Transcript anthrax as a biological weapon

Association of Occupational and
Environmental Clinics
Worker Preparedness
and Response
to Bioterrorism
Edward W. Cetaruk, M.D.
Toxicology Associates
University of Colorado Health Sciences Center
Denver, Colorado, USA
Section 1
An Overview of Biological Weapons
Objectives:
1) To be able to list biological agents that may be
weaponized
2) To describe the process of weaponization
3) To develop an understanding of the
bioterrorist threat
4) To be able to recognize a biological attack
Probability vs. Potential Impact
BIOLOGICAL
AGENT
NUCLEAR
WEAPON
IMPROVISED
NUCLEAR
DEVICE
POTENTIAL
IMPACT
RADIOACTIVE
MATERIAL
PROBABILITY/LIKELIHOOD
CHEMICAL AGENT
OR TOXIC
INDUSTRIAL
CHEMICAL
History of Biological Warfare
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Oldest of the NBC triad of agents
Used for > 2,000 years
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Sieges of middle ages
Smallpox blankets given to Native
Americans
Germany in World War I
Japan in World War II
Modern Bioterrorism
Aum Shinrikyo Cult
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Sarin Nerve Agent attacks 1994 and 1995
Attempted Botulinum Toxin release multiple times
Anthrax released multiple times
Attempted to obtain Ebola virus in Zaire
Anthrax Letters
United States
Weaponized Biowarfare
Agents
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Anthrax
Botulinum Toxin A
Brucellosis
Glanders
Marburg Virus
Plague
Q Fever
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Salmonella
Smallpox
Staph Enterotoxin B
Monkey Pox
Ricin
Tularemia
VEE
VHFs
Biological Agents of Highest Concern
Category A
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Variola major (Smallpox)
Bacillus anthracis (Anthrax)
Yersinia pestis (Plague)
Francisella tularensis (Tularemia)
Botulinum toxin (Botulism)
Filoviruses and Arenaviruses (Viral hemorrhagic fevers)
ALL suspected or confirmed cases should be reported to
health authorities immediately
Incubation Periods of Selected
Biological Agents
Anthrax
1-5 Days++
Plague
2-3 Days
Q Fever
10-40 Days
Tularemia
2-10 Days
Smallpox
7-17 Days
Viral encephalitides
V(2-6d); E&W (7-14 d)
VHFs
4-21 Days
Botulinum toxin
1-5 Days
Staph. enterotoxin B
1-6 Hours
Infective Aerosol Doses of Selected
Biological Agents
Anthrax
spores
8,000 (or fewer)
Plague
100-500 organisms
Q Fever
1-10 organisms
Tularemia
10-50 organisms
Smallpox
10-100 organisms
Viral encephalitides
10-100 organisms
VHFs
1-10 organisms
Botulinum toxin
0.001 ug/kg
Aerosol Size and Infectivity
The ideal aerosol
contains a
homogeneous
population
of 2 or 3 micron
particulates that contain
one or more
viable organisms
Maximum human
respiratory infection
is a particle that
falls within the 1 to 5
micron size
Particle Size Infection
(Micron, Mass
Severity
Median Diameter)
18-20
Less
Severe
15-18
7-12
4-6
(bronchioles)
1-5 (alveoli)
More
Severe
Epidemiologic Clues
•
Large epidemic with high illness and death rate
• Immunocompromised 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
Epidemiologic Information
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Travel history
• Local
• Distant
Infectious contacts
Employment history
Activities over the
preceding 1 to 2
weeks
Section 2
Bioterrorism and the Workplace
Objectives:
1) To be able to develop practices and
procedures to defend workers and the
workplace from a bioterrorist attack
2) To respond the unique risks faced by first
responders
3) To be able to choose and use the correct
PPE needed for biological weapons
Bioterrorism Educational Needs
of the Worker
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Awareness
Fundamental understanding of biowarfare
agents
Recognition and handling of suspicious
mail or dissemination devices
PPE and workplace safety
Recognition of bioterrorist attack
Post exposure management
Bioterrorism:
Who are First Responders?
