1 bioweapons diseases, detection, and doctrine. 2 i. guillemin: points to remember a.three phases in...

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Bioweapons

Diseases, Detection, and Doctrine

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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?

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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?

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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

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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

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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?

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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…)

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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

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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)

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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

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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

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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.

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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

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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)

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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

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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?

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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

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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

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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)

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1. Bioweapons: Design Choices

Pathogens

ContagiousNon-

Contagious

Lethal Nonlethal Lethal Nonlethal

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2. Bioweapons: Strategic Choices

Pathogens

ContagiousNon-

Contagious

Mass Killing

EconomicDisruption

AreaDenial

Incapacitation

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3. Bioweapons: Selected Examples

Pathogens

ContagiousNon-

Contagious

Smallpox Influenza Anthrax Q Fever

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IV. In Depth: Four BW Agents

• Selected as examples of general classes of BW agents

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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)

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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

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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

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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

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b. Likely effects of attack

• Nonimmune population• <20% of U.S. with substantial immunity

• Potential for more potent attack• Engineered resistance to vaccine

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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

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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

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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

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• Day 1: Initial rash

appears minor

b. Symptoms of smallpox from day one of symptoms (not infection)

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• Day 2: Papules

appear


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• Day 3: Rash is

distinct; papules

are raised evenly


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• Day 4: Vesicles

have become firm

and filled with

liquid (highly

infectious)


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• Day 5: Vesicles

have become

pustules. Fever

rises.


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• Day 7:

Unmistakeable

smallpox rash (note

that the chest / torso

usually have less

pox than face /

extremities – unlike

chicken pox)


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• Day 8-9: Pustules

reach maximum

size.


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• Day 10-19: Pox dry

up and scab over.

Scabs contain live

smallpox virus.

Victim is still

highly infectious.


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• Day 20: Victim

ceases to be

infectious, but is

likely to be

scarred for life


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• Again, note that torso has fewer pox

than face / extremities:


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c. Outcomes of smallpox

• Historical data from limited-immunity populations

•

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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)

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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

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a. 1918-1919: The worst recent pandemic

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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.”

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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

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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.

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iii. An unusual flu – it killed military-age people

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iv. Temporal and Spatial Extent:

Armstrong, et al. JAMA 1999;281:61-66.

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b. The 1957 “Asian Flu”i. Key facts:

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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

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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

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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

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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

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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

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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

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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

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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]

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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

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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

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Growing Q Fever:

The “8-Ball”Ft. Detrick, MD ca. 1968

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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 %)

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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

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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

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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

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ii. Accidental release: Sverdlovsk, April-May 1979

Cause now known to be failure to replace air filter

94 infections, 64 deaths

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iii. 1993: Aum Shinrikyo attack

• Japanese religious cult• “Supreme truth”

• No human injuries. Why?

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• 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

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• 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

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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

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Anthrax Cases, 2001

• 7 month old boy• Visited ABC Newsroom• Cutaneous lesion• Initial diagnosis:

• spider bite

• Punch biopsies confirmed anthrax

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2. Human Transmission

• Cutaneous• Contact with infected

tissues, wool, hide, soil• Biting flies

• Inhalational• Tanning hides,

processing wool or bone• Gastrointestinal

• Undercooked meat

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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

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Day 2

Day 6

Day 4

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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.

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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)

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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

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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

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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

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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

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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

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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)

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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

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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…

117

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)

118

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

1 bioweapons diseases, detection, and doctrine. 2 i. guillemin: points to remember a.three phases in...

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