Anthrax Akaki 20161129
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Zoonotic disease caused by Bacillus anthracis Infects primarily herbivores- goats, sheep, cattle, horses and swine Human infections - contact with infected animals or contaminated animal products Human infections rarely via the respiratory or gastrointestinal tracts
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Anthrax Akaki 20161129
- 1. Bacillus anthracis: Introduction, Microbiology and Epidemiology, Treatment, Prevention
- 2. Anthrax • Zoonotic disease caused by Bacillus anthracis • Infects primarily herbivores- goats, sheep, cattle, horses and swine • Human infections - contact with infected animals or contaminated animal products • Human infections rarely via the respiratory or gastrointestinal tracts
- 3. Microbiology • Bacillus anthracis - derives from Greek work for coal (anthrakis) – Disease causes black coal-like skin lesions • B. anthracis - large Gram-positive spore- forming bacillus (1-1.5 μm x 3-10 μm) • Grows readily on sheep blood agar
- 6. Anthrax Epidemiology • Anthrax occurs virtually worldwide • Abundant rainfall after a period of drought may enhance spore density in soil • Resistant spores can survive for extended periods – 40 years in soil – 80 years in a vial – 200 years from bones from an archeological site Friedlander A.M. 2000. Curr. Clin. Topics. Infect. Dis 20:335349
- 9. Epidemiology • Modes of Transmission (human cases) – Contact with infected tissues of dead animals (butchering) leading to cutaneous anthrax – Consumption of contaminated undercooked meat leading to gastrointestional or oropharyngeal anthrax – Contact with contaminated hair, wool or hides which can lead to either inhalational or cutaneous anthrax
- 10. Epidemiology • Modes of Transmission (human cases) – Laboratory exposure – Person to person transmission- • Rarely reported with cutaneous anthrax
- 11. Anthrax Toxins Edema Factor (EF) Protective Antigen (PA) Lethal Factor (LF) Edema Toxin Lethal Toxin MW 89,000 MW 83,000 MW 90,000
- 12. Anthrax Pathogenesis • Infection begins with introduction of spore through the skin or mucosa • Spore germinates into bacillus after ingestion by macrophages at the local site • Bacillus replicates, producing toxins and capsule • Organism can spread to the draining lymph node
- 13. Clinical Syndromes of Anthrax • Clinical presentation varies by route of infection • Clinical syndrome:* – Cutaneous – Gastrointestinal – Oropharyngeal – Inhalation or Pulmonary/Mediastinal • Can obviously see mixtures/combinations of above *Meningitis can be initial presentation, but resulting from one of the described syndromes
- 15. Cutaneous Anthrax • Most common clinical form of anthrax in natural human disease – 95% of human cases • Caused by inoculation of spores (or bacilli?) into compromised skin • Very low number of spores required for transmission
- 16. Cutaneous Anthrax • Incubation period: 5 days (range 1 - 12) • Local symptoms: Painless or pruritic palpule or pustule ⇒ vesicular or ulcerative lesion ⇒ black eschar • Varying degrees of edema, may have satellite vesicles (1 - 3 mm)
- 17. Cutaneous Anthrax • Systemic symptoms: Fever, malaise, headache, regional lymphadenopathy • Lesion: Black eschar develops and over 2 - 3 weeks the eschar separates, leaving a scar • Septicemia rare • Mortality if untreated: up to 20% • Mortality if treated: < 1%
- 18. Cutaneous Anthrax Images from US CDC http://www.bt.cdc.gov/agent/anthrax/anthrax- images/cutaneous.asp
- 19. Cutaneous Anthrax Images from US CDC http://www.bt.cdc.gov/agent/anthrax/anthrax- images/cutaneous.asp
- 22. Cutaneous Anthrax Management • Antibiotics – Single drug usually adequate – may consider multiple if evidence of bacteremia/sepsis – May not alter clinical progression of lesion, but prevents systemic spread • Corticosteroids – controversial – Theoretical benefit in reducing edema – Most experts do not recommend routinely • DO NOT INCISE or DEBRIDE!
