FM 3-11.9 POTENTIAL MILITARY CHEMICAL/BIOLOGICAL AGENTS AND COMPOUNDS (JANUARY 2005) - page 7

 

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FM 3-11.9 POTENTIAL MILITARY CHEMICAL/BIOLOGICAL AGENTS AND COMPOUNDS (JANUARY 2005) - page 7

 

 

h. PD Profile. Table H-77 provides toxicity estimates for a lethal dose from an
inhalation/ocular vapor exposure to PD.
Table H-77. PD Profile Estimates (Lethal Dose, Inhalation/Ocular)1
Ct Profile (15L MV)
MV Profile (2-Minute Exposure)
Exposure Duration (min)
LCt50 (mg-min/m3)
Concentration (mg/m3)
MV (L)
LCt50 (mg-min/m3)
2
2600
1300
10
3900
10
2600
260
15
2600
30
2600
85
30
1300
60
2600
45
50
780
120
2600
20
240
2600
10
360
2600
5
Selected Toxicology Information
Probit Slope: Unknown
TLE: 1 (Assumed)
DOC: Low
i.
CX Profile. Table H-78 provides toxicity estimates for a lethal dose from an
inhalation/ocular vapor exposure to CX.
Table H-78. CX Profile Estimates (Lethal Dose, Inhalation/Ocular)1
Ct Profile (15L MV)
MV Profile (2-Minute Exposure)
Exposure Duration (min)
LCt50 (mg-min/m3)
Concentration (mg/m3)
MV (L)
LCt50 (mg-min/m3)
2
3200
1600
10
4800
10
3200
320
15
3200
30
3200
105
30
1600
60
3200
55
50
960
120
3200
25
240
3200
15
360
3200
10
Selected Toxicology Information
Probit Slope: Unknown
TLE: 1 (Assumed)
DOC: Low
6.
Respiratory Irritants
Table H-79 provides toxicity estimates for a lethal dose from an inhalation/ocular
vapor exposure to DM.
Table H-79. DM Profile Estimates (Lethal Dose, Inhalation/Ocular)1
Ct Profile (15L MV)
MV Profile (2-Minute Exposure)
Exposure Duration (min)
LCt50 (mg-min/m3)
Concentration (mg/m3)
MV (L)
LCt50 (mg-min/m3)
2
11,000
5500
10
16,500
10
11,000
1100
15
11,000
30
11,000
365
30
5500
60
11,000
185
50
3300
120
11,000
90
240
11,000
45
Selected Toxicology Information
Probit Slope: Unknown
TLE: 1 (Assumed)
DOC: Low
NOTES
1Sharon Reutter, et al., Review and Recommendations for Human Toxicity Estimates for FM 3-
11.9, ECBC-TR-349, September 2003.
H-32
Appendix I
PROPERTIES OF SELECTED BIOLOGICAL AGENTS
This appendix provides information on the properties of selected biological agents.
I-1
Table I-1. Properties of Selected Biological Agents
Likely Methods of
Transmissibility
BW Agents1
Infectivity
Lethality2
Stability2
Dissemination
Person-to-Person
Anthrax (Inhalation)
Spores in aerosols
None
Moderate
High
Spores are highly stable
Brucellosis
1. Aerosol
None
High
Low
Long persistence in wet soil and
2. Sabotage (food supply)
food
Cholera
1. Sabotage (food/water supply)
Unstable in aerosol and pure
Negligible
Low
Moderate to high
2. Aerosol
water; more so in polluted water
Glanders
Aerosol
DNA
DNA
DNA
DNA
Melioidosis
Aerosol
Negligible
High
Variable
Stable
Plague (Pneumonic)
1.
Aerosol
High
High
Very high
Less important because of high
2.
Infected Vectors
transmissibility
Psittacosis
Aerosol
Negligible
Moderate
Very low
Stable
Shigellosis
Sabotage (Food/Water Supply)
DNA
DNA
DNA
DNA
Tularemia
Aerosol
Negligible
High
Moderate if untreated
Not very stable
Typhoid Fever
1. Sabotage (food/water supply)
Negligible
Moderate
Moderate if untreated
Unknown
2. Aerosol
Q Fever
1. Aerosol
None
High
Very low
Stable
2. Sabotage (food supply)
Rocky Mountain Spotted Fever
1. Aerosol
None
High
High
Not very stable
2. Infected Vectors
Trench Fever
1. Aerosol
None
DNA
Low
DNA
2. Vector
Typhus Fever
1. Aerosol
None
High
High
Not very stable
2. Infected vectors
Chikungunya
Aerosol
None
High
Very low
Relatively stable
Crimean-Congo Hemorrhagic Fever
Aerosol
Moderate
High
High
Relatively stable
Dengue Fever
Aerosol
None
High
Low
Relatively unstable
Eastern Equine Encephalitis
Aerosol
None
High
High
Relatively unstable
Western Equine Encephalitis
Aerosol
None
High
Low
Relatively unstable
Ebola Fever
Aerosol
Moderate
High
High
Relatively unstable
Far Eastern Tick-borne Encephalitis
1. Aerosol
None
High
Moderate
Relatively unstable
2. Milk
Hantaan Virus (Korean HFV)
Aerosol
None
High
Moderate
Relatively stable
Juinn Hemorrhagic Fever
Aerosol
DNA
DNA
DNA
DNA
Table I-1. Properties of Selected Biological Agents (Continued)
Likely Methods of
Transmissibility
BW Agents1
Infectivity
Lethality2
Stability2
Dissemination
Person-to-Person
Machuo Hemorrhagic Fever
Aerosol
DNA
DNA
DNA
DNA
Lassa Fever
Aerosol
Low to moderate
High
Unknown
Relatively stable
Lymphocytic Choriomeningitis
Aerosol
None
DNA
Low
DNA
Monkeypox
Aerosol
DNA
Rift Valley Fever
1. Aerosol
Low
High
Low
Relatively stable
2. Infected vectors
Smallpox
Aerosol
High
High
High
Stable
Venezuelan Equine Encephalitis
1. Aerosol
Low
High
Low
Relatively unstable
2. Infected vectors
Yellow Fever
Aerosol
None
High
High
Relatively unstable
Botulinum Toxin
1. Sabotage (food/water supply)
None
N/A
High
Stable
2. Aerosol
Clostridium Perfringens Toxins
1. Sabotage
None
N/A
Low
Stable
2. Aerosol
Conotoxins
1. Aerosol
None
N/A
High
DNa
2. Sabotage (food/water)
Shigatoxins
1. Aerosol
DNA
N/A
DNA
DNA
2. Sabotage (food/water)
Microcystin
1. Aerosol
None
N/A
DNA
DNA
2. Sabotage (food/water)
Ricin
Aerosol
None
N/A
High
Stable
Saxitoxin
1. Sabotage
None
N/A
High
Stable
2. Aerosol
Staphylococcal Enterotoxin B
1. Aerosol
None
N/A
Low
Stable
2. Sabotage
Tetrodotoxin
1. Sabotage
None
N/A
High
Stable
2. Aerosol
Trichothecene Mycotoxins
Aerosol
None
N/A
High
Stable
NOTES
1FM 8-9/NAVMED P-5059/AFJMAN 44-151, NATO Handbook on the Medical Aspects of
NBC Defense Operations AMEDP-6(B), 1 February 1996.
