Korean haemorrhagic fever 1951
Dengue haemorrhagic fever 1953
Argentine haemorrhagic fever 1953
Kyasanu Forest fever 1956
Human babesiosis 1957
O'nyong - nyong fever 1959
Bolivian haemorrhagic fever 1960
La Crosse encephalitis 1965
Marburg disease 1967
Intestinal capillariasis 1967
Pontiac fever 1968
Lassa fever 1969
Human toxoplasmosis 1970
Lyme fever 1975
Ebola fever 1976
Legionnaires disease 1976
Adult T-cell leukemia 1977
Rift valley fever 1977
Toxic shock syndrome 1980
Escherichia coli O157:H7 1982
Brazilian purpuric fever 1984
Human ehrlichiosis 1986
Venezuelan haemorrhagic fever 1989
Toxic shock like syndrome 1989
"Meat-eating" disease 1989
Hantavirus pulmonary syndrome 1993
Why South America and Africa?
Korean haemorrhagic fever (Seoul hantavirus) (causes internal bleeding, shock and
Dengue (occurs in South America - a child killer)
Argentine h.f. (Juni virus - killed 20% of victims)
Human babesiosis (a malaria like condition spread from cattle; Yugoslavia)
O'nyong - nyong fever (Uganda; mild)
Oropouche (Brazil; mild)
La Crosse encephalitis (Wisconsin)
Marburg disease (Zaire and Sudan; 31 workers in Marburg, Germany - 7 died)
Pontiac fever (mild legionnaires)
Lassa fever (Nigeria)
Lyme fever (tick borne)
Ebola fever (death rate: 50-90%)
Legionnaires disease (50000 cases annually in USA)
Toxic shock syndrome (S. aureus toxins on tampons)
Escherichia coli O157:H7 (food!)
Toxic shock like syndrome*
* Streptococcus A
ORIGIN OF DISEASE
• Extraterrestrial source!
• From other species:
• smallpox probably from dogs and cattle
• haemorrhagic fevers from rodents and monkeys
• TB from cattle and birds
• common cold from horses
• AIDS probably from African monkeys
• Routes of transmission
• mosquitoes, ticks
• Disease is old (~0.5 billion years)
• fossil plants have fossil fungus infections
• ancient jellyfish and molluscs have signs of parasites
• 250 million old dinosaur bones with signs of bacterial infection
• remains of mastodons and sabre-tooth tiger with bacterial infections
• Hosts are initially susceptible to new diseases (= no immunity)
• In Central and South America, mosquitoes infect tree top monkeys with yellow
fever virus, which remains in tree canopy. Loggers fell trees; mosquitoes descend,
bite loggers and transmit virus. Loggers spread virus in cities.
• Trichinosis is spread by contaminated undercooked pork (now a problem in
• Scrapie in sheep to BSE in cattle
• Bovine TB, an ancient disease of cattle, spread to humans with domestication
• Brucella, present in ungulates, spreads in farm herds, causing spontaneous
• Trypanosoma brucei strikes domesticated herds in Africa
[Agriculture has resulted in new ills!]
ORIGINS OF DISEASE
Some diseases pass between humans and animals, e.g. malaria, yellow fever, influenza.
• Influenza virus may have originated in birds and swine. With domestication, strains have
been exhcanged and mutated, resulting in human only stains, and occasional pandemics,
• Measles is akin to canine distemper virus [= likely originator], rinderpest of cattle, and a
form of swine fever
• lyme fever from deer ticks
• bubonic plague from fleas of rodents
• Africans, clearing land, have contracted haemorrhagic fever from monkeys and wild rats
(and possibly AIDS from monkeys)
• Thomas Hull estimates that humans have contracted diseases from dogs (65), cattle
(45), sheep/goats (46), pigs (42), horses (35), rats/mice (32), poultry (26)
• Mosquitoes carry Plasmodium ovale - a mild form of malaria. West Africans cleared
land for farming; disrupted the mosquitoes carrying P. ovale. The niche was taken by
Anopheles gambiae, which transmits P. falciparum; the cause of malignant subtertian
malaria - responsible for ~95% of all malaria deaths.
• A genetic adaptation (sickle-cell trait) offers P. falciparum a starvation diet giving
rise to a lighter infection and fewer symptoms.
• This trait gives other problems- weak children, who are debilitated and have early
• "Mystery disease of Pudoc" - Philippines, 1965
• In the village of Pudoc, people (particularly men) developed a wasting intestinal
disease, many of whom died.
• By 1979, 2000 cases in Philippines (100? deaths)
• No bacteria or viruses (supernatural!)
