Transcript Preparedness Against Biological Weapons: A Module for

Biological Weapons: Essential
Information on Category B Agents
Felissa R. Lashley, RN, PhD, FAAN, FACMG
Professor, College of Nursing, and
Interim Director, Nursing Center for Bioterrorism and
Infectious Disease Preparedness
College of Nursing
Rutgers, The State University of New Jersey
This module on the use of biological
agents as bioweapons covers general
material, the classification of biological
agents as to their use in bioterrorism and
gives the most important information
regarding the Category B Agents
according to the Centers for Disease
Control and Prevention (CDC)
classification. Separate modules address
Category A and Category C agents and
details re isolation precautions. This
module was supported in part by
USDHHS, HRSA Grant No. T01HP01407.
The format and information in this module
focuses on the use of the agent or outbreak of
disease particularly in regard to bioterrorism
including emphasis on management with
nursing applications and infection control
material. Detailed material on general
transmission of disease, infection control and
isolation precautions is in a separate module
and this should be consulted. Aspects of
preparedness are also in a separate module.
Note that for the care of persons exposed to
any biological agent, the nurse should be sure
he/she is adequately protected first.
Objectives
At the completion of this module, participants
will be able to:
1. Identify at least 10 factors that make a biological
agent or biological toxin suitable for use as a
bioterror agent.
2. List the 3 CDC categories for critical biological
agents and why they are so categorized.
3. Identify and list CDC Category B biological agents
with potential for use in a bioterrorism attack.
4. Describe the signs and symptoms of infection
with Category B agents.
5. Discuss isolation precautions for each Category B
agent.
Using Biological Agents as
Bioweapons
Biological Agents and Bioterrorism


Includes microorganisms, especially
certain bacteria and viruses, and biological
toxins such as botulinum toxin, which act
like chemical agents.
May be directed at humans, plants,
animals, and be a threat to crops,
livestock, food products (agroterrorism)
during processing, distribution, storage
and transportation which could cause
illness and also have severe economic
consequences such as bovine spongiform
encephalopathy, and foot and mouth
disease.
Biological Agents and Bioterrorism-2

Biological agents can be used as weapons
in:
• Biocrimes
• Bioterrorism
• Biowarfare

Definition: North Atlantic Treaty
Organization (NATO) defines a biological
weapon as “the provision of any infectious
agent or toxin by any means of delivery in
order to cause harm to humans, animals,
or plants.”
Biological Agents and Bioterrorism-3

Various definitions for bioterrorism
have been given. The following may
be used: “the intentional use or
threat of use of biological agents on
a population to achieve political,
social, religious, ethnic, or ideological
ends by causing illness, death and
wide scale panic and disruption.” The
aim may not be maximum damage
but rather a political statement.
Biological Agents and Bioterrorism-4



The technology exists to modify existing
biological agents, or weaponize them, to,
for example, make it easier to disseminate
and/or cause greater harm in their
dissemination.
The use of biological agents for
bioterrorism has been referred to as the
“poor man’s nuclear bomb.”
All involve the use of biological agents in
order to obtain an outcome: political,
social, economic, theological, personal.
Agents with Potential for USE in
BIOTERRORISM






Varies according to source
NATO handbook lists 39 agents
World Health Organization (WHO) has another list
CDC lists biological agents in various categories, A,
B, and C
National Institute for Allergy and Infectious Diseases
(NIAID), National Institutes of Health (NIH) also lists
categories A, B, and C, but they differ somewhat
from how CDC categorizes agents and lists a greater
number of agents
Others
The Following are Desirable Characteristics for
Biological Agents to be Used for Harmful Intent








Generate high levels of panic among
poulation
Easy to obtain
Inexpensive
Easy to produce in mass quantities
Can be relatively easily “weaponized” or
altered for maximum effect (even with
genetic manipulation)
High infectivity
High person-to-person contagion
High mortality
The Following are Desirable Characteristics for
Biological Agents to be Used for Harmful Intent-2



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Lack of effective treatment
Need for intensive care, straining
resources
High potential for casualties/morbidity
Result in lengthy illness with prolonged
care needed
Non-specific symptoms, especially early,
delaying recognition
Long incubation periods
Hard to diagnose
Great degree of helplessness from effect
Examples of Historical Uses of the
Deliberate Release of Biological Agents



Known as early as the 6th century BC
Soldiers dropped corpses of those who
died of plague over city walls during siege
of Kaffa to start a plague epidemic and
force surrender.
British soldiers used variola contaminated
blankets to spread smallpox to American
Indians during the French and Indian Wars
(1754-1767).
Examples of Historical Uses of the
Deliberate Release of Biological
Agents-2


Followers of Bhagwan Shree Rajneesh
intentionally contaminated salad bars in the The
Dalles, Oregon with Salmonella. The purpose was
to keep people from voting in a local election in
November, 1984. More than 750 people were
affected.
The Aum Shinrikyo group in Japan attempted to
carry out attacks using aerosolized anthrax
spores and botulinum toxin before releasing sarin
in the Tokyo subway in 1995.
Examples of Historical Uses of the
Deliberate Release of Biological
Agents-3

Intentional
distribution of anthrax
spores mainly through
the US mail to various
people occurred in the
fall of 2001. In all,
there were 22 known
cases of anthrax; 11
were inhalational.
Picture from CDC. Inhalational
anthrax.
Categories of Critical Biological
Agents as Specified by CDC