2Lethality and stability information is based on studies of natural, endemic strains of these
agents. There is potential that the lethality and/or stability of some agents may be changed
through various laboratory alterations and/or the use of stabilizing chemicals.
I-4
Appendix J
SELECTED ANIMAL PATHOGENS
1.
Background
This appendix provides summaries of animal diseases listed in The Biological and
Chemical Warfare Threat (1999). The information generally addressed in this appendix
provides descriptions, treatment, and control measures. The military role, if any, would
likely be in a consequence management support role, and the brief descriptions provided
furnish an awareness of the agents that could be used. For further information, contact the
Army Medical Department (AMEDD).
2.
Animal Diseases
a.
African Swine Fever (ASF).1
(1)
ASF is a tick-borne and contagious disease of swine caused by a virus and
characterized by hemorrhages of internal organs, high fever, moderate anorexia, and
leukopia. Mortality rates may reach 100 percent. It occurs in Africa and on the island of
Sardinia.
(2)
There is no treatment available.
(3)
Control. Slaughter and disposal of all acutely infected pigs, widespread
testing and elimination of all seropositive animals, and good herd isolation and sanitary
practices can accomplish control and eradication of ASF in developed countries. There is no
vaccine.
(4)
Human beings are not susceptible to ASF.
b.
Avian Influenza (AI) (Fowl Plague).2
(1)
AI is a disease of viral etiology that ranges from a mild or even
asymptomatic infection to an acute, fatal disease of chickens, turkeys, guinea fowls, and
other avian species, especially migratory waterfowl. Highly pathogenic AI viruses have
periodically occurred in recent years in Australia, England, South Africa, Scotland, Ireland,
Mexico, Pakistan, and the US. It is generally accepted belief that waterfowl, sea birds, or
shore birds are generally responsible for introducing the virus into poultry. Death may
occur within 24 hours of first signs of disease, frequently within 48 hours, or can be delayed
for as long as a week.
(2)
The practice of accepted sanitation and biosecurity procedures in the
rearing of the poultry is of utmost importance. In areas where waterfowl, shore birds, or
sea birds are prevalent, the rearing of poultry on open range is incompatible with a sound
AI prevention program. Cleaning and disinfection procedures are critical.
(3)
The AI viruses are Type A influenza viruses, and the possibility exists that
they could be involved in the development, through genetic reassortment, of new
mammalian strains. The infection and deaths of 6 of 18 humans infected with an AI virus
in Hong Kong in 1997 has resulted in a reconsideration of the role that the avian species
have on the epidemiology of human influenza.
J-1
(4)
The AI viruses are Type A influenza viruses, and the possibility exists that
they could be involved in the development, through genetic reassortment, of new
mammalian strains.
c.
Bluetongue (Sore Muzzle).3
(1)
Bluetongue is an acute, noncontagious, insect-borne disease of sheep, goats,
cattle, and wild ruminants caused by a virus. Occurrence is probably worldwide. Cattle
and goats with inapparent infections are important reservoirs of the virus.
(2)
The only applicable treatment available is to minimize animal stress and
administer broad-spectrum antibiotics to combat secondary infections.
(3)
A live attenuated vaccine is available for use in sheep in the US.
(4)
There is only one documented human infection, and that was a laboratory
worker.
d.
Foot-and-Mouth Disease (FMD).4
(1)
FMD is a highly contagious disease of cloven-footed domestic and wild
animals caused by a virus. The morbidity is essentially 100 percent, and the mortality is
less than 1 percent. Great economic loss results from the effects of the disease, which
include lameness, low milk production, weight loss, mastitis, debilitation, and abortion.
FMD occurs in many major livestock-producing countries.
(2)
A number of inactivated vaccines, including those prepared in cell cultures
containing the appropriate types or subtypes, are used in countries where the disease is
endemic. The duration of immunity may be as short as 4 months. Treatment to prevent
and cope with secondary infection may be necessary.
(3)
In countries free of FMD, a policy of quarantine and slaughter is usually
practiced with the goal of complete eradication.
(4)
In a review of the zoonotic aspects of FMD by K. Bauer in 1997, he reported
that, since 1921, the FMD virus has been isolated and typed from slightly over 40 human
cases. The cases occurred on three continents: Europe, Africa, and South America.
Because infection is uncommon, FMD is not considered to be a public health problem.
e.
Sheep Pox and Goat Pox.5
(1)
Sheep pox and goat pox, in fully susceptible animals, are highly contagious
and often fatal diseases caused by a capripoxvirus and characterized by fever and pox. The
diseases are endemic in Africa, the Middle East, the Indian subcontinent, and much of Asia.
Transmission is by direct and indirect contact, and the viruses can survive on contaminated
premises for many months.
(2)
There is no treatment available.
(3)
When a new case is confirmed, the area should be quarantined, infected
and exposed animals should be slaughtered, and the premises cleaned and disinfected.
Vaccination of susceptible animals on premises surrounding the infected flock should be
considered.
(4)
There is no conclusive evidence that SGPV infects humans.
f.
Aujeszky’s Disease (AJD) (Pseudorabies).6
J-2
(1)
AJD is caused by porcine herpesvirus-1. Pigs are the main host, but
sporadic cases have occurred in cattle, sheep, goats, horses, dogs, cats, foxes, and rodents.
AJD is highly contagious and is principally spread via the respiratory route. It is endemic
in the swine of many countries. It occurs frequently in the US, but not in Canada and
Australia.
(2)
There is no treatment available.
(3)
Live attenuated and inactivated virus vaccines are available to reduce
losses in herds in which the disease is a continuing problem. Vaccination does not
necessarily prevent infection or shedding of the virus.
(4)
There is no transmission to humans.
g.
