2/14 Bacterial Skin infections Flashcards

(41 cards)

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
What is this and what is it caused by?
Cellulitis - caused by S. pyogenes and/or S. aureus
26
How is cellulitis acquired? What does it affect? What can it be complicated by?
- 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
What is the clinical presentation of cellulitis? What can occur in children?
- 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
How do you diagnose and treat cellulitis?
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
What is this and what is it caused by?
**Erysipelas** - caused by **S. pyogenes** H. influenze can cause similar facial infections in non-immunized children; requires IV antibiotics
30
What is the clinical picture of erysipelas?
- Superficial **cellulitis** with **significant lymphatic involvemen**t (lymphadenopathy) - **well-demarcated** painful erythema, usually on face, with **peau d’orange texture** * *- rapidly progressive**
31
How is erysipelas treated?
penicillin
32
What is this and what is it caused by?
Necrotizing Fasciitis “Flesh-eating bacteria” Syndrome **Polymicrobial (Strep, S. aureus, E. coli, Bacteroides spp, Clostridium spp)** - 10% due to group A streptococcus alone
33
What are some of the clinical features of Necrotizing Fasciitis? (trauma? complications/mortality? illnesses that predispose one to this?
- 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
How is Necrotizing Fasciitis diagnosed and treated?
diagnosis: MRI, surgical exploration treatment: - extensive **surgical debridement** - IV **broad spectrum antibiotics** * *- hyperbaric oxygen** therapy (controversial)
35
What is this and what is it caused by?
Lyme disease **Borrelia burgdorferi**, a tick-borne illness that is common in the NE
36
What are some complications of Lyme disease? (4)
- Bell’s palsy - arthritis - myocarditis - meningoencephalitis BAMM wha wha...
37
What is the clinical presentation of Lyme disease?
**“bulls eye rash” erythema migrans** rash because it enlarges rather than remaining static
38
How do you diagnose and treat Lyme disease?
**ELISA** test for antibodies followed by Western Blot if positive **Doxycycline** for 10 to 21 days (**amoxicillin** for children and pregnant women)
39
What is this and what is it caused by?
Syphilis - Treponema pallidum
40
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?
**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
How is syphillis diagnosed and treated?
Nontreponemal serology: **VDRL, RPR Treponemal test** Non-Treponemal test **- ****Flourescent treponemal antibody-absorpsion (FTA-ABS)** **Penicillin G benzathine** for all stages of syphilis