Transcript Biological Casualties - Arkansas Hospital Association

The Biologic Incident
Management of Biological
Casualties
DPT 8.0
Hospital Management of
Biological Casualties
DPT 8.0
Biological Warfare Agents
Terminal Objective
• Be able to describe the various types of
biological warfare agents and recognize the
signs and symptoms of exposure.
• Be able to describe how to properly manage and
treat infectious victims
• Know which agents are a risk for secondary
transmission and how to protect against this
spread using personal protective equipment
(PPE) and isolation measures.
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Biological Warfare (BW) Agents - History
• Oldest of the NBC triad of
agents
• Used for > 2,000 years
– Sieges of middle ages
– Smallpox blankets given to
Native Americans
– Germany in World War I
– Japan in World War II
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Aerosol / Infectivity Relationship
Particle Size
The ideal aerosol contains a
homogeneous population
of 2 or 3 micron particulates
that contain one or more
viable organisms
(Micron, Mass
Median Diameter)
18-20
Infection
Severity
Less
Severe
15-18
7-12
Maximum human
respiratory infection is
a particle that falls
within the 1 to 5 micron
size
4-6
(bronchioles)
1-5 (alveoli)
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More
Severe
BW - Epidemiologic Clues
• Large epidemic with high illness and death rate
• HIV(+) individuals may have first susceptibility
• Respiratory symptoms predominate
• Infection non-endemic for region
• Multiple, simultaneous outbreaks
• Multi-drug-resistant pathogens
• Sick or dead animals
• Delivery vehicle or intelligence information
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BW - Epidemiological Information
• Travel history
• Infectious contacts
• Employment history
• Activities over the
preceding 3 to 5
days
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Biological Agents - Types and Characteristics
• Bacteria
• Viruses
• Toxins
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Bacteria as Biological Agents
• Bacteria
– Single celled microorganism
– Invade tissue; cause inflammatory
reaction or produce toxins
– May form spores
• Anthrax
• Plague
• Tularemia
• Q Fever
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Anthrax - Microbiology
• Bacillus anthracis - gram +,
spore-forming bacillus
• Endemic infection in animals
• Humans develop infection
naturally from handling
contaminated fluids or hides
(“Woolsorters Disease”)
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Anthrax - Pathogenesis
• Inoculation, ingestion, or inhalation of spores which
may travel to the regional lymph nodes
• Vegetative bacteria produce edema factor and lethal
factor (toxins)
• Inhalation route has highest mortality and is most likely
route to be used by terrorists
• Inhaled anthrax causes a mediastinitis rather than a
pneumonia
• Untreated skin infection - 21% mortality if septicemia
develops (treated 1%)
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Cutaneous Anthrax
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Gastrointestinal Anthrax
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Inhalational Anthrax
• 2 to 6-day incubation period followed
by fever, myalgias, cough, and fatigue
• Initial improvement followed by abrupt
onset of respiratory distress, shock,
and death in 24 to 36 hours
• Physical findings are nonspecific,
pneumonia is rare
• Chest x-ray - may show widened
mediastinum with or without a bloody
pleural effusion
• 50 % of cases have associated
hemorrhagic meningitis
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Prevention of Secondary Anthrax Transmission
• No documented cases of
person-to-person
transmission of
inhalational anthrax has
ever occurred
• Cutaneous
transmissions are
possible
• Universal precautions
required
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Anthrax - Soviet Incident
Biological
Warfare research,
production and
storage facility
An accident at a Soviet
military compound in
Sverdlovsk (microbiology
facility) in 1979 resulted
in an estimated 66 deaths
downwind.