• Small intestine found to be packed with microscopic helminths, dubbed Capillaria
philippiensis = intestinal capillariasis
• Source: fish (possibly as a secondary host)
• The reason for the disease: consumption of raw seafood and the raw vital organs of
terrestrial animals (goats/cows).
• It is not in the interest of a pathogen/parasite to kill its major host!
• When a pathogen strikes a new population, they are not discriminating but attack
most individuals of all ages, and damage many organs. Yet, as host and pathogen
adapt to each other, the disease tends to become less acute with milder symptoms in
fewer organs. For example [AIDS?]:
• Syphilis. First appeared in Europe in C15, causing repulsive pustules over the entire
body and attacking many organs. Death occurred within a few years. 50 years later,
symptoms were less severe, being restricted to the genital, face and nervous system.
Death took many years.
• Measles. Evolved from canine distemper, adapting to humans. Death rate still 10%
in poor countries (1 million deaths/yr).
• Leprosy (the first "new" disease)
• TB - resurgence in the 90's.
• Possibly the pathogens originated in the sea, and became adapted to fish and reptiles.
• Leprosy - thought to have mutated from an ancestor in mice.
• Fiennes believed that humans first acquired leprosy from Asian water buffalo by
using its hide.
• Leprosy probably arose in the area bounded by India and East Africa (4000 yrs ago),
then spread to China, to Egypt, etc.
• Leprosy only occurs naturally in humans (artificially infects armadillos and the
footpads of mice)
• Leprosy is a difficult disease to transmit (despite all the myths).
• The disease may take decades to damage humans, and decades to exert its worst
• Leprosy eventually disfigures - swellings to the face, skin lesions, weakness, paralysis
and mutilated fingers and toes (lepers have ben loathed by society).
• Oldest proof is in Egyptian skeletons, dated AD500.
• By C13, 200 leper houses in England, then leprosy started to decline in Europe - it
still affects 15 millions, worldwide.
• Cross immunity with TB.
• 4000 yrs ago M. bovis probably mutated to M. tuberculosis, which thrives in oxygen
rich tissues in human lungs; transmitted by coughing.
• Rickettsia typhi lodges in rat fleas and rats, causing little harm.
• Rat fleas meet humans, and pass on the rickettsias, giving typhus.
• R. typhi probably evolved into R. prowazeckii that infected humans and their lice
giving epidemic typhus.
• R. prowazeckii infects head and pubic lice and occasionally body lice.
• Typhus takes advantage of malnutrition, dirt, overcrowding and hunger - referred to
as "prison fever", "camp fever", "ship fever", "famine fever". Previously, it struck
along with dysentery, typhoid, and scurvy.
• May have been responsible for the epidemics in Greco-Roman times.
• Begins with headache, high fever and a body rash; face darkens and swells, delirium
follows, and then a stupor (typhos in Greek for haze/smoke). The rash leads to
sores, to gangrene in toes and fingers.
• Victims rot alive, giving off a hideous stench.
• At the start of WW1, typhus wiped out 150 000 soldiers in Serbia. From 1917-21, it
killed 3 million Russians.
• Over 500 known, of which 100 cause human diseases.
• Many cause encephalitis and/or haemorrhagic fevers
• Strikes forestry workers, campers and children who play in woodland.
• Begins with fever, headache and stiff neck, then inflammation in the brain, resulting
in lethargy, seizure and death. Survivors may be paralysed, retarded, deaf or blind.
• Eastern equine encephalitis can kill up to 80% of its victims, and leave many survivors
• May pass from birds via mosquitos.
• among the deadliest human diseases.
• Symptoms include fever, headache, pains in muscles, joints and abdomen. Then, rash
caused by small haemorrhages under the skin.
Blood leaks through walls of blood vessels, and flows from internal organs, nose, mouth,
rectum and eyes; kidney failure; inflammation and bleeding in the brain.
• Best known are yellow fever and dengue - spread from West Africa.
• Natural reservoir of yellow fever - monkeys.
• First appeared in Old Lyme, Connecticut
• Transmitted via deer ticks
• Causal agent: Borrelia burgdorferi
• Symptoms: fever, headache, sore throat, nausea, fatigue, swollen glands, stiff neck,
• The disease can subside during a long latent period, and re-appear to attack gonads,
heart and nervous system.
• Incidence in USA: 500 in 1982; 10000 in 1992
• Surfaced slowly and insidiously in developed nations during the 80's, when doctors in
California and NY noticed that some homosexual men suffered from rare disorders,
including Kaposi's sarcoma (a skin cancer) and Pneumocyctis carinii pneumonia, and
toxoplasmosis (a protozoan brain infection). Eventually the immune system collapsed,
and patients died of these and other opportunistic diseases, e.g. TB
• Initially called GRID (gay related immune disease) = "gay cancer"
• By 1982, AIDS coined, and was recognised in Haiti, Europe, Central Africa and USA
• In Africa, AIDS is spread mainly by heterosexual intercourse, especially prostitution
• AIDS is also a killer of haemophiliacs and intravenous drug users.
