Hospital Medicine

Impetigo

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I. What every physician needs to know.

Impetigo is a superficial skin infection most commonly caused by gram-positive bacteria such as S. aureus and group A beta-hemolytic streptococcus. Community acquired methicillin resistant staphylococcal aureus (CA-MRSA) has also been known to be a causative pathogen in certain communities. Although impetigo occurs most often in children 2 to 5 years old, it can occur in patients of any age. Impetigo is highly contagious and can rapidly spread through day care centers and schools from close contact and poor hygiene. It is often characterized by the development of honey-colored crusted lesions around the mouth, nose, chin, and other parts of the face.

There are two types of impetigo: non-bullous impetigo also called impetigo contagiousa and bullous impetigo.

Non-bullous impetigo is the more frequently seen form of impetigo. In non-bullous impetigo, a superficial bacterial infection causes a localized inflammatory reaction to form small vesicles and pustules on the skin surface. Eventually, these pustules rupture leaving behind liquid debris that dries upon exposure to air causing the characteristic honey-colored crusting. These lesions usually can be found around the peri-oral areas and nasolabial folds but can spread to other sites through autoinoculation.

Bullous impetigo, on the other hand, is an intra-epidermal variant caused by toxin-producing S. aureus that results in the development of flaccid bullae on the skin surface. These large collections of fluid also rupture and leave a honey-colored, crusted residue visibly overlying the skin. Sometimes the roof of the ruptured bullae can also be visualized. The pathophysiology behind the formation of subcorneal bullae in bullous impetigo is secondary to an exfoliative toxin produced by S. aureus that targets the desmosome adhesion protein desmoglein 1. Loss of desmosome adhesion consequently causes intra-epidermal separation and bulla formation similar to the mechanism seen in pemphigous vulgaris.

Most cases of impetigo are due to staphylococcus bacteria, but group A beta-hemolytic streptococcus are responsible for infection in a minority of cases. In cases of streptococcal impetigo, post-streptococcal glomerular nephritis has been described. As such, it is imperative that clinicians have a high degree of suspicion for a post-streptococcal glomerular nephritis in patients presenting with edema, hypertension, and tea-colored urine following a localized skin infection.

II. Diagnostic Confirmation: Are you sure your patient has Impetigo?

The diagnosis of both bullous and non-bullous impetigo is primarily clinical and seldom requires additional laboratory or histological confirmation. Nevertheless, gram stains of material from underneath a scraped crust usually demonstrate gram-positive cocci. Bacterial culture of debris or bulla fluid would typically grow S. aureus. Sensitivities may aid when a diagnosis of MRSA is suspected, in treatment failure, or when considering resistance patterns in some settings. However, it must be reiterated that these tests are not needed for diagnosis or treatment in most circumstances. Furthermore, biopsies samples are not necessary to make the diagnosis.

A. History Part I: Pattern Recognition:

Non-bullous impetigo usually presents with honey-colored or light brown crusts around the mouth, nose, chin, and other parts of the face. Autoinoculation may spread the infection to other parts of the body, as well. The infection begins with an erythematous macule or papule that quickly becomes a vesicle or pustule that eventually ruptures its contents to leave behind a honey-colored crust. In bullous impetigo a toxin causes intra-epidermal cleavage. This variant of impetigo usually begins as a vesicle that quickly enlarges into a flaccid bulla filled with fluid. These large bullae then rupture and leave behind fluid that also crusts over and develops an orange-brown hue. Oftentimes the roof of the bulla can be visualized on the skin once the bulla ruptures.

B. History Part 2: Prevalence:

A British study demonstrated that the annual incidence of impetigo was about 3% in children less than 4 years old and close to 2% in children 5 years old through the early teen years. In a Dutch study, the annual incidence of impetigo was found to be 16.5 – 20.6 per 1000 person years under 18 years old. Moreover, impetigo is the most common bacterial skin infection in children and is the third most common skin disease in children. Impetigo is rare in adults but can be seen in homeless populations and in immune compromised individuals. Up to 70% of impetigo cases are non-bullous in nature. CA-MRSA is also commonly involved as a primary pathogen in impetigo in certain settings and communities.

C. History Part 3: Competing diagnoses that can mimic Impetigo.

Numerous dermatological conditions can mimic both non-bullous and bullous impetigo. Ecthyma, also called streptococcal pyoderma can similarly present with crusting. The key difference being that ecythma is characteristically a much deeper infection and removal of the crust often reveals an ulceration of the skin with moderate amounts of surrounding erythema. Impetigo is a very superficial infection and crust removal shows only mild skin erosion without extensive surrounding erythema.

