Impetigo

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Usama Talib, BSc, MD [2]

Impetigo is a contagious superficial, bacterial skin infection most common among children age 2–6 years. People who play close contact sports such as rugby, American football and wrestling are also susceptible, regardless of age. The name derives from the Latin impetere (“assail”). It is also known as school sores. Skin is normally colonized with a large number of pathogens. When the pathogens increase in number on the skin or when there is a break in the continuity ofthe skin, they can lead to an infection.^[1][2]

In 1880, Alexander Ogston for the first time wrote about the involvement of Staphylococci in skin infections.In 1863, R. W. Dunn of Porrigo described lesions of impetigo as dirty, flat, irregular spots that are straw coloured.^[3] The first epidemic in the nurseries was reported in 1989.^[4]

Impetigo can be classified in various ways. It can be classified as bullous, non-bullous and ecthyma. It can also be classified as primary or secondary to a disease or process. Another classification pattern is with respect to the involved pathogen as staphylococcal or streptococcal impetigo. Non-bullous impetigo also known as “impetigo contagiosa” is caused by both Staphylococci and Streptococci and is estimated to make almost 70% of its cases.^[5]

Impetigo is spread by direct lesion contact. 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 Stapphylococcus aureus. The toxins are of two types, A and B, and lead to the production of bullae in the superficial layer of epidermis.^[6]

Impetigo is usually caused by Staphylococcus aureus. Streptococci (e.g. Streptococcus pyogenes) have been associated with the non-bullous form of impetigo and ecthyma.Streptococci can either infect individually or co-infect with Staphylococcus aureus. Non-bullous impetigo makes 70% of all the caess of impetigo.^[7][8][9][5]

Impetigo must be differentiated from other diseases that cause pustules surrounded by erythematous skin, including chickenpox, herpes zoster, erythema multiforme, among others. It should be differentiated from scabies, contact dermatitis, lupus (discoid type), herpes simplex, burns, necrotizing faciitis.^[10]

In 2010, 140 million people suffered from impetigo. Impetigo is more common among children. Impetigo is more prevalent in tropical and pacific countries.^[11][12][13]

Impetigo is often associated with insect bites, cuts, and other forms of trauma to the skin. Humidity, obesity, corticosteroid use, chemotherapy, dysglobulinemias, leukemias and malnutrition are some other risk factors for impetigo.^[14] Handwashing decreseas the incidence of impetigo by 34%.^[15]

The United States Preventive Services Task Force (USPSTF) has not issued any guidelines for the screening of impetigo.

If left untreated, most cases of non-bullous impetigo resolve within 1-2 weeks. The complications of impetigo include poststreptococcal glomerulonephritis and rheumatic fever.^{[16][17][18][19][20]}

PImptigo has a conatgious course. People who suffer from cold sores have shown higher chances of suffering from impetigo. Patients with impetigo usualy have a history of recurrent lesions, immunodeficiency and trauma or abrasions. Symptoms may vary from vesicles to bullae that can be seen localized in early disease or spread to trunk and extremities if not taken care of. Fever and fatigue are important symtoms associated with seeking medical attention.^[5][21]

Patients may present with one or more pimple-like lesions surrounded by reddened skin. Lesions fill with pus, then break down over 4–6 days and form a thick crust. Impetigo is often associated with insect bites, cuts, and other forms of trauma to the skin. Itching is common.^[5]

The diagnosis of impetigo is primarily clinical. A thorough physical examination plays an important role in the diagnosis of impetigo along with a detailed history taking.Bullae, papules, pustules or ulcers may be visible depicting various types of impetigo.^[19][5]

Impetigo is primarily diagnosed clinically. Some laboratory tests can also be used to confirm the involved pathogen and to focus the treatment on that pathogen in particular. These include gram stain and culture and senstivity.^[19][2]

Xrays do not contribute in the diagnosis of impetigo.

CT scan does not contribute in the diagnosis of impetigo.

MRI does not contribute in the diagnosis of impetigo.

Ultrasound does not contribute in the diagnosis of impetigo.

Other imaging findings do not contribute in the diagnosis of impetigo.

Immunodeficiency can be evaluated in case of recurrence of impetigo. Other aspects may involve a detailed review of conditions like malnutrition, leukemia and diabetes.

