SSTIs Flashcards

1
Q

Purulent SSTIs

A
  • Impetigo
  • Cutaneous abcesses
  • Inflamed epidermoid cysts
  • Furuncles
  • Carbuncles
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2
Q

What is Impetigo?

A
  • Highly contagious infection of epidermis
  • Typically transmitted through direct contact
  • Occurs most commonly in children
  • Most frequently affects face and extremities
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3
Q

What are the two types of Impetigo?

A

Nonbullous (~70% of cases)
Bullous

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4
Q

What are the predisposing factors of Impetigo?

A
  • Group A Strep skin colonization or S. aureus nasal colonization.
  • Hot, humid summer weather
  • Areas with poor hygiene and in crowded living conditions
  • Minor trauma (insect bite, abrasion)
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5
Q

What is Nonbullous Impetigo?

A
  • Caused by: Strep pyogenes (Group A) or Staph aureus
  • Small, fluid filled vesicles → pustules → pustules rupture → golden yellow crusts over an erythematous base
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6
Q

What is Bullous Impetigo?

A
  • Caused by: Staphylococcus aureus
  • Vesicles → bullae with clear, yellow fluid → bullae rupture, forming thin, light brown crusts
  • Usually affects neonates and children < 5 yo
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7
Q

Ecthyma

A
  • Ulcerative form of impetigo causing painful fluid- or pus-filled sores; heals with scarring
  • Requires abx tx
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8
Q

Topical Treatment of Impetigo

A
  • Topical therapy is as effective as systemic therapy
  • Mupirocin or retapamulin applied to lesions
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9
Q

Duration of Topical Treatment of Impetigo

A

5 days

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10
Q

Systemic Treatment of Impetigo (suspicion or confirmation of MRSA)

A
  • Clindamycin
  • Doxycycline
  • TMP/SMX
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11
Q

Systemic Treatment of Impetigo (no suspicion of MRSA)

A
  • Dicloxacillin
  • Cephalexin
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12
Q

Duration of Systemic Treatment of Impetigo

A

7 days

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13
Q

What is Folliculitis?

A
  • Pyoderma located within hair follicles
  • Small (<5mm), erythematous (sometimes pruritic) papules usually covered by central pustule
  • Develops in areas of friction and perspiration (armpits, groin, etc.)
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14
Q

What are the causative organisms of Folliculitis?

A
  • S. aureus (most common)
  • P. aeruginosa (swimming pools, hot tubs, whirlpools)
  • Candida spp (prolonged antibiotics or corticosteroids)
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15
Q

What is the treatment for Folliculitis?

A
  • Saline compresses (promotes drainage)
  • Topical therapy with antibacterials or antifungals sufficient
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16
Q

What are Furuncles (Boils)?

A
  • Deep inflammatory nodule that typically develops from preceding folliculitis.
  • Lesions often rupture and drain spontaneously
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17
Q

What is the treatment for Furuncles?

A

Application of moist heat to promote drainage

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18
Q

What are Carbuncles?

A
  • When infection extends to involve several adjacent follicles producing a coalescing inflammatory mass with pus draining from multiple follicular orifices.
  • Progression from furuncles
  • Typically found at nape of neck, face, armpits, buttocks
  • Fever and malaise usually present
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19
Q

What is the causative organism of Furuncles and Carbuncles?

A

S. aureus

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20
Q

What are the predisposing factors for Furuncles and Carbuncles?

A
  • Diabetes, obesity
  • Inadequate personal hygiene
  • Close contact with others with furuncles
  • Anterior nares colonization with S. aureus (recurrent cases)
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21
Q

What is the treatment for Furuncles and Carbuncles?

A
  • Incision and drainage (I&D)
  • Systemic antibiotics rarely required unless fever or multiple furuncles/carbuncles
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22
Q

Causative Organism of Cutaneous Abcesses and Inflamed Epidermoid Cysts

A

S. aureus

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23
Q

Treatment of Cutaneous Abcesses and Inflamed Epidermoid Cysts

A
  • Incision and evacuation of pus and debris
  • Systemic antibiotics usually NOT recommended
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24
Q

When to use systemic abx for purulent SSTI

A
  • Systemic signs of infection (fever, etc.)
  • Multiple abcesses
  • Lack of response to I & D
  • Immunocompromised
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25
Q

Duration of Systemic Abx Therapy for Purulent SSTI

A

5 days

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26
Q

When is MRSA coverage warranted for purulent SSTI?