- 23. Treatment of Cutaneous AnthraxPrimary Treatment • Adults: Ciprofloxacin 500mg PO BID or Doxycycline 100mg PO BID (7 - 10 days) • Children: Ciprofloxacin 10 - 15mg/kg q 12hrs (<1gm/day) • Pregnant women: Ciprofloxacin 500mg PO BID or Doxy (only serious) • Immunocompromised persons: Same as above • If penicillin sensitive: Amoxicillin 80mg/kg PO TID
- 25. Gastrointestinal Anthrax • Transmitted by consumption of contaminated meat – Probably ingestion of vegetative organisms • Cannot produce disease with spores in animal models – Probably requires large inoculum of organisms • Incubation: 1 - 6 days • Causes hemorrhagic necrotizing enteritis, necrotizing mesenteric lymphadenitis, bacteremia/septicemia • Case fatality rate: 25 - 60%
- 26. Anthrax: Gastrointestinal Small bowel necrosis and necrotizing mesenteric lymphadenitis
- 28. Orophayngeal Anthrax • Rare form of anthrax – Somewhat artificially separated from “lower” gastrointestinal anthrax • Often occurs in clusters associated with ingestion of tainted meat • Ingestion of vegetative organisms implicated – Role of ingestion of spores is debatable
- 29. Orophayngeal Anthrax • Sometimes referred to as “cutaneous anthrax of the oropharynx” – Similar constellation of local necrotic lesion, edema, regional adenitis – More severe systemic symptoms • Relatively high mortality (>25%)
- 30. 0 5 10 15 20 Days Incubation Period 1 to 6 days (usually 2-5 days) Week 1 Week 2 Clinical Timeline: Oropharyngeal AnthraxExposureExposure ~ Fever ~ Severe sore throat ~ Severe pharyngitis ~ Unilateral neck edema ~ Dysphagia ~ Lesion(s) in the posterior oropharynx (often the tonsils) ~ Central necrosis and ulceration of the lesions ~ Tan or grey pseudomembrane covers the ulcer ~ Possible airway compromise
- 32. Inhalational Anthrax • Transmitted by inhalation of spore form • Incubation period 1-6 days (can be ≥ 43 days?) • Hemorrhagic meningitis seen in up to 50% of cases • GI hemorrhage in up to 80% • Mortality >85% historically
- 34. Gram stain of blood smear in macaque with inhalational anthrax
- 35. Gram stain of cerebrospinal fluid showing B. anthracis. Emerging Infectious Diseases vol 7(6): 2001
- 36. B. anthracis from nasal swab. 24 hrs growth on sheep blood agar. Courtesy of G. Martin, MD, R. Paolucci.
- 37. Diagnosis of Anthrax • Microbiologic confirmation – Colony morphology – γ- phage lysis – DFA for cell wall and/or capsule – Biochemical testing • Other laboratory methods – PCR – usually for pX01 and/or pX02 – Serologic • ELISA (or other method) for antigen - not widely used in US • Antibody testing – only for retrospective dx and epi
- 38. Anthrax Prevention – Infection Control • Standard universal precautions adequate for infection control – Handwashing – Gloves – Eye protection for expected splatter • Respiratory/droplet precautions not necessary
- 39. Anthrax Vaccine - AVA • Given to veterinarians and laboratory workers other persons working with animal hides/products to protect against naturally occurring disease • Given to hundreds of thousands of U.S. military personnel since 1998 to protect against the use of anthrax as a bio-weapon
Notas del editor
- Slide shows a cartoon of anthrax environment cycle in ruminants. Background information: Ruminants: Sudden death, bleeding from orifices, subcutaneous hemorrhage, without prior symptoms or following a brief period of fever and disorientation should lead to suspicion of anthrax. At death in most susceptible species (the pig being a notable exception), the blood contains 10e7 to 10e8 bacilli per ml provided the animal has not been treated (numbers may also be lower in immunized animals which succumb to the disease). For reasons unknown, numbers of B. anthracis at death are very low in pigs (hundreds per milliliter or less). The worst case natural contamination in the environment is found at the carcass sites of animals that have died of anthrax. In a study in Namibia of 106 such sites, the highest contamination level found was just over 1 million anthrax spores per gram of soil, but 79% had less than 1000 per gram and 25% less than 10 per gram (Lindeque and Turnbull, 1994). Levels in other types of inadvertently contaminated environments (soils at tannery sites, horsehair plaster, etc.) rarely exceed a few units or tens of spores per gram (Turnbull, 1996). Natural environmental exposure to infectious doses in the normal course of human life and endeavor is, therefore, a fairly unlikely event.
