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HSE420Module2Chapter3Slides.pptxBiosecurity & Bioterrorism: Containing and Preventing Biological Threats
Chapter 3
Category A Diseases and Agents
Learning Objectives
List and explain the criteria used to define Category A agents.
Describe the signs and symptoms of anthrax, plague, tularemia, smallpox, viral hemorrhagic fever, and botulism.
Describe the clinical manifestations of anthrax, plague, tularemia, smallpox, viral hemorrhagic fever, and botulism.
Discuss prophylaxis and medical treatment strategies used to counter anthrax, plague, tularemia, smallpox, viral hemorrhagic fever, and botulism.
Understand the challenges that public health officials and emergency management practitioners face when an intentional release of a Category A agent occurs in their community.
Key Terminology
Anthrax
Botulism
Plague
Smallpox
Tularemia
Viral Hemorrhagic Fever (VHF)
HHS Category A Criteria
Easily disseminated
Transmitted from person-to-person
High mortality rates
May cause panic or social disruption
Special action for public health preparedness
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Since you’re starting here, we can cover the criteria for putting certain agents in Category A. If a biological agent is easily disseminated or transmitted from person-to-person; has a high mortality rate; may cause panic or social disruption; and, would require special actions for public health you’ll find it here.
Category A Agents & Diseases
| Disease | Agent | Type of Agent | Zoonoses | Contagious Person-to-Person |
| Anthrax | Bacillus anthracis | Bacteria | Yes | No |
| Plague | Yersinia pestis | Bacteria | Yes | Yes, in pneumonic form |
| Tularemia | Francisella tularensis | Bacteria | Yes | No |
| Smallpox | Variola major | Virus | No | Yes |
| Viral Hemorrhagic Fever | Several from Arenaviridae, Filoviridae, Bunyaviridae and Flaviviridae | Virus | Yes | Yes |
| Botulism | Botulinum toxin from Clostridium botulinum | Toxin | No | No |
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This is what we’ll be covering in our discussion of Category A agents. The agents and the disease or syndrome they cause are listed above. This is an important point. Are diseases transmitted or are their agents? To be exact, we should put it this way:
The etiologic agent of Anthrax is Bacillus anthracis. In the 2001 Amerithrax incident we often hear that “anthrax was sent through the mail”. This is a pet peeve of mine. We should say that Bacillus anthracis spores were sent through the mail, but it’s so common to put it the other way that it’s now accepted by most agencies.
So, let’s get on with it.
Anthrax
Image courtesy of CDC PHIL
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Bacillus anthracis
Large, gram positive non-motile rod
Vegetative form and spores
Nearly worldwide distribution
Over 1,200 strains
Image courtesy of CDC PHIL
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The Spore
Sporulation requires
Poor nutrient conditions
Presence of oxygen
Spores
Very resistant to extremes
Survive for decades
Taken up by host and germinate
Lethal dose 2,500 to 55,000 spores
Image courtesy of CDC PHIL
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3 Clinical Manifestations
Cutaneous
Inhalation
Gastrointestinal
Images courtesy of CDC PHIL
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Human Transmission
Most human cases are occupationally related
Tanneries
Textile mills
Wool sorters
Bone processors
Slaughterhouses
Ceremonial drum makers
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Human Transmission
Cutaneous
Contact with infected tissues, wool, hide, soil
Biting flies
Inhalational
Tanning hides, processing wool or bone
Gastrointestinal
Consumption of undercooked meat from infected animals
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Cutaneous Anthrax
95% of all cases globally
Incubation: 3-5 days (up to 12 days)
Spores enter skin through open wound or abrasion
Case fatality rate 5-20%
Untreated – septicemia and death
Edema can lead to death from asphyxiation
Image courtesy of CDC PHIL
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Gastrointestinal Anthrax
Severe gastroenteritis
Incubation: 2-5 days after consumption of undercooked, contaminated meat
Case fatality rate: 25-75%
GI anthrax never documented in U.S.
Suspected cases in 2000
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Inhalation Anthrax
Incubation: 1-7 days
Initial phase
Nonspecific - Mild fever, malaise
Second phase
Severe respiratory distress
Dyspnea, stridor, cyanosis, mediastinal widening, death in 24-36 hours
Case fatality: 60-90% (untreated)
Image courtesy of CDC
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Anthrax in U.S.
