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Bullous Impetigo

Bullous impetigo is a contagious bacterial cutaneous infection with characteristic bullae. Impetigo can be divided into bullous and nonbullous type, both of which have different pathophysiologies and presentations.


Presentation

Bullous impetigo typically presents with superficial bullae of varying sizes which are transient and rupture spontaneously even before presentation. The lesions usually affects face, trunk, extremities, buttocks and the perineal regions. It could affect more than one part of the body by spread through autoinoculation. The lesions occur on intact skin with minimal erythema and no peripheral adenopathy. However, it could infect preexisting skin lesions causing secondary infections.

Patients with bullous impetigo usually have a history of contact either with an infected individual or one who is a chronic carrier of S. aureus. There is also a history of residing in hot, humid environments, poor hygiene practices, or engagement in contact sports [15]. Immunosuppressive states such as chemo or radiation therapy, steroid treatment, diabetes mellitus, and infection with HIV predispose individuals to impetigo. However, recurrent impetigo occurs in the absence of predisposing factors in the setting of a congenital immune deficiency [16].

Bullous impetigo typically presents with thin-roofed, fragile and transparent blisters which contain clear fluid initially, but which becomes cloudy and deep yellow with time. These blisters or bullae rupture within 1-3 days leaving crusts or collarette of scale over an erythematous floor which becomes visible when the crust is removed. Bullous impetigo rarely involves the oral mucosa and it is not associated with regional adenopathy as opposed to nonbullous impetigo. Worth noting, however, is the fact that bullous impetigo is not as contagious as the nonbullous type [17]. In infants, there are generalized symptoms including fever, diarrhea, and malaise.

