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Applied Pathophysiology > Skin & Soft Tissue Infections (SSTIs) > Flashcards

Skin & Soft Tissue Infections (SSTIs) Flashcards

1
Q

Bacterial skin infections are classified as:

A
  • Primary: areas of previously HEALTHY skin
  • often caused by a single pathogen
  • MONOmicrobial
  • Secondary: areas of DAMAGED skin
  • often POLYmicrobial (many pathogens)
  • i.e. 1 antimicrobial may not be sufficient

(typ. cutaneous layer)

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2
Q

Soft tissues =

A

tissues that connect, support, or surround other structures and organs of the body
- once infection gets in these delicate areas it can spread & can lead to amputation

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3
Q

SSTIs are also classified as:

A

uncomplicated and complicated

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4
Q

Complicated infections involve:

A

deeper skin structures (eg. fascia (CT that lines all areas), muscle layers)
* need surgical interventions (esp. if damage becomes too severe - may need amputations)
* Occurs frequently in patients with wounds or compromised immune functions (eg. diabetes, HIV infection)

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5
Q

Other categories that are crucial for successful SSTI treatment are the differentiation of:

A
  • purulent vs non-purulent
  • Suspicion of necrotizing fasciitis (NF)
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6
Q

Purulent vs non-purulent:

A
  • consisting of, containing, or discharging pus (composition of WBCs, damaged tissue, infectious agents, etc. - body is trying to fight/remove)
  • Abscess: painful collection of pus, usually caused by a bacterial infection
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7
Q

Abscess:

A

painful collection of pus, usually caused by a bacterial infection

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8
Q

Necrotizing fasciitis (NF):

A

is the death of cells in tissues or organs caused by an infection
- want to avoid & is the worst case scenario - complicated treatment
- won’t get proper BF

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9
Q

SSTIs are the most common infections seen in…

A

community and hospital settings
* Most are treated in an outpatient setting, making it difficult to accurately quantify community-acquired SSTIs
* Most common among those 70 years of age and older (but some target children)
* Community acquired (CA)–MRSA is on the rise
* In US and Canada almost half (46%) of all culture-positive SSTIs are caused by MRSA
- tend to form outbreaks & more complicated to treat

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10
Q

What is the SSTIs etiology?

A
  • Most SSTIs are caused by Gram-POSITIVE organisms present on the skin surface
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11
Q

Approximately 30% to 35% of healthy individuals are reported to be colonized with ______ on the skin or in the anterior nares

A

S. aureus
(may not become a problem, but could be carrying it)

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12
Q

_________ species, can be found in moist intertriginous areas (eg. groin, toes, axilla)

A

Acinetobacter

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13
Q

______ and _______ are the top 2 most frequent CA SSTIs

A

S. aureus and S. pyogenes (in primary infections)

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14
Q

What is the common skin flora (already populating)?

A

Gram-POSITIVE bacteria
* Coagulase-negative Staphylococci
* Streptococci
* Micrococci (Micrococcus luteus)
* Corynebacterium species
(diphtheroids)
* Propionibacterium species

Gram-NEGATIVE bacteria
* Acinetobacter species

FUNGI
Malassezia species Candida species

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15
Q

5 Risk factors for developing SSTIs:

A
  1. DAMAGE TO THE EPIDERMAL LAYER allowing for bacterial
    penetration
  2. HIGH CONCENTRATIONS OF BACTERIA > 10^5 microorganisms
    - hard to be sterilant b/c they are also protecting since birth
    - less wastes can cause more
  3. EXCESSIVE MOISTURE of the skin
    - in more tropical areas
  4. INADEQUATE BLOOD SUPPLY
    - therefore, produce less WBCs that can help defend infections
  5. AVAILABILITY OF bacterial NUTRIENTS
    - too much of nutrients from bath products for ex can be bad/too much
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16
Q

What are other risk factors for SSTI’s (aside from the 5)

A
  • Other risk factors are co-morbidities: obesity, diabetes, disabilities limiting movement, heart problems
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17
Q

Folliculitis:

A

is inflammation of the hair follicle
* SUPERFICIAL (surface level) infection with pus present only in the epidermis (with or without pus) (cutaneous + ~subcutaneous)
- 1st line of infection

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18
Q

Furuncle:

A

(aka boil) is a walled-off mass of purulent material arising from a hair follicle
* involve DEEPER areas of skin (SUBCUTANEOUS tissue)

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19
Q

Abscess:

A

is a painful collection of pus, usually
caused by bacterial infection (red and swollen)

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20
Q

Carbuncles:

A

are a COLLECTION OF FURUNCLES that
coalesce to form a single inflamed area
* form deep masses that OPEN and DRAIN through sinus
tracts
- if not treated could get into sinuses or lymphatic tissue

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21
Q

______ is the most common cause of folliculitis,
furuncles, and carbuncles

A

S. aureus

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22
Q

P. aeruginosa common in…

A

in unsanitized hot tub/ pool outbreaks ( ↓ [chlorine])
- or chemicals that are meant to disinfect

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23
Q

What is the treatments for Folliculitis, Furuncles & Carbuncles?