• Health workers referred to AIDS victims as the 4-H club (homosexuals, Haitians,
heroin users and haemophiliacs)
• As death toll mounted, a growing trickle of heterosexually transmitted cases occurred
in the West
• Earliest case: 1950s - from blood samples and clinical records
• First appeared in Africa in the 60's
• 1985; pandemic in USA and Africa
• 1990; epidemic in Europe, Asia and Latin America
• Estimated predictions: millions of infections in USA early next century
• seems to be always fatal
• 1983; human immunodeficiency virus (HIV) - a retrovirus [RNA] discovered (a
related virus occurs in cats; FIV)
• "Related retroviruses": adult T-cell leukemia (ATL) [Japan in 1977; also spread
primarily by sex, contaminated needles and blood
transfusions. Virus may lie dormant for 20-40 years before triggering fatal leukemia.
Cause: human T-cell lymphotrophic virus (HTLV-1)
- hairy cell leukemia; cause HTLV2
• HIV only occurs naturally in humans
• HIV has affinity for T-cells
• Likely origin: African monkeys
• From genetic studies: HIV1 evolved in Central Africa; HIV2 arose in West Africa. Both
related to simian immunodeficiency virus (SIV), which infects African monkeys without
apparent symptoms; SIM kills Asian monkeys
• SIV, HIV1 and HIV2 probably evolved from a common ancestor - the green monkey and
• Once in human body, HIV keeps mutating to evade the host defences
• Although a single sexual contact can transmit HIV, it more often takes dozens if not 100's
• Spread from monkeys (pets, partially cooked or raw meat)
• 60's - live monkeys were a major export product. Villagers caught monkey, but were
bitten and scratched. During transport, interchange of pathogens, and so to humans..
• Promiscuity spread the disease in Africa (multiple wives, prostitutes) and needles which
were not sterilized between use.
• The HIV equivalent of Typhoid Mary was an airline employee, who knowing to be
infected, had unprotected sex with 100's of partners, worldwide
SLOW VIRUSES? (PRIONS)
• Creutzfeldt-Jakob disease
• Visma (a sheep disease like human multiple sclerosis)
• Kuru (in New Guinea)
• Bovine spongiform encephalopathy (BSE)
Common sign = spongy degeneration of the brain
• First in 1986; mad cow disease
• By 1994, tens of thousand of cattle had died
• Passes from pregnant female to foetus
• Similar disease appeared in domestic cats, elk, deed and American mink
• Thought source was sheep carcasses (scrapie?)
- sheep carcasses rendered at lower temperature; scrapie agent survived
- extraction of sheep fat with solvents stopped (solvents were germicidal)
• 1982; Stanley Prusiner suggested that the cause is not an ordinary retrovirus but
protein molecule - PRION. This molecule invades the body and evades the immune
system; possibly hijacks host genes
• Oncoviruses (cancer)
- Rous Sarcoma virus causes tumours in birds
- Epstein Barr virus causes Bukitts lymphoma or nasopharyngeal cancer
Definition: It is contended that any attempts to define terrorism are futile and only
confuse. Most definitions are either too broad or too narrow. Between 1936 and 1980
there were >100 definitions coined for terrorism. Seth Carus defines a terrorist as “a non-
state actor who uses violence on behalf of a political cause without reference to the moral
or political justice of the cause. This includes non-state actors who operate in organized
military units (as with guerillas) if the use of biological agents is undertaken covertly
using improvised delivery systems.
Bioterrorists may include:
First recorded use - the Romans, who used dead animals to foul the water supply
of their enemies. This killed enemy numbers and lowered morale.
The Tartars infected the enemy by catapulting bodies infected with bubonic
plague over the walls of the city of Kaffa in 1346. Some believe that this was the
cause of the epidemic of plague that swept across medieval Europe killing 25
In 1710 during the war between Russia and Sweden, Russian troops are said to
have used the cadavers of plague victims to provoke an epidemic with the enemy.
1767 The French and Indian War was fought in North America between France
and England during the period of 1754-1767. Both sides relied heavily on the
support of Indian allies. The English attacked Ft. Carillon twice and were repulsed
with heavy losses. An English general, Sir Jeffery Amherst, surreptitiously
provided the Indians loyal to the French with blankets infected with smallpox
virus. The resulting epidemic decimated the Indians. Shortly thereafter, General
Amherst successfully attacked Ft. Carillon and renamed it Ft. Ticonderoga. By
deduction, the small pox epidemic played a significant role in the victory.