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Primary Care Personnel
Hospital ER Staff
Public Health Professionals
Emergency Response Personnel
Laboratory Personnel
Law Enforcement
Public
Military
First Responders
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Often dealing with unknown agent(s)
May be exposed to infectious agent
May be exposed to infectious patients
May be targeted with secondary devices
May be first to notice the epidemiological
pattern of a bioweapons attack
Emergency Plan
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All Hazards Approach
Identify areas with risk of exposure
Develop controls to minimize risk
• Engineering Controls
• Administrative Controls
• Housekeeping Controls
PPE for workers
Develop response and recovery plan
Training and Exercises
Emergency Plan
Exposure to Biological Agent
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Policies and Procedures for handling
suspicious mail or packages
Plan for facility response
Plan for involving appropriate authorities
Medical Surveillance
Training and Exercises
Handling of Suspicious Mail
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Do not shake, empty contents
Do not carry, show others, or allow others to
examine it
Do not sniff, touch, look closely at it, or any
contents that may have spilled
Leave on stable surface, alert others, leave
area, close doors, shut off ventilation
Wash hands with soap and water
Notify law enforcement
Create list of persons with potential contact
Personal Protective Equipment
 Level A
• SCBA, Encapsulation
• Level of protection for entering contaminated,
unsecured scene
 Level
B
 Level C
 Level D
Personal Protective Equipment
Respirators
Powered Air-Purifying Respirator (PAPR)
• HEPA filter face masks (N95, N100)
• Respirators must be in compliance with
OSHA respiratory standard
(29 CFR 1910.134)
• Respirators must be fit tested
Powered Air Purifying Respirator
(PAPR)
PPE
Respirators
• Respirators should be used in accordance with a
respiratory-protection program that complies with
the OSHA respiratory-protection standard (29 CFR
1910.134).
N95
N100
Personal Protective Equipment
Respirators
 The respirator is properly positioned over your
nose and mouth at all times
 The top strap or head harness assembly is
positioned high on the back of the head
 The lower strap is worn at the back of the neck
below the ears
 The straps are snug enough to keep the respirator
from moving but not overly tight
 Nothing (beards, head coverings, etc.) passes
between the skin of the face and the respirator’s
sealing edge
PPE
Dermal Protection
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Disposable
Reusable
Overgarments, Booties, Hoods, Gloves
All PPE should be decontaminated prior to
leaving potentially contaminated area
PPE should be removed and discarded prior
to removing face mask
Section 3
Anthrax as a Biological Weapon
Objectives:
1) To understand the microbiology and
epidemiology of anthrax
2) To understand the pathophysiology of the
different anthrax clinical syndromes
3) To be able to recognize cutaneous anthrax
4) To be able to recognize an intentional
anthrax release
5) To be able to treat patients with anthrax
Anthrax
Microbiology & Epidemiology
•
Bacterium
• Spores may survive > 100 yrs
• Worldwide soil distribution
• Common disease of herbivores
• Herbivores in USA vaccinated
• Man infected via animal products
• Woolsorter’s Disease
Anthrax
Worldwide Occurrence
Source: WHO World Anthrax Data Site
Anthrax
Pathophysiology
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Spore enters skin, GI tract, or lung
• Germinates in macrophage
• Transported to regional lymph nodes
• Local production of toxins
• Swelling and Tissue Death
• Toxemia
Anthrax
Clinical Syndromes
Cutaneous
• Gastrointestinal
• Inhalational
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Multiple forms can be
seen as the result of a BW attack
Anthrax
Gastrointestinal
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Abdominal pain, usually accompanied by
bloody vomiting or diarrhea, followed by
fever and signs of sever infection
GI anthrax is sometimes seen as mouth
and throat ulcerations with tender neck
glands and fever
Develops after ingestion of contaminated,
poorly cooked meat.
