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Emerging Infections and Bioterrorism Lecture

Emerging Infections and Bioterrorism Lecture

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  • 1. Emerging Infections and Bioterrorism
    Jeffrey Gehring, MD
    Department of Emergency Medicine
    February 12, 2009
  • 2. Goals and Objectives
    Introduction of emerging and re-emerging infections
    Introduction to potential agents of bioterrorism
  • 3. Emerging and Re-Emerging Infectious Diseases
    Fall into one of three categories
    1. Diseases that have not previously affected humans (SARS)
    2. Diseases that occurred previously, but only affected a small number of people (Ebola)
    3. Diseases that have occurred previously, but have only recently been determined to be caused by distinct infectious agents (Lyme disease)
    Slaven, Stone, and Lopez. Infectious Diseases Emergency Department Diagnosis and Management. McGraw-Hill Companies, Inc., 2007
  • 4.
  • 5. Severe Acute Respiratory Syndrome (SARS)
    Previously unknown disease entity
    Causative virus is a coronavirus: SARS coronavirus (SARS-CoV)
    Coronaviridae is second most common cause of the common cold
    First emerging infection of the 21st century
  • 6. SARS
    “Near” Pandemic between November 2002 and July 2003
    8,096 known infected cases with 774 deaths
    9.6% fatality rate (as compared to annual influenza fatality rate of 0.6%)
    Originated in Guandong province of China
    Spread to 37 countries around the world
    Epidemic controlled by July 5, 2003
  • 7. SARS
    Spread by respiratory droplets
    2-7 day asymptomatic incubation period
    Incubation followed by 3-7 days of fever, malaise myalgia, headache, and anorexia (much like influenza)
    Dry cough, SOB, progressive hypoxia and respiratory failure
    Patients most contagious late in the illness course which accounts for high incidence of healthcare workers infected
  • 8. SARS
    History and physical exam suggestive of influenza or other respiratory tract infections (Non-specificity makes diagnosis difficult; reliance on trends)
    Contact with someone diagnosed with SARS within 10 days
    Travel to regions affected with SARS
    CXR abnormal in 60% of cases initially.
    CXR, when abnormal, reveals patchy interstitial infiltrates
    Lower lung fields affected preferentially as disease progresses
  • 9. SARS
    Laboratory Testing
    None available during acute illness
    ELISA able to detect antibodies 21 days after illness
    Largely supportive
    Isolation in negative pressure rooms
    Complete barrier precautions
    Anecdotal reports of effectiveness of ribavirin and steroids, but some research shows detrimental effects
    Some feel most serious damage is caused by overreaction of the immune system
    Chinese researchers have developed a vaccine that has been tested on 36 individuals with 24 showing immunity
  • 10. West Nile Virus
  • 11. West Nile Virus
    First discovered in Uganda’s West Nile district in 1937
    First outbreak in the United States started in New York in August, 1999
    Belongs to the Flaviviridae family of viruses that also includes dengue fever virus
    Mainly infects birds which are the reservoir
    Disease spread to humans by mosquitoes (Primarily the Culex species)
    In 2007 there were 3,630 cases with 124 deaths (Less than 4% fatality which is probably an overestimate because most cases are not severe)
    Elderly and patients with history of organ transplantation are most at risk
  • 12. West Nile Virus
    Three different effects on humans
    Asymptomatic infection
    West Nile Fever (mild febrile syndrome)
    West Nile meningitis or encephalitis
    Febrile stage
    has incubation of 2-8 days followed by headache, fever/chills, and other “flu” like symptoms.
    Resolution of symptoms in 7-10 days
    West Nile Meningitis/Encephalitis
    Signs and symptoms of meningitis or encephalitis
    May present as flaccid paralysis with progressive limb weakness over 48hrs
  • 13. West Nile Virus
    CSF analysis
    WNV – specific IgM antibodies detected with enzyme-immunoasay
    Serum tests more useful if acute and convalescent samples taken
    No vaccine available
    Avoidance of mosquito bites
  • 14. Influenza
  • 15. Influenza
    “It killed more people in twenty-four weeks than AIDS has killed in twenty-four years, more in a year than the Black Death killed in a century.” John M. Barry. The Great Influenza. Penguin Books, Ltd. 2005
    Approximately a third of the population was infected in the 1918-1919 pandemic with estimated deaths between 50 and 100 million people
    Fatality rate was greater than 2.5%
  • 16. Influenza
    Caused by an RNA virus in the family Orthomyxoviridae
    Two types: Influenza A and Influenza B
    Influenza A subdivided based on two surface antigens
    Hemagglutinin (H)
    Neuraminidase (N)
    The 1918 pandemic was caused by H1N1, and all subsequent pandemics are descendents of the H1N1 except for human infection caused by avian viruses such as H5N1
    Reemerges each year due to anigenicdrift which is caused by point mutations during replication, whereas antigenic shift is a major change in the virus leading to novel hemagglutinin or neuraminidase proteins.
