Impetigo is spread by direct contact with the lesion. The incubation period is 1–3 days and 4-10 days for for Streptococci and Staphylococci respectively. Bullous impetigo is caused by exfoliative toxins which are released by Staphylococcus aureus. The toxins are of two types, A and B, and lead to the production of bullae in the superficial layer of epidermis.^[1]

Impetigo, the infection of epidermis, can either be primary or secondary to scratches, injuries, bites or conditions that lead to a break in the continuity of the skin. The breaks in the continuity are potential sites for the pathogens to enter and infect.^[2][3][4][5]

• The D and E strains of emm protein act as a virulence factor for group A streptococci.^[2][6]
• Group A Streptococci have great invasive potential. They can be isolated from the skin 10 days before an infection and from the oropharynx, 2-3 weeks after the appearance on the skin.^[7]

Staphylococci cause toxin mediated impetigo in the following way:^[8]

• Staphylococci produce toxins that act as superantigens.
• These superantigens can activate T-lymphocytes.
• The exfoliative toxins produced can hydrolyze desmoglein 1 and thus weaken the desmosomes.
• They can also produce IL-1 and IL-6 and tumor necrosis factor alpha (TNF-a).
• These lymphokines can act on the skin producing bullous impetigo.

The following are important aspects in the pathogenesis of bullous impetigo:^[9][10][4]

• Bullous impetigo is caused by exfoliative toxins which are released by Stapphylococcus aureus.
• The exfoliative toxins can hydrolyze desmoglein 1 and thus weaken the desmosomes.
• The toxins are of two types, A and B, and lead to the production of bullae in the superficial layer of epidermis.
• These bullae are flaccid and can rupture easily.

The pathogenesis of non-bulbous impetigo involves:^[11]

• Staphylococcus aureus is involved in almost 80% cases.
• Group A streptococci also contribute in the pathogenesis either alone or in combination with Staphylococcus aureus.
• Toxins are produced by the bacteria which act as superantigens.
• Activation of T-lymphocytes and the production of IL-1, IL-6 and TNF-a is mediated by the toxins.
• These lead to exfoliative skin changes and thus impetigo.

The pathogenesis of ecthyma involves:^[12]

• Infection is usually caused by Streptococcus pyogenes.
• Immunodeficient individuals have a higher risk of ecthyma.
• The deficiency of antibody that opsonizes the S. pyogenes M protein is main step in pathogenesis.
• The lesions are painful and filled with pus.
• The lesions extend into the epidermis and thus an ulcer is formed after the rupture of the lesion.
• The surface of the ulcer is covered with a brown scab.

Impetigo associated with group A streptococci is understood to have a genetic basis and is associated with subfamilies of emm gene.^[6]

The conditions associated with impetigo include:^[13][11]

• Diabetes
• Immunodeficiency
• Eczema
• Diseases associated with rash
• Cellulitis
• Dermatological disorders of all kinds
• Trauma
• Atopic dermatitis
• Contact dermatitis
• Pediculosis

Microscopic pathology findings are not significant for the diagnosis or treatment of impetigo.