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1
Bioweapons
Diseases, Detection, and Doctrine
2
I. Guillemin: Points to RememberA. 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?
3
I. Guillemin: Points to Remember
D. The Development of BW as WMD1. Note the US progress in WW II2. The “Immunity Deal” with Japanese
scientists and Cold War Research3. Bureaucratic politics and the need to
match atomic-scale devastation (competition for scarce resources)
E. Arms races1. “Looking Glass” justifications and
overestimation of opponents2. The surprising unilateral renunciation of
Nixon – What explains it?
4
I. Guillemin: Points to RememberF. Offense-defense overlap
1. Vaccines as keys to offensive BW2. Project Whitecoat and the misuse of
conscientious objectors
G. The dilemma of verification – the weakness of the BWC
1. The Soviet program2. US resistance to verification3. Merits and risks of secrecy4. Responsible/Irresponsible nations
distinction and international law
5
II. Supplements to Guillemin
A. Use in World War II1. 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
6
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?
7
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…)
8
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 BW
9
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)
10
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
11
B. A broad definition of bioweapons
1. Pathogens: Cause illness2. 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
12
13
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.
14
3. Antiplant: A neglected hazard
a. US stockpiled fungi (wheat stem rust, rye stem blast, rice blast) until 1972 for use against crops
b. Most existing fungi have some corresponding fungicides – ineffective unless transport / industry destroyed
c. Monoculture increases vulnerability – use of GEOs (genetically engineered organisms) increases risk because generally are cloned/engineered and patented.
d. Potential devastation. Examples = Irish potato famine, American chestnut blight
15
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)
16
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
17
B. The Ideal Mass Killer: Characteristics1. Persistence: Spores or local animal reservoir2. Highly lethal (% infected that die), with little
immunity3. 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 periodc. Asymptomatic infection: Infectious before symptoms
emerged. Vague onset symptoms
5. Widespread dispersal
6. Low ID50 – Amount needed to infect 50% of people (median infective dose)
• Which pathogens come close?
18
Agent Persist / Animal Host?
Lethality If Not Treated
Treat-ment?
Commun-icable?
Incuba-tion?
Asymp-tomatic Infection?
Anthrax Yes > 90% Lim No 1-6d No
Smallpox 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 No 5-15d No
Plague Yes 100% Yes Yes 2-6d No
Tularemia Yes 30-60 Yes No 2-10d No
Marburg Yes 25-90 No Lim 3-9d No
Typhus Yes 10-60 Lim No 6-16d No
CCHF Yes 15-30 No Yes 1-6d No?
Influenza Yes .1-3% Lim Yes 1-4d Yes
19
C. Do BW Superweapons Exist?1. No natural disease qualifies2. 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
20
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)
21
1. Bioweapons: Design Choices
Pathogens
ContagiousNon-
Contagious
Lethal Nonlethal Lethal Nonlethal
22
2. Bioweapons: Strategic Choices
Pathogens
ContagiousNon-
Contagious
Mass Killing
EconomicDisruption
AreaDenial
Incapacitation
23
3. Bioweapons: Selected Examples
Pathogens
ContagiousNon-
Contagious
Smallpox Influenza Anthrax Q Fever
24
IV. In Depth: Four BW Agents
• Selected as examples of general classes of BW agents
25
A. Smallpox (Variola virus)
1. Historya. 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)
26
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
27
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
28
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
29
b. Likely effects of attack
• Nonimmune population• <20% of U.S. with substantial immunity
• Potential for more potent attack• Engineered resistance to vaccine
30
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
31
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
32
3. Symptoms and Outcomes
a. Incubation: Four-day period before rash develops
Onset of rash
FEVE
R
RA
SH
Pre-eruption Papules-Vesicles Pustules Scabs
Days – 4 – 3 – 2 – 1 1 2 3 4 5 6 7 8 9 10 11 12 13 14 21
33
• Day 1: Initial rash
appears minor
b. Symptoms of smallpox from day one of symptoms (not infection)
34
• Day 2: Papules
appear
b. Symptoms of smallpox from day one of symptoms (not infection)
35
• Day 3: Rash is
distinct; papules
are raised evenly
b. Symptoms of smallpox from day one of symptoms (not infection)
36
• Day 4: Vesicles
have become firm
and filled with
liquid (highly
infectious)
b. Symptoms of smallpox from day one of symptoms (not infection)
37
• Day 5: Vesicles
have become
pustules. Fever
rises.