  • 17. Avian Influenza
    Wild birds are the host of influenza A
    January 2003: influenza A (H5N1) reported in Asian poultry
    Greater than one million birds died or were killed due to the disease
    Humans infected by this highly virulent strain, but humans not highly contagious at this time
    Fear is of coinfectionwith an avian strain and a highly contagious human strain which could lead to genetic realignment
  • 18. Avian Influenza
    Symptoms show spectrum of typical influenza infection to acute respiratory distress
    CXR nonspecific
    Suspect in any person with contact with poultry or people in an affected region and a temperature greater than 38° C with cough, sore throat, or SOB
    Nasopharyngeal swab for influenza A
    Virus isolation only biosafety level 3+ facility
  • 19. Avian Influenza
    Supportive measures
    Two classes of antivirals
    M2 inhibitors (amantadine and rimandadine) H3N2 has shown 91% resistance in 2005. Always ineffective against influenza B
    Neuraminidase inhibitors: Oseltamivir (Tamiflu) and zanamivir (Relenza) have been shown to be beneficial with no known resistance
  • 20. Bioterrorism
    Characteristics of bioterrorism weapons
    Ease of dissemination
    Ability to cause panic and social disruption
  • 21. Anthrax
  • 22. Anthrax
    First disease with a definite microbial origin established by Robert Koch in 1876
    First disease with a vaccine created by Louis Pasteur in 1881
    Investigated as a biological weapon by 5 countries
    Former Soviet Union is known to have created weaponized anthrax with antibiotic resistant strains
    Used as biological weapon in October of 2001 when 22 cases of clinical anthrax were caused by contaminated mail
  • 23. Anthrax
    Bacillus anthracis is an aerobic, gram-positive, non-motile spore former
    Zoonosis which occurs in mammas such as sheep, goats, cattle, and horses
    Infection is caused by endospores which enter the body through the skin/mucosa or through inhalation
    Spores are infectious, but bacilli are not—so no known cases of human to human transmission
  • 24. Anthrax
    Three routes of infection
    95% of naturally occurring cases are cutaneous
    Three factors are the leading causes of virulence
    Edema toxin: calmodulin-dependent adenylatecyclase that leads to cell edema
    Lethal toxin: zinc metalloprotease which inhibits cell and cytokine response and causes the release of TNF and IL-1B which leads to toxicity and sudden death
    Capsule Production: inhibits phagocytosis of vegetative forms
  • 25. Anthrax
    Cutaneous Anthrax
    Incubation period of 3-5 days
    Bacterial proliferation and toxin release cause local edema and necrosis
    Begins a pruriticmacule or papule which ruptures causing a necrotic ulcer
    Antibiotics don’t help with cutaneous manifestation, but help prevent systemic spread
    20% mortality if left untreated, but death rare if treated
  • 26. Anthrax
    Gastrointestinal Anthrax
    Caused by ingestion of undercooked contaminated meat
    Two forms: abdominal or oropharyngeal
    Abdominal type: N/V, bloody diarrhea, abdominal pain, hematemesis, shock and death
    Oropharyngeal: edema, lymphadenopathy, sepsis, death
  • 27. Anthrax
    Inhalation Anthrax
    “Wool sorters’ Disease”
    Rapid onset of symptoms in 2-3 days post-exposure
    Spores ingested by macrophages and carried to mediastinallymphnodes leading to hemorrhagic mediastinitis
    Not considered true pneumonia
    Biphasic clinical syndrome
    Initial phase is a non-specific flu-like illness
    Second phase represented by severe sepsis, MODS and death usually within 3 days
  • 28. Anthrax
    Clinical suspicion
    Widened mediastinum on CXR (hemorrhagic mediastinitis), pleurual effusions
    Gram stain of peripheral blood (Gram positive bacilli) or of vesicular fluid
    CSF Gram stain and culture (Up to 50% of patients with inhalation anthrax will have meningitis)
  • 29. Anthrax
    Early initiation of antibiotics: ciprofloxacin, clindamycin, rifampin, doxycycline
    Triple antibiotic coverage recommended
    Barrier precautions
    No documented cases of person-person spread
    No need for exposure prophylaxis for ED staff
    Vaccine is available
  • 30. Smallpox
  • 31. Smallpox
    Estimated to have caused 300 million deaths in the 20th century
    Up to 80% mortality in non-immune populations
    Last recorded natural case in Somalia in 1977. Routine vaccination in the US stopped in 1972
    Two known sources of the virus
