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Bacteriology Lectures > Clostridium, Actinomyces, Nocardia, Aeromonas/Plesiomonas > Flashcards

Clostridium, Actinomyces, Nocardia, Aeromonas/Plesiomonas Flashcards

1
Q

Clostridium organism and appearance

A

Gram positive rods

rounded ends, in pairs or short chains

*spores often wider than the cell

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2
Q

Clostridium metabolism

Can be found in ____

A

Strict anaerobe

Found in soil

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3
Q

C. botulinum clinical presentation

A

bilateral cranial nerve palsies

descending flaccid paralysis

dysphagia/diplopia/ptosis

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4
Q

Sources of C. botulinum

A

Home canned foods

Alaskan native food

Entry via wounds, needles (IV drugs)

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5
Q

Major source of “floppy baby syndrome” (C. botulinum)

A

Ray honey - up to 70% of cases

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6
Q

Serotypes of C. botulinum

A

7 serotypes, A through G

A, B, E in humans

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7
Q

C. botulinum pathogenic factor

A

AB neurotoxin

B binds to NMJ

A cleaves synaptobrevin –> blocks fusion –> blocks Ach release

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8
Q

Control/Tx of C. botulinum

A

Antitoxin injection (A-G) as soon as you suspect botulism in the differential

*No ABX!

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9
Q

C. tetani clinical presentation

A

Spasms (Jaw then back)

Death occurs when spasms interfere with breathing

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10
Q

C. tetani sources

A
  • soil + **animal feces **(introduced by fomites penetrating the skin)
  • Neonatal = from umbilical infections
  • IV drug use
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11
Q

C. tetani pathogenic factor

A

AB neurotoxin = Tetanospasmin (plasma encoded)

  • asorbed at NMJ, retrograde transport to cell body of motor neuron
  • binds irreversibly
  • reuptaken by presynaptic membrane of inhibitory neurons
  • cleaves synaptobrevin –> prevents GABA release
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12
Q

C. tetani control (vaccine, treatments, antibiotics)

A
  • VAX with tetanus toxoid – boosters every 10 years
  • Antitoxin (Tetanus Immune Globulin) = only works if given early
  • Early tracheostomy, avoid stimulation
  • Muscle relaxants
  • ABX = Mzole (preferred over Penicillin)
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13
Q

C. perfringens strains

A

5 strains based on toxin profile

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14
Q

C. perfringens clinical presentation

A

1-3 days until it starts from a wound

–> Tissue necrosis, toxemia, shock, death

*Can also present as food poisoning (1-2 days) if ingested (“enteritis necroticans”)

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15
Q

How is C. perfringens acquired

A

Tramautic injury coupled with anaerobic conditions (i.e. ischemia)

**other organisms that are present will help facilitate anaerobic environment

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16
Q

C. perfringens pathogenic factors (5)

A
  • Alpha-toxin (lecithinase = phospholipase)
  • Hyaluronidase + Collagenase
  • Beta-toxin (food poisoning = e. necroticans)
  • Enterotoxin (in some strains)
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17
Q

C. perfringens pathogenic process

A

Gas fermentations –> tissue distension –> compress vessels and stops bloodflow –> necrosis

*Necrotic tissue induces toxemia

18
Q

C. perfringens control (treatment, antibiotics,)

A

Surgical debridement or amputation

ABX (to stop multiplying) = Mzole, penicillin, clindamycin

19
Q

C. diff major disease

A

pseudomembranous colitis

20
Q

C. diff usually beigins when?

How is it acquired?

Main cause of symptoms?

A
  • 4-10 days after broad-spec ABX - Beta Lactams and Clindamycin are big offenders
  • Infects via nosocomial route, associated with PPI use
  • Main cause = disruption of native gut flora
21
Q

C. diff disease progression

A
  • Early Sx = watery diarrhea
  • leukocytes and cells form exudate = pseudomembrane
  • May involve part or entire length of colon
22
Q

______ leads to asymptomatic carriage of C. diff

A

Ingestion of spores without dysbiosis (fancy word for native bacterial disruption)

23
Q

is C. diff normal flora?