Path of
airborne
Anthrax
MOSCOW
Sverdlovs
k
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Inhalational Anthrax - Sverdlovsk
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Inhalational Anthrax Post Mortem - Sverdlovsk
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BW Anthrax - Diagnosis
• Clinical picture of sudden onset of respiratory
distress with mediastinal widening on x-ray
• A small number of patients may present with GI or
cutaneous anthrax
• Gram stain of blood and blood cultures - but these
may be late findings in the course of the illness
• ELISA and immunohistology testing may confirm
diagnosis but samples must go to reference
laboratory
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Anthrax - Treatment
Acute Treatment
• Usually futile in severe
mediastinitis patients
who inhaled or ingested
spores
• Ciprofloxacin - 400 mg
IV q 8 to 12 hr
• Doxycycline - 100 mg IV
q 12 hr X 4 wks
• Vaccination begins at
the start of drug therapy
Post-exposure
• Oral prophylaxis
– Ciprofloxacin (500 mg po
q 12 h) X 4 wks until 3
doses of vaccine
– Doxycycline (100 mg po
q 12 h) X 4 wks until 3
doses of vaccine
• FDA licensed vaccine
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Anthrax - Pediatric Treatment
Prophylaxis
• Penicillin
• Doxycycline
IV Therapy
• Penicillin
• Doxycycline
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Anthrax Disease Complex Summary
Inhalational
Tracheobronchial
Lymphadenitis
1-6
days
Hemorrhagic
Meningitis
50%
Cutaneous
ABRUPT
ONSET
Mediastinitis, cyanosis,
stridor, pulmonary
edema
Papule  vesicle
edema + eschar
24 - 36 hours
GI
Toxic shock
and
Death
20%
Resolve
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Plague - Microbiology
• Yersinia pestis - gram(-), nonmotile, non-spore forming bacillus
• Fleas living on infected rodents
spread infection to humans
• Recovery offers temporary
immunity
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Plague - Pathogenesis
• Produces disease by being
consumed by macrophages
and transported to regional
lymph nodes, causing
regional adenitis
• Bacteremia - spread to other
organs (lungs, spleen, liver,
and brain)
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Plague Transmission
Fleas
(active or dormant)
Aerosol
PNEUMONIC
Surface contact
Rodent
BUBONIC
and
SEPTICEMIC
SECONDARY
PNEUMONIC and
OROPHARYNGEAL
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Pneumonic Plague
Prevention of Secondary Infection
• Secondary transmission is
possible and likely
• Standard, contact, and
aerosol precautions for
at least 48 hrs until
sputum cultures are
negative or pneumonic
plague is excluded
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Plague Endemic Counties
Counties with Plague-Positive Samples
1970 - 1994
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Inhalational (Pneumonic) Plague
Signs and Symptoms
• 2 to 3 day incubation period followed by high fever,
myalgias, chills, HA, and cough with bloody sputum
• In contrast to anthrax, pneumonia and sepsis develop
acutely and may be fulminant with patients developing
dyspnea, stridor, cyanosis, and circulatory collapse
• Patchy infiltrates or consolidation seen on chest x-ray
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Bubonic Plague
Signs and Symptoms
• Erythema, fever, rigors
• Bubo formation in
regional lymph nodes
• Bubo aspiration and
gram stain is diagnostic
– Differentiate from
• Tularemia
• Cat-scratch fever
• Staph-strep
lymphadenitis
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Acral Gangrene
Acral gangrene may be a
late complication of
pneumonic or septicemic
plague, and may occur in
the finger, toes, earlobes,
nose, and penis.
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Plague - Acral Gangrene
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Plague - Diagnosis
• Gram stain and culture
of lymph node
aspirates, sputum, or
CSF samples
• Bipolar staining “Safety
Pin” may be present
• Immunoassays are also
available
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Plague - Treatment
Respiratory isolation mandatory for at
least the first 48 hours of treatment
•
•
•
•
Care is otherwise supportive
Vaccine effective only for bubonic plague
Prophylaxis - tetracycline or doxycycline
Antibiotics must be started within 24 hours of symptoms to
impact survival
• Streptomycin (30 mg/kg/day IM divided BID for 10 days)
• Doxycycline (100 mg IV BID for 10 days)
• Chloramphenicol for plague meningitis
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Plague - Pediatric Treatment
Prophylaxis
• Doxycycline
• Trimethoprim/Sulfamethoxazole
IV Therapy
• Streptomycin (over 1 year of age)
• Gentamicin
• Chloramphenicol
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Plague Disease Complex
Erythema
Fever/rigors
Inhalational
Pharyngitis
2 -3 Sudden
days onset
Fever,
URI syndrome
APTT
ecchymosis
DIC
Tender bubo
1 - 10 cm
9%
24 hrs
Liver
enzymes
Fulminant
Pneumonia
6% late
meningitis
2 - 10 days
Stridor, cyanosis,
productive cough,
bilateral infiltrates
Leukemoid
reaction
Systemic
Toxicity
Respiratory failure
& circulatory collapse
Gram - ve
rods in sputum
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Viruses as Biological Agents
• Smallpox
• Viral Hemorrhagic
Fevers (VHF)
• Venezuelan Equine
Encephalitis (VEE)
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Viruses - General Characteristics