b. Symptoms of smallpox from day one of symptoms (not infection)
38
• Day 7:
Unmistakeable
smallpox rash (note
that the chest / torso
usually have less
pox than face /
extremities – unlike
chicken pox)
b. Symptoms of smallpox from day one of symptoms (not infection)
39
• Day 8-9: Pustules
reach maximum
size.
b. Symptoms of smallpox from day one of symptoms (not infection)
40
• Day 10-19: Pox dry
up and scab over.
Scabs contain live
smallpox virus.
Victim is still
highly infectious.
b. Symptoms of smallpox from day one of symptoms (not infection)
41
• Day 20: Victim
ceases to be
infectious, but is
likely to be
scarred for life
b. Symptoms of smallpox from day one of symptoms (not infection)
42
• Again, note that torso has fewer pox
than face / extremities:
b. Symptoms of smallpox from day one of symptoms (not infection)
43
c. Outcomes of smallpox
• Historical data from limited-immunity populations
•
44
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 partially-immune populations
• Danger is greater outside developed countries (little residual immunity)
45
B. Influenza: A potential WMD?1. History: Disease distinguished recently
Timeline of Emergence of Timeline of Emergence of Influenza A Viruses in HumansInfluenza A Viruses in Humans
1918 1957 1968 1977 19971998/9
2003
H1
H1H3
H2
H7H5H5
H9
SpanishInfluenza
AsianInfluenza
RussianInfluenza
AvianInfluenza
Hong KongInfluenza
46
a. 1918-1919: The worst recent pandemic
47
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.”
48
i. US deaths from influenza greater than US killed in any war
0
100
200
300
400
500
600
700
800
900
Civil WWI 1918-19 WWII Korean Vietnam
War Influenza War War
Thousands
49
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.
50
iii. An unusual flu – it killed military-age people
51
52
iv. Temporal and Spatial Extent:
Armstrong, et al. JAMA 1999;281:61-66.
53
54
55
56
57
58
b. The 1957 “Asian Flu”i. Key facts:
59
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)
ii. “Asian Flu” Timeline
60
iii. Temporal and Spatial Diffusioniii. Temporal and Spatial Diffusioniii. Temporal and Spatial Diffusioniii. Temporal and Spatial Diffusion
69,800 US deaths69,800 US deaths69,800 US deaths69,800 US deaths
Spread of H2N2 Influenza in 1957Spread of H2N2 Influenza in 1957“Asian Flu“Asian Flu””
Spread of H2N2 Influenza in 1957Spread of H2N2 Influenza in 1957“Asian Flu“Asian Flu””
Feb-Mar 1957Apr-May 1957Jun-Jul-Aug 1957
61
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
63
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
64
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
66
Estimated hospitalizations due to influenza pandemic
0
200
400
600
800
1000
1200
1400
15% 20% 25% 30% 35%
National, 1 year gross attack rate
Ho
spit
aliz
atio
ns
('00
0)
95th percentile
5th percentile
Source: Meltzer et al. EID 1999;5:659-71
Mean
67
Estimated deaths due to influenza pandemic
0
50
100
150
200
250
300
350
400
15% 20% 25% 30% 35%
National, 1 year gross attack rate
Dea
ths
('00
0)
95th percentile
5th percentile
Source: Meltzer et al. EID 1999;5:659-71
Mean
68
69
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]
70
Cases of Q fever in Humans Reported by State Health Departments, 1978-2004
* Years in which Q fever was a Nationally Reportable Disease
0
10
20
30
40
50
60
70
80
1978
1979
1980
1981
1982
1983
1984
1985
1986
1987
1988
1989
1990
1991
1992
1993
1994
1995
1996
1997
1998
1999
2000
*20
01*
2002
*20
03*
2004
*
Year
Nu
mb
er o
f Cas
es
71
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
72
Growing Q Fever:
The “8-Ball”Ft. Detrick, MD ca. 1968
73
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 %)
74
D. Anthrax
1. Historya. 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
75
0
10
20
30
40
50
60
70
1955 1960 1965 1970 1975 1980 1985 1990 1995 2000
Cas
es
Anthrax—United States, 1951-2002
Animal vaccine
Human vaccineBioterrorism
7620,000-100,000 cases estimated globally/yearhttp://www.vetmed.lsu.edu/whocc/mp_world.htm
77
e. Anthrax Attacksi. 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
78
ii. Accidental release: Sverdlovsk, April-May 1979
Cause now known to be failure to replace air filter
94 infections, 64 deaths
79
iii. 1993: Aum Shinrikyo attack
• Japanese religious cult• “Supreme truth”
• No human injuries. Why?
