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PHARM/MHD EXAM - 3 > L11 MHD: Gram Positive/Negative Anaerobic Bacteria > Flashcards

L11 MHD: Gram Positive/Negative Anaerobic Bacteria Flashcards

1
Q

Which clostridium is responsible for the following:

  1. Gas gangrene – toxin
  2. Intra-abdominal infections - vegetative and toxin
  3. Food poisoning- toxin
A

Clostridium Perfringens

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2
Q

Structure of C. Perfringens:

  1. Gram (+ or -)
  2. Motile?
  3. Encapsulated?
  4. forms _____
  5. ___ Appearance
A
  1. Gram +
  2. Non - motile
  3. Encapsulated
  4. SPORES
  5. Box car appearance
  • double zone hemolysis
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3
Q

Gas gangrene by C. Perfringens:

  1. Requires ____ with devitalized tissue/muscle
  2. What organism spores germinate quickly?
A
  1. TRAUMA with devitalized tissue/muscle
2. Spores of :
C. perfringens, 
C. novyi, 
C. septicum,
 C. ramosum germinate quickly
  • Extremities, endometrium, abdominal wall
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4
Q

Which type is most common of C. Perfringens that causes gas gangrene?

What are the function of alpha & beta toxins?

Which causes muscle cell necrosis?

A

Type A most common cause of human disease in U.S

  • alpha = lecithinase (phospholipase C) lyses inflammatory cells, RBCs, platelets, & destroys tissue
  • abscess does not have any leukocytes since lysed by the organism

= MUSCLE CELL NECROSIS –> ALPHA

Beta toxin:
- Necrotizing enteritis (pig bel)
= food poisoning

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5
Q

What is the first order of therapy of gas gangrene?

What are the systemic symptoms of Gas gangrene?

Clinical presentation?

A

REMOVE THE DEBRIS
= debridement! (TEST)

(before antibiotics)

Systemic:

  • shock
  • hyper or hypothermia
  • rapid onset
  • NECROSIS of muscle
    tense edema
    bullae formation
    gas formation (fermentation)
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6
Q

How does clindamycin affect C. Perfringens?

What antibiotics should be given for C. Perfringens (after debridement)?

A
  • inhibits protein synthesis and decreases toxin production

2. Penicillin, B - lactam inhibitor (Unasyn)

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7
Q

C. Perfringens food poisoning occurs because of what toxin?

How long after ingestion?

A
  1. Enterotoxin
  • toxin B
  • HEAT RESISTANT spores survive (gravy/soup)
  • produce an enterotoxin following germination
  1. 8-24 hours after eating
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8
Q

What is the treatment for C. Perfringens food poisoning?

A

SELF - LIMITED disease

culture not needed

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9
Q
  1. Clostridium Tetani enters via
    what? Specifically for infants?
  2. Local germination without ____
  3. What is Tetanospasmin and what does it to?
A
  1. puncture wounds, burns
    infants = UMBILICUS
  2. No necrosis = no pus or inflammation!
  3. Tetanospasmin:
    - neurotoxin that blocks post-synaptic inhibition of spinal motor reflexes (GABA + glycine)

= SPASMOTIC CONTRACTIONS

  • toxin found on plasmid
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10
Q

C. Tetani:

  1. Gram + or -
  2. Aerobic or Anaerobic
  3. How does it appear on gram stain? (shape)
A
  1. Gram +
  2. Anaerobic
  3. tennis racket shapes
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11
Q

The following describes:

  1. Gram positive
  2. SPORE forming
  3. Obligate anaerobic bacilli
A

CLOSTRIDIA!

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12
Q

C. Tetani:
GENERALIZED symptoms

  1. What is the initial symptom of C. Tetani?
  2. The tone of ____ muscle increases.
  3. Arm/flexion leg extension is called ____
  4. The most dangerous clinical symptom of tetanus is what?
A
  1. TRISMUS
    - lock jaw
  2. Risus Sardonicus = increased tone of Orbicularis Oris
  3. Opisthotonus
  4. RESPIRATORY OBSTRUCTION
    - spasms of the diaphragm
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13
Q

What is Risus Sardonicus and what anaerobic gram positive bacteria is it associated with?