Hog Cholera (Swine Fever).7
(1)
Hog cholera, a highly contagious disease, is caused by a virus and is
characterized in fully susceptible pigs by high mortality. The disease occurs in many
countries of Europe, Africa, and Asia. It has been eradicated in Australia, Canada, and the
US. The disease is spread by direct and indirect contact.
(2)
There is no treatment available.
(3)
A strict regimen of vaccination will reduce the number of outbreaks to a
level at which complete eradication by sanitary measure alone will be feasible.
(4)
Human beings are not susceptible to Hog Cholera infection.
h. Lyssa Virus (Rabies).8
(1)
Rabies infections are usually established following introduction of virus-
infected saliva into a bite or scratch, although animals can also be infected by the oral and
nasal (olfactory) routes. Bat-infested caves may result in infectious aerosols; nonbite
transmission of the disease from this source has been reported in a number of animal
species, including humans. The disease generally takes one of two forms: “furious,” with
sporadic episodes of rage; or “dumb,” in which there is an early progressive paralysis. Both
forms almost invariably result in death. A normally lively and sociable dog, for example,
may become anorexic, withdrawn, irritable, or restless. This behavior may suddenly
change, with the animal becoming highly affectionate. At this stage, the dog may try
repeatedly to lick the hands and face of its owner or handler. As the disease progresses,
the animal may appear to have difficulty swallowing, as if a bone were caught in its throat.
Any attempt to alleviate the problem manually exposes the handler to considerable risk,
either through a bite or the deposition of virus-infected saliva on mucous membranes or
minor scratches. The dog’s bark becomes high pitched and hoarse, indicating the onset of
paralysis. The animal drools saliva. Convulsive seizures and muscular incoordination
become apparent, followed by progressive paralysis, usually terminating in death within 7
days of the onset of symptoms. In about 25 to 50 percent of cases, apparently as a result of
limbic lobe dysfunction, dogs with rabies develop the furious form of the disease. Affected
animals may eat abnormal objects, and during paroxysms of rage, will attack almost
anything. Rabies is present in most of Europe, throughout Africa, the Middle East, and
most of Asia and the Americas. The UK, Ireland, parts of Scandinavia, Japan, Singapore,
Australia, New Zealand, Papua New Guinea, and the Pacific Islands are free of rabies.
(2)
There is no treatment available.
J-3
(3)
Once a virulent strain of rabies virus has established itself in the CNS of an
infected animal, the outcome is almost always death. At a practical level, however, the only
ways of preventing rabies are by preexposure immunization.
(4)
All warm blooded animals, including humans, are susceptible.
i.
Velogenic Newcastle Disease (VND) (Exotic Newcastle Disease, Asiatic
Newcastle disease).9
(1)
VND is likely the most serious disease of poultry throughout the world. In
chickens it is characterized by morbidity rates near 100 percent and mortality rates as high
as 90 percent in susceptible chickens.
(2)
The establishment of a strict quarantine, destruction of all infected and
exposed birds followed by thorough cleaning, and disinfection of the premises are the main
actions necessary for eradication of VND virus. VND virus has been recovered from
effluent water for as long as 21 days and from carcasses for 7 days when the daytime
temperatures were over 90 degrees.
(3)
Although people may become infected with VND virus, the resulting
disease is typically limited to conjunctivitis. Recovery is usually rapid, and the virus is no
longer present in eye fluids after 4 to 7 days. Infections have occurred mostly in laboratory
workers and vaccinating crews, with rare cases in poultry handlers. No instance of
transmission to humans through handling or consuming of poultry products is known.
Individuals with conjunctivitis from VND virus should not enter poultry premises or come
in contact with live avian species.
j.
Peste Des Petits Ruminants (PPR) (Pest of Small Ruminants).10
(1)
PPR is an acute or subacute disease of sheep and goats caused by a virus.
The disease is not contagious, and transmission requires close contact. The mortality,
depending on the form, varies form 50 to 80 percent. The disease has been reported from
west and central Africa, the Middle East, and the Indian subcontinent.
(2)
There is no specific treatment for PPR. Drugs that control bacterial and
parasitic complications may decrease mortality.
(3)
Eradication is recommended when PPR appears in new areas. Methods
should include quarantine, slaughter, and proper disposal of carcasses and contact fomites;
decontamination; and restrictions on importation of sheep and goats from affected areas.
(4)
PPR is not infectious to humans.
k.
Swine Vesicular Disease (SVD).11
(1)
SVD is a contagious disease of swine. This disease produces lesions that
are grossly indistinguishable from those of FMD. In the natural disease, the prognosis is
favorable; however, in most countries, as soon as it is recognized, the pigs are slaughtered.
This disease, which has been reported from several European countries and Asia, does not
occur in North America.
(2)
There is no treatment available.
(3)
Preventive measures include control of animals imported from infected
areas and sanitary disposal of garbage from international aircraft and ships. Eradication
J-4
measures consist of quarantining infected farms and areas, slaughtering and disposing of
infected and exposed pigs, and cleaning and disinfecting infected premises.
(4)
Human infection has been reported in laboratory personnel working with
the virus. Caution should be taken when working with infected material.
l.
Rinderpest.12
(1)
Rinderpest is a contagious viral disease of cattle, domestic buffalo, and
some species of wildlife. The disease is found only in the Indian subcontinent, Near East,
and sub-Saharan Africa. Transmission is by direct and indirect contact. Aerosol
transmission is not a significant means of transmission except in confined areas and over
short distances. In fully susceptible cattle, the mortality may approach 100 percent with
some virulent strains.
(2)
There is no treatment available.
(3)
If an outbreak occurs, the area should be quarantined, infected and exposed
animals slaughtered and buried or burned, and ring vaccination considered.
(4)
There are no reports of Rinderpest infection in humans.
m. Enterovirus Encephalomyelitis (Porcine Polioencephalomyelitis, Teschen
Disease, Talfan Disease).13
(1)
These diseases are caused by several closely related enteroviruses. They
occur in pigs of all ages and are characterized by a fever and convulsions, stiffness, spasms,
and paralysis. The highly virulent strain (Teschen Disease) has a mortality rate of 70 to 90
percent. Transmission is made by direct or indirect contact, swill feeding, and fomites.
Teschen disease is found in central and eastern Europe, Madagascar, and Uganda.
(2)
There is no treatment available for this pathogen.
(3)
Live attenuated and inactivated vaccines are effective in controlling the
disease. Quarantine and hygienic measures should be applied. In the US, strict import
regulations must be followed for Teschen disease.