In 1900, A U.S. doctor researching in the Philippines infected prisoners with the
plague. He continued by inducing Beriberi in another 29 prisoners. The
experiments resulted in two known fatalities.
In 1915, A doctor in Mississippi produced Pellagra in 12 white Mississippi
inmates in an attempt to discover a cure for the disease.
In 1917, there is evidence that German agents inoculated horses and cattle with
glanders in the USA before they were shipped to France. Although horsepower
was a major component of logistics during World War I, the German use of BW
obviously was not successful in altering the course of the war.
In 1918, the Japanese formed a special section of the Army (Unit 731) dedicated
In, 1925 the Geneva Convention governing wartime conduct bans biological
weapons. Japan refuses to approve treaty.
In 1931, Japan took over part of Manchuria ,and Unit 731 (Shiro Ishii – a
physician) secured "an endless supply of human experiment materials."
Essentially all prisoners of war were available for BW experiments.
In 1931, The Puerto Rican Cancer Experiment was undertaken by Dr. Cornelius
Rhoads. Under the auspices of the Rockefeller Institute for Medical
Investigations, Rhoads purposely infected his subjects with cancer cells. Thirteen
of the subjects died. Rhoads went on to establish U.S. Army Biological Warfare
facilities in Maryland, Utah, and Panama. He later was named to the U.S. Atomic
Energy Commission and was at the heart of the recently revealed radiation
experiments on prisoners, hospital patients, and soldiers.
In 1932, The Tuskegee Syphilis Study began. 200 poor black men with syphilis
began a long term experiment in which those men were to be studied. They were
never told of their illness, and treatment was denied them. > 100 died as a direct
or indirect result of the illness. The wives and children of the subjects also
suffered as a result of the disease.
In the 1940’s, a crash program to develop new drugs to fight Malaria led to
doctors in the Chicago area infecting ~ 400 prisoners with the disease. Although
the Chicago inmates were given general information that they were helping with
the war effort, they were not provided adequate information in accordance with
the later standards set by the Nuremberg War Crimes Tribunal. Nazi doctors on
trial at Nuremberg cited the Chicago studies as precedents to defend their own
behaviour in aiding the German war effort.
In 1941, Japanese planes sprayed bubonic plague over parts of China. Tens of
thousands may have died.
In 1942 "bacterial bombs" were deployed on mainland China but determined to be
The Japanese released thousands of plague infested rats prior to their surrender,
with unknown consequences.
The Japanese tested on American POW's, and the U.S. Government apparently
knew, but did nothing (perhaps a worse atrocity.)
The USA offered immunity to would-be Japanese war criminals in exchange for
BW became intimately linked to the Cold War.
The UK developed a programme in BW, focusing on anthrax spores and their
viability and "range of spread " when delivered with a conventional bomb.
Gruinard Island off the coast of Scotland was used.
The data was used by the UK and the U.SA to develop bombs that were better
able to effectively disperse spores.
An outbreak of anthrax in sheep and cattle occurred in 1943 on the coast of
Scotland that directly faced Gruinard, and the British stopped testing.
Gruinard Island was contaminated with Bacillus anthracis spores for 50-years
until decontaminated recently.
Programme started in 1942.
With Japanese data and the increased tensions of the cold war, the U.S.
programme accelerated in activity and grew in size.
1950 – 1953. Feathers infected with anthrax, fleas and mosquitoes dosed with
Plague and Yellow Fever, and rodents infected with a variety of diseases were
allegedly used against North Korea.
In 1955, The Tampa Bay area of Florida experienced a sharp rise in Whooping
Cough cases, including 12 deaths, after a CIA test where a bacteria withdrawn
from the Army's Chemical and Biological Warfare arsenal was released into the
environment. Details of the test are still classified.
In 1956 the former Soviet Union accused the U.S. of using biological weapons in
Korea. This changed the focus of the U.S. program to a more defensive one.
One of the biggest experiments involved the use of Serratia marcescens being
sprayed over San Francisco. At one point, 5000 particles/minute were sprayed
from the coastal areas inward. During this time, one man died (in the hospital) and
10 others became infected in what was described as "a mystery to doctors."
It has been shown that during periods following spraying tests, there were 5-10
times the normal infections reported.
Tests in Minneapolis were disguised as "smoke screen tests" because residents
were told a harmless smoke was being tested so that cities might be 'hidden' from
radar guided missiles.
In 1966 Bacillus subtilis was released into the subway system of New York City
to determine how vulnerable it was to attack. Results showed that the entire
underground tunnel system could be infected by release in only one station due to
the winds created by the trains.
