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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 • • 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 Modern Bioterrorism Aum Shinrikyo Cult • • • • 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 • • • • • • • Anthrax Botulinum Toxin A Brucellosis Glanders Marburg Virus Plague Q Fever • • • • • • • • Salmonella Smallpox Staph Enterotoxin B Monkey Pox Ricin Tularemia VEE VHFs Biological Agents of Highest Concern Category A • • • • • • • 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 • • • • 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 • • • • • • 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? • • • • • • • • Primary Care Personnel Hospital ER Staff Public Health Professionals Emergency Response Personnel Laboratory Personnel Law Enforcement Public Military First Responders • • • • • 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 • • • • • • 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 • • • • • 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 • • • • • • • 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 • • • • • 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 • 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 • Multiple forms can be seen as the result of a BW attack Anthrax Gastrointestinal • • • • • 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 • • 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 • • • • 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 • • 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) • Laboratory Workers Decontamination and Disinfection Effective sporicidal solutions: • • • 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 • • • 200,000,000 deaths Biblical (I Sam.) - 1320 BC, Philistines Major Pandemics • 541 - Plague of Justinian • 1346 - ‘Black Death’ • 1894 - Modern Pandemic Plague Distribution • 1894 - Began in China • 1898 - Southwest to India • 1898 - South to Vietnam • 1900 - Trans-Pacific to United States Plague Epidemiology Vector: fleas, >80 species • • • • • 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. • • Rattus rattus (Black rat) Ground squirrels, prairie dogs, cats Plague Pathogenesis • • • • 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 • • Incubation 1-8 days (mode 3-5 days) Sudden onset of flu-like syndrome • • Bubo formation - within 24 hours • • (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 • • 2 to 3 day incubation period followed by high fever, muscle aches, chills, headache Cough with bloody sputum within 24 hours • • • • 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 • • • 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: • • • • 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 • • • • 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 • • • 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 • 1763- French & Indian War • • • World War II • • Fort Ticonderoga Lord Jeffrey Amherst Unit 731 experiments in China Cold War • USSR arsenal Why would smallpox Make A Good Biological Weapon? • Infectious via aerosol • Vaccination discontinued • Decreased potency of vaccine stocks • Severe morbidity and mortality • Transmissible • Clinical inexperience • “Brand-name” recognition Clinical Smallpox Prodrome • • • • • • 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 • • Enanthem Exanthem • • • • 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 • Variola Major • 30% fatal in unvaccinateds • 3% fatal in vaccinateds • • • • • 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 • • • • 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 • Normal host • Inadvertent Autoinoculation (skin, eye) • Generalized vaccinia • Erythema multiforme • Encephalitis • • • 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 • • • • • 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) • • • 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 • • • • • • • 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 • • • • • • 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) • • • • 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 • • Descending paralysis Bulbar Palsies • • • • • • • • 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 • • • • • 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) • • • 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 • 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 • • • • Supportive Care: Oxygenation Hydration Most victims will recover No vaccine available No antibiotic is effective