Three Categories of Agents:
• Category A Agents: Pose the greatest
threat to national security
• Category B Agents: Second highest
priority to national security.
• Category C Agents: Third highest
priority agents include emerging
pathogens that could be engineered for
mass dissemination in the future.
Category A Agents

Pose a threat to national security
because they:
• Can be easily disseminated or
transmitted person-to-person
• Cause high mortality with potential for
major public health impact
• Might cause public panic and social
disruption
• Require special action for public health
preparedness
Category B Agents

Second highest priority to national
security:
• Are moderately easy to disseminate
• Cause moderate morbidity and low
mortality
• Require specific enhancements of CDC’s
diagnostic capacity and enhanced
disease surveillance
Category C Agents

Third highest priority agents include
emerging pathogens that could be
engineered for mass dissemination in
the future because of:
• Availability
• Ease of production and dissemination
• Potential for high morbidity and
mortality and major health impact
CDC Category B Agents

These agents include the following
organisms with the disease in
parentheses.
• Alphaviruses


Eastern and western equine
encephalomyelitis
Venezuelan encephalomyelitis
• Brucella species (brucellosis)
• Burkholderia mallei (glanders)
CDC Category B Agents-2
• Clostridium perfringens epsilon toxin
• Coxiella burnetti (Q fever)
• Ricin toxin from Ricinus communis, the
castor bean
• Staphyloccus enterotoxin B
• A subset of Category B agents includes
food- or water-borne pathogens.
CDC Category B Agents-3

The following are food or waterborne
pathogens that are a subset of Category B
agents that includes but are not limited
to:
•
•
•
•
•
Cryptosporidium parvum (cryptosporidiosis)
Escherichia coli O157:H7
Salmonella species
Shigella dysenteriae (dysentery)
Vibrio cholerae (cholera)
Source: CDC. (2000). Biological and chemical terrorism:
Strategic plan for preparedness response. MMWR, 49 (RR
-04), 1-14.
ALPHAVIRUSES
Venezuelan Equine Encephalitis (VEE) Complex
Eastern Equine Encephalitis (EEE)
Western Equine Encephalitis (WEE)

Description:
• Alphaviruses in the Togaviridiae family.
• Are closely related, and cause illness,
ranging from mild flu-like symptoms to
encephalitis.
• Are listed as Category B agents by CDC,
and Category C agents by NIAID.
• VEE was tested as a potential
biowarfare agent in the 1950s and
1960s.
Alphaviruses-2

Epidemiology:
• VEE, WEE, and EEE cause encephalitis in
equines (horses, donkeys) and humans.
• EEE can produce illness in some birds such as
pheasants, quails, and ostriches as well as
puppies, and the virus transmission cycle is
between birds and mosquitoes.
• WEE has been isolated from various mammals
and pheasants and sparrows.
• Human cases are relatively infrequent in the
non-bioterrorism context.
• Those below 15 years of age and over 50 years
of age are at greatest risk.
Alphaviruses-3

Epidemiology cont.:
• VEE occurs in Central and South America,
Mexico, and along the Gulf Coast of the US.
• EEE occurs in the Eastern seaboard of the US,
the Gulf Coast and some inland midwest
locations.
• WEE occurs mainly in the western US, South
America, and Canada, but the virus has been
isolated in Wyoming and Nebraska.
Alphaviruses-4

Transmission:
• Usually transmitted by mosquito bite.
• Could be transmitted by aerosol if
weaponized.
• Only 10-100 VEE organisms are needed
to produce infection in humans.
• No direct human-to-human or horse-tohuman transmission has been
documented, but is theoretically
possible through respiratory droplets.
Alphaviruses-5

Incubation period:
• 4-10 days

Clinical manifestations:
• EEE



Sudden onset of fever, myalgia and
headache.
Some persons progress to encephalitis,
seizures and coma.
In those who survive, many develop
permanent brain damage which may be
severe enough to require permanent care.
Alphaviruses-6

Clinical manifestations cont.:
• WEE

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

Most infections are asymptomatic or are mild
and nonspecific.
Others present with a sudden onset with fever,
headache, nausea, vomiting, anorexia and
malaise which may be followed by altered
mental status, photophobia, weakness and
meningeal irritation with neck rigidity and
paralysis.
Children under 1 year of age are most
vulnerable to severe infection.
Permanent sequelae occur in 5 to 30% of
children.
Alphaviruses-7

Clinical manifestations cont.:
• VEE
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
Usually manifests as a mild flu-like illness but can
progress to fatal encephalitis.
Symptoms include spiking fevers, chills, malaise,
severe headache, photophobia, leg pain, back pain
followed by nausea, vomiting, cough, sore throat and
diarrhea.
Conjunctival injection may be seen.
About 4% of children and less than 1% of adults
develop CNS signs.
In those children who recover, seizure disorders and
neurological defects may be seen.
Infection in pregnancy can lead to spontaneous
abortions, stillbirths and congenital anomalies in the
fetus.
Alphaviruses-8

Mortality rate:
• EEE – about 35%.
• WEE – about 3-10%.
• VEE – about 1% overall, but 35% of children
and 10% of adults who develop encephalitis
will die.