Incubation period: 1–7 days
Case-fatality: 25–90% (role of early
antibiotic treatment is undefined)
Anthrax:
Cutaneous
• Begins as a papule, progresses through a
vesicular stage to a depressed black necrotic ulcer
(eschar)
• Edema, redness, and/or necrosis without
ulceration may occur
• Form most commonly encountered in naturally
occurring cases
• Incubation period: 1–12 days
• Case-fatality:
• Without antibiotic treatment:
20%
• With antibiotic treatment:
1%
Cutaneous
Anthrax
Hospital
Day 5
Hospital
Day 12
2 months
after
discharge
JAMA. 2002;287:869-874
Inhalational Anthrax
Clinical Presentation
•
Incubation Period: 1-6 days
• A brief prodrome resembling a “viral-like”
illness, characterized by muscle aches, fatigue,
fever, with or without respiratory symptoms,
nausea, vomiting, abdominal pain
• Early Symptoms: malaise, fever, fatigue, nonproductive cough, chest discomfort
• Confusion, neck stiffness, and headache suggest
meningitis (seen in 50% of patients)
Inhalational Anthrax
Clinical Presentation
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After initial onset of illness, symptoms may
remain mild or even improve slightly before
worsening
Terminal Phase: dyspnea, stridor, cyanosis,
shock, chest wall edema, meningitis,
widened mediastinum with effusion with
overall toxic/septic clinical picture
Presenting Symptoms
Symptoms
Fever, chills
Sweats, often drenching
Fatigue, malaise, lethargy
Cough
Nausea or vomiting
Dyspnea
Chest discomfort or pleurisy
Myalgias
Headache
Confusion
Abdominal pain
Sore throat
Rhinorrhea
n=10
10
7
10
9
9
8
7
6
5
4
3
2
1
Emerg Infect Dis vol.7, no. 6, 2001
Anthrax Diagnosis
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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, FA, PCR and immunohistology testing
may confirm diagnosis but samples must go to
reference laboratory
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
• Vaccination
Post-exposure
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Oral prophylaxis
•
Ciprofloxacin (500 mg
PO q12 h) X 60 days and
until 3 doses of vaccine
•
Doxycycline (100 mg PO
q12 h) X 60 days and
until 3 doses of vaccine
Vaccination
Anthrax Vaccine
•
FDA approved 1970
• Cell Free filtrate (NO organisms, dead or alive)
• Adverse effects 1-3%
• Bioport Corporation
Laboratory Workers
Increased number of highly pathogenic
bacterial and viral samples
• Increased need for universal precautions
• Increased need for security, including
maintaining chain of custody for forensic
samples
• Increased need for decontamination procedures
• Laboratory Response Network (LRN)
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Laboratory Workers
Decontamination and Disinfection
Effective sporicidal solutions:
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Commercially-available bleach diluted to
0.5% Sodium hypochlorite (1 part household
bleach to 9 parts water)
Rinse off concentrated bleach to avoid
caustic effects
Approved sporicidal agents
Section 4
Plague as a Biological Weapon
Objectives:
1) To be able to describe the pathophysiology
and epidemiology of plague.
2) To be able to recognize and treat the
different clinical forms of plague.
3) To be able to control the secondary
transmission of plague
Plague
History
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200,000,000 deaths
Biblical (I Sam.) - 1320 BC, Philistines
Major Pandemics
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541 - Plague of Justinian
• 1346 - ‘Black Death’
• 1894 - Modern Pandemic
Plague Distribution
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1894 - Began in China
• 1898 - Southwest to India
• 1898 - South to Vietnam
• 1900 - Trans-Pacific to United States
Plague
Epidemiology
Vector: fleas, >80 species
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Xenopsylla cheopis (Oriental rat flea)
Fleas feed on plague-infected mammal
Bacteria multiply in gut
Coagulum blocks gut
Plague organisms are
regurgitated into bite
wound with next feeding
Photo: Ken Gage, Ph.D., CDC, Fort Collins, CO
Plague
Epidemiology
Reservoir: mammals, >200 species.
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Rattus rattus (Black rat)
Ground squirrels, prairie dogs, cats
Plague
Pathogenesis
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Yersinia pestis - a Gram negative, nonmotile,
nonsporulating bacteria
Size: 0.5–0.8 × 1.5–2.0 µm
Normally a disease of rodents
Virulence Factors: antiphagocytic fraction 1
capsule, pH 6 antigen, antiphagocytic Yops H
and E, V antigens, Yop M, and plasminogen
activator
Plague
Pathophysiology
Inoculation or inhalation
(1-10 organisms)
(100-20,000 organisms)
Macrophage
Lymphatics
Regional lymph nodes
Blood
Lung
Meninges
Liver
Spleen
Bubonic Plague
Clinical Presentation
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Incubation 1-8 days (mode 3-5 days)
Sudden onset of flu-like syndrome
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Bubo formation - within 24 hours
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(Fever, rigors, malaise, myalgias, nausea)
Swollen, infected lymph node (very painful!)
