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Introductory Microbiology > Skin and Soft Tissue Infections > Flashcards

Skin and Soft Tissue Infections Flashcards

1
Q

What is the epidermis?

A
  • thin outer portion consisting of several epithelial cell layers
  • outermost layer is composed of dead cells containing keratin
  • when unbroken, an effective physical barrier against microbes
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2
Q

What is the dermis?

A
  • thick inner portion
  • provides strength and flexibility and supports growth of epidermis
  • blood vessels, nerve endings, hair follicles, sweat and oil glands
  • follicles and glands can serve as passageways for microorganisms
  • risk for bacteremia
  • normal flora repopulates up and out of hair follicles
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3
Q

In what ways is the skin surface inhospitable for microbial growth?

A
  • covered in salt, sweat, and sebum which contain antimicrobials
  • outer layers of epidermis sloughed off and replaced every month
  • normal flora must be resistant to drying and high salt concentrations
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4
Q

The concentration of microbes varies with…

A

available nutrients, moisture, pH, temperature, salt and sebum levels

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5
Q

Is hand washing effective in removing normal flora?

A

No; will reestablish through hair follicles and sweat glands

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6
Q

What is a benefit and a risk of the normal flora of the skin?

A

Benefit - offers microbial antagonism

Risk - entry into other tissues can result in infection

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7
Q

The normal skin flora is composed of…

A
  • mainly Gram positives and some yeasts
  • 90% Staphylococcus epidermidis (coagulase negative)
  • diphtheroids (ex. Proprionibacterium)
  • Staphylococcus aureus (coagulase positive), Lactobacillus spp., and sometimes Gram negatives in warm, moist areas of body
  • in perineal region “gut” bugs may be found
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8
Q

When is S. epidermidis pathogenic?

A

When skin barrier is broken or invaded

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9
Q

What are the most common areas where skin flora is found?

A

Under arms and between legs

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10
Q

What is a skin rash?

A

Any change in the colour or texture of the skin; very non-specific

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11
Q

What are the two types of rashes?

A

1) Exanthem: skin rash accompanied by systemic symptoms such as fever, malaise and headache
2) Enanthem: rash on mucous membranes accompanied by systemic symptoms such as fever, malaise and headache

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12
Q

Rashes are most commonly associated with…

A
  • most commonly associated with infection
  • reaction to a toxin, damage to the skin by a microorganism, immune response to a pathogen
  • also associated with drug reactions, allergy, autoimmune diseases
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13
Q

What are the eight types of skin rashes?

A

1) Macule - flat lesion that cannot be palpated, like a freckle
2) Vesicle - very fragile, appears to be a blister, filled with clear fluid under epidermis
3) Papule - raised lesion, not fluid-filled, results from accumulation of debris in the dermis
4) Pustule - pus-filled raised lesion, fragile
5) Nodule - a large papule that travels deeper into the skin
6) Bullae - a large vesicle; will rupture easily to the touch, fluid is clear, associated with necrotizing fasciitis
7) Wheal - a raised, itchy area of skin; sign of allergy
8) Plaque - a large raised area that forms a plateau; associated with psoriasis

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14
Q

What is a skin ulcer?

A

An open sore of the skin often caused by an initial abrasion, and generally maintained by 1) inflammation, 2) infection, and/or 3) medical conditions which impede healing

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15
Q

How does skin normal flora interfere with sampling?

A

Normal flora will colonize the wound; different from the bacteria deeper in the wound which are true pathogens

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16
Q

Why are swabs not optimal for sampling?

A
  • only sample surface of wound
  • do not account for anaerobic bacteria
  • do not collect enough specimen
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17
Q

What sampling techniques exist for wounds?

A
  • skin scraping
  • biopsy and needle aspiration (pus and tissue)
  • swabs useful if sample contains suspected pathogen (ie: from leading edge, or deep inside specimen)
  • samples stored in a sterile container for immediate transport
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18
Q

Skin infections can arise from…

A
  • superficial structures of skin (hair follicles)
  • hematogenous spread
    (disseminated infection e.g. gonococcal infections)
  • exogenous penetration
    via trauma (skin abrasions, etc…), surgery, animal and insect bites
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19
Q

What is Staphylococcus aureus?

