Transcript Bioweapons - Texas A&M University–Central Texas

Bioweapons
Diseases, Detection, and Doctrine
1
I. Guillemin: Points to
Remember
A. Three phases in the history of BW
B. Difficulty of effective employment –
1. US/UK difficulties in efficient aerosol dispersion.
2. USSR incidents in Kazakhstan and Sverdlovsk
3. Japanese program backfires (perhaps kills more
Japanese soldiers than Chinese!)
4. Nonstate programs numerous but rarely
effective: Criticisms of “Dark Winter” scenarios
C. No “Golden Age” of bioweapon use –
defenses kept pace with offense.
Chemicals more commonly used. Why?
2
I. Guillemin: Points to
Remember
D. The Development of BW as WMD
1. Note the US progress in WW II
2. The “Immunity Deal” with Japanese
scientists and Cold War Research
3. Bureaucratic politics and the need to
match atomic-scale devastation
(competition for scarce resources)
E. Arms races
1. “Looking Glass” justifications and
overestimation of opponents
2. The surprising unilateral renunciation of
Nixon – What explains it?
3
I. Guillemin: Points to
Remember
F. Offense-defense overlap
1. Vaccines as keys to offensive BW
2. Project Whitecoat and the misuse of
conscientious objectors
G. The dilemma of verification – the
weakness of the BWC
1.
2.
3.
4.
The Soviet program
US resistance to verification
Merits and risks of secrecy
Responsible/Irresponsible nations
distinction and international law
4
II. Supplements to Guillemin
A. Use in World War II
1. The case of Stalingrad…
a. Suspicious outbreak of tularemia at
Stalingrad
b. Kenneth Alibek (Soviet weapons scientist)
alleges USSR used bioweapons
c. Other scientists believe outbreak was natural
5
2. Japan’s Unit 731
a. Guillemin lowballs the figures for Chinese
deaths. But Langford (Introduction to
Weapons of Mass Destruction, 2004, p.142)
says 250,000 Chinese killed by Japanese
BW, mainly plague.
b. A few thousand – 250,000 is a big range.
Can we narrow down the effectiveness of the
Japanese program?
6
i. Testimony of Hayashi Shigemi
(October 7, 1954)
• "In 1943…(we) spread cholera once in Shantung
Province... The germ was first dumped into the Wei
River, then the dike was destroyed to let the water flow
into a larger area to rapidly spread the germ. I personally
participated in this mission. I handed the germ to
Kakizoe Shinobu, an Army medical doctor. He then in
turn sent someone else to spread the germ. According to
my knowledge, in our local area there were twenty five
thousand two hundred ninety one Chinese people who
died from this. How many died altogether I do not know,
because it was top-secret information. Our mission was
to murder Chinese people in mass, to test the
effectiveness of the cholera germ, and to be ready to use
it in fighting the Russians.“
• Problem: Unable to locate source of testimony (reprinted
on highly nationalist web sites – but no trials in 1954…)
7
ii. Sources of evidence
• Estimate of 3000 = testimony of one official
who witnessed about 600 deaths/year for 5
years at Ping Fan
• Now considered “gross underestimate”
because excludes other camps
• Prisoners not issued unique IDs: 101-1500
used as ID numbers, then recycled with next
batch of prisoners. X-Rays destroyed by end
of war.
• NONE of these estimates include the actual
plague outbreaks in China. But can those be
blamed on Japanese BW, or were they
natural?
• Ishii had incentives to exaggerate effects of
8
BW
iii. Possible BW-caused epidemics,
1939-1942
• 1939-1940: Typhoid (near Harbin) from
well poisonings
• 1940: Cholera (near Changchun)
• 1942: Paratyphoid A and Anthrax (near
Nanking)
• 1939-1942: Plague epidemics near
Ningbo (possibly from infected rats
released in cities by Japanese troops)
9
c. Bureaucratic Politics?
