13: Anaerobes

Question 1

Define anaerobes.

Answer 1

• Bacteria requiring anaerobic conditions to initiate and sustain growth
• Strict (obligate): unable to grow if > 0.5% O2.
• Moderate: can grow between 2-8% O2.
• Microaerophilic: grow in presence of O2, but better in anaerobic conditions
• Facultative: grow in presence/absence of O2.

Question 2

What are the roles of anaerobes?

Answer 2

• Prevent colonization & infection by pathogens
• Contribute to host physiology (e.g., b. fragilis synthesizes vitK and deconjugates bile acids)

Question 3

Identify the virulence factors of anaerobes.

Answer 3

• Attachment & adhesion: polysaccharide capsules and pili
• Invasion: aerotolerance
• Establishment of infection:
  
  • Polysaccharied capsule resists opsonization/phagocytosis
  • Synergize with aerobes
  • Spore formation (Clostridium)
• Tissue damage: elaboration of enzymes, toxins

Question 4

Identify the anaerobic gram positive bacilli by spore/non-spore formation.

Answer 4

No spore formation:

• Propionibacterium
  
  • P. acnes
• Actinomyces
  
  • A. israelii
• Lactobacillus
• Mobiluncus

Spore formation:

• Clostridium
  
  • C. perfringens
  • C. difficile
  • C. tetani
  • C. botulinum

Question 5

Describe the propionbacterium.

Answer 5

• Produce propionic acid
• P. acnes: acne, on prosthetics

Question 6

Describe actinomyces.

Answer 6

• Cervicofacial actinomycosis: normal mucosal barriers disrupted (dental procedure); endogenous, indolent
• Dx via infected fluid:
  
  • Macroscopic colonies of organisms resembling grains of sand (sulfur granules)
• Tx: surgical debridement, prolonged penicillin

Question 7

Describe lactobacillus.

Answer 7

• GI and GU tract; now in probiotics
• Clinical disease: bacteremia from GU source, bacteremia in immunocompromised host, endocarditis

Question 8

Describe colstridium.

Answer 8

• Pathogenesis: spore formation, rapid growth in O2 deprived, nutrionally-enriched environment, toxin elaboration (histolytic toxins, enterotoxins, neurotoxins)
• C. perfringens:
• C. difficile
• C. botulinum
• C. tetani

Question 9

Describe colstridium perfringes.

Answer 9

• Type A in soil, water contaminated w/ feces; causes human infx
• Type B-E in GI of animals
• Pathogenesis: alpha-toxin (lecithinase lyses cells –> vascular permeability, hemolysis); beta-toxin (necrotizing activity); entertoxin (incr. membrane permeability)
• Sx: gastroenteritis; crepitant cellulitis –> fascitis –> myonecrosis (gas gangrene)
• Tx: surgical debridement, penicillin, hyperbaric O2

Question 10

Describe colstridium difficile.

Answer 10

• Overgrowth via cephalosporins, clindamycin, ampicillin/amoxicillin, fluoroquinolones
• Enterotoxin (toxin A): cytokines, fluid hypersecretion, hemorrhagic necrosis
• Cytotoxin (toxin B): loss of actin-based cytoskeleton
• Colitis: profuse, watery diarrhea, pseudomembranous colitis: leukocytosis, exudates on scope
• Diagnosis: Toxin A/B ELISA or PCR for toxin B gene
• Rx: Metronidazole (PO/IV) or vancomycin (PO); pooled human IVIG; probiotics, fecal microbial transplant

Question 11

Describe colstridium tetani.

Answer 11

• Spores in soils, GI tracts of animals; disease in un-vaccinated/inadequately immunized; disease does not induce immunity
• Spores inoculate wound –> tetanospasmin (heat-labile neurotoxin) –> retrograde axonal transport in CNS –> block release of inhibitory NT (e.g., GABA) (irreversible) –> unregulated excitatory synapse
• Clinical (4 types):
  
  • Generalized
    
    • Trismus (lockjaw), risus sardonicus (spastic grin), opisthotonos (spasm of paraspinal muscles)
    • Sweating, hyperthermia, cardiac arrythmias, labile blood pressures
  • Cephalic (cranial nerves only)
  • Localized (muscles in primary area of injury)
  • Neonatal (infected umbilical stump)
• Tx: debride, metronidazole, tetanus immunoglobulin, vaccination w/ tetanus toxoid

Question 12

Describe colstridium botulinum.

Answer 12

• Commonly isolated in soil, water
• Human disease with botulinum toxin A, B, E, F
• Pathogenesis: block NT at peripheral cholinergic synapse, prevent ACh release –> muscle relaxation
• Recovery depends on regeneration of nerve endings
• Clinical syndromes:
  
  • Foodborne botulism
    
    • Home-canned foods (A, B)
    • Preserved fish (E)
    • Onset of symptoms 1-2 days (blurred vision, dilated pupils, dry mouth, constipation, bilateral descending weakness of peripheral muscles; death due to respiratory failure)
  • Infant botulism
    
    • Consume foods contaminated with botulinum spores (e.g., honey)
    • Neurotoxin produced in vivo
    • Onset of sx 3-10 days
  • Wound botulism
  • Asymptomatic adult carriage
• Ddx: Symmetric cranial nerve palsies, symmetric flaccid paralysis, ID toxin/organism in stool/serum, electromyography
• Tx: Gastric lavage, metronidazole or penicillin, botulinum immunoglobulin (BIG), trivalent equine immunoglobulin (ABE)

Question 13

Identify the anaerobic gram negative bacilli.

Answer 13

• Bacteroides
  
  • B. fragilis
  • B. thetaiotaomicron
• Fusobacterium
• Prevotella
• Porphyromonas

Question 14

Describe bacteroides fragilis.

Answer 14

• 80% of intra-abdominal infections (peritonitis, intrabdominal abscesses), diabetic foot ulcers
• Pathogenesis: polysaccharide capsule (adhesion, abscess formation), superoxide dismutase & catalase, enzyme elaboration, synergistic infx w/ aerobes

Question 15

Describe abscess formation.

Answer 15

1. Inital phase: introduce bacteria, inflammatory exudates (esp. fibrin)
2. Microbial persistence (localization): impair bacterial clearance, phagocytic functin, neutrophil migration/killing
3. Development of mature abscess: central core of necrotic debris, dead cells, bacteria; surrounded by neutrophils and macrophages