A
  • Gram positive cocci, catalase positive, coagulase positive
  • colonizes nasopharynx, axillae, rectum, skin (20% of people)
  • causes a variety of infections; skin and soft tissue, bone, joint, heart valves, kidneys, lungs, brain bacteremia, food poisoning
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20
Q

What is group A Streptococci?

A
  • beta-hemolytic, Gram positive cocci, catalase negative
  • colonizer of skin and nasopharynx
  • causes a variety of disease including skin and soft tissue infections (NF), bone and joint infections, strep throat, scarlet fever, rheumatic fever, bacteremia, glomerulonephritis
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21
Q

How does S. aureus compare to S. epidermidis in terms of virulence factor?

A

S. aureus is much more virulent in terms of enzymes, factors that inhibit phagocytosis, and toxins

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22
Q

What is folliculitis?

A
  • localized infection of the hair follicle (red, swollen and pus filled)
  • associated with pain, tenderness and localized edema at the site of infection
  • lesions vary in size and may scar despite resolution
  • causative pathogens: Staphylococcus aureus, Psuedomonas aeruginosa, Candida albicans
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23
Q

How is folliculitis treated?

A
  • depends on extent of infection
  • antibacterial soap to affected area, warm compresses
  • clean and drain abscess of pus, if possible
  • multiple lesions: topical mupirocin
  • severe multiple lesions: oral dicloxacillin (abx)
  • resolves in 1-2 weeks
24
Q

What is a furuncle?

A
  • also called a boil
  • large, painful, raised nodular lesion
  • extension of folliculitis into surrounding hypodermis
  • grows larger and more painful (5-7 days) before developing yellow-white tip that then ruptures and drains
25
Q

What is a carbuncle?

A
  • cluster of boils; often hard, round and deep infection of multiple hair follicles (multiple furuncles)
  • often occurs on back of neck, shoulders or thighs, especially in older men, where skin is thick
  • sometimes associated with fever, more slow to heal
26
Q

What is staphylococcal scaled skin syndrome?

A
  • specific strains of S. aureus produce exfoliative exotoxins
  • cause cells within the outer epidermis to separate from each other and from underlying tissues – systemic effect (toxemia)
  • redness and wrinkling of the skin appears first on the mouth, then spreads across entire body, followed by the formation of clear, fluid filled blisters
  • exotoxin travels from site of infection through the bloodstream causing wide spread epidermal response to the exotoxin
  • epidermis falls away within 2 days of symptom onset, and resolves within 7 – 10 days
  • does not scar but vulnerable to infection
27
Q

Who is at risk for staphylococcal scalded skin syndrome?

A
  • those < 5 years old
  • elderly
  • immunocompromised
28
Q

How is staphylococcal scalded skin syndrome treated?

A
  • wound care team needs to get involved
  • treat like a burn
  • IV naficillin or oxacillin therapy
29
Q

What is impetigo?

A
  • also called pyoderma
  • affects epidermis
  • no scarring
  • small, flattened, red patches on face and limbs; develop into thin walled vesicles and pustules that rupture and crust over (golden brown, sticky crust)
  • lesions are highly contagious and itchy until healed
  • vesicles present in various stages simultaneously on the skin
  • causative pathogens: S. aureus (80%) and S. pyogenes (20%)
  • resolves in 1-2 weeks
  • “macular vesicular rash”
30
Q

What allows for skin infections to occur?

A
  • loss of skin integrity in some way allows for portal of entry
31
Q

Who is at risk for impetigo?

A
  • 2-5 years old, especially in summer months
32
Q

How is impetigo treated?

A
  • depends on extent of infection
  • if limited: topical mupirocin
  • if multiple severe lesions: PO clindamycin or doxycycline
33
Q

What two pathogens are the most common cause of bacterial skin infections?