(4)
Pigs are the only susceptible species.
n. Vesicular Stomatitis.14
(1)
Vesicular stomatitis is a contagious disease of cattle, horses, and pigs. The
disease occurs in North and Central America and the northern part of South America. The
incubation period is usually 24 hours; and direct contact, biting insects, and fomites spread
the disease rapidly. Humans may be infected by contact and by aerosol.
(2)
There is no treatment except the use of mild antiseptics and astringents on
the mucosa of the mouth.
(3)
Infected and exposed animals should be quarantined. A vaccine is
available in some countries.
(4)
Vesicular stomitis (New Jersey and Indiana) infection frequently occurs in
man and causes influenza-like symptoms, but rarely results in vesicles. Other vesicular
stomitis viruses (Piry, Isfahan, and Chandipura) are much more infectious for man.
o.
Contagious Bovine Pleuropneumonia (CBPP).15
J-5
(1)
CBPP is caused by Mycoplasma mycoides and primarily affects cattle. The
principal mode of infection is by inhalation. The disease occurs in Africa and some regions
of Asia (especially India and China), with occasional outbreaks in Europe.
(2)
Treatments are generally ineffective for this pathogen.
(3)
CBPP is a notifiable disease in most countries. A live attenuated vaccine is
employed in areas where eradication is not feasible.
(4)
There is no evidence to indicate that humans are susceptible to this
disease.
p.
Contagious Equine Metritis (CEM).16
(1)
CEM is a highly contagious disease of horses. It has been reported from
Australia, Ireland, a number of European countries, Japan, Belgium, Denmark,
Netherlands, Norway, Sweden, Switzerland, and Luxembourg. The disease has been
eradicated from the US.
(2)
Treatment of mares with antimicrobial drugs is not always effective, even
though the disease-causing organism is generally susceptible to antibiotics.
(3)
This is a reportable disease in North America. Quarantine or isolation with
attempts to eliminate actively infected animals and positive carriers is generally used.
(4)
There is no evidence that man is affected by the CEM.
q.
Heartwater (Cowdriosis).17
(1)
Heartwater is a disease of ruminants caused by rickettsia and transmitted
by ticks. It occurs in Africa, Madagascar, Guadeloupe, and other islands of the Caribbean.
Cattle, sheep, and goats are affected; and indigenous breeds are more resistant than
imported ones.
(2)
Treatment involves administering tetracyclines.
(3)
Preventive measures include control of ticks. Simultaneous infection with
infectious blood and treatment with tetracyclines provides protection against some strains.
(4)
Humans are not known to be affected by Heartwater.
r.
Screwworm Myiasis.18
(1)
Myiasis is the infestation of live vertebrate animals with larvae, which for
at least a certain period, feed on the host’s dead or living tissue, liquid body substances, or
ingested food. Screwworm larvae penetrate deeply into a wound of a warm-blooded animal
and feed on living tissue and body fluid.
(2)
Screwworm myiasis is treated with topical application of an approved
larvacide directly into the infested wound.
(3)
Where screwworm is endemic, animals must be inspected at least every 3 to
4 days to discover and treat cases of screwworm myiasis.
(4)
Humans are susceptible to screwworm myiasis.
s.
Enterovirus Infections of Swine (Virus Infection of Swine).19
J-6
(1)
This virus causes stillbirths, mummification, embryonic death, and
infertility. These infections can be widespread where swine are raised intensively.
(2)
There is no treatment for this virus.
(3)
Enterovirus can be controlled by comingling new replacement boars or gilts
by fence-line contact or exchange of manure for 30 days before breeding begins.
NOTES
1 C.A. Mebus, “African Swine Fever (Peste porcine Africaine, fiebre porcina Africana,
maladie de Montgomer),” Foreign Animal Diseases “The Gray Book”, 1998 ed.,
2 C.W. Beard, “Avian Influenza (Fowl Plague),” Foreign Animal Diseases “The Gray Book”,
3 O.L Stott, “Bluetongue and Epizootic Hemorrhagic Disease (Sore muzzle, pseudo foot-and-
mouth disease, muzzle disease),” Foreign Animal Diseases “The Gray Book”, 1998 ed.,
4 James House and C.A. Mebus, “Foot-and-Mouth Disease (Afta epizootica, Bek-en-klouseer,
Fiebra aftosa, Fievre aphteuse, Maul-und-Klauenseuche),” Foreign Animal Diseases “The
Gray Book”, 1998 ed., http://www.vet.uga.edu/vpp/gray_book/FAD/fmd.htm (31 March
2003).
5 James A. House, “Sheep and Goat Pox”, Foreign Animal Diseases “The Gray Book”, 1998
6 Alexandre Fediaevsky, “B052-Aujeszky’s Disease,” Manual for the Recognition of Exotic
Diseases of Livestock, 17 December 2002,
G. Garner and Peter Saville).
7 Gilles C. Dulac, “Hog Cholera (Classical swine fever, peste du porc, colera porcina,
Virusschweinepest),” Foreign Animal Diseases “The Gray Book”, 1998 ed.,
8 Alexandre Fediaevsky, “B058-Rabies,” Manual for the Recognition of Exotic Diseases of
Livestock, 17 December 2002,
(Developed by G. Garner and Peter Saville).
9 Charles W. Beard, “Velogenic Newcastle Disease (Exotic Newcastle disease, Asiatic
Newcastle disease),” Foreign Animal Diseases “The Gray Book”, 1998 ed.,
10 J.T. Saliki, “Peste Des Petits Ruminants (Pest of Small Ruminants, stomatitis-
pneumoenteritis complex or syndrome pseudorinderpest of small ruminants and kata
[Pidgin English for catarrh]),” Foreign Animal Diseases “The Gray Book”, 1998 ed.,
J-7
11 C.A. Mebus, “Swine Vesicular Disease,” Foreign Animal Diseases “The Gray Book”, 1998
12 C.A. Mebus, “Rinderpest,” Foreign Animal Diseases “The Gray Book”, 1998 ed.,
13 Alexandre Fediaevsky, “B256-Enterovirus Encephalomyelitis (Previsously Teschen
Disease),” Manual for the Recognition of Exotic Diseases of Livestock, 17 December 2002,
http://www.spc.int/rahs/Manual/Porcine/PEVE.HTML (1 April 2003).(Developed by G.
Garner and Peter Saville).
14 C.A. Mebus, “Vesicular Stomatitis,” Foreign Animal Diseases “The Gray Book”, 1998 ed.,
15 Corrie Brown, “Contagious Bovine Pleuropneumonia,” Foreign Animal Diseases “The
Gray Book”, 1998 ed., http://www.vet.uga.edu/vpp/gray_book/FAD/CBP.htm (31 March
2003).
