Microbiology-Anaerobes Flashcards
(39 cards)
Special precautions to take when handling anaerobes
Keep them protected from oxygen when taking them to diagnostics, otherwise they’ll die
Characteristics of anaerobes
Can’t use O2 as final e- acceptor, unable to break down H2O2 because they lack catalase, in the presence of O2 (except bacteroides), superoxide accumulates because they lack superoxide dismutase (except bacteroides)
Toxin-mediated anaerobic infections
Clostridia: C. botulinum (food-borne, infant, infection) is preformed. C. difficile, C. perfringens (gas gangrene and food poisoning) and C. tetani are formed in vivo.
More common source of anaerobic infection? Where else can anaerobic infections come from?
Normal flora, although most infections are mixed. Regions of the body most susceptible have low O2, warm, moisture and substrate (like mucous membranes)Less common sources are exogenous where spores are kicked up in dirt or on contaminated foreign bodies that germinate on infection.

What things create an opportunity for anaerobic infection?
Injury and poor perfusion (like in a dog bite)
Why are anaerobic infections difficult to treat?
They are often mixed infections

Areas in the body with high concentrations of anaerobes
GI tract

Clinical characteristics of anaerobic infections
Aspiration, brain abscesses, foul-smelling pus, anaerobic sinusitis
Anaerobic infections above the waist (like sinusitis)
Typically related to poor dentition and are more susceptible to antibiotics.
Why is sinusitis commonly associated with anaerobic infection after a URI?
URI results in blockage of the sinuses from inflammation, decreases O2 content and allows for anaerobic growth.
Anaerobic infections below the waist
Typically related to GI and GI. Less susceptible to antibiotics. Use metronidazole, clindamycin, augmentin.
Which species of clostridia are shown below?

Left) Tetani Middle) Perfringens Right) Botulinum. Note that they are all gram + rods.

Most common cause of invasive clostridial infections
C. perfringens (myonecrosis and gas gangrene). Often mixed with facultative organisms like E. coli that use up the oxygen in the environment that allow anaerobes to proliferate.
C. perfringens virulence factors
Lecithinase: phospholipase that kills cells and hemolyzes RBCs (hemolytic and blood agar and egg yolk). This leads to muscle necrosis (reddish blue-black tissue) with ABSENT PMNs.

What happens when you incubate C. perfringens with milk?
Stormy fermentation with lots of gas production.

Pathogenesis of C. perfringens infection.
Contaminated wound -> Spores germinate where O2 is low -> Exotoxins (lecithinase) made -> Tissue necrosis and deeper penetration -> Rapid spread across fascial planes
Anaerobe found in the oral flora that are gram-positive non-spore forming rods that grow in chains and in a molar formation.

Actinomyces
Sulfur granules
Macro colonies that resemble grains of sand that are frequently seen in abscesses and sinus tracts. Associated with actinomyces.

What microbe most likely caused this?

Note the suppurative and granulomatous inflammation of the cervico-facial region. This is most often due to poor oral hygiene after invasive dental surgery by actinomyces.
Gram-positive, non-spore former that causes acne and infection of prosthetic devices
Propionibacterium

Most common gram-negative non-spore forming rods
Bacteroides and fusobacterium. Bacteroides are commonly pathogenic after GI surgery because it is very prevalent in the colon and urogenital tract, causes intra-abdominal abscesses (below the waist!)
Virulence factors of bacteroides fragilis
Polysaccharide capsule is anti-phagocytic.
How do you treat bacteroides?
Not with penicillins because most below the waist anaerobes make beta lactamase
Lab diagnosis of bacteroides
Grow in bile and turn bile black when they grow on it




