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MHD 1 > L29 Gram Negative and Gram Positive Anaerobes > Flashcards

L29 Gram Negative and Gram Positive Anaerobes Flashcards

1
Q

What are the medically important Gram positive rod anaerobes?

A
  1. Clostridium spp.
  2. Eubacterium
  3. Lactobacillus
  4. Actinomyces
  5. P. acnes
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2
Q

What are the medically important Gram negative rod anaerobes?

A
  1. Bacteroides fragilis group
  2. Prevotella spp.
  3. Porphyromonas spp.
  4. Fusobacterium spp.
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3
Q

What are the medically important Gram positive cocci anaerobes?

A
  1. Peptostreptococci
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4
Q

What are the 4 important Clostridium species?

A
  1. Perfringens
  2. Tetani
  3. Botulinum
  4. Difficile
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5
Q

What is caused by C. perfringens?

A
  1. Gas gangrene (toxin)
  2. Intra-abdominal infections (vegetative and toxin)
  3. Food poisoning (toxin)
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6
Q

What are the major structural features of C. perfringens?

A
  1. Gram positive
  2. Non-motile
  3. Encapsulated
  4. Forms spores
  5. Double zone hemolysis
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7
Q

Describe the shape of Clostridium species on a Gram stain.

A

Box car Gram positive rods

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8
Q

Describe the pathogenesis of gas gangrene.

A

A trauma occurs and leads to devitalized tissue/muscle. Spores of C. perfringens (and several similar species) germinate quickly. It can affect extremities, endometrium, and the abdominal wall.

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9
Q

What is the most common type of gas gangrene caused by C. perfringens in the U.S.?

A

Type A

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10
Q

What are the 5 toxins associated with gas gangrene and what do they do?

A
  1. Alpha: lecithinase (PLC), lysis of inflammatory cells, tissue destruction
  2. Beta: enteritis necroticans
  3. Iota: necrosis and vascular permeability
  4. Epsilon: systemic vascular permeability
  5. Theta: cardiotoxic
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11
Q

What are the symptoms of gas gangrene caused by C. perfringens?

A
  1. Tense edema
  2. Bullae formation (filled with substance of a greyish, dish water appearance)
  3. Necrosis of muscle and skin
  4. Gas formation
  5. Can lead to systemic shock and/or hypo- or hyper-thermia
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12
Q

Describe the onset of gas gangrene.

A

Rapid (6-72 hours)

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13
Q

How is gas gangrene diagnosed?

A

Clinically (suspicion, Gram stain, culture to confirm)

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14
Q

How is gas gangrene treated?

A

Debridement (removal of damaged tissue or foreign objects from wound) and antibiotics (penicillin, beta-lactam + inhibitor) + clindamycin to shut down the toxins

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15
Q

Why can C. perfringens cause food poisoning?

A

Heat resistant spores survive and germinate, leading to enterotoxin production

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16
Q

What is the clinical presentation of food poisoning caused by C. perfringens?

A

Nausea, abdominal pain, diarrhea 8-24 hours after ingestion

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17
Q

Desribe the difference between food poisoning caused by Staph and by C. perfringens.

A

Staph: pre-formed toxin is already in the food

C. perfringens: spores germinate in the body and produce the toxin

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18
Q

How is C. perfringens diagnosed?

A

Clinically, culture to confirm

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19
Q

How is C. perfringens treated?

A

Self-limiting; supportive care only

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20
Q

How is C. tetani spread?

A

Puncture wounds, burns, umbilicus, local germination without necrosis

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21
Q

What is the neurotoxin associated with C. tetani and how does it function?

A

Tetanospasmin; blocks post-synpatic inhibition of spinal motor reflexes (GABA), leading to spasmotic contractions

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22
Q

Describe the clinical presentation of C. tetani.

A

Trismus (lockjaw), risus sardonicus (increased tone of the orbicularis oris), opisthotonus (arm flexion and leg extension), respiratory issues (obstruction, diaphragm)

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23
Q

How does the toxin of C. tetani travel?