• Japanese forces were decentralized (Unit 731, Unit 100,
Eu 1644, other units)
• Ishii-Kitano rivalry created incentives to overestimate
BW effectiveness by both researchers
• Hypothesis: Ishii and Kitano deliberately avoided use of
controls (i.e. comparison to plague deaths in non-BW
areas) in order to produce results (think US BMD tests
or manufacturers’ tests of effectiveness for parallels)
• Hypothesis suggests deaths were >10,000 (killed directly) but
<250,000 (because that ascribes all epidemics to BW, which is
probably false)
• Proven BW-induced epidemics killed <1000 in each case,
sometimes < 100
• Accordingly, real figures more likely to be in 20,000-50,000
range
• Problem: No evidence with which to test hypothesis.
Much was destroyed and most of the rest is STILL
classified by the US
10
B. A broad definition
of bioweapons
1. Pathogens: Cause illness
2. Toxins:
a. Produced by biological organisms or
synthesized in the labs
b. Generally worse than “chemical
weapons”
c. Also prohibited by treaty -- “biological and
toxin weapons” different from CW even if
toxins are synthetic
11
12
C. Types of Pathogens
1. Antipersonnel – To kill or disable
people. Focus of most writers.
2. Antianimal – To kill livestock or pack
animals. Less useful with
mechanization, but still economic
weapon.
13
3. Antiplant: A neglected
hazard
a.
b.
c.
d.
US stockpiled fungi (wheat stem
rust, rye stem blast, rice blast) until
1972 for use against crops
Most existing fungi have some
corresponding fungicides –
ineffective unless transport / industry
destroyed
Monoculture increases vulnerability
– use of GEOs (genetically
engineered organisms) increases
risk because generally are
cloned/engineered and patented.
Potential devastation. Examples =
Irish potato famine, American
chestnut blight
14
4. Antimateriel
• Microbes can attack
petroleum (developed for
cleaning up oil spills)
• Other microbes produce
rust and degrade rubber
(less useful against
modern alloys and
plastics)
15
III. Biological Weapons: The
Threat
A. Characteristics: Dependent on type of agent
and dispersal mechanism
1. Types
•
•
•
•
Major Categories: Bacteria, Viruses, Toxins
Persistent (Anthrax) vs. non-Persistent (Influenza)
Lethal (Botulism) vs Incapacitating (Q Fever)
Contagious (Smallpox) vs. non-Contagious (Anthrax)
2. How powerful are bioweapons? Answer depends
on goals of program. Needed: BW strategy and
doctrine
16
B. The Ideal Mass Killer: Characteristics
1. Persistence: Spores or local animal reservoir
2. Highly lethal (% infected that die), with little
immunity
3. No effective treatment (i.e. reducing mortality or
enabling productivity)
4. Factors encouraging epidemic formation
a. Communicable between people (usually trades off against
persistence – ideal is BOTH animals and people as
carriers)
b. Relatively long incubation period
c. Asymptomatic infection: Infectious before symptoms
emerge
d. Vague onset symptoms
5. Widespread dispersal
6. Low ID50 – Amount needed to infect
50% of people (median infective dose)
•
Which pathogens come close?
17
Agent
Persist /
Animal
Host?
Lethality
If Not
Treated
Anthrax
Yes
Smallpox
Commun- Incubaicable?
tion?
Asymptomatic
Infection?
> 90% Lim
No
1-6d
No
No
20-40 No
Yes
12d
No
HIV
No
100% Yes
Lim
9 yrs
Yes
Ebola
Yes
80-90 No
Lim
5-10d No
West Nile Yes
10%
No
5-15d No
Plague
Yes
100% Yes
Yes
2-6d
Tularemia Yes
30-60 Yes
No
2-10d No
Marburg
Yes
25-90 No
Lim
3-9d
Typhus
Yes
10-60 Lim
No
6-16d No
CCHF
Yes
15-30 No
Yes
1-6d
Influenza
Yes
Treatment?
No
.1-3% Lim
Yes
1-4d
No
No
No?
Yes
18
C. Do BW Superweapons
Exist?
1. No natural disease qualifies
2. Genetic engineering can increase lethality
and virulence – but usually not persistence
or communicability
3. Tendency for reduced virulence over time –
disease that kills 100% usually burns out
before infecting all possible hosts. Result =
evolution to weaker forms over time.
