Impetigo is a common skin infection, generally effecting children more so then adults. Statistics indicate that approximately 10% of skin infections/problems that occur in the US are cases of impetigo.

The exception is the lymphedema patient. Due to the immunocompromised condition of our lymphedematous limb, we are much more susceptible to infections. In fact, if discussions in our online support groups is any indication, impetigo is the third most common infection we come down with. It is very much one of those infections associated with lymphedema. So it is important that we understand what it is and how we can effectively treat it.

Years ago, my daughter and I caught impetigo from what we thought was an immaculate swimming pool. Hers was quickly brought under control, while mine just as quickly turned into an incredibly severe form of cellulitis.

There are two types of impetigo. They are bullous impetigo and non bullous impetigo

Bullous impetigo results from invasion by phage group 2 S aureus onto either intact or disrupted skin. This occurs after colonization of the upper respiratory tract, usually involving the nares. Invasion is believed to be a result of an epidermolytic toxin that disrupts epidermal cell attachments.

Bullous impetigo usually has a history of thin-roofed bullae that spontaneously rupture without a history of localized lymphadenopathy or cutaneous disruption.(1)

Bullous lesions

• Thin-roofed bullae that spontaneously rupture are present.

• Bullous lesions usually spread locally in the face, trunk, extremities, buttocks, or perineal regions.

• These lesions may secondarily invade preexisting lesions (eg, eczema) to cause generalized lesions.

• Minimal or no surrounding erythema occurs.

• No regional lymphadenopathy occurs.

In nonbullous impetigo, a tiny pustule or honey-colored crusted plaque with rapid spread, occasional pruritus, and regional lymphadenopathy may follow a break in the skin. (1)

Nonbullous lesions

• Lesions start as tiny pustules that evolve rapidly into honey-colored crusted plaques, which usually measure less than 2 cm in diameter.

• A rash is usually found in exposed areas of the face and extremities where bites, abrasions, lacerations, scratches, burns, or trauma have occurred.

• Rapid spread occurs.

• Lesions are usually asymptomatic, with occasional pruritus.

• Little or no surrounding erythema or edema is present.

• Regional adenopathy is common.

Causes of impetigo include Staphylococci (staph) and less frequently Streptocci (Strep). A person becomes infected through any opening, crack, lesion or cut in the skin. These “breaks” can include insect bites, animal bites, or human bites, or other injury or trauma to the skin. Impetigo may occur on skin where there is no visible break

• Cellulitis

• Lymphangitis

• Suppurative Lymphadenitis

• Staphylococal scalded skin syndrome

• Scarlet fever

• Osteomyelitis

• Pneumonia

• Septicemia

• Guttatre psoriases

Impetigo is highly contagious and is quickly spread through contact with an infected person.

This contact can include even sharing towels with an infected person.

It is also transmitted by direct contact with the lesions.

Impetigo begins as an itchy red sore that blisters, oozes and finally crusts. It then spreads quickly unless promptly treated.

Generalized symptoms include:

Skin lesion on the face or lips, or on the arms or legs, spreading to other areas. Typically this lesion begins as a cluster of tiny blisters which burst, followed by oozing and the formation of a thick honey- or brown-colored crust that is firmly stuck to the skin.

Itching blister:

• Filled with yellow or honey-colored fluid

• Oozing and crusting over

• Rash (may begin as a single spot, but if person scratches it, it may spread to other areas).

• In infants, a single or possibly multiple blisters filled with pus, easy to pop and – when broken – leave a reddish raw-looking base.

• Lymphadenopathy – local lymph nodes near the infection may be swollen.

All but the most complicated case of impetigo are treated on an outpatient basis.

Treatment itself generally consists of a topical antibiotics, for example Bactroban or Altabax.

While oral antibiotics used includes the cephalexin class of antibiotics (Keflex), Amoxicillin and clavulanate (Augmentin); Dicloacillin (Dycil, Dynapen) and less commonly now erythromycin.

Uncomplicated case generally respond rapidly to antibiotic therapy.

Because impetigo responds rapidly to antibiotic therapy, the prognosis is excellent although it can reoccur.

Generally the lesions seldom scar, except in the most severe of cases.