A

Associated with ORBICULARIS ORUS

  • pulling the corners of the mouth up

C. TETANI

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14
Q

How is tetanus treated? (4)

A
  1. Human tetanus immunoglobulin (anti-toxin)
    - only effective if haven’t toxins haven’t adhered to tissues
  2. Sedation w/ diazepams
  3. Supportive (tracheotomy ) to aid with breathing
  4. BOOSTER

DEBRIDEMENT OF WOUND + PCN

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15
Q

What is the prophylactic treatment of tetanus?

How is it prevented?

A
  1. 3 doses of DPT
    - revaccinated every 10 years (booster)
  2. PASSIVE IMMUNIZATION
    - HTIG for appropriate wound
  • hyperimmunoglobulin injected to bind toxin around the site!!!
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16
Q

Clostridium Botulinum:

  1. Associated with ____ foods
  2. Entry via ____ from contaminated food
  3. Avoid giving ____ to infants less than 1years of age.
A
  1. HOME CANNING!! (test)
    - fruits/vegetables
    - fish
  2. PREFORMED TOXIN from contaminated food
  3. no HONEY to babies less than 1
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17
Q

The following describes what toxin?

  1. Cleaved by bacterial protease
  2. MOST POTENT in nature
  3. BLOCKS ACh
  4. prevents NT release leading to FLACCID PARALYSIS
  5. Heat labile (can autoclave/heat to kill the toxin)
A

C. Botulinum TOXIN
(bacteriophage born)

  • synapse permanently damaged
  • C. Botulinum for BOTOX
  • no release of ACH due to inhibition of snares
    = FLACCID PARALYSIS
18
Q

What are the 3 most important clinical presentations of BOTULISM?

A
  1. GI (nausea, dry mouth, diarrhea)
    - usually in infants
  2. DESCENDING PARALYSIS
    (flaccid)
    -start with cranial nerves 3,4,6
  3. Wound botulism (local paralysis in a wound)
19
Q

How is Botulism often diagnosed?

What is the prevention/ tx?

A
  1. TOxin assays
  2. avoid contaminated food
    - heating of food (boiling)
    - antitoxin
    - SUPPORTIVE treatment (ventilator)
20
Q

C. Difficile:

Use of ____ usually precedes the disease.

T/F: Not part of our normal flora

What are the 2 important toxins?

A
  1. ANTIBIOTIC THERAPY
    - wiping out the normal flora due to the use of BROAD SPECTRUM ANTIBIOTICS
    - acquired from hospital

FALSE: part of our normal flora

Toxin A
(enterotoxin, inflammatory)
- causeses GI upset
- bidns to BRUSH BORDER of intestines –> inflammation + cell death & water diarrhea (A for apple brush on apple)

Toxin B - Cytotoxic
- kills mucosal cells
- B for licorice –> disrupts cytoskeleton integrity by DEPOLYMERIZING actin
- enterocyte death & necrosis
= PSEUDOMEMBRANOUS COLLITIS (look for toxin in stool via PCR)

21
Q

What causes diffuse hemorrhagic colitis & pseudomembrane formation?

A

C. Difficile Cytotoxin & Enterotoxin

22
Q

Which C. Difficile toxin is responsible for

  1. Pseudomembranous colitis via cytoskeletal disruption & actin depolymerization
  2. Which binds to the brush border of the gut?

What is a classic clinical finding of C. Difficile?

A
  1. Cytotoxin B
  2. ENTEROTOXIN –> Toxin A

BI (Nap1) Strain: (enterotoxin)
Increased Toxin A production
Higher mortality, especially elderly (>80)
Up to 50% of isolates  DOMINANT strain

  1. LEUKOCYTOSIS!!! (TEST)
23
Q

What test has higher specificity for C. Difficile

PCR or ELISA?