4. Who would build one – and why?
Conclusion: Assessing risk requires
analysis of strategic choice
19
D. The Strategic Choice of
Antipersonnel BW Agents
• Two key choices = whether pathogen will
spread on its own (communicability) and
whether disease kills or merely sickens
(lethality)
20
1. Bioweapons: Design Choices
Pathogens
Contagious
Lethal
Nonlethal
NonContagious
Lethal
Nonlethal
21
2. Bioweapons: Strategic Choices
Pathogens
Contagious
Mass
Killing
Economic
Disruption
NonContagious
Area
Denial
Incapacitation
22
3. Bioweapons: Selected Examples
Pathogens
Contagious
Smallpox
Influenza
NonContagious
Anthrax
Q Fever
23
IV. In Depth: Four BW Agents
• Selected as examples of general
classes of BW agents
24
A. Smallpox (Variola virus)
1. History
a. Most deaths of any infectious
disease (500 million deaths in 20th
Century alone)
b. Natural disease eradicated
•
•
•
•
Last U.S. case – 1949 (imported)
Last international case – 1978
Declared eradicated in 1979
Officially, only two stocks remaining
(US and Russia)
25
c. Use of smallpox in war
i. French and Indian Wars (1754-1767)
• British gave Native Americans infected
blankets
• Outbreaks ensued, some tribes lost 50%
ii. Allegations of use in U.S. Civil War
iii. Alleged use by Japanese in China in
WWII
26
d. Why worry about an eradicated
disease?
• Former Soviet Union scientists
have confirmed that smallpox was
successfully weaponized for use in
bombs and missiles
• Active research was undertaken to
engineer more virulent strains
• Possibility of former Soviet Union
virus stock in unauthorized hands
27
2. Bioweapon Potential
a. Features making smallpox a likely agent
•
•
•
•
•
•
•
Can be produced in large quantities
Stable for storage and transportation
Known to produce stable aerosol
High mortality
Highly infectious
Person-to-person spread
Most of the world has little or no immunity
28
b. Likely effects of attack
• Nonimmune population
• <20% of U.S. with substantial immunity
• Potential for more potent attack
• Engineered resistance to vaccine
29
c. Paths to attack
• Airborne route known effective mode
• Initially via aerosol in BT attack
• Then person-to-person
• Hospital outbreaks from coughing patients
• Highly infectious
• <10 virions sufficient to cause infection
• Aerosol exposure <15 minutes sufficient
30
d. Epidemiology of smallpox
• Person-to-person
transmission
• Secondary Attack Rate (SAR)
• 25-40% in unvaccinated contacts
• Relatively slow spread in
populations (compared to
measles, etc.)
• Higher during cool, dry conditions
• Historically 3-4 contacts infected
• May be 10-20 in unvaccinated
population
• Usually requires face-to-face
contact
• Very high potential for
iatrogenic spread

31
3. Symptoms and Outcomes
FEVER
a. Incubation: Four-day period before rash
develops
6
7
8
Pustules
9
10 11 12 13 14
21
Scabs
RASH
Days – 4 – 3 – 2 – 1 1 2 3 4 5
Pre-eruption Papules-Vesicles
Onset of rash
32
b. Symptoms of smallpox from day
one of symptoms (not infection)
• Day 1: Initial rash
appears minor
33
b. Symptoms of smallpox from day
one of symptoms (not infection)
• Day 2: Papules
appear
34
b. Symptoms of smallpox from day
one of symptoms (not infection)
• Day 3: Rash is
distinct; papules
are raised evenly
35
b. Symptoms of smallpox from day
one of symptoms (not infection)
• Day 4: Vesicles
have become firm
and filled with
liquid (highly
infectious)
36
b. Symptoms of smallpox from day
one of symptoms (not infection)
• Day 5: Vesicles
have become
pustules. Fever
rises.
37
b. Symptoms of smallpox from day
one of symptoms (not infection)
• Day 7:
Unmistakeable
smallpox rash (note
that the chest / torso
usually have less
pox than face /
extremities – unlike
chicken pox)
38
b. Symptoms of smallpox from day
one of symptoms (not infection)
• Day 8-9: Pustules
reach maximum
size.
