zajtchuk, et al. (eds), Textbook of Military Medicine: Medical Aspects of
Chemical and Biological Warfare, Office of the Surgeon General, 1997, Chapter 29, “Viral
Hemorrhagic Fevers.”
15CDC, Monkeypox, “Fact Sheet: Basic Information About Monkeypox,” 12 June 2003,
16Yvan J.F. Hutin (CDC), et. al., “Research: Outbreak of Human Monkeypox, Democratic
Republic of Congo, 1996-1997,” Emerging Infectious Diseases, Vol. 7, No. 3, May-June 2001.
17CDC, Monkeypox, “Updated Interim Infection Control and Exposure Management
Guidance in the Health-Care and Community Setting for Patients with possible Monkeypox
IV-29
2 September 2003.
18CDC, Monkeypox, “Fact Sheet: Smallpox Vaccine and Monkeypox,” 9 July 2003,
19BG Russ Zajtchuk, et al. (eds), Textbook of Military Medicine: Medical Aspects of
Chemical and Biological Warfare, Office of the Surgeon General, 1997, Chapter 33,
“Botulinum Toxins.”
20CDC, HHS, “Regulatory Impact Analysis: 42 CFR Part 73: Select Biological Agents and
Toxins, Interim Final Rule (Draft),” 9 December 2002.
21National Cancer Institute (NCI) Nomination Submitted to the National Toxicity Program
(NTP), “Blue-Green Algae,” September 2000.
22BG Russ Zajtchuk, et al. (eds), Textbook of Military Medicine: Medical Aspects of
Chemical and Biological Warfare, Office of the Surgeon General, 1997, Chap. 30, “Defense
Against Toxin Weapons.”
23Ingrid Chorus and Jamie Bartram ed., Toxic Cyanobacteria in Water: A guide to their
public health consequences, monitoring and management, Geneva, WHO, 1999.
24BG Russ Zajtchuk, et al. (eds), Textbook of Military Medicine: Medical Aspects of
Chemical and Biological Warfare, Office of the Surgeon General, 1997, Chap. 32, “Ricin
Toxin.”
25BG Russ Zajtchuk, et al. (eds), Textbook of Military Medicine: Medical Aspects of
Chemical and Biological Warfare, Office of the Surgeon General, 1997, Chap. 34,
“Trichothecene Mycotoxins.”
26Office of the US President, The Biological and Chemical Warfare Threat, 1999.
IV-30
Chapter V
TOXIC INDUSTRIAL CHEMICALS AND THEIR PROPERTIES
1. Background
In April 1915, the Germans released 150 tons of a TIC (chlorine gas) across a 4-mile
front in one of the first gas attacks of WWI. It is estimated that up to 5,000 allied soldiers
were killed and 20,000 became casualties. In addition to chlorine, other gases were used
against the Allies in other periods during this war. Arsine, cyanogen chloride, hydrogen
cyanide, phosgene, and hydrogen sulfide were used during WWI. In most cases, these gases
were first developed for industrial purposes, but the potential of these chemicals as war
gases was recognized. In Bhopal, India, in December 1984, an accidental release of methyl
isocyanate from a production facility killed an estimated 2,500 persons and left many
thousands injured.1
a.
Potential Hazard. The US troops—through the deliberate release, accidental
release, or as a result of collateral damage—could encounter TIC. Military personnel are
trained to operate in an environment in which CW weapons may be used. However, the
potential hazards of TIC are a relatively new threat. These forces must be able to safely
operate, survive, and sustain operations in those instances where they may be exposed to
toxic industrial hazards. Commanders have direct responsibility for protecting their forces
against these threats and, therefore, must become aware of and plan for defense against the
potential release of TIC in their AO. In future operations, failure to properly plan for the
release of TIC may result in significant casualties, disruption of operations, and mission
degradation.
b.
Characteristics. A number of hazards are associated with a release of TIC.
Some key factors are—
(1)
Certain chemicals have the ability to bypass or penetrate current military
protective equipment and, in many cases, are not detectable by current military equipment.
(2)
Exposure can be through several routes, including inhalation, ingestion, or
surface contact with the material.
(3)
Many of these chemicals cause a variety of immediate and delayed
symptoms that make detection, diagnosis, and treatment difficult.
(4)
Symptoms are often difficult to trace back to a specific chemical.
(5)
Determining the exposure level that constitutes a hazard for the individual
is often difficult due to the variances of susceptibility among individuals.
c.
Protection. It is important that commanders and troops be aware that the best
defense against TIC is to escape the path of the TIC immediately. The military field
protective mask can provide limited protection and should only be used to escape the
hazard area. Personnel or equipment that have been contaminated with TIC can be
decontaminated by washing with large amounts of cold, soapy water. Contaminated
clothing should be immediately removed and disposed of in a safe manner.
V-1

 

 

 

 

 

 

 

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