A

Yes, seems to be inportant for Treg cell development in colon

24
Q

C. diff acquired by what route? Where does this normally happen?

A

Nosocomial

In health care settig (94% of cases)

25
Q

C. diff pathogenesis

A

Toxin A = Enterotoxin –> fluid accumulation

*Toxin B* = Cytotoxin –> Kills gut epithelial cells

26
Q

______ antibodies are useful in C. diff diagnosis

A

Anti-ToxinB

(anti-cytotoxin)

27
Q

C. diff control (treatments, antibiotics, vaccine

A

Stop ABX if possible

  • Probiotic, fluid replacement, FECAL TRANSPLANT
  • ABX = Vancomycin + Mzole
    • Fidaxomycin (RNApol inhibitor) = for recurrent infection
  • Vax = toxoid against toxins A and B
28
Q

Actinomyces israelii organism and appearance

Metabolism?

A

Gram positive branching, fragmenting filaments

Faculatative anaerobes (like higher CO2)

Grow Slowly –> molar tooth colonies

29
Q

Actinomycosis clinical presentation

A
  • Lumpy Jaw (pyogenic abcess)
  • occurs at cervicofacial, thoracic, abdominal, skin (feet)

**Sulfur granules = Actinomyces surrounded by PMN’s

30
Q

Actinomyces normal flora?

Infection epidemiology?

A

Yes

Infection is usually just in IC patients and is non-communicable

31
Q

Actinomyces acquisition?

A

Tooth extraction, bad hygeine, aspiration (lungs), perforated gut/ruptured appendix

*Food infection is found from soil bacteria

32
Q

Actinomyces control (Tx, ABX) and prophylaxis

A

Drainage of abcess

PenG for a few weeks (I.M.) and then oral for 6-12 months

**Tetracycline, erythromycin, clindamycin can be used with a penicillin allergy

Prophylactic Pen = with recurring infection or before oral surgery

33
Q

Nocardia asteroides organism

Nocardia metabolism

A

actinomycete morphology

(= Gram positive branching, fragmenting filaments)

Partially acid fast (produces shorter mycolic acids)

Aerobic (lives in surface soil)

34
Q

Nocardiosis presentation

A

Lobar PNA, usually in alcoholics or IC patients

  • abcess in lung lobe –> can spread to CNS (Meningitis or Abcess)
35
Q

Nocardiosis can also occur…

A

on the foot from soil-based infections

36
Q

Nocardia lung infection from _____.

Disseminates to _____ and ______

A

From Aspiration

Dissemination to CNS and Kidneys

37
Q

Nocardia control

A

Bactrim

(also carbapenems + amikacin)

38
Q

Aeromonas and Plesiomonas organism and origin

A

Gram negative rod, facultative anaerobe, motile

*Common fish pathogens

  • Aeromonas = Freshwater*
  • Plesiomonas = Saltwater*
39
Q

Aeromonas and Plesiomonas…most common presentation?

A

Gastroenteritis

Watery (cholera-like) or Bloody (dysenteric) diarrhea

**Also cellulitis and myonecrosis

40
Q

Aeromonas and Plesiomonas often acquired from…

A

fish-hook injury, SCUBA activity (??)

41
Q

Aeromonas and Plesiomonas pathogenic factors

A
  • Typical Gram negative stuff (LPS, PG tox)
  • Pili for attachment
  • ACT Toxin = “aerolysin-cytotoxin-enterotoxin”

—> lyses cells + upregulates cAMP

42
Q

Aeromonas and Plesiomonas control and Tx?

A

Avoid undercooked fish

IC patients and wound cellulitis = Bactrim or Tetracycline

(Diarrhea is self limiting)

Bacteriology Lectures (14 decks)

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