A
  • S. aureus

- S. pyogenes (GAS)

34
Q

What is erysipelas?

A
  • acute infection of the dermis and dermal lymphatics
  • requires a portal of entry, most common in children & elderly (face, arms, legs)
  • causative pathogen; Streptococcus pyogenes
  • 5% of patients develop bacteremia, which carries a high rate of mortality if left untreated
  • characterized by a demarcated area of painful erythema and induration (raised margin)
  • on the face, erysipelas often presents as a “butterfly wing” lesion
  • often preceded by impetigo/streptococcal pharyngitis and concomitant fever
35
Q

How is erysipelas treated?

A
  • PO or IV penicillin therapy
36
Q

What are signs and symptoms of erysipelas?

A
  • steep textural raise
  • swollen lymph nodes
  • pain, fever, chills
  • increased WBCs
  • risk of bacteremia
37
Q

What is cellulitis?

A
  • acute spreading infection of subcutaneous fatty tissues (hypodermis)
  • increased pain and risk bacteremia and sepsis
  • commonly affects legs
  • no area of induration
  • signs include warmth, tenderness, pain, redness, and edema
  • lymphadenopathy
  • may also see chills, fever, malaise
  • causative pathogens: S. aureus or S. pyogenes (other pathogens in immunocompromised hosts)
  • resolves in 1-2 weeks but can reoccur
  • be alert in cases of GAS (may invade fascia causing necrotizing fasciitis)
38
Q

Who is at risk for cellulitis?

A
  • diabetics, those with chronic venous stasis, those having previous infection
39
Q

How is cellulitis treated?

A
  • oral or IV antibiotic therapy (in complicated cases)
  • area of erythema can spread over the first 24-48 hours of treatment due to poor perfusion; monitor for systemic symptoms
40
Q

What other pathogens may cause cellulitis?

A
  • Vibrio spp. (salt water)
  • Pseudomonas aeruginosa (hot-tub and whirlpools)
  • Ersipelothrix rhusiopathiae (saltwater fish, shellfish, animal hides)
41
Q

What is the greatest risk factor for invasive GAS infection?

A
  • varicella

- also diabetes, cancer, and HIV

42
Q

What are the two types of necrotizing skin infections?

A

1) Type 1: Mixed infection (non-GAS), post surgical setting and previously ill patients, nosocomial
2) Type 2: : GAS isolated alone or in combination with other bacteria (most commonly S. aureus), community acquired infection

43
Q

What is necrotizing fasciitis?

A
  • rare, life-threatening infection located in the deep fascia & necrosis of subcutaneous tissues
  • associated with trauma or recent surgery, and
    S. pharyngitis and varicella (chicken pox)
  • frequently accompanied by streptococcal toxic shock syndrome
  • diagnosis made surgically with tissue biopsies
44
Q

What are the “clues” to necrotizing fasciitis?

A
  • rapidly progressive (centimeters in an hour)
  • pain disproportionate to apparent tissue damage because damage is under the surface
  • prominent systemic symptoms/signs
  • anesthesia of affected area due to nerve damage
45
Q

What are the symptoms of necrotizing fasciitis and how does it progress?

A
  • begins with area of erythema that quickly spreads over the course of hours to days
  • margins of infection move into normal skin without being raised or sharply demarcated
  • as it progresses, a dusky purplish colour develops near site of injury
  • necrosis more advanced that appearance suggests
  • simultaneous presence of hemorrhagic bullae
  • eventual anesthesia of affected area
  • signs of systemic toxicity including fever, tachycardia, hypotension
  • elevated WBC count, pain
46
Q

How is necrotizing fasciitis treated?

A
  • Type I - broad spectrum coverage of both aerobes and anaerobes (IV piperacillin/tazobactam or meropenem)
  • Type II - GAS is universally susceptible to penicillins, (IV penicillin - drug of choice)
  • clindamycin added to decrease toxin production
  • IVIg - given in cases meeting clinical criteria for streptococcal toxic shock syndrome (ie: hypotension, renal impairment, coagulopathy, acute respiratory distress syndrome)
  • amputation of affected limb may be necessary
47
Q

How does clindamycin decrease toxin production?