Cutaneous anthrax
Early 1900’s: 200 cases annually
Late 1900’s: 6 cases annually
Inhalation anthrax
20th century: 18 cases/16 fatal
2001 Amerithrax
22 cases (11 cutaneous, 11 inhalation); 5 deaths all from inhalation cases
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Anthrax in the U.S.
Outbreaks in soil endemic areas
Alkaline soil
Grass or vegetation damaged by flood-drought sequence
Wet spring that leads to grass kill followed by hot, dry period in summer or fall
“Anthrax weather”
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Diagnosis in Humans
Isolation of Bacillus anthracis
Blood, skin
Respiratory secretions
Serology
ELISA
Nasal swabs
Screening tool
Images courtesy of CDC PHIL
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Treatment
Penicillin
Has been the drug of choice
Some strains resistant to penicillin and doxycycline
Ciprofloxacin
Chosen as treatment of choice in 2001
No strains known to be resistant
Doxycycline may be preferable
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Plague
The Black Death
Image courtesy of CDC PHIL
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Yersinia pestis
Bacteria
Destroyed by
Sunlight & Desiccation
Survival
1 hour in air
Briefly in soil
1 week in soft tissue
Years when frozen
Image courtesy of CDC PHIL
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Brief History of Plague
540-590 AD: Justinian’s pandemic
10,000 deaths per day
Fall of the Roman Empire
1346~1400: Black Death pandemic
Quarantine
1/3 of European population died
Fall of the feudal system
1665: Great Plague of London
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Plague in the United States
1899: Hawaii
From ship rats to sylvatic rodents
Spread throughout the western U.S.
1924/5: Los Angeles
Last person-to-person case
32 pneumonic cases
31 deaths
Currently established in southwest
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Plague as a Disease
Class 1 quarantinable disease (WHO)
CDC Division of Quarantine
Reportable disease
Image courtesy of CDC PHIL
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Epidemiology Natural Reservoirs
Bites of infected flea
Most common vector – Oropsylla montana
Blood meal from bacteremic animal
Regurgitates into human/ animal host
Common reservoirs
Deer mice
Ground squirrels
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Urban Plague
Infected fleas or rodents move to urban area
Commensal (domestic) rodents infected
Roof rat, Norway rat
Rapid die off
Fleas seek new host
Domestic cats or humans
Poverty, filth, homelessness
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Epidemiology - Transmission
Bite of infected flea
Respiratory droplets
Direct contact (6 feet)
Direct skin/mucous membrane less common
BT event – Respiratory droplets or aerosols
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Plague Incidence United States,1970-2012
Endemic to US
Bubonic Most Common
83% Bubonic
2% Primary Pneumonic
15% Septicemic
5 to 15 cases per year
Greatest Concentrations
Arizona, Colorado, New Mexico, Utah
Image courtesy of CDC
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Plague Incidence Worldwide, 1970 - present
All inhabited continents, but Australia
1,500 to 3,000 cases annually
Greatest Concentrations
Asia
South America
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Transmission
Flea bite (78%)
Direct animal contact (20%)
Tissues, body fluids, scratches, bites
Enters through break in skin
Aerosol (2%)
Human cases
April-November (93%)
Increased activity of fleas and hosts
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Clinical Syndromes
Bubonic
Septicemic
Pneumonic
Plague Meningitis
Pharyngeal
Ocular
“Safety Pin” Y. pestis in blood
Image courtesy of CDC PHIL
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Bubonic Plague
80-90% of cases
Incubation: 2-6 days
Clinical signs
Fever, malaise, chills, headache
Bubo: swollen, painful lymph node
vomiting, abdominal pain, nausea, petechiae
Mortality (untreated): 50-60%
Image courtesy of CDC PHIL
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Bubonic Plague
Infected flea bite
Exposure through break in skin
No person-to-person
Untreated progresses to pneumonic
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Septicemic Plague
Systemic spread
Clinical signs
Similar to bubonic, plus
Prostration, circulatory collapse, septic shock, organ failure, hemorrhage, DIC
Necrosis of extremities
Microthrombi blocking capillaries
Mortality (untreated): 100%
Image courtesy of CDC PHIL
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Pneumonic Plague
Inhalation of plague bacteria
Disease progression
Respiratory failure
Shock
Rapid death
Person-to-person transmission
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Pneumonic Plague
Incubation: 1-6 days
Primary - Y. pestis inhaled
Secondary - septicemic form spreads
Clinical signs
Fever, chills, headache, septicemia
Respiratory distress, hemoptysis
Person-to-person possible
Quarantine!
