bacillus anthracis spring 2011

32
Morphology and Physiology 1) Gram positive, encapsulated bacilli (single or paired) 2) Large (1-8μm to 1-1.5μm); sporeforming, nonmotile, facultative anaerobe bacilli. 3) Spore size: 1-2 μm; central or terminal. Germinate readly in an environment at 37° C, rich in amino acids, nucleosids, and glucose

Upload: kayal-vizhi

Post on 24-May-2015

802 views

Category:

Documents


0 download

TRANSCRIPT

Page 1: Bacillus anthracis spring 2011

Morphology and Physiology

• 1) Gram positive, encapsulated bacilli• (single or paired)• 2) Large (1-8μm to 1-1.5μm); sporeforming,• nonmotile, facultative anaerobe bacilli.• 3) Spore size: 1-2 μm; central or terminal.• Germinate readly in an environment at • 37° C, rich in amino acids, nucleosids, • and glucose

Page 2: Bacillus anthracis spring 2011

• 4) Endospores can survive for decades.• 5) Capsule: poly-D-glutamic acid.

Immunogenic.• 6) Colonies: Nonhemolytic “curled-hair”

white to gray.

• B.- Taxonomy:

Genus: Bacillus (Group B. cereus)

Species: B. anthracis, B. cereus,

B. mycoides, B. thuringiensis

Page 3: Bacillus anthracis spring 2011
Page 4: Bacillus anthracis spring 2011
Page 5: Bacillus anthracis spring 2011
Page 6: Bacillus anthracis spring 2011
Page 7: Bacillus anthracis spring 2011
Page 8: Bacillus anthracis spring 2011
Page 9: Bacillus anthracis spring 2011

C.- Virulence Factors:• 1.- Capsule: Antiphagocytic• 2.- Exotoxins: Three components combine

to form two binary toxins.• a) Edema toxin: Protective antigen (bin_

ding to host cell) and edema factor

(calmodulin-dependent adenylate cy-

clase).

Massive edema, inhibit Neutrophils

function.

Page 10: Bacillus anthracis spring 2011

• b) Lethal toxin: Protective antigen and

lethal factor (Zinc metalloprotease)

Stimulates macrophages to release

TNF-α and IL-1 β

• D.- Epidemiology:

1) B. Anthracis primarily infects

herbivorous.

2) Humans are infected through exposure to spores from animal hair and wool.

Page 11: Bacillus anthracis spring 2011

• 3) Reservoir: Animals, carcases, soil.• 4) Routes:• a.- Inoculation of spores through skin:• 95% of cases.• b.- Ingestion: Common in hervivorous• very rare in humans.• c.- Inhalation (Wool-sorters’ disease).• LD50: 2,500 to 55,000 spores.

Page 12: Bacillus anthracis spring 2011

E.- Clinical Manifestations:1.- Pathogenesis:

*Endospores are phagocytosed by macropha_

ges and carried to regional lymph nodes.

*Endospores germinate inside the macropha_

ges and vegetative bacteria are then released.

*Bacillus multiply in the lymphatic system

and cause bacteremia then massive septcemia

2.- Cutaneous anthrax:

*Occupational exposure to spores that are intro_

duced subcutaneously through a cut or abrasion

Page 13: Bacillus anthracis spring 2011

• *After 3 to 5 days: Painless, pruritic macule or papule, then a vesicle undergoes to

central necrosis and drying leaving a black eschar, surrounded by edema and purplish vesicles.

Page 14: Bacillus anthracis spring 2011
Page 15: Bacillus anthracis spring 2011
Page 16: Bacillus anthracis spring 2011
Page 17: Bacillus anthracis spring 2011
Page 18: Bacillus anthracis spring 2011
Page 19: Bacillus anthracis spring 2011
Page 20: Bacillus anthracis spring 2011
Page 21: Bacillus anthracis spring 2011
Page 22: Bacillus anthracis spring 2011
Page 23: Bacillus anthracis spring 2011

• 3.- Gastrointestinal and Oropharyngeal Anthrax:

*Two to five days after the ingestion of endospore-contaminated meat.

• *Bacilli is seen in mucosal and submucosal lymphatic tissue (mesenteric lymphadenitis).

• *Massive edema and mucosal necrosis in the terminal ileum or

cecum.

Page 24: Bacillus anthracis spring 2011

• *Nausea, vomiting, and malaise, progressing to • bloody diarrhea, acute abdomen or sepsis. As_• citis, blood loss, fluid and electrolytes imbalan_• ces, shock.• *Death results from intestinal perforation or • anthrax toxemia.

• 4.- Inhalation Anthrax:• *Two to 43 days after exposure to spores.• *Endospores are engulfed by alveolar

Page 25: Bacillus anthracis spring 2011

• macrophages and transported to the mediastinal

and peribronchial lymph nodes, after multiply,

causes hemorrhagic mediastinitis and then

bacteremia.• *Two days to six weeks after exposure: Fever,

nonproductive cough, myalgia, and malaise.

Chest X-rays show a widened mediastinum and

marked pleural effusions.

After one to three days: dyspnea, strident cough,

chills, and death.

Focal, hemorrhagic necrotizing pneumonitis,

Page 26: Bacillus anthracis spring 2011

• with similar lesions in peribronchial lymph

nodes.• 5.- Anthrax meningitis:

*Bacillus can spread to CNS by hematogenous or

lymphatic routes in all types of anthrax.

*Fatal: 1 to 6 days after the onset of illness.

*Meningeal symptoms and nuchal rigidity plus

fever, fatigue, myalgia, headache, nausea, vo_

miting, and sometimes agitation, seizures and

delirium. Followed by rapid neurologic degene_

ration and death.

Page 27: Bacillus anthracis spring 2011

• *Hemorrhagic meningitis, with extensive edema, inflammatory infiltrates, and numerous bacilli in the leptomeninges.

• CSF is often bloody with many bacilli.

Page 28: Bacillus anthracis spring 2011
Page 29: Bacillus anthracis spring 2011
Page 30: Bacillus anthracis spring 2011

• F.- Laboratory diagnosis:• 1) Exudates, blood, CSF, aspirates

fluids, tissues.• *Direct microscopy exam: Gram

stain• *Culture: Blood agar,nonhemolytic

colonies grow rapidly and are firmly adherent to the agar.

“Medusa heads”, serpentine chains of bacilli.

• *PCR

Page 31: Bacillus anthracis spring 2011
Page 32: Bacillus anthracis spring 2011

• 2) Serologic and Immunologic test:

• *ELISA: Antibodies anti-capsule or exotoxins.

• G.- Treatment and Prophylaxis:

1) Ciprofloxacin or Levofloxacin

2) Doxycycline, or Erythromycin, or Chloramphenicol.

Amoxicillin in pregnant women.

• 3) Corticosteroid therapy for severe edema

• 4) Antitoxin therapy

• *** Vaccine.