Blistering Distal Dactylitis

Etiology

Typically, BDD is caused by group A beta-hemolytic Streptococcus infection.

Group B streptococcus, Staphylococcus aureus, and more recently even methicillin-resistant Staphylococcus aureus (MRSA) have been reported as etiological agents.[2][3][4] Hays and Mullard proposed that autoinoculation of the finger from nose-picking was the instigating cause of BDD in children, although any reservoir of the bacteria could be a source of infection.

The organisms tend to invade the skin through open wounds from insect bites, traumatic cuts, erosions, and burns or through abnormalities of skin appendages such as nails. The actual pathogenesis of the blister is not very clear. Streptococcus does not seem to cause the development of bullae, through a toxin-mediated or another indirect mechanism. S. aureus, however, does secrete toxins that can cause epidermal splitting. It should be noted that Streptococcus and S. aureus-associated BDD are clinically indistinguishable, and this makes the role of toxins in BDD uncertain.

Epidemiology

Children between the ages of two and 16 years of age are most commonly affected. There have been case reports of BDD occurring in children younger than one year of age and even in adults. BDD has also been reported in immunocompromised individuals, including human immunodeficiency virus (HIV)-positive cases and in people with diabetes.

History and Physical

The term ‘dactylitis’ indicates inflammation of a digit and is attributed to inflammatory infectious or non-infectious causes as well as certain contagious agents.

This inflammatory process may affect only the bone (as in sickle cell dactylitis, syphilitic dactylitis), the bone, soft tissues, and skin (as in tuberculous dactylitis, sarcoid dactylitis), or only the skin as in BDD.

BDD presents as a single, or sometimes multiple, oval-shaped tense bullae containing seropurulent fluid on an erythematous base over the palmar aspect of the finger which may extend dorsally to involve lateral nail folds. The lesions usually range in size from 10 mm to 30 mm. Darkening of the skin may be noticed a few days before the actual onset of the blisters. The bull progresses to form bullae with central erosions or simple erosion with adherent layers of skin. Some reports have shown that the infection may also affect the toes. Even more rarely, lesions might affect the palmar or dorsal hand and feet.[5][6]The presence of a thick stratum corneum and also stratum lucidum over palms and soles could be the reason for the eruption of blisters in BDD. Multiple blisters appear to be a predictor of BDD triggered by Staphylococcus aureus. Some patients may complain of pain and tenderness in the area, and they may be febrile. Bacterial infections of the eye, upper respiratory tract, the gastrointestinal or genitourinary tract may occasionally coexist which underlines the need for systemic antibiotic therapy.Isolated case reports of recurrent BDD associated with an ingrown toenail and cases coexisting with herpetic whitlow have been described. Anthropophilic transmission of BDD has also been reported.

 Differential diagnosis

• Herpetic whitlow: HSV infection can resemble BDD with grouped vesicular lesions. A Tzanck smear from the vesicle shows viral cytopathic effects. PCR for HSV as well as antibodies to HSV-1 and HSV-2 can be sent for confirmation in suspected cases. It has been suggested that blistering distal dactylitis and herpetic whitlow could coexist at the distal phalanx. One hypothesis for this is an autoinoculation due to thumb sucking in children, and also when infants are exposed when their fingers tend to explore the mouth of infected adults. Clinical response to antibiotics makes herpetic whitlow unlikely and can be used to differentiate from BDD.
• Friction blisters including those due to thumb sucking (and in the case of toes, secondary to friction due to new shoes)
• Thermal and chemical burns
• Insect bites
• Contact dermatitis and pompholyx

A detailed history of thumb sucking, insect bites, or contact with chemicals or heat gives clues to differentiate these conditions from BDD.

• Bullous impetigo: The vesicles are more superficial although the etiology is same as BDD. A bacterial culture more commonly grows Staphylococcus than Streptococcus.
• Blistering disorders like Epidermolysis bullosa simplex (EBS), localized bullous pemphigoid (BP)-EBS occurs commonly over the exposed trauma-prone sites; histopathology including direct immunofluorescence can confirm BP. Other tools like antigen mapping also help in diagnosis.
• Acute paronychia

Course and Prognosis

BDD usually resolves rapidly with the appropriate antibiotics and local dressing without any complications or sequelae. There is a report of digital amputation post BDD which emphasizes the need to treat infections aggressively, especially in HIV positive individuals.

Evaluation

The fluid can be collected after puncturing or deroofing the blister. Fluid is then examined for gram-stain smear and bacterial culture and sensitivity for confirmation of the diagnosis and for starting appropriate antibiotics.[7][8]

A histopathological examination has not been done in published case reports, but Weedon writes that the blistering results from massive subepidermal edema. The presence of erosions in some cases suggests that the split in the epidermis is superficial. [9][10]The severe necrosis that occurs in toxic shock syndrome, which results in the formation of acral bullae, has not been described in BDD.

Treatment / Management

If bullae are tense and tender, incision and drainage followed by wet dressing are recommended. Bullae may also be deflated with a sterile needle, leaving the blister roof intact. Wet compresses are helpful for rapid resolution of the bulla followed by topical antibiotics. BDD can coexist with and may be secondary to clinically indiscernible bacterial infections of the upper and lower respiratory or gastrointestinal tract, which underlines the need for systemic antibiotic therapy.

Topical antibiotics alone are inadequate in most cases. Systemic antibiotics are commonly recommended to avert the development of new lesions and the spread of infection to other sites. Oral antibiotics also decrease the chances of spread to other people. B-Lactamase-resistant antibiotics (flucloxacillin, dicloxacillin, cloxacillin) are the drug of choice because S. aureus is often resistant to penicillin. For cases that show MRSA positivity along with systemic signs, intravenous vancomycin is indicated.

Differential Diagnosis

• Ankylosing spondylitis

• Axial spondyloarthritis

• Chronic gout

• Enteropathic arthritis

• Gout

• Histiocytosis

• Histoplasmosis

• Osteoarthritis

• Plantar fasciitis

• Psoriatic arthritis

• Reactive arthritis

• Reiter’s disease