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Treatment
With early treatment – Survival ~100%
Supportive
Antibiotics
Aminoglycosides
Streptomycin, kanamycin
Doxycycline, tetracycline, chloramphenicol
Penicillins and cephalosporins are NOT effective
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Contact Management
Contact – Within 6-7 feet, or 2 meters, of patient in prior 7 days
Evaluate contacts with fever or cough
7 days prophylaxis and symptom monitoring
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Critical Thinking
Consider a case of bubonic plague in the Emergency Room of a New York City hospital. Why would this be a “red flag” event for public health officials?
Tularemia
Rabbit Fever
Deer Fly Fever
Image courtesy of CDC PHIL
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Tularemia is also known as Rabbit Fever and Deer Fly Fever. The etiologic agent of tularemia is one of the most infectious bacterial agents known to man. Less than 10 cells inhaled into the lungs is sufficient to produce a lethal infection. The Russians used it against the attacking German army in the battle for Stalingrad.
The Organism
Francisella tularensis
Gram negative
Intracellular pathogen
Macrophages
Survival-persistence
3-4 months in mud, water, dead animals
>3 years in frozen meat
Easily killed by disinfectants
Inactivated by heat
Image courtesy of CDC PHIL
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History
1907: First described in humans
1911: California ground squirrels
1930-1940’s
Large waterborne outbreaks
Europe and the Soviet Union
1950-1960’s
US biological warfare program
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Transmission
Reservoirs
Many mammals, ticks, and some birds
Rabbits, hares, beavers, muskrats, domestic animals, hard ticks
Ticks and rabbits most important
Rodent-mosquito cycle in Russia, Sweden
Infectious dose
Small for inoculation or inhalation (10-50)
Large for oral (108)
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Transmission
Vector-borne
Ticks
Transovarial transmission
14 species
Dermacentor andersonii
Dermacentor variabilis
Amblyomma americanum
Mosquitoes, flies
Infrequent
Chrysops discalis (Deer fly)
Image courtesy of CDC PHIL
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Transmission
Direct
Contact with tissues of rabbits or other infected mammals
Skinning, necropsy
Handling contaminated skins, paws
Ingestion
Undercooked meat
Contaminated water
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Transmission
Aerosol
Contaminated dust
Hay, grain or soil
Laboratory testing procedures
Bites or scratches (rare)
Not person-to-person
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Epidemiology
Northern hemisphere only
North America, Europe, Russia, China, Japan, Mexico
Nationally notifiable in the United States
About 100 cases per year
Summer – tick/deerfly abundance
Early winter – rabbit hunting season
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Tularemia in the U.S. - 2008
Image courtesy of CDC
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Human Disease
Incubation
3-15 days
Varies with virulence of strain and dose
Initially all forms start with
Sudden fever
Chills
Headache
Myalgia
6 clinical syndromes
Ulceroglandular
Glandular
Oculoglandular
Oropharyngeal
Typhoidal
Pulmonary
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Human Disease
Ulceroglandular
Most common
Ulcer and regional lymphadenopathy
Ulcer 1 week-months
Glandular
Regional lymphadenopathy, no ulcer
Second most common
75-85% of all cases
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Human Disease
Oculoglandular
Conjunctiva infected
By contaminated fingers
Contaminated material splashed into eye
Conjunctivitis
Regional lymphadenopathy
Severe form
Ulceration of conjunctiva
Ocular discharge
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Human Disease
Oropharyngeal
Ingestion
Hand-to-mouth
Consumption of undercooked meat or water
Pharyngitis, diarrhea, abdominal pain, vomiting, GI bleeding, nausea
Pseudo-membrane may develop over tonsils
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Human Disease
Typhoidal
Acute
Septicemia
Without lymphadenopathy or ulcer
Pulmonary
Inhalation of aerosol
Spread through bloodstream
Complications from other forms
Case-fatality (untreated): 30-60%
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Treatment and Prognosis