• RNA or DNA within a
protein coat
• Require a host to
function and survive
• Many viruses attack a
specific type of cell
causing disease or
cancer
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Viruses - General Characteristics
• May cause disease through direct cytopathic effect,
immune complex deposition and other effects
• May result in end-organ system failure, vascular
damage
• Few antiviral medications available
• Vaccination is the most effective means of preventing
infection
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Smallpox - Microbiology
• Variola (Var-ï-óla) virus, an
Orthopox virus, both minor and
major forms of smallpox exist
• Structure is a large DNA virus
• Declared eradicated in 1980 and
the U.S. stopped its civilian
vaccination in 1981, U.S. military
stopped in 1985
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Smallpox - Pathogenesis
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Smallpox - Case Study
• In 1963, en route by air from Australia to Sweden, a
seaman stops in Djakarta, Singapore, Rangoon,
Calcutta, Karachi, Teheran, Damascus, and Zurich
• Fifteen days later he develops a fever and rash
• Diagnosed with smallpox; 19 cases identified
• More than 300,000 vaccinated worldwide
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Smallpox - Diagnosis & Treatment
DIAGNOSIS
TREATMENT
• Clinical presentation
• Supportive
• Demonstrate virus from
vesicular sampling via
electron microscopy
• Vaccine still available
from CDC
• Confirmation by tissue
culture
• Immune globulin may
also be available from
CDC
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Smallpox - Prevention of Secondary Infection
• Contagious
• All contacts are
quarantined for at
least 17 days
• Infectious until all
scabs are healed over
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Monkeypox Virus
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Smallpox / Monkeypox - Clinical Course Summary
Exanthema on
face, arms, hands
Inhalational
Replication in regional node of airways
12 day incubation
Flat Smallpox
variants
Hemorrhagic
Smallpox
rapid death before
typical lesions
Macules papules 
pustular vesicles
8 - 10 days
2 - 3 days
Scabs separate
+ pt non-infective
Viremia
Acute malaise, fever,
rigors, headache
+ mental status changes
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Viral Hemorrhagic Fevers (VHF) - Microbiology
• RNA viruses causing high
fevers and generalized
vascular damage
• Human infections by
insect bites or by contact
with blood and body fluids
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VHF Pathogenesis
• Fever, myalgias, prostration
• Cases evolve into shock and generalized
mucous membrane hemorrhage
• Conjunctival injection, petechial hemorrhage, and hypotension
• Abnormal renal and LFT - poor prognosis
• Mortality varies; 50 - 80% Ebola Zaire
• Disease severity and survival depends on various host factors;
target organ is the vascular bed.
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VHF Treatment
• Hemodynamic resuscitation and monitoring
– Invasive Swan Gantz catheter as feasible
• Careful fluid management
– use of colloid
• Vasopressors and cardiotonic drugs
• Cautious sedation and analgesia
• No anti-platelet drugs or IM injections
• Coagulation studies and replacement of clotting
factors / platelet transfusions
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Prevention of Secondary VHF Transmission
• No vaccine is available at this time
• Single room w/ adjoining anteroom as only entrance
– handwashing facility with decontamination solution
• Negative air pressure if possible
• Strict barrier precautions
– gloves, gown, mask. shoe covers, protective
eyeware/faceshield
– consider HEPA respirator for prominent hemorrhage,
vomiting, diarrhea, cough
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Prevention of Secondary VHF Transmission
• Chemical toilet
• All body fluids disinfected
• Disposable equipment/sharps into rigid containers and
autoclaved/incinerated
• Double-bag refuse-outside bag disinfected
• Electronic/mechanical equipment can be
paraformaldehyde disinfected
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Prevention of Secondary VHF Transmission
• Wash / irrigate wound site immediately
• Mucous membranes (eye, mouth, nose)
– Continuous irrigation with rapidly flowing water or sterile
saline for >15 minutes
• Skin
– Scrub for >15 minutes while copiously soaking the wound
with detergent solution
– Germicidal solution
(Dilute 1 part laundry bleach with 9 parts tap water)
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The VHF RNA Viruses
Acute onset
febrile illness
High fever, myalgia,
GI disturbances
Ebola
Marburg
Major
organ
necrosis
Severe systemic illness
coagulation abnormalities
Lassa
Oropharangeal
lesions
Machupo
Hantaan
Renal
failure
Pulmonary
Syndrome
Severe bleeding
ecchymosis
Congo fever
7 days
Rapid progression into
shock and death
Jaundice
Syndrome
Four Corners Agent
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Yellow fever
Dengue (2x)
Rift Valley
Ebola Case Study
• April 5, 1995 - Zaire laboratory worker - fever and
bloody diarrhea
• May 17 - 93 cases - 92% fatality - most cases were in
health care providers
• June 25 - 296 cases
When institutional barrier precautions were
implemented by WHO/CDC - the infection rate
among health care workers dramatically decreased.