Treatment:
• Supportive.
• May need anticonvulsants, maintenance of
fluid and electrolyte balance, maintain
adequate respiration, and analgesics for pain.
Alphaviruses-9

Nursing considerations:
• Supportive including maintenance of fluid and electrolytes,
maintenance of adequate respiration, and analgesia for
pain.
• Observe carefully.
• Prevent secondary bacterial infections.
• Standard isolation precautions are considered adequate
since patient-to-patient transmission has not been proven.
• Some recommend droplet precautions for VEE since personto-person transmission is theoretically possible via
respiratory droplets.

Vaccination:
• Equine vaccine available for EEE and one is investigational
for humans.
• For WEE and VEE, vaccines are available for laboratory
workers but has frequent side effects.
Brucella species (Brucellosis)
Also known as undulant fever, Malta fever, &
Mediterrean fever

Etiology:
• Brucella melitensis; also Brucella abortus; B.
suis; and B. canis.
• Tiny gram-negative aerobic coccobacilli are
non-spore forming.

Epidemiology:
• About 100 human cases per year in US, but is
common in other parts of the world.
• Mostly from California, Florida, Texas, and
Virginia.
• B. abortus responsible for abortions in animals.
• Transmission by skin contact is considered an
occupational hazard for vegetarians, farmers,
butchers, workers, and animal handlers.
Brucellosis-2

Transmission:
• Ingestion-especially of unpasteurized milk and
milk products
• Direct skin contact when handling infected
material, including animal material, tissue and
fluids
• Aerosols
• No direct person-to-person transmission
except rarely. Has been transmitted via
banked sperm and sexual contact.
• Has occurred in lab worker as recently as
2006.
Brucellosis-3

Infective dose:
• 10-100 organisms

Incubation period:
• 5 days to more than 6 months
Brucellosis-4
Clinical manifestations:

Acute (less than 8
weeks) – are nonspecific and flu-like
and may begin
insidiously:
• Fever
• Profuse sweating
(typically 101o F to
104o F), often with
foul odor
• Malaise
•
•
•
•
•
•
•
•
•
Headache
Muscle pain
Back pain
Abdominal pain
Generalized
weakness
Diarrhea or
constipation
Vomiting
Leukocyte count
may be lower or
normal
Splenomegaly
Brucellosis-5
Clinical manifestations:

Chronic – can
occur more than 1
year from onset;
symptoms may
include:
• Chronic fatigue
syndrome
• Depression
• Arthritis

Undulant form –
less than 1 year
from onset;
symptoms may
include:
•
•
•
•
Fever
Arthritis
Orchitis in males
Neurological
symptoms in up to
5%
Brucellosis-6
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Treatment:
In 2008 the most effective treatment was known
to be doxycyline-aminoglycoside-rifampin with
the aminoglycoside given for 7-14 days and
doxycycline and rifampin given for 6-8
weeks(Skalsky et al. 2008).
• Other therapies recommended are oral therapy with
doxycycline and rifampin for 6 weeks but other
combinations, such as doxycycline and gentamicin or
doxycycline for 6 weeks with IM steptomycin for 2
weeks have been used.
• In cases of meningoencephalitis or endocarditis
complications, then some recommend long term triple
drug therapy with rafampin, a tetracycline and an
aminoglycoside.
• Chemoprophylaxis may be recommended in a
bioterrorism context or for high risk exposures, but is
not usually recommended for possible exposure to
endemic disease.
Brucellosis-7

Mortality:
• Less than 5%

Nursing considerations:
• Standard isolation precautions are
recommended.
• Contact precautions may be needed for the
draining lesions.
• General support and comfort measures
depending on manifestations.

Other notes:
• Studied under biosafety level 3 conditions.
Burkholderia mallei (Glanders)

Etiology:
• Burkholderia mallei, a gram-negative
bacterium.

Epidemiology:
• Primarily infects horses, donkeys and mules
but can also infect goats, dogs and cats.
• Until 2000, no human cases described in
English medical literature since 1949.
• Sporadic cases occur in Asia, Africa, the Middle
East and South America.
Glanders-2

Epidemiology cont.:
• In 2000, a microbiologist at US Army Medical
Research Institute for Infectious Diseases
(USAMRIID), working on the microbiology of B.
mallei acquired glanders.
• Glanders is considered to be a potential agent
of biological warfare, and had been used by
Germany during WWI.
• May be seen among those who work with
equines, such as veterinarians, abbattoir
workers, and caretakers of horses, donkeys
and mules.
Glanders-3

Transmission:
• Inhalation.
• Direct contact with infected animals through
nasal, oral mucosa, conjunctiva or through
open skin lesions.
• Human-to-human transmission has been
reported in family caretakers and possibly
through sexual transmission.
• Only a few organisms are needed to produce
infections.
• The high attack rate leading to severe disease
and high mortality make this a powerful
potential bioterrorism agent.
Glanders-4

Incubation period:
• Few days to several weeks.

Clinical manifestations:
• May be acute, subacute or chronic forms.
• Symptoms depend on the route of infection.
• In localized suppurative infection, a nodule can
form with regional lymphadenopathy usually
within 1 to 5 days.
• Infection of the eyes, nose or respiratory tract
can cause mucopurulent drainage with later
lesions that may ulcerate.
Glanders-6

Clinical manifestations cont.:
• In the case of aerosolized acquired infections,
symptoms include pneumonia, pulmonary
abscesses and may include pleural effusion.
• Cough and pleuritic pain occur.
• In the septicemic form either as a primary
route or secondary to infection from another
site, fever, myalgias, rigors, malaise,
photophobia, lacrimation, sweating, diarrhea
and pleuritic chest pain may occur along with
cervical adenopathy and lesions on the face
and limbs followed by generalized pustular
lesions.
Glanders-7

Clinical manifestations cont.:
• Suppurative disease can be seen in liver,
spleen, lungs or subcutaneous tissues and high
swinging features.
• The chronic form may include cutaneous
abscesses as well as in muscles of arms and
legs and in liver and spleen, and include
regional lymphadenopathy, nasal discharge
and ulceration.