A

Inside the axon, ascends

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24
Q

What are the 3 types of tetanus?

A
  1. Localized - rigidity of muscles at site of sporulation (usually precedes generalized)
  2. Cephalic (cranial nerve musculature)
  3. Neonatal (failure of aseptic technique)
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25
Q

How is tetanus diagnosed?

A

Clinically

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26
Q

How is tetanus treated?

A

Human tetanus immunoglobulin, sedation, control of spasms, supportive (airway)

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27
Q

How is tetanus prevented?

A

3 doses of DTaP in infancy and re-vaccination every 10 years

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28
Q

C. botulinum spores are heat resistant and thus are often found in ___.

A

Home canning fruits/vegetables, fish

29
Q

Describe entry of C. botulinum into the human.

A
  1. Preformed toxin from contaminated food

2. Spores in honey (infants)

30
Q

Describe the C. botulinum toxin.

A
  1. Large single polypeptide
  2. Cleaved by bacterial protease
  3. Most potent toxin in nature
  4. Blocks ACh, no transmitter is released, leads to paralysis, can damage synapses permanently
  5. Can travel through axons
  6. Heat labile
31
Q

Describe the clinical presentation of botulism.

A 
1. GI (first symptoms -
 nausea and dry mouth, diarrhea)
2. Descending paralysis (flaccid) beginning from CN III, IV, VI 
3. Afebrile
4. Symmetric neurologic effects
5. Patients i conscious
6. Heart rate is normal
7. No sensory deficits
32
Q

How is botulism diagnosed and what are some differential considerations?

A

Clinically and toxin assays

Myasthenia gravis, Eaton Lambert, tick paralysis, Guillain-Barre’

33
Q

How is botulism prevented and treated?

A

Avoid contaminated food, heat food, anti-toxin, supportive care

34
Q

___ therapy usually precedes disease caused by C. difficile.

A

Antibiotic

35
Q

What are the two toxins associated with C. difficile?

A
  1. Toxin A: enterotoxin, inflammatory response

2. Toxin B: cytotoxic

36
Q

Describe the clinical presentation of C. diff.

A
  1. Pseudomembranous colitis
  2. Diarrhea (water, severe, bloody)
  3. Abdominal pain
  4. Leukocytosis
  5. Fever
  6. Toxic megacolon
37
Q

Describe the BI (Nap1) strain of C. difficile.

A

Increased Toxin A production, higher mortality, especially in elderly people

38
Q

How is C. Diff diagnosed?

A

PCR to amplify the toxin region; detection of toxin A in stool; culture (not routinely recommended); sigmoidoscopy/colonoscopy

39
Q

How is C. diff treated?

A
  1. Stop antibiotics
  2. Metronidazole - mild/moderate (oral preferred)
  3. Vancomycin (oral only)
  4. Fidaxomycin (primary and relapse)
  5. Colon resection
  6. Lactobacillus
  7. Fecal transplant
40
Q

What is caused by C. septicum?

A

Non-traumatic myonecrosis and bacteremia (likely the result of a break in bowel mucosa integrity)

41
Q

What is C. septicum highly associated with?

A

Colon cancer, leukemia

42
Q

C. sordelli is seen in which situations?

A

Abortion (11%), pregnancy (18%), IVDA (22%), other (43%)

43
Q

Profound ___ is observed in C. sordelli; it has a 50-100% mortality.

A

Leukocytosis

44
Q

Describe the characteristics of actinomyces.

A
  1. Gram positive rods
  2. Anaerobic
  3. Non-spore forming
  4. Filamentous hyphae
  5. Sulfur granules (yellow sand colonies)
  6. Non-acid fast
  7. Slow growing
45
Q

Describe the clinical presentation of Actinomyces.

A

Slow-growing, suppurative, oral-associated; cervicofacial, thoracic, pelvic, intra-abdominal

46
Q

How is infection with Actinomyces diagnosed?