39
b. Symptoms of smallpox from day
one of symptoms (not infection)
• Day 10-19: Pox dry
up and scab over.
Scabs contain live
smallpox virus.
Victim is still
highly infectious.
40
b. Symptoms of smallpox from day
one of symptoms (not infection)
• Day 20: Victim
ceases to be
infectious, but is
likely to be
scarred for life
41
b. Symptoms of smallpox from day
one of symptoms (not infection)
• Again, note that torso has fewer pox
than face / extremities:
42
c. Outcomes
of smallpox
• Historical
data from
limitedimmunity
populations
•

43
d. Predicting fatalities: Relevant
Factors
• S-shaped curve is known –
but how many are in initial
population exposed (first
generation of cases)
determines upper bound.
• Any delay in notification
logarithmically increases
total cases (and deaths)
• About 15% of those who get
smallpox die in partiallyimmune populations
• Danger is greater outside
developed countries (little
residual immunity)
44
B. Influenza: A potential WMD?
1. History: Disease distinguished recently
Timeline of Emergence of
Influenza A Viruses in Humans
Avian
Influenza
Russian
Influenza
Asian
Influenza
Spanish
Influenza
H1
1918
H9
H5
H7
H5
H1
H3
H2
Hong Kong
Influenza
1957 1968 1977
1997 2003
45
1998/9
a. 1918-1919: The worst recent
pandemic
46
From America’s Forgotten
Pandemic by Alfred Crosby
“The social and medical importance
of the 1918-1919 influenza pandemic
cannot be overemphasized. It is
generally believed that about half of
the 2 billion people living on earth in
1918 became infected. At least 20
million people died. In the Unites
states, 20 million flu cases were
counted and about half a million
people died. It is impossible to
imagine the social misery and
dislocation implicit in these dry
statistics.”
47
i. US deaths from influenza greater than US
killed in any war
Thousands
900
800
700
600
500
400
300
200
100
0
Civil
War
WWI
1918-19
Influenza
WWII
Korean
War
Vietnam
War
48
ii. Military Effects
• Slowed delivery of US troops on the
Western front.
• 43,000 deaths in US armed forces.
• Slow down and eventual failure of the
last German offensive (spring and
summer 1918) attributed to influenza.
49
iii. An unusual flu – it killed
military-age people
50
51
iv. Temporal and Spatial Extent:
52
Armstrong, et al. JAMA 1999;281:61-66.
53
54
55
56
57
b. The 1957 “Asian Flu”
i. Key facts:
58
ii. “Asian Flu” Timeline
February 1957
• Outbreak in Guizhou Province, China
April-May 1957
• Worldwide alert
• Vaccine production begins
October 1957
• Peak epidemic, follows school openings
December 1957
• 34 million vaccine doses delivered
• Much vaccine unused
January-February 1958
• Second wave (mostly elderly)
59
iii. Temporal and Spatial Diffusion
Spread of H2N2 Influenza in 1957
“Asian Flu”
Feb-Mar 1957
Apr-May 1957
Jun-Jul-Aug 1957
69,800 US deaths
60
2. Avian Flu: A potential BW Agent?
a. Recent outbreaks
• 1997: H5N1 in Hong Kong
• 18 hospitalizations and 6 deaths
• 1999: H9N2 in Hong Kong
• 2 hospitalizations
• 2003: H5N1 in China
• 2 hospitalizations, 1 death
• H7N7 in the Netherlands
• 80 cases, 1 death
61
b. Ability to Vaccinate?
• Annual vaccine is trivalent (3 strains),
pandemic vaccine will be monovalent.
