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
Q

Development of Clostridium difficile associated diarrhea requires what two things

A
  1. presence of C diff

2. disruption of native flora

26
Q

Who gets Clostridium difficile?

A

People on antibiotics or PPIs

27
Q

Normal influence of Clostridium difficile on the colon?

A

Important for T-reg development

28
Q

Most Clostridium difficile patients are infected where?

A

A Health Care Setting

29
Q

Pathogenesis of Clostridium difficile?

A

Enterotoxin (Toxin A) – Fluid Acc

Cytotoxin (Toxin B) – Kills gut epithelial cells

30
Q

How is Clostridium difficile controlled/treated?

A
Stop previous antibiotics if you can
Replenish gut flora
Vancomycin, Metronidazole
Fecal transplant
Fluid Replacement
31
Q

Physical structure of Actinomyces israelii

A

G+

Branching, Fragmenting Filaments

32
Q

Oxygen sensitivity of Actinomyces israelii?

A

Facultative anerobes

33
Q

Actinomyces israelii colonies are in what shape?

A

Molar tooth

34
Q

Clinical presentation of Actinomyces israelii?

A

Swollen, pyogenic abscess with draining fistulae (lumpy jaw)
“Sulfur granules” apparent in collected pus
Common in face/neck, lungs, ab, skin

35
Q

How do people typically get Actinomyces israelii infection?

A

Tooth extraction or poor oral hygiene
Thoracic inf from aspiration
abdominal inf from perforated gut/appendix
Foot from soil bacteria

36
Q

Who gets Actinomyces israelii?

A

IC patients

37
Q

How is Actinomyces israelii treated?

A

Surgical drainage of abscess

Parenteral Pen G for a few weeks

38
Q

Unique physical traits of Nocardia asteroides?

A

Actinomycete
Shorter mycolic acids, partially acid fast
aerobic, lives in soil

39
Q

Clinical presentation of Nocardia asteroides?

A

Lobar Pneumonia in Alcoholics or IC
Lung abscesses
Can spread to brain –> meningitis, brain abscess
In foot from soil

40
Q

How do people get Nocardia asteroides infection?

A

Opportunistic infection

Lung aspiration of vomit

41
Q

How is Nocardia asteroides treated?

A

SxT

42
Q

Physical structure of Aeromonas hydrophilia, plesiomonas shigelloides?

A

G- Rod
Fac. anerobe
Motile

43
Q

Where are Aeromonas hydrophilia, plesiomonas shigelloides found?

A

Common Fish Pathogens
Aeromonas hydrophilia - Fresh
Plesiomonas shigelloides - Salt

44
Q

Clinical presentation of Aeromonas hydrophilia, plesiomonas shigelloides infection?

A

Gastroenteritis – can be watery or blood and mucas
Cellulitis from infected wounds
Myonecrosis

45
Q

How do people typically get Aeromonas hydrophilia, plesiomonas shigelloides?

A

Infected food, water
Tissue entry after trauma (fish-hook)
SCUBA biofilms

46
Q

Pathogenesis of Aeromonas hydrophilia, plesiomonas shigelloides?

A

LPS, PG toxicity
ACT toxin
Pili grab onto gut epithelium

47
Q

How is Aeromonas hydrophilia, plesiomonas shigelloides controlled?

A

Avoid undercooked seafood

48
Q

How do you treat Aeromonas hydrophilia, plesiomonas shigelloides?

A

SxT, Tetracycline