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2/14 Bacterial Skin infections Flashcards

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Dermatology Board Prep flashcards
1
Q

Agent that causes Impetigo

A
  • Staph aureus
  • Strep (group A - ß hemolytic)
  • or Both
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2
Q

Agent that causes Staphylococcal Scalded Skin Syndrome

A

exfoliatin, ET-A, ET-B produced by Staph aureus (phage II strain)

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3
Q

Agent that causes folliculitis, furuncles, carbuncles

A

S. aureus (predilection for hair follicles)

Pseudomonas aeruginosa (hot tub/swimming pool folliculitis)

Yeasts: Candida and Pityrosporum

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4
Q

Agent that causes MRSA

A

S. aureus

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5
Q

Agent that causes Cellulitis

A

S. pyogenes and/or S. aureus

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6
Q

Agent that causes Erysipelas

A

S. pyogenes

H. influenze can cause similar facial infections in non-immunized children

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7
Q

Agent that causes Necrotizing Fasciitis

A

Polymicrobial (Strep, S. aureus, E. coli, Bacteroides spp, Clostridium spp)

10% due to group A streptococcus alone

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8
Q

Agent that causes Lyme disease

A

Borrelia burgdorferi

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9
Q

Agent that causes Syphillis

A

Treponema pallidum

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10
Q

What is this and what are the forms that are present?

What are some defining features of each? (bacteria caused by each one)

A

Impetigo

  • *Non-bullous (crusted)**
  • S. aureus, and occasionally by Strep (group A, beta-hemolytic)
  • Moist, honey colored crusts on erythematous base
  • Fever, systemic symptoms are rare (usually due to Strep, which progresses rapidly from impetigo -> cellulitis -> fever)
  • May be preceded by skin trauma; located around nose and mouth
  • Often complicates atopic dermatitis (secondary impetiginization)
  • *Bullous (Non-crusted)**
  • caused by S. aureus, phage II, type 71 – produces exfoliatin that produces the bullae)
  • may arise without obvious trauma
  • large flaccid bullae may develop and rupture, leaving shiny shallow erosions
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11
Q

What are some characteristic features of impetigo?

Be sure to touch upon:
age of patients
predisposing factors
contagiousness
source of infection

A
  • Young children
  • Predisposing factors: heat, humidity, crowding, poor hygiene
  • Occurs year round
  • Contagious - spreads via direct contact, autoinoculation
  • Nasal and/or perineal areas may be the source of infection (S. aureus
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12
Q

How do you diagnose and treat Impetigo? (mild cases, widespread/complicated cases, and recurrent cases)

A

culture/sensitivities - recommended due to rise of resistant organisms

Mild cases: topical mupirocin

Widespread, complicated cases:

  • **penicillinase-resistant penicillins
  • first generation cephalosporin**

Recurrent cases:

  • treat nares (mupirocin) and body (chlorhexidine)
  • bleach baths
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13
Q

What is this? What is it caused by?

A

SSSS - exfoliatin, ET-A, ET-B produced by S. aureus (phage II strain) circulate systemically and split the skin at the superficial granular layer

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14
Q

What are some characteristic features of SSSS? (typical patients, prognosis)

A

Children <6 yo, good prognosis

Immunosuppressed adults, esp. with renal failure (rare), BAD prognosis

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15
Q

What is the clinical presentation of SSSS?

A
  • Site of infection may or may not be apparent
  • Prodrome of malaise, fever, irritability
  • skin becomes tender, symmetrical sunburn-like erythema develops around facial orifices, neck, flexures
  • superficial skin blisters, which sloughs and leaves behind moist skin, scales
  • heals without scarring 10-14d
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16
Q

How is SSSS diagnosed and treated?

A

Diagnosis is primarily based on clinical presentation (cultures are negative because the symptoms are caused by teh exfoliatins that S. aureus secretes!!!)

Trmt:
oral penicillinase-resistant penicillin
1st generation cephalosporin

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17
Q

What other syndrome must you differentiate SSSS from?

A

from toxic epidermal necrolysis (TEN),

  • drug-induced reaction that causes full thickness skin sloughing that leads to widespread denudation
  • mucosa is involved, high mortality, treat with burn units +/- IVIg
18
Q

What is the difference between all of these and what causes it?

A

S. aureus (predilection for hair follicles)

Pseudomonas aeruginosa (hot tub/swimming pool folliculitis)

Yeasts: Candida and Pityrosporum

19
Q

What are some defining characteristics of folliculitis, furuncles, carbuncles? What is it and how are they different? How what are some predisposing factors?

A

Bacterial infection (pustules) of hair follicle

Predisposing factors: trauma, maceration, occlusion, diabetes, immunosuppression

depth of infection determines lesion

  • superficial/small pustules at orifice: folliculitis
  • entire follicle and surrounding tissue (a red, warm, painful, nodule): furuncle
  • multiple coalescing furuncles, deep tissues (a really large, bad, ugly, complicated “boil”) carbuncle
20
Q

How is Folliculitis, furuncles, carbuncles diagnosed and treated?

A

furuncles: compression or spontaneous rupture may be enough
Superficial Folliculitis: Topical mupirocin
Abscesses: may rupture or require incision/drainage
widespread involvement or lesions in critical areas or patients: antibiotics

  • **penicillinase-resistant penicillins (dicloxicillin)
  • 1st generation cephalosporin (culture recommended)**
  • fluoroquinolone for hot-tub folliculitis
  • seek and treat for nasal / perineal colonization if recurrent

NOTE: if it is due to community-acquired MRSA (causes very painful, virulent furuncles): **culture it!! **

21
Q

What is MRSA?