16 T.W. Swerczek, “Contagious Equine Metritis,” Foreign Animal Diseases “The Gray Book”,
17 C. John Mare, “Heartwater (Cowdriosis),” Foreign Animal Diseases “The Gray Book”,
18 James E. Novy, “Screwworm Myiasis (Gusanos, Mosca Verde, Gusano barrendor,
Gusaneras),” Foreign Animal Diseases “The Gray Book”, 1998 ed.,
19 Alex Hogg and Donald G Levis, “Swine Reproductive Problems: Infectious Causes),”
NebGuide, February 1997, http://www.ianr.unl.edu/pubs/swine/g926.htm (8 April 2003).
J-8
Appendix K
SELECTED PLANT PATHOGENS
1.
Background
The purpose of this appendix is to provide a brief summary of select plant diseases
listed in The Biological and Chemical Warfare Threat (1999). The military could
potentially be involved in a consequence management support role, and brief descriptions
are provided to furnish an awareness of these agents. For further information, contact
AMEDD.
2.
Bacterial Diseases
a.
Xanthomonas albilineans.1
(1)
Description. Leaf Scald (Sugar Cane).
(2)
Specific Bacteria. Xanthomonas albilineans.
(3)
Symptom. The initial characteristic symptom is one or more narrow, white
“pencil lines” running longitudinally down the leaf blade into the sheath. Under severe
disease conditions, entire plants may die.
(4)
Transmission. The bacterium lives from year to year in infected plants. It
is spread by the harvester and possibly by other cultivation practices that cause plant
wounding. The disease can be spread aerially in windblown rain.
(5)
Control Measures. The main control measures are use of disease-free or
treated seed and crop rotation. Additionally, the disease is kept out of production areas
through quarantine of varieties introduced from other areas.
b.
Xanthomonas campestris pv. citri.2
(1)
Description. Citrus Canker (citrus plants).
(2)
Specific Bacteria. Bacterium-Xanthomonas campestris pv. citri.
(3)
Symptom. On leaves, first appearance is as oily-Looking, 2- to 10-mm
circular spots. The lesions are often similarly sized. Later, they become white or yellow
spongy pustules. The pustules darken and thicken into tan to brown corky cankers.
Sunken craters are noticeable on fruits. Defoliation occurs on severely infected trees.
(4)
Transmission. The bacterium is spread primarily by wind-driven rain,
overhead irrigation, and contaminated equipment. Citrus canker seems to be much more
severe in areas in which the periods of high rainfall coincide with the period of high mean
temperature (such as Florida and other Gulf Coast states).
(5)
Control Measures. In canker-free, citrus-producing areas, strict quarantine
measures are practiced. When the canker bacterium is found in such an area, control is
attempted by burning all infected and adjacent trees to prevent the spread of the pathogen.
c.
Xanthomonas campestris pv. oryzae.3
K-1
(1)
Description. Bacterial Leaf Blight (rice).
(2)
Specific Bacteria. Bacterium-Xanthomonas campestris pv. oryzae.
(3)
Symptom. The first symptom of the disease is a water-soaked lesion on the
edges of the leaf blades near the leaf tip.
(4)
Transmission. High rainfall and strong winds are thought to provide
conditions for the bacteria to multiply and enter the leaf through injured tissue.
(5)
Control Measures. Fall plowing or rolling of stubble to hasten decay of the
rice debris should help to manage the disease by destroying the tissue in which the
bacterium is maintained.
d.
Xylella fastidiosa (grapevines).4
(1)
Description. Pierce’s disease (PD) (grapevines).
(2)
Specific Bacteria. Bacterium-Xylella fastidiosa.
(3)
Symptom. In grapes, symptoms appear as a sudden drying and scorching
of much of the margin area of the leaf while the rest of the leaf is still green. Grape clusters
on vines with leaf symptoms stop growing, wilt, and dry up. The bacterium also causes leaf
scorching in the American elm, maple, mulberry, and plum. In the peach and alfalfa
plants, the bacterium slows and stunts growth.
(4)
Transmission. The pathogen is transmitted by certain kinds of leafhoppers
known as sharpshooters. The leafhopper vectors transmit the bacteria from diseased to
healthy plants.
(5)
Control Measures. There is no practical control of Pierce’s disease of grapes
in the field. All commercial grape varieties are susceptible to the disease.
3.
Fungal Diseases
a.
Colletotrichum Coffeanum.5
(1)
Description. Coffee Berry Disease (CBD) (coffee).
(2)
Specific Fungi. Colletotrichum Coffeanum.
(3)
Symptom. CBD attacks the green tissues at the beginning stage of berry
development, often penetrating into the interior of the berry and destroying the bean.
(4)
Transmission. Infected berries are the major source of transmission. Rain
is also a major factor responsible for spreading spores. Windblown rain also results in local
dispersal from tree to tree or over relatively short distances. If an infected seed is planted,
systemic seed-borne inoculum could easily infect the bark of young seedlings and become
established in mature orchards.
(5)
Control Measures. Since CBD is limited to Africa, precautions should be
taken with coffee seeds from this region.
b. Cochiliobolus miyabeans (Helminthosporium oryzae).6
(1)
Description. Brown Spot (rice).
(2)
Specific Fungi. Cochliobolus miyabeanus (Helminthosporium oryzae).
K-2
(3)
Symptom. Leaf spots initially appear as small circular to oval spots on the
first seedling leaves. Leaf spots are observed throughout the growing season and can vary
in size, shape, and color. Small spots are dark brown to reddish brown while large spots
have a light, reddish-brown or gray center surrounded by a dark to reddish-brown margin.
Older spots may have a bright yellow halo surrounding the lesion. Severely infected leaves
will produce lightweight or chalky kernels.
(4)
Transmission. The disease spreads from plant to plant in the field by
airborne spores. Disease development is favored by high relative humidity (86 to 100
percent) and temperatures between 68 and 78 degrees F. Leaves must be continuously wet
for 8 to 24 hours for infection to occur.
(5)
Control Measures. The best management strategy is balanced nutrition
because plants that grow in soils with nutritional deficiencies or in soils where nutrient
uptake is hindered are more susceptible to infection. Fungicidal seed treatment has proven
very effective in reducing seedling brown spot disease.
c.
Microcyclus ulei.7
(1)
Disease. South American Leaf Blight (Hevea species only, yields latex).
(2)
Specific Fungi. Microcyclus ulei (M. ulei).
(3)
Symptom. The symptoms vary with the age of the leaves; however, on
young leaves up to 10 days old, slightly colored hypertrophic deformations are visible 3 to 4
days after inoculation.
