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Anthrax Sung Chul Hwang, M.D. Dept. of Pulmonary and Critical Care Medicine Ajou University School of Medicine.

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Presentation on theme: "Anthrax Sung Chul Hwang, M.D. Dept. of Pulmonary and Critical Care Medicine Ajou University School of Medicine."— Presentation transcript:

1 Anthrax Sung Chul Hwang, M.D. Dept. of Pulmonary and Critical Care Medicine Ajou University School of Medicine

2 Definition Acute bacterial disease caused by Bacillus anthracis, occurrs most frequently in herbivourous animals Humans become infected when the spores are introduced into the body by direct contact with infected animals or contaminated animal products Very rarely by consumption of contaminated meat products

3 Three Human forms of Anthrax Cutaneous Anthrax Localized skin lesion, central eschar plus surrounding edema Inhalation Anthrax Hemmorrhagic mediastinitis, rapidly progressive, high mortality Gastrointestinal Anthrax Rare and high mortality

4 Etiology Bacillus Anthracis Large : 1.5  x 4-10 Non motile Encapsulated, chain forming, aerobic gram positive rods Forms centrally located, oval spores Oxygen required for sporulation but not for germination Sporulation does not take place in living animals

5 Epidemiology The distribution is world wide Most prevalent among domestivc herbivores (cattle, sheep, horses, goats) Spores  Grazing in contaminated area  Severe anthrax with bacteremia  bleeding from nose, mouth, GI tracts  contamination of soil and water  subsequent sporulation


7 Virulence factors (1) Anthrax toxins  lethal in sterile state Protective Antigen (PA) Encoded by pX01plasmid  184.5 kbp binds plasma membrane and cleaves into two fragments ( PA 20 & PA 63). PA63 provides binding& entry sites for EF and LF Edema Factor (EF) : Calmodulin dependent adenylcyclase, depress PMN Lethal Factor (LF) : cell deaths by inhibiting MAP kinase 1 & 2

8 Virulence Factor (2) Capsular polypeptide : poly D- glutamic acids Encoded by pX02 plasmid  95.3 kbp Avidly phagocytized by PMN cells Antiphagocytic activity

9 Cutaneous Anthrax Introduction of spores through the skin by cuts or abrasions or biting flies Most common (95%) Small red macule  papule, vesicle, pustular stage  formation of an ulcer  blackened eschar with expanding zone of brawny edema Painful reactive lymphadenitis Afebrile or mild constitutional symptoms

10 Inhalation Anthrax About 5 % of cases “ Woolsorter’s Disease” Similar symptoms with severe viral URI In 1 to 3 days increasing fever, dyspnea, stridor, hypoxia, and hypotension Lesding to death within 24 hours Hemorrhagic mediastinitis

11 Gastrointestinal Anthrax Variable symptoms Fever, nausea, vomiting, abdominal pain, rapidly developing ascites Occasionally, massive diarrhea Hemoconcentration and hypotension Grave prognosis

12 Cutaneous Anthrax

13 Diagnosis of Anthrax Gram staining Direct Fluorescent Antibody staining Cultures of cutaneous lesion, blood Bloody CSF containing large number of B. anthracis ELISA test for B. anthracis

14 Treatment of Anthrax Cutaneous : Penicillin G 2 million Unit q 6 hrs until edema subsides  oral penicillin 7 to 10 days Inhalation or GI anthrax : High dose Penicillin  2 million Unit q 2 hrs

15 Prevention Control animal anthrax with live avirulent vaccine( Pasteur spore vaccine- loss of PA plasmid or Sterne spore vaccine- loss of plasmid for capsular poly peptide) Proper disposal of infected animals PA toxoid and PA produced vaccine for humans for the protection Good personal hygienic measures Use of protective clothing and respirators Proper cooking of meat

16 Prognosis Untreated cutaneous anthrax : 10 – 20 % mortality Treated cutaneopus anthrax : very low Inhalation anthrax : 100 % Gastrointestinal anthrax : 50%

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