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
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
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
4
Q
The concentration of microbes varies with…
A
available nutrients, moisture, pH, temperature, salt and sebum levels
5
Q
Is hand washing effective in removing normal flora?
A
No; will reestablish through hair follicles and sweat glands
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
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
8
Q
When is S. epidermidis pathogenic?
A
When skin barrier is broken or invaded
9
Q
What are the most common areas where skin flora is found?
A
Under arms and between legs
10
Q
What is a skin rash?
A
Any change in the colour or texture of the skin; very non-specific
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
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
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
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
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
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
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
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
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
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
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
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
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
What is a carbuncle?
- 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
What is staphylococcal scaled skin syndrome?
- 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
Who is at risk for staphylococcal scalded skin syndrome?
- those < 5 years old
- elderly
- immunocompromised
28
How is staphylococcal scalded skin syndrome treated?
- wound care team needs to get involved
- treat like a burn
- IV naficillin or oxacillin therapy
29
What is impetigo?
- 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
What allows for skin infections to occur?
- loss of skin integrity in some way allows for portal of entry
31
Who is at risk for impetigo?
- 2-5 years old, especially in summer months
32
How is impetigo treated?
- depends on extent of infection
- if limited: topical mupirocin
- if multiple severe lesions: PO clindamycin or doxycycline
33
What two pathogens are the most common cause of bacterial skin infections?
- S. aureus
| - S. pyogenes (GAS)
34
What is erysipelas?
- 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
How is erysipelas treated?
- PO or IV penicillin therapy
36
What are signs and symptoms of erysipelas?
- steep textural raise
- swollen lymph nodes
- pain, fever, chills
- increased WBCs
- risk of bacteremia
37
What is cellulitis?
- 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
Who is at risk for cellulitis?
- diabetics, those with chronic venous stasis, those having previous infection
39
How is cellulitis treated?
- 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
What other pathogens may cause cellulitis?
- Vibrio spp. (salt water)
- Pseudomonas aeruginosa (hot-tub and whirlpools)
- Ersipelothrix rhusiopathiae (saltwater fish, shellfish, animal hides)
41
What is the greatest risk factor for invasive GAS infection?
- varicella
| - also diabetes, cancer, and HIV
42
What are the two types of necrotizing skin infections?
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
What is necrotizing fasciitis?
- 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
What are the "clues" to necrotizing fasciitis?
- 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
What are the symptoms of necrotizing fasciitis and how does it progress?
- 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
How is necrotizing fasciitis treated?
- 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
How does clindamycin decrease toxin production?
- protein synthesis inhibitor; will reduce production of the superantigen, a protein
48
What is the pathophysiology of necrotizing fasciitis?
- 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
What pathogenic factors do GAS strains causing NF possess?
- streptokinase, hyaluronidase
- M proteins, Streptolysin S
- exotoxin A (a super-antigen)
50
What is varicella?
- 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
What is shingles?
- 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
What is Herpes Simplex Virus 1 (HSV-1)?
- 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
What is Herpes Simplex Virus 2 (HSV-2)?
- 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
Antivirals work by...
Reducing viral replication and viral shedding
55
What is the pathophysiology of HHV?
- 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
What is ringworm?
- 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