(4)
Transmission. Plants older than 4 to 5 years normally change leaves once a
year at the onset of the dry season. This change behavior is very important for an epidemic
of M. ulei because leaves are only susceptible when they are less than 10 to 15 days old.
The spores of M. ulei are disseminated mainly by rain splash or wind.
(5)
Control Measures. The disease threatens the rubber cultivation in the
tropical regions of the globe.
d.
Puccinia graminis tritici.8
(1)
Disease. Wheat Stem Rust (wheat; some varieties of barley, oats, and rye;
wild barley; and goat grass).
(2)
Specific Fungi. Puccinia graminis.
(3)
Symptom. Wheat stem rust is encountered during growing season and may
occur on any aboveground parts. Rust spots are very small, circular or elongated, and vivid
orange-red in color. Later in the year, the rust pustules darken because of the production of
dark brown spores that are the over-wintering stage of the rust.
(4)
Transmission. Virtually all of the stem rust infections come by way of
spores blown in from infected fields of other regions.
(5)
Control Measures. Plant-resistant wheat varieties are available. If
necessary, apply a foliar fungicide at the very early stage of disease development.
e.
Puccinia striiformis.9
(1)
Disease. Stripe Rust of Wheat (mainly wheat, can occasionally infect
barley, triticale, and cereal rye).
K-3
(2)
Specific Fungi. Puccinia striiformis.
(3)
Symptom. Initially, small areas 1 to 10 meters in diameter will appear as
yellow patches in paddocks. Infected leaves develop yellow-orange spore masses (pustules)
in long stripes on the leaves, but rarely on the stems and heads. As the crop matures, the
spore masses turn from yellow to black stripes.
(4)
Transmission. The disease, like leaf rust, develops from spores blown in
from other wheat-growing areas. Stripe rust spores can be spread on contaminated
clothing.
(5)
Control Measures. Resistant varieties can be selected if this disease
becomes serious. Foliar fungicides also are labeled for stripe rust.
f.
Pyricularia grisea.10
(1)
Disease. Rice Blast (rice).
(2)
Specific Fungi. Pyricularia grisea.
(3)
Symptom. Lesions that occur on the leaf are usually diamond-shaped with
a gray or white center and brown or reddish brown border. Panicle lesions are usually
brown, but may also be black.
(4)
Transmission. Shortly after the fungus infects and produces a lesion on
rice, fungal strands called “conidiophores” grow and produce spores called “conidia.” These
conidia are dispersed in the air. The disease is favored by long periods of free moisture,
high humidity, little or no wind at night, and night temperatures between 63 and 73
degrees F. Leaf wetness from dew or other sources is required for infection. Sporulation is
greatest when relative humidity is above 93 percent.
(5)
Control Measures. Resistant varieties are available. Continuous flooding
is recommended to limit blast development. Avoid field drainage, especially for extended
periods because it allows the formation of nitrate and may cause drought stress.
g.
Deuterophoma tracheiphila.11
(1)
Disease. Citrus.
(2)
Specific Fungi. Deuterophoma tracheiphila.
(3)
Symptom. The first symptoms appear in the spring, followed by a dieback
of twigs and branches. Gradually, the pathogen affects the entire tree, and it eventually
dies.
(4)
Transmission. Prunings containing affected twigs or branches can be a
source of inoculum for several weeks. The fungus can survive within infected twigs in the
soil for more than 4 months. The disease can also be transmitted by rain, hail, and wind.
Dissemination by birds and contaminated insects is also suspected.
(5)
Control Measures. Resistant varieties of lemon trees are available.
h. Moniliophthora roreri.12
(1)
Disease. Monilia Pod Rot (cocoa).
(2)
Specific Fungi. Moniliophthora roreri.
K-4
(3)
Symptom. Moniliophthora roreri completes its entire life cycle on the pods
in the tree. There will be conspicuous bumpy swellings on the pod surfaces. Sporulation
begins over the pod causing a tan discoloration within 12 days after pod swellings.
(4)
Transmission. To monitor for Moniliophthora Pod Rot, “sanitation sweeps”
are made through the planting after pod set and should be continued on 7- to 10-day
schedules. This is well within infected pod surface sporulation, which disperses spores
throughout the trees during rainy periods.
(5)
Control Measures. Detection of cocoa-infected pods and their removal is the
real and only key to pest management. Good surface drainage and removal of weeds should
be practiced on a regular basis.
4.
Viral Diseases
a.
Barley Yellow Dwarf (BYD) Virus.13
(1)
Disease. BYD (wheat, barley, and oat).
(2)
Specific Virus. BYD.
(3)
Symptom. Symptoms include uneven, blotchy leaf discoloration in various
shades of yellow, red, or purple, progressing from leaf tip to base and margin to midrib.
The most striking symptoms occur on older leaves Wheat and barley leaves usually turn
yellow, while oat leaves are more red.
(4)
Transmission. Transmitted by more than 20 aphid species (e.g., corn leaf
aphid).
(5)
Control Measures. The main hope of control of BYD is the use of resistant
varieties. Most of the commercial varieties of oats, barley, and wheat are susceptible to
BYD, but some are less susceptible than others. A number of varieties have been found or
developed that show some tolerance or resistance to BYD. Also, avoid very early or very
late planting dates during active aphid populations.
b.
Banana Bunchy Top Virus (BBTV).14
(1)
Disease. BBTV (bananas).
(2)
Specific Virus. BBTV.
(3)
Symptom. New leaves of infected plants develop dark green streaks. On
mature plants, new leaves emerge with difficulty, are narrower than normal, are wavy
rather than flat, and have yellow leaf margins. They appear to be “bunched” at the top of
the plant.
(4)
Transmission. BBTV is transmitted from plant to plant by aphids and
transmitted from place to place by people transporting planting materials obtained from
infected plants.
(5)
Control Measures. The most important factors in controlling this disease
are killing the aphid vector and removing and destroying infected banana plants.
K-5
NOTES
1Kenneth Witam, et al., “Field Crops: Sugarcane” 2001 Plant Disease Control Guide, 2001,
2Dean W. Gabriel, Citrus Canker Disease, 5 August 2002,
3Texas Extension Plant Pathologists, “Bacterial Leaf Blight Symptoms on Rice,” February
4A.H. Purcell, “An Introduction to Pierce’s Disease,” Xylella Fastidiosa Web Site, November
5Stephen A. Ferreira and Rebecca A. Boley, “Colletrotrichum Coffeanum,” Crop Knowledge
1, 2003).
