Are You Confident of the Diagnosis?

Blistering distal dactylitis (BDD) results from and was initially described in group A β-hemolytic Streptococcus (GABHS) infections that manifested with bullae on acral skin.

  • Characteristic findings on physical examination

In BDD the acral oval bullae are typically 10-30mm in diameter. BDD most commonly occurs as bullae on the volar fat pads of the fingers but can occur on the proximal phalangeal and palmar areas of the hands and even the forearm and can manifest as multiple bullae. The bullae sometimes evolve into erosions over the course of several days or stay as bullae. BDD can coexist with and may be secondary to clinically imperceptible infections of the nasopharynx, conjunctiva, or anus, which underlines the need for systemic antibiotic therapy.

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Reports in recent years have linked BDD to Staphylococcus aureus (SA). It seems that currently SA is a more common cause of BDD than GABHS. Multiple bullae appear to be a predictor that SA is the causative agent of a case of BDD. This is interesting because typically, GABHS primarily causes the related condition of bullous impetigo and the development of the bullae of bullous impetigo is attributed to the certain toxins and qualities of GABHS that SA might not have.

A report in 2011 noted associated methicillin-resistant Staphylococcus aureus (MRSA) resulting in blistering distal dactylitis in an infant.

  • What to be alert for in the history

The key element to the diagnosis of BDD is the history of rapid development of bullae on acral areas that persists over days. The diagnosis of BDD is confirmed with a Gram stain and culture. If the diagnosis is entertained, therapy should be instituted and tests should be obtained for confirmation. Typically, in BDD there are tense bullae on one or more of the digits.

  • Expected results of diagnostic studies

A Gram stain demonstrates gram-positive bacteria. A culture would show SA or GABHS. The cultures are typically positive, more so than with bullous impetigo.

  • Diagnosis confirmation

Unlike bullous impetigo, the blisters of BDD are not fragile, which is likely a result of the thickness and nature of acral skin. Bullae are distinct from those of bullous tinea, dyshydrotic eczema, an insect bite, or contact dermatitis (in particular from poison ivy), a bullous disease; additionally, the history is suggestive of the diagnosis of BDD. The bullae of BDD might have a little more surrounding erythema than dyshydrotic eczema but they may still resemble the other conditions mentioned in the previous sentence.

Another condition that resembles BDD is herpetic whitlow. Cultures help to distinguish herpetic whitlow from BDD. Also, whitlow often has a more herpetic appearance, with white material (usually pus) in its blisters whereas there is seldom pus in the bullae of BDD. Epidermolysis bullosa resemble BDD in pictures but clinically one is a chronic complex genetic condition and the other is an acute infectious condition. BDD and bullous impetigo overlap, but the former has firm bullae in its early stages and the latter flaccid fragile blisters. BDD and friction blisters differ in that the former is a firm inflammatory bullae surrounded by erythema most commonly occurring on the tips of digits, and the latter is bland bullae that occurs at sites of friction.

Who is at Risk for Developing this Disease?

Anyone can develop BDD or bullous impetigo. BDD seems to usually be a disease of children. It is of equal prevalence in males and females. It would be expected that BDD occurs on the hands and feet and thus people whose hands and feet touch those of others might be at increased risk for getting the disease.

What is the Cause of the Disease?

  • Etiology

  • Pathophysiology

Group A β-hemolytic Streptococcus infections of acral skin. Recent reports link BDD to SA. Presumably the bacteria and the toxins that they produce cause dyshesion of the keratinocytes.

Systemic Implications and Complications

Typically, the infection is limited and evolves over days. Cases that evolve into abscesses or cellulitis have not been reported but could occur. BDD could evolve into impetigo or bullous impetigo or recur, but this is not well-reported.

Treatment Options


The first-line of treatment for BDD is amoxicillin/clavulanate potassium or a similar antibiotic at the appropriate dose and frequency for simple skin and skin structure infections as assessed by age and weight.


The usual adult dose is one 500 mg tablet every 12 hours or one 250 mg tablet every 8 hours. For more severe infections and infections of the respiratory tract, the dose should be one 875 mg tablet every 12 hours or one 500 mg tablet every 8 hours.

Patients with impaired renal function do not generally require a reduction in dose unless the impairment is severe. Severely impaired patients with a glomerular filtration rate of less than 30 mL/min should not receive the 875 mg tablet. Patients with a glomerular filtration rate of 10-30 mL/min should receive 500 mg or 250 mg every 12 hours, depending on the severity of the infection. Patients with a less than 10 mL/min glomerular filtration rate should receive 500 mg or 250 mg every 24 hours, depending on the severity of the infection.