Diagnosis:
• Isolation of organism in blood, lesions, or
urine.
• Complement fixation tests.
Glanders-8

Mortality rates:
• Mortality in the septicemic form is over
50% with treatment and 95% without
treatment.
• Mortality can be 20% even in treated
localized disease.

Vaccination:
• No vaccine is currently available.
Glanders-9

Treatment:
• Information is limited.
• Imipenem and doxycycline were used to
effectively treat the infected laboratory worker.
• In vitro tests indicate that ceftrazidime,
gentamicin, ciprofloxacin, and a combination of
sulfazine and trimethoprim would be effective.
• Need several weeks of intensive therapy and
then eradication of the organism which can
take as long as 3 to 6 months with oral
antibiotics as indicated.
Glanders-10

Nursing and management
considerations:
• In hospital setting, standard precautions plus
contact precautions may be observed,
including:
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Washing hands after patient contact,
Wearing gloves when entering the room,
Placing patient in private room if possible or cohort
with patient with same pathogen,
Wearing gown when entering room if contact with
patient is anticipated or there is wound drainage
without dressing,
Glanders-11

Nursing and management
considerations cont.:
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Use mask and eye protection during any
procedures which may generate splashes or
sprays of blood, body fluids, and/or
secretions or excretions,
Limit movement or transport of patient from
the room,
Handle used patient care equipment and
linen in manner that prevents transfer of
microorganisms to people or equipment,
Use care when handling sharps,
Glanders-12

Nursing and management
considerations cont.:

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Use mouthpiece or other ventilation device
as alternative to mouth-to-mouth
resuscitation,
Ensure that patient care items, bedside
equipment and frequently touched surfaces
receive daily cleaning,
Dedicate use of patient care equipment such
as stethoscopes to single patient or patients
with same pathogen or be careful to ensure
adequate disinfection between patients.
These are described in module on infection
control.
Clostridium perfringens e-Toxin


As a potential agent for bioterrorism,
Clostridium perfringens e-toxin, is thought
to have potential for dissemination by
aerosolization.
Etiology:
• Produced by the bacteria Clostridium
perfringens (a Gram positive spore forming
rod) types B and D.

Transmission:
• Ingestion
• Inhalation
e-Toxin-2

Clinical manifestations:
• Ingestion –
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In animals who ingest this toxin, intestinal
permeability is enhanced.
Hyperemic kidneys, pulmonary edema and pericardial
fluid accumulation may be seen.
Can cause neurological dysfunction such as
nervousness, seizures, or opisthotonos.
There is a veterinary vaccine for animals for
protection.
• Inhalation –

Inhalation could cause pulmonary edema, and renal,
cardiac and central nervous system damage but
information about human illness is sparse.
e-Toxin-3

Treatment:
• Supportive care
• Antibiotics not indicated

Nursing considerations:
• Standard precautions
• Supportive care
Coxiella burnetti (Q fever)

Etiology:
• Coxiella burnetti, a rickettsial bacterium.
• Has sometimes been called Query fever or 9mile fever.

Epidemiology:
•
•
•
•
Widespread in livestock worldwide.
Is considered a zoonosis.
Primary reservoirs are cattle, sheep and goats.
Other affected animals include cats, dogs, wild
rodents, and birds.
Q fever-2

Epidemiology cont.:
• Ticks may also be affected.
• Infected animals shed organisms in birth
products such as amniotic fluid and placenta as
well as milk, urine, feces and other body tissue
or fluid.
• The bacterium can survive for long periods in
the environment.
• Certain occupational workers, such as abattoir
workers, meat packers, farmers, veterinarians,
and laboratory workers are at risk.
Q fever-3

Transmission:
• Inhalation, for example, of
contaminated dust,
• Direct contact with infected animals, or
• Contact with contaminated materials,
such as bedding or hay.
• Transmission may also occur through
blood transfusion or injection.
Q fever-4

Transmission cont.:
• If used as a biological weapon might be
used in aerosol form or through
contaminated food or water.
• Rare cases have followed sexual contact
and vertical transmission.
• Is highly infectious as just one organism
can produce disease.
Q fever-5

Incubation
period:
• Variable.
• Most commonly 2
to 3 weeks after
exposure.
Q fever-6

Clinical manifestations:
• In about 50% of those who are infected, no
symptoms are seen.
• In others, flu-like symptoms may occur initially,
including high fever, headache, malaise,
sweating, chills, abodominal pain, possible
photophobia, and myalgia.
• Cough may be present with x-ray evidence of
pneumonia.
• Nausea and vomiting may occur.
• May see transient thrombocytopenia.
• Weight loss may be seen, and fever may last
more than a week.
• Up to half of those with symptoms develop
pneumonia.
Q fever-7

Clinical manifestations cont.:
• Hepatitis may occur, sometimes only
detectable by abnormal lab tests.
• Some develop chronic Q fever either within a
year or up to 20 years later.
• This consists of endocarditis, occurring in more
than 7%.
• Mortality is high if endocarditis develops.
• In addition, a syndrome similar to chronic
fatigue syndrome with fatigue, myalgia,
arthralgia, sweating and changes in mood and
sleep may be seen.
Q fever-8

