Anaerobes (1/17) Flashcards
What are anaerobes?
strict, moderate, microaerophilic, facultative
Bacteria that require anaerobic conditions to grow
Strict = unable to grow in O2
moderate = can grow between 2-8% O2
Microaerophillic = grows in presence of O2 but better in anaerobic conditions
Facultative = grows both in presence and absence of O2
What are medically important anaerobes & how are they classified?
• Gram positive cocci
– Peptostreptococcus
• Gram negative cocci
– Veillonella
• Gram positive bacilli
– Clostridium perfringens, tetani, botulinum, difficile (form spores)
– Propionibacterium (P. acnes)
– Actinomyces (A. israelii)
– Lactobacillus
– Mobiluncus
• Gram negative bacilli
– Bacteroides fragilis, thetaiotaomicron
– Fusobacterium
– Prevotella
– Porphyromonas
Where can endogenous infections of anaerobes exist?
– Indigenous microflora
• Skin: Propionibacterium, Peptostreptococcus
• Upper respiratory: Propionibacterium
• Mouth: Fusobacterium, Actinomyces
• Intestines: Clostridium, Bacteroides, Fusobacterium
• Vagina: Lactobacillus
Note that they are also part of the normal flora of skin, moth, intestinal, and GU tracts.
– Flora can be profoundly modified to favor anaerobes
• Medications: antibiotics, antacids, bowel motility agents
• Surgery (blind loops)
• Cancers
What is the role of anaerobes in humans?
(1) Prevent colonization & infection by
pathogens
• Bacterial interference through elaboration of toxic
metabolites, low pH, depletion of nutrients
• Interference with adhesion
(2) Contributes to host physiology
• Bacteroides fragilis synthesizes vitamin K and
deconjugates bile acids
How do anaerobic infections form?
The source of infecting micro-organism is
the endogenous flora of host
Alterations of host’s tissues provide
suitable conditions for development of
opportunist anaerobic infections
Anaerobic infections are generally
polymicrobial
Abscess formation
Exotoxin formation
What are important virulence factors in anaerobic infection development?
Polysaccharide capsules and pili aid in attachment/adhesion
Aerotolerance aids in capacity to invade
Polysaccharide capsule resists opsonization and phagocytosis
They can synergize with aerobes or form spores
They damage tissue by making enzymes/toxins
What does P. acnes do? Where does it colonize?
Produces propionic acid from fermentation
Colonizes skin, conjuctiva, external ear, oropharynx, female GU tract
P. acnes causes acne (resides in sebaceous follicles, releases low molecular weight peptide, stimulates inflammation) and can cause opportunistic infeciton on prosthetic devices
What does Actinomyces do?
What disease does it cause?
It’s a strict anaerobe that colonizes the upper resp tract, GI, and female GU tract
Causes actinomycosis: an endogenous disease (no person to person spread)
Low virulence– developments when normal mucosal barriers are disrupted i.e. during dental procedure, poor oral hygeine. Can form chronic granulomatous lesions that become suppurative and form sinus tracts
Diagnose by examining infected fluid
Treat with surgical debridement & prolonged penicillin
Lactobacillus– what is it? What disease does it cause?
Strict anaerobe, colonize Gi and GU tract
Clinical disease results from transient bacteremia from GU source –> endocarditis
What is Colstridium?
Present in normal flora in GI tract
Forms spores –> heat resistant, can survive long time
Rapid growth in O2 deprived, nutritionally rich environ.
Toxin elaboration
Clostridium perfringens
Where is its reservoir?
What is the pathogenesis? Which strain is responsible for pathogenesis?
What is the clinical manifestation?
Lives in GI tract
Type A = responsible for most human infections & comes from soil/water contaminated with feces
Alpha toxin (lyses erythrocytes, platelets, and ET cells –> increased vascular permeability), beta toxin (necrotizing activity), and enterotoxin (increases membrane permeability) –> pathogenesis
Leads to self-limited gastroenteritis, soft tissue infections (cellulitis, fascities, myonecrosis)
What is Clostridium difficile?
What’s the pathogenesis?
It colonizes GI tract in 5% of healthy individuals
Antibiotic exposure can lead to overgrowth of C. difficile
Can also come from spores in hospital rooms of infected patients
Pathogenesis comes from an enterotoxin (toxin A) –> hemorrhagic necrosis
Cytotoxin (toxin B) –> polymerization of actin with loss of cellulary cytoskeleton
What’s the clinical manifestation of C. diff & how do you diagnose/treat it?
You can get no symptoms, antibiotic-associated diarrhea, or pseudomembranous colitis
Diagnose by isolating the toxin & culturing
Treat by discontinuing antiboitics, giving metronidazole/oral vancomycin, pooled human IV Ig, probiotics
Relapse in 20-30% bc spores are resistant
What’s Clostridium tetani?
Pathogenesis?
Spores found in soil, GI tract
Disease in unvaccinated individuals & disease doesn’t induce immunity
Spore –> wound –> tetanospasmin (heat-labile neurotoxin, retrograde axonal transport to CNS, doesn’t allow you to control your synapes –> muscle spasms; irreversible binding)
What is the clinical manifestation of tetanus?
4 types: generalized (trismus= lock jaw,risus sardonicus = facial spasm, opisthotonos = rigid body, arched back) + autonomic involvement, , cephalic (cranial nerves only), localized (near injury site), neonatal (infected umbilical stump– generalized)
Treat with debridement of wound, metronidazole, tetanuse Ig, vaccination