A

Culture

47
Q

How is infection with Actinomyces treated?

A

Pencillin is best (can also use clindamycin or erythromycin)

48
Q

Propionobacterium acnes is a slow-growing anaerobe. Is the one of the most common ___.

A

Contaminants of blood cultures

49
Q

Propionobacterium acnes infection is associated with what issues?

A

Infection of prosthetic devices or hardware, opportunitistic infections, and acne

50
Q

What is the treatment for Propionobacterium acnes?

A

Penicillin as well as other agents except metronidazole

51
Q

Were is peptostreptococcus normally found?

A

Normal flora of the mouth, GI tract, pelvis

52
Q

What does peptostreptococcus cause?

A

Contiguous infections intra-abdominally, endometritis, pulmonarily, brain abscess

53
Q

How is peptostreptococcus diagnosed?

A

Culture

54
Q

How is peptostreptococcus treated?

A

Debridement and penicillin, metronidazole, carbapenems, clindamycin

55
Q

What are the features of the Bacteroides fragilis group?

A
  1. Non-spore forming
  2. Non-motile
  3. Requires enriched media to grow
  4. Normal inhabitant of the GI tract (colon) - may provide protection from invasion
56
Q

What is the hallmark pathogenesis of the B. fragilis group?

A

Abscess formation

57
Q

What are the virulence factors of the B. fragilis group?

A
  1. Polysaccharide capsule (adherence, resist phagocytosis, resist T-cell/humoral immunity)
  2. Oxygen tolerance (superoxide dismutase, catalase)
  3. Toxins: defective endotoxin (not associated with sepsis)
58
Q

What infections are associated with the B. fragilis group?

A
  1. Intra-abdominal
  2. Female genital tract
  3. Aspiration pneumonia
  4. Empyema
  5. Otitis media
  6. Brain abscess
  7. SSTIs
59
Q

What are the features of the Prevotella spp?

A
  1. Normal flora of the mouth, GI tract, and pelvis
  2. Gram negative
  3. Obligate anaerobes
  4. Require enriched media (with blood)
  5. Non-motile
  6. Non-encapsulated
  7. Unknown virulence
60
Q

What is the pathogenesis of Prevotella spp.?

A

Abscess formation

61
Q

What infections are caused by Prevotella spp?

A
  1. Female genital tract infections (P. bivia, P. disiens)
  2. Oral and pleuropulmonary infections (p. oris, P. buccae, P. oralis)
  3. Oral cavity, UG, GI tract (P. melaninogenica, P. corporis, P. denticola, P. intermedia, P. loescheii, P. nigrescens)
62
Q

What infections are caused by Porphyromonas spp?

A
  1. Oral

2. Periodontal

63
Q

What infections are caused by F. nucleatum?

A
  1. Aspiration pneumonia
  2. Lung abscess
  3. Empyema
  4. Chronic liver abscess
64
Q

What infections are caused by F. necrophorum?

A
  1. Lemierre’s syndrome
  2. Post-anginal sepsis
  3. Widespread metatstatic infection
65
Q

What is the important virulence factor of F. necrophorum?

A

Potent endotoxin

66
Q

What are the most actives antibiotics for bacteroides?

A
  1. Metronidazole
  2. Ampicillin/sulbactam
  3. Piperacillin/tazobactam
  4. Carbapenems
  5. Chloramphenicol
67
Q

What antibiotics used to be active against bacteroides?

A

Cefoxitin, clindamycin, piperacillin

68
Q

What are the most active antibiotics for fusobacterium?

A
  1. Metronidazole
  2. Ampicillin/sulbactam
  3. Piperacillin/tazobactam
  4. Clindamycin
  5. Cefoxitin

Some activity: piperacillin, penicillin

69
Q

What are the most active antibiotics for peptostreptococcus?

A
  1. Penicillin
  2. Clindamycin
  3. Ampicillin/sulbactam
  4. Piperacillin/tazobactam
  5. Metronidazole (some are resistant)

MHD 1 (58 decks)

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