• Production using current technologies
would likely take 4-5 months  may not
be available before 1st pandemic wave
• There will be vaccine shortages initially
• 2 doses may be necessary to ensure
immunity
63
c. Control: antiviral medications
• Uses
• Prophylaxis
• Treatment
• Issues
• Limited supply
• Need for prioritization (among risk groups
and prophylaxis versus treatment)
• Unlikely to markedly affect course of
pandemic
64
Estimated hospitalizations due to
influenza pandemic
Hospitalizations ('000)
1400
1200
95th percentile
1000
800
Mean
600
400
200
5th percentile
0
15%
20%
25%
30%
35%
National, 1 year gross attack rate
Source: Meltzer et al. EID 1999;5:659-71
66
Estimated deaths due to influenza
pandemic
400
Deaths ('000)
350
95th percentile
300
250
Mean
200
150
100
50
5th percentile
0
15%
20%
25%
30%
35%
National, 1 year gross attack rate
Source: Meltzer et al. EID 1999;5:659-71
67
68
C. Q Fever, aka “Query Fever”
1. Characteristics:
Worldwide endemic
disease in animals
• Caused by Coxiella
burnetii
• Shed in birthing
fluids, excreta, milk
• Humans infected via
inhalation, ingestion
Electron micrograph showing an infected
monkey cell with one large vacuole
harboring about 20 Coxiella burnetii
bacteria. [Credit: R Heinzen, NIAID] 69
Cases of Q fever in Humans Reported
by State Health Departments, 1978-2004
80
60
50
40
30
20
10
0
1978
1979
1980
1981
1982
1983
1984
1985
1986
1987
1988
1989
1990
1991
1992
1993
1994
1995
1996
1997
1998
1999
2000*
2001*
2002*
2003*
2004*
Number of Cases
70
* Years in which Q fever was a Year
Nationally Reportable Disease
70
2. Assets of Q Fever for BW
• Shed in the environment in a small cell form
that is very hardy (“spore-like”)
• Resistant to pH changes, desiccation, UV light
• Resistant to some common disinfectants
• Remains viable in soil, dust for months to years
- isolated from barns, soil – culture, PCR
71
Growing Q
Fever:
The “8-Ball”
Ft. Detrick, MD
ca. 1968
72
3. Acute Q fever
• 1-3 week incubation
• Asymptomatic infections occur
• Nonspecific flu-like illness: fever, severe
headache, fatigue, nausea, vomiting, etc.
• Pulmonary Syndrome (~30%)
• Hepatitis (30-60%)
• Chronic fatigue-like illness
• Following acute infection in Australian
slaughterhouse workers (10%)
• Antibiotics may shorten course
• Low mortality (< 1 %)
73
D. Anthrax
1. History
a. Disease is ancient
b. Disease most common in agricultural
areas (cattle and sheep)
c. Industrial Revolution: Woolworkers’
disease
d. Animal vaccine developed: Cases
dropped in developed world
74
Anthrax—United States, 1951-2002
70
Animal vaccine
60
Cases
50
Human vaccine
Bioterrorism
40
30
20
10
0
1955
1960
1965
1970
1975
1980
1985
1990
1995
200075
20,000-100,000 cases estimated globally/year
http://www.vetmed.lsu.edu/whocc/mp_world.htm
76
e. Anthrax Attacks
i.
South Africa and Rhodesia 1978-1980:
Anthrax probably used by apartheid
forces
•
•
•
•
•
•
Thousands of cattle died
10,738 human cases (largest known
outbreak of human anthrax in history)
182 known deaths
Black-inhabited Tribal Lands only
White populations untouched
South Africans admit involvement to Truth
and Reconciliation Commission in 1998 77
ii. Accidental release:
Sverdlovsk, April-May 1979
Cause now known
to be failure to
replace air filter
94 infections, 64
deaths
78
iii. 1993: Aum Shinrikyo attack
• Japanese religious
cult
• “Supreme truth”
• No human injuries.
Why?
79
Answer: They used the wrong strain
• Disease-causing strain carries 2
plasmids each containing a different
toxin gene.
• Both genes must be expressed to
cause disease.
Toxin gene 2
Bacillus anthracis
Toxin gene 1
80
Answer: They used the wrong strain
• Strain produced and disseminated by
terrorists in Tokyo carried only one of
the plasmids, so it was not pathogenic.
Strain was actually used for vaccine
research.
• Bioterrorists are not knowledgeable in
the molecular biology of disease.