Impetigo, impetigo contagiosa, impetigo bullosa, streptococcal impetigo, staphylococcal impetigo, nonbullous impetigo, bullous impetigo, crusted tetter, pyoderma, group A beta hemolytic streptococci, GABHS

Pat

Impetigo is a skin disorder caused by bacterial infection and characterized by crusting skin lesions.

Impetigo is a common skin infection. It is most common in children, particularly children in unhealthy living conditions. In adults, it may follow other skin disorders. Impetigo may follow a recent upper respiratory infection such as a cold or other viral infection. It is similar to cellulitis, but is more superficial, involving infection of the top layers of the skin with streptococcus (strep), staphylococcus (staph), or both.

The skin normally has many types of bacteria on it, but intact skin is an effective barrier that keeps bacteria from entering and growing within the body. When there is a break in the skin, bacteria can enter the body and grow there, causing inflammation and infection. Breaks in the skin may occur with insect bites, animal bites, or human bites; or other injury or trauma to the skin. Impetigo may occur on skin where there is no visible break.

Impetigo begins as an itchy, red sore that blisters, oozes and finally becomes covered with a tightly adherent crust. It tends to grow and spread. Impetigo is contagious. The infection is carried in the fluid that oozes from the blisters. Rarely, impetigo may form deeper skin ulcers.

Skin lesion on the face/ lips, or on the arms or legs, spreading to other areas. Typically this lesion begins as a cluster of tiny blisters which burst, followed by oozing and the formation of a thick honey or brown colored crust that is firmly stuck to the skin.

Itching blister:

• Filled with yellow or honey-colored fluid

• Oozing and crusting over

Rash (may begin as a single spot, but if child digs at it, it may spread to other areas).

In infants, a single or possibly multiple blisters filled with pus, easy to pop and when broken leave a reddish raw-looking base.

Lymphadenopathy – local lymph nodes near the infection may be swollen.

Diagnosis is based primarily on the appearance of the skin lesion. A culture of the skin or mucosal lesion usually grows streptococcus or staphylococcus.

The goal is to cure the infection and relieve the symptoms.

A mild infection is typically treated with a prescription antibacterial cream such as Bactroban. Oral antibiotics (such as erythromycin or dicloxacillin) are also frequently prescribed and result in rapid clearing of the lesions.

Wash the skin several times a day, preferably with an antibacterial soap, to remove crusts and drainage.

Use a clean washcloth and towel each time. Do not share towels, clothing, razors, and so on with other family members. Wash the hands thoroughly after touching the skin lesions.

The sores of impetigo heal slowly and seldom scar. The cure rate is extremely high, but they often come back in young children.

• The infection could spread to other parts of the body. This is common.

• Children often have multiple patches of impetigo.

• A systemic infection could lead to kidney failure (post-streptococcal glomerulonephritis). This is a rare occurrence.

• Permanent skin damage and scarring (also extremely rare).

Good general health and hygiene help to prevent infection. Minor abrasions or areas of damaged skin should be thoroughly cleansed with soap and clean water. A mild antibacterial agent may be applied if desired.

Impetigo is contagious, so avoid skin contact with drainage from impetigo lesions.

Update Date: 4/15/2003

Medline Plus

Br J Dermatol. 2007 Dec

Durupt F, Mayor L, Bes M, Reverdy ME, Vandenesch F, Thomas L, Etienne J. INSERM, U851, 69008 Lyon, France; Université Lyon 1, Centre National de Référence des Staphylocoques, Faculté Laennec, 69008 Lyon, France, and Service de Dermatologie, Hôtel Dieu & Université Lyon 1, 69288 Lyon cedex 02, France.

Background The precise role of Staphylococcus aureus toxins and nasal carriage in common skin infections remains unclear.

Objectives To seek correlations between toxin expression, S. aureus nasal carriage and clinical manifestations in patients with community-acquired furuncles and impetigo.

Methods From November 2004 to August 2005, we studied clinical data and bacteriological samples prospectively collected from 121 patients presenting with furuncles or impetigo.

