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Microbiology Unit 3 > 4 Bacterial Skin Infections > Flashcards

4 Bacterial Skin Infections Flashcards

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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
Q

Superficial skin infection with crusting or bullae

A

Impetigo (pyoderma)

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26
Q

Causative agents of impetigo

A

Staphylococci, streptococci, or both

S. aureus currently #1, with MRSA in about 20%

Strep pyogenes is a possible coinfection

27
Q

Ulcerative form of impetigo

A

Ecthyma

28
Q

Risk factors for impetigo/ecthyma

A

Moist environment, poor hygiene, or chronic nasopharyngeal carriage of agents

29
Q

Nonbullous impetigo is characterized by…

A

Clusters of vesicles that rupture and crust over

30
Q

Bullous impetigo is characterized by …

A

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
Q

How do you manage impetigo?

A

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
Q

What is Ritter’s Disease?

A

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
Q

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)

A

Ritter’s Disease, or Staphylococcal Scalded Skin Syndrome

Slight pressure disrupts skin (Nikolsky’s sign), skin peels easily, desquamated areas look scalded.

34
Q

Patients with Ritter’s Disease become very ill with systemic disease manifestations, but…

A

Mortality rate is low and often caused by secondary infections (esp with children <6, infants)

35
Q

How is Ritter’s disease diagnosed?

A

Confirmation of dx may require biopsy, but clinical presentation is important

Skin culture seldom positive, bullae are sterile

36
Q

How do you treat Ritter’s disease?

A

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
Q

Acute infection of skin and deeper subcutaneous tissues

A

Cellulitis

Pain, rapidly spreading erythema and edema, fever and lymph node enlargement

38
Q

Although many agents can produce cellulitis, ________ and _______ account for >90% of cases

A

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
Q

What is erysipelas?

A

Superficial cellulitis with focal dermal lymphatic involvement

Usually caused by group A strep

40
Q

Most common location for cellulitis?

A

Lower extremities, unilateral

41
Q

Cellulitis results from…

A

Infected skin break or endogenous seeding (wound may not be evident) —> acute inflammation

42
Q

Hallmarks of cellulitis

A

HEET - areas of Heat, Erythema, Edema, and Tenderness

Localized sunburn-like area

Borders blend in elevation and color to surrounding tissue

43
Q

Symptoms of cellulitis are due to…

A

Bacterial toxins and inflammatory response

44
Q

What is MRSA?

A

Methicillin-resistant Staph. aureus

Multiple abx resistance, difficult to treat due to usual delay in recognition

45
Q

____% of the general population are carriers for MRSA

A

2%

Problematic in health care facilities

Hospitals may screen patients to ID carriers

46
Q

Typical signs of MRSA infection

A

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
Q

How is cellulitis diagnosed?

A

By clinical exam - cultures rarely identify etiologic agent

Abx Treatment usually leads to quick resolution (empiric, against most probable agent)

48
Q

Why should you avoid NSAIDs with cellulitis?

A

May mask pain of developing myonecrosis and interfere with response to agent

49
Q

Hallmarks of necrotizing subcutaneous infections?

A

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
Q

Causative agent of necrotizing fasciitis…

A

Streptococcal gangrene

Infection of deeper tissues with destruction of muscle fascia and overlying structures

51
Q

How does necrotizing fasciitis usually spread?

A

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
Q

How do you treat necrotizing fasciitis?

A

IV fluids and abx and AGGRESSIVE SURGERY

53
Q

Type 1 necrotizing fasciitis is…

A

Polymicrobic - group A strep (pyogenes) and anaerobes

Risk factors = diabetes, surgery, immune compromise

54
Q

Type 2 necrotizing fasciitis…

A

“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
Q

Clinical manifestations of necrotizing fasciitis

A

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
Q

What differentiates necrotizing fasciitis from cellulitis?

A

Failure to respond to abx therapy (cellulitis usually improves in 24-48 hours)

57
Q

What causes gas gangrene?

A

Clostridium perfringens type A —> clostridial myonecrosis

C. perfringens is spore-forming, gram-positive

58
Q

Pathogenesis of gas gangrene

A

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
Q

Clinical manifestations of myonecrosis (gas gangrene)

A

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
Q

How do you diagnosis myonecrosis?

A

Gram stain of biopsy shows muscle necrosis, gram-variable rods, and tissue destruction

61
Q

What is Toxic Shock Syndrome?

A

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
Q

Who is at increased risk for Streptococcal TSS?

A

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
Q

Staphylococcal TSS occurs…

A

Commonly without pre-existing skin infections

Menstrual - linked to tampon use

Surgery

Microbiology Unit 3 (10 decks)

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