A

PCR!

Elisa is sensitive, but not specific

24
Q

What are the 3 major treatments of C. Difficile?

A
  1. Stop antibiotics if possible
  2. Metronidazole (ORAL) for mild to moderate
  3. Vancomycin***
25
Q

Propionobacterium acnes is present in contaminated ____

Cause of infection?

Tx?

A
  1. Blood cultures (along with staph)
  2. Prosthetic devices or hardware
  3. tx: PENICILLIN
    (No metronidazole)
26
Q

All the anaerobic bugs mentioned in this lecture are part of the normal flora except what?

What is the cause of dental infection that forms abscesses?

A

Clostridium (soil)

Peptostreptococcus

  • pathogen when out of normal environment associated with DENTAL infection + BRAIN ABCESS (tooth infection can get bacteremia & cross the BBB - form an abscess)

ANYTHING THAT FORMS abscesses = DEBRIDEMENT is necessary

27
Q

B. Fragilis is found _____ not in the small intestine.

  1. Spores?
  2. Motile?
  3. What is its role in GI?
A
  1. COLON!!
  2. No spores
  3. Not motile
  4. PROTECT FROM INVASION (ex: C Diff)
28
Q

What is the hallmark of B. Fragilis?

A

ABSCESS formation

  • mixed infection (like peptostreptococcus)
  • bacteria attract neutrophils
29
Q

What are the 2 the main virulence factors of B. Fragilis?

A
  1. Polysaccharide capsule
    -Adherence to peritoneal cavity
    Resists phagocytosis
    Resistance to T cell and humoral immunity
  2. Oxygen tolerance
    - superoxide disputes breaks down oxygen into H20 and CO2
    - growth suspended during presence of OXYGEN
30
Q

What toxin does B. Fragilis produce?

What are the 2 main infections it causes?

A

DEFECTIVE ENDOTOXIN

  • not associated with sepsis
    (not virulence factor)

TEST

  1. Intra-abdominal infection (peritonitis)
  2. Wuund infection = SKIN & SOFT TISSUE
31
Q

What is the most important aerobe that causes intra-abdominal infections?

Anaerobe?

A
  1. E. Coli (colon)
  2. B. Fragilis!!! (colon)

(TEST)

32
Q

What soft tissue & skin infection does B. Fragilis cause?

A

Fournier Gangrene

33
Q

Besides B. Fragilis, what clostridium bacteria can cause soft tissue infection?

A

C. Perfringens

= MIXED INFECTION

  1. Staph Aureus
34
Q

What is the main anaerobic organism isolated from diabetic foot infections?

A

B. Fragilis!

Bacteroides arise by contamination of a wound with feces

35
Q

What bacteria is most commonly found in BRAIN ABSCESSES?

A

Prevotella (& peptostreptococcus)

36
Q

The following describes what:

  1. gram negative obligate anaerobe
  2. Non - motile
  3. not encapsulated
  4. ABCESS formation
A

Prevotella!!

37
Q

If oral contents were aspirated, what gram negative anaerobic bacteria would likely be present?

A

PREVOTELLA!

  • cause brain access
  • fluid abcess
38
Q

State which Fusobacterium (F. Nucleatum or F. Necrophorum) is responsible for the following:

A:

  1. aspiration pneumonia
  2. lung abcess
  3. Chronic otitis liver abcess
  4. sinusitis
B)
- LEMIERRE's syndrome
post anginal sepsis
- widespread metastatic infection
- Highly virulent – potent endotoxin
A

F. Nucleatum

B) F. Necrophorum!

39
Q

Porphyromonas causes ____ infections

A

Oral, periodontal

Ginitvitis

40
Q

What antibiotic is most active for Bacteroides?

What is ineffective?

A

METRONIDAZOLE!

  • also use B - lactam inhibitor
  • resistant to penicillin and is likely one of the most resistant gram negative anaerobe

PHARM/MHD EXAM - 3 (21 decks)

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