In 1979, there was an explosion in Sverdlosk – and airborne leak of material - and
an outbreak of anthrax followed. The disease affected 94 people and killed at
least 64, with the first victim dying after 4-days, and the last after 6-weeks. The
story was admitted by Boris Yeltsin in 1992.
Human diseases: anthrax, bubonic plaque, cholera, tularaemia, haemorrhagic fevers,
encephalitis, smallpox, SEB
Description of Agent: Anthrax is a highly lethal infection caused Bacillus anthracis.
Organisms usually gain entrance through skin wounds (causing a localized infection), but
may be inhaled or ingested. Intentional release would presumably involve the aerosol
route - spore form is stable and possesses characteristics ideal for aerosols.
Signs and Symptoms: The incubation period for inhalation anthrax is 1-6 days. Fever,
malaise, fatigue, cough, and mild chest discomfort are rapidly followed by severe
respiratory distress. Shock and death occur within 24-36 hours of the onset of severe
symptoms. In cases of cutaneous anthrax, a papule develops, then vesicles, then a black
eschar surrounded by moderate to severe oedema. The lesions are usually painless.
Without treatment, the disease may progress to septicaemia and death, with a case-fatality
rate of 20%. With treatment, fatalities are rare.
Treatment: Although usually ineffective in inhalational cases, once symptoms are
present, antibiotic treatment with high-dose penicillin, ciprofloxacin, or doxycycline may
Defense: A licensed vaccine is available. Vaccination is undertaken at 0, 2, and 4 weeks
(initial series), followed by booster doses at 6, 12, 18 months and then yearly. Oral
ciprofloxacin or doxycycline is useful in cases of known or imminent exposure.
Following confirmed exposure, all unimmunized individuals should receive three doses
of vaccine over 30 days, while those vaccinated with < 3 doses prior to exposure should
receive an immediate booster. Anyone vaccinated with the initial 3-dose series in the
previous 6 months does not require boosters. All exposed personnel should continue
antibiotic therapy for 4 weeks. If vaccine is unavailable, antibiotics may be continued
beyond 4 weeks and should be withdrawn only under medical supervision.
Decontamination and Isolation: Drainage and secretion precautions should be
practiced. Anthrax is not known to be transmitted via the aerosol route from person to
person. Following invasive procedures or autopsy, instruments and surfaces should be
thoroughly disinfected with a sporicidal agent (e.g. iodine or 0.5% sodium hypochlorite).
Outbreak Control: Although anthrax spores may survive in the environment for many
years, secondary aerosolization of such spores (such as by pedestrian movement or
vehicular traffic) generally presents no problem for humans. The carcasses of animals
dying in such an environment should be burned, and animals subsequently introduced
into such an environment should be vaccinated. Meat, hides, and carcasses of animals in
affected areas should not be consumed or handled by untrained and/or unvaccinated
This might be a candidate for use as a biological warfare agent. Indeed, the USA began
development of B suis as a biological weapon in 1942. The agent was formulated to
maintain long-term viability, placed into bombs, and tested in field trials during 1944–
1945 using animal targets. By 1967, the USA terminated its offensive programme for
development and deployment of Brucella as a biological weapon. Although the munitions
developed were never used in combat, the studies reinforced the concern that Brucella
might be used against U.S. troops as a biological warfare agent.
Brucellosis is a zoonotic infection of domesticated and wild animals. Humans become
infected by ingestion of animal food products, direct contact with infected animals, or
inhalation of infectious aerosols.
Brucellosis in humans has a strong association with military medicine.
Q fever is a zoonosis caused by Coxiella burnetii, a rickettsia-like organism of
low virulence but remarkable infectivity.
A single organism may initiate infection.
Despite the fact that C burnetii is unable to grow outside host cells, there is a
sporelike form that is extremely resistant to heat, pressure, desiccation, and many
antiseptics; this allows C burnetii to persist in the environment for long periods
under harsh conditions. This persistence, coupled with transmission by inhalation
allows for the development of acute infection following only indirect exposure to
an infected source. The acute clinical disease is usually a benign, although a
temporarily incapacitating, illness in humans.
Without treatment, the vast majority of patients recover.
The primary reservoir infection is livestock, particularly parturient females. (eg,
calving or lambing).
Treatment: Tetracyclines are effective.
Prevention: Formalin-killed, whole-cell vaccine. Prior skin testing to exclude immune
individuals is necessary to avoid severe local reactions to the vaccine.
Since 1937, 1000’s of cases involving military personnel have been reported.
A possible problem when troops are present in an area with infected animals.
The potential is directly related to infectivity. It has been estimated that 50 kg of
dried, powdered C. burnetii would produce casualties a rate equal to that of
similar amounts of anthrax or tularemia.