A

Methicillin-Resistant Staph Aureus (MRSA) - S. aureus strain that is resistant to penicillinase-resistant penicillins (ie dicloxicillin) and other commonly used oral medications traditionally used to treat staph infections (ie cephalosporin, amoxicillin)

22
Q

What are 5 characteristics that facilitate the transmission of MRSA?

A
  • Crowding
  • Frequent skin-to-skin Contact
  • Compromised skin (cuts, abrasions)
  • Contaminated surfaces and other items (fomites)
  • Lack of Cleanliness
23
Q

How do you tell a MRSA infection from a non-MRSA infection?

A

they are clinically indistinguishable from one another (i.e. a furuncle caused by 
an MRSA strain looks like one cause by a non-MRSA staph strain)

24
Q

How is MRSA treated?

A
  • Sulfonamides (TMP/SMX) and tetracyclines
  • Clindamycin is an option but some strains are prone to inducible clindamycin resistance
  • Topical meds (esp to address nasal carriage): mupirocin (Bactroban) or silver-containing compounds.
  • Chlorhexidine (Hibiclens) scrubs are useful for skin colonization, use as body wash
  • Bleach baths are cheap and effective
25
Q

What is this and what is it caused by?

A

Cellulitis - caused by S. pyogenes and/or S. aureus

26
Q

How is cellulitis acquired? What does it affect? What can it be complicated by?

A
  • Infection of deep dermis and subcutaneous tissues
  • Infects skin either from break in the skin (immunocompetent pts) or hematogenous spread (immunosuppressed pts)
  • damage to lymphatic system may predispose to recurrent infections -> lymphadema
  • strep cellulitis can be complicated by glomerulonephritis, lymphadentis, lymphatic scarring, endocarditis
27
Q

What is the clinical presentation of cellulitis? What can occur in children?

A
  • red, warm, painful and swollen
  • ill-defined
  • can blister
  • associated fever, chills, malaise common
  • *borders are not well demarcated**

streptococcal perianal disease: recurrent bright perianal erythema in otherwise-healthy children

28
Q

How do you diagnose and treat cellulitis?

A

diagnosis is based on clinical picture because cultures are usually negative

oral antibiotics (**penicillinase-resistant pen, 1st gen. cephalosporins**)
 if systemically ill, consider **IV antibiotics**
29
Q

What is this and what is it caused by?

A

Erysipelas - caused by S. pyogenes

H. influenze can cause similar facial infections in non-immunized children; requires IV antibiotics

30
Q

What is the clinical picture of erysipelas?

A
  • Superficial cellulitis with significant lymphatic involvement (lymphadenopathy)
  • well-demarcated painful erythema, usually on face, with peau d’orange texture
  • *- rapidly progressive**
31
Q

How is erysipelas treated?

A

penicillin

32
Q

What is this and what is it caused by?

A

Necrotizing Fasciitis “Flesh-eating bacteria” Syndrome

Polymicrobial (Strep, S. aureus, E. coli, Bacteroides spp, Clostridium spp)

  • 10% due to group A streptococcus alone
33
Q

What are some of the clinical features of Necrotizing Fasciitis? (trauma? complications/mortality? illnesses that predispose one to this?

A
  • skin trauma may or may not precede symptoms
  • underlying illnesses predispose including OH, DM, vascular + cardiac disease
  • complications common: mortality, deformity, TSS
  • resembles cellulitis early on, but pain may be unusually severe!
  • progresses rapidly with necrosis developing within 24-36 hrs
  • systemic illness can be profound
  • usually involves extremities
  • Fournier’s gangrene - involvement of perineum and genitalia
34
Q

How is Necrotizing Fasciitis diagnosed and treated?

A

diagnosis: MRI, surgical exploration
treatment:
- extensive surgical debridement
- IV broad spectrum antibiotics
* *- hyperbaric oxygen** therapy (controversial)

35
Q

What is this and what is it caused by?

A

Lyme disease Borrelia burgdorferi, a tick-borne illness that is common in the NE

36
Q

What are some complications of Lyme disease? (4)

A
  • Bell’s palsy
  • arthritis
  • myocarditis
  • meningoencephalitis

BAMM wha wha…

37
Q

What is the clinical presentation of Lyme disease?

A

“bulls eye rash” erythema migrans rash because it enlarges rather than remaining static

38
Q

How do you diagnose and treat Lyme disease?

A

ELISA test for antibodies followed by Western Blot if positive

Doxycycline for 10 to 21 days (amoxicillin for children and pregnant women)

39
Q

What is this and what is it caused by?

A

Syphilis - Treponema pallidum

40
Q

What are the 4 stages of syphillis and what parts of the body does it affect?

What happens if the fetus contracts syphillis from the mother?

A

Primary – painless chancre on genitals; highly infectious

Secondary – (4-10wks after chancre) spirochete spreads throughout body; maculopapular rash on** palm, soles, and mucous membranes** (most contagious)

Latent – asymptomatic, but pts may have secondary syphilis skin lesions

Tertiary – cardiovascular and CNS involvement (ie degeneration of DCML columns in spine** -> TABES DORSALIS)**

Congenital syphilis – high rates of spontaneous abortion and stillbirth

41
Q

How is syphillis diagnosed and treated?

A

Nontreponemal serology: VDRL, RPR
Treponemal test
Non-Treponemal test **- **Flourescent treponemal antibody-absorpsion (FTA-ABS)

Penicillin G benzathine for all stages of syphilis

x DERM (22 decks)

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