Cutaneous findings in 25% of cases
• Mortality:
Untreated 60%
Treated <5%
Bubonic Plague
Photographs: Ken Gage, Ph.D., Centers for Disease Control and Prevention, Fort Collins, CO
Pneumonic Plague
Clinical Presentation
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2 to 3 day incubation period followed by high fever,
muscle aches, chills, headache
Cough with bloody sputum within 24 hours
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pneumonia progresses rapidly – shortness of breath, stridor,
cyanosis, difficulty breathing, chest pain
respiratory failure, shock, bleeding
In contrast to anthrax, Plague pneumonia and sepsis
develop acutely and may be fulminant
Patchy lung infiltrates or consolidation seen on chest
x-ray
Pneumonic Plague
Photograph by Ken Gage, Ph.D., Centers of Disease Control and Prevention, Fort Collins, CO.
Plague Transmission
Fleas
(active or
dormant)
Aerosol
PNEUMONIC
Surface
contact
Rodent
BUBONIC
and
SEPTICEMIC
SECONDARY
PNEUMONIC
and
OROPHARYNGEAL
Plague
Diagnosis
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Photomicrograph: Ken Gage, Ph.D., Centers for
Disease Control and Prevention, Fort Collins, CO.
Gram stain and culture
of lymph node
aspirates, sputum, or
CSF samples
Bipolar staining
“Safety Pin” may be
present
Immunoassays are also
available
Plague - Treatment
Antibiotic Therapy:
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Streptomycin (choice)15-30 mg/kg IM bid x
10 days
Gentamicin - 2 mg/kg IV then 1.0-1.5 mg/kg
q8h or 5 mg/kg IV q24h x 10 days
Doxycycline - 200 mg IV then
100 mg bid x 10-14 days
Ciprofloxacin - 400 mg IV q12h x 10 days
Plague
Control of Secondary Transmission
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
Section 5
Smallpox as a Biological Weapon
Objectives:
1) To be able to describe the epidemiology
and microbiology of smallpox
2) To be able to recognize clinical smallpox
3) To be able control the secondary
transmission of smallpox
4) To describe treatment and vaccination
options for smallpox.
Smallpox
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The world’s first eradicated disease
1977- last endemic case in Somalia
1978- two laboratory cases in Britain
1980- WHO declares global
eradication of smallpox
Smallpox
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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
Smallpox as a Bioweapon
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1763- French & Indian War
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World War II
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Fort Ticonderoga
Lord Jeffrey Amherst
Unit 731 experiments in China
Cold War
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USSR arsenal
Why would smallpox Make A
Good Biological Weapon?
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Infectious via aerosol
• Vaccination discontinued
• Decreased potency of vaccine stocks
• Severe morbidity and mortality
• Transmissible
• Clinical inexperience
• “Brand-name” recognition
Clinical Smallpox
Prodrome
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Incubation 7-17 days (mean 12)
Infection of respiratory mucosa
Minor viremia: seeding of liver, spleen
Major viremia: seeding of skin
Acute onset fever, rigors, headache,
vomiting
Virus cultured from blood
Clinical Smallpox
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Enanthem
Exanthem
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begins on face, hands, forearms
spreads to lower extremities
centrifugal distribution
Macules  papules  vesicles 
pustules  scabs/crusts  scars
Breman & Henderson, NEJM, 346(17), April, 2002
Smallpox
Day 3 of Rash
From: Fenner F, Henderson DA, Arita I, Jezek Z, Ladnyi ID. Smallpox and Its Eradication.
Geneva, Switzerland: World Health Organization; 1988: 10–14. Photographs by I. Arita.
Smallpox
Day 5 of Rash
From: Fenner F, Henderson DA, Arita I, Jezek Z, Ladnyi ID. Smallpox and Its Eradication.
Geneva, Switzerland: World Health Organization; 1988: 10–14. Photographs by I. Arita.
Smallpox
Day 7 of Rash
From: Fenner F, Henderson DA, Arita I, Jezek Z, Ladnyi ID. Smallpox and Its Eradication.