Diagnosis:
• Is typically
serological by
indirect
immunofluorescence
assay.
• DNA amplification by
PCR may also be
used.
Q fever-9

Treatment:
• Doxycycline 100 mg. po or iv every 12 hours for 2
weeks for acute Q fever is treatment of choice.
• The acute form may be self-limited with recovery
without treatment, especially if not seriously ill.
• Doxycycline may also be used in chronic Q fever,
sometimes with hydroxychloroquine orally for as long as
18 months.
• In a mass casuality situation, doxycycline may be the
drug of choice for 5 to 7 days.
• Doxycycline is contraindicated in pregnancy
• Special considerations and therapies are suggested for
pregnant women, children and those with complications.
Q fever-10

Nursing considerations:
• Use of standard precautions that includes masks,
gloves, and gowns unless aerosolized in the case
of bioterrorism attack.
• Need to protect against droplet and direct
contact.
• May be resistant against normal disinfectants.
• Prophylaxis not considered necessary for the
general public but might be used for essential
individuals.
Q fever-11

Vaccination:
• Vaccine is available.
• Used frequently in
Australia.
• In case of terrorist
attack, might use
vaccine preexposure.
Q fever-12

Other:
• May have been used as biological weapon in
WWII.
• May be used as a biological weapon because it
is:





Widely available,
Is easily transmitted by aerosol,
Could be aerosolized easily,
Is environmentally stable, and
Could be produced in large quantities.
• Is believed that morbidity could be high with
long convalescence and debilitation.
Ricin Toxin

Etiology:
• Is a cytotoxin derived from Ricin
communis, the castor bean plant.
• Ricin is part of waste left over from
castor bean processing.
• Ricin has potential medical uses.
• Its action is to inhibit protein synthesis
in the cell.
Ricin Toxin-2

Description:
• Can be prepared in large quantities relatively
easily without great technological capacity or
expense.
• May appear as a white powder which can be
dissolved.
• As a potential bioterror attack agent, is not as
toxic as botulinum toxin or Staphlococcus
Enterotoxin B but has reportedly been used in
at least one instance.
• As a potential attack agent, could be used to
contaminate food or water, be aerosolized for
inhalation, or be injected.
• Is very stable.
Ricin Toxin-3

Transmission:
• Inhalation
• Injection (very rare)
• Ingestion
• Dermal and ocular exposures are not
thought to cause systemic toxicity
• No person-to-person transmission
Ricin Toxin-4

Epidemiology:
• In October 2003, a threatening note in an
envelope with a sealed container was processed
at a mail facility in South Carolina. Ricin was
found present in the container. No ricinassociated illness was identified among workers.

Incubation period:
• Ingestion – within 6 hours
• Inhalation – symptoms begin with a few hours
• In February, 2008, a 57 year old men contacted
emergency personnel because of breathing
difficulties. He was found to have ricin vials
present in his room.
Ricin Toxin-5

Clinical manifestations:
• Vary with route of exposure.
• Severe allergic reactions may occur
especially after inhalation.
• May be fatal.
• Ingestion of ricin toxin:



Symptoms occur within 1-4 hours of ingestion.
Include nausea, vomiting, abdominal pain,
cramping, diarrhea, gastrointestinal bleeding,
low or absent urinary output, fever, thirst, sore
throat, headache, vascular collapse, and shock.
Can see necrosis of gastrointestinal epithelium,
as well as hepatic, splenic and renal necrosis.
Ricin Toxin-6

Clinical manifestations cont.:
• Inhalation of ricin toxin (most symptoms may
begin in 4 to 8 hours but be preceded by
allergic reaction):



Symptoms include fever, cough, wheezing, chest
tightness, dyspnea, nausea, heavy sweating and
arthralgias.
Pulmonary edema, adult respiratory distress
syndrome (ARDS), and respiratory failure,
multisystem organ failure as well as death may occur
within 36 to 72 hours.
Eye and skin exposure to powder or mist may cause
pain and redness of eyes.
Ricin Toxin-7

Mortality:
• Death often occurs within 36 to 72 hours after
exposure.
• If death does not occur in 3-5 days, person
often recovers.

Diagnosis:
• Detection of ricin in environmental samples
with clinically compatible signs and symptoms.
• Methods are not available for ricin detection in
biological fluids.
Ricin Toxin-8

Treatment:
• Varies as to route of exposure.






Can adhere to skin or clothing, so need
decontamination.
If eyes or skin exposed, wash or shower with soap
and water.
Remove clothing if contaminated – do not pull off
head, cut off instead.
Place clothing in plastic bag touching as little as
possible preferably using stick or gloves and seal in
bag. Double bag and dispose of properly.
Remove contact lenses. Flush eyes if exposed – do
NOT reinsert. Eyeglasses can be thoroughly washed
and put back on if needed.
Discourage any hand-to-mouth or eye activities.
Ricin Toxin-9

Treatment cont.:
• Immediate care for exposure:

Ingestion –
• Treatment may include lavage (controversial) and
one dose of activated charcoal early if no
vomiting.
• Aggressive IV fluid and electrolyte replacement.
• Treat any effects such as seizures.
• Supportive care which may include respiratory
support and cardiac monitoring.

