Clostridium, Actinomyces israelii, Nocardia asteroides, Aeromonas, Plesiomonas Flashcards

1
Q

Describe the physical structure of Clostridium

A

G+ Rods, Usually Rounded Ends
Pairs/Short Chains
Sporulatin

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2
Q

Describe the oxygen sensitivity of Clostridium

A

Anerobic

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3
Q

Clinical presentation of Clostridium botulinum

A

18-24 hour incubation

Bilateral Cranial Nerve Palsies with Progressive Descending Flaccid Paralysis

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4
Q

How do people die of Clostridium botulinum?

A

Involvement with heart or diaphragm

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5
Q

Main sources of Clostridium botulinum infection?

A

Home-Canned Foods, Rarely commercial

Entry Woulds, like needles (botox, black tar heroin)

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6
Q

How does Clostridium botulinum manifest in children?

A

Rapidly colonizes gut, replaces developing flora
Floppy Baby Syndrome
Caused by spores in honey

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7
Q

Pathogenesis of Clostridium botulinum?

A

AB neurotoxin
- B binds neuron end plates, A blocks ACh release
No ACh = Flaccid Muscle Paralysis

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8
Q

How does Clostridium botulinum block ACh release?

A

Cleaving synaptobrevin

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9
Q

How is Clostridium botulinum controlled?

A

Use Antitoxin from CDC as early as possible

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10
Q

Clinical presentation of Clostridium tetani

A

Rigid Paralysis

Eventually Death from Inability to Breathe

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11
Q

Epidemiology of Clostridium tetani?

A

Spores in soil/feces

Introduces by fomites in skin

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12
Q

How do neonates get Clostridium tetani?

A

Umbilical stump infection

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13
Q

Pathogenesis of Clostridium tetani?

A

A-B neurotoxin, tetanospasmin

 - Absorbed at neuromusc. junction, retrograde transport to motor neuron
 - Binds irreveribly to and re-uptaken by presynaptic mem. of inhib neurons
 - Cleaves synaptobrevin, no GABA release
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14
Q

How is Clostridium tetani controlled?

A

DTaP, Tdap

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15
Q

What can you do for a tetanus patient?

A
Tetanus Immune Globulin antitoxin
avoid stimulation
Early tracheostomy to prevent laryngospasm suffication
Muscle Relaxants
Metronidazole
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16
Q

Describe the presentation of Clostridium perfringens

A

Infected wound suppurating
Foul Discharge, Tissue Necrosis
Toxemia, Shock Death
Also – can present as food poisoning –> gut necrosis

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17
Q

Epidemiology of Clostridium perfringens

A

Traumatic Tissue Injury, Esp if anaerobic conditions

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18
Q

Why is Clostridium perfringens typically polymicrobial?

A

Other infection will produce the anoxic environemnt Clostridium perfringens requires

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19
Q

Pathogenesis of Clostridium perfringens?

A

Extracellular enzyme secretions destroy tissue, allow invasion
- alpha toxin
- hyaluronidase, collagenase
- beta-toxin
- enterotoxin
Gas from ferm. causes tissue distention, compressed vessels

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20
Q

What does alpha toxin do?

A

Its a lecithinase (phospholipase)

21
Q

How is Clostridium perfringens controlled?

A

Prompt surgical debridement

22
Q

How is Clostridium perfringens treated?

A

Metronidazole, Penicillin, and Clindamycin stop growth

23
Q

Clinical presentation of Clostridium difficile?

A

Usually following antibiotics
Watery Diarrhea early
Leukocytes penetrate connective tissue of bowel
- Form pseudomembrane

24
Q

Which anti-biotics are most prone to cause Clostridium difficile development?

A

beta-lactams, clindamycin

25
Development of Clostridium difficile associated diarrhea requires what two things
1. presence of C diff | 2. disruption of native flora
26
Who gets Clostridium difficile?
People on antibiotics or PPIs
27
Normal influence of Clostridium difficile on the colon?
Important for T-reg development
28
Most Clostridium difficile patients are infected where?
A Health Care Setting
29
Pathogenesis of Clostridium difficile?
Enterotoxin (Toxin A) -- Fluid Acc | Cytotoxin (Toxin B) -- Kills gut epithelial cells
30
How is Clostridium difficile controlled/treated?
``` Stop previous antibiotics if you can Replenish gut flora Vancomycin, Metronidazole Fecal transplant Fluid Replacement ```
31
Physical structure of Actinomyces israelii
G+ | Branching, Fragmenting Filaments
32
Oxygen sensitivity of Actinomyces israelii?
Facultative anerobes
33
Actinomyces israelii colonies are in what shape?
Molar tooth
34
Clinical presentation of Actinomyces israelii?
Swollen, pyogenic abscess with draining fistulae (lumpy jaw) "Sulfur granules" apparent in collected pus Common in face/neck, lungs, ab, skin
35
How do people typically get Actinomyces israelii infection?
Tooth extraction or poor oral hygiene Thoracic inf from aspiration abdominal inf from perforated gut/appendix Foot from soil bacteria
36
Who gets Actinomyces israelii?
IC patients
37
How is Actinomyces israelii treated?
Surgical drainage of abscess | Parenteral Pen G for a few weeks
38
Unique physical traits of Nocardia asteroides?
Actinomycete Shorter mycolic acids, partially acid fast aerobic, lives in soil
39
Clinical presentation of Nocardia asteroides?
Lobar Pneumonia in Alcoholics or IC Lung abscesses Can spread to brain --> meningitis, brain abscess In foot from soil
40
How do people get Nocardia asteroides infection?
Opportunistic infection | Lung aspiration of vomit
41
How is Nocardia asteroides treated?
SxT
42
Physical structure of Aeromonas hydrophilia, plesiomonas shigelloides?
G- Rod Fac. anerobe Motile
43
Where are Aeromonas hydrophilia, plesiomonas shigelloides found?
Common Fish Pathogens Aeromonas hydrophilia - Fresh Plesiomonas shigelloides - Salt
44
Clinical presentation of Aeromonas hydrophilia, plesiomonas shigelloides infection?
Gastroenteritis -- can be watery or blood and mucas Cellulitis from infected wounds Myonecrosis
45
How do people typically get Aeromonas hydrophilia, plesiomonas shigelloides?
Infected food, water Tissue entry after trauma (fish-hook) SCUBA biofilms
46
Pathogenesis of Aeromonas hydrophilia, plesiomonas shigelloides?
LPS, PG toxicity ACT toxin Pili grab onto gut epithelium
47
How is Aeromonas hydrophilia, plesiomonas shigelloides controlled?
Avoid undercooked seafood
48
How do you treat Aeromonas hydrophilia, plesiomonas shigelloides?
SxT, Tetracycline