Fever
  • The patient was also having fever and refused any oral intake. At this point, a probable diagnosis of bacterial skin infection was considered and the patient was admitted.[ukm.pure.elsevier.com]
  • Fever persisted, not too high, around 38. She was only taking cefalexin and the topical ointments. We were saving money and felt we didn't need the claricort.[patient.info]
  • A 21-month-old African American presented to the pediatric emergency department at our institution with complaints of a "rash" on the buttocks, fever, and unwillingness to walk. His mother stated that he had been in the[jamanetwork.com]
  • Children with localized exfoliative staphylococcal infections, such as bullous impetigo , were excluded from the study. isolates isolates Furuncles 7 7 (100) Abscess 9 8 (89) Carbuncle 26 20 (77) Cellulitis 25 19 (76) Staphylococcal scarlet fever 27 17[freethesaurus.com]
  • It may cause scarlet fever in severe case of infection. About 10% of the children with bullous impetigo can get lymphangitis or cellulitis. Diagnosis : The doctor can detect impetigo through blisters or lesions on the skin.[diseaseslab.com]
Fishing
  • Great sources are wild-caught fish like salmon, tuna, and halibut. Three servings per week will suffice. Stay away from sugary snacks and fried foods. Eat minimal red meats.[healdove.com]
Blister
  • Furthermore, epidemolysin was measured in the blister fluid of 3 of 5 children with bullous impetigo but not in blister fluid from control patients with other blistering eruptions.[ncbi.nlm.nih.gov]
  • PubMed was used to search the following terms, separately and in combination: blister, blistering, bullous, gestationis, herpes, herpetiformis, impetigo, pemphigoid, pregnancy, pregnant, psoriasis, pustular, virus.[ncbi.nlm.nih.gov]
  • Exfoliative toxin A, produced by Staphylococcus aureus, causes blisters in bullous impetigo and its more generalized form, staphylococcal scalded-skin syndrome.[ncbi.nlm.nih.gov]
  • Painless, Delicate Blisters In Bullous Impetigo pain is very rare. These blisters are usually painless. Bullous Impetigo rashes are delicate and rupture often.[primehealthchannel.com]
  • Bullous impetigo is at the mild end of a spectrum of blistering skin diseases caused by a staphylococcal exfoliative toxin that, at the other extreme, is represented by widespread painful blistering and superficial denudation (the staphylococcal scalded[ncbi.nlm.nih.gov]
Eruptions
  • Furthermore, epidemolysin was measured in the blister fluid of 3 of 5 children with bullous impetigo but not in blister fluid from control patients with other blistering eruptions.[ncbi.nlm.nih.gov]
  • It is important to distinguish benign physiological rashes from significant pathological eruptions. A case of generalized pustular eruption due to Staphylococcus aureus in a neonate is reported.[ncbi.nlm.nih.gov]
  • Bullous impetigo is a blistering eruption caused by Staphylococcus aureus. The earliest lesion is a vesicle, which rapidly evolves into a bulla.[skincareguide.ca]
  • The disease has a chronic benign, relapsing course and the pustular eruption has the distinctive histology of a subcorneal bulla containing neutrophils.[drmhijazy.com]
  • The eruption appears clinically similar to non-bullous impetigo. Usually S. aureus is involved. The underlying skin disease may improve with successful treatment of the impetigo, and the converse may also be true.[pedclerk.bsd.uchicago.edu]
Pruritus
  • Rarely, patients may report burning and pruritus. The diagnosis of impetigo is mostly based on the characteristic appearance of the lesions.[steadyhealth.com]
  • Anti Histamin, Generasi 2 Jika pruritus signifikan, antihistamin dapat diresepkan untuk membantu meminimalkan kemungkinan menggaruk. Menghindari trauma pada kulit dapat mencegah atau membatasi penyebaran impetigo oleh autoinokulasi.[de.slideshare.net]
  • Pruritus is common; scratching may spread infection, inoculating adjacent and nonadjacent skin. Diagnosis Diagnosis of impetigo and ecthyma is by characteristic appearance.[merckmanuals.com]
  • Pemphigus herpetiformis is a rare variant of vulgar pemphigus, clinically resembling dermatitis herpetiformis (vesicles, papules, strong pruritus) and histologically is characterized by acantholysis and positive immunofluorescence finding.[atlases.muni.cz]
Nikolsky's Sign
  • sign (sheet-like removal of epidermis with sliding pressure) Highly contagious; may occur in outbreaks ( Antonie Van Leeuwenhoek 2009;95:387 , Euro Surveill 2009;14:19372 ) May affect caregivers ( Cutis 2008;81:115 ) Usually indicates penicillin resistance[pathologyoutlines.com]
  • […] bullae , which go on to rupture and form thin, brown crusts Lateral traction causes sloughing of the skin ( positive Nikolsky sign ) Localization : trunk and upper extremities Ecthyma : ulcerative impetigo that extends into the dermis ; ( coin-sized[amboss.com]
  • Associated systemic involvement Staphylococcal scalded skin syndrome Cutaneous tenderness, positive Nikolsky sign, large areas of desquamation or exfoliation. Infection spreads hematogenously because of absence of protective antitoxin antibodies.[ncbi.nlm.nih.gov]
  • The result is erythematous, tender and desquamating areas of skin, usually with a positive Nikolsky’s sign.[cirp.org]
  • The erythematous skin wrinkles and peels off at sites of minor trauma or with minimal lateral pressure with the examiner's fingertip, illustrating the positive Nikolsky's sign (also found in TEN).[barnardhealth.us]
Alopecia
  • Alopecia areata Diffuse alopecia Defluvium Pseudopelade of Brocq Alopecia in lupus erythematodes Follicular mucinosis (alopecia mucinosa) Primary follicular mucinosis Secondary follicular mucinosis in mycosis fungoides Alopecia androgenica Trichotillomania[atlases.muni.cz]
  • The face and scalp are also a common site of involvement in secondary syphilis in which individuals develop moth-eaten alopecia , scaly or moist papules around the nose and at the angles of the mouth.[barnardhealth.us]
  • (Flaccid Bullae) Fig.283-1 Pemphigus (Nicoklysk's signe ve) Fig. 283-2 Pemphigus vulgaris(infected bullae) Fig.283 Pemphigus vulgaris Fig.283-4 Pemphigus-Subungual bullae Fig. 283-5 Pemphigus vulgaris Fig.283-2 Pemphigus of the scalp and cicatricial alopecia[drmhijazy.com]
  • Chronic forms show acanthosis with only minimal spongiosis and resemble psoriasis. 5.2.35.1 Pityriasis amiantacea Clinical signs: sticky, asbestos-like scales location: scalp may be complicated by alopecia often accompanied by seborrhoic dermatitis Histology[atlases.muni.cz]
Crusts On Face
  • The resulting erosive lesions may be covered by a yellow crust.[dermis.net]
  • The disease is characterized by fragile vesicles and flaccid blisters, most often presenting as erosive lesions covered by a yellow crust. The face, trunk and extremities of children under 5 years of age (particularly neonates) are mainly affected.[orpha.net]
  • The resulting erosive lesions may be covered by a yellow crust. The face, trunk and extremities of infants and children are mainly affected when there is Bullous Impetigo . Bullous Impetigo is also known as Impetigo Contagiosa Staphylogenes.[impetigo-treatment.learnandenjoy.com]
  • My face was really raw afterwards though, and I have some post inflammation hyperpigmentation (where the skin darkens from the inflammation) but this can be covered in makeup and will fade in good time.[earthclinic.com]

Workup

Diagnosis of bullous impetigo is made by the history and physical examination of the lesions. There is almost always a history of contact with infected persons and predisposing factors such as residing in hot humid and crowded environment.