Inhalation –
• Provide fresh air, rest, half-upright position, and
oxygen if necessary.
• Supportive care with management similar to
pulmonary edema.
Ricin Toxin-10

Nursing and management
considerations:
• Standard isolation precautions for
patient care.
• Secondary aerosols not expected to be
problematic.
• Be sure immediate exposure care has
occurred.
• Supportive, precise care depends on
clinical picture.
Ricin Toxin-11

Other notes:
• For inhalation situations, pressure
demand, self-contained breathing
apparatus and in other situations,
powered air purifying respirator with
HEPA filters are needed for workers at
site.
Staphylococcal Enterotoxin B

Etiology:
• Is an exotoxin produced by various types of
Staphylococcus aureus, a bacterium.

Transmission:
• Ingestion
• Inhalation
• Food poisoning by this toxin is considered one of
the most common causes of outbreaks of food
poisoning.
• The enterotoxins are usually preformed in the
food, especially unfrigerated meats, dairy and
bakery products.
• In a bioterror episode, could be used to
contaminate water supplies or be put in food but
inhalation is considered the greater possibility.
Staphylococcal Enterotoxin B-2

Clinical manifestations:
• Ingestion –






Symptoms can begin 1 to 8 hours after ingestion.
Manifestations of staphylococcal enterotoxin ingestion
include severe nausea, diarrhea, vomiting, abdominal
cramps, and low grade fever.
Prostration may occur.
Usually resolves spontaneously within 20 hours but fluid
and electrolyte management might be desirable.
Fatalities are not usual, and may occur in those who are
immunocompromised, in the elderly or in infants.
Some cases are so mild they do not come to attention.
Staphylococcal Enterotoxin B-3

Clinical manifestations cont.:
• Inhalation –




Would likely begin with significant shortness of breath
and chest pain after latent period of 3-12 hours.
Clinical manifestations of staphylococcal enterotoxin
inhalation could result in respiratory disease leading to
pulmonary edema.
Symptoms could include fever, headache, mylagia, nonproductive cough, chest pain (retrosternal), and
dyspnea.
Lung fields may be clear with no effusion or
consolidation.
Staphylococcal Enterotoxin B-4

Complications:
• After inhalation exposure, cough could
persist as long as a month.

Mortality:
• Rarely fatal with appropriate hydration.
Staphylococcal Enterotoxin B-5

Treatment:
• Supportive with appropriate fluid and
electrolyte management.
• If ingested, most cases are self-limited
resolving in under 24 hours.
Staphylococcal Enterotoxin B-6

Nursing considerations:
• Supportive as above.
• Standard isolation precautions.
• No secondary transmission from
patients.
Staphylococcal Enterotoxin B-7

Vaccination:
• No human vaccine
currently available.
Cryptosporidiosis

Etiology:
• A parasite, Cryptosporidium parvum,
and other Cryptosporidium species.
• Are coccidian protozoa.

Description:
• A disease with largely gastrointestional
and generalized symptoms resulting
from Cryptosporidium ingestion.
Cryptosporidiosis-2

Epidemiology:
• Cryptosporidium are found in a variety of
biological hosts including snakes, lizards, fish,
amphibians, birds, rodents, cats, dogs, sheep,
pigs, deer, and humans.
• Food sources implicated in outbreaks have
included a variety of raw vegetables, basil,
cilantro, unpasturized apple juice and cider,
shellfish and chicken salad.
• The most well known outbreak occurred in
Milwaukee in 1993 when about 430,000 people
were affected from contamination in water
treatment plants.
Cryptosporidiosis-3

Transmission:
• Generally through the fecal-oral route
through oocyst contaminated drinking
water, recreational water, food, or
through close contact with infected
humans or other hosts, such as animals
in petting zoos as well as through
contact with contaminated surfaces.
• The parasite may live in soil, water,
food or surfaces contaminated with
feces from infected humans or animals.
Cryptosporidiosis-4

Incubation
period:
• 2 to 14 days with a
median of 7 days.
Cryptosporidiosis-5

Clinical manifestations:
• The major manifestation is diarrhea that
can last a median duration of 9 days with
a median of 12 stools per day
accompanied by a copious loss of fluids,
abdominal cramps, nausea, loss of
appetite, fatigue, nausea, chills, sweating,
myalgia, headache, and vomiting.
• Symptoms may cycle.
• Persons with weakened immune systems
are at greater risk for severe disease.
Cryptosporidiosis-6

Treatment:
• In immunocompetent persons, is selflimited.
• Symptomatic treatment consists of oral
rehydration and antimotility drugs.
• Nitazoxanide is a new broad spectrum
antimicrobial agent being used for
therapy especially in children.
Cryptosporidiosis-7

Nursing considerations:
• Supportive care.
• Observe for dehydration and treat
appropriately.
• Standard isolation precautions with
excellent handwashing and patient
education on handwashing.
• Contact precautions may be necessary if
patient is in diapers or incontinent.
Cryptosporidiosis-8

Management:
• Prevention consists of environmental
controls, good personal hygiene, and
the safety of water and food.
• The oocysts are resistant to many
chemical disinfections, such as chlorine,
iodine and lysol, and heat-sensitive
medical equipment, such as endoscopes
can be fomites for nosocomial
transmission.
Cryptosporidiosis-9

Management cont.:
• Thus, the institution must determine which of
the effective chemical disinfectants will be
used for instrument and surfaces.
• Handwashing is of major importance,
especially after exposure to feces, after diaper
changes, and after using the toilet as well as
before handling food or providing patient care.