    CDC in Atlanta
    Russian State Research Center of Virology and Biotechnology in Koltsovo, Russian Federation
    Humans are only known host with no known animal reservoir
    Mortality estimates are 20-40% in unvaccinated individuals and 1-3% in vaccinated individuals
  • 32. Smallpox
    DNA virus of the orthopox virus genus
    Variola major
    Variola minor (milder form less associated with morbidity and mortality)
    Transmission is person to person by respiratory droplets and through infectious fomites
    People are infectious from onset of rash until resolution of all lesions
  • 33. Smallpox
    3-4 days of asymptomatic to nonspecific symptomatic viremia follows initial exposure
    Second cycle of viremia occurs at 7-17 days post-exposure, and is marked by signs and symptoms of toxemia
    Rash follows second phase by 48hrs
    Death occurs 1-2 weeks after onset of illness
    Classically described as acute fever followed by rash in 1-2 days
  • 34. Smallpox
    First noted on oral mucosa, pharynx, followed by head, face, proximal extremities, distal extremities and trunk
    Involvement of palms and soles
    Initially maculopapular and then progresses to vessicles in 1-2 days, and become umbilicated in another 1-2 days
    Pustules scab over in an additional 2 days
    Scabs slough off in 8-17 days
    All lesions in one area of the body are in the same stage of development which distinguishes it from varicella
  • 35. Smallpox
    Initial diagnosis is clinical
    High clinical suspicion
    Confirmation by electron microscopy
    Culture and PCR (only available at CDC)
    Cidofivir shows in vitro activity
    Negative pressure isolation
    Patient contact only by vaccinated individuals
    Clothing is potential fomite carrier
    Vaccine available
  • 36. Plague
  • 37. Plague
    “Black Death”
    Three pandemics with a deaths exceeding 100 million people
    First used as a biologic weapon in the Crimean War in 1346
    Used as a biologic weapon by Japan in World War II by aerial dropping of infected fleas on Chinese villages
    Former Soviet Union created large quantities of genetically engineered Y. pestis that could be delivered by aerial munitions
    Disease is endemic to 17 western states
  • 38. Plague
    Yersiniapestis: gram negative, non-motile, coccobacillus
    “Safety Pin” appearance
    Virulence due to multiple plasmid encoded proteins
    Natural reservoir is rats, prairie dogs, chipmunks, and multiple other animals
    Transmission is by bite of infected flea
    Three principle forms
    Bubonic (84% of cases with 14% mortality)
    Septicemic (13% of cases with 22% mortality)
    Primary Pneumonic (2% of cases with 57% mortality)
    Bacteria transported to regional lymph nodes and created classic “bubo”
  • 39. Plague
    Untreated infection will lead to systemic involvement with resultant septicemia
    Systemic spread to the lungs results in “secondary” pneumonic plague
    About 13% of people present with systemic infection without adenopathy (primary septicemic plague) with about twice the mortality
    Primary pneumonic plague results from direct inhalation of infected particles which is more virulent than secondary pneumonic plague—this is the form feared in a bioterrorism attack
  • 40. Plague
    Aerosolized plague would result in a rapidly progressive primary pneumonic plague or septicemic picture
    Bubonic plague presents after 1-8 days incubation period (Could present if infected fleas used as bioterror threat)
    Initial symptoms non-specific
    Follow rapidly by painful adenopathy at location near inoculation site
    Bubos differentiated by other diseases by rapid onset, extremely painful, absence of lymphangitis, and toxicity
    Septicemia in 2-6 days if left untreated
  • 41. Plague
    Common complication is DIC which leads to acral ischemia and gangrene—”Black Death”
    Primary pneumonic plague has incubation of 1-6 days, and is the most deadly form of the disease
    Clinical suspicion
    Rapidly progressive adenitis or severe pneumonia and sepsis in normally healthy individuals
    Blood cultures, cultures of bubos
    CBC often markedly elevated especially in children (50,000-100,000)
    Nonspecific CXR
  • 42. Plague
    Streptomycin, tetracycline, doxycycline (FDA approved)
    Gentamicin appears equally effective in animal models
    Chloramphenicol effective, especially in cases of meningitis
    Respiratory precautions
    Vaccine available
  • 43. On The Bright Side