Q fever has been evaluated as a potential
biological warfare agent by the USA
Description of Agent: Tularemia is an infection caused by the Gram-negative
coccobacillus, Francisella tularensis. Two biogroups are known; biogroup tularensis,
also known as type A, is the more virulent form, and is endemic in much of North
America. Naturally-acquired tularemia is contracted through the bites of insects (ticks
and deerflies), or via contact with infected rabbits, muskrats, and squirrels. Intentional
release by belligerents would presumably involve aerosolization of living organisms.
Although naturally-acquired tularemia has a case-fatality rate of ~5%, the pneumonic
form of the disease, which would predominate in the setting of intentional release, would
likely have a greater mortality rate.
Signs and Symptoms: Naturally-acquired tularemia frequently has an ulceroglandular
presentation, although a significant minority of cases involve the typhoidal or pneumonic
forms. The incubation period averages 3-5 days, but varies widely. Use of tularemia as a
weapon would likely lead to a preponderance of pneumonic and typhoidal cases, and
large aerosolized innocula would be expected to shorten the incubation period.
Ulceroglandular disease involves a necrotic, tender ulcer at the site of inoculation,
accompanied by tender, enlarged regional lymph nodes. Fever, chills, headache, and
malaise often accompany these findings. Typhoidal and pneumonic forms often involve
significant cough, abdominal pain, substernal discomfort, and prostration in addition to
prolonged fever, chills, and headache.
Diagnosis: Clinical suspicion. Laboratory tests are unhelpful, and F. tularensis does not
typically grow in standard blood cultures, although special media are available for the
culturing of blood, sputum, lymph node material, and wound exudates if the diagnosis is
suspected. Serology is available to confirm the diagnosis in suspected cases.
Treatment: Streptomycin is the drug of choice. Gentamicin is also used. Relapses are
more common with tetracycline therapy, although this alternative may be employed in
patients who cannot tolerate aminoglycosides.
Defense: A live, attenuated vaccine is available. It may be given to those at high risk of
exposure. A single dose is administered by scarification. I.M. streptomycin will prevent
disease following documented exposure, but is not recommended following tick bites or
Decontamination and Isolation: Tularemia is not transmitted person-to-person via the
aerosol route, and infected persons should be managed with secretion and drainage
precautions. Heat and common disinfectants (such as 0.5% hypochlorite) will readily kill
Outbreak Control: Following intentional release of F. tularensis in a given area, it is
possible that local fauna, especially rabbits and squirrels, will acquire disease, setting up
an enzootic mammal-arthropod cycle. Persons entering such an area should avoid
skinning and eating meat from such animals. Water supplies and grain in such areas
might likewise become contaminated, and should be boiled or cooked before
consumption. Organisms contaminating soils are unlikely to survive for significant
periods of time and present little hazard.
The causal agent of cholera.
Control: The mainstay of therapy is fluid and electrolyte replacement. This may be
accomplished through the use of oral rehydration salts or diluted juice in less severe
cases, whereas IV fluids are often required in cases of severe dehydration. Antibiotics
shorten the duration of diarrhoea and thereby decrease fluid loss; tetracycline or
doxycycline are reasonable used. Concerns over tetracycline resistance have recently
arisen, and ciprofloxacin, erythromycin, or furazolidone may also be considered.
A licensed, killed vaccine is available but only modestly effective, providing about 50%
protection lasting for no more than 6 months. Vaccinations are given at 0 and 4 weeks,
with booster doses every 6 months. The limited efficacy of the preparation has led most
public health authorities to recommend against vaccination under most circumstances.
Description of Agent: Causes bubonic and pneumonic plague. Naturally-occurring
plague is acquired by the bite of a flea which had previously fed on infected rodents. In
such cases, plague classically presents as a localized abscess with secondary formation of
very large, fluctuant regional lymph nodes known as buboes (bubonic plague). Plague
may also be transmitted via aerosol and by inhalation of sputum droplets from coughing
patients. In such instances, a primary pneumonic form may develop and, in the absence
of prompt therapy, progress rapidly to death within 2-3 days. Intentional release by
belligerents or terrorist groups would presumably involve aerosolization, but could also
involve the release of infected fleas.
Signs and Symptoms: Pneumonic plague has an incubation period of 2-3 days, and
begins with high fever, chills, and headache. Death results from respiratory failure,
circulatory collapse, and internal bleeding. Bubonic plague has an incubation period of 2
to 10 days, and presents with malaise, high fever, and tender lymph nodes (buboes).
Bubonic plague may progress spontaneously to the septicaemic form, with spread to the
CNS, lungs, and elsewhere.