The treatment of impetigo is primarily medical.

The mainstay of therapy for impetigo is antimicrobial therapy. Empiric therapy for mild disease includes either Mupirocin or Retapamulin applied topically. Empiric therapy for numerous lesions or poststreptococcoal glomerulonephritis includes either Dicloxacillin, Amoxicillin-Clavulanate, or Cephalexin. Penicillin is the drug of choice for impetigo caused by Streptococcus. Patients with impetigo caused by Methicillin-resistant Staphylococcus aureus are treated with either Doxycycline, Clindamycin, or Sulfamethoxazole-Trimethoprim. Non-bullous impetigo is self resolving and usually takes 1-2 weeks.^[5][22]Topical or oral antibiotics are usually prescribed.

Medical therapy is the primary mode of treatment for impetigo. Surgery is not usually required. Biopsy may sometimes be required if there is recurrence of lesions and the diagnosis of impetigo is not confimed.^[23]

Primary prevention of impetigo involves various aspect of ensuring hygiene including avoiding prolonged exposures to dirty environments , handwashing and regular bathing. Handwashing alone can decrease the incidence of impetigo by 34%.^[15]

The measure for secondary prevention of impetigo include avoidance of scratching, keeping the lesions covered, nails must be cut to avoid spread and keepig towel separate is also recommended.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Usama Talib, BSc, MD [2]

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.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Usama Talib, BSc, MD [2]

Impetigo is usually caused by Staphylococcus aureus. Streptococci (e.g. Streptococcus pyogenes) have been associated with the non-bullous form of impetigo and ecthyma.Streptococci can either infect individually or co-infect with Staphylococcus aureus. Non-bullous impetigo makes 70% of all the caess of impetigo.^[1][2][3][4]

It was previously believed that non-bullous impetigo is caused by group A streptococci whereas Staphylococcus aureus causes the bullous subtype of impetigo. Both bullous and non-bullous subtypes of impetigo are now understood to be primarily caused by S. aureus. Streptococci have been associated with the non-bullous form and ecthyma.^[3][5][6][7]

The common causes of impetigo include:^{[8][9][10][11]}

• Staphylococcus aureus
  • Methicillin-resistant Staphylococcus aureus (MRSA)
  • Gentamicin-resistant Staphylococcus aureus

• Streptococcus pyogenes

• Staphylococcus aureus

• Staphylococcus aureus
• Group A, beta-hemolytic Streptococcus (Streptococcus pyogenes)

• Group A, beta-hemolytic Streptococcus (Streptococcus pyogenes)

• Artemether and lumefantrin
• Secukinumab

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2], Usama Talib, BSc, MD [3]

Impetigo must be differentiated from other diseases that cause pustules surrounded by erythematous skin, including chickenpox, herpes zoster, erythema multiforme, among others. It should be differentiated from scabies, contact dermatitis, lupus (discoid type), herpes simplex, burns, necrotizing fasciitis.^[1][2]

Different rash-like conditions can be confused with impetigo and are thus included in the differential diagnosis. The various conditions that should be differentiated from impetigo include:^{[1][2][3][4][5][6][7]}

