Sir,

Scabies is a parasitic skin infestation caused by Sarcoptes scabiei, affecting people of all ages, ethnicities, and climates [1]. Although more common among the young, there are no major differences in gender or race susceptibility [2]. Risk factors include overcrowding, migration, poor hygiene, malnutrition, dementia, and immunocompromised states [3]. Intense nocturnal pruritus is characteristic, although asymptomatic cases exist [4]. Bullous scabies (BS), first reported in 1974 [5], is a rare variant mimicking autoimmune blistering diseases such as bullous pemphigoid or epidermolysis bullosa (EB). We report a case of BS in a patient with hereditary EB, highlighting diagnostic and therapeutic challenges.

An 18-year-old man with simple hereditary EB, diagnosed at age four, presented with generalized intense nocturnal pruritus and new-onset bullae for four months. Initial treatment with topical corticosteroids and antihistamines failed. Laboratory tests revealed hypereosinophilia (1850/mm³).

On examination, there was diffuse dry erythroderma, multiple post-bullous erosions, and tense bullae (0.2–1.4 cm) mainly on the trunk and hands (Figs. 1a, 1b, 1c). Burrows were visible between the fingers. Dermoscopy revealed the delta sign (Fig. 1d). Microscopic evaluation confirmed Sarcoptes scabiei. Skin biopsy showed subepidermal bullae without immune deposits. The diagnosis of bullous scabies was made. Oral ivermectin (two doses, 15 days apart) led to complete resolution.

Figure 1: (a) Scattered erosions of varying size with surrounding mild inflammation.(b) Multiple tense blisters and bullae (0.2–1.4 cm in diameter) filled with clear fluid, surrounded by erythema, and scattered across the affected area.(c) Lesions primarily located on the dorsal aspect of the hands, with extension into the interdigital spaces, consistent with scabetic involvement. (d) Dermoscopic examination showing the delta sign and the characteristic sinuous burrow of the Sarcoptes scabiei mite.

Bullous scabies represents less than 5% of scabies cases and can mimic autoimmune bullous diseases, complicating diagnosis [6]. Histopathology often shows subepidermal blisters with eosinophilic and neutrophilic infiltration, similar to bullous pemphigoid [7]. Direct immunofluorescence may occasionally detect immune deposits, but negative results, as seen in our patient, support an infectious rather than autoimmune cause.

Superinfection and mite-induced alteration of basement membrane proteins could trigger blister formation. In patients with hereditary EB, new bullous lesions accompanied by intense pruritus and visible burrows should prompt suspicion of scabies. The use of ivermectin proved highly effective, underlining its value in complex presentations of bullous scabies.

Clinicians should consider bullous scabies in hereditary EB patients presenting with worsening bullous lesions and severe pruritus. Early recognition and treatment with ivermectin can avoid unnecessary immunosuppressive therapies and improve outcomes.

ACKNOWLEDGEMENTS

The authors would like to express their sincere gratitude to all the medical and laboratory staff involved in the diagnosis and management of this case. Special thanks to the dermatology department for their valuable support and expertise. We also acknowledge the contributions of the pathology team for their assistance in histological and immunofluorescence analysis. Finally, we extend our appreciation to the patient and their family for their cooperation and trust throughout the diagnostic and treatment process.

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