6Lawrence E. Datnoff and Richard S. Lentini, “Brown Spot in Florida Rice,” May 1994,
7The International Rubber Research and Development Board, “South American Leaf
8J.E. Partridge, “Stem Rust of Wheat,” University of Nebraska-Lincoln, Department of Plant
Pathology, 1997,
2003).
9Department of Agriculture-Western Australia, “Stripe Rust of Wheat: Puccinia striiformis
f.sp. tritici,” August 2002,
10R.K. Webster, “Rice: Rice Blast,” UC Pest Management Guidelines, July 2000,
11Data Sheets on Organisms Cuarentenarios for the Paises Members of the Cosave Card
Cuarentenaria, “Xanthomonas campestris (Pammel) Dowson pv. Oryzae (Ishiyama) Dye,”
12 “Monilia (Moniliophthora roreri),” http://www.oardc.ohio-state.edu/cocoa/monilia.htm (1
April 2003).
13R.M. Davis, “Small Grains: Barley Yellow Dwarf,” University of California Statewide
Integrated Pest Management Program, December 2002,
14College of Tropical Agriculture & Human Resources, University of Hawaii, “Banana
Bunchy Top Virus,” Plant Disease, December 1997,
K-6
Appendix L
DISSEMINATION OF BIOLOGICAL AGENTS
1.
Background
The term “dissemination” refers to the intentional release of a biological agent by an
adversary so that it will reach the portals of entry of target personnel in a viable and
virulent state. Based on the portals of entry, the characteristics of agents used, and the
results desired, certain methods of dissemination are feasible for biological attacks. The
effectiveness of these methods is determined by physical and environmental factors that
limit the ability of the agent to establish infection. Dissemination methods are related to
the routes of entry through which pathogens may be introduced into the body to establish
infection.1 These routes of entry are inhalation, percutaneous, and oral.
2.
Inhalation or Aerosol Route of Entry
The primary route of exposure to biological agents is through the respiratory tract.
This would be accomplished by disseminating the agent as an aerosol. An aerosol is
comprised of finely divided particles, either liquid or solid, suspended in a gaseous medium.
Examples of common aerosols are dust, fog, and smoke. A biological agent aerosol is
defined as an airborne suspension of particles containing biological agents.
a.
Characteristics of Aerosol Dissemination.
(1)
Difficulty of Detection. A biological agent aerosol in field concentrations
cannot be detected by the physical senses.
(2)
Capability of Penetration. Aerosol particles tend to diffuse in much the
same manner as a gas. The aerosol cloud travels with the wind and is capable of diffusing
into nonairtight structures that are not equipped with adequate filtering devices.
(3)
Difficulty of Diagnosis. The classical symptoms of a disease associated with
a particular agent can mimic the symptoms of diseases, such as the flu.
(4)
Increased Severity and Mortality Rate. Certain diseases have altered
incubation periods and incapacitation times and increased mortality rates when the agent
enters the body through the respiratory tract. This is the result of the organism diffusing
directly into the bloodstream and being carried by the blood directly to the body tissues.
(5)
Massive Overdoses. Personnel might be exposed to massive overdoses of an
agent through the use of an aerosol. Thus, the acquired immunities of target personnel
might be overcome by the use of selected agents.
(6)
Increased Susceptibility. Man has a constant requirement for oxygen;
therefore, he is breathing continually. This increases the probability of contacting an
airborne organism.
b.
Particle Size. For the biological agent aerosol to be effective, it must reach target
personnel. Particle size is a critical factor in lung infections. Particles in the size range
from 1 to 5 microns are much more capable of passing through the defensive barriers of the
L-1
upper respiratory tract and of being retained in the lungs than those below or above this
size range.
c.
Formation of Aerosol Particles. Particles in the proper size range can be formed
by physically breaking up a substance. This can be accomplished by release through a
nozzle or a spray or by an explosive force. There are three general methods of forming
biological agent aerosols—
(1)
Generator. Particles can be formed by forcing the wet (slurry form) agent
through a nozzle at a regulated pressure. The amount of pressure, the size of the orifices,
the viscosity of the agent, and the relative humidity determine particle size. Size control of
solid particles (dry form of agent) can be achieved by presizing before dissemination.
(2)
Spray. Releasing the agent in slurry form into a high-velocity air stream
can produce aerosol particles in the proper size range.
(3)
Explosive Force. Biological agents can be disseminated by explosive means.
The use of an explosive means for aerosol production is feasible because large numbers of
organisms can be packaged in a munition. The total volume and agent concentration will
support low efficiencies and still produce aerosols that result in adequate area coverage
with high infective dose concentrations.
d.
Agent Aerosol Stability. From the instant an aerosol is created, certain physical
and environmental factors affect its stability. Aerosols eventually diffuse and become too
dilute to be effective; environmental conditions cause the agent in the aerosol to gradually
lose its ability to establish infection. This decline in aerosol effectiveness is called the
“aerosol decay rate,” which is usually expressed as percent decay (death) of microorganisms
per minute. The decay rate differs from agent to agent and for meteorological conditions.
Some of the factors that determine aerosol stability are—
(1)
Settling. The rate of fall of the particle is directly related to its size. The
terminal velocity of a 1- to 5-micron particle is relatively small (5 inches per hour for a 1-
micron-diameter particle in still air). This slow settling rate and the presence of convection
currents within the target area cause fallout of 1- to 5-micron particles to be negligible.
(2)
Impaction. As the aerosol cloud moves downwind from its release point,
particles within the cloud strike and stick to objects in their path. While a number of
particles will impact, the overall effect is negligible.
(3)
UV Radiation. The UV radiation in sunlight kills microorganisms. In spite
of the low penetrating power of UV radiation, its killing effect for most pathogens is
complete and takes place in a relatively short period of time upon direct contact.
(4)
Wind Direction and Speed. These determine the direction in which the
aerosol cloud will travel and the size of the area that it will cover. Aerosols of biological
agents with a high decay rate can be employed effectively at high wind speeds (8 to 18
knots). At these speeds, the aerosol may be carried over extensive areas during the agent’s
survival period. Low wind speeds decrease downwind travel, which reduces area coverage.
However, low wind speeds also tend to lengthen the time the aerosol is on the target and
thereby increase the inhaled dose in target personnel.
