Anaerobic Bacteria WITH Sketchy, Schaeters and Lecture Material Flashcards
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 Sketchymedical.com 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
Structure and the two most common effects for E. Coli
Structure: Gm (-) Rod, facultative anaerobe, encapsulated (K antigen in capsule), Catalase Positive, Fimbriae that allow it to cause UTIs (#1 cause, 80% of UTIs), LPS endotoxin (#1 cause of sepsis)
Discuss culturing of E.Coli
Cx: Lactose fermenter (pink on MacConkey), Green on EMB Agar
When does E. Coli cause meningitis?
Sx: Neonatal meningitis when + for K antigen in the capsule
How does the EHEC form of E.Coli cause damage?
EHEC - From undercooked meat, usually hamburgers. Causes bloody diarrhea. Cx: Only E.Coli that doesn’t ferment sorbitol. Shiga-like toxin that damages endothelial cells in capillaries of glomerulus → Damages endothelium leading to area becoming thrombogenic = Platelet aggregation and decrease in platelet count → Aggregates of platelets shear RBCs as they pass by = Hemolysis. O157:H7 antigen is associated with outbreaks
Tell me about Traveler’s Diarrhea
ETEC - “Traveler’s Diarrhea” - Transmitted via water sources, often from Mexico (Montesuma’s Revenge). Toxins: Heat labile toxin that increases cAMP and a heat stable toxin that increases cGMP. Sx: Watery diarrhea
Structure and special culturing for E. Faecalis
Structure: Gm (+) cocci, facultative anaerobe
Cx: Resists 6.5% NaCl
Factors: Bile resistance
Trifecta of sadness we see due to E. Faecalis
Sx: UTIs, biliary tree infections (bile resistant), endocarditis
Treatment for E. Faecalis
Tx: Linezolid or Tigecycline just to be safe
What makes E. Faecium different from E. Faecalis?
Less common but worse
Cause: Nosocomial infection, resistant to almost all antibiotics (VRE = Vancomycin Resistant Enterococcus)
DEFINITELY treat with Linezolid and Tigecycline
Structure and labs for Pseudomonas Aeruginosa
Lab: Oxidase +, Catalase +
Structure: Gm (-), obligate aerobe, encapsulated
Discuss the pathophys for the Pseudomonas Aeruginosa toxin
Pathophys of Toxins: ADP ribosylation of E2F (nearly identical to diptheria) to inhibit protein synthesis and cause cell death
Discuss the culture for P. Aeruginosa
Cx: Blue green when plated (pyocyanin and pyoverdin produced by P.A.). Makes purple grape smell (fruity smell).
Symptoms of P. Aeruginosa
1 Cause of gram negative nosocomial pneumonia
Common cause of pulmonary infection and respiratory arrest in Cystic Fibrosis patients due to bad chloride channel pumps
Osteomyelitis in IV drug abusers (directly inject P.A.)and diabetics (more likely to have traumatic wounds in feet)
Skin lesions
- Pruitic papulopustular folliculitis secondary to underchlorinated hot tubs
- After sepsis it can lead to necrosis of skin = Ecthyma gangrenosum
Otitis externa = Swimmer’s ear
Who is at risk for P. Aeruginosa infection
At risk: Chronic Granulomatous Disease pts, Dangerous for patients with burn wounds and catheters/UTIs
Treating P. Aeruginosa
Tx: Piperacillin and tazobactam. Less common: Aminoglycosides and fluoroquinolones (Cipro and Levo)
