2/14 Bacterial Skin infections Flashcards
Agent that causes Impetigo
- Staph aureus
- Strep (group A - ß hemolytic)
- or Both
Agent that causes Staphylococcal Scalded Skin Syndrome
exfoliatin, ET-A, ET-B produced by Staph aureus (phage II strain)
Agent that causes folliculitis, furuncles, carbuncles
S. aureus (predilection for hair follicles)
Pseudomonas aeruginosa (hot tub/swimming pool folliculitis)
Yeasts: Candida and Pityrosporum
Agent that causes MRSA
S. aureus
Agent that causes Cellulitis
S. pyogenes and/or S. aureus
Agent that causes Erysipelas
S. pyogenes
H. influenze can cause similar facial infections in non-immunized children
Agent that causes Necrotizing Fasciitis
Polymicrobial (Strep, S. aureus, E. coli, Bacteroides spp, Clostridium spp)
10% due to group A streptococcus alone
Agent that causes Lyme disease
Borrelia burgdorferi
Agent that causes Syphillis
Treponema pallidum
What is this and what are the forms that are present?
What are some defining features of each? (bacteria caused by each one)
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
What are some characteristic features of impetigo?
Be sure to touch upon:
age of patients
predisposing factors
contagiousness
source of infection
- 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
How do you diagnose and treat Impetigo? (mild cases, widespread/complicated cases, and recurrent cases)
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
What is this? What is it caused by?
SSSS - exfoliatin, ET-A, ET-B produced by S. aureus (phage II strain) circulate systemically and split the skin at the superficial granular layer
What are some characteristic features of SSSS? (typical patients, prognosis)
Children <6 yo, good prognosis
Immunosuppressed adults, esp. with renal failure (rare), BAD prognosis
What is the clinical presentation of SSSS?
- 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
How is SSSS diagnosed and treated?
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
What other syndrome must you differentiate SSSS from?
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
What is the difference between all of these and what causes it?
S. aureus (predilection for hair follicles)
Pseudomonas aeruginosa (hot tub/swimming pool folliculitis)
Yeasts: Candida and Pityrosporum
What are some defining characteristics of folliculitis, furuncles, carbuncles? What is it and how are they different? How what are some predisposing factors?
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
How is Folliculitis, furuncles, carbuncles diagnosed and treated?
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!! **
What is MRSA?
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)
What are 5 characteristics that facilitate the transmission of MRSA?
- Crowding
- Frequent skin-to-skin Contact
- Compromised skin (cuts, abrasions)
- Contaminated surfaces and other items (fomites)
- Lack of Cleanliness
How do you tell a MRSA infection from a non-MRSA infection?
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)
How is MRSA treated?
- 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
What is this and what is it caused by?
Cellulitis - caused by S. pyogenes and/or S. aureus
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
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
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**
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
What is the clinical picture of erysipelas?
- Superficial cellulitis with significant lymphatic involvement (lymphadenopathy)
- well-demarcated painful erythema, usually on face, with peau d’orange texture
- *- rapidly progressive**
How is erysipelas treated?
penicillin
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
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
How is Necrotizing Fasciitis diagnosed and treated?
diagnosis: MRI, surgical exploration
treatment:
- extensive surgical debridement
- IV broad spectrum antibiotics
* *- hyperbaric oxygen** therapy (controversial)
What is this and what is it caused by?
Lyme disease Borrelia burgdorferi, a tick-borne illness that is common in the NE
What are some complications of Lyme disease? (4)
- Bell’s palsy
- arthritis
- myocarditis
- meningoencephalitis
BAMM wha wha…
What is the clinical presentation of Lyme disease?
“bulls eye rash” erythema migrans rash because it enlarges rather than remaining static
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)
What is this and what is it caused by?
Syphilis - Treponema pallidum
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
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