Disease	Features
Impetigo	It commonly presents with pimple-like lesions surrounded by erythematous skin. Lesions are pustules, filled with pus, which then break down over 4-6 days and form a thick crust. It’s often associated with insect bites, cuts, and other forms of trauma to the skin.
Insect bites	The insect injects formic acid, which can cause an immediate skin reaction often resulting in a rash and swelling in the injured area, often with formation of vesicles.
Kawasaki disease	Commonly presents with high and persistent fever, red mucous membranes in mouth, “strawberry tongue“, swollen lymph nodes and skin rash in early disease, with peeling off of the skin of the hands, feet and genital area.
Measles	Commonly presents with high fever, coryza and conjunctivitis, with observation of oral mucosal lesions (Koplik’s spots), followed by widespread skin rash.
Monkeypox	The presentation is similar to smallpox, although it is often a milder form, with fever, headache, myalgia, back pain, swollen lymph nodes, a general feeling of discomfort, and exhaustion. Within 1 to 3 days (sometimes longer) after the appearance of fever, the patient develops a papular rash, often first on the face. The lesions usually develop through several stages before crusting and falling off.
Rubella	Commonly presents with a facial rash which then spreads to the trunk and limbs, fading after 3 days, low grade fever, swollen glands, joint pains, headache and conjunctivitis. The rash disappears after a few days with no staining or peeling of the skin. Forchheimer’s sign occurs in 20% of cases, and is characterized by small, red papules on the area of the soft palate.
Atypical measles	The symptoms commonly begin about 7-14 days after infection and present as fever, cough, coryza and conjunctivitis. Observation of Koplik’s spots is also a characteristic finding in measles.
Coxsackievirus	The most commonly caused disease is the Coxsackie A disease, presenting as hand, foot and mouth disease. It may be asymptomatic or cause mild symptoms, or it may produce fever and painful blisters in the mouth (herpangina), on the palms and fingers of the hand, or on the soles of the feet. There can also be blisters in the throat or above the tonsils. Adults can also be affected. The rash, which can appear several days after high temperature and painful sore throat, can be itchy and painful, especially on the hands/fingers and bottom of feet.
Acne	It is typical of teenagers, usually appears on the face and upper neck, but the chest, back and shoulders may have acne as well. The upper arms can also have acne, but lesions found there are often keratosis pilaris, not acne. The typical acne lesions are comedones and inflammatory papules, pustules, and nodules. Some of the large nodules were previously called “cysts“
Syphilis	It commonly presents with gneralized systemic symptoms such as malaise, fatigue, headache and fever. Skin eruptions may be subtle and asymptomatic It is classically described as: Non-pruritic bilateral symmetrical mucocutaneous rash Non-tender regional lymphadenopathy Condylomata lata and Patchy alopecia.
Molluscum contagiosum	The lesions are commonly flesh-colored, dome-shaped, and pearly in appearance. They are often 1-5 millimeters in diameter, with a dimpled center. Generally not painful, but they may itch or become irritated. Picking or scratching the lesions may lead to further infection or scarring. In about 10% of the cases, eczema develops around the lesions. They may occasionally be complicated by secondary bacterial infections.
Mononucleosis	Common symptoms include low-grade fever without chills, sore throat, white patches on tonsils and back of the throat, muscle weakness and sometime extreme fatigue, tender lymphadenopathy, petechial hemorrhage and skin rash.
Toxic erythema	It is a common rash in infants, with clustered and vesicular appearance.
Rat-bite fever	It commonly presents with fever, chills, open sore at the site of the bite and rash, which may show red or purple plaques.
Parvovirus B19	The rash of fifth disease is typically described as “slapped cheeks,” with erythema across the cheeks and sparing the nasolabial folds, forehead, and mouth.
Cytomegalovirus	The common symptoms include sore throat, swollen lymph nodes, fever, headache, fatigue, weakness, muscle pain and loss of appetite.
Scarlet fever	It commonly includes fever, punctate red macules on the hard and soft palate and uvula (Forchheimer’s spots), bright red tongue with a “strawberry” appearance, sore throat and headache and lymphadenopathy.
Rocky Mountain spotted fever	The symptoms may include maculopapular rash, petechial rash, abdominal pain and joint pain.
Stevens-Johnson syndrome	The symptoms may include fever, sore throat and fatigue. Commonly presents ulcers and other lesions in the mucous membranes, almost always in the mouth and lips but also in the genital and anal regions. Those in the mouth are usually extremely painful and reduce the patient’s ability to eat or drink. Conjunctivitis of the eyes occurs in about 30% of children. A rash of round lesions about an inch across, may arise on the face, trunk, arms and legs, and soles of the feet, but usually not on the scalp.
Varicella-zoster virus	It commonly starts as a painful rash on one side of the face or body. The rash forms blisters that typically scab over in 7-10 days and clears up within 2-4 weeks.
Chickenpox	It commonly starts with conjunctival and catarrhal symptoms and then characteristic spots appearing in two or three waves, mainly on the body and head, rather than the hands, becoming itchy raw pox (small open sores which heal mostly without scarring). Touching the fluid from a chickenpox blister can also spread the disease.
Meningococcemia	It commonly presents with rash, petechiae, headache, confusion, and stiff neck, high fever, mental status changes, nausea and vomiting.
Rickettsial pox	The first symptom is commonly a bump formed by a mite-bite, eventually resulting in a black, crusty scab. Many of the symptoms are flu-like including fever, chills, weakness and muscle pain but the most distinctive symptom is the rash that breaks out, spanning the person’s entire body.
Meningitis	It commonly presents with headache, nuchal rigidity, fever, petechiae and altered mental status.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Usama Talib, BSc, MD [2]

