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bioterrorism

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Information about bioterrorism
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Published on January 4, 2008

Author: Emma

Source: authorstream.com

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Bioterrorism: Dentistry’s Role In Recognizing And Responding To The Threat:  Bioterrorism: Dentistry’s Role In Recognizing And Responding To The Threat Louis G. DePaola, DDS, MS Bioterrorism:  Bioterrorism The unlawful use, or threatened use, of microorganisms or toxins derived from living organisms to produce death or disease in humans, animals, or plants. The act is intended to create fear and/or intimidate governments or societies in the pursuit of political, religious, or ideological goals. Dissemination may cover large area Difficult to detect release Symptoms occur days or weeks later Some agents capable of secondary transmission Infectious from infected person to uninfected person Use can cause panic 2002 The Johns Hopkins University, Center for Civilian Biodefense Strategies http://www.hopkins-biodefense.org/ Bioterrorism: A Legitimate Threat:  Bioterrorism: A Legitimate Threat Many agents successfully weaponized Anthrax, smallpox, plaque, tularemia, botulism, viral hemorrhagic fever Former Soviet scientists confirm active research was undertaken to engineer more virulent and antibiotic resistant strains State sponsorship of terrorism With the collapse of the Soviet Union, microbe stock & technology has possibly landed in hands of terrorists At least 17 nations are known to have offensive biological weapons programs 2002 The Johns Hopkins University, Center for Civilian Biodefense Strategies http://www.hopkins-biodefense.org/ Delivery Mechanisms:  Delivery Mechanisms Aerosol delivery most probable dissemination method for the majority of agents Agents bioengineered for aerosol delivery Easiest to disperse Highest number of people exposed Most efficient, most contagious route of infection Food / Waterborne less likely Only effective for some agents Deliberate infection of terrorist(s) with transmissible agent in attempt to infect others person to person Agent would have to be highly infectious Probably would not infect large numbers of people 2002 The Johns Hopkins University, Center for Civilian Biodefense Strategies http://www.hopkins-biodefense.org/ Epidemiology of Bioterrorism:  Epidemiology of Bioterrorism Clues suggesting a bioweapon release Large numbers present at once (epidemic) Clusters of severe disease with similar symptoms Previously healthy persons affected High morbidity and mortality Severe pneumonia, dyspnea, septic shock Unusual syndrome or pathogen for region Recent terrorist claims or activity Unexplained epizootic of dead, sick animals 2002 The Johns Hopkins University, Center for Civilian Biodefense Strategies http://www.hopkins-biodefense.org/ Biological Agents Category-A:  Agent Disease Variola Major Bacillus anthracis Yersinia pestis Clostridium botulinum Francisella tularensis Filoviruses and Arenaviruses Biological Agents Category-A Smallpox Anthrax Plague Botulism Tularemia VHF Viral hemorrhagic fever Ebola, Lassa Fever EID 2002,8(2): 225-30 Biological Agents Category-B:  Biological Agents Category-B Agent Coxiella burnetii Brucella spp. Burkholderia mallei Burkholderia pseudomallei Alphaviruses Rickettsia prowazekii Toxins Ricin, Staph. enterotoxin B Chlamydia psittaci Food safety threats Salmonella, spp; E. coli Water safety threats Vibrio cholerae; Cryptosporidium parvum Disease Q fever Brucellosis Glanders Melioidosis Encephalitis Typhus fever Toxic syndromes Psittacosis EID 2002,8(2): 225-30 Indications of Intentional Release of a Biologic Agent Include: :  Indications of Intentional Release of a Biologic Agent Include: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5041a2.htm Anthrax:  Serious bacterial infection caused by endospores of Bacillus anthracis Spores enter body by: Abrasions/cuts on skin Inhalation Ingestion Three forms of the disease: Cutaneous Pulmonary/Inhalational GI/Oropharyngeal Meningitis in about 50% of advanced cases Anthrax Dixon et al; N Engl J Med 1999; 41(11):815-826. Pathogenesis B. anthracis:  Pathogenesis B. anthracis Disease requires entry of spores into body Exact infection rate unknown Varies