- Slide shows compontents of the 2 anthrax toxins: Full virulence requires: 1. Antiphagocytic capsule - plasmid coded 2. 3 toxin components - plasmid coded a. Protective antigen. Forms heptamers on cell surface, facilitating entry of edema factor and lethal factor into cells b. Lethal factor. Zinc metolloprotease (like botulinum and tetanus toxins). Causes release of TNF-alpha, IL-1beta. Serves as a mitogen activated protein kinase kinase, disrupting phagocytic cytokine signaling pathways. This may not be the toxin’s only effect on cells, however. c. Edema factor…eukaryotic calmodulin-dependent adenylate cyclase, homologous to Pertussis toxin. Increases cAMP in many cells. Impairs neutrophil function and impairs water homeostasis, leading to edema.
- When the spores are ingested, they can germinate in the intestines and form hemorrhagic lesions in the gastrointestinal tract or the lymphoid tissue. Here is a lesion in the GI tract caused by anthrax.
- Another form of anthrax that occurs after ingestion of contaminated meat, although much less frequently, is orophyarngeal anthrax. After an incubation period of 1 to 6 days, the patient experiences fever and symptoms that reflect the location of the infection – severe sore throat and pharyngitis, edema of the neck that is often unilateral, dysphagia and lesions that can be seen in the posterior oropharynx and are often on the tonsils. Without treatment, these symptoms progressively worsen and the lesions begin to necrose and ulcerate. A tan or grey pseudomembrane can cover the ulcer, as seen in this picture on the right. Edema may become so severe that the airway can be compromised.
- Self explanatory slide.
- Widened mediastinum
- From Literature - Figure 2 from: Emerging Infectious Diseases vol 7(6): gram stain of CSF showing B. anthracis: Case #1 (bioterrorism cases2001)
- Slide shows close up of anthrax colonies on SBA. Anthrax colonies behave as “beaten egg white” when lifted from the agar…likely due to adhesion from long, hair like chains of bacilli which form in vitro (not in vivo) Supporting Data: Colony characteristics of B. anthracis a. After incubation of SBA plates for 15-24 h at 35-37°C, well isolated colonies of B. anthracis are 2-5 mm in diameter. The flat or slightly convex colonies are irregularly round, with edges that are slightly undulate (irregular, wavy border), and have a ground-glass appearance. There may be often comma-shaped projections from the colony edge, producing the &quot;Medusa-head&quot; colony. b. B. anthracis colonies on SBA usually have a tenacious consistency. When teased with a loop, the growth will stand up like beaten egg white; refer to Fig. A5. In contrast to colonies of B. cereus and B. thuringiensis, colonies of B. anthracis are not â-hemolytic; refer to Fig. A6. However, weak hemolysis may be observed under areas of confluent growth in aging cultures and should not be confused with â-hemolysis. c. When examining primary growth media, it is important to compare the extent of growth on SBA plates with that on MAC. B. anthracis grows well on SBA but does not grow on MAC. d. B. anthracis grows rapidly; heavily inoculated areas may show growth within 6-8 h and individual colonies may be detected within 12-15 h. This trait can be used to isolate B. anthracis from mixed cultures containing slower-growing organisms.