[3] Three main clinical manifestations of histoplasmosis are pulmonary, progressive disseminated and chronic cavitory forms: all may be accompanied with skin lesions, or rarely, the disease manifests as PCH.[4] PCH in immunocompetent individuals itself is very rare, with hardly three case reports, and selleck bio can present with nodules, ulcers and abscesses.[3,5] Confirmation of etiology in our case is credited to histopathology and good response to the approved antifungal itraconazole. Absence of lymphadenopathy and hepatosplenomegaly, normoglycemic status, a normal hemogram and renal biochemical parameters and a normal chest X-ray, rule out systemic involvement. Puckering of skin amidst the area of involvement was probably due to healing of inflamed and ulcerated lesions following administration of itraconazole.

Source and route of infection are undetermined in our case. The probable route of infection may be through direct inoculation of spores through skin with splinter injury or thorn pricks.[5] Cutaneous presentation without any systemic involvement, florid inflammation and ulceration, normal CD4 count, HIV seronegative status of the patient and prompt response to appropriate treatment are the notable features of our case. The differential diagnosis of nodulo-ulcerative lesions should include skin and lymphocutaneous malignancies and other systemic mycoses. CONCLUSION Though histoplasmosis is reported to be endemic in West Bengal, there are no reports of primary cutaneous histoplasmosis accompanied with extensive inflammation in HIV seronegative individual from West Bengal, till date.

In our case, early diagnosis and accurate treatment would have relieved the patient of morbid stress much earlier. Such cases with unusual clinical presentation may pose diagnostic challenge. Footnotes Source of Support: Nil Conflict of Interest: None declared.
A continuous process of teeth eruption and shedding replaces the exfoliated Dacomitinib deciduous teeth with succedaneous teeth, i.e., permanent incisors, canine, and premolar. Impaired tooth eruption, where this process is disturbed may manifest either as delayed or complete absence of eruption, resulting in impacted, embedded permanent teeth, or retained deciduous teeth.[1] Differential gene expressions by dental follicle needed for osteoclastogenesis, osteogenesis, and pressure from underlying succedaneous teeth are responsible for timely shedding and eruption process of succedaneous teeth[2] and several local, systemic causes including syndromes (cleidocranial dysplasia and Gardner’s syndrome) and metabolic or hormonal diseases have been attributed in literature for impacted and embedded teeth.