A

Many FOLLICULAR INFECTIONS RESOLVE SPONTANEOUSLY without medical or surgical intervention, BUT SOME NEED:

Mild (Folliculitis):
- moist heat + topical agents

Moderate/high risk patients (Furuncles):
- lesion incision + drainage (sterically - popping with fingers just adds more bacteria & drainage b/c keeping it there can make it get worse & spread)
- systemic antibiotic therapy

Severe (Carbuncles):
- recurrent infectious: cultures + AST* (= antimicrobial susceptibility testing)
- trying to identify the microorganisms so you can better treat

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24
Q

Why is moist heat good for folliculitis?

A

opens up hair follicles which can help infectious agents to drain

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25
Q

What are primary SSTIs:

A
  • Erysipelas
  • Impetigo
  • Lymphangitis
  • Cellulitis
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26
Q

What is Erysipelas caused by?

A

Group A β-hemolytic streptococci (GABHS) = Streptococcus pyogenes

(a primary SSTIs)

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27
Q

What is Impetigo caused by?

A

Staphylococcus aureus (including methicillin-resistant strains = MRSA), occasionally GABHS

(a primary SSTIs)

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28
Q

What is Lymphangitis caused by?

A

GABHS; occasionally S. aureus

(a primary SSTIs)

29
Q

What is Cellulitis caused by?

A

GABHS, S. aureus (potentially including MRSA strains); occasionally other Gram-POSITIVE cocci, Gram-NEGATIVE bacilli, and/or anaerobes

(a primary SSTIs)

30
Q

Cellulitis:

A

is an acute SSTI that BEGINS UNDER THE SKIN in the epidermis/ dermis and then spreads to superficial fascia/ subcutaneous layers = the CONNECTIVE TISSUES

  • bacteria enter via break in epidermis/dermis → infection
  • secondary b/c of the break therefore damage
  • 30% OF BLOOD WORK TAKEN FROM CELLULITIS patients have BACTEREMIA
  • to make sure it isn’t spreading
31
Q

What are the symptoms of Cellulitis?

A

Non-elevated lesion with edema (swelling), erythema (redness) with have POORLY DEFINED MARGINS → affected area feels hot, tender, and painful
- use a marker to see how fast it’s growing

32
Q

Lymphangitis:

A

is inflammation involving the LYMPHATIC VESSELS/CHANNELS (cutaneous + subcutaneous)
* BLOOD POISONING
cellulitis
lymphangitis
* usually occurs from puncture wounds, infected blisters, or other skin lesions→often originates from CELLULITIS

33
Q

What are the symptoms of Lymphangitis?

A

subcutaneous red line(s) in skin extending from site of injury/ infection→SERIOUS AND RAPID
- b/c once it gets into circulatory system & drainage system it’ll be serious & perhaps impossible

34
Q

Erysipelas:

A

is an acute distinct form of CELLULITIS involving superficial layers of the skin and cutaneous lymphatics; BLOCKAGE OF DERMAL LYMPHATICS
* common name “St. Anthony’s fire”
- b/c so bright red & B-hemolysis infections (lysing BC’s)

35
Q

What are the symptoms of Erysipelas? & who is it common in?

A

skin rash, ELEVATED LESION, erythema (redness), edema (swelling), pain, tenderness, and fever
- & DEFINED borders

Erysipelas is common in infants, young children, the elderly, and patients with nephrotic syndrome (kidney damage)
- b/c dealing with damage from lymphatic system

36
Q

Impetigo:

A

is a superficial EPIDERMAL skin infection that is seen most commonly *in children

  • common –> non-bullous
  • neonates –> bullous (fluid filled) - don’t pop
37
Q

What is diff. about Impetigo?

A

is highly communicable, spreads through close contacts, especially siblings and children in daycare centers and
schools (~military, dorms, etc.)

38
Q

What primary SSTI treatments are there for Cellulitis?

A
  1. moist heat + topical agents
    - (non-purulent +/- abscess)
  2. Lesion incision + drainage
    - both (esp. if there’s a large purulent mass)
  3. Systemic antibiotic therapy
    - purulent +/- abscess + fever bacteriemia variable treatments
    - ask if in hot tub etc.

b/c severe

39
Q

What primary SSTI treatments are there for Lymphangitis?

A

not the 1st two (i.e. moist heat + topical agents & Lesion incision + drainage) b/c it’s UNDER the skin

therefore:
systemic antibiotic therapy –> Penicillin G/VK or Lincosamide* (penicillin allergy treatment)

40
Q

What primary SSTI treatments are there for Erysipelas?

