Bullous impetigo

Bullous impetigo
Bullous impetigo after rupture of the blister
Specialty	Dermatology
Symptoms	Large blisters that rupture and leave a yellow crust, fever, enlarged lymph nodes
Complications	Ecthyma, poststreptococcal glomerulonephritis, scarlet fever, staphylococcal scalded skin syndrome (SSSS)
Usual onset	Under age of two
Causes	Staphylococcus aureus
Risk factors	Close contact with someone affected
Diagnostic method	Based on symptoms, confirmed by bacterial culture
Differential diagnosis	Drug reaction, insect bite, contact dermatitis, bullous pemphigoid, pemphigus vulgaris, erythema multiforme
Treatment	Antibiotics by mouth (cephalexin, amoxicillin/clavulanate, doxycycline)
Frequency	3% of rashes in children

Bullous impetigo is a bacterial skin infection that results in the formation of large blisters. The number often increases over time, and when they pop they leave a yellow crust. They may be tender or itchy. Often areas were the skin rubs together are affected, such as the groin. Other symptoms may include fever or enlarged lymph nodes. Complications may include skin ulceration, known as ecthyma.

It is caused by Staphylococcus aureus that produces specific toxins that disrupt connections between cells in the uppermost layer of the skin. It is contagious and spread through close contact. Diagnosis is often based on symptoms and examination, with confirmation by bacterial culture. A biopsy may be useful in unclear cases.

Treatment is generally with antibiotics by mouth such as cephalexin, amoxicillin/clavulanate, or doxycycline. Outcomes are generally good with resolution within 3 weeks; though, rarely scarlet fever, staphylococcal scalded skin syndrome (SSSS), or kidney issues, specifically poststreptococcal glomerulonephritis, may occur.

Bullous impetigo is relatively common, accounting for about 3% of rashes in children. It accounts for 30% of cases of impetigo, with the other 70% being non-bullous impetigo. Most cases occur in children under the age of two. When it occurs in adults, testing for poor immune function, including HIV/AIDS should occur.

Signs and symptoms

Bullous impetigo can appear around the diaper region, axilla, or neck. The bacteria causes a toxin to be produced that reduces cell-to-cell stickiness (adhesion), causing for the top layer of skin (epidermis), and lower layer of skin (dermis) to separate. Vesicles rapidly enlarge and form the bullae which is a blister more than 5mm across. Bullae is also known as staphylococcal scalded skin syndrome. Other associated symptoms are itching, swelling of nearby glands, fever and diarrhea. Pain is very rare.

Long-term once the scabs on the bullous have fallen off, scarring is minimal. Possible long-term effects may include kidney disease.

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  Bullous impetigo

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  Bullous impetigo

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  Bullous impetigo

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  Bullous impetigo on the arm

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  Bullous impetigo

Cause

Exposure is most commonly seen in hospital wards and nurseries, and can be passed from person to person in other settings, such as close contact sports. Therefore, the patient is advised to try to limit human contact as much as possible to minimize the risk of spreading the infection.

Infectious period

After 48 hours the disease is considered no longer contagious assuming the proper antibiotic treatments have been administered.

Pathogenesis

Exfoliating toxins are serine proteases that specifically bind to and cleave desmoglein 1 (Dsg1). Previous studies suggested that exfoliating toxins bind to gangliosides, causing a release of protease by keratinocytes acting as superantigens in stimulating the skin's immune system. A more recent proposal states there are three known exfoliating toxins; ETA, ETB, and ETD which act as a glutamic acid-specific serine protease with concentrated specificity. Which results in the cleavage of human Dsg1 at a unique site after glutamic acid residues causing deactivation. Proteolysis of the peptide bond leading up to the dysfunction of Dsg1 and the desmosome allows for an understanding as to why the bullous forms, making the peptide bond crucial for proper function if Dsg1.

S. aureus

A phyogenic non-motile Gram-positive cocci which forms into grape like clusters. Just like other forms of staph, S. aureus has a variety of virulence factors which include surface proteins involved in adherence, secretion of enzymes that degrade proteins, and secrete toxins which damage the host's cells.

S. aureus expresses surface receptors for fibrinogen, fibronectin, and vitronectin. These surface receptors allow a bridge to be formed which binds to host endothelial cells. Lipases allow for the degradation of lipids on the skin surface and its expression can be directly correlated with its ability of the bacteria to produce abscesses.

Diagnosis

Observing the skin's physical appearance, or swabbing a culture of the lesion for S. aureus. Nasal swabs from the patient's immediate family members are necessary to identify them as being asymptomatic nasal carriers of S. aureus.

Histology

The epidermis is composed of four layers, stratum basale, stratum spinosum, stratum granulosum, and stratum corneum.

Normal H&E

H&E of Bullous Impetigo

The cleavage plane can be found either subcorneally or within the upper stratum granulosum. The roof of the pustule is parakeratotic stratum corneum, and the floor is formed of keratinocytes, which may or may not be acantholytic. Neutrophils begin to fill the pustule. Toxins are produced by S. aureus and target desmoglein, which is a desmosomal cell-cell adhesion molecule found in the upper levels of the epidermis. This correlates with the subcorneal localization of the bullae.

Uncommon variants

• Erythema multiform
• Systemic lupus erythematosus
• Stevens–Johnson syndrome
• Pemphigus vulgaris

Differential

• HPV
• insect bites
• burns
• Herpes simplex 1/2

Prevention

Since the common pathogens involved with impetigo are bacteria naturally found on the skin, most prevention (especially in children), is targeted towards appropriate hygiene, wound cleaning, and minimizing scratching (i.e. by keeping nails trimmed and short). Avoiding close contact and sharing of items such as towels with potentially infected individuals is also recommended.

Management

Antibiotic creams are the preferred treatment for mild cases of impetigo, despite their limited systemic absorption. Such prescribed ointments include neosporin, fusidic acid, chloramphenicol and mupirocin. More severe cases of impetigo however (especially bullous impetigo) will likely require oral agents with better systemic bioavailability, such as cephalexin. Cases that do not resolve with initial antibiotic therapy or require hospitalization may also be indicative an MRSA infection, which would require the use of agents specifically able to treat it, such as clindamycin.

Antibiotic treatment typically last 7–10 days, and although highly effective some cases of methicillin resistant S. aureus (MRSA) may require longer therapy depending on the severity of infection and how much it has spread.

See also

• Skin lesion
• List of conditions caused by problems with junctional proteins

External links

Classification	ICD-10: Xxx.x ICD-9-CM: 684