81
iv. The Anthrax Letters, 2001
• 22 cases
• 11 cutaneous
• 11 inhalation
• 5 deaths (all inhalation)
•
•
•
•
Index case in Florida
2 postal workers in Maryland
Hospital supply worker in NYC
Elderly farm woman in Connecticut
82
Anthrax Cases, 2001
•
•
•
•
7 month old boy
Visited ABC
Cutaneous lesion
Initial diagnosis:
Newsroom
• spider bite
• Punch biopsies confirmed anthrax
83
2. Human Transmission
• Cutaneous
• Contact with infected
tissues, wool, hide, soil
• Biting flies
• Inhalational
• Tanning hides,
processing wool or bone
• Gastrointestinal
• Undercooked meat
84
a. Cutaneous
Anthrax
• 95% of all cases globally
• Incubation: 3-5 days (up to 12 days)
• Spores enter skin through open wound or
abrasion Large skin ulcer created
• Fever and malaise  5% - 20% mortality
• Untreated – septicemia and death. Edema
(swelling due to lymphatic fluid) can lead to
death from asphyxiation if lesion is near
neck
85
Day 2
Day 4
Day 6
86
b. Gastrointestinal
Anthrax
• Severe gastroenteritis
• Incubation: 2-5 days after
consumption of
undercooked,
contaminated meat
• Case fatality rate: 25-75%
• GI anthrax never
documented in U.S.
87
c. Inhalation Anthrax
• Incubation: 1-7 days
• Initial phase
• Nonspecific - Mild
fever, malaise
• Second phase
• Severe respiratory
distress
• Cyanosis, death in
24-36 hours
• Case fatality: 75-90%
(untreated)
88
3. Vaccination and
Treatment
a. Vaccine – available but
effectiveness unproven in
humans (only monkeys)
•
•
•
5-35% experience systemic side
effects
No long-term side effects proven
Six shots plus annual booster
required
89
b. Treatment
i. Penicillin
• Has been the drug of choice
• Some strains resistant to penicillin
ii. Ciprofloxacin
• Chosen as treatment of choice in 2001
• No strains known to be resistant
90
4. Anthrax BW: Possible Effects
a. Worst-case scenario (Office of
Technology Assessment)
• 50 kg of spores
• Urban area of 5 million
• 250,000 cases of anthrax
• 100,000 deaths
• 100 kg of spores
• Upwind of Wash D.C.
• 130,000 to 3 million deaths
91
b. Why have previous releases failed
to generate mass casualties?
• Imperfect dispersal – low volume
(Sverdlovsk) or limited volume of
aerosol (2001 letters)
• Availability of antibiotics – Allows
prophylaxis unless attack is both
massive and undiscovered before
symptoms
92
V. Biodefense: Prevention
A. Preventing state use of BW
1. Mass vaccination is impractical (unless
one has time – i.e. intends to use them
first)
2. Deterrence – Threaten retaliation with
something that exceeds benefits of BW
use (thus increased BW effectiveness
increases threat needed to deter)
3. Nonproliferation – Prevent the spread of
capability (more on this later…)
93
B. Preventing Bioterrorism
1. Access control. US data and
regulations:
• >300 registered institutions
with bioweapons agents
• >16,000 registered
individuals with bioweapons
agents
• Only security requirement is
a lock on the door
• No requirement to exclude
non-screened personnel for
labs
• No requirement for secure
transport
94
2. Anticipation: Ideal Characteristics
for Potential Biological Terrorism
Agent
•
•
•
•
•
•
Inexpensive, easy to produce
Can be aerosolized (1-10 µm)
Survives sunlight, drying, heat
Cause lethal or disabling disease
No effective treatment or prophylaxis
Person-to-person transmission (to make
the most of small amounts of agent)
95
Agent
Ease to
Acquire
Lethality
If Not
Treated
Anthrax
Easy
Smallpox
Commun- Incubaicable?
tion?
Treatment
> 90% Yes
No
1-6d
Lim
Hard
20-40 Yes
Yes
12d
No
HIV
Easy
100% No
Lim
9 yrs
Yes
Ebola
Hard
80-90 Yes
Lim
5-10d No
West Nile Hard
10%
No
5-15d No
Plague
Med
100% Yes
Yes
2-6d
Tularemia Med
30-60 Yes
No
2-10d Yes
Marburg
Hard
25-90 Yes
Lim
3-9d
Typhus
Med
10-60 Yes
No
6-16d Lim
CCHF
Med
15-30 No
Yes
1-6d
Influenza
Easy
Aerosol?