The bullae are seen in bullous impetigo, although most patients present after these have ruptured and crusted. The presence of abcesses and cellulitis increase the suspicion of MRSA.

Laboratory studies are not necessary in the diagnosis of bullous impetigo unless MRSA is suspected. In this case, skin swabs should be taken for cultures and sensitivities. Hematology tests are usually normal and, therefore, not indicated in diagnosis of bullous impetigo.

Treponema Pallidum
  • Further differentiated on the basis of culture characteristics and biochemical tests Treponema pallidum Diffuse erythematous lesions containing large number of treponemes.[ncbi.nlm.nih.gov]

Treatment

Most cases of bullous impetigo resolve spontaneously without treatment. However, standard treatment for bullous impetigo in the absence of systemic involvement is topical antibiotics. Intranasal antibiotics may be used to treat chronic nasal carriage of S aureus. Systemic antibiotics are indicated if there is systemic involvement or if there's no response to topical treatment. However, there are certain treatment recommendations based on the age of the patient and the severity of the disease.

Neonatal bullous impetigo is best treated with parenteral antibiotics including nafcillin, oxacillin, or clindamycin. In cases caused by MRSA, vancomycin is best. In adults, children, and infants with local disease without systemic manifestations, topical mupirocin or retapamulin is recommended. Adults, children, and infants with widespread skin lesions are treated with oral antibiotics including dicloxacillin, erythromycin, or a first generation cephalosporin such as cephalexin. In cases where MRSA is suspected, clindamycin, trimethoprim/sulfamethoxazole, or doxycycline is recommended.

Parenteral antibiotic treatment with nafcillin, oxacillin, or clindamycin is indicated in patients, including children and infants with systemic and deep cutaneous involvement of bullous impetigo. Parenteral vancomycin is preferred if MRSA is suspected.

Skin hygiene is critical in the management of bullous impetigo. Bathing twice daily with an antiseptic soap is recommended for all patients with impetigo. Adults and older children may use chlorhexidine to clean the affected area to reduce bacterial colonization, however this is not recommended for neonates and young children because of potential toxicity.

Prognosis

Impetigo may cause serious complications in neonates and infants and, therefore, requires adequate and timely treatment. Immunocompromised patients are also at a significant risk of developing complications from impetigo and unresponsiveness to treatment. Complications of bullous impetigo include cellulitis, stapylococcal scalded skin syndrome (SSSS), sepsis, and septic arthritis.

Etiology

Bullous impetigo is exclusively caused by staphylococcus aureus. Group II coagulase positive staphylococcus aureus, particularly the phage type 71, is by far the most common cause of bullous impetigo. This strain is particularly associated with scalded skin syndrome. Furthermore, methicicllin resistant staphylococcus aureus (MRSA) has been implicated in 20% of cases of bullous impetigo [3]. MRSA could be community-acquired or hospital-acquired.

Factors which predispose to hospital-acquired MRSA include prolonged placement of an indwelling catheter or other medical instruments and working in a hospital. On the other hand, community acquired MRSA is commonly seen in closely crowded institutions such as prisons and day care centres, and in immunosuppressed individuals or those with pre-existing skin diseases.

Epidemiology

Generally, impetigo is the commonest bacterial skin infection and accounts for 10% of all dermatological cases in Amrican pediatric clinics, something that makes it the third most common skin condition in children in the United States [2]. Always in the United States, peak incidence of impetigo occurs during summer and fall [4]. The disease is also predominant in the warmer southeastern part of the country.

Impetigo is seen more often in the tropics basically because of the warm humid climate, predominance of poor hygiene and crowded living conditions in those regions. Studies done in the Netherlands show that impetigo is also the third most common skin disease seen in primary care clinics [5] [6]. A study in Germany also indicated an increase in the yearly incidence of impetigo in children under 18 years of age [7]. A study conducted in Queensland, Australia observed that among 60 children who presented with bacterial skin infections, 27 were diagnosed with impetigo, 38% of which  were boys. The median age of the infection among the diagnosed children was 19 years [8]. Studies analysing the global prevalence of impetigo indicated that the highest incidence of impetigo complicating scabies is in Australian aboriginal regions [9].

Impetigo has no racial or gender predilections. While it occurs in persons of all ages, it is commonest in children between 2-5 years of age because of the predominant risk in daycare centers and nurseries. Bullous impetigo predominantly affects children under 2 years of age and could occur in neonates born from infected mothers.

