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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
What are primary SSTIs:
- Erysipelas - Impetigo - Lymphangitis - Cellulitis
26
What is Erysipelas caused by?
Group A β-hemolytic streptococci (GABHS) = Streptococcus pyogenes (a primary SSTIs)
27
What is Impetigo caused by?
Staphylococcus aureus (including methicillin-resistant strains = MRSA), occasionally GABHS (a primary SSTIs)
28
What is Lymphangitis caused by?
GABHS; occasionally S. aureus (a primary SSTIs)
29
What is Cellulitis caused by?
GABHS, S. aureus (potentially including MRSA strains); occasionally other Gram-POSITIVE cocci, Gram-NEGATIVE bacilli, and/or anaerobes (a primary SSTIs)
30
Cellulitis:
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
What are the symptoms of Cellulitis?
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
Lymphangitis:
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
What are the symptoms of Lymphangitis?
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
Erysipelas:
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
What are the symptoms of Erysipelas? & who is it common in?
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
Impetigo:
is a superficial EPIDERMAL skin infection that is seen most commonly *in children - common --> non-bullous - neonates --> bullous (fluid filled) - don't pop
37
What is diff. about Impetigo?
is highly communicable, spreads through close contacts, especially siblings and children in daycare centers and schools (~military, dorms, etc.)
38
What primary SSTI treatments are there for Cellulitis?
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
What primary SSTI treatments are there for Lymphangitis?
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
What primary SSTI treatments are there for Erysipelas?
1. moist heat + topical agents 2. Lesion incision + drainage 3. Systemic antibiotic therapy - Penicillin G/VK or Lincosamide* (penicillin allergy treatment)
41
What primary SSTI treatments are there for Impetigo?
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) 3. Systemic antibiotic therapy - Variable: Dicloxacillin, Penicillin G/VK
42
What are the Secondary SSTIs?
- Animal Bites - Human Bites - Pressure Sores - Necrotizing Fasciitis (NF) - Burn Wounds
43
What are Animal Bites caused by?
Pasteurella spp., S. aureus, streptococci, Bacteroides spp.
44
What are Human Bites caused by?
Eikenella corrodens, S. aureus, streptococci, Corynebacterium spp., Bacteroides spp., Peptostreptococcus spp.
45
What are Pressure sores caused by?
S. aureus including MRSA, streptococci, Enterobacteriaceae, Bacteroides spp., Peptostreptococcus s pp, Pseudomonas aeruginosa
46
What are Necrotizing Fasciitis (NF) caused by?
Anaerobes (Bacteroides spp., Peptostreptococcus spp.) and facultative bacteria (streptococci, Enterobacteriaceae) Clostridium perfringens, Group A streptococci
47
Pressure Sores & NF have similar features b/c of?
similar causative agents
48
What are Burn wounds caused by?
P. aeruginosa, Enterobacteriaceae, S. aureus, streptococci
49
Pressure sores:
* 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
What is the Pressure Sore Treatment?
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
Pressure sore staging indicates severity and depth of infection:
* 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
Necrotizing Fasciitis:
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
What are the 2 different NF types?
* FAST + RARE MONOmicrobial: Clostridium perfringens, MRSA, Group A streptococci (S. pyogenes) * SLOW + COMMON POLYmicrobial: anaerobes - fecal-oral route
54
Different terms are used to classify NF types based on:
* 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
What is the NF Diagnostic tests?
* 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
What are NF treatments?
* 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
Bite Wounds:
* 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
What are the most common bites?
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
What are the symptoms of bite wounds?
Edema (swelling) + erythema (redness) → cellulitis or lymphangitis is common around wound site
60
What is the treatment of ALL bite wounds?
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
What is the treatment of more extensive injuries?
(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
Greater edema =
less successful antibiotic therapy
63
Purulent injury + erythema + edema→
drainage and broad- spectrum antimicrobial treatment (oral or IV depending co- morbidities/ risk)
64
Burn wounds:
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
Burn wound infection severity is determined by:
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
More eschar present...
more likely you'll need debriment & surgical removal (& also dealing with inflammation & burn)
67
What is the burn wound treatment for 1st to 2nd (superficial) degree?
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
What is the burn wound treatment for 2nd (deep) to 3rd degree?
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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