Antibiotic treatment
Streptomycin (drug of choice)
Prognosis
Untreated
Symptoms last 1-4 weeks to months
<8% mortality overall (all cases)
Case-fatality for typhoidal and pneumonic (30-60%)
Treated
<1% mortality overall (all cases)
Type A has higher case-fatality rate
Long-term immunity
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Smallpox
Variola major
Rotting Face
Image courtesy of CDC PHIL
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The Organism
Double stranded DNA
Orthopoxvirus
Variola, cowpox, vaccinia, monkeypox,
Variola major or minor
Stable outside host
Retains infectivity
Last case, 1977
WHO declared eradicated, 1980
Image courtesy of CDC PHIL
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History of Smallpox
First appeared in Northeastern Africa around 10,000 BC
Skin lesions on mummies
1570-1085 BC
Ramses V
Image courtesy of CDC PHIL
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History of Smallpox
1763, Sir Jeffrey Amherst
Smallpox in blankets for Indians
18th century Europe
400,000 deaths
Case fatality, 20-60%
Scars, blindness
Infants, 80-98% CF
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Variolation
Ground scabs, pus, vesicles used to vaccinate
China, powdered scabs blown into nostrils
Pills from fleas of cows
India, application of scab or pus to scarified skin
Children exposed to mild smallpox
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Edward Jenner
1796, England, May
Inoculated James Phipps with fluid from milkmaid’s pustule
Subsequent variolation of boy produced no reaction
Development of vaccine using cowpox
Protective for smallpox
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Smallpox Vaccine
Vaccine comes from vaca, Latin for cow
Cows used in early 19th century for vaccine production
Image courtesy of USDA
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Smallpox Eradication
1967-1980, $300 million
1967
10 million cases
2 million deaths
1972
Last U.S. vaccination
Image courtesy of CDC PHIL
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Eradication Success
Vaccine available
No animal reservoir
Vaccinees easily identifiable
Vaccinees could “vaccinate” close contacts
Diseased easily identifiable
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Smallpox Transmission
Person-to-person
Inhalation of droplets
Direct contact
With infected body fluids
Scabs
Contaminated objects
Bedding, clothing, bandages
Aerosol
Rarely
Image courtesy of CDC PHIL
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Smallpox Transmission
Spread more easily in cool, dry winter months
Can be transmitted in any climate
No transmission by insects or animals
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Smallpox Transmission
Transmission from a smallpox case
Prodrome phase, less common
Fever, no rash yet
Most contagious with rash onset
First 7-10 days
Contagious until last scab falls off
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Smallpox Clinical Disease
Incubation period 7-17 days
Range 12-14 d
Initial signs
Small red spots in mouth and on tongue
Rash on face
Spreads to arms, legs, hands, feet (centrifugal)
Entire body within 24 hours
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Clinical Forms of Smallpox
Variola major
Most common and severe form
Extensive rash, higher fever
Ordinary (discrete, confluent, semi-confluent)
Modified
Flat
Hemorrhagic (early and late)
Variola minor
Less common, less severe disease
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Treatment
If exposed but not showing signs, vaccinate
Within 3 days, lessens severity
Within 4-7 days, some protection
Quarantine
If showing clinical signs
Isolate patient
Supportive therapy
Cidofovir?
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Smallpox and Animals
Animals do not show signs of disease
No animal reservoir for smallpox
Not zoonotic
Some animals naturally susceptible to pox viruses
Cats and cowpox
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The Smallpox Vaccine
Vaccinia virus
Protects against variola virus
Origins unknown
Live vaccine
Used in US until 1972
Immunity high for 3-5 years
Potentially protective much longer
Images courtesy of CDC PHIL
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Viral Hemorrhagic Fevers
Image courtesy of CDC PHIL
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What is Viral Hemorrhagic Fever?