Results Sixty-four patients (31 with furuncles and 33 with impetigo) had S. aureus-positive skin culture. Panton-Valentine leukocidin (PVL) genes were present in 13 of 31 (42%) isolates from furuncles and were associated with epidemic furunculosis. Exfoliative toxin genes were present in 10 of 10 (100%) and 12 of 21 (57%) bullous and nonbullous impetigo isolates, respectively. Nasal carriage of S. aureus was found in 58% of patients overall. It was strongly associated with chronic furunculosis but not with simple furuncles (88% vs. 29%, P < 0.007). Skin and nose isolates from a given patient always had identical characteristics. Methicillin-resistant S. aureus accounted for four of 64 (6%) positive skin cultures.

Conclusions PVL is not involved in all types of furuncles but is associated with epidemic furunculosis. Both bullous and nonbullous forms of impetigo are associated with exfoliative toxins. Staphylococcus aureus nasal carriage is associated with the chronicity of furuncles.

PMID: 17916211 PubMed - in process]

Br J Dermatol. 2007

Rørtveit S, Rortveit G. Municipal Health Services of Austevoll Kommune, 5399 Bekkjarvik, Norway.sverre.rortveit@aknett.net

BACKGROUND: Little is known about incidence and natural variation of impetigo in general populations.

OBJECTIVES: To investigate the natural course of impetigo in a well-defined population, and to study the resistance pattern of the causal bacteria over time.

METHODS: This is a population-based incidence study in Austevoll, an island community of 4457 inhabitants in Norway, in the years 2001-2005. Incidence rates are given as events per person-year. Epidemic periods were identified by statistical process-control analyses.

RESULTS: The incidence rate of impetigo for the whole study period was 0.017 events per person-year, corresponding to a total of 334 cases. The incidence rates were 0.009, 0.026, 0.019, 0.016 and 0.009 in the years 2001, 2002, 2003, 2004 and 2005, respectively. Three epidemics were identified, starting in August of 2002, 2003 and 2004, lasting for 11, 11 and 5 weeks, respectively. Incidence rates in these epidemic periods were 0.099, 0.045 and 0.074, respectively. In epidemic periods, Staphylococcus aureus was the causal bacterium in 89% (117/132) of cases, while this proportion was 68% (84/123) in nonepidemic periods (P < 0.01). Staphylococcus aureus was resistant to fusidic acid in 84% (98/117) and 64% (54/84) of impetigo cases in epidemic and nonepidemic periods, respectively (P < 0.01). When investigating all types of infections caused by S. aureus in the study period, the proportion of fusidic acid resistance in impetigo cases (152/201, 76%) differed significantly from fusidic acid resistance in other infections (18/116, 16%) (P < 0.01).

CONCLUSIONS: Distinctive epidemic outbreaks occurred during the summer of three of the five follow-up years. In outbreaks, S. aureus was more frequently the causal agent and the sensitivity to fusidic acid decreased significantly.

PMID: 17553056 PubMed - indexed for MEDLINE]

http://www.nlm.nih.gov/medlineplus/impetigo.html

http://www.skinsite.com/info_impetigo.htm

http://www.dermnetnz.org/bacterial/impetigo.html

http://www.emedicine.com/emerg/topic283.htm

http://www.emedicine.com/ped/topic1172.htm (1)

http://www.netdoctor.co.uk/diseases/facts/impetigo.htm

http://edcp.org/factsheets/impetigo.html

http://dermatlas.med.jhmi.edu/derm/result.cfm?Diagnosis=16

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17367045&ordinalpos=35&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

American Family Physicians

http://www.aafp.org/afp/20070315/859.html

ICD-9-CM Diagnosis 684

Impetigo

A common superficial bacterial infection caused by STAPHYLOCOCCUS AUREUS or group A beta-hemolytic streptococci.

Characteristics include pustular lesions that rupture and discharge a thin, amber-colored fluid that dries and forms a crust. This condition is commonly located on the face, especially about the mouth and nose.

684 is a specific code that can be used to specify a diagnosis

684 contains 14 index entries

• 680 Carbuncle and furuncle

• 681 Cellulitis and abscess of finger and toe

• 682 Other cellulitis and abscess

• 683 Acute lymphadenitis

• 684 Impetigo

• 685 Pilonidal cyst

• 686 Other local infections of skin and subcutaneous tissue

L01 - Impetigo

Excludes: impetigo herpetiformis ( L40.1 ) pemphigus neonatorum ( L00 )

L01.0 - Impetigo [any organism] [any site]

Bockhart's impetigo

L01.1 - Impetiginization of other dermatoses

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