ASB in Blood Cultures (1): Bacillus

Microbiology:

Bacillus anthracis:

Background:

• Infection occurs by tranmission of the spores, which are shed in the terminal stages of infection.
• Infection is spread from a dead or dying host.
• Spores can survive in the environment for long periods of time.
• Spores are never found in tissues but can appear when the organism is shed or grown on artificial media.
• Relatively resistant to chemicals.
• Killed by pressured autoclaving 121 C @ 15mins.

Pathogenesis:

• Inoculation through the skin by handling infected animals/products.
• Cutaneous anthrax: malignant pustule. Coagulation at the centre leads to the purple eschar. This is then surrounded by vesicles containing serous fluid -> extensive oedema & induration.
• Poor prognosis if patients become toxic.
• Wool-sorter's disease: inhalation of dust or wool fibres containing spores
• Rapid multiplication of bronchial innoculum leads to widespread dissemination.. This leads to inflammation, haemorrhage & sepsis.
• Bacterial load & toxin production lead to endotoxic shock.
• many susceptible animals esp. guinea pigs (REM: mouse model).

Virulence determinants:

• D-glutamic acid containing capsule inhibiting opsonophagocytosis
• Triple protein plasmid encoded toxin complex:
  • Protective antigen: binds the complex to receptors on the macrophage surface
  • Oedema Factor & Lethal Factor (released after endocytosis): block adenyl cyclase
  • This complex leads to increased vascular permeability

Diagnosis:

• Clinical appearance of cutaneous leisons.
• Fluid aspirated from the vesicles surrounding the eschar may yield bacilli.
• Gram stain appearance and colonial morphology as above.
• Isolation from the environment can be difficlu due to numerous other species.
• Laboratory tests:
  • non-motility
  • gelatin liquefaction
  • growth in straight chains (enhanced aerobically)
  • inverted fir tree appearance in the gelatin stab
  • toxin production: gene probe etc.

Treatment:

• Penicillin is the treatment of choice as beta-lactam producing strains are rare.
• Ciprofloxacin as prophylaxis or early treatment - as during a biological attack a genetically modified penicillin resistant strain would probably not be used.
• In the later stages supportive treatment of shock is more important than antimicrobial therapy.
• The role of isolation has been questioned as human-to-human transmission is uncommon and appropriate use of antibiotics render patients free of bacilli.
• Highest risk from the dead or dying.
• Vaccination with alum-precipitated toxoid has been used to immunize workers at risk. Rapidly declining antibodies means regular boosting.

Bacillus anthracoides differs from Bacillus anthracis in the folowing:

• Motile cell
• No capsule
• Effective haemolysis
• Not pathogenic to guniea pigs (?)

Bacillus cereus:

Microbiology:

• Large Gm+ bacillus.
• Motile.
• Lacks glutamic acid capsule.
• Saprophytic/environmental pathogen.
• Large grey irregular colonies.

• Large innocula cause death in laboratory animals, but without the haemorrhagic appearance of anthrax.
• McFadyean's -ve.

Pathogenesis:

• Toxin producing, heat resistance spores.
• Found in raw food, cereals & rice.
• Usually causes vomiting within 6 hours of ingestion. The toxin is heat and acid stable and is resistant to proteolytic enzymes, and is preformed.
• When diarrhoea occurs 8-24 hours after ingestion, this enteric picture is due to an enterotoxin formed in the gut.
• Post traumatic ophthalmitis caused by B. cereus requires local aggressive Rx.

Diagnosis:

• High numbers of B. cereus in the absence of other enteric pathogens is diagnostic.
• Characteristic colonial morphology.

Treatment:

• Supportive, both forms are self-limiting.

Other Bacillus spp.

• B. subtilis, B. pumilis & B. licheniformis can cause food-poisoning similar to B. cereus. These do not form toxins, but produce antibacterial peptides, allowing disturbance of bowel flora.
• They may be found in wounds or tissues of immunocompromised or burnt patients.

AMH