1) Bacillus anthracis is a gram-positive, spore-forming bacterium that causes anthrax. It forms large encapsulated bacilli that can survive as dormant spores for decades. 2) B. anthracis infects humans through contact with infected animals or inhalation of spores. Clinical manifestations vary depending on route of infection but commonly include lesions, edema, and sepsis. 3) Diagnosis involves microscopy, culture, and PCR to detect the bacteria along with serologic tests to detect antibodies. Treatment involves antibiotics and sometimes antitoxins or corticosteroids. Vaccination can provide prophylaxis.

1. 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

2. • 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

9. 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.

10. • 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.

11. • 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.

12. 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

13. •
• *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.

23. • 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.

24. •
• *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

25. • 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,

26. • 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.

27. •
• *Hemorrhagic meningitis, with extensive
edema, inflammatory infiltrates, and
numerous bacilli in the leptomeninges.
• CSF is often bloody with many bacilli.

30. • 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

32. • 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.