Anaerobic Bacteria Flashcards
General characteristics of anaerobic bacteria
Lack SOD
Generally lack catalase
Ferment
Cannot use O2 as terminal e- acceptor
Facultative = enterobacter
Obligate = ABC (Actinomyces, Bacteroides, Clostridium)
Where is anaerobic bacteria predominant within the body?
On ALL mucocutaneous surfaces
Orgal cavity, skin, GI, GU (female)
What “opportunity” does anerobic bacteria require before they cause an infection?
Tissue injury
+
Poor perfusion
Usually polymicrobial b/c other organisms help reduce O2 levels
Endogenous vs Exogenous infections
Greater amount of endogenous infections (trauma displaces anaerobes into places they are not normally found/deeper sites)
Tx for Anaerobic Bacteria
Surgical Debridement
Tissue drainage
Broad spectrum abx (clindamycin, cefazolin, etc.)
Gram (+), spore-forming rod
Obligate anaerobe
Non-motile
Clostridium perfringens
Most common invasive obligate anerobe
C. perfringens
Clinical presentation:
Cellulitis or
Gas gangrene or
Food poisoning
Clostridium
Pathobiology of gas gangrene
Spores in soil, introduced via deep muscle laceration (military wounds, automobile accidents, crude abortions, etc.), grows in anaerobic environment, and releases:
-
Alpha toxin (lecithinase) = muscle cell necrosis
- Type of phospholipase that acts on lecithin
- Degradative enzymes = subcutaneous bubbles (crepitus)
Look for tissue necrosis with NO PMNs
Gram (+)
Beaded Filaments
Not acid fast
Obligate anaerobe
Actinomyces israelii
Clinical presentation:
Abscesses (mouth, lung, GI tract, GU tract)
Draining sinus tracts
Actinomyces israelii
Pathobiology of actinomyces
NO PERSON-PERSON TRANSMISSION
(normal flora of oral cavity, GI tract, female GU tract)
Trauma/surgery disrupts mucosal barrier, local infection and inflammation, yellow sulfur granules develop (filamentous bacteria lined by proteinaceous coat) surrounded by PMNs, forms pus-filled abscess
Slow expansion to contiguous tissue (sinus tracts form, possible hematogenous spread)
Risk factors for actinomyces
Poor oral hygiene
Recent dental surgery (i.e., lumpy jaw after tooth infection)
Tx of actinomyces
Penicillin G
Surgical drainage of abscesses
“Most misdiagnosed disease”
Actinomyces is often confused with neoplasms
Forms long, branching filaments that resemble hyphae or fungi
Males 3x more likely to develop actinomycosis; for women, IUDs are a risk factor
Distiniguishing b/w Nocardia (only A. israelii forms sulfur granules and only Nocardia is acid-fast)
Gram (-)
Strict anaerobe
Bacteroides fragilis
Clinical presentation:
peritonitis
GI or pelvic abscesses (“below the diaphragm”)
B. fragilis
Typically seen after a bout of appendicitis or diverticulitis
Pathobiology of B. fragilis
Normal GI flora, ruptured intestinal mucosa (trauma, surgery, perforation), spills into peritoneum along with GI facultative anaerobes, survives oxygen environment via catalase and SOD, facultative anaerobes eventually deplete all oxygen, organism thrives and becomes numerically dominant
Local inflammation, purulent abscess formation (abscess serves as reservoir for organisms, which may spread causing shock)
Can B. fragilis cause DIC?
(Disseminated Intravascular Coagulation)
No
It lacks typical Gram (-) endotoxin (i.e., LPS)
Only gram (-) without typical endotoxin, similar to how listeria is the only gram (+) with endotoxin
Normally makes vitamin K for host (within GI flora)
Bacteroides species
Anti-phagocytic polysaccharide capsule
B-lactamase producing
Can grow in bile
B. fragilis
Prevotella melaninogenica (previously known as Bacteriodes melaninogenicus)
gram (-) rod anaerobe (along with Fusobacterium nucleatium)
Found in the upper airways and can cause pulmonary abscesses (Tx = penicillin G)
Tx of B. fragilis
Drain abscess
Repair lesions
Abx (metronidazole, clindamycin)
Thrombophlebitis of the jugular vein caused by
gram (-) rod anaerobes
Septic Emboli + Metastatic Infection
Lemierre’s syndrome (specifically caused by Fusobacterium species, which are indigenous to the oral cavity)
Occurs in young patients by progression from pharyngitis or dental infections and can be treated w/ ampicillin-sulbactam
If a patient presents with Lemierre’s syndrome (or was recently infected with Fusobacterium nucleatum) what disease might you be worried about in the future?
Linked to COLON CANCER
Antimicrobial tx of wounds (in the military) has lead to the emergence of what type of infections later on?
Invasive fungal infections
Above waist anaerobic infection
Most likely dental origin (e.g., recent tooth infection)
Gram + : Peptostreptococcus, Proprionobacterium, Actinomyces
Gram - : Porphyromonas, Prevotella
Organisms typically sensitive to Abx
Below waist anaerobic infection
Endogenous origin from GI (and GU for females)
Gram + : Peptostreptococcus, Clostridium species
Gram - : Bacteroides
C. tetani
Produces tetanus toxin (tetanospasmin)
Neurotoxin that cleaves SNARE proteins (specifically synaptobrevin), preventing the release of GABA and glycine, which are inhibitor neurotransmitters
Result = sustained muscle contraction (i.e., tetany)
C. botulinum
Produces botulism exotoxin (heat labile A-B neurotoxin)
Targets SNARE protein (specifically SNAP25), which prevents the release of acetylcholine. Symptoms include paralysis and respiratory compromise.
At risk population: consumption of improperly canned foods, traumatic injury, or babies ingest spores from honey (floppy baby syndrome)
Treatment = antitoxin and supportive therapy
Is there natural immunity to C. tetani or C. botulinum?
No, they are too potent