Vaccination:
• None available
Escherichia coli O157:H7

Etiology:
• E. coli are gram-negative, non-spore forming,
rod shaped bacteria of the Enterobacteriaceae
family that are capable of surviving in food and
soil for long periods.
• They are part of the normal organisms in the
intestine.
• There are various pathogenic strains and
serotypes.
• E. coli O157:H7 is a strain that produces Shiga
toxin and adhere closely to mucosa.
• A few organisms can cause infection (10-100).
Escherichia coli O157:H7-2

Description:
• Infection with E. coli O157:H7 can result
in hemolytic uremic syndrome (HUS)
especially in those under 5 years of age
or in the elderly.
Escherichia coli O157:H7-3

Epidemiology:
• Animals, such as cattle, sheep, pigs, and deer,
can carry E. coli O157:H7 and discharge them
in their feces to contaminate soil, food, or
water.
• Food vehicles such as undercooked
hamburger, unpasteurized apple cider,
uncooked vegetables and sprouts have been
the source of infection.
• Infection has occurred when visiting petting
zoos or dairy farms or when swimming in
contaminated water.
• Mainly reported in industrialized countries.
Escherichia coli O157:H7-4

Transmission:
• Fecal-oral route.
• May be foodborne, waterborne or
spread through animal-to-human or
person-to-person contact.
• Nosocomial transmission has occurred.
• Household contacts may become
infected, and person-to-person
transmission is predominant in group
settings, such as day care facilities or
nursing homes.
Escherichia coli O157:H7-5

Incubation period:
• Typically 1 to 14 days.

Clinical manifestations:
• Infection may be asymptomatic or
symptomatic.
• Initial clinical signs include diarrhea,
which may become blood-streaked or
overtly bloody, vomiting (in about
50%), and abdominal pain which is
often cramping.
Escherichia coli O157:H7-6

Clinical manifestations cont.:
• There is usually little or no fever.
• Most people recover in about a week,
but HUS may occur, especially in
children or the elderly.
• HUS usually occurs 4 to 13 days after
initial diarrhea.
• It is believed that in children, HUS is
one end of a gradient of coagulation
abnormalities that occur after E. coli
O157:H7 associated colitis.
Escherichia coli O157:H7-7

Clinical manifestations cont.:
• HUS manifestations may include
thrombotic thrombocytopenic purpura,
microangiopathic anemia, acute renal
failure and CNS manifestations.
• Chronic renal failure, stroke, blindness,
seizures and coma may be complications.
• Long-term sequelae in regard to renal
disease, effects of colonic resection if
needed to treat HUS or cognitive
impairment may be seen.
Escherichia coli O157:H7-8

Diagnosis:
• Stool culture usual in those with afebrile
bloody diarrhea particularly.

Treatment:
• Antibiotics and antimotility agents are not
recommended, and antibiotic treatment in
children may be associated with HUS
development.
• Generally supportive measures recommended
including correcting and maintaining fluids and
electrolytes, monitoring hemoglobin
concentration and treating any anemia;
dialysis if renal complications occur with HUS.
Escherichia coli O157:H7-9

Nursing management:
• Appropriate infection control including
standard precautions and contact
precautions when diarrhea present or
for diapered or incontinent persons.
• Supportive care including observation
for dehydration and fluid and electrolyte
maintenance, and comfort measures.
Salmonella Species (spp)

Description:
• Various members (over 2,000) of the
Salmonella spp. may cause illness and are
considered Category B agents by CDC.

Etiology:
• Salmonella are enteric bacteria.
• Salmonella are gram-negative rod-shaped
bacilli.
• Most well known for causing severe illness is S.
serogroup Typhi (typhoid fever).
• S. Enteritidis and S. typhimurium are the two
serotypes causing about 50% of salmonellosis
in the US. S. Newport is a serotype increasing
in incidence.
Salmonella-2

Epidemiology:
• For salmonellosis, infections are found
worldwide with about 1.4 million cases
per year in the US.
• About 400 cases of typhoid fever occur
each year in the US, most acquired
abroad.
• Worldwide about 17 million cases of
typhoid fever occur each year.
• All age groups may be affected.
Salmonella-3

Transmission:
• Contaminated food or water through
fecal-oral route.
• Salmonellosis may also be acquired
through contact with infected animals,
especially reptiles or exotic pets.
• In typhoid fever, a chronic carrier state
may occur in about 5% of infected
persons.
Salmonella-4

Incubation period:
• Typically 12 hours to 3 days.