with: Amount and duration of inoculation Portal of entry Host immunity Inhalation Anthrax Phagocytosed by alveolar macrophages Migrate to mediastinal/hilar lymph nodes Germinate into vegetative bacilli May be delayed up to 60 days Antibiotic exposure may contribute Delayed germination after antibiotic suppression Pathogenesis Inhalation Anthrax:  Pathogenesis Inhalation Anthrax Vegatative B. anthracis produces active toxin Hemorrhagic necrotizing mediastinitis Does NOT cause pneumonia Hallmark of inhalational anthrax Widened mediastinum on CXR Followed by high-grade bacteremia Seeding of multiple organs, including meninges Toxin production Has usually begun by time of early symptoms Stimulates cascade of inflammatory mediators Sepsis Multi-organ failure DIC Death www. Hopkins-biodefense.org Anthrax:  Cutaneous lesion: Painless reddish papule develops on exposed area. Pruritus and burning may be present Mimics a mosquito bite. The initial papule enlarges, becomes edematous and in 1-2 days it progresses to developing a central pustule or blister Known as “malignant pustule” The surrounding tissue becomes more erythematous and a brawny, gelatinous, non-pitting edema develops. Anthrax Bartlett J, et al. Clinical Anthrax: Primer For Physicians, 2001, AETC National Resource Center Anthrax:  Inhalation Anthrax: Incubation period: Usually 1-7 days; Biphasic clinical features: The prodrome is described as: Flu-like with malaise, fever, headache, nonproductive cough, substernal pain, myalgias, nausea, and abdominal pain. In contrast to flu and other common respiratory infections there has been no coryza with inhalation anthrax. Anthrax Bartlett J, et al. Clinical Anthrax: Primer For Physicians, 2001, AETC National Resource Center Anthrax:  Inhalation Anthrax: The second phase of inhalation anthrax is fulminant and often fatal Severe dyspnea and shock; About 50% with advanced disease have meningitis and compromised consciousness. In the 1979 Sverdlovsk epidemic of inhalation anthrax, the average duration of symptoms prior to admission was 4 days, The average survival after hospitalization was 1 day. Anthrax Bartlett J, et al. Clinical Anthrax: Primer For Physicians, 2001, AETC National Resource Center Treatment of Anthrax:  Treatment of Anthrax Immediately treat presumptive cases IV antibiotics Empiric until sensitivities are known cases Prior to confirmation Rapid antibiotics may improve survival Differentiate between cases and exposed Cases: Potentially exposed with any signs/symptoms Exposed: Potentially exposed but asymptomatic Provide Post-Exposure Prophylaxis Intensive supportive care PRN Postexposure Prophylaxis:  Postexposure Prophylaxis Who should receive PEP? Anyone exposed to anthrax! Not for contacts of cases, unless also exposed Antibiotic therapy Treat ASAP Prompt therapy can improve survival Continue for 60 days Potential adverse effects Hypersensitivity Neurological side effects, especially elderly Bone/cartilage disease, tooth staining in children Oral contraceptive failure Development of antibiotic resistance CDC Health Advisory Updated Recommendations for Handling Suspicious Packages or Envelopes :  CDC Health Advisory Updated Recommendations for Handling Suspicious Packages or Envelopes The following are updated CDC interim recommendations: October 25, 2001 Update: Investigation of bioterrorism-related anthrax and interim guidelines for exposure management and antimicrobial therapy. MMWR 2001; 50: 909-919. Smallpox:  Smallpox Incubation period 12-14 days No symptoms, not contagious at this time Sudden flu-like symptoms: Fever, malaise, headache, back pain Within 2-3 days fever decreases and characteristic rash appears Lesions develop in nose and mouth and rapidly ulcerate releasing large amounts of virus into the mouth and throat Highly contagious at this time WHO; 2001; 76(44):337-343 Smallpox:  Characteristic macular rash forms Most prominent of face and extremities Lesions progress from macules to: Papules to Vesicles to Pustules 8-14 days after onset of symptoms pustules form scabs Leave depressed, depigmented scars upon healing Smallpox WHO; 2001; 76(44):337-343 Smallpox Epidemiology:  Smallpox Epidemiology All ages and genders affected Incubation period from infection to onset of prodrome Range 7-17 days; Average 12-14 days Transmission Airborne via aerosol in BT attack