Yes
.1-3% Yes
Yes
1-4d
Yes
No
No
Lim
96
Ideal Agents for Terrorists
• Smallpox is ideal but well-guarded
• Anthrax has only limited treatment
(must treat before symptoms to save
inhalational cases) and isn’t
communicable but is otherwise the best
• Third best is probably plague, especially
if many people are rapidly infected
97
3. Estimated Casualties From
an Undetected Bioterrorist
Release
• WHO data (Health Aspects of Chemical
and Biological Weapons, 1970)
• Assumes urban area of 500,000 people
• Assumes 110 pounds (50 kg) of dried
agent released in a one mile (2 km) line
upwind of the city
• Assumes attack is initially undetected
98
• Assumes developed country
3. Estimated Casualties From
an Undetected Bioterrorist
Release
Agent
Rift Valley Fever
Typhus
Brucellosis
Plague
Q Fever
Tularemia
Anthrax
* Includes deaths
Downwind
Reach (km)
Dead
Sick*
1
5
10
10
20
20
20
100
2,500
150
6,500
50
4,500
24,000
10,000
30,000
27,000
27,000
60,000
60,000
60,000
99
4. Challenges of Detection
a. Initial Symptoms too vague to know
attack has occurred
Agent
Anthrax
Clinical
Effect
Mediastinitis
Plague
Pneumonia
Q fever
Pleuritis,
hepatitis
Tularemia
Pneumonia
Smallpox
Pustules
Initial
Symptoms
}
Headache
Fever
Malaise
Cough
100
b. Epidemiologic Clues
• Tight cluster of cases
• High infection rate
• Unusual or localized
geography (rural
disease in urban area)
• Unusual time of year
(i.e. flu-like symptoms
in midsummer)
• Dead animals (for
some diseases)
101
4. Which groups are capable?
a. Requirements
• Virulent strain of agent
• Equipment and expertise to culture agent
safely
• Equipment and expertise to stockpile agent
until use
• Equipment and expertise to generate right
size aerosol OR access to processed food
/ water supplies
102
b. Intent:
Which
groups
try?
103
C. Defense against accidental
release
1. Encourage other countries to
implement safeguards, esp. on
government programs
2. US: High security for BW research but
not private research.
Universities: Essentially no safety
regulations (voluntary only, apply to NIH
grants for recombinant-DNA research
only)
104
VI. Proliferation of BW
A. What are the incentives to build BW?
105
1. Advantages of Bioweapons
• Small amount needed
• Pathogens grow inside host
• Extremely toxic
• Botox: Dot of an “i” kills 10
• Easy/inexpensive to grow
• Cheese making equipment
(viruses more difficult than
bacteria / toxins)
• Large amount produced in
short period of time
• Days to weeks
• Potential for panic
106
2. Disadvantages of Bioweapons
• Protection of Workers and Public
• Release into environment (Sverdlovsk was state
of the art!)
• Quality control
• Particles must be aerosolized (1 micron or so)
• Delivery problems
• Rain, wind, UV light
• Bombs, bomblets, and shells produce poor,
localized aerosols
• Heat and shock waves (explosions) kill most
organisms
• Poor storage survival
• Difficult to control release – “boomerang
effects”
107
B. Patterns of Proliferation
108
1. CBW Proliferation (Official)
109
2. Suspected BW Proliferation
110
3. Causes of BW Proliferation
a. Portfolio Strategy: Every BW aspirant
has also pursued Chemical and/or
Nuclear Weapons. What does this
suggest?
b. Cost-Effectiveness: BW cheaper than
other WMD
c. Ease of acquisition: offensive BW relies
on dual-use technology
d. Difficult to detect: Weakness of BWC,
permissibility of defensive research
111
4. Predicting BW Proliferation
• Best predictors are security variables:
• Enduring Rivalry Increases Risk
• Dispute Involvement Increases Risk
• Defense Pact Decreases Risk
• Large states more likely to develop BW
• Other predictors include:
• Democracy Decreases Risk
• IO Membership Slightly Increases Risk
• Wealth Increases Risk
112
C. Proliferation: The Risks
1. Risk of state use –
Relationship depends on
balance between deterrence
and escalation
a. Deterrence – Use of threats to
prevent BW
b. Escalation – Use of BW to
achieve dominance in war
c. Little evidence to test
comparisons – State BW use has
always been rare. Only
examples are cases where no
retaliation was possible.
