Bullous impetigo

Bullous impetigo
Bullous impetigo after rupture of the bullae
Specialty	Infectious disease/dermatology

Bullous impetigois a bacterial skin infection caused byStaphylococcus aureusthat results in the formation of large blisters calledbullae,usually inareas with skin foldslike the armpit, groin, between the fingers or toes,beneath the breast,and between the buttocks. It accounts for 30% of cases ofimpetigo,the other 70% being non-bullous impetigo.

The bullae are caused by exfoliative toxins produced byStaphylococcus aureusthat cause the connections between cells in the uppermost layer of the skin to fall apart.Bullous impetigo in newborns, children, or adults who are immunocompromised and/or are experiencingkidney failure,can develop into a more severe and generalized form calledstaphylococcal scalded skin syndrome(SSSS). The mortality rate is less than 3% for infected children, but up to 60% in adults.

Signs and symptoms

Bullous impetigo on the arm

Bullous impetigo

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 asstaphylococcal scalded skin syndrome.Other associated symptoms are itching, swelling of nearby glands, fever and diarrhea. Pain is very rare.

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

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 cleavedesmoglein1 (Dsg1). Previous studies suggested that exfoliating toxins bind togangliosides,causing a release of protease by keratinocytes acting assuperantigensin 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 pyogenic non-motile Gram-positive cocci which forms into grape like clusters. Just like other forms of staph,S. aureushas 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. aureusexpresses surface receptors forfibrinogen,fibronectin,andvitronectin.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,andstratum corneum.

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 beacantholytic.Neutrophils begin to fill the pustule. Toxins are produced by S.aureusand 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.

Clinical Differential

• Insect bites
• bullous erythema multiforme
• fungal infections/bullous fungal
• 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 includeneosporin,fusidic acid,chloramphenicolandmupirocin.More severe cases of impetigo however (especially bullous impetigo) will likely require oral agents with better systemicbioavailability,such ascephalexin.Cases that do not resolve with initial antibiotic therapy or require hospitalization may also be indicative an MRSA infection, which would require consultation with a local microbiologist.

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

See also

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