Clinical manifestations:
• Typhoid fever –


Usually begins with fever reaching 103o to
104o F, chills, malaise, headache, loss of
appetite, myalgia, abdominal pains, and
possibly constipation.
Diarrhea is not typical and if vomiting occurs
it is not severe.
Salmonella-5

Clinical manifestations cont.:
• Typhoid fever cont. –




Some people get a flat, rose-colored rash.
There is little to distinguish it from many
other infectious diseases at first.
In severe cases, intestinal perforation,
confusion, delirium and even death may
occur.
Without treatment, duration of illness may
be 3 to 4 weeks.
Salmonella-6

Clinical manifestations cont.:
• Salmonellosis –



Fever, diarrhea and abdominal cramps.
Most persons recover without treatment and
symptoms usually resolve within a week.
Mortality rates:
• Typhoid fever may be 12 to 30%.
• Salmonellosis - negligible
Salmonella-7

Treatment:
• In severe cases of either, appropriate
hydration and supportive care is indicated.
• Typhoid fever

Antibiotics such as ampicillin, trimethoprimsulfamethoxazole, quinolones, and
ciprofloxacin are usually given.
• Salmonellosis



Antibiotics are not usually indicated unless
illness is severe or there is extra-intestinal
spread.
Usually resolve in 5-7 days.
If diarrhea is severe, rehydration may be
needed.
Salmonella-8

Nursing considerations:
• Supportive care
• Observation for dehydration and appropriate
fluid and electrolyte replacement.
• Good handwashing techniques are important,
and should be taught to patients as well as pet
handling precautions if secondary infected pet.
• Infection control: Contact precautions if person
is incontinent or in diapers, otherwise standard
precautions. Contact precautions may also be
used to control institutional oubreaks.

Vaccination:
• Typhoid vaccine available.
Salmonella-9

Complications:
• Typhoid fever 
2% of cases are complicated by chronic
arthritis or Reiter’s syndrome.
Shigella dysenteriae

Etiology:
• Shigella dysenteriae are gram-negative
bacteria.
• They can cause shigellosis.

Epidemiology:
• Shigellosis is most common in children,
particularly 2 to 4 years of age, and the
elderly.
• May be commonly seen in developing
countries and in child care settings.
Shigella dysenteriae-2

Transmission:
• Fecal-oral route
• Person-to-person transmission.
• May be acquired from contaminated
food or contaminated water which is
drunk or used for bathing.

Incubation period:
• 24 to 48 hours is usual.
Shigella dysenteriae-3

Clinical manifestations:
• Some are asymptomatic.
• In others, one or two days after
exposure, diarrhea (usually bloody),
fever, malaise, and abdominal cramping
occurs.
• The diarrhea may be severe enough to
require hospitalization.
• However, usually resolution occurs in 5
to 7 days.
Shigella dysenteriae-4

Treatment:
• Antibiotic therapy shortens the illness
and is used in severe cases.
• Preferred antibiotics include nalidixic
acid or other quinolones.
• Some antibiotic-resistant strains have
been noted.
• Usually antidiarrheal agents should be
avoided.
• Supportive care.
Shigella dysenteriae-5

Nursing and management
considerations:
• Infection control: contact precautions if
patient is incontinent or diapered to
control an institutional outbreak
otherwise standard precautions.
• Supportive care.
• In the bioterrorism context, prevention
centers around appropriate
handwashing and basic hygiene.
Cholera

Etiology:
• Vibrio cholerae, a gram-negative, curved, rodshaped bacteria with many serogroups,
including the well known El Tor and 01 and
0139 pandemic strains.

Epidemiology:
• Is endemic in some areas such as India.
• Several pandemics have occurred.
• Is usually transmitted via contaminated water
and food, especially contaminated
undercooked or raw seafood.
• Poor sanitation, use of water from wells, using
stored water which are contaminated by
contaminated hands are all ways transmission
occurs.
Cholera-2

Transmission:
• Generally food- and water-borne,
usually transmitted through fecal-oral
route.
• Person-to-person contact is rare
because large doses of the organism are
needed to cause illness.

Incubation period:
• 18 hours to 5 days usual.
Cholera-3

Clinical manifestations:
• Acute onset with vomiting which tends
to be clear and watery, and watery
diarrhea of great volumes ranging from
500 to 1000 mL that resembles rice
water.
• Dehydration occurs rapidly with
associated signs and symptoms such as
poor skin turgor, deficient tears, and
sunken eyes.
• Complications can include tachycardia,
hypotension and vascular collapse.
Cholera-4

Treatment:
• Rehydration with rapid replacement of
fluids.
• In severe dehydration, patients may
require replacement intravenously but
usually oral rehydration solutions are used
especially for mild cases.
• Requires rapid replacement of fluids,
correction of any electrolyte imbalances
including metabolic acidosis and potassium
imbalances, replacement of any continuing
fluid losses and maintenance.
Cholera-5

Treatment cont.:
• Antibiotics are generally used after fluid
replacement.
• Single dose Azithromycin appears to be
effective for treatment in adults.
• In outbreaks, the antibiotic of choice will
depend on antibiotic resistance patterns.
• Antibiotic treatment shortens symptoms
and decreases the needs for fluid
replacement and generally shortens care
and the need for resources.
Cholera-6

Mortality:
• Without treatment can be as high as
50%.
• With treatment, is often less than 1%.
• Recovery with hydration and without
antibiotics is typically 4 to 5 days and 2
to 3 days with antibiotics.
Cholera-7

Nursing considerations:
• Assess patient for hydration status, and assure
appropriate replacement; observe for additional
symptoms.
• For isolation, standard precautions are
recommended except for infants and young
children or incontinent persons in which case
contact precautions are recommended.
• In emergencies, the cholera cot has been used
which consists of a bucket placed under a bed
with a hole in the middle of the mattress which is
protected by plastic with a sleeve draining from
the hole into the bucket.
• Hand washing is important for staff, patients and
visitors
Cholera-8

Vaccination:
• Oral vaccine available but not 100%
effective and used under certain
circumstances.

Other notes:
• In the bioterrorism context, cholera is
often very debilitating and unpleasant,
but not usually fatal in developed
countries.
Sources: See CDC