Superficial fungal infections are also in the differential diagnosis for a patient with impetigo. Some superficial fungal infections can also cause pustule formation. Fungal infections, however, can easily be diagnosed by a positive potassium hydroxide (KOH) stain. A well-demarcated, annular patch with scale rather than crust usually identifies dermatophyte infections. Other entities also to consider include candidiasis that can characteristically present with beefy red papules and plaques most commonly in the intertriginous area. Atopic dermatitis, contact dermatitis, and insect bites may also present similarly although these will lack the characteristic honey-colored crusts of impetigo.

Any dermatological disease with bullae formation is potentially in the differential diagnosis when considering bullous impetigo. Bullous pemphigoid and pemphigous vulgaris are two blistering diseases that may resemble bullous impetigo. These diseases would be more appropriate to consider with the formation of bullae in multiple areas, bullous impetigo not responsive to therapy, or in patients with chronic bullae. Staphylococcal scaled skin syndrome also results in flaccid bullae formation. However, gram stain and culture of fluid from intact bullae in patients with staphylococcal scaled skin syndrome are sterile. Furthermore, these patients have very tender, erythematous, often desquamated skin. More pronounced systemic symptoms such as fever, leukocytosis, and tachycardia are commonly seen.

Contact dermatitis, insect bites, and thermal burns can also produce bullae whose contents may rupture and cause crusting. These may be difficult to distinguish from bullous impetigo by exam alone but a careful history will often be quite revealing.

D. Physical Examination Findings.

Honey-colored or light brown crusts around the mouth, nose, chin, and other parts of the face characterize non-bullous impetigo. Removal of the dried liquid debris or crusts reveals a superficial, shining base. In bullous impetigo the physical exam is often notable for flaccid bullae with well-defined margins that may be intact or may have ruptured also leaving behind honey-colored crusts. Sometimes, ruptured bullae leave behind a thin, membrane-like structure called a “collarette of scale” which is the remnant of the bullae roof. Regional lymphadenopathy may occur but is not common.

E. What diagnostic tests should be performed?

The diagnosis of both bullous and non-bullous impetigo is primarily clinical and seldom requires additional laboratory or histological confirmation. Routinely, studies are not performed to make the diagnosis of impetigo. However, it is reasonable to obtain gram stains, cultures, and sensitivities of the material underneath crusts or liquid inside a bulla when a diagnosis of MRSA is suspected, in treatment failure, or when considering resistance patterns in some settings.

Additional tests may be ordered when excluding competing diagnoses. Such testing may include KOH stain, patch tests, HSV testing, and direct and indirect immunoflorescence. A urinalysis, ASO titers, and ant-DNase B may be useful in patients with suspected post-streptococcal glomerular nephritis.

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Laboratory studies are not required to make the diagnosis of impetigo, as it is a clinical diagnosis. However, the following laboratory findings may be found if these studies are obtained:

  • CBC may reveal mild leukocytosis, depending on the area of skin that is impetiginized.

  • Wound gram stain and culture may reveal Staphylococcus aureus, MRSA, or group A Streptococcus.

  • ESR may be elevated if the area of involvement is extensive.

  • ASO titers may be positive/elevated.

  • Anti-DNAse B and direct and indirect immunofluoresence of the skin may be positive for infection.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

None

F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.

Wound cultures are often unnecessary as this disease, in the eye of a trained clinician, can be diagnosed clinically.

III. Default Management.

Most cases of non-bullous impetigo can ideally be treated with topical antibiotics. Oral antibiotics can be used for more extensive disease, bullous impetigo, suspected MRSA, or when the application of topical agents is not practical. The agent selected for treatment should have activity against both staphylococcal and streptococcus bacteria. Currently, the first line treatment for limited, non-bullous impetigo is 1% mupirocin cream or ointment applied three times per day. More recently, retapamulin 1% ointment was found to be an excellent alternative to mupirocin.

Numerous oral antibiotic regiments are outlined below. It is important to note that several meta-analyses demonstrated the superiority of topical antibiotics to placebo and found topical antibiotics to be more effective than oral erythromycin for treatment of limited disease. Currently, there is a lack of evidence to support the use of topical disinfectant solutions for the treatment of impetigo.

A. Immediate management.

Limited Disease: mupirocin 2% cream/ointment TID to affected site. Retapamulin 1% ointment applied BID to affected site.

Systemic treatment: dicloxacillin 250- 500 mg PO QID x 7-10 days (adults), dicloxacillin 25 mg/kg/d PO QID x 7-10 days (children), cephalexin 250- 500 mg PO QID x 7-10 days (adults), cephalexin 40 -50 mg/kg/d x 7-10 days (children).

Systemic treatment (CA-MRSA): minocycline 100 mg PO BID x 7-10 days (adults), doxycycline 100mg PO BID x 7-10 days (adults), TMP-SMX 160 mg TMP + 800 mg SMX BID x 7-10 days (adults), clindamycin 300–450 mg PO QID x 7-10 days (adults), clindamycin 15 mg/kg/d x 7-10 days (children), linezolid 600 mg PO BID x 7-10 days (adults).