A
  1. moist heat + topical agents
  2. Lesion incision + drainage
  3. Systemic antibiotic therapy
    - Penicillin G/VK or Lincosamide* (penicillin allergy treatment)
41
Q

What primary SSTI treatments are there for Impetigo?

A
  1. moist heat + topical agents

NOT Lesion incision + drainage - b/c it’ll move infection further & spread since it’s highly communicable (so let body absorb it)

  1. Systemic antibiotic therapy
    - Variable: Dicloxacillin, Penicillin G/VK
42
Q

What are the Secondary SSTIs?

A
  • Animal Bites
  • Human Bites
  • Pressure Sores
  • Necrotizing Fasciitis (NF)
  • Burn Wounds
43
Q

What are Animal Bites caused by?

A

Pasteurella spp., S. aureus, streptococci, Bacteroides spp.

44
Q

What are Human Bites caused by?

A

Eikenella corrodens, S. aureus,
streptococci, Corynebacterium spp., Bacteroides spp., Peptostreptococcus spp.

45
Q

What are Pressure sores caused by?

A

S. aureus including MRSA, streptococci, Enterobacteriaceae, Bacteroides spp., Peptostreptococcus s pp, Pseudomonas aeruginosa

46
Q

What are Necrotizing Fasciitis (NF) caused by?

A

Anaerobes (Bacteroides spp., Peptostreptococcus spp.) and facultative bacteria (streptococci, Enterobacteriaceae) Clostridium perfringens, Group A streptococci

47
Q

Pressure Sores & NF have similar features b/c of?

A

similar causative agents

48
Q

What are Burn wounds caused by?

A

P. aeruginosa, Enterobacteriaceae, S. aureus, streptococci

49
Q

Pressure sores:

A
  • A.K.A. DECUBITUS ULCER or BED SORE
  • decubitus is rooted in latin meaning
    “lying down” (can cause sores b/c of increased BF, circulation, moisture – should be turned around to help this if bed ridden)
  • Frequently occur at bone joints and areas of highest pressure

MAJORITY CONCENTRATED AROUND HIP BONE

  • Includes DIABETIC FOOT INFECTIONS (DFIs) (increase risk)
  • common among chronically debilitated persons, diabetics, and the elderly (>70 yr olds)
  • Mild cases/sores are often MONOMICROBIAL
  • more SEVERE SORES are typically POLYMICROBIAL; up to 60% of hospitalized patients

Worried b/c:
* Untreated sores and DFIs increases the risk of OSTEOMYELITIS
- b/c hip bones, scapula, feet where tissue:bone ratio is lower in these areas

50
Q

What is the Pressure Sore Treatment?

A

Mild:
- Sore wound cleansing (+/- debridement –> removal of dead tissue that can be a food source

Moderate:
- Deep culture biopsy/needle aspiration at wound base for AST (access how severe)
+ Antibiotics

Severe:
- Bone culture biopsy from wound base for AST
+ Antibiotics
- go deep into inf. to see what is happening b/c surface has too many common things need bone biopsy

51
Q

Pressure sore staging indicates severity and depth of infection:

A
  • Stage 1: dermis +
    epidermis (mono-
    microbial)
  • Stage 2: sub-cutaneous
    skin tissue and fat
  • Stage 3: muscle and fascia
  • Stage 4: bone
    (polymicrobial)
  • risk for polymicrobial increase b/c may have less O2
52
Q

Necrotizing Fasciitis:

A

is a RARE but SEVERE INFECTION of the SUBCUTANEOUS TISSUES (fat, fascia, muscle, organs)→GANGRENE AND NECROSIS
* when body tissue dies due to a loss of blood supply

53
Q

What are the 2 different NF types?

A
  • FAST + RARE MONOmicrobial: Clostridium perfringens, MRSA, Group A streptococci (S. pyogenes)
  • SLOW + COMMON POLYmicrobial: anaerobes
  • fecal-oral route
54
Q

Different terms are used to classify NF types based on:

A
  • Co-morbidities
  • skin appearance and etiologic agent
    *gasproduction; Clostridial myonecrosis (gas gangrene
  • muscle involvement and systemic toxicity
  • how deep & how far has it spread
  • amputation becomes an option
55
Q

What is the NF Diagnostic tests?

A
  • Hard to distinguish CELLULITIS and NF in early stages
  • TISSUE SAMPLES taken for histologic examination, culture, and
    antimicrobial susceptibility testing (AST)
  • BLOOD SAMPLES should be collected for complete blood count and chemistry profile, as well as for bacterial culture.
56
Q

What are NF treatments?