Sex distribution
Age distribution

Pathophysiology

Bullous impetigo is caused by staphylococcus aureus in the presence of factors which promote its colonization on the skin, including hot humid environment, preexisting skin disease and deranged skin bacterial flora by antibiotic use. Immunosuppression is also a potent risk factor for bacterial proliferation on the skin, therefore, steroids, IV drug abuse, diabetes, and HIV increase the risk of bullous impetigo.

One-third of the population are carriers of S aureus in the anterior nares while 10% of the population have perineal, pharyngeal, and axillary carriage of the organism. Nasal carriers of the S aureus may develop impetigo on the nose and lips and may transmit the infection to close contacts. After transmission of the bacteria, the lesions develop after about 7-14 days. 

Skin diseases which are mostly associated with colonization and proliferation of S aureus include atopic dermatitis (with up to 90% colonization rate), scabies, dermatophytosis, and pediculosis. As shown in one study in atopic dermatitis, proteins involved in skin barrier and moisture production were under-expressed and there was over-expression of epidermal fatty acid-binding proteins which may be involved in the inflammatory response involved in impetigo [10]. Unlike the nonbullous type, bullous impetigo occurs on intact skin.

S aureus produces exfoliative toxins A and B which cause loss of cell adhesion in the dermal layer separating it from the dermal layer forming blisters. Exfoliative toxin A destroys desmoglein I, a substance which promotes cell adhesion. An exfoliative toxin D has been identified to be involved in the pathophysiology of impetigo [11].

Incidence of MRSA-associated impetigo has been on the rise over the last years. Most strains of community-acquired MRSA contain a unique exotoxin called panton-valentine leucocidin (P-VL) which is highly virulent. This exotocin causes necrosis of dermal tissues and lysis of leucocytes. These strains of S aureus are more often associated with abscesses and cellulitis [12] [13] [14]. This toxin is the cause of hematogenous spread of the disease causing generalized sequelae such as staphylococcal scalded skin syndrome.

Prevention

Proper hand washing and bathing with antiseptic soaps reduce bacterial colonization. Chronic nasal and perineal carriage of staphylococcal aureus should be treated with topical antibiotics. Contact with infected persons should be strictly avoided and infected children should be adequately treated before returning to schools since impetigo is highly contagious. Administration of zinc supplements to undernourished pregnant women reduces the incidence of impetigo in infants.

Summary

Bullous impetigo is a highly contagious, blistering infection of the superficial layer of the skin [1]. Bullous impetigo is caused by staphylococcus aureus. The blisters or bullae are fluid-filled lesions of over 0.5 cm in diameter and are characteristic of bullous impetigo. The bullae are caused by destruction and seperation of the skin layers by toxins released from S aureus. Another characteristic feature of bullous impetigo is the occurrence of the lesions on unbroken skin.

Impetigo most commonly occurs in children, especially in a setting of a chronic nasal carriage of staphylococcus aureus, residency in humid living environment, poor hygiene and immunosuppression. Bullous impetigo makes up 30% of all cases of impetigo [2]. In the management of bullous impetigo, good skin hygiene and proper hand washing are key to preventing further spread of the disease. However, antibiotics are the mainstay of treatment.

Patient Information

Overview.

Bullous impetigo is a highly contagious skin infection caused by the bacterial species, such as staphylococcus aureus, and is characterized by the presence of blisters on the skin. This disease affects all age groups but it is most commonly seen in children between the ages of 2 to 5 years.

Etiology.

Bullous impetigo is an infection caused by the bacterial species like staphylococcus aureus after colonizination and overgrowth in the skin. This bacteria releases a toxic substance which destroys skin cells and separates the outer from the inner layer of the skin forming blisters. Factors which may promote this bacterial colonization include poor hygiene, hot humid climates, poor hand washing practices, compromised immune system from HIV, diabetes, steroid use, cancer treatment, and cancers.

Prognosis.

Although most cases of this disease may resolve even without treatment, in babies less than one month old and in patients whose immune systems have been compromised such as those infected with HIV, diabetes, cancer, or those taking steroids, it could lead to serious complications if left untreated.

Presentation.

Bullous impetigo typically presents with blisters in different areas of the body particularly the arms, trunks, face, and legs. The blisters are painless and rupture fast releasing the fluid they contained. On rupturing, the skin around the blisters become red and itchy. In some cases, especially in infants, the disease may spread through the blood causing other symptoms such as fever and diarrhea.

Workup.

