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Lechiguana is a disease of cattle caused by an interaction between Dermatobia hominis warble and the bacteria Manheimia granulomatis. It is characterized by subcutaneous swellings that grow rapidly and result in death after 3 to 8 months. The objective of this paper was to investigate some vascular and fibrogenic changes of the disease at different lesion stages by histochemical and immunohistochemical techniques. A peculiar histopathological aspect observed during a proliferative phase (before treatment) was the intense vasculitis, described as degenerative and fibro-proliferative, expressed by the oncogene p53, possibly caused by the presence of bacteria in close contact with enthotelial cells, along with dense accumulations of lymphoid cells around venules. The synthesis of collagen fibers during the development of Lechiguana lesions assume a structural aspect of star arrangement with fiber radiation centers that gradually interconnect to design the Extracellular Matrix (ECM) framework, seen by Confocal Laser Scanning Microscopy (CSLM). Angiogenesis was the most characteristic finding in both proliferative and regressive stages as seen by the immunohistochemical expression of cytoskeleton proteins and von Willebrand (Factor VIII-Related Antigen). Additionally, in all tissues samples, active ECM elements like Metalloproteinases (MMPs), Tissue Inhibitors Metalloproteinases (TIMP) and Fibronectin (FN) were mainly associated to vessels structures. The extraordinary regression of exuberant granulation tissue after treatment is undoubtedly associated to the maintenance of the vascular components observed during the regressive phase.

This work aimed to investigate some aspects related to the pathogenicity of Lechiguana, a bovine fibroproliferative lesion characterized by rapid collagen accumulation. Light and transmission electron microscopy and in situ hybridization studies were performed in order to elucidate the fibrogenic activity of this lesion. The characterization of fibroblastic plasticity in the lesion was done by immunohistochemical study for alpha-smooth-muscle cell actin. The ovoid-shaped cells presented positive reaction for alpha-smooth-muscle cell actin in their cytoplasm and, at the electron-microscopic level demonstrated basal lamina-like material adjacent to the external surface and collagen fibrils that corresponded to a cell population phenotypically similar to the myofibroblast. We also investigated alpha1 collagen type I mRNA at different times of evolution of Lechiguana lesions, using isotopic and non-isotopic in situ hybridization. The results strongly suggest the involvement of a myofibroblast-like cell population that expresses mRNA for type I collagen and is probably associated with the increase of collagen deposition.

Lechiguana is a disease of cattle characterized by large, hard, subcutaneous swellings that grow rapidly and result in death after 3-11 months in untreated animals. Cattle treated with antibiotics recover. The disease has been reported from five states in south and southeastern Brazil. Histologically, the lesion consists of focal proliferation of fibrous tissue infiltrated by plasma cells, eosinophils, lymphocytes and sometimes neutrophils. The primary lesion is an eosinophilic lymphangitis, which results in eosinophilic abscesses, with occasional rosettes containing bacteria in their centres. Much experimental and epidemiological evidence, reviewed in this article, supports the suggestion that lechiguana is caused