Hemodialysis patients should receive 500 mg or 250 mg every 24 hours, depending on the severity of the infection. They should receive an additional dose both during and at the end of dialysis. Hepatically impaired patients should be dosed with caution and hepatic function monitored at regular intervals.

For pediatric patients 3 months and older, based on the amoxicillin component (600mg/5mL), the recommended dose of AUGMENTIN ES-600 is 90 mg/kg/day divided every 12 hours, administered for 10 days (see Table I).

Table I.
Body Weight (kg) Volume of AUGMENTIN ES-600 providing 90 mg/kg/day
8 3.0 mL twice daily
12 4.5 mL twice daily
16 6.0 mL twice daily
20 7.5 mL twice daily
24 9.0 mL twice daily
28 10.5 mL twice daily
32 12.0 mL twice daily
36 13.5 mL twice daily

Use of cephalexin or cefdinir might possibly suffice, but this needs to be assessed in each clinical situation. Use of quinolone or tetracycline in children is not suggested. The fact that MRSA has now been shown to cause BDD should not yet change treatment for children, but, in adults, it should cause consideration of the combination of amoxicillin/clavulanate potassium with trimethoprim and sulfamethoxazole, which is effective against MRSA. Both of these medications can cause drug eruptions so treatment must be considered carefully.

It is important to recall that trimethoprim and sulfamethoxazole is not effective for GABHS. It is not recommended for use in pediatric patients less than 2 months of age.



The usual adult dosage in the treatment of skin infection is one trimethoprim/sulfamethoxazole DS (double strength) tablet or two trimethoprim/sulfamethoxazole tablets every 12 hours for 10-14 days.


Table II. Sulfamethoxazole/trimethoprim: Dosage for children 2 months of age or older

Table II.
Weight Dose every 12 hours
lb kg Tablets
22 10
44 20 1
66 30
88 40 2 or 1 DS tablet

The recommended dose for children with skin infection with MRSA is 40 mg/kg sulfamethoxazole and 8 mg/kg trimethoprim for 24 hours, given in two divided doses every 12 hours for 10 days. Table II provides a guideline for the attainment of this dosage. Pediatric patients 40 kg and heavier can be treated like adults for dosing purposes.

As MRSA can easily develop resistance to clindamycin, its use is disfavored.

Optimal Therapeutic Approach for this Disease

BDD is best treated with oral antibiotics. Newer data suggests that due to the increase in prevalence of MRSA, all cases of BDD should be treated with trimethoprim/sulfamethoxazole and a cephalosporin (e.g., cefdinir), or penicillin (e.g., ampicillin or amoxicillin) to cover for Group A β-hemolytic Streptococcus.

Patient Management

When BDD is suspected, treatment involves (1) incision and drainage of bullae, (2) wet-to-dry compresses to dry the eroded areas, and (3) a course of antibiotics. It has been suggested that beta-lactamase-resistant antibiotics are necessary because SA, now found to be a common cause of BDD, is usually resistant to penicillin.

Treatment failures heretofore have not been well-reported. With the documentation that MRSA can cause BDD, the role of incision and drainage and culture before antibiotic treatment is more important than ever. Incision and drainage can be complicated in children.

Unusual Clinical Scenarios to Consider in Patient Management

Any recently formed bullae on the digits could be BDD. While dyshydrotic eczema and bullous tinea are more common, BDD should be considered in all cases, both pediatric and adult, of digital blisters. Herpetic whitlow can mimic BDD so if possible a tzanck smear and appropriate testing should be done to distinguish these entities.

What is the Evidence?

Fretzayas, A, Moustaki, M, Tsagris, V, Brozou, T, Nicolaidou, P. “MRSA blistering distal dactylitis and review of reported cases”. Pediatr Dermatol. 2011;Mar 25. (First report of MRSA causing BDD. This underlines the need for culture and the use of appropriate antibiotics if initial treatment does not succeed or is inappropriate.)

Scheinfeld, N. “A review and report of blistering distal dactylitis due to Staphylococcus aureus in two HIV-positive men”. Dermatol Online J. vol. 13. 2007. pp. 8(A review of two cases of BDD caused by SA in HIV-positive patients. Both have good outcomes with standard therapy.)

Scheinfeld, NS. “Is blistering distal dactylitis a variant of bullous impetigo”. Clin Exp Dermatol. vol. 32. 2007. pp. 314-6. (Review of cases and pathophysiology.)

Cohen, R, Levy, C, Cohen, J, Corrard, F. “Diagnostic of group A streptococcal blistering distal dactylitis”. Arch Pediatr. vol. 21. 2014. pp. S93-6.

Kollipara, R, Downing, C, Lee, M, Guidry, J. “Blistering Distal Dactylitis in an Adult”. J Cutan Med Surg. vol. 19. 2015. pp. 397-9. (Comprehensive review of BDD and treatment approaches.)