A
  • Long-term care facility
  • IV drug abuse
  • HIV
  • MSM
  • Incarceration
  • Military
  • Native American
  • Sharing razors or sports equipment
  • History of MRSA infection/colonization
  • Current MRSA infection elsewhere
  • Failed initial abx therapy
  • Penetrating trauma
  • Markedly impaired host defenses
  • Severe infection with systemic sxs and/or hypotension
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27
Q

Duration of Therapy for Purulent SSTI if concern for MRSA

A

5-7 days

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28
Q

PO Antibiotics for MSSA Purulent SSTI

A
  • Dicloxacillin
  • Cephalexin
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29
Q

IV Antibiotics for MSSA Purulent SSTI

A
  • Nafcillin/Oxacillin
  • Cefazolin
  • Clindamycin (if pt has beta-lactam allergy)
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30
Q

PO Antibiotic Therapy for MRSA Purulent SSTI

A
  • Doxycycline
  • TMP/SMX
  • Clindamycin (need to do D-test first to check susceptibility)
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31
Q

IV Antibiotics for MRSA Purulent SSTI

A
  • Vancomycin (DOC)
  • Linezolid
  • Ceftaroline
  • Daptomycin
  • Oritavancin (preferred for outpatient)
  • Dalbavancin (preferred for outpatient)
  • Tedizolid
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32
Q

Treatment of Recurrent S. aureus SSTI

A
  • Nasal decolonization: Mupirocin 2% intranasal x 5-10 days
  • Topical decolonization: Chlorhexidine or bleach bath
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33
Q

What is Cellulitis?

A
  • Acute, spreading infection of skin that involves epidermis and dermis.
  • Local tenderness/pain, swelling, warmth, erythema
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34
Q

What is the location of Cellulitis?

A

Commonly on lower legs

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35
Q

What are the systemic manifestations of Cellulitis?

A

Fever, tachycardia, confusion, hypotension, leukocytosis

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36
Q

Erysipelas

A

Superficial form of cellulitis with clearly defined borders of inflammation

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37
Q

What are the predisposing factors for Cellulitis?

A
  • Previous trauma (laceration, puncture wound)
  • Conditions that cause skin to be more fragile or local host defenses less effective (obesity, diabetes, previous cutaneous damage, edema (from venous insufficiency or lymphatic obstruction), surgical procedures, eczema)
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38
Q

Common Pathogens Causing Cellulitis

A
  • S. pyogenes (Group A) - most common
  • S. aureus
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39
Q

How to Differentiate Between Cellulitis Caused by S. pyogenes or S. aurues

A

S. aureus infection usually has pus, purulence, or abcess

S. pyogenes infection does not

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40
Q

Diagnosis of Cellulitis

A
  • Done by physical exam
  • Routine diagnostic testing NOT recommended
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41
Q

Symptoms of Mild Cellulitis

A
  • No purulence
  • No systemic sxs, AMS, or hemodynamic instability
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42
Q

Treatment of Mild Cellulitis

A
  • Outpatient tx
  • Penicillin
  • Augmentin
  • Cephalexin
  • Clindmycin (if beta-lactam allergy)
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43
Q

Signs/Symptoms of Mederate-Severe Cellulitis

A
  • Deeper infection
  • Poor adherence
  • Systemic sxs
  • Failed outpatient therapy
  • Immunocompromised
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44
Q

Treatment of Moderate-Severe Cellulitis

A
  • Inpatient tx
  • Penicillin IV
  • Cefazolin or ceftriaxone
  • Clindamycin (if beta-lactam allergy)
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45
Q

Duration of Cellulitis Treatment (regardless of severity)

A

5 days

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46
Q

When is MRSA coverage indicated for cellulitis?

A
  • Penetrating trauma
  • Evidence of MRSA infection elsewhere
  • Nasal colonization with MRSA
  • Injection drug use
  • Purulent drainage
  • Severe infection (necrotizing)
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47
Q

PO Treatment for MRSA Cellulitis

A
  • TMP/SMX
  • Doxycycline
  • Clindamycin
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48
Q

IV treatment for MRSA Cellulitis

A
  • Vancomycin (DOC)
  • Linezolid
  • Daptomycin
  • Ceftaroline
  • Tigecycline
  • Telavancin
  • Tedizolid
  • Oritavancin
  • Dalbavancin
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49
Q

Cellulitis Treatment if Coverage for Strep and MRSA Needed

A
  • Clindamycin
  • TMP/SMX + Beta-Lactam
  • Doxycycline + Beta-Lactam
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50
Q

Non-Medication therapy for Cellulitis

A

Elevation of affected area

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51
Q

Adjunctive Treatment for Cellulitis

A

Systemic corticosteroids x 7 days in non-diabetic adults

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52
Q

Recurrent Cellulitis

A
  • 2+ discrete SSTIs over a 6 month period
  • 3-4 SSTIs/year
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53
Q

Prophylactic antibiotics for Recurrent Cellulitis

A
  • Penicillin V
  • Erythromycin
  • Benzathine penicillin
54
Q

Duration of Cellulitis Prophylaxis

A

Continue therapy for as long as predisposing factors are present

55
Q

What is some general information about Bite Wounds?

