Lecture 16

Question 1

Shape and stain of clostridium

Answer 1

GramPos rods with rounded ends

In pairs or short chains (shorter than bacillus though)

Question 2

How does clostridium survive

Answer 2

Endospores

Question 3

Clostridium O2 needs

Answer 3

Anaerobic

Question 4

C. botulinum clinical manifestation

Answer 4

18-24 hour incubation
Bilateral CN palsy with progressive descending flaccid paralysis
Death via heart and diaphragm involvement
Floppy baby syndrome (honey)-botulism inhabits the gut before other native flora can

Question 5

Main ways. C. botulism is spread

Answer 5

Home canned foods
Infected wounds
Black tar heroin

Question 6

How does C. botulism cause illness

Answer 6

From phage conversion
B part binds motor end plates
A part blocks release of acetylcholine –> flaccid paralysis

Question 7

C. botulism treatment

Answer 7

Heptavalent antitoxin
Administered early
No antibiotics because it’s an intoxication

Question 8

C. tetani clinical manifestation

Answer 8

4 days-4 weeks incubation
Rigid paralysis first of jaws then back
Eventually death with respiration impairment

Question 9

C. tetani pathogenesis

Answer 9

AB toxin, plasmid encoded
Tetanospasm for retrograde transport to CNS
Binds irreversibly to inhibitory neurons
Prevents GABA release

Question 10

C. tetani control

Answer 10

Tetanus immunoglobulin
Antitoxin works only if given early enough
Early trach
Muscle relaxants
Metronidazole to reduce bacterial population

Question 11

Clostridium perfringens causes what?

Answer 11

Gas gangrene
1-3 days until infected wound begins suppurating
Can also be a food poisoning
Commonly from traumatic tissue injury if anaerobic tissue conditions are present

Question 12

Clostridium perfringens pathogenesis

Answer 12

Extracellular enzyme destroys tissues
Lecithinase
Hyaluronidase, collegenase
Some produce enterotoxin (diarrhea like B. cereus)

Question 13

What is main way tetanus is now spread in US

Answer 13

IV drug use

Tattoos

Question 14

Why does C. perferingens cause gas in tissues?

Answer 14

Gas from fermentation of destructed tissues

Compresses blood flow and creates more necrosis

Question 15

C. perfringen control

Answer 15

Prompt surgical debridement

Metronidazole, PCN, clindamycin

Question 16

C. diff causes

Answer 16

Usually after 4-10 days of broad spectrum oral antibiotic use
Also with excessive PPI

Question 17

What does the inside of bowel look like with C diff?

Answer 17

Leukocytes penetrate CT layer and forms a gray, white, yellow pseudomembrane (pseudomembrane colitis)

Question 18

What is main spread of C diff

Answer 18

Nosocomial

Question 19

C diff pathogenesis

Answer 19

2 toxins:
Enterotoxin (toxin A)-fluid accumulation
Cytotoxin (toxin B)-kills gut epithelium

Question 20

C diff control

Answer 20

Stop previous Abx if you can
Fecal transplant form healthy donor
Vanc, metronidazole
Fidaxomycin

Question 21

Actinomyces israelii shape and stain

Answer 21

G+, branching, fragmenting filaments

ONLY ONE THAT’S A FILAMENT

Question 22

Actinomyces israelii O2 requirement

Answer 22

Facultative anaerobe

Question 23

Actinomyces israelii clinical manifestations

Answer 23

Swollen, pyogenic draining abscess (lumpy jaw)
Can manifest in face, lungs, abdomen, skin
Sulfur granules in collected pus

Question 24

Actinomyces israelii is found where?

Answer 24

Part of normal mouth and gut flora
Oral-from tooth extraction or poor hygiene
Lungs-aspiration
Abdomen-perforation

Question 25

Actinomyces israelii mainly affects who?

Answer 25

Immunocompromised PTs

Question 26

Actinomyces israelii control

Answer 26

Surgical drainage if possible PenG for 6-12 months Tetra or other if PT is allergic Prophylactic if PT has recurring infection

Question 27

Nocardia asteroides stain?

Answer 27

Looks like actinomycete morphology | Also has short mycolic acids so partially acid-fast

Question 28

Nocardia asteroides O2 requirement

Answer 28

Aerobic

Question 29

Nocardia asteroides lives were

Answer 29

Surface soil

Question 30

Nocardia asteroides clinical manifestations

Answer 30

Lobar pneumonia in alcoholics of immunocompromised Abscess formation in lung May spread to CNS and brain (meningitis, brain abscess) Also on foot from soil

Question 31

Nocardia asteroides control

Answer 31

SxT

Question 32

Aeromonas and Plesiomonas shape and stain

Answer 32

GramNeg rod

Question 33

Aeromonas and Plesiomonas O2 requirement

Answer 33

Anaerobe

Question 34

Aeromonas and Plesiomonas is found where?

Answer 34

Aquatic environment

Question 35

Aeromonas and Plesiomonas clinical manifestation

Answer 35

Cholera-type (watery) diarrhea Dysentery type-blood and mucous Also cellulitis and myonecrosis

Question 36

Aeromonas and Plesiomonas transfer

Answer 36

Infected sea food Fish hook Scuba equipment (biofilms)

Question 37

Aeromonas and Plesiomonas pathogenesis

Answer 37

LPS, PG ACT toxin-lyses cells and ↑ cAMP Pili for attachment to gut epithelium

Question 38

Aeromonas and Plesiomonas treatment

Answer 38

Avoid undercooked seafood Diarrhea-usually self limiting Immunocompromised and wound cellulitis Tx with SxT, clinda