Clostridium, Actinomyces, Nocardia, Aeromonas/Plesiomonas

Question 1

Clostridium organism and appearance

Answer 1

Gram positive rods

rounded ends, in pairs or short chains

*spores often wider than the cell

Question 2

Clostridium metabolism

Can be found in ____

Answer 2

Strict anaerobe

Found in soil

Question 3

C. botulinum clinical presentation

Answer 3

bilateral cranial nerve palsies

descending flaccid paralysis

dysphagia/diplopia/ptosis

Question 4

Sources of C. botulinum

Answer 4

Home canned foods

Alaskan native food

Entry via wounds, needles (IV drugs)

Question 5

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

Answer 5

Ray honey - up to 70% of cases

Question 6

Serotypes of C. botulinum

Answer 6

7 serotypes, A through G

A, B, E in humans

Question 7

C. botulinum pathogenic factor

Answer 7

AB neurotoxin

B binds to NMJ

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

Question 8

Control/Tx of C. botulinum

Answer 8

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

*No ABX!

Question 9

C. tetani clinical presentation

Answer 9

Spasms (Jaw then back)

Death occurs when spasms interfere with breathing

Question 10

C. tetani sources

Answer 10

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

Question 11

C. tetani pathogenic factor

Answer 11

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

Question 12

C. tetani control (vaccine, treatments, antibiotics)

Answer 12

• 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)

Question 13

C. perfringens strains

Answer 13

5 strains based on toxin profile

Question 14

C. perfringens clinical presentation

Answer 14

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”)

Question 15

How is C. perfringens acquired

Answer 15

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

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

Question 16

C. perfringens pathogenic factors (5)

Answer 16

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

Question 17

C. perfringens pathogenic process

Answer 17

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

*Necrotic tissue induces toxemia

Question 18

C. perfringens control (treatment, antibiotics,)

Answer 18

Surgical debridement or amputation

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

Question 19

C. diff major disease

Answer 19

pseudomembranous colitis

Question 20

C. diff usually beigins when?

How is it acquired?

Main cause of symptoms?

Answer 20

• 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

Question 21

C. diff disease progression

Answer 21

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

Question 22

______ leads to asymptomatic carriage of C. diff

Answer 22

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

Question 23

is C. diff normal flora?

Answer 23

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

Question 24

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

Answer 24

Nosocomial

In health care settig (94% of cases)

Question 25

C. diff pathogenesis

Answer 25

Toxin A = Enterotoxin --\> fluid accumulation \*Toxin B\* = Cytotoxin --\> Kills gut epithelial cells

Question 26

\_\_\_\_\_\_ antibodies are useful in C. diff diagnosis

Answer 26

Anti-ToxinB (anti-cytotoxin)

Question 27

C. diff control (treatments, antibiotics, vaccine

Answer 27

_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

Question 28

Actinomyces israelii organism and appearance Metabolism?

Answer 28

Gram positive branching, fragmenting filaments Faculatative anaerobes (like higher CO2) Grow Slowly --\> molar tooth colonies

Question 29

Actinomycosis clinical presentation

Answer 29

* Lumpy Jaw (pyogenic abcess) * occurs at cervicofacial, thoracic, abdominal, skin (feet) \*\***_Sulfur granules_** = Actinomyces surrounded by PMN's

Question 30

Actinomyces normal flora? Infection epidemiology?

Answer 30

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

Question 31

Actinomyces acquisition?

Answer 31

Tooth extraction, bad hygeine, aspiration (lungs), perforated gut/ruptured appendix \*Food infection is found from soil bacteria

Question 32

Actinomyces control (Tx, ABX) and prophylaxis

Answer 32

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_

Question 33

Nocardia asteroides organism Nocardia metabolism

Answer 33

_actinomycete morphology_ (= Gram positive branching, fragmenting filaments) **Partially acid fast** (produces shorter mycolic acids) **Aerobic** (lives in surface soil)

Question 34

Nocardiosis presentation

Answer 34

**Lobar PNA**, usually in alcoholics or IC patients * _abcess in lung lobe_ --\> can spread to **CNS** (Meningitis or Abcess)

Question 35

Nocardiosis can also occur...

Answer 35

on the foot from soil-based infections

Question 36

Nocardia lung infection from \_\_\_\_\_. Disseminates to _____ and \_\_\_\_\_\_

Answer 36

From _Aspiration_ Dissemination to _CNS_ and _Kidneys_

Question 37

Nocardia control

Answer 37

Bactrim (also carbapenems + amikacin)

Question 38

Aeromonas and Plesiomonas organism and origin

Answer 38

Gram negative rod, facultative anaerobe, motile \*Common fish pathogens * Aeromonas = Freshwater* * Plesiomonas = Saltwater*

Question 39

Aeromonas and Plesiomonas...most common presentation?

Answer 39

Gastroenteritis Watery (cholera-like) or Bloody (dysenteric) diarrhea \*\*Also cellulitis and myonecrosis

Question 40

Aeromonas and Plesiomonas often acquired from...

Answer 40

fish-hook injury, SCUBA activity (??)

Question 41

Aeromonas and Plesiomonas pathogenic factors

Answer 41

* Typical Gram negative stuff (LPS, PG tox) * Pili for attachment * **_ACT Toxin_** = "aerolysin-cytotoxin-enterotoxin" ---\> _lyses cells_ + _upregulates cAMP_

Question 42

Aeromonas and Plesiomonas control and Tx?

Answer 42

Avoid undercooked fish IC patients and wound cellulitis = **Bactrim** or **Tetracycline** (Diarrhea is self limiting)