(5)
Relative Humidity and Evaporation. Liquid particles in a biological aerosol
may be reduced in size by evaporation. A decrease in the amount of liquid in the particle
creates a corresponding increase in the percentage of salts remaining in the liquid
L-2
surrounding the agent. This results in increased osmotic pressure, which tends to draw
fluids out through the cell membrane and results in dehydration of the living
microorganisms. The rate of evaporation is dependent upon the relative humidity and the
temperature in the environment surrounding the particle. Disseminating the agents
affected during conditions of high relative humidity reduces the rate of evaporation. Low
relative humidity is conducive to the stability of some biological agents. These agents
would be disseminated during conditions of low relative humidity.
(6)
Temperature. Temperature has little direct effect on the living portion of a
biological aerosol. Indirectly, however, an increase in temperature is normally followed by
an increase in evaporation rate. High temperatures (170 to 180 degrees F) tend to kill most
vegetative bacteria as well as the viral and rickettsiae agents; however, these temperatures
are not normally encountered under field conditions. Subfreezing temperatures tend to
freeze the aerosol (if it is in liquid form) after its dissemination. This freezing tends to
preserve the agent and decrease its rate of decay.
(7)
Air Stability. The temperature gradient conditions of lapse, inversion, and
neutral affect the biological agent aerosol in much the same manner as they affect a
chemical agent cloud. Inversion and neutral conditions are most effective for aerosol travel
because the cloud is kept at a height conducive to inhalation by target personnel.
Turbulence, which occurs during lapse conditions, will cause vertical diffusion of the cloud
with a resulting loss of agent to higher altitudes and a reduction of area coverage.
(8)
Precipitation. Heavy and prolonged precipitation will substantially reduce
the number of agent particles in the air. The high relative humidity associated with very
light rain makes it less important in aerosol effectiveness than the rainout effect of heavy
rainfall.
e.
Effects of Terrain on Cloud Travel. Terrain affects cloud travel of biological
agent aerosols in the same general manner as it affects chemical agent clouds. The ground
contour of rough terrain creates wind turbulence, which in turn influences the vertical
diffusion of the aerosol cloud. Soil will have an effect only as related to heat absorption and
reflection, which aid in determining temperature gradients.
3.
Percutaneous Route of Entry
A second portal of entry that can be utilized for biological agent employment is the
skin. Penetration of the skin can be accomplished by the bite of an arthropod vector
(carrier), injection, or absorption.
a.
Arthropod Vector. These insects are capable of transferring pathogens to man
through breaks in the skin. For the purpose of this manual, the definition of “vector” is
limited to the arthropods. The spread of pathogens by arthropod vectors to man is well-
established in history. Some examples of vectors and the pathogens that they have shown
to be capable of transmitting are as follows:
(1)
Mosquitoes. The virus of yellow fever is transmitted from man to man by
the bite of a mosquito. Other important mosquito-borne viral diseases are dengue fever and
several types of encephalitis.
(2)
Flies. Most varieties of true flies have sucking mouthparts, but those few
that have mouthparts capable of piercing the skin of man or animals carry pathogens that
cause some of the most feared human diseases. The sucking flies introduce pathogens
L-3
through previously injured body surfaces or mechanically transport them on their body
surfaces to exposed food and water. Typhoid fever, bacillary and amoebic dysentery, and
Asiatic cholera are examples of diseases that may be spread mechanically by nonbiting
flies. Pathogens transported by the biting flies include those that cause the dreaded
African sleeping sickness—an infection of man, domestic animals, and wild game. The
vector responsible for this disease is the tsetse fly (Glossina morsitans). Tularemia, a
bacterial disease of man and wild animals, is sometimes transmitted by the deer fly.
(3)
Lice. Lice are sucking, dorsoventrally flattened, wingless insect parasites
of the skin of mammals and birds. The human body louse, Pediculis humanus, is the vector
for the rickettsiae that cause epidemic typhus and trench fever.
(4)
Fleas. Fleas are small, wingless insect parasites of the skin of mammals
and birds. Their bodies are flattened laterally, and they have mouthparts for piercing the
skin. While different species show preferences for certain hosts, when hungry they will
attack any warm-blooded animal. This habit increases their potential to transmit disease
to man. The common rat flea, Xenopsylla cheopis, is the vector of endemic typhus.
(5)
Ticks and Mites. These arthropod vectors are known as acarids and are not
true insects. As adults, they possess eight legs while insects have six. Most of these are
merely parasitic skin pests of land vertebrate animals, but a few are important disease
vectors. Certain mites transport the causative organism of scrub typhus. The wood tick,
Dermacentor andersoni, indigenous to the western US, is known to transmit to man the
rickettsia of Rocky Mountain spotted fever, the bacterium of tularemia, and the virus of
Colorado tick fever.
b.
Injection. Biological agents can be injected through the skin. In 1978, Bulgarian
exile Georgi Markov, was attacked in London, England, with a device disguised as an
umbrella. The weapon discharged a tiny pellet in the subcutaneous tissue of his leg while
he was waiting for a bus. He died days later. The pellet, which contained Ricin, was found
during autopsy.2 A Flechette is another penetrating device.
c.
Absorption. Biological agents may be absorbed through the skin or placed on the
skin to do damage to the integument.
4.
Oral Route of Entry
Another possibility is through the oral route by ingestion of contaminated food or
water supplies. Contamination with toxins of chlorinated water, rivers, lakes, or reservoirs
would be difficult because of dilution effects.5
5.
Covert Dissemination1
a.
Characteristics. Biological agents lend themselves well to covert or hidden
operations because of detection difficulties, the variety of potential agents, the ways they
might be employed, and the small amounts of materials required to cause infection.
Sabotage is the direct application, by a person, of material to the target. It is generally
covert in nature.
b.
Targets. Covert use of biological agents might be aimed primarily at the
respiratory tract and secondly at the digestive tract. Since many pathogens are spread
naturally in food and water, these provide proven vehicles in which the saboteur could
employ an agent. The respiratory tract is an excellent target for the small-scale
employment of a biological antipersonnel agent aerosol.
L-4
NOTES
1TM 3-216/AFM 355-6, Technical Aspects of Biological Defense, January 1971.
2BG 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.”
3BG Russ Zajtchuk et al. (eds), Textbook of Military Medicine: Medical Aspects of Chemical
and Biological Warfare, Office of the Surgeon General, 1997, Chapter 32, “Ricin Toxin.”
4BG Russ Zajtchuk et al. (eds), Textbook of Military Medicine: Medical Aspects of Chemical
and Biological Warfare, Office of the Surgeon General, 1997, Chapter 20, “Use of Biological
Weapons.”
21BG Russ Zajtchuk et al. (eds), Textbook of Military Medicine: Medical Aspects of Chemical
and Biological Warfare, Office of the Surgeon General, 1997, Chapter 30, “Defense Against
Toxic Weapons.”
L-5
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