Geneva, Switzerland: World Health Organization; 1988: 10–14. Photographs by I. Arita.
Smallpox
Smallpox
Clinical Forms
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Variola Major
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30% fatal in unvaccinateds
• 3% fatal in vaccinateds
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Variola Minor
Flat-Type Smallpox
Hemorrhagic Smallpox
Modified-Type Smallpox
Variola Sine Eruptione
Variola
Minor
From: Fenner F, Henderson DA, Arita I, Jezek Z, Ladnyi ID. Smallpox and Its Eradication.
Geneva, Switzerland: World Health Organization; 1988: 10–14. Photographs by I. Arita.
Flat-type Smallpox
From Fenner F, Henderson DA, Arita I, Jezek Z, Ladnyi ID. Smallpox and Its Eradication.
Geneva, Switzerland: World Health Organization; 1988: 33. Photograph by F. Dekking
Hemorrhagic Smallpox
From Herrlich A, Mayr A, Munz E, Rodenwaldt E. Die pocken; Erreger, Epidemiologie
und klinisches Bild. 2nd ed. Stuttgart, Germany: Thieme; 1967.
Smallpox vs. Chickenpox
Incubation
Prodrome
Distribution
Evolution
Scabs Form
Scabs Separate
Infectivity
Variola
7-17 days
2-4 days
centrifugal
synchronous
10-14 days
14-28 days
separation
Varicella
14-21 days
minimal
centripetal
asynchronous
4-7 days
<14 days
scabbing
Smallpox
Management of Contacts
• Immediate vaccination or boosting
• VIG 0.6 ml/kg
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Pregnant patients
Dermatoses patients
?? Normal hosts
Limited data: Vaccine + VIG better than
vaccine alone?
• STRICT quarantine x 17 days
Vaccination
•
Employs Vaccinia virus
• Given by scarification
• One dose protective for 5-10 years
• Must keep vaccinia immunoglobulin
(VIG) on hand to treat complications
of vaccination
Complications of Vaccination
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Normal host
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Inadvertent Autoinoculation (skin, eye)
• Generalized vaccinia
• Erythema multiforme
• Encephalitis
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Pregnancy - fetal vaccinia
Dermatoses/Burns - eczema vaccinatum
Immunocompromised - vaccinia necrosum
Ocular
Vaccinia
From Fenner F, Henderson DA, Arita I, Jezek Z, Ladnyi ID. Smallpox and Its Eradication.
Geneva, Switzerland: World Health Organization; 1988: 298. Photograph by C. H. Kempe
Vaccinia
Necrosum
From Fenner F, Henderson DA, Arita I, Jezek Z, Ladnyi ID. Smallpox and Its Eradication.
Geneva, Switzerland: World Health Organization; 1988: 298. Photograph by C. H. Kempe
Eczema Vaccinatum
N Engl J Med, Vol. 346, No. 17, April 25, 2002
Smallpox
Therapy
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Public health emergency
Supportive care
Vaccinia Immunoglobulin
Strict quarantine until scabs off
• At least 17 days
Codofovir
Section 6
Other Viruses as Biological Weapons
Objectives:
1) To become familiar with viral hemorrhagic
fever viruses (VHFs) and Venezuelan equine
encephalitis virus pathophysiology
2) To be familiar with necessary PPE to able to
limit the secondary spread of VHF
3) To be able to treat victims of these biological
agents
Viral Hemorrhagic Fevers
Microbiology
•
RNA viruses causing
high fevers and
generalized vascular
damage
• Filoviruses (Ebola,
Marburg)
• Human infections by
insect bites or by
contact with blood
and body fluids
Photograph: Robert Swanepoel, PhD, DTVM, MRCVS,
National Institute of Virology, Sandringham, South Africa.
Viral Hemorrhagic Fevers
(VHFs)
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RNA viruses causing high fevers and
generalized vascular damage
May be spread by aerosol, on fomites, and by
oral secretions and eye drainage in animals
Human infections by contact with blood and
body fluids
VHF Pathogenesis
•
Fever, muscle aches, prostration
• Cases evolve into shock and generalized mucous
membrane hemorrhage
• Conjunctival injection, petechial hemorrhage, and
hypotension
• Abnormal kidney and liver function tests  poor
prognosis
• Mortality varies; 50 - 80% Ebola Zaire
• Disease severity and survival depends on various
host factors; target organ is the blood vessel system.