A
  • Immediate COMBINATION BROAD-SPECTRUM intravenous(IV) ANTIBIOTICS: Piperacillin–tazobactam + vancomycin or β-lactam (penicillin) + lincosamide (clindamycin)
  • all tissue affected has to be removed so it doesn’t spread & become septic
  • immediate and aggressive surgical debridement of all necrotic tissues is essential in all patients with suspected or confirmed NF
  • means amputation b/c don’t want infection to spread & become systemic
  • > 14 hours after NF diagnosis see an increase patient mortality; increased risk of death in patients with septic shock
57
Q

Bite Wounds:

A
  • Most bite infections are POLYMICROBIAL, with an average 3 to 9 bacterial isolates per culture→ (often b/c of) oral microflora of biter
  • complicated to treat
58
Q

What are the most common bites?

A
  1. DOG TEETH (not as sharp) can exert a pressure
    of 200 - 450 lb/in2 (~1,400 to 3,100 kPa)→ results in serious crush injuries
  2. CAT TEETH (sharp and slender) easily penetrate to bones and joints→higher incidence of septic arthritis and osteomyelitis
  3. HUMAN TEETH: generally more serious and more prone to infection than animal bites, particularly clenched-fist to face injuries
    - b/c you’re open to all the infections like HIV etc. depending on who it was
59
Q

What are the symptoms of bite wounds?

A

Edema (swelling) + erythema (redness) → cellulitis or lymphangitis is common around wound site

60
Q

What is the treatment of ALL bite wounds?

A

irrigated thoroughly with a copious volume of sterile water or saline and soap or antiseptic to reduce bacteria in the wound

  • IMMUNIZATION OF BITER→determine if antiviral/ antiretroviral therapy or immunization is also needed
  • PROPHYLACTIC ANTIMICROBIAL THERAPY for early, non- infected animal bite wounds remains CONTROVERSIAL - b/c don’t want to increase antimicrobial resistance
61
Q

What is the treatment of more extensive injuries?

A

(human and dog wounds) may require surgical debridement and immobilization of the affected area
* Greater edema = less successful antibiotic therapy
* Purulent injury + erythema + edema→drainage and broad- spectrum antimicrobial treatment (oral or IV depending co- morbidities/ risk)

62
Q

Greater edema =

A

less successful antibiotic therapy

63
Q

Purulent injury + erythema + edema→

A

drainage and broad- spectrum antimicrobial treatment (oral or IV depending co- morbidities/ risk)

64
Q

Burn wounds:

A

Burns damage the body’s mechanical barriers, neutrophil function and immune responses
* Result in FLUID AND ELECTROLYTE IMBALANCES
* wounds are sterile immediately after the burn is inflicted,
but become POLYMICROBIAL within hours

65
Q

Burn wound infection severity is determined by:

A
  1. Size of burn surface
    * Superficial burns <30% of total body area→treatable with topical antimicrobials
    - & if they don’t penetrate they can be treated even in outpatients
  2. Depth of the burn
    * ESCHAR is non-viable (dead) skin debris on the surface of deep burns
    * INFECTIONS FROM ESCHAR and can invade deeper tissues over time and
    concentration of infection→cause LYMPHANGITIS AND BACTEREMIA (more widespread)
    * 1st to 3rd DEGREE BURNS HAVE SIMILAR STAGES AS PRESSURE SORES but with increased eschar in 2nd degree (deep) to 3rd degree burns
  3. Age and pre-existing conditions of the patient
    * Young children < 5 yrs are at risk due to immunological status and risk of re-infection (keeping the area clean)
    * older > 55 patients are most at risk due to immunological status and co-morbidities (diabetes, heart disease, etc.)
66
Q

More eschar present…

A

more likely you’ll need debriment & surgical removal (& also dealing with inflammation & burn)

67
Q

What is the burn wound treatment for 1st to 2nd (superficial) degree?

A

superficial/ cutaneous layer damage
* Topical antibiotic (1st) or parenteral antiseptic therapy (2nd)
- b/c of damaged skin so it’s open to infectious agents
* Frequent changes of dressing
- b/c don’t want eschar to form (therefore will prevent it & keep it clean)

68
Q

What is the burn wound treatment for 2nd (deep) to 3rd degree?

A

subcutaneous→muscle/ bone
* Oral or IV antibiotic treatment of 3 most common infections
* Streptococci: Penicillins, Erythromycin and Vancomycin
* Staphylococci: flucloxacillin or a glycopeptide (if MRSA suspected)
* P. aeruginosa: aminoglycoside (tobramycin) + β-lactam (ceftazidime/ imipenem (becoming more popular)
* Wound debridement +/- purulence abscess drainage * Frequent dressing changes > 2 times daily (so it doesn’t spread)
* Surgical skin grafts - depends on candidate

Applied Pathophysiology (34 decks)

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