Impetigo overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
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]
Historical Perspective
Classification
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.[3]
Pathophysiology
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.[4]
Causes
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.[5][6][7][3]
Differentiating Impetigo from other Diseases
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.[8]
Epidemiology and Demographics
In 2010, 140 million people suffered from impetigo. It is more common among children aged 2 to 5 years.[9]
Risk Factors
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.[10] Handwashing decreseas the incidence of impetigo by 34%.[11]
Screening
The United States Preventive Services Task Force (USPSTF) has not issued any guidelines for the screening of impetigo.
Natural History, Complications and Prognosis
If left untreated, most cases of non-bullous impetigo resolve within 1-2 weeks. The complications of impetigo include poststreptococcal glomerulonephritis and rheumatic fever.[12][13][14][15][16]
Diagnosis
History and Symptoms
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.[3][17]
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.[3]
Physical Examination
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.[15][3]
Laboratory Findings
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.[15][2]
Xray
Xrays do not contribute in the diagnosis of impetigo.
CT Scan
CT scan does not contribute in the diagnosis of impetigo.
MRI
MRI does not contribute in the diagnosis of impetigo.
Ultrasound
Ultrasound does not contribute in the diagnosis of impetigo.
Other Imaging Findings
Other imaging findings do not contribute in the diagnosis of impetigo.
Other Diagnostic Studies
Immunodeficiency can be evaluated in case of recurrence of impetigo. Other aspects may involve a detailed review of conditions like malnutrition, leukemia and diabetes.
Treatment
Medical Therapy
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.[3][18]Topical or oral antibiotics are usually prescribed.
Surgery
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.[19]
Primary Prevention
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%.[11]
Secondary Prevention
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.
References
- ↑ Oumeish I, Oumeish OY, Bataineh O (2000). "Acute bacterial skin infections in children". Clin Dermatol. 18 (6): 667–78. PMID 11173202.
- ↑ 2.0 2.1 Ibrahim F, Khan T, Pujalte GG (2015). "Bacterial Skin Infections". Prim Care. 42 (4): 485–99. doi:10.1016/j.pop.2015.08.001. PMID 26612370.
- ↑ 3.0 3.1 3.2 3.3 3.4 3.5 Cole C, Gazewood J (2007). "Diagnosis and treatment of impetigo". Am Fam Physician. 75 (6): 859–64. PMID 17390597.
- ↑ "ISDH: Impetigo".
- ↑ Darmstadt GL, Lane AT (1994). "Impetigo: an overview". Pediatr Dermatol. 11 (4): 293–303. PMID 7899177.
- ↑ Demidovich CW, Wittler RR, Ruff ME, Bass JW, Browning WC (1990). "Impetigo. Current etiology and comparison of penicillin, erythromycin, and cephalexin therapies". Am J Dis Child. 144 (12): 1313–5. PMID 2244610.
- ↑
- ↑ Hartman-Adams H, Banvard C, Juckett G (2014). "Impetigo: diagnosis and treatment". Am Fam Physician. 90 (4): 229–35. PMID 25250996.
- ↑ Vos T, Flaxman AD, Naghavi M, Lozano R, Michaud C, Ezzati M; et al. (2012). "Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010". Lancet. 380 (9859): 2163–96. doi:10.1016/S0140-6736(12)61729-2. PMID 23245607.
- ↑ Carroll JA (1996). "Common bacterial pyodermas. Taking aim against the most likely pathogens". Postgrad Med. 100 (3): 311–3, 317–22. doi:10.3810/pgm.1996.09.84. PMID 8795661.
- ↑ 11.0 11.1 Luby SP, Agboatwalla M, Feikin DR, Painter J, Billhimer W, Altaf A; et al. (2005). "Effect of handwashing on child health: a randomised controlled trial". Lancet. 366 (9481): 225–33. doi:10.1016/S0140-6736(05)66912-7. PMID 16023513. Review in: Evid Based Med. 2006 Jun;11(3):88
- ↑ McDonald MI, Towers RJ, Andrews RM, Benger N, Currie BJ, Carapetis JR (2006). "Low rates of streptococcal pharyngitis and high rates of pyoderma in Australian aboriginal communities where acute rheumatic fever is hyperendemic". Clin Infect Dis. 43 (6): 683–9. doi:10.1086/506938. PMID 16912939.
- ↑ Weinstein L, Le Frock J (1971). "Does antimicrobial therapy of streptococcal pharyngitis or pyoderma alter the risk of glomerulonephritis?". J Infect Dis. 124 (2): 229–31. PMID 4942062.
- ↑ Cohen PR (2016). "Bullous impetigo and pregnancy: Case report and review of blistering conditions in pregnancy". Dermatol Online J. 22 (4). PMID 27617460.
- ↑ 15.0 15.1 15.2 Duggal SD, Bharara T, Jena PP, Kumar A, Sharma A, Gur R; et al. (2016). "Staphylococcal bullous impetigo in a neonate". World J Clin Cases. 4 (7): 191–4. doi:10.12998/wjcc.v4.i7.191. PMC 4945591. PMID 27458596.
- ↑ Eison TM, Ault BH, Jones DP, Chesney RW, Wyatt RJ (2011). "Post-streptococcal acute glomerulonephritis in children: clinical features and pathogenesis". Pediatr Nephrol. 26 (2): 165–80. doi:10.1007/s00467-010-1554-6. PMID 20652330.
- ↑ Adams BB (2002). "Dermatologic disorders of the athlete". Sports Med. 32 (5): 309–21. PMID 11929358.
- ↑ Koning S, van der Sande R, Verhagen AP, van Suijlekom-Smit LW, Morris AD, Butler CC; et al. (2012). "Interventions for impetigo". Cochrane Database Syst Rev. 1: CD003261. doi:10.1002/14651858.CD003261.pub3. PMID 22258953.
- ↑ Geria AN, Schwartz RA (2010). "Impetigo update: new challenges in the era of methicillin resistance". Cutis. 85 (2): 65–70. PMID 20349679.