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Microbiology Unit 3 > 4 Bacterial Skin Infections > Flashcards

4 Bacterial Skin Infections Flashcards

(63 cards)

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1
Q

Flat, nonpalpable lesions

A

Manuel’s

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2
Q

Palpable bumps

A

Papules

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3
Q

Fluid filled

A

Vesicles

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4
Q

Pus-filled

A

Pustules

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5
Q

Uncomplicated bacterial skin infections …

A

Respond readily to abx and wound care

Have potential to become more serious

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6
Q

Skin infections are considered complicated if…

A

Pre-existing wound involved

Deeper tissues involved

Requires surgery

Is unresponsive to therapy or recurrent

Associated with underlying disease (ie diabetes)

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7
Q

_________ are normal skin and mucous membrane inhabitants

A

Staphylococci

Often introduced through breaks in skin, but inoculum is usually not large, meaning proper cleansing and disinfection with germicidal soup or other agents will prevent disease in persons of normal health

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8
Q

In what conditions does the infectious dose of staphylococci drop dramatically?

A

If foreign body is present - ie splinter or stitches

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9
Q

Gram positive, anaerobic bacillus that causes acne vulgaris

A

Propionibacterium acnes

Normal skin flora, colonizers sebaceous follicles to produce acne in teens and young adults

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10
Q

What triggers proprionibacterium acnes?

A

Androgen hormones

Disease may progress from noninflammatory state to far more severe condition that extends beyond follicles into dermis and surrounding tissue

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11
Q

Though it usually causes acne, P. acne’s can also cause…

A

Disease in subjects with prostheses such as artificial heart valves and joints and indwelling catheters

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12
Q

What is the pathogenesis for acne?

A

P. acne’s bacteria growing in follicles produce low molecular weight peptides which attract leukocytes

After phagocytosis, bacterial enzymes stimulate an inflammatory response

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13
Q

How do you treat acne?

A

Disease NOT related to skin cleansing b/c inflammatory action is in the sebaceous follicles

Topical application of BENZOYL PEROXIDE and ABX are effective

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14
Q

Folliculitis is usually caused by…

A

Staph aureus

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15
Q

Mild pain, itching/irritation with pustules or nodules surrounding hair follicles

A

Folliculitis

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16
Q

How do you treat folliculitis?

A

Topical treatments (clindamycin ointment or benzoyl peroxide wash) usually sufficient

If empiric abx Treatment fails to cure, gram stain to rule out gram negative etiology or MRSA

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17
Q

What are the two primary pathogens for superficial folliculitis?

A

Staphylococcus aureus (majority of abscess-like infections)

Pseudomonas aeruginosa (opportunistic pathogen)

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18
Q

How do you recognize folliculitis that is caused by Pseudomonas aeruginosa?

A

Pyocyanin/Pyoverdin - blue (pus) and green (fluorescent) pigments

Gram-negative rods

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19
Q

Hot Tub Folliculitis

A

Appears 8-48 hours after exposure

Contaminated water is source (inadequate chlorine)

Typical signs - areas of itchy maculopapular rash, some pustules

Caused by Pseudomonas aeruginosa

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20
Q

What are furuncles?

A

Boils

Abscesses caused by S. aureus involving a hair follicle and surrounding tissue

Often on neck, thighs, buttocks, and face

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21
Q

What are carbuncles?

A

Clusters of furuncles (boils) with subcutaneous connections, extend into dermis and subcutaneous tissue

May be accompanied by fever and prostrations

Common locations - back of neck, back and thighs

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22
Q

Both furuncles and carbuncles can affect healthy young persons but are more common in…

A

Obese, immunocompromised, diabetic, and elderly patients

Diagnosis by direct exam

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23
Q

How do you treat carbuncles and furuncles?

A

Abscesses are incised and drained. Hot compresses aid drainage

Abx if lesions >5 mm, do not resolve with drainage, if evidence of spreading, or if immunocompromised or at risk of endocarditis

Patients with fever, multiple abscesses or carbuncles are given more aggressive combo therapy with RIFAMPIN 😳

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24
Q

Because furuncles are often recurrent, you can prevent them by…

A

Use of liquid soap containing chlorhexidine/isopropyl alcohol and maintenance abx