A
  • protein synthesis inhibitor; will reduce production of the superantigen, a protein
48
Q

What is the pathophysiology of necrotizing fasciitis?

A
  • S. pyogenes releases exotoxins which act as superantigens
  • superantigens produce a non-specific and uncontrolled immune response, resulting in widespread tissue damage
  • uncontrolled immune response causes over-production of cytokines that over-stimulate macrophages
  • macrophages release massive amounts of oxygen free radicals, causing rapid tissue damage
  • IVIg administration and clindamycin may reduce the effects of the exotoxin
49
Q

What pathogenic factors do GAS strains causing NF possess?

A
  • streptokinase, hyaluronidase
  • M proteins, Streptolysin S
  • exotoxin A (a super-antigen)
50
Q

What is varicella?

A
  • causative pathogen: human herpes virus 3 varicella-zoster
  • incubation period of 2-3 weeks
  • highly contagious (airborne & direct contact) even 1-2 days prior to rash onset
  • pleomorphic rash preceded (1 – 2 days) by fever, malaise, headache and abdominal pain
  • trunk (abundant), face, arms, legs, may affect mouth, pharynx and vagina
  • stages: macule, papule, vesicles, pustules, then scab/crust within 4-7 days of rash onset
  • patient remains contagious until vesicles are crusted over
  • vaccine: Varivax
51
Q

What is shingles?

A
  • reactivation of herpes virus varicella-zoster (15 – 20 % of people)
  • usually associated with altered immune responses
  • virus enters peripheral nerves; viral DNA becomes dormant in dorsal root ganglion
  • reactivated virus moves along the peripheral nerves into the cutaneous sensory nerves of the skin
  • pain and eruptions follow a dermatomic pattern
  • clinical signs: fever, pain, clusters of red macules that become papules, vesicles and then crusts; typically distributed around the trunk
  • treatment: oral antiviral agents (acyclovir)
  • vaccine: Zostavax & Shingrix (different from chickenpox vaccine)
52
Q

What is Herpes Simplex Virus 1 (HSV-1)?

A
  • HSV-1 transmitted most commonly via oral routes
  • infections typically occur in childhood leading to “cold sores” in 20% of those infected
  • painful short lived vesicles that occur near the margins of the lips – reoccurrence triggered by emotional upset, stress, hormonal fluctuations, sunlight, disease
  • initial infections may also be accompanied by flu-like symptoms (malaise, fever, muscle pain)
  • antiviral drugs are available to shorten healing time & protect cells
53
Q

What is Herpes Simplex Virus 2 (HSV-2)?

A
  • HSV-2 transmitted primarily by sexual contact
  • infections typically occur between the ages of 15 – 29 years
  • first episode associated with painful lesions, followed by recurrences that are typically less severe
  • Valacyclovir can help reduce the frequency of eruptions and shorten healing time; no cure
  • HSV-1 and HSV-2 and swap easily
54
Q

Antivirals work by…

A

Reducing viral replication and viral shedding

55
Q

What is the pathophysiology of HHV?

A
  • enters and remains dormant in trigeminal, sacral, and other nerve ganglia
  • reactivation associated with stressors
  • two thirds of patients with HHV 1 and 2 will experience activation of latent infection
  • as often as every 2 weeks for some clients
  • recurrent lesions are more mild than primary infection
  • manifests as whitlow, genital, ocular, etc.
56
Q

What is ringworm?

A
  • dermatomycoses
  • ascomycetes (fungi) transmitted via direct contact and fomites
  • appear commonly on face and arms
  • erythematous and scaling patches that are round or oval
  • lesions start small, then expand outward; open at the center with a raised and scaly border
  • diagnosed by skin scrapings and processed in the lab using potassium hydroxide (KOH)
  • KOH dissolves epithelial tissue, allowing a clear view of the fungal hyphae
  • treatment: topical antifungal medication

Introductory Microbiology (11 decks)

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