Anaerobic Bacteria WITH Sketchy, Schaeters and Lecture Material

Question 1

Why do anaerobes hate O2 so much?

Answer 1

• 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)

Question 2

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

Answer 2

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

Question 3

Tell me about the structure for Clostridium Botulinum

Answer 3

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

Question 4

How do we transmit Clostridium Botulinum?

Answer 4

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)

Question 5

What virulence factor is used by Clostridium Botulinum?

Answer 5

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

Question 6

What symptoms do we see with clostridium botulinum?

Answer 6

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

Question 7

Structure of Clostridium Difficile

Answer 7

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

Question 8

Discuss the presentation and virulence toxins we see with clostridium difficile

Answer 8

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

Question 9

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

Answer 9

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

Question 10

Structure for Clostridium perfringes

Answer 10

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

Question 11

Discuss the lifecycle and pathophys of C. Perfringens

Answer 11

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.

Question 12

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

Answer 12

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)

Question 13

What lab/histo will we see with C. Perfringens

Answer 13

Histo: Muscle necrosis, reddish to black with no PMNs

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

Question 14

What special enzyme does C. Perfringens make

Answer 14

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

Question 15

How do we treat C. Perfringens

Answer 15

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

Question 16

Structure for C. Tetani

Answer 16

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

Question 17

Discuss the transmission pathway for C. Tetani

Answer 17

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.

Question 18

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).

Answer 18

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

Opisthotonus = Exaggerated arching of the back

Question 19

Treatment for C. Tetani

Answer 19

Tx: Toxin conjugated to a protein vaccine

Question 20

Structure of Actinomyces Israeli

Answer 20

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)

Question 21

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

Answer 21

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

Question 22

Treating A. Israeli?

Answer 22

Tx: Penicillin G

Question 23

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?

Answer 23

Gm (+) rod, anaerobic, non spore former

Sx: Acne and infection of prosthetic devices

Question 24

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

Answer 24

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

Question 25

Tell me about the virulence factors of B. Fragilis

Answer 25

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

Question 26

Most common causative agent for intra-abdominal abscess

Answer 26

B. Fragilis

Question 27

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?

Answer 27

Gm (+) rods

Location: Indigenous to the human oral cavity

Complications: Linked to colorectal cancer

Question 28

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

Answer 28

Eikenella Corrodens

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

Cause: Bite wounds on faculty exam

Question 29

Common sinus pathogen

Answer 29

Strep Intermedius

Question 30

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

Answer 30

Prevotella Oralis

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

Question 31

Structure and the two most common effects for E. Coli

Answer 31

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)

Question 32

Discuss culturing of E.Coli

Answer 32

Cx: Lactose fermenter (pink on MacConkey), Green on EMB Agar

Question 33

When does E. Coli cause meningitis?

Answer 33

Sx: Neonatal meningitis when + for K antigen in the capsule

Question 34

How does the EHEC form of E.Coli cause damage?

Answer 34

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

Question 35

Tell me about Traveler’s Diarrhea

Answer 35

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

Question 36

Structure and special culturing for E. Faecalis

Answer 36

Structure: Gm (+) cocci, facultative anaerobe

Cx: Resists 6.5% NaCl

Factors: Bile resistance

Question 37

Trifecta of sadness we see due to E. Faecalis

Answer 37

Sx: UTIs, biliary tree infections (bile resistant), endocarditis

Question 38

Treatment for E. Faecalis

Answer 38

Tx: Linezolid or Tigecycline just to be safe

Question 39

What makes E. Faecium different from E. Faecalis?

Answer 39

Less common but worse

Cause: Nosocomial infection, resistant to almost all antibiotics (VRE = Vancomycin Resistant Enterococcus)

DEFINITELY treat with Linezolid and Tigecycline

Question 40

Structure and labs for Pseudomonas Aeruginosa

Answer 40

Lab: Oxidase +, Catalase +

Structure: Gm (-), obligate aerobe, encapsulated

Question 41

Discuss the pathophys for the Pseudomonas Aeruginosa toxin

Answer 41

Pathophys of Toxins: ADP ribosylation of E2F (nearly identical to diptheria) to inhibit protein synthesis and cause cell death

Question 42

Discuss the culture for P. Aeruginosa

Answer 42

Cx: Blue green when plated (pyocyanin and pyoverdin produced by P.A.). Makes purple grape smell (fruity smell).

Question 43

Symptoms of P. Aeruginosa

Answer 43

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

1. Pruitic papulopustular folliculitis secondary to underchlorinated hot tubs
2. After sepsis it can lead to necrosis of skin = Ecthyma gangrenosum

Otitis externa = Swimmer’s ear

Question 44

Who is at risk for P. Aeruginosa infection

Answer 44

At risk: Chronic Granulomatous Disease pts, Dangerous for patients with burn wounds and catheters/UTIs

Question 45

Treating P. Aeruginosa

Answer 45

Tx: Piperacillin and tazobactam. Less common: Aminoglycosides and fluoroquinolones (Cipro and Levo)