Diagnosis: To facilitate prompt therapy, plague must be suspected clinically. A
presumptive diagnosis may also be made by Gram or Wayson stain of lymph node
aspirates, sputum, or CSF. The plague bacillus may be readily cultured from aspirates of
buboes or from the blood of septicaemic patients.
Treatment: Early administration of antibiotics is quite effective, but must be started
within 24 hours of onset of symptoms in pneumonic plague. The treatment of choice is
streptomycin (30 mg/kg/day IM in 2 divided doses x 10 days) or gentamicin. Intravenous
doxycycline is also effective; chloramphenicol should be added in cases of plague
meningitis. Supportive therapy for pneumonic and septicaemic forms is typically
Defense: A licensed, killed vaccine is available. The primary vaccination series consists
of a 1.0 ml IM dose initially, followed by 0.2 ml doses at 1-3 months and 3-6 months.
Booster doses are given at 6, 12 and 18 months and then every 1-2 years. As this vaccine
appears in animal experiments to offer no protection against aerosol exposure, victims of
a suspected attack with aerosolized plague, or respiratory contacts of coughing patients,
should be given doxycycline.
Decontamination and Isolation: Drainage and secretion precautions should be
employed in managing patients with bubonic plague; such precautions should be
maintained until the patient has received antibiotic therapy for 48 hours and has
demonstrated a favourable response to such therapy. Care must be taken when handling
or aspirating buboes to avoid aerosolizing infectious material. Strict isolation is necessary
for patients with pneumonic plague.
Outbreak Control: In the event of the intentional release of plague into an area, it is
possible that local fleas and rodents could become infected, thereby initiating a cycle of
enzootic and endemic disease. Such a possibility would appear more likely in the face of
a breakdown in public health measures (such as vector and rodent control) which might
accompany armed conflict. Care should be taken to rid patients and contacts of fleas
utilizing a suitable insecticide; flea and rodent control measures should be instituted in
areas where plague cases have been reported.
Clostridium botulinum toxin
Description of Agent: Botulinum toxins are a group of 7 related neurotoxins (types A-G)
produced by Clostridium botulinum. They are typically formed in canned foods and
subsequently ingested, although the spore form of the organism may occasionally gain
access to the body through wounds or through the GI tract before germinating and
producing toxin. Intentional release by belligerents or terrorists would likely involve
aerosolization of pre-formed toxin, which could then produce disease via the inhalational
route. Deliberate contamination of food supplies is possible. Botulinum toxins block
acetylcholine release at the neuromuscular junction, and in the central and peripheral
nervous systems. In the face of large numbers of casualties and/or in the absence of
prompt, intensive, and long-term medical management, botulism can be thought of as a
Signs and Symptoms: Generalized weakness, dizziness, dry mouth and throat, blurred
vision, followed by paralysis and the development of respiratory failure. Symptoms may
begin as early as 12-36 hours following ingestion or inhalation, but may require as long
as several days in some cases.
Diagnosis: The diagnosis is made clinically, as there are no specific laboratory findings,
and a limited differential diagnosis. Assays for toxin are not widely available. Intentional
release should be suspected if numerous co-located casualties present with progressive
descending bulbar, muscular, and respiratory weakness.
Treatment: Supportive care consists chiefly of intubation and ventilatory assistance for
respiratory failure; tracheostomy may be required. A licensed trivalent equine botulinum
antitoxin (types A, B, and E) is available through the CDC and should be administered as
soon as possible in order to bind toxin remaining in the circulation. Skin testing should be
performed before administration of equine antitoxins (to detect sensitivity).
Defense: A pentavalent toxoid (types A, B, C, D, and E) is available for those at high risk
of exposure. Doses (0.5 ml) are given at 0, 2, and 12 weeks, with yearly boosters.
Decontamination and Isolation: Decontamination of surfaces contaminated by toxin
may be accomplished using soap and water, or 0.5% hypochlorite. Spores are best killed
by pressure-cooking of foodstuffs to be canned. Toxin is not dermally active (although
spores may enter through skin wounds) and secondary aerosols from affected patients
pose no risk of botulism transmission.
Outbreak Control: Intentionally-released aerosols of botulinum toxin probably pose
little risk beyond the immediate period of release. In the event that contamination of
foodstuffs is suspected, pre-formed toxin may be destroyed by boiling for 10 minutes.
Staphylococcal enterotoxin B
Description of Agent: Staphylococcal enterotoxin B (SEB) is one of several toxins
produced by Staphylococcus aureus. SEB is a common contributor to staphylococcal
food poisoning but could be employed by belligerents or terrorist groups as an
aerosolized inhalational agent. It is incapacitating, but would rarely kill.
