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

Micro Exam #2 > Clostridium, Actinomyces israelii, Nocardia asteroides, Aeromonas, Plesiomonas > Flashcards

Flashcards in Clostridium, Actinomyces israelii, Nocardia asteroides, Aeromonas, Plesiomonas Deck (48)
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1

Describe the physical structure of Clostridium

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

2

Describe the oxygen sensitivity of Clostridium

Anerobic

3

Clinical presentation of Clostridium botulinum

18-24 hour incubation
Bilateral Cranial Nerve Palsies with Progressive Descending Flaccid Paralysis

4

How do people die of Clostridium botulinum?

Involvement with heart or diaphragm

5

Main sources of Clostridium botulinum infection?

Home-Canned Foods, Rarely commercial
Entry Woulds, like needles (botox, black tar heroin)

6

How does Clostridium botulinum manifest in children?

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

7

Pathogenesis of Clostridium botulinum?

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

8

How does Clostridium botulinum block ACh release?

Cleaving synaptobrevin

9

How is Clostridium botulinum controlled?

Use Antitoxin from CDC as early as possible

10

Clinical presentation of Clostridium tetani

Rigid Paralysis
Eventually Death from Inability to Breathe

11

Epidemiology of Clostridium tetani?

Spores in soil/feces
Introduces by fomites in skin

12

How do neonates get Clostridium tetani?

Umbilical stump infection

13

Pathogenesis of Clostridium tetani?

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

14

How is Clostridium tetani controlled?

DTaP, Tdap

15

What can you do for a tetanus patient?

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

16

Describe the presentation of Clostridium perfringens

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

17

Epidemiology of Clostridium perfringens

Traumatic Tissue Injury, Esp if anaerobic conditions

18

Why is Clostridium perfringens typically polymicrobial?

Other infection will produce the anoxic environemnt Clostridium perfringens requires

19

Pathogenesis of Clostridium perfringens?

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

20

What does alpha toxin do?

Its a lecithinase (phospholipase)

21

How is Clostridium perfringens controlled?

Prompt surgical debridement

22

How is Clostridium perfringens treated?

Metronidazole, Penicillin, and Clindamycin stop growth

23

Clinical presentation of Clostridium difficile?

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

24

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

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