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Micro > Lecture 16 > Flashcards

Lecture 16 Flashcards

1
Q

Shape and stain of clostridium

A

GramPos rods with rounded ends

In pairs or short chains (shorter than bacillus though)

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2
Q

How does clostridium survive

A

Endospores

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3
Q

Clostridium O2 needs

A

Anaerobic

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4
Q

C. botulinum clinical manifestation

A

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

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5
Q

Main ways. C. botulism is spread

A

Home canned foods
Infected wounds
Black tar heroin

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6
Q

How does C. botulism cause illness

A

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

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7
Q

C. botulism treatment

A

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

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8
Q

C. tetani clinical manifestation

A

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

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9
Q

C. tetani pathogenesis

A

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

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10
Q

C. tetani control

A

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

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11
Q

Clostridium perfringens causes what?

A

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

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12
Q

Clostridium perfringens pathogenesis

A

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

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13
Q

What is main way tetanus is now spread in US

A

IV drug use

Tattoos

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14
Q

Why does C. perferingens cause gas in tissues?

A

Gas from fermentation of destructed tissues

Compresses blood flow and creates more necrosis

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15
Q

C. perfringen control

A

Prompt surgical debridement

Metronidazole, PCN, clindamycin

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16
Q

C. diff causes

A

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

17
Q

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

A

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

18
Q

What is main spread of C diff

A

Nosocomial

19
Q

C diff pathogenesis

A

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

20
Q

C diff control

A

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

21
Q

Actinomyces israelii shape and stain

A

G+, branching, fragmenting filaments

ONLY ONE THAT’S A FILAMENT

22
Q

Actinomyces israelii O2 requirement

A

Facultative anaerobe

23
Q

Actinomyces israelii clinical manifestations

A

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

24
Q

Actinomyces israelii is found where?

A

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

25
Q

Actinomyces israelii mainly affects who?

A

Immunocompromised PTs

26
Q

Actinomyces israelii control

A

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

27
Q

Nocardia asteroides stain?

A

Looks like actinomycete morphology

Also has short mycolic acids so partially acid-fast

28
Q

Nocardia asteroides O2 requirement

A

Aerobic

29
Q

Nocardia asteroides lives were

A

Surface soil

30
Q

Nocardia asteroides clinical manifestations

A

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

31
Q

Nocardia asteroides control

A

SxT

32
Q

Aeromonas and Plesiomonas shape and stain

A

GramNeg rod

33
Q

Aeromonas and Plesiomonas O2 requirement

A

Anaerobe

34
Q

Aeromonas and Plesiomonas is found where?

A

Aquatic environment

35
Q

Aeromonas and Plesiomonas clinical manifestation

A

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

36
Q

Aeromonas and Plesiomonas transfer

A

Infected sea food
Fish hook
Scuba equipment (biofilms)

37
Q

Aeromonas and Plesiomonas pathogenesis

A

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

38
Q

Aeromonas and Plesiomonas treatment

A

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

Micro (13 decks)

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