Anaerobic Bacteria WITH Sketchy, Schaeters and Lecture Material Flashcards Preview

Final Multisystems Microbiology > Anaerobic Bacteria WITH Sketchy, Schaeters and Lecture Material > Flashcards

Flashcards in Anaerobic Bacteria WITH Sketchy, Schaeters and Lecture Material Deck (45)
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Why do anaerobes hate O2 so much?

- Can’t use O2 as final electron acceptor
- Can’t break down H2O2 because they lack Catalase (except Bacteroides)
- In presence of O2, toxic superoxide anions accumulate.
- Strict anaerobes also lack the enzyme superoxide dismutase (except Bacteroides)


What general type of bacteria is most frequent in the gut?

Anaerobes - Predominant flora type in mucocutaneous surfaces (outnumber aerobic 1000:1 in gut)


Tell me about the structure for Clostridium Botulinum

Structure: Gm (+), spore forming, obligate anaerobe


How do we transmit Clostridium Botulinum?

Transmission: Improper canning of food, make a bunch of preformed toxin in the can. Can’t cross BBB but toxin gets absorbed in gut and travels in peripheral motor nerves.

Babies: Get spores from eating honey, their environment is perfect for growing anaerobic bacteria since they don’t have other gut flora competing (babies don’t eat canned food)


What virulence factor is used by Clostridium Botulinum?

Virulence Factor: SNARE protease: Inhibits fusion of the vesicle with the presynaptic nerve terminal so ACh can’t leave the presynaptic neuron → paralysis, since ACh is needed for excitement


What symptoms do we see with clostridium botulinum?

Sx: Flaccid descending paralysis (absence of muscle contraction). Begins with eye problems like ptosis and diplopia. Same in baby (Flaccid Baby Syndrome).


Structure of Clostridium Difficile

Structure: G(+) bacilli, obligate anaerobe, spore forming


Discuss the presentation and virulence toxins we see with clostridium difficile

Pathophys: nosocomial diarrhea from abx use

virulence factors:
exotoxin A- cell death of brush border intestinal cells= watery diarrhea
exotoxin B- depolymerizes actin in cytoskeleton =pseudomembranous colitis


How do we diagnose C. Diff and then how do we treat it?

Lab: toxin in stool
Tx: oral vancomycin (important, ORAL vancomycin, not IV or stick)


Structure for Clostridium perfringes

Structure: Gm (+) rods, spore forming, obligate anaerobe


Discuss the lifecycle and pathophys of C. Perfringens

Life-cycle: Spores found in soil, organisms in intestinal tract of humans and animals

Patho: Surgery/Trauma puts soil in wound → Spores germinate and organism multiplies under conditions of low oxidation reduction potential. Rapid disease spread.


Two types of symptoms we see with those infected with C. Perfringens

Highly metabolically active, make abundant gas in vitro and in vivo (gas gangrene = clostridiomyomycosis) → Crackling crepitus on palpation of area

Food poisoning (lots of spores ingested, toxins then generated in the gut to cause diarrhea. Takes a while so this is a late presentation)


What lab/histo will we see with C. Perfringens

Histo: Muscle necrosis, reddish to black with no PMNs

Lab: Lysis of RBCs, digests egg yolk in agar. Stormy fermentation in milk


What special enzyme does C. Perfringens make

Lecithinase - Phospholipase that kills cells and hemolyzes RBCs in vitro and in vivo (alpha toxin breaks lecithin in lipid membrane) → Double zone of RBC hemolysis on blood agar


How do we treat C. Perfringens

Tx: IV Penicillin G for Gas Gangrene, nothing for diarrhea (transient symptom)


Structure for C. Tetani

Structure: Gm (+), obligate anaerobe, spore forming


Discuss the transmission pathway for C. Tetani

Transmission: Into anaerobic environment, typically via a puncture from a rusty nail → organism vegetates and stays at the site of infection → Tetanus toxin travels retrograde in neurons to spinal cord → SNARE Protease stops release of Glycine and GABA from Renshaw cells (monitor contractions) = No inhibitors.


Discuss the symptoms we see with C. Tetani

(if you find yourself taking a while with these cards, watch Sketchy Micro. If you don't know what that is, Stop, close this tab, grab your wallet, go to and start watching videos. If your grade doesn't go up 10% then you went to the wrong site).

Sx: Spastic paralysis (relentless contractions).
Rheesus Sardonicus = “Evil Grin” = Lock Jaw = Jaw won’t open.

Opisthotonus = Exaggerated arching of the back


Treatment for C. Tetani

Tx: Toxin conjugated to a protein vaccine


Structure of Actinomyces Israeli

Structure: Gm (+), obligate anaerobic, non-spore forming, branching rods that form chains. Make macrocolonies that resemble grains of sand and can be seen in abscesses and draining sinus tracts (sulfur granules, look like yellow pus)


Where are A. Israeli on the body and how does it begin presentation

Location: Cervico-facial region (poor oral hygiene/ after invasive oral surgery). Begins as infected tooth/ “lumpy jaw.”


Treating A. Israeli?

Tx: Penicillin G


Alright so this one was brought up in the infection clinical lecture. Nothing in Schaeter's or Robbins so this is as low yield as it gets. But if you find yourself with extra brainspace:

What is the structure and symptoms for Propionibacterium Acnes?

Gm (+) rod, anaerobic, non spore former

Sx: Acne and infection of prosthetic devices


Tell me about what makes Bacteroides so special when compared to other Gram Negatives

G(-) rod, non-spore-forming

Structure: Strict anaerobe HOWEVER unlike other anaerobes, this guy can survive in oxygen environments due to oxidative stress enzymes that protect it from oxygen radicals. Due to this it can release into the peritoneal cavity (higher PO2 than colon)

Superoxide dismutase - Detoxifies oxygen radicals

Catalase - Breaks down H2O2→ H2O + O2


Tell me about the virulence factors of B. Fragilis

Polysaccharide capsule = antiphagocytic, hinders complement (gives it access to blood) and helps it to bind to mesothelium of peritoneum

B- Lactamases

Neuraminidase - Required in order to make abscess

Polysaccharide A - Zwitterionic molecule (positive and negative ends) that induces an immune response by CD4+ cells that makes an abscess in the peritoneum


Most common causative agent for intra-abdominal abscess

B. Fragilis


A weird bacterium that probably won't be on the final is Fusobacterium nucleatum.

Where do I find this and what is a very common and worrisome complication of it?

Gm (+) rods

Location: Indigenous to the human oral cavity

Complications: Linked to colorectal cancer


If I see bite wound on the faculty exam, and I've eliminated all other options, what weird bacterium could be left?

Eikenella Corrodens

Structure: Gram negative Bacillus, facultative (likes more CO2)

Cause: Bite wounds on faculty exam


Common sinus pathogen

Strep Intermedius


A pathogen to keep in mind with neck infections on the faculty exam

Prevotella Oralis

Structure: Gm (-) Bacillus
Virulence: Beta lactamases
Sx: Neck infections