Ebola Virus
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1976 - First reported case in Sudan
1989 - Reston, VA health facility
among imported monkeys
April 1995 - Ebola epidemic Kikwit, Zaire
1996 - Ebola outbreak in Alice, TX - monkeys
1996 - Gabon patient infection transferred to
Johannesburg clinic healthcare worker
50 to 80% mortality rate in humans - extensive
hemorrhage, shock, and end organ failure
2002 – Gabon – most recent outbreak
VHF
Treatment
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Blood pressure resuscitation and monitoring
Careful fluid management
• Use of colloids (e.g. plasma)
Vasopressors and inotropes
Cautious sedation and analgesia
No anti-platelet drugs or IM injections
Coagulation studies and replacement of
clotting factors, platelet transfusions
Prevention of Secondary VHF
Transmission
•
Animal studies indicate aerosol transmission possible
•
Single room with adjoining anteroom as only
entrance
•
•
•
Handwashing station with decontamination solution
Negative air pressure room if possible
Strict barrier precautions (PPE):
•
Gloves, gown, mask. shoe covers, protective
eyeware/faceshield
• Consider HEPA respirator (e.g. N95) for severe
hemorrhage, vomiting, diarrhea, cough
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 must be
disinfected
Venezuelan Equine Encephalitis
(VEE)
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Alphavirus spread by mosquitoes
Endemic to Central and South America,
Mexico, and Florida
Highly infectious - 100% of exposed
individuals develop symptoms
Low mortality rate - 1%
Section 7
Toxin Weapons
Objectives:
1) To be able to explain how each of the
presented toxin weapons act
2) To be able to recognize victims to toxin
weapon poisoning
3) To understand that toxin weapons are
NOT infectious and CANNOT be
secondarily spread
Botulinum Toxin
•
•
•
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
Botulinum Toxin
Normal Muscle Contraction
NMJ
Acetylcholine
Motor Nerve
MUSCLE CONTRACTION
Muscle
Botulinum Toxin
Botulinum-Paralyzed Muscle
NMJ
Motor Nerve
B
O
T
O
X
NO MUSCLE CONTRACTION
Muscle
Botulism
Signs & Symptoms
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Descending paralysis
Bulbar Palsies
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Blurred vision
Dilated pupil
Double vision
Drooping eyelids
Light intolerance
Difficulty swallowing
Difficulty speaking
Respiratory failure
“Floppy” baby flaccid paralysis
Botulism
Diagnosis and Treatment
•
•
•
•
•
Clinical diagnosis: bulbar palsies with
descending paralysis
Mouse neutralization assay confirms diagnosis
Treatment is supportive
• Long-term mechanical ventilation
Antitoxins are available but must be
administered early to be effective
CDC vaccine protective for A,B and E toxins
Ricin
•
•
•
Potent toxin - a protein
byproduct of castor bean
processing for castor oil
5 times more toxic per
weight than VX
Blocks protein synthesis
within the cell, causes
cell death, and airway
tissue death and swelling
when inhaled
Ricin
Diagnosis & Treatment
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•
•
•
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Fever, chest tightness, cough.
Shortness of breath, nausea, and joint pain.
Ingestion causes severe diarrhea,
hemorrhage, and necrosis of the liver, spleen,
and kidneys - shock and death within 3 days
Treatment is supportive, including airway
management
No antitoxin or vaccine available
Staphylococcal Enterotoxin B
(SEB)
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Common cause of food poisoning in
improperly handled foods
80% of exposed individuals develop
symptoms
Symptoms vary by route of exposure can be aerosolized or introduced into
food system
SEB
Signs & Symptoms
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Sudden onset of high fever, headache, chills,
muscle aches, and non-productive cough, and
malaise.
Inhalational: Severe shortness of breath &
chest pain with larger doses
Ingestion:
Nausea, vomiting, and diarrhea
SEB
Treatment
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Supportive Care: Oxygenation
Hydration
Most victims will recover
No vaccine available
No antibiotic is effective