Severe multisystem syndrome
Damage to overall vascular system
Symptoms often accompanied by hemorrhage
Rarely life threatening in itself
Includes conjunctivitis, petechia, echymosis
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Viral Hemorrhagic Fever
Viruses of four distinct families
Arenaviruses
Filoviruses
Bunyaviruses
Flaviviruses
RNA viruses
Enveloped in lipid coating
Survival dependent on an animal or insect host, for the natural reservoir
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Arenaviridae
Junin virus
Machupo virus
Guanarito virus
Lassa virus
Sabia virus
Image courtesy of CDC PHIL
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Arenaviridae History
First isolated in 1933
1958: Junin virus - Argentina
First to cause hemorrhagic fever
Argentine hemorrhagic fever
1963: Machupo virus – Bolivia
Bolivian hemorrhagic fever
1969: Lassa virus – Nigeria
Lassa fever
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Arenaviridae Transmission
Virus transmission and amplification occurs in rodents
Shed virus through urine, feces, and other excreta
Human infection
Contact with excreta
Contaminated materials
Aerosol transmission
Person-to-person transmission
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Arenaviridae Epidemiology
Africa
Lassa
South America
Junin, Machupo, Guanarito, and Sabia
Contact with rodent excreta
Case fatality: 5 – 35%
Explosive nosicomial outbreaks with Lassa and Machupo
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Arenaviridae in Humans
Incubation period
10–14 days
Fever and malaise
2–4 days
Hemorrhagic stage
Hemorrhage, leukopenia, thrombocytopenia
Neurologic signs
78
Bunyaviridae
Rift Valley Fever virus
Crimean-Congo Hemorrhagic Fever virus
Hantavirus
Image courtesy of CDC PHIL
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Bunyaviridae History
1930: Rift Valley Fever – Egypt
Epizootic in sheep
1940s: CCHF - Crimean peninsula
Hemorrhagic fever in agricultural workers
1951: Hantavirus – Korea
Hemorrhagic fever in UN troops
5 genera with over 350 viruses
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Bunyaviridae Transmission
Arthropod vector
Exception – Hantaviruses
RVF – Aedes mosquito
CCHF – Ixodid tick
Hantavirus – Rodents
Less common
Aerosol
Exposure to infected animal tissue
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Bunyaviridae Epidemiology
RVF - Africa and Arabian Peninsula
1% case fatality rate
CCHF - Africa, Eastern Europe, Asia
30% case fatality rate
Hantavirus - North and South America, Eastern Europe, and Eastern Asia
1-50% case fatality rate
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Bunyaviridae Humans
RVF
Incubation period – 2-5 days
0.5% - Hemorrhagic Fever
CCHF
Incubation period – 3-7 days
Hemorrhagic Fever - 3–6 days following clinical signs
Hantavirus
Incubation period – 7–21 days
HPS and HFRS
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Bunyaviridae Animals
RVF
Abortion – 100%
Mortality rate
>90% in young
5-60% in older animals
CCHF
Unapparent infection in livestock
Hantaviruses
Unapparent infection in rodents
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Filoviridae
Marburg virus
Ebola virus
Image courtesy of CDC PHIL
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Filoviridae History
1967: Marburg virus
European laboratory workers
1976: Ebola virus
Ebola Zaire
Ebola Sudan
1989 and 1992: Ebola Reston
USA and Italy
Imported macaques from Philippines
1994: Ebola Côte d'Ivoire
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Filoviridae Transmission
Reservoir is believed to be bats
Intimate contact
Nosocomial transmission
Reuse of needles and syringes
Exposure to infectious tissues, excretions, and hospital wastes
Aerosol transmission
Primates
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Filoviridae Epidemiology
Marburg – Africa
Case fatality – 23-33%
Ebola - Sudan, Zaire and Côte d'Ivoire – Africa
Case fatality – 53-88%
Ebola – Reston – Philippines
Pattern of disease is UNKOWN
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Filoviridae Humans
Most severe hemorrhagic fever
Incubation period: 4–10 days
Abrupt onset
Fever, chills, malaise, and myalgia
Hemorrhage and DIC
Death around day 7–11
Painful recovery
89
Filoviridae Animals
Hemorrhagic fever
Same clinical course as humans
Ebola Reston
High primate mortality - ~82%
90
Flaviviridae
Dengue virus
Yellow Fever virus
Omsk Hemorrhagic Fever virus
Kyassnur Forest Disease virus
Image courtesy of CDC PHIL
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Flaviviridae History
1648 : Yellow Fever described
17th–20th century
Yellow Fever and Dengue outbreaks
1927: Yellow Fever virus isolated
1943: Dengue virus isolated
1947: Omsk Hemorrhagic Fever virus isolated
1957: Kyasanur Forest virus isolated
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Flaviviridae Transmission
Arthropod vector
Yellow Fever and Dengue viruses
Aedes aegypti
Sylvatic cycle
Urban cycle
Kasanur Forest Virus
Ixodid tick
Omsk Hemorrhagic Fever virus
Muskrat urine, feces, or blood
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Flaviviridae Epidemiology