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25
Superficial skin infection with crusting or bullae
Impetigo (pyoderma)
26
Causative agents of impetigo
Staphylococci, streptococci, or both S. aureus currently #1, with MRSA in about 20% Strep pyogenes is a possible coinfection
27
Ulcerative form of impetigo
Ecthyma
28
Risk factors for impetigo/ecthyma
Moist environment, poor hygiene, or chronic nasopharyngeal carriage of agents
29
Nonbullous impetigo is characterized by...
Clusters of vesicles that rupture and crust over
30
Bullous impetigo is characterized by ...
Vesicles that enlarge to form bacteria-colonized fluid-filled bullae created by action of exfoliating toxin that disrupts epidermal cell connections Toxin impacts do not disseminate belong the local sites of infection Specific strains of toxin-producing S. aureus exclusively
31
How do you manage impetigo?
Dx by clinical presentation Culture if patient doesn’t respond to therapy Wash with soap/water, use topical abx (systemic abx may be needed for patients with extensive lesions or resistant lesions)
32
What is Ritter’s Disease?
Staphylococcal Scalded Skin Syndrome Acute extensive epidermolysis due to action of staph toxin (exfoliation) that splits the skin just beneath the granule cell layer
33
Abrupt onset of perioral redness which involves entire body within 2 days —> large fluid-filled bullae (contain no organisms or leukocytes, as it’s toxin mediated)
Ritter’s Disease, or Staphylococcal Scalded Skin Syndrome Slight pressure disrupts skin (Nikolsky’s sign), skin peels easily, desquamated areas look scalded.
34
Patients with Ritter’s Disease become very ill with systemic disease manifestations, but...
Mortality rate is low and often caused by secondary infections (esp with children <6, infants)
35
How is Ritter’s disease diagnosed?
Confirmation of dx may require biopsy, but clinical presentation is important Skin culture seldom positive, bullae are sterile
36
How do you treat Ritter’s disease?
Prompt dx and therapy with penicillinase-resistant anti-staphy abx, be aware drug resistance is rampant and agent has high potential to spread between persons Skin healing without scarring in a few days to a week If extensive, treat as you would burns
37
Acute infection of skin and deeper subcutaneous tissues
Cellulitis Pain, rapidly spreading erythema and edema, fever and lymph node enlargement
38
Although many agents can produce cellulitis, ________ and _______ account for >90% of cases
S. aureus S. pyogenes (GAS) Streptococci more likely to create diffuse, swiftly spreading infections due to expression of tissue destructive enzymes Be alert for MRSA
39
What is erysipelas?
Superficial cellulitis with focal dermal lymphatic involvement Usually caused by group A strep
40
Most common location for cellulitis?
Lower extremities, unilateral
41
Cellulitis results from...
Infected skin break or endogenous seeding (wound may not be evident) —> acute inflammation
42
Hallmarks of cellulitis
HEET - areas of Heat, Erythema, Edema, and Tenderness Localized sunburn-like area Borders blend in elevation and color to surrounding tissue
43
Symptoms of cellulitis are due to...
Bacterial toxins and inflammatory response
44
What is MRSA?
Methicillin-resistant Staph. aureus Multiple abx resistance, difficult to treat due to usual delay in recognition
45
____% of the general population are carriers for MRSA
2% Problematic in health care facilities Hospitals may screen patients to ID carriers
46
Typical signs of MRSA infection
Usual skin infection signs (redness, swelling, warmth, pain) with... Fluctuate (evidence of fluid) Yellow or white center Central point (head) Draining pus or ability to aspirate pus with syringe
47
How is cellulitis diagnosed?
By clinical exam - cultures rarely identify etiologic agent Abx Treatment usually leads to quick resolution (empiric, against most probable agent)
48
Why should you avoid NSAIDs with cellulitis?
May mask pain of developing myonecrosis and interfere with response to agent
49
Hallmarks of necrotizing subcutaneous infections?
Mixed infection of aerobes and anaerobes —> necrosis of subcutaneous tissue/fascia Tissues become red, hot, and swollen with PAIN OUT OF PROPORTION to clinical signs Poor prognosis w/o quick and aggressive intervention
50
Causative agent of necrotizing fasciitis...
Streptococcal gangrene Infection of deeper tissues with destruction of muscle fascia and overlying structures
51
How does necrotizing fasciitis usually spread?
Spreads along muscle fascia, but muscle tissue with good oxygen supply is spared Initially overlying tissue appears unaffected, which makes diagnosis difficult without surgical intervention
52
How do you treat necrotizing fasciitis?
IV fluids and abx and AGGRESSIVE SURGERY
53
Type 1 necrotizing fasciitis is...
Polymicrobic - group A strep (pyogenes) and anaerobes Risk factors = diabetes, surgery, immune compromise
54
Type 2 necrotizing fasciitis...
“Flesh eating Bacteria” - group A strep pyogenes (monomicrobic) Exposure often not found - can follow blunt trauma, bug bite, chickenpox, IVDU, surgery, strep throat Risk factors not clear - no significant past med Hx, any age group
55
Clinical manifestations of necrotizing fasciitis
Usually acute onset Affected area - HEET and shiny Pain out of proportion with rapid progression over several days Skin changes color - red-purple —> patches of blue-gray After 3-5 days —> skin breakdown with bullae, thick pink/purple fluid, cutaneous gangrene, no longer tender (cutaneous anesthesia)
56
What differentiates necrotizing fasciitis from cellulitis?
Failure to respond to abx therapy (cellulitis usually improves in 24-48 hours)
57
What causes gas gangrene?
Clostridium perfringens type A —> clostridial myonecrosis C. perfringens is spore-forming, gram-positive
58
Pathogenesis of gas gangrene
Intro of anaerobic cells or spores into tissues Reduced oxygen tension from trauma or other bacteria Production of exotoxins and insoluble H2 gas —> promotes splitting and invasion of nearby tissue
59
Clinical manifestations of myonecrosis (gas gangrene)
Rapid onset of symptoms - emergency! Sudden onset of pain due to toxin-mediated ischemia Skin develops a bronze appearance, becomes tense (edema), intensely tender, and crediting (H2 gas) Overlying bullae - clear, red, blue, or purple Can be similar in presentation to necrotizing fasciitis
60
How do you diagnosis myonecrosis?
Gram stain of biopsy shows muscle necrosis, gram-variable rods, and tissue destruction
61
What is Toxic Shock Syndrome?
Multi-organ system toxicity Produced by some strains of staph aureus and strep pyogenes Fever and whole body sunburn-like rash with desquamated Toxins act as superantigens that nonspecifically over-stimulate immune system response
62
Who is at increased risk for Streptococcal TSS?
HIV, cancer, diabetes, VZV, flu, childbirth, surgery, heart/pulmonary patients These patients often have pre-existing skin infections, are bacteremic and have necrotizing fasciitis
63
Staphylococcal TSS occurs...
Commonly without pre-existing skin infections Menstrual - linked to tampon use Surgery

Microbiology Unit 3 (10 decks)

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