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Toxins as Biological Agents
• Botulinum
• Ricin
• Staphylococcal
Enterotoxin B (SEB)
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Toxins
General Characteristics
• Naturally produced poisons
• More toxic per weight than manmade chemical
agents
• Non-volatile
• Minimal absorption in intact skin
• Not prone to person-to-person transmission
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Botulinum Toxin - Characteristics
• Neurotoxin produced by
Clostridium botulinum Botulism
• Most lethal compound
per weight (15,000 times
more toxic than the nerve
agent VX)
• Different toxicity if inhaled
or ingested
Bot A Toxin
HN
Hc
neutralizing
epitopes
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light chain
Botulism - Pathogenesis
• Blocks the release of ACh at 3
places in the presynaptic
terminal of the neuromuscular
junction and autonomic
nervous system
• Bulbar palsies and skeletal
muscle weakness
MUSCLE
NERVE
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Botulism - Signs & Symptoms
• Descending paralysis
• Bulbar palsies
–
–
–
–
–
–
–
blurred vision
mydriasis
diplopia
ptosis
photophobia
dysphagia
dysarthria
“Floppy” baby
flaccid paralysis
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Botulism - Diagnosis and Treatment
• Clinical diagnosis - bulbar palsy with descending
paralysis
• Mouse neutralization assay can confirm diagnosis
• Treatment is supportive
– Long-term mechanical ventilation
• Antitoxins are available; must be administered early
• CDC vaccine protective for A and B toxins
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Ricin - Characteristics
• Toxic by multiple routes
of exposure
• Can be dispersed as an
aerosol
• Effective orally, by
injection, or inhalation
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Ricin - Pathogenesis
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Ricin - Signs & Symptoms
• Fever, chest tightness, cough, SOB, nausea, and joint
pain 4 to 8 hours after inhalation
• Airway necrosis and edema leads to death in 36 to
72 hours
• Ingestion causes N,V, severe diarrhea, GI hemorrhage,
and necrosis of the liver, spleen, and kidneys - shock and
death within 3 days
• Injection causes marked necrosis of muscles and lymph
nodes with multiple organ failure leading to death
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Ricin - Diagnosis & Treatment
DIAGNOSIS
• Difficult
• Routine labs are
nonspecific
• ELISA of blood
TREATMENT
• Supportive oxygenation and
hydration
• No antitoxin or vaccine
available
• Immunohistochemical
tests may confirm
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Teaching Points
•
•
BW EXPOSURE: WET OR DRY AGENT AEROSOLS
BACTERIAL AGENTS
– LETHAL: Anthrax, Tularemia, Plague
– NON-LETHAL: Q Fever
•
VIRAL AGENTS
– LETHAL: Smallpox / Monkeypox, Viral Hemorrhagic
Fevers
– NON-LETHAL: Venezuelan Equine Encephalitis
•
TOXINS
– LETHAL: Ricin, Botulinum Toxin A
– NON-LETHAL: Staphyloccal Enterotoxin B
•
SECONDARY INFECTION IS POSSIBLE WITH
– Plague, Smallpox/Monkeypox, and VHF
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Biological Agents
Case Study
Emergency departments always seem busier during a full moon
despite evidence to the contrary. Tonight was no exception. Over a
6-hour period, it seemed that almost half of the patients presented
with similar complaints of high fever, cough, shortness of breath,
and generalized ill feeling. Five young, previously healthy
individuals required intubation and mechanical ventilation for
severe respiratory distress. Strangely, most of the patients knew
each other from work and none of their family members were
suffering similar symptoms. At 11 p.m., the only other community
hospital in the area went on diversion because all of their intensive
care unit (ICU) beds were full and their need for mechanical
ventilators was at a critical level. The public health officer on call
was not aware of any recent infectious outbreak.
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Biological Agents
• What might the causative agent be?
• How could you identify common factors which might relate
the patients to each other?
• How long ago might the attack have occurred?
• If you are suspicious that patient illnesses could be the
result of a biological attack, whom should you notify?
• What precautions should you and other healthcare
providers take?
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