Bullous pemphigoid (BP) is an acquired autoimmune blistering disorder of unknown etiology uncommon in childhood. Unlike adult BP, infantile BP shows acral distribution and resolves rapidly with systemic steroids. We report three infants with infantile BP presenting shortly after vaccination for diphtheria, pertussis, tetanus, poliomyelitis, hepatitis B, Haemophilus influenzae B, and meningococcus C. Our cases further reinforce the causal association between childhood BP and vaccination.

Congenital malignant melanoma within a pre-existing large congenital melanocytic naevus (CMN) is exceedingly rare. Its incidence is difficult to determine due to the small number of reported cases and because of problems associated with diagnosis. Some benign nodular proliferations (called proliferative nodules) arising in CMN, while rare, are significantly more common and can mimic malignant melanoma clinically or histologically. There are no reported cases of congenital melanoma or benign proliferative nodules in CMN in patients who also had eruptive disseminated Spitz naevi. We describe a girl who was noted to have a dark-brown plaque with several large erythematous nodules affecting the scalp at delivery, in addition to multiple erythematous dome-shaped papules that developed in a disseminated manner over several months, beginning at 10 days of age. It was difficult, not only clinically but also histologically, to determine the benign or malignant nature of all of these lesions. As primary cutaneous melanoma, atypical proliferative nodules in CMN, bland CMN or CMN with foci of increased cellularity and Spitz naevi show clear differences in the genetic aberration patterns, comparative genomic hybridization (CGH) could be a diagnostic help in ambiguous cases such as this. CGH performed on this patient showed multiple DNA copy number changes in the most atypical nodule, but such alterations could not be found in the remainder of the lesions. CGH showed differences between the nodular lesions that occurred in the CMN and helped us in supporting the diagnosis of this unique case of benign proliferative nodules and a possible congenital melanoma arising in a large CMN, associated with multiple widespread eruptive Spitz naevi.

A 40-year-old human immunodeficiency virus (HIV)-positive man had three relapses of visceral leishmaniasis (VL). In the third he developed nodular skin lesions of three types, some reminiscent of Kaposi's sarcoma. Biopsy of each type disclosed abundant dermal macrophages with a huge number of intracellular and extracellular Leishman-Donovan bodies. Rapid improvement of lesions was achieved after antiparasitic treatment. AIDS leads to atypical forms of leishmaniasis. Leishmania has been detected both in normal and pathological skin of these patients due to dissemination during VL. It is suspected that a considerable proportion of the population may be infected in endemic areas, Leishmania being opportunistic in immunosuppressed individuals. It is important to recognize the range of lesions that may occur in patients with HIV and VL, many of which are non-specific and may cause diagnostic difficulty.

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1357mucosal lesions have been reported on the mouth, labia majora, and oesophagus. In addition, verrucoid papules infrequently occur, 2 which, when on the genital areas, may resemble warts. Langenbery et al. 2 reviewed the literature and concluded that all verrucoid genital lesions with the histological features of HHD may represent familial benign chronic pemphigus (HHD). The authors thought that this rare clinical entity, verrucoid HHD, was not associated with HPV infection. In our patient, however, verrucoid papules were found on the surface of the erythematous patch clinically, and HPV type 6 DNA was detected in the verrucoid lesions. These findings therefore differ from Langenbery's conclusion. The argument that our patient had condyloma on the genital skin, which happened to have a subclinical anatholytic process of HHD, is unjustified because the base of the verrucoid papules was an erythematous, erosive patch, representing an active lesion of HHD. It seems more likely that our patient had a newly developed HHD lesion superimposed with HPV type 6 infection on the genitalia.The role of infection in inducing lesions of HHD is controversial. 3,4 Herpes virus hominis has been reported to cause a severe exacerbation of HHD. 5 Candidal or bacterial infection may or may not initiate lesions but the subsequent inflammation certainly potentiates acantholysis. 3 On the other hand, some investigators consider that such microbes are secondary invaders rather than primary aetiological agents. 4 In our case, we surmise a possible role of HPV infection in the provocation or induction of skin lesions of HHD. Therefore, biopsy and detection of HPV genome are necessary when verrucoid papules on genital lesions of HHD are encountered.