Signs and Symptoms: Symptoms begin 3-12 hours after aerosol exposure, and consist of
sudden onset of fever, chills, headache, myalgia, and nonproductive cough. Some patients
may develop shortness of breath and chest pain. Fever may last 2 to 5 days, and cough
may persist for up to 4 weeks. Patients ingesting toxin might present with nausea,
vomiting, and diarrhoea. Very high exposure levels may lead to pulmonary oedema and,
Diagnosis: Largely clinical. As inhalational disease is not encountered naturally, its
presence indicates intentional aerosolization.
Treatment: Treatment is limited to supportive care. Artificial ventilation may be
required in very severe cases, and attention to fluid management is important. Antibiotics
are of no benefit, and no antitoxin has been developed.
Defense: There is currently no human vaccine available to prevent SEB intoxication. As
with all potential inhalational biological agents, protective masks such as those employed
by military units offer excellent protection in those individuals alert to the possibility of
Decontamination and Isolation: Decontamination of most surfaces may be
accomplished with soap and water or with 0.5% hypochlorite solution. Food which may
have been contaminated should be destroyed.
Outbreak Control: Prolonged environmental contamination would not be expected
following release of aerosolized SEB.
British colonial commanders considered distributing blankets from smallpox
victims among Native Americans as a biological weapon.
In the years leading up to and during World War II, the Japanese military
explored weaponization of smallpox during the operations of Unit 731 in
Mongolia and China.
Yet, the actual potential of variola virus as a biological weapon remains
Given the ease of administration and the availability of the vaccinia virus as a
vaccine against smallpox, some have argued that smallpox would have limited
biological warfare potential.
CDC maintains over 12 million doses of vaccine in storage, and WHO has in
storage enough vaccine to protect 200 to 300 million people.
However although allegedly eliminated:
viable variola virus could be recovered from scabs up to 13 years after collection,
and it is conceivable that cadavers preserved in permafrost or dry crypts could
release the virus.
Virus specimens from the smallpox-eradication campaign may remain
unrecognized or unreported.
Using the published sequence of variola and its significant homology with other
Orthopoxviruses, a malevolent laboratory could theoretically engineer a
recombinant virus exhibiting variola virus’s virulence by starting with
Selection criteria for antilivestock and antipoultry agents:
The agent should be:
1. Highly infectious and contagious
2. Good ability to survive in the environment
3. Predictable clinical disease pattern, including morbidity and mortality
4. Pathogenic for livestock or poultry
5. Available and easy to acquire or produce
6. Attributable to a natural outbreak, ensuring plausible deniability
7. Not harmful to perpetrator
8. Easily disseminated
The following agents pose the greatest potential threats:
1. Foot-and-mouth disease virus
2. Classical swine fever virus
3. African swine fever virus
4. Rinderpest virus
5. Rift Valley fever virus
6. Avian influenza virus
7. Velogenic viscerotropic Newcastle disease (VVND) virus
8. Venezuelan equine encephalomyelitis virus
9. Bluetongue virus
10. Sheep and goat pox viruses
11. Pseudorabies virus (Aujeszky’s disease)
12. Vesicular stomatitis virus
13. Teschen disease virus (porcine enterovirus 1)
14. Porcine enterovirus type 9
15. Lyssaviruses and rabies viruses
16. Lumpy skin disease virus
17. Porcine reproductive and respiratory syndrome virus
18. African horse sickness virus
19. Bacillus anthracis (anthrax)
20. Chlamydia psittaci (ornithosis, psittacosis, chlamydiosis)
21. Cowdria ruminantium (heartwater, cowdriosis)
22. Screwworm (myiasis)
Foot and Mouth Disease (of concern in the USA)
The mouth of an infected animal may be wiped with a cloth, which may be readily
concealed and used to spread the inoculum to other animals (an early means of
“vaccination” – some animals would become infected others would develop immunity)
DISSEMINATION OF AGENTS
Not ideal as at high altitude, winds can blow agents off course.
A first choice - produce a fine, high-concentration mist at ground level, making
inhalation much easier, causing high casualty rate.
Will release a cloud of the agent, but do not have a very great range. Usually, a cloud
emitted by a canister will stay within 20 feet of the area in which it was sprayed. Users
may become infected . Canisters are among the easiest methods of delivery because of
their small size and simplicity to open. Another benefit is that they are very concealable.
When released in a small contained area, a subway system for example, a large area can
be infected if the agent is concentrated enough because the winds created by the moving
trains would help carry it to other stops.
Deliberate distribution of contaminated vectors (e.g. rodents) of or infected humans
Use of masks
Use of protective clothing
There will be difficulty in acquiring the organism (easier for microbiologists!)
There will be difficulty with growing the pathogen in sufficient quantity and in
extracting toxins, etc.
There will be problems with dissemination
Easier for nations than individuals