Skin and Soft Tissue Infections

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skin, soft tissue, bone and joint, prosthetics and animal bites

Last updated 12:18 AM on 10/4/26
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89 Terms

1
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What are the usual pathogens in SSTIs?

S. aureus and S. pyogenes

2
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What is the drug of choice for treating SSTI that is caused by GAS?

Penicillins BUT only if we are targetting GAS alone.

3
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T/F: Empirically we will be covering for both staph and strep.

True

4
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What are our oral options for treating MSSA SSTIs?

  • amox/clav

  • dicloxacillin

  • cephalexin


5
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What is an IV option for treating MSSA SSTIs?

Cefazolin

6
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What are our oral options for treating MRSA SSTIs?

  • doxycycline

  • TMP/SMX

  • Linezolid


7
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What happens when we use doxycycline in treating SSTIs?

We lose our GAS coverage and often need to add another agent to cover for it.

8
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Why don’t we use clindamycin for SSTI?

Resistance in staph is increasing and its just a bad choice empirically

9
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What are the major side effects we need to be aware of with Amox/clav?

GI (diarrhea) and hypersensitivity

10
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What are the major side effects we need to be aware of with Cephalexin/Cefazolin?

allergic reactions

11
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What are the AE we need to be aware of with doxycycline?

Photosensitivity and chelation DDIs

12
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What are the AE we need to be aware of with TMP/SMX?

Rash, allergic reactions, hyperkalemia

13
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What are the AE we need to be aware of with Linezolid and what should we do about it?

Thrombocytopenia, we should monitor platelets if our duration of therapy is going to be >7 days.

14
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T/F: we will not be using FQs in this disease state

True, basically never.

15
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What are signs and symptoms of Impetigo?

Red papules or bumps that will rapidly evolve into vesicles containing clear fluid and pustules that contain pus. They will then rupture and the dried discharge will form honey-colored scabs on the base of papules.

16
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What are the main players in Impetigo?

Strep pyogenes (usually) and also s. aureus.

17
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How do we treat Impetigo?

Topical mupirocin

18
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What do we do if the impetigo becomes extensive and outbreak worthy>

Switch to oral antibiotics for 5-7 days.

19
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What is Ecythema?

A form of impetigo that causes ulcers to form deeper in the dermis. They look punched out and sometimes contain pus.

20
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How do we treat Ecythema?

Oral antibiotics targeting GAS and S. aureus for 5-7 Days

21
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What are furuncles?

Infections of the hair follicle leading to a small abscess.

22
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What are carbuncle?

Several furuncles fused into a single inflammatory mass.

23
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How do we treat furuncles and carbuncles?

Incision and Drainage (I&D).

24
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What are abscesses?

Deeper collections of pus within dermis and deeper skin tissues.

25
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How do we treat abscesses?

I&D AND oral antibiotics that will target MRSA and S. pyogenes for 5 days.

26
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T/F: We treat abscesses after we get cultures and focus on definitive therapy

False, we treat empirically.

27
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What are erysipelas?

Superficial skin infection limited to the upper dermis,

28
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What is the key player in erysipelas?

S. pyogenes

29
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What is the difference between erysipelas and cellulitis in terms of inflammation??

Erysipelas has more defined borders.

30
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How long do we treat Erysipelas?

5-7 days of antibiotics

31
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What is cellulitis?

An infection of the epidermis, deeper dermis and SQ fat layer. Lesions are usually hot, painful and red, with non-elevated, poorly defined margins.

32
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What are the main players in cellulitis?

S. pyogenes and S. aureus

33
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How do we track control of cellulitis?

After starting a patient on antibiotics, we can draw a line around the edge to track if redness, swelling and warmth are expanding.

34
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How long do we wait for lack of expansion and if it doesn’t occur what do we do in cellulitis?

We should see a lack of expansion at ~48-72h and if not, we need further examination.

35
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What is severe cellulitis?

failure of oral antibiotics or irrigation and debridement as well as systemic symtpoms.

36
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What are the systemic symptoms that would contribute to severe cellulitiis?

Fever, tachycardia, tachypnea, leukocytosis

37
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Which population of cellulitis should we get site of infection and blood cultures?

Severe

38
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T/F: In severe cellulitis, IV therapy is often indicated.

True

39
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When targeting MSSA in severe cellulitis, what do we use?

Cefazolin

40
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When targeting MRSA in severe cellulitis, what do we use?

Vancomycin but we can also use alternatives such as dapto, linezolid and dalbavancin

41
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When should we employ MRSA coverage in severe cellulitis, should we do it all the time?

NO, only when there is sepsis or septic shock going on or in a risk factor for MRSA i.e is purulent, previous MRSA infection, etc.

42
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How long do we treat cellulitis for as a standard in uncomplicated states?

5 days

43
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How long do we treat cellulitis for if IV therapy was started and the patient is showing delayed response?

Extend to 10 days

44
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If we start on IV therapy for cellulitis, can we step down to oral treatment?

Yes if there is rapid response/improvement.

45
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Should we be going longer than 10 days of therapy for cellulitis?

Only if there is bone and joint involvement, we then go up to weeks.

46
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When should we reassess response in all cellulitis?

48h

47
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What is necrotizing fasciitis?

A deep infection involving the fascial later and potentially muscle compartments.

48
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What is the initial presentation of necrotizing fasciitis?

Often presents like cellulitis

49
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What are the systemic signs of infection of necrotizing fasciitis?

After progressing, it will include high temperatures, sepsis/shock, disorientation and lethargy.

50
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What are the key players in necrotizing fasciitis?