A
  • Most bites are due to dogs or cats
  • Cat bite wounds are usually more severe and have higher proportion of osteomyelitis and septic arthritis
  • Human bite wounds are typically more serious than animal bites
  • Predominant pathogens: oral flora, skin flora
56
Q

What are the complications caused by bite wounds?

A

Septic arthritis, osteomyelitis, subcutaneous abscess formation, tendonitis, bacteremia (rarely)

57
Q

What is the bacteriology of Dog/Cat bite wounds?

A
  • Pasteurella - most common
  • Capnocytophaga canimorsus: causes bacteremia and fatal sepsis especially in asplenia or underlying hepatic disease patients
58
Q

What is the bacteriology of Human bite wounds?

A
  • Strep (esp. viridans)
  • Staph
  • Eikenella corrodens - most common
  • Anaerobes present in > 60% of cases
59
Q

What are some vaccines that can be used for Bite Wounds?

A

Tetanus. Rabies (for all feral, wild animal bites, areas with high prevalence of rabies)

60
Q

Drug of Choice for Treatment of Bite Wounds

A

Beta-lactam + Beta-lactamase inhibitor

  • Augmentin
  • Ampicillin/sulbactam
  • Piperacillin/tazobactam
61
Q

When should IV therapy be used for bite wounds?

A
  • Failed initial oral abx
  • Bite involves hand, head, joint
  • Presence of lymphatic spread
62
Q

Bite Wound Treatment (beta-lactam allergy)

A

2nd or 3rd generation cephalosporin, TMP/SMX, levofloxacin, ciprofloxacin

PLUS

Metronidazole

OR

Single-Agent Options: carbapenem, moxifloxacin, doxycycline

63
Q

Duration of Treatment for Bite Wounds

A

5 days

64
Q

What should be avoided in the treatment of Bite Wounds?

A

1st generation CEPHs and Penicillinase-Resistant PCNs (oxacillin, nafcillin, dicloxacillin), Macrolides, Clindamycin

65
Q

Wound closure for Bite Wounds

A

Wound closure is NOT recommended unless affected area involves face

66
Q

What are Necrotizing Skin and Soft Tissue Infections?

A
  • Aggressive subcutaneous infection of the fascial and/or muscle compartments
  • Can cause major tissue destruction and death
  • Usually develops from an initial skin break from trauma or surgery
  • Life threatening emergency - requires surgery and broad spectrum abx
67
Q

What are the clinical features of Necrotizing Fasciitis

A
  • Severe pain disproportional to clinical findings
  • Hard, wooden feel of subcutaneous tissue
  • Crepitus (including gas in tissue)
68
Q

Type II (Monomicrobial) Necrotizing Fasciitis

A
  • Commonly affects lower extremities
  • Common cause: S. pyogenes
69
Q

Type I (Polymicrobial) Necrotizing Fasciitis

A
  • Common in IV drug users (at injection site)
  • Originates from bowel or genitourinary flora
  • Polymicrobial: average of 5 pathogens per wound
70
Q

Diagnosis of Necrotizing Fasciitis

A
  • Definitive diagnosis via surgical exploration
  • Culture and gram stain of deep tissue sample from surgery
71
Q

Treatment of Necrotizing Fasciitis

A

Emergent surgery intervention followed by debridement every 24-36 hours

72
Q

Empiric Therapy for Nectrotizing Fasciitis

A
  • Broad spectrum (including MRSA and anaerobes)
  • Vanco PLUS piperacillin/tazobactam (or carbapenem)
73
Q

Directed Therapy for Necrotizing Fasciitis (Strep)

A

PCN + clindamycin

74
Q

Directed Therapy for Necrotizing Fasciitis (Staph)

A
  • MSSA: 1st generation cephalosporin or oxacillin
  • MRSA: Vanco
75
Q

Duration of Treatment for Necrotizing Fasciitis

A

Until debridement is no longer necessary

76
Q

Clinical Features of Infectious Gangrene

A
  • Gas production leading to crepitus
  • Muscle necrosis
  • Progression within hours
77
Q

What is Trauma-Associated Clostridial Gas Gangrene?