Yellow Fever Virus – Africa and Americas
Case fatality rate – varies
Dengue Virus – Asia, Africa, Australia, and Americas
Case fatality rate – 1-10%
Kyasanur Forest virus – India
Case fatality rate – 3–5%
Omsk Hemorrhagic Fever virus – Europe
Case fatality rate – 0.5–3%
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Flaviviridae Humans
Yellow Fever
Incubation period – 3–6 days
Short remission
Dengue Hemorrhagic Fever
Incubation period – 2–5 days
Infection with different serotype
Kyasanur Forest Disease
Omsk Hemorrhagic Fever
Lasting sequela
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Flaviviridae Animals
Yellow Fever virus
Non-human primates – varying clinical signs
Dengue virus
Non-human primates – No symptoms
Kyasanur Forest Disease Virus
Livestock – No symptoms
Omsk Hemorrhagic Fever Virus
Rodents – No symptoms
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Disease in Humans
97
Clinical Symptoms
Differ slightly depending on virus
Initial symptoms
Marked fever
Fatigue
Dizziness
Muscle aches
Exhaustion
Image courtesy of CDC PHIL
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Clinical Symptoms
More severe
Bleeding under skin
Petechiae, echymoses, conjunctivitis
Bleeding in internal organs
Bleeding from orifices
Blood loss rarely cause of death
99
Diagnosis
Specimens must be sent to
CDC
U.S. Army Medical Research Institute of Infectious Disease (USAMRIID)
Serology
PCR
IHC
Viral isolation
Electron microscopy
100
Treatment
Supportive treatment, mostly
A number of experimental drugs in clinical trials
Convalescent-phase plasma
Argentine HF, Bolivian HF and Ebola
Strict isolation of affected patients is required
Report to health authorities
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Botulism
Image courtesy of CDC PHIL
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Organism
Clostridium botulinum
Gram positive
Obligate anaerobic bacillus
Spores
Ubiquitous
Resistant to heat, light, drying and radiation
Specific conditions for germination
Anaerobic conditions
Warmth (10-50oC)
Mild alkalinity
Image courtesy of CDC PHIL
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Neurotoxins
Seven different types: A through G
Different types affect different species
All cause flaccid paralysis
Only a few nanograms can cause illness
Binds neuromuscular junctions
Toxin: Destroyed by boiling
Spores: Higher temperatures to be inactivated
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History
1793, Justinius Kerner
“Wurstgift”
“Botulus” = Latin for sausage
1895, Emile von Ermengem
Isolated organism during Belgium outbreak
U.S. outbreaks led to improved industry processing
105
Transmission
Ingestion
Organism
Spores
Neurotoxin
Wound contamination
Inhalation
Person-to-person not documented
106
Epidemiology
In U.S., average 110 cases each year
Approximately 25% food-borne
Approximately 72% infant form
Remainder wound form
Case-fatality rate
5-10%
Infective dose- few nanograms
107
Epidemiology
1977, Largest botulism outbreak
Michigan - 59 people
Poorly preserved jalapeno peppers
Alaska
27% of U.S. foodborne botulism cases
1950-2000
226 cases from 114 outbreaks
108
Human Disease
Three forms
Foodborne
Wound
Infant
All forms fatal and a medical emergency
Incubation period: 12-36 hours
109
Foodborne Botulism
Preformed toxin ingested from contaminated food
Most common from home-canned foods
Asparagus, green beans, beets, corn, baked potatoes, garlic, chile peppers, tomatoes; type A
Improperly fermented fish (Alaska); type E
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Infant Botulism
Most common form in U.S.
Spore ingestion
Germinate then toxin released and colonize large intestine
Infants < 1 year old
94% < 6 months old
Referred to as “floppy baby syndrome”
Spores from varied sources
Honey, food, dust, corn syrup
111
Wound Botulism
Organism enters wound
Develops under anaerobic conditions
From ground-in dirt or gravel
It does not penetrate intact skin
Associated with addicts of black-tar heroin
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Adult Clinical Signs
Nausea, vomiting, diarrhea
Double vision
Difficulty speaking or swallowing
Descending weakness or paralysis
Shoulders to arms to thighs to calves
Symmetrical flaccid paralysis
Respiratory muscle paralysis
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Infant Clinical Signs
Constipation
Lethargy
Poor feeding
Weak cry
Bulbar palsies
Failure to thrive
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Diagnosis
Clinical signs
Toxin in serum, stool, gastric aspirate, suspected food
Culture of stool or gastric aspirate
Takes 5-7 days
Electromyography also diagnostic
Mouse neutralization test
Results in 48 hours
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Treatment
Intensive care immediately
Ventilator for respiratory failure
Botulinum antitoxin
Derived from equine source
CDC distributes
Used on a case-by-case basis
Botulism immune globulin
Infant cases of types A and G
116
Critical Thinking
Discuss the reasons why each of the Category A agents discussed here is a threat to society. Apply the four Category A criteria to each of the agents and diseases.