S. pyogenes, s. aureus, V. vulnificus, A. hydrophila

51
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T/F: Necrotizing fasciitis is only monomicrobial

False it can be mono or polymicrobial

52
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What are the key pathogen in gas gangrene?

Clostridium perfringens

53
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What is gas gangrene often associated with?

Traumatic injuries

54
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What two key principles of treating necrotizing fasciitis should we do?

  1. EMPIRIC BROAD SPECTRUM THERAPY with later narrowing based on culture results (wound and blood)

  2. SURGICAL INTERVENTION


55
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What are our empiric regimens and what will we need to cover upfront for necrotizing fasciitis?

We need to cover MRSA, Gram (-) and anaerobes.

- Linezolid + Pip/tazo OR

  • Vanco + Pip/tazo (or Cefepime/Metro combination) + Clindamycin or linezolid


56
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What is our definitive option for clostridial necrotizing fasciitis and gas gangrene?

Clindamycin + Penicillin

57
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What if we get a mixed organism culture in necrotizing fasciitis and gas gangrene?

We need to tailor our broad spectrum therapy to the most definitive one that will also cover the organisms.

58
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What is the most common pathogen in necrotizing fasciitis and why is it unique to the disease state?

S. pyogenes and because a lot of the damage is done by toxin production of strep.

59
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Based on the nature of infection in necrotizing fasciitis with GAS, what was historically the treatment of choice and why don’t we use it anymore?

Penicillin PLUS clindamycin for the toxin suppression effect. Now, GAS exhibits high rates of resistance to clindamycin.

60
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What do we use now for both EMPIRIC and DEFINITIVE management of GAS necrotizing fasciitis? (STANDARD)

Linezolid

61
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What are diabetic foot ulcers?

A complication of diabetes.

62
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T/F: We should always treat diabetic foot ulcers.

False, we only should treat with antibiotics if signs of infection are present (local include redness, swelling, warmth, pus, tenderness/pain or systemic think septic presentation).

63
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Even though pathogens vary wildly in diabetic foot ulcers, what is the most predominant?

Gram positive organisms including MRSA.

64
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As the diabetic ulcers progress and get deeper, what other pathogens can we expect to see?

EPK gram negatives and potentially anaerobes.

65
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T/F: We always should get a deep culture of an infected diabetic foot ulcer.

True because our pathogen can be just about anything.

66
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Empirically, what do we use in the treatment of diabetic foot ulcers?

Vancomycin ± Ceftriaxone is an example but we really want to cover a lot of pathogens so many regimens are used.

67
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Do we always target pseudomonas in diabetic foot ulcers?

No, it’s only included in patients with a history of p. aeruginosa infection, those who are/were in subtropical climates or those who are septic.

68
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How long do we treat diabetic foot ulcers for?

  • Mild infection: 1-2 weeks

  • Moderate-Severe infection: 2-4 weeks

  • Osteomyelitis (bone involvement): 4-6 weeks


69
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T/F: In diabetic foot ulcers we must treat until the ulcer fully heals.

False, we only need to treat until the infection resolves.

70
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Why do we sometimes see bone infections more in pediatric patients?

If they have bacteremia (in the blood) it can be delivered to the bone in a way because of enhanced blood flow as kids are still growing.

71
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What are some other secondary causes of bone infections?

Progression of skin infections most commonly in those with deep diabetic foot ulcers or bed sores.

72
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What are the most common pathogens in bone and joint infections?

S. aureus, s. epidermidis, s. pyogenes

73
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T/F: Anything can be a player in bone and joint infections.

True

74
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What is the general treatment paradigm for bone and joint infections?

We use IV therapy to start but if we can use Linezolid, TMP/SMX or doxy and FQs instead we can. We can also using dalbavancin where two doses will provide an entire course.

75
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How long do we treat joint infections?

Generally 3 weeks, can be 4 in pseudomonas and 6-12 for prosthetics

76
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How long do we treat ostomyelitis (bone) infections?

4-6 weeks generally but if pseudomonas we extend to 6 weeks.

77
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Will we add on fluoroquinolones or ags for pseudomonal treatment of bone and joint infections?

NO, the IV B lactam is ENOUGH!

78
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Can we step down to FQs if the patient is responding to IV B lactam therapy in bone and joint infections?

Sure

79
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What pathogen loves to form biofilms on prosthetics?

Staph aureus

80
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What drug will we most commonly add-on to Cefazolin or Vanco with a s. aureus prosthetic infection?

Rifampin

81
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Will we ever use rifampin monotherapy? Why?

NO because it is bad as monotherapy due to lots of resistance with single point mutations. Basically only good for adding on for biofilm penetration

82
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What concerns do we have with rifampin?

MANY DDIs with CYP, and AE of hepatotoxicity and red stained bodily fluids.

83
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If we have a septic arthritis infection due to N. gonnorhoeae, what drug do we use?

Ceftriaxone

84
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With animal bites, what is the key pathogens we need to cover for?

Pasturela Multicoda (MAIN), s. aureus, s. pyogenes, anaerobes

85
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What are the standard oral and IV therapies for animal bites?

Oral: Amox/clav

IV: Amp/Sul

86
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What are alternatives we can use if the patient is allergic to penicillins in animal bites?

Doxycycline or Moxifloxacin

87
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Who gets antibiotics in animal bite setting?

Anyone who is infected and thos needing prophylaxis: deep puncture (basically all cat bites), mod-severe injury with a crush wound, on the hand face or genitalia, near prosthetics, involves the bone or joint and if they are immunocompromised.

88
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How long do we treat infected animal bite patients?

5-7 days

89
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How long do we treat patients for animal bite prophylaxis?

3-5 days