In 2010, 140 million people suffered from impetigo. Impetigo is more common among children. Impetigo is more prevalent in tropical and pacific countries.^[1][2][3]

• In 2010, 140 million people suffered from impetigo.^[3]

• The prevalence of impetigo in Australian Aboriginal communities is 49%.^[2]
• The prevalence of impetigo in Solomon Islands is 43%.^[4]
• Impetigo is more prevalent in tropical and pacific countries.^[1][2]
• In 2006-2007, 25.6% school going children and 12.2% infants had active impetigo in Fiji.^[1]

• Impetigo is more common among young children between age 2 to 5. Particularly those who attend school or daycare centers.^[5][6][1]
• A study showed that almost 69% of children below the age of 16 were affected by impetigo.^[2]
• Non-bullous impetigo is rare in children under 2 years.^[7]

• The distribution of impetigo is not effected by gender of the patient.

• Impetigo is very common in Australian Aboriginal communities and Solomon Islands.^[2]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Usama Talib, BSc, MD [2]

Impetigo is often associated with insect bites, cuts, and other forms of trauma to the skin. Humidity, obesity, corticosteroid use, chemotherapy, dysglobulinemias, leukemias and malnutrition are some other risk factors for impetigo.^[1] Handwashing decreseas the incidence of impetigo by 34%.^[2]

Risk factors for impetigo include:^{[1][3][4][5][6][7][8]}

• Abrasions
• Trauma
• Insect bite
• Herpes
• Scabies
• Children attending daycare
• Basic skin pH
• Lack of sebaceous secretions
• Humidity
• Obesity
• Corticosteroid use
• Chemotherapy
• Dysglobulinemias
• Leukemia
• Contact sports
• Chronic granulomatous disease
• Diabetes
• Malnutrition
• Congenital or acquired immunodeficiencies e.g. AIDS
• Temperature around 37 C
• Surgery
• Poor hygiene

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Usama Talib, BSc, MD [2]

If left untreated, most cases of non-bullous impetigo resolve within 1-2 weeks. The complications of impetigo include poststreptococcal glomerulonephritis and rheumatic fever.^{[1][2][3][4][5]}

If left untreated, most cases of non-bullous impetigo resolve within 1-2 weeks. All forms of impetigo start as a lesion which then ruptures leading to variable pattern of crusting.^[5][6][7][8]

• Non-bullous impetigo begins as a vesicle with erythematous base.
• The lesions are 1-2cm each and distant lesions can be seen because of its contagious nature.
• The vesicle ruptures easily forming a yellow exudate on the surface.
• This exudate dries to form a golden brown crust.
• Lymphadenopathy and fever may be observed.
• This is followed by complete recovery of the lesion.
• If left untreated, most cases of non-bullous impetigo resolve within 1-2 weeks.

• Bullus impetigo begins as smaller vesicles which form flaccid blisters.
• If left untreated the bullae are filled with clear fluid which turns yellow and less clearer later.
• Rupture of the bullae leaves a ring of golden crust.
• The bullous impetigo lesions are painful and associated with itching.
• The lesions of bullous impetigo are commonly seen on the trunk and the extremities.
• Bullous impetigo when left untreated for long, may lead to cellulitis, poststreptococcal glomerulonephritis or rheumatic fever.

• Ecthyma starts as pus filled, painful lesions on the extremities.
• The lesions rupture to form a hard crust along with an ulcer that can involve deeper layers.
• The lesions of ecthyma may form a scar after their resolution.

The complications of impetigo include:^{[1][2][3][4][5][6]}

• Recurrent impetigo
• Poststreptococcal glomerulonephritis
• Rheumatic fever
• Cellulitis

The prognosis of non-bullous impetigo is very good.

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