113
d. BW Doctrines as Evidence
(Planning the Unthinkable)
i. Realism: States use BW to alter the
balance of power with rivals. Implies
BW good for the weak side in
asymmetric dyads, bad for the strong
side in asymmetric dyads, and good for
balanced dyads. Problem = balance of
capabilities appears to increase war
risk!
114
ii. Organization theory
• Military organizations pursue autonomy
and therefore develop offensive
strategies
• Undermines ability of BW to deter
(realism) because militaries are partially
independent of political calculations that
drive civilians to avoid war
115
iii. Strategic culture theory
• Civilians also pursue goals other than
national security – i.e. re-election
• Militaries differ in the degree to which
they seek autonomy
• No clear conclusions about whether
more BW is dangerous
• Which theory is correct? Read the case
studies…
116
2. Risk of nonstate use
• Proliferation should increase
risk of nonstate use, ceteris
paribus. Why?
• However, hypothesis is difficult
to test because all is not equal:
Role of nonstate actors in
politics changes over time
(increase in foreign military
intervention by nonstate actors)
117
3. Risk of accidental use
a. Risk is not zero – remember
Sverdlovsk
b. Risk increases with each new BW
state
c. Safety measures can slow the
increase but not avert it.
118
4. The danger of proliferation
a. The nonstate dimension: We don’t need to
assume “rogue states” are any different in
order to conclude that more BW is
dangerous. Majority of BW uses have been
nonstate or accidental releases!
b. State-level deterrence fails: does not deter
nonstate actors and has only limited effect
on accidental releases (provides incentive
for strong safety systems)
c. Conclusion: Deterrence alone is insufficient.
Efforts to reduce proliferation or roll back
BW programs necessary to decrease BW
risk
119
D. Anti-Proliferation Strategies
1. Nonproliferation: Arms Control
(See Assignment 2 and in-class
exercises for details on the BWC and
its effect on proliferation)
120
a. The 5th Review Conference of the
BWC
i.
ii.
US scuttles the conference (Guillemin) BUT
Russia also tried to undermine BWC
through definition of dozens of terms (would
create legal loopholes to enable “everything
but” BW programs)
iii. NAM (led by China and including Pakistan
and India) sought to strengthen Article X
(sharing technical expertise) at the expense
of Article III (export controls) and even
inspections
121
b. The
th
6
Review Conference
• Ended December 8, 2006
• Only significant accomplishment was
agreement on annual meetings before
the next Review Conference in 2011
• (The 2011 meeting is our simulation)
122
2. Counterproliferation:
Compellence as a strategy
a. Rejects deterrence alone – must have
ability to coerce states or groups with
BW into renouncing it, not just to
refrain from using it
b. Distinct from arms control – includes
use of force; associated with
reluctance to make concessions
(bargain)
123
3. Paradoxes of Anti-Proliferation
a. Counterproliferation can undermine
nonproliferation – Threat of pre-emptive
war may encourage WMD development.
New counterproliferation strategies
threaten first use of nuclear weapons
(new bunker busters). See the Sagan
article for why this might be a bad idea.
124
b. The deterrence dilemma
• Deterrence cannot roll back BW,
because BW programs built in full
knowledge of the deterrent threat (i.e.
already taken into consideration)
• Increased ability to deter increases
threat (primary driver of proliferation)
125
c. The nonproliferation paradoxes
i.
Rewarding bad behavior: Incentives
to renounce BW may encourage
others to build BW as bargaining chips
ii. Substitution effect: Verification on one
dimension of WMD may increase
appeal of other dimensions
126