Your doctor can make a diagnosis of bullous impetigo just by examining the skin and by seeking from certain information which suggest that you or your child might have been exposed to an infected person. However, tests could be ordered sometimes to check for the presence of the bacteria in the skin disease by growing cultures of swabs taken from the blisters.

Treatment.

Antibiotics are the mainstay of treatment of bullous impetigo. The antibiotics could be given as ointments, tablets, capsules, syrups, or intramuscular/intravenous injections depending on the severity of the disease and the age of the patient.

Home remedies.

  1. Bathing with antiseptic soaps at least twice daily to reduce the amount of bacteria in the skin and to remove the crusts from the skin.
  2. Avoid touching the blisters to prevent persistence of the infection or spread to other parts of the body.
  3. Avoid loose fitting clothes to reduce pressure on the affected skin area.
  4. Proper hand washing, bathing with antiseptic soaps, and restricting infected children from attending school till completion of treatment help to prevent bullous impetigo.

References

Article

  1. James WD, Berger TG, Elston DM. Andrews' Diseases of the Skin: clinical Dermatology. Saunders Elsevier; 2006.
  2. Cole C, Gazewood J. Diagnosis and treatment of impetigo. Am Fam Physician. 2007 Mar 15. 75(6):859-64.
  3. Geria AN, Schuartz RA. Impetigo Update: New Challenges in the Era of Methicillin Resistance. Cutis. 2010. 85(2):65-70.
  4. Loffeld A, Davies P, Lewis A, Moss C. Seasonal occurrence of impetigo: a retrospective 8-year review (1996-2003). Clin Exp Dermatol. 2005 Sep. 30(5):512-4.
  5. Koning S, Verhagen AP, van Suijlekom-Smit LW, et al. Interventions for impetigo. Cochrane Database Syst Rev. 2004. CD003261. 
  6. Razmjou RG, Willemsen SP, Koning S, et al. Determinants of regional differences in the incidence of impetigo. Environ Res. 2009 Jul. 109(5):590-3.
  7. Treating impetigo in primary care. Drug Ther Bull. 2007 Jan. 45(1):2-4.
  8. Spurling G, Askew D, King D, Mitchell GK. Bacterial skin infections--an observational study. Aust Fam Physician. 2009 Jul. 38(7):547-51.
  9. Romani L, Steer AC, Whitfeld MJ, Kaldor JM. Prevalence of scabies and impetigo worldwide: a systematic review. Lancet Infect Dis. 2015 Aug. 15 (8):960-7.
  10. Broccardo CJ, Mahaffey S, Schwarz J, et al. Comparative proteomic profiling of patients with atopic dermatitis based on history of eczema herpeticum infection and Staphylococcus aureus colonization. J Allergy Clin Immunol. 2011 Jan. 127(1):186-93, 193.e1-11.
  11. Yamasaki O, Tristan A, Yamaguchi T, et al. Distribution of the exfoliative toxin D gene in clinical Staphylococcus aureus isolates in France. Clin Microbiol Infect. 2006 Jun. 12(6):585-8.
  12. Daskalaki M, Rojo P, Marin-Ferrer M, Barrios M, Otero JR, Chaves F. Panton-Valentine leukocidin-positive Staphylococcus aureus skin and soft tissue infections among children in an emergency department in Madrid, Spain. Clin Microbiol Infect. 2010 Jan. 16(1):74-7. 
  13. Geng W, Yang Y, Wu D, et al. Molecular characteristics of community-acquired, methicillin-resistant Staphylococcus aureus isolated from Chinese children. FEMS Immunol Med Microbiol. 2010 Apr. 58(3):356-62. 
  14. Liu Y, Kong F, Zhang X, Brown M, Ma L, Yang Y. Antimicrobial susceptibility of Staphylococcus aureus isolated from children with impetigo in China from 2003 to 2007 shows community-associated methicillin-resistant Staphylococcus aureus to be uncommon and heterogeneous. Br J Dermatol. 2009 Dec. 161(6):1347-50.
  15. Ludlam H, Cookson B. Scrum kidney: epidemic pyoderma caused by a nephritogenic Streptococcus pyogenes in a rugby team. Lancet. 1986 Aug 9. 2(8502):331-3. 
  16. Belgemen T, Suskan E, Dogu F, Ikinciogullari A. Selective immunoglobulin M deficiency presenting with recurrent impetigo: a case report and review of the literature. Int Arch Allergy Immunol. 2009. 149(3):283-8.
  17. Hirschmann JV. Impetigo: etiology and therapy. Curr Clin Top Infect Dis. 2002. 22:42-51.

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Last updated: 2018-06-22 08:49