Then person-to-person Hospital outbreaks from coughing patients Highly infectious <10 virions sufficient to cause infection Aerosol exposure <15 minutes sufficient Infectious Material Saliva, vesicular fluid, scabs Conjunctival fluid, urine, possibly blood Transmission via fomites: hospital linens, blankets Slide22:  In an outbreak setting of atypical or variant rashes Smallpox must be considered until proven otherwise! Smallpox Vaccine :  Smallpox Vaccine Vaccinia virus Related to cowpox and variola Source – calf lymph Now cell culture methods available Strains Lister used by WHO for eradication campaign New York Board of Health only U.S. strain Newer more attenuated Japanese strain Vaccine administration Bifurcated needle High efficacy, sterilizable, simple, rapid (1500/day) Uses less vaccine: Used for the WHO eradication campaign Jet gun Rapid; High maintenance Photo: National Archives Smallpox Vaccine :  Smallpox Vaccine Duration of efficacy – single dose Probably 5-10 years Some immunity >20 years Lower morbidity & mortality (3 fold) Revaccination leads to >30 years protection Vaccine efficacy Nearly complete protection for responders Effective for all ages except neonates Reduces secondary attack rate 10 fold Supply/Production No current active production New vaccine production scheduled for 2004 7-15 million doses in U.S. as of 1999 >20 years old; Controlled by CDC Smallpox Vaccination:  Smallpox Vaccination Serious complications Occur in 74-250 per million (1/10,000) 3-4 fold higher risk in infants <1 y.o. Highest risk in primary vaccinees Types of reactions: Severe cutaneous Most common; Associated with vaccinia viremia Encephalitis 1 in 300,000 Vaccinia gangrenosum/necrosum Original lesion spreads and does not heal Mortality 100% in untreated, 20-36% treated Highest risk in immunocompromised Treatment Vaccinia immunoglobulin (VIG); thiosemicarbazone Plague Yersinia pestis:  Caused by the bacteria Yersinia pestis Historical cause of “Black Death” Techniques developed to directly aerosolize plague particles leading to pneumonic plague. Highly lethal and potentially contagious form of plague. A modern attack would most probably occur via aerosol dissemination of Y. pestis, and the ensuing outbreak would be almost entirely pneumonic plague. The first sign of a bioterrorist attack with plague would most likely be a sudden outbreak of patients presenting with severe symptoms. The mortality of untreated pneumonic plague approaches 100%. Plague Yersinia pestis JAMA. 1999;281:1735-1745 Bubonic/Pneumonic Plague:  Symptoms: Develop 2-8 days post-exposure Sudden onset of fever, chills, malaise Acutely painful and swollen lymph node (bubo) Large 1-10cm, pain often limits movement Buboes usually found in groin, axilla or cervical area Necrosis of small blood vessels results in gangrene Commonly found on nose, fingers and toes Bloodstream spread of organisms to lungs Severe secondary pneumonia Chest pain, dyspenia, cough and hemoptysis Pneumonic plague 10-15 % of naturally occurring cases Pneumonic plague is highly infectious & often fatal! Bubonic/Pneumonic Plague JAMA 2000, 283(17): 2281-90. Centers for Disease Control and 2002 The Johns Hopkins University, Center for Civilian Biodefense Strategies http://www.hopkins-biodefense.org/ Bubonic Plague:  Bubonic Plague Organism: Y. pestis Highly infectious gram negative, non-motile bacillus Significant human pathogen, cause of “Black Death” Pandemics AD 541, 1356 and 1855 Transmission: Bite(s) from plague-infected fleas Pathogenesis: Bubonic plague Introduced bacteria migrate by cutaneous lymphatics to regional lymph nodes Y. pestis resists phagocytosis Rapidly multiply Destroy integrity of lymph nodes Results in bacteremia, septicemia, endotoxemia Death results from septic shock JAMA 2000, 283(17): 2281-90. 