Human hemorrhagic pulmonary leptospirosis: pathological findings and pathophysiological correlations.

BACKGROUND: Leptospirosis is a re-emerging zoonosis with protean clinical manifestations. Recently, the importance of pulmonary hemorrhage as a lethal complication of this disease has been recognized. In the present study, five human necropsies of leptospirosis (Weil's syndrome) with extensive pulmonary manifestations were analysed, and the antibodies expressed in blood vessels and cells involved in ion and water transport were used, seeking to better understand the pathophysiology of the lung injury associated with this disease. PRINCIPAL FINDINGS: Prominent vascular damage was present in the lung microcirculation, with decreased CD34 and preserved aquaporin 1 expression. At the periphery and even inside the extensive areas of edema and intraalveolar hemorrhage, enlarged, apparently hypertrophic type I pneumocytes (PI) were detected and interpreted as a non-specific attempt of clearence of the intraalveolar fluid, in which ionic transport, particularly of sodium, plays a predominant role, as suggested by the apparently increased ENaC and aquaporin 5 expression. Connexin 43 was present in most pneumocytes, and in the cytoplasm of the more preserved endothelial cells. The number of type II pneumocytes (PII) was slightly decreased when compared to normal lungs and those of patients with septicemia from other causes, a fact that may contribute to the progressively low PI count, resulting in deficient restoration after damage to the alveolar epithelial integrity and, consequently, a poor outcome of the pulmonary edema and hemorrhage. CONCLUSIONS: Pathogenesis of lung injury in human leptospirosis was discussed, and the possibility of primary non-inflammatory vascular damage was considered, so far of undefinite etiopathogenesis, as the initial pathological manifestation of the disease.

Revisiting Langerhans cells in paracoccidioidomycosis: expression of CD207/langerin in human cutaneous and mucosal lesions.

Langerhans cells are identified by the expression of langerin. We detected this molecule in cutaneous and mucosal lesions in paracoccidioidomycosis, an important infection in Latin America. Langerin+ cells were scarcely distributed, with short dendrites in epidermis and epithelium and were frequent in the dermis and corium, in the inflammatory infiltrate and granulomas. Mucosal lesions presented a higher expression of langerin in lesions with loose granulomas. For the first time we presented the expression of langerin in paracoccidioidomycosis. Positive cells in dermis and corium could represent migrating Langerhans cells or a new subset of langerin+ cells with a role in paracoccidioidomycosis.