A
  • C. perfringens most frequent cause
  • Skin initially pale –> bronze –> purplish red.
  • Signs of systemic toxicity: tachycardia, fever, diaphoresis –> shock and multiple organ failure
78
Q

What is Spontaneous Clostridial Gas Gangrene?

A
  • C. septicum most frequent cause
  • Neutropenic and GI malignancy patients
79
Q

Diagnosis of Infectious Gangrene

A

Diagnosis by surgical exploration during emergent debridement

80
Q

Treatment of Infectious Gangrene

A

Emergent surgical debridement + appropriate abx

81
Q

Empiric Antibiotic Therapy for Infectious Gangrene

A
  • Broad spectrum (including MRSA and anaerobes)
  • Vanco PLUS piperacillin/tazobactam
82
Q

Directed Antibiotic Therapy for Infectious Gangrene (Clostridial)

A

PCN + Clindamycin

83
Q

What are the general characteristics of Diabetic Foot Infections?

A

Usually arise from a skin ulceration that occurs as a consequence of peripheral neuropathy or wound from trauma

84
Q

Risk Factors for Diabetic Foot Infections

A
  • Peripheral neuropathy
  • Peripheral vascular disease
  • Poor glycemic control
  • Foot deformities
  • Ulcer present > 30 days
  • History of recurrent foot infections
  • Previous lower extremity amputation
  • Walking barefoot
85
Q

Diagnosis for Diabetic Foot Infections

A

Purulent secretions OR

2 classic signs or symptoms of inflammation: erythema, warmth, tenderness, pain, or induration

Definitive Diagnosis: culture and sensitivity

MRI to rule out abscess or osteomyelitis

Labs - WBC, ESR, CRP, Procal

86
Q

What organisms cause the acute/superficial (typically monomicrobial) diabetic foot infections?

A
  • S. aureus
  • S. epidermidis
  • Beta-hemolytic strep (Group A, B, C, G)
87
Q

What organisms cause chronic/deep (typically polymicrobial) diabetic foot infections?

A
  • S. aureus
  • Strep
  • Enterococcus
  • Enterobacteriaceae
  • Pseudomonas
  • Anaerobes
88
Q

What organisms cause necrosis, gangrene, or malodorous drainage in diabetic foot infections?

A
  • Anaerobic Strep
  • Bacteroides
  • Clostridium
89
Q

Mild Diabetic Foot Infection

A
  • Local infection
  • Erythema 0.5-2 cm
90
Q

Moderate Diabetic Foot Infection

A
  • Local infection
  • Erythema > 2 cm
  • Deeper infections
91
Q

Severe Diabetic Foot Infection

A

Local infection with systemic signs of infection

92
Q

Diabetic Foot Infections Requiring Hospitalization

A
  • Severe infection
  • Moderate infection with complicating features (severe PAD, poor social support)
  • Poor compliance with or failing outpatient therapy
93
Q

Treatment of Diabetic Foot Infections

A

Debridement, proper wound care, + appropriate abx

94
Q

Uninfected diabetic foot ulcers

A

Avoid antibiotic use

95
Q

Mild-moderate diabetic foot infections

A
  • Narrow spectrum agent: aerobic GPC coverage
  • High bioavailability PO agents may be sufficient (Augmentin)
96
Q

Severe or chronic diabetic food infections

A
  • Broad spectrum agents: GPC (+MRSA), GNR, anaerobes
  • Vanco PLUS Zosyn, Carbapenem, Cefepime, Ceftazidime, or Aztreonam
  • Parenteral therapy (may switch to PO when stable)
97
Q

Duration of treatment be for mild diabetic foot infections

A

1-2 weeks

98
Q

Treatment duration for moderate-severe diabetic foot infections

A

2-3 weeks

99
Q

Wound care for diabetic foot infections

A
  • Dressed in a manner that allows daily inspection and encourages a moist wound-healing environment.
  • Removal of pressure from foot wound is necessary for healing.
  • Accuzyme: topical debriding agent
100
Q

Need for surgery with diabetic foot infections

A

-I/D of necrotic tissue

Revascularization of lower extremity

-Urgent amputation for extensive necrosis or life-threatening infection

101
Q

What is Osteomyelitis?