80
• Disease-causing strain carries 2 plasmids each containing a different toxin gene.
• Both genes must be expressed to cause disease.
Bacillus anthracis Toxin gene 1
Toxin gene 2
Answer: They used the wrong strain
81
• 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.
Answer: They used the wrong strain
82
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
83
Anthrax Cases, 2001
• 7 month old boy• Visited ABC Newsroom• Cutaneous lesion• Initial diagnosis:
• spider bite
• Punch biopsies confirmed anthrax
84
2. Human Transmission
• Cutaneous• Contact with infected
tissues, wool, hide, soil• Biting flies
• Inhalational• Tanning hides,
processing wool or bone• Gastrointestinal
• Undercooked meat
85
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
86
Day 2
Day 6
Day 4
87
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.
88
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)
89
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
90
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
91
4. Anthrax BW: Possible Effectsa. 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
92
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
93
V. Biodefense: Prevention
A. Preventing state use of BW1. 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…)
94
B. Preventing Bioterrorism1. 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
95
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)
96
Agent Ease to Acquire
Lethality If Not Treated
Aerosol? Commun-icable?
Incuba-tion?
Treatment
Anthrax Easy > 90% Yes No 1-6d Lim
Smallpox 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% Yes No 5-15d No
Plague Med 100% Yes Yes 2-6d Yes
Tularemia Med 30-60 Yes No 2-10d Yes
Marburg Hard 25-90 Yes Lim 3-9d No
Typhus Med 10-60 Yes No 6-16d Lim
CCHF Med 15-30 No Yes 1-6d No
Influenza Easy .1-3% Yes Yes 1-4d Lim
97
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
98
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• Assumes developed country
99
3. Estimated Casualties From an Undetected Bioterrorist Release
AgentAgent
Rift Valley FeverRift Valley FeverTyphusTyphusBrucellosisBrucellosisPlaguePlagueQ FeverQ FeverTularemiaTularemiaAnthraxAnthrax
Downwind Downwind ReachReach (km) (km)
1155
10101010202020202020
DeadDead
1001002,5002,500
1501506,5006,500
50504,5004,500
24,00024,000
Sick*Sick*
10,00010,00030,00030,00027,00027,00027,00027,00060,00060,00060,00060,00060,00060,000
* Includes deaths
100
4. Challenges of Detection
AnthraxAnthrax
PlaguePlague
Q feverQ fever
Tularemia Tularemia
SmallpoxSmallpox
AgentAgent
MediastinitisMediastinitis
PneumoniaPneumonia
Pleuritis, Pleuritis, hepatitishepatitis
PneumoniaPneumonia
PustulesPustules
Clinical Clinical EffectEffect
}HeadacheHeadache
FeverFever
MalaiseMalaise
CoughCough
InitialInitial SymptomsSymptoms
a. Initial Symptoms too vague to know attack has occurred
101
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)
102
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
103
b. Intent: Which groups try?
104
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)
105
VI. Proliferation of BW
A. What are the incentives to build BW?
106
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
107
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”
108
B. Patterns of Proliferation
109
1. CBW Proliferation (Official)
110
2. Suspected BW Proliferation
111
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
112
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
113
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.
114
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!
115
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
116
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…
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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)
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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.
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4. The danger of proliferationa. 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
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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)
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a. The 5th Review Conference of the BWC
i. US scuttles the conference (Guillemin) BUT
ii. 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
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b. The 6th 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)
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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)
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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.
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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)
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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