Implications for Public Health
In the Wake of Amerithrax
Pneumonic Plague
Inhalation Tularemia
Reemergence of Smallpox
The Deadly Ebola
Botulism Delivered
Intentional Release & Estimated Effects of Anthrax
50 kg of spores
Urban area of 5 million
250,000 cases of anthrax
100,000 deaths
100 kg of spores
Upwind of Wash D.C.
130,000 to 3 million deaths
119
South Africa, 1978-1980
Anthrax used by Rhodesian and South African apartheid forces
Thousands of cattle died
10,738 human cases
182 known deaths
Black Tribal lands only
White populations untouched
“Operation Coast”
120
Anthrax Cases, 2001
22 cases
11 cutaneous
11 inhalation
5 deaths (all inhalation)
Index case in Florida
2 postal workers in Maryland
Hospital supply worker in NYC
Elderly farm woman in Connecticut
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Amerithrax 2001
CDC survey of health officials following 9-11-01
7,000 reports regarding anthrax
4,800 phone follow-ups
1,050 led to lab testing
1996-2000
Less than 180 anthrax inquiries
122
Anthrax Cases, 2001
Antimicrobial prophylaxis
Ciprofloxacin
5,342 prescribed
60 day regime
44% compliance
57% suffered side effects
Diarrhea
Abdominal pain
Dizziness
Nausea & Vomiting
123
Plague Bioterrorism Scenario
Most dangerous as an aerosol
Outbreak of pneumonic
Possibly pharyngeal or ocular
Report all suspect cases to public health immediately
124
Human Cases of Plague
New York, 2002
Married couple from New Mexico
Fever, unilateral inguinal adenopathy
Bubonic plague diagnosed
Antibiotic treatment
Deteriorated (septicemic spread)
Sent to ICU
Recovered after 6 weeks
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Importance of Case
NMDPH and CDC investigation
Trapped rodents and fleas around home
Y. pestis isolated
Importance
Plague out of endemic area
Should raise suspicions
Prompt detection important
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Tularemia as a Biological Weapon
History
WHO estimate
50 kg virulent F. tularensis particles aerosolized
City of 5 million people
250,000 people ill
19,000 deaths
CDC estimate
$5.4 billion/100,000 people exposed
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VHF Agents as Biological Weapons
Outbreak of undifferentiated febrile illness 2-21 days following attack
Could include
Rash, hemorrhagic diathesis and shock
Diagnosis could be delayed
Unfamiliarity
Lack of diagnostic tests
Ribavirin treatment may be beneficial
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VHF Agents as Biological Weapons
Most are not stable in dry form
Most have uncertain stability and effectiveness in aerosol form
Arenaviruses have tested effectiveness in aerosol form
Marburg and Ebola have high case fatality rates
Rift Valley is the most stable VHF in liquid or frozen state
VHFs do pose a threat as aerosolized agents
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Botulism Delivered
Aum Shinrikyo cult
Extremely potent and lethal
Easily produced and transported
Signs of deliberate aerosol or foodborne release of toxin
No common source
Large number of acute cases clustered
Uncommon toxin type (C, D, F, G)
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Potential Bioterrorism Threat
Point source aerosol release
Incapacitate or kill 10% of persons within 0.5 km downwind
CDC surveillance system
Prompt detection of botulism related events
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Discussion Questions
What are the four criteria of HHS Category A?
Why would a single case of smallpox be considered an Incident of National Significance, indeed an incident of international significance?
In what ways could plague be used as a biological weapon?
What is the most deadly biological toxin and how could it be practically employed to affect a large number of people?
Chapter 3 Summary
Category A contains the agents of greatest concern
Be certain you know the criteria!
Know why each agent has been placed within the category – apply the criteria
Realize the potential that each agent has to cripple the public health infrastructure within a community
