Leprosy, a disease caused by Mycobacterium leprae, has polymorphic neurocutaneous manifestations strongly correlated with the host immune response. Peripheral neural damage can lead to sensory and motor losses, as well as deformities of the hands and feet. Both innate and acquired immune responses are involved, but the disease has been classically described along a Th1/Th2 spectrum, where the Th1 pole corresponds to the more limited presentations and the Th2 to the multibacillary ones. The aim of this review is to discuss this dichotomy in light of the current knowledge of the cytokines, T helper subpopulations, and regulatory T cells involved in each presentation of leprosy. The text will also address leprosy reactions related to increased inflammatory activity in both limited and multibacillary presentations, leading to exacerbation of chronic signs and symptoms and/or the development of new ones. Despite the efforts of many research groups around the world, there is no standardized serological test/biological marker for diagnosis so far, even in endemic areas, which could contribute to the eradication of leprosy.

Biopsy specimens of the skin were taken from 10 patients with acute meningococcemia who exhibited mainly maculopurpuric lesions. The specimens were studied by light, electron, and immunofluorescent microscopy in an attempt to obtain information on the pathogenesis of vascular injury. Light microscopy disclosed a large number of Neisseria meningitidis organisms, both in the endothelial cells and being phagocytized by neutrophils. Vascular injury was characterized (by means of both light and electron microscopy) by endothelial necrosis, thrombosis, and necrosis of other elements of the vascular wall, such as muscle cells and pericytes. Immunoglobulins and complement were also found in the vascular wall in most cases. Hypercoagulability was demonstrated in some patients. These findings suggest that the cutaneous lesions of meningococcemia fulfill most of the gross and histologic criteria of the local Shwartzman reaction, but that immunological factors probably contribute to pathogenesis.

Leprosy is a chronic infectious disease whose evolution involves complex immune mechanisms of the host that influence the clinical presentation of the disease. For many years, the main interpretation of the host defense response was based on characterization of the established immune paradigm between T helper (Th) 1 and Th2 lymphocytes. However, with advances in the knowledge of immunology, new approaches have emerged along with the development of new immunological pathways that have changed the interpretation of the long-established paradigm of the polar forms of the disease, especially with the identification of new subtypes of T lymphocytes such as Th9, Th17, Th22, and Tregs. Thus, this review discusses the role of these new subtypes of T helper lymphocytes and how the development of the immune response of these cells modifies the pattern of the Th1/Th2 response in the immunopathogenesis of leprosy.

A case of hyalohyphomycosis caused by Paecilomyces lilacinus is described in a renal transplant patient. Infection was localized on the left forearm. Two separate cultures of the lesions yielded the same organism. Histological sections disclosed hyaline elements in the tissue. The infection responded well to therapy with oral griseofulvin (500 mg daily) and the patient was cured within 45 days. Forty-six cases of human infection due to Paecilomyces species have been reported previously in the literature, most of them occurring in conjunction with prosthesis implants or immunosuppression. The antifungal sensitivity of Paecilomyces varies widely among the species but the general trend is for Paecilomyces variotii isolates to be almost universally sensitive to amphotericin B and 5-fluorocytosine, while P. lilacinus and Paecilomyces marquandii isolates are resistant to these antifungals but sensitive to the imidazoles.