A
  • Progressive infectious process that can involve one or multiple components of bone
  • Characterized by inflammatory destruction of bone, necrosis, and new bone formation
102
Q

Signs and Symptoms of Osteomyelitis

A
  • Dull pain at involved site
  • Local inflammation (tenderness, warmth, erythema, swelling)
  • Systemic symptoms may be present
103
Q

Cierny and Mader Stage 1

A
  • Medullary: likely seen on MRI
  • Hematogenous seeding
  • Can be treated with antimicrobial therapy alone
104
Q

Cierny and Mader Stage 2

A
  • Superficial
  • Contiguous spread
  • Requires surgical intervention + systemic abx
105
Q

Cierny and Mader Stage 3

A
  • Localized
  • Hematogenous or contiguous
  • Requires surgical intervention + systemic abx
  • Resection required
106
Q

What is Cierny and Mader Stage 4?

A
  • Diffuse osteo
  • Requires surgical intervention + systemic abx
  • Resection required
107
Q

How is Osteomyelitis diagnosed?

A

Confirmation by imaging studies +/- growth of microorganism from bone biopsy or surgical sampling

108
Q

What labs are abnormal in Osteomyelitis?

A

ESR and CRP elevated

109
Q

What imaging studies are done for Osteomyelitis?

A

X-ray: quickest

MRI: gold-standard

110
Q

Acute Osteomyelitis

A
  • Onset: days to weeks
  • Necrotic bone usually absent
111
Q

Chronic Osteomyelitis

A
  • Onset: weeks to months (may persist for years)
  • Necrotic bone present
112
Q

Age of Onset for Contiguous Osteomyelitis

A

Adults > 50 yo

113
Q

What is the age of onset like for Osteomyelitis due to vascular insufficiency?

A

Adults > 40 years

114
Q

What is the age of onset like for Hematogenous Osteomyelitis?

A

Mostly in children (age < 20 yrs), adults > 50 yrs

115
Q

Sites of Infection in Contiguous Osteomyelitis

A

Femur, tibia, skull, mandible

116
Q

What are the sites of infections for Contiguous Osteomyelitis?

A

Femur, tibia, skull, mandible

117
Q

What are the sites of infections for Hematogenous Osteomyelitis?

A

Long bones (tibia and femur) in children

Vertebrae (spondylodiskitis) in adults

118
Q

What are the risk factors for Contiguous Osteomyelitis?

A
  • Trauma
  • Surgery
  • Insertion of joint prosthesis
  • Cellulitis
119
Q

What are the risk factors for Osteomyelitis due to vascular insufficiency?

A
  • DM > 10 yrs
  • Poor glucose control
  • Peripheral neuropathy
  • Peripheral vascular disease
120
Q

What are the risk factors for Hematogenous Osteomyelitis?

A

Bacteremia or endocarditis

121
Q

What are the typical microorganisms that cause Contiguous Osteomyelitis?

A

Usually polymicrobial

Most common: S. aureus

122
Q

What are the typical microorganisms that cause Osteomyelitis due to vascular insufficiency?

A

Usually polymicrobial

Most common: S. aureus and Beta-Hemolytic Strep

123
Q

What are the typical microorganisms that cause Hematogenous Osteomyelitis?

A

Usually monomicrobial

Neonates: S. aureus, Group B Strep, E. coli

Children: S. aureus and S. pneumoniae

Adults: S. aureus and S. epidermidis

Elderly: GNRs

IVDU: P. aeruginosa

124
Q

Duration of Antimicrobial Therapy for Osteomyelitis (no surgical intervention)

A

At least 6 weeks of IV abx

125
Q

Duration of Antimicrobial Therapy for Osteomyelitis (following radical resection of infected tissue of diabetic foot osteomyelitis)

A

2-5 days

126
Q

Duration of Antimicrobial Therapy for Osteomyelitis (persistent infected or necrotic bone)

A

At least 4 weeks

127
Q

Duration of Antimicrobial Therapy for Osteomyelitis (acute, hematogenous infection)

A

At least 4-6 weeks of IV abx

128
Q

Duration of Antimicrobial Therapy for Osteomyelitis (chronic infection)

A

Months (IV followed by PO)

129
Q

What is the treatment for Hematogenous osteomyelitis like?

A
  • S. aureus: cefazolin or oxacillin
  • MRSA or S. epidermidis: Vancomycin
  • GNB: 3rd gen ceph
130
Q

What is the treatment for Contiguous or vascular insufficiency osteomyelitis like?

A
  • Polymicrobial: Pip/tazo OR 3rd gen ceph + metronidazole or clindamycin
  • Pseudomonas coverage: Pip/tazo, Ceftazidime or cefepime, Ciprofloxacin