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Bullous arthropod assault
Insect-bite reactions are commonly seen in dermatology practice. Most often, they present as pruritic papules. Vesicles and bullae can be seen as well but are less common. Flea bites are the most likely to cause blisters.1 Lesions may be grouped or in a linear pattern. Children tend to have more severe reactions than adults. Body temperature and odor may make some people more susceptible than others to bites. Of note, patients with chronic lymphocytic leukemia tend to have more severe, bullous reactions.2 The differential diagnosis includes bullous pemphigoid, bullous impetigo, bullous tinea, bullous fixed drug, and bullous diabeticorum.
In general, bullous arthropod reactions begin as intraepidermal vesicles that can progress to subepidermal blisters. Eosinophils can be present. Flame figures are often seen in patients with chronic lymphocytic leukemia.3 Histopathology in this patient revealed a subepidermal vesicular dermatitis with minimal inflammation. Periodic acid–Schiff (PAS) stain was negative. Direct immunofluorescence was negative for IgG, C3, IgA, IgM, and fibrinogen. Of note, systemic steroids may alter histologic and immunologic findings.
Bullous pemphigoid is an autoimmune blistering disorder where patients develop widespread tense bullae. Histopathology revealed a subepidermal blister with numerous eosinophils. Direct immunofluorescence study of perilesional skin showed linear IgG and C3 deposits at the basal membrane level. Systemic steroids, tetracyclines, and immunosuppressive medications are a mainstay of treatment. In bullous impetigo, the toxin of Staphylococcus aureus causes blister formation. It is treated with antistaphylococcal antibiotics. Bullous tinea reveals hyphae with PAS staining. Topical or systemic antifungals are used for treatment.
In severe cases, systemic steroids can be used as well. Bacterial culture was negative in this patient. The patient was treated with 1 week of oral prednisone prior to biopsy and topical betamethasone ointment. Her lesions subsequently resolved with no recurrence.
This case and photo were submitted by Brooke Resh Sateesh, MD, San Diego Family Dermatology.
Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.
References
1-3. “Dermatology” 2nd ed. (Maryland Heights, Mo.: Mosby, 2008).
Bullous arthropod assault
Insect-bite reactions are commonly seen in dermatology practice. Most often, they present as pruritic papules. Vesicles and bullae can be seen as well but are less common. Flea bites are the most likely to cause blisters.1 Lesions may be grouped or in a linear pattern. Children tend to have more severe reactions than adults. Body temperature and odor may make some people more susceptible than others to bites. Of note, patients with chronic lymphocytic leukemia tend to have more severe, bullous reactions.2 The differential diagnosis includes bullous pemphigoid, bullous impetigo, bullous tinea, bullous fixed drug, and bullous diabeticorum.
In general, bullous arthropod reactions begin as intraepidermal vesicles that can progress to subepidermal blisters. Eosinophils can be present. Flame figures are often seen in patients with chronic lymphocytic leukemia.3 Histopathology in this patient revealed a subepidermal vesicular dermatitis with minimal inflammation. Periodic acid–Schiff (PAS) stain was negative. Direct immunofluorescence was negative for IgG, C3, IgA, IgM, and fibrinogen. Of note, systemic steroids may alter histologic and immunologic findings.
Bullous pemphigoid is an autoimmune blistering disorder where patients develop widespread tense bullae. Histopathology revealed a subepidermal blister with numerous eosinophils. Direct immunofluorescence study of perilesional skin showed linear IgG and C3 deposits at the basal membrane level. Systemic steroids, tetracyclines, and immunosuppressive medications are a mainstay of treatment. In bullous impetigo, the toxin of Staphylococcus aureus causes blister formation. It is treated with antistaphylococcal antibiotics. Bullous tinea reveals hyphae with PAS staining. Topical or systemic antifungals are used for treatment.
In severe cases, systemic steroids can be used as well. Bacterial culture was negative in this patient. The patient was treated with 1 week of oral prednisone prior to biopsy and topical betamethasone ointment. Her lesions subsequently resolved with no recurrence.
This case and photo were submitted by Brooke Resh Sateesh, MD, San Diego Family Dermatology.
Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.
References
1-3. “Dermatology” 2nd ed. (Maryland Heights, Mo.: Mosby, 2008).
Bullous arthropod assault
Insect-bite reactions are commonly seen in dermatology practice. Most often, they present as pruritic papules. Vesicles and bullae can be seen as well but are less common. Flea bites are the most likely to cause blisters.1 Lesions may be grouped or in a linear pattern. Children tend to have more severe reactions than adults. Body temperature and odor may make some people more susceptible than others to bites. Of note, patients with chronic lymphocytic leukemia tend to have more severe, bullous reactions.2 The differential diagnosis includes bullous pemphigoid, bullous impetigo, bullous tinea, bullous fixed drug, and bullous diabeticorum.
In general, bullous arthropod reactions begin as intraepidermal vesicles that can progress to subepidermal blisters. Eosinophils can be present. Flame figures are often seen in patients with chronic lymphocytic leukemia.3 Histopathology in this patient revealed a subepidermal vesicular dermatitis with minimal inflammation. Periodic acid–Schiff (PAS) stain was negative. Direct immunofluorescence was negative for IgG, C3, IgA, IgM, and fibrinogen. Of note, systemic steroids may alter histologic and immunologic findings.
Bullous pemphigoid is an autoimmune blistering disorder where patients develop widespread tense bullae. Histopathology revealed a subepidermal blister with numerous eosinophils. Direct immunofluorescence study of perilesional skin showed linear IgG and C3 deposits at the basal membrane level. Systemic steroids, tetracyclines, and immunosuppressive medications are a mainstay of treatment. In bullous impetigo, the toxin of Staphylococcus aureus causes blister formation. It is treated with antistaphylococcal antibiotics. Bullous tinea reveals hyphae with PAS staining. Topical or systemic antifungals are used for treatment.
In severe cases, systemic steroids can be used as well. Bacterial culture was negative in this patient. The patient was treated with 1 week of oral prednisone prior to biopsy and topical betamethasone ointment. Her lesions subsequently resolved with no recurrence.
This case and photo were submitted by Brooke Resh Sateesh, MD, San Diego Family Dermatology.
Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.
References
1-3. “Dermatology” 2nd ed. (Maryland Heights, Mo.: Mosby, 2008).