B. Physical Examination Tips to Guide Management.

Once antibiotic therapy is initiated with either topical or oral agents impetigo usually clears without cosmetic disfigurement. Persistent lesions, the formation of new vesicles, pustules, or bullae should alert the physician of a potential treatment failure that may be due to resistance, inadequately dosed antibiotics, or alternative diagnoses. Edema, leg swelling, and dark colored urine are highly suspicious for post-streptococcal glomerularnephritis.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

Laboratory testing is typically not needed to monitor response to therapy for most cases of impetigo. However, laboratory testing would be indicated in cases of persistent lesions, suspicion for alternative diagnoses, treatment failures, and for post-streptococcal glomerularnephritis. In these cases it would be advisable to obtain: gram-stain of lesions, culture and sensitivities, ASO titers, UA, anti-DNase B, and if necessary direct and indirect immunofluorescence.

D. Long-term management.

Continuation of antibiotics until the disease has cleared and good hygiene are mainstays of long-term therapy.

E. Common Pitfalls and Side-Effects of Management.

Discontinuing antibiotics prior to complete resolution of the disease may result in recurrence or spread. Secondary cellulitis may also occur if there are open wounds within or surrounding the impetiginized areas of skin.

IV. Management with Co-Morbidities.

Patients with diabetes may have elevated blood glucose levels during the infection, so appropriate management of their hyperglycemia is indicated.

Patients with underlying immunocompromising diseases such as HIV or on immunosuppressive therapy should have close monitoring to ensure early diagnosis and timely resolution of their infection.

A. Renal Insufficiency.

Systemic antibiotics that are renally cleared should be dosed according to GFR.

B. Liver Insufficiency.

Systemic antibiotics that are hepatically metabolized should be used with caution in patients with liver disease.

C. Systolic and Diastolic Heart Failure.

No change in standard management.

D. Coronary Artery Disease or Peripheral Vascular Disease.

No change in standard management.

E. Diabetes or other Endocrine issues.

No change in standard management.

F. Malignancy.

No change in standard management.

G. Immunosuppression (HIV, chronic steroids, etc).

No change in standard management.

H. Primary Lung Disease (COPD, Asthma, ILD).

No change in standard management.

I. Gastrointestinal or Nutrition Issues.

No change in standard management.

J. Hematologic or Coagulation Issues.

No change in standard management.

K. Dementia or Psychiatric Illness/Treatment.

It is important to ensure compliance in patients who may not be able to care for themselves.

V. Transitions of Care.

A. Sign-out considerations While Hospitalized.

Hospitalization is usually not indicated.

B. Anticipated Length of Stay.

N/A

C. When is the Patient Ready for Discharge.

N/A

D. Arranging for Clinic Follow-up.

Follow up with the patient's PCP in 3 days is important to ensure resolution/improvement of the condition.

1. When should clinic follow up be arranged and with whom.

Follow-up with the patient's PCP is recommended. Occasionally, for severe bullous impetigo, it may be helpful to have a dermatolgist also follow up the patient.

2. What tests should be conducted prior to discharge to enable best clinic first visit.

None

3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit.

None

E. Placement Considerations.

N/A

F. Prognosis and Patient Counseling.

Prognosis is usually good, with complete resolution of the symptoms. Occassionally, patients may have post-inflammatory hyper or hypo pigmentation of the affected skin. However, patients should be counselled that this often fades with time.

VI. Patient Safety and Quality Measures.

A. Core Indicator Standards and Documentation.

N/A

B. Appropriate Prophylaxis and Other Measures to Prevent Readmission.

Prophylaxis is rarely indicated. Good hygiene and avoiding direct contact with infected lesions can help reduce transmission of this condition.

VII. What's the evidence?

Bolaji, RS, Dabade, TS, Gustafson, CJ. "Treatment of impetigo: oral antibiotics most commonly prescribed". J Drugs Dermatol. vol. 11. 2012. pp. 489-94.

Cole, C, Gazewood, J. "Diagnosis and treatment of impetigo". Am Fam Physician. vol. 75. 2007. pp. 859-64.

Bernard, P. "Management of common bacterial infections of the skin". Curr Opin Infect Dis. vol. 21. 2008. pp. 122-8.

Darmstadt, GL, Lane, AT. "Impetigo: an overview". Pediatr Dermatol. vol. 11. 1994. pp. 293-303.

Geria, AN, Schwartz, RA. "Impetigo update: new challenges in the era of methicillin resistance". Cutis. vol. 85. 2010. pp. 65-70.

Konin, S, Van Der Wouden, JC, Chosidow, O. "Efficacy and safety of retapamulin ointment as treatment of impetigo: randomized double-blind multicentre placebo-controlled trial". Br J Dermatol. vol. 158. 2008. pp. 1077-82.

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