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Aesthetic Medicine • May 2014

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Dr Patrick Treacy shares some of his most challenging cases

Dr Treacy’sCASEBOOK

DR PATRICK TREACYis chairman of the Irish Association of Cosmetic Doctors and Irish regional representative of the British Collage of Aesthetic Medicine (BCAM). He is European medical advisor to Network Lipolysis and Consulting Rooms and holds higher qualifications in dermatology, laser technology and skin resurfacing. In 2012 and 2013 he won awards for ‘Best Innovative Techniques’ for his contributions to facial aesthetics and hair transplants. Dr Treacy also sits on the editorial boards of three international journals and features regularly on international television and radio programmes. He was Faculty IMCAS Paris 2013, AMWC Monaco 2013, EAMWC Moscow 2013 and keynote speaker for the American Academy of Anti-Ageing Medicine in Mexico City this year.

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A75-year-old Irishman presented with a week history of an inflamed thoracic and upper limb area, populated by fragile 3cm fluid-filled vesicles and flaccid blisters. He had previously been in Dubai where he had seen two dermatologists who had prescribed steroids, anti-inflammatories and Aldara cream. The patient said that the bullae ruptured easily; leaving

a reddened base but now they were turning browny black and causing the patient some distress. The patient was a newspaper magnate who was leaving to Toronto that evening. He was otherwise healthy and denied any history of recent infection or trauma. Apparently, recent full blood count and blood chemistry in Dubai was within normal range. He had no other medical problems, except mild diarrhea and was not taking any systemic medications.

On physical examination, there was evidence of numerous bullae containing a clear, yellow fluid along his thorax and in his intertriginous areas. The chest area contained some cloudy and dark yellow bullae mostly the lesions appeared to have a brownish crust at the periphery. Removal of this crust in one instance revealed a moist, red base. There was no surrounding erythema or edema present between the lesions or evidence of regional adenopathy. There was no involvement of the buccal mucous membranes and no ??

Sentance finishes strangelyA punch biopsy was taken

from the thoracic area to aid in the diagnosis. Histology showed skin with >

“On physical examination, there was

evidence of numerous bullae containing a clear, yellow fluid

along his thorax and in his intertriginous areas. The chest area contained some cloudy

and dark yellow bullae.”

Will finalise layout once text is sorted

38 Aesthetic Medicine • May 2014

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subcorneal bulla formation and overlying parakeratosis. The superficial and mid dermis contained a moderate inflammatory infiltrate composed predominantly of lymphocytes with occasional neutrophils. Gram stain highlighted gram-positive cocci in fragments of detached scale crust.

COMMENT Based on the clinical findings a provisional diagnosis of bullous impetigo was made. The diagnosis of impetigo is usually based solely on history and clinical appearance. Impetigo is an acute, highly contagious gram-positive bacterial infection of the superficial layers of the epidermis. Bacterial culture and sensitivity are recommended to identify possible methicillin-resistant Staphylococcus aureus (MRSA). Impetigo occurs most commonly in children, especially those who live in hot, humid climates. It presents in two forms: bullous and nonbullous. Nonbullous impetigo is the more common form, constituting approximately 70% of impetigo cases1. It tends to affect skin on the face or extremities that has been disrupted by bites, cuts, abrasions, other trauma, or diseases such as varicella2.

The rarer variant, bullous impetigo is commonly due to exfoliative toxins of S aureus termed exfoliatins A and B. These exotoxins cause a loss of cell adhesion in the superficial dermis, which, in turn, causes blisters and skin sloughing by cleaving of the granular cell layer of the epidermis3. It is characterized by fragile fluid-filled vesicles and flaccid blisters and is caused by pathogenic strains of Staphylococcus aureus4. 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 skin syndrome).5

Impetigo has been associated crowded living conditions, poor personal hygiene, or an unhygienic work environment encourages contamination of the skin by pathogenic bacteria. It is also associated with hot humid weather and even participation in contact sports, such as rugby6. Conditions such as HIV infection, post transplantation, diabetes mellitus, hemodialysis, chemotherapy, radiation therapy, or systemic corticosteroid treatment increase susceptibility7.

Topical therapy should constitute either fusidic acid (Fucidin, Leo Pharma Ltd) as a first-line treatment or mupirocin (Bactroban, GlaxoSmithKline) in proven cases of bacterial resistance. First-line systemic therapy is oral or intravenous flucloxacillin (Floxapen, GlaxoSmithKline). Nasal swabs from the patient and immediate relatives should be performed to identify asymptomatic nasal carriers of Staphylococcus aureus. In the case of outbreaks on wards and in nurseries, healthcare professionals should also be swabbed8, 9. AM

REFERENCES 1. Cole C, Gazewood J. Diagnosis and treatment of impetigo.

Am Fam Physician. Mar 15 2007;75(6):859-64.

2. Moulin F, Quinet B, Raymond J, Gillet Y, Cohen R. [Managing children skin and soft tissue infections]. Arch Pediatr. Oct 2008;15 Suppl 2:S62-7.

3. 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. Jun 2006;12(6):585-8.

4. Amagai M, Matsuyoshi N, Wang ZH, Andl C, Stanley JR (November 2000). “Toxin in bullous impetigo and staphylococcal scalded-skin syndrome targets desmoglein 1”. Nat. Med. 6 (11): 1275–7.

5. Yasushi, Hanakawa. “Molecular mechanisms of blister formation in bullous impetigo and staphylococcal scalded skin syndrome.” journal of Clinical Investigation. 110.1 (2002): 53-60.

6. Ludlam H, Cookson B. Scrum kidney: epidemic pyoderma caused by a nephritogenic Streptococcus pyogenes in a rugby team. Lancet. Aug 9 1986;2(8502):331-3.

7. Mancini AJ. Bacterial skin infections in children: the common and the not so common. Pediatr Ann. Jan 2000;29(1):26-35.

8. Koning S, Verhagen AP, van Suijlekom-Smit LW, et al. Interventions for impetigo. Cochrane Database Syst Rev. 2004;CD003261

9. George A, Rubin G. A systematic review and meta-analysis of treatments for impetigo. Br J Gen Pract. Jun 2003;53(491):480-7.

HISTOLOGY REPORTHistology showed skin with subcorneal bulla formation and overlying parakeratosis. The superficial and mid dermis contained a moderate inflammatory infiltrate composed predominantly of lymphocytes with occasional neutrophils. A Gram stain (not photographed) highlighted gram-positive cocci in fragments of detached scale crust. The histopathology features are consistent with bullous impetigo.

Prof. Kieran Sheahan, Consultant Histopathologist, St. Vincent’s University Hospital, Elm Park, Dublin 4.

Dr Linda Mulligan, Pathology Registrar, St. Vincent’s University Hospital, Elm Park, Dublin 4.

“Impetigo has been associated with

crowded living conditions, poor personal hygiene, or an

unhygienic work environment encourages contamination of

the skin by pathogenic bacteria.”

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