2002 The Johns Hopkins University, Center for Civilian Biodefense Strategies http://www.hopkins-biodefense.org/ Bubonic/Pneumonic Plague:  Symptoms: Develop 2-8 days post-exposure Sudden onset of fever, chills, malaise Acutely painful and swollen lymph node (bubo) Large 1-10cm, pain often limits movement Buboes usually found in groin, axilla or cervical area Necrosis of small blood vessels results in gangrene Commonly found on nose, fingers and toes Bloodstream spread of organisms to lungs causes severe secondary pneumonia Pneumonic plague 10-15 % of cases Severe pneumonia, chest pain, dyspenia, cough and hemoptysis Pneumonic plague is highly infectious & often fatal! Bubonic/Pneumonic Plague JAMA 2000, 283(17): 2281-90. Pneumonic Plague: Bioterrorist Release:  Diagnosis: No available rapid tests, > 24-48 hrs for cultures Diagnosis will require vigilance and high level of suspicion for plague First evidence would be sudden cluster(s) of severe pneumonia and sepsis Treatment: Vaccine discontinued in 1999 Antibiotics: Streptomycin, gentamicin, doxycycline, ciprofloxacin No controlled trials to confirm efficacy Historic treatment- streptomycin Reduces mortality to 5-14% range In short supply in USA Pneumonic Plague: Bioterrorist Release JAMA 2000, 283(17): 2281-90. Tularemia :  Tularemia Caused by infection with Francisella tularensis One of the most infectious pathogenic bacteria Infection with as few as 10 organisms F. tularensis considered to be a dangerous potential biological weapon because of: Extreme infectivity Ease of dissemination Substantial capacity to cause illness and death Previous use as a bioagent Japanese in China during WW2 Eastern front WW1 and WW2 JAMA. 1999;281:1735-1745 Tularemia:  Tularemia Clinical manifestations: Abrupt onset of fever, chills, headache, body aches, coryza, and sore throat Oropharyngeal tulmaremia: Consumption of contaminated food or water Stomatitis, exudative pharyngitis or tonsillitis Pronounced cervical and/or retropharyngeal lymphadenopathy common Tularemia pneumonia: Direct from inhalation of organism Secondary by hematogenous spread Treatment: Streptomycin, gentamicin, doxycycline, ciprofloxacin JAMA 2000, 285(21): 2763-73. Botulism Toxin:  Botulism Toxin A major bioweapons threat because of its extreme potency and lethality The single most poisonous substance known. Easy to produce, transport and misuse The average incubation period is 12-72 hours after ingestion. Patients with botulism typically present with difficulty speaking, seeing and/or swallowing. Prominent neurologic findings include ptsosis, diplopia, blurred vision, dysarthria and dysphagia. Patients typically are afebrile and do not have an altered level of consciousness. Patients may initially present with gastrointestinal distress, nausea, and vomiting preceding neurological symptoms. JAMA. 1999;281:1735-1745 Botulism Clostridium botulinum:  Botulism Clostridium botulinum Symptoms: Acute, afebrile, symmetric, decending paralysis of facial musculature, multiple cranial nerve palsies Onset and severity dependent on amount of toxin absorbed Incubation variable 2 hrs to 8 days after ingestion Neurologic symptoms: Ptosis, diplopia, blurred vision, loss of head control Deep tendon reflexes diminish Death results from airway obstruction; Respiratory and diaphragmatic muscle paralysis Diagnosis: Index of suspicion for botulism; clusters of cases Treatment: Supportive care and administration of passive equine antitoxin JAMA 2001, 285(8): 1059-70. Hemorrhagic Fever:  Hemorrhagic Fever http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5041a2.htm Bleeding manifestations, such as petechiae, ecchymoses, and hemorrhages, occur as the disease progresses. Ebola Chemical Agents:  Chemical Agents Nerve agents Disrupt the transmission of nerve impulses in the body The effects of nerve agents appear almost immediately. In a large group of exposed people, these effects will range from relatively minor effects to very severe effects that may lead to death. Blister agents Cause skin burns and blisters May damage the eyes, airways, lungs & other internal organs Pulmonary agents Agents inhaled Result in varying degrees of pulmonary edema Usually after a symptom-free period that varies in duration with the amount inhaled. Other agents http://www.bt.cdc.gov/Agent/AgentlistChem.asp Bioterrorism Dentistry’s Response :  Bioterrorism Dentistry’s Response Role of Dental Practitioners:  Role of Dental Practitioners Have a high level of suspicion Keep bioterrorist agents in differential diagnosis Recognize typical bioterrorist disease syndromes Some bioagents have: Oral/facial Cervical Head & neck manifestations Be aware of unusual clinical presentation Index cases may be atypical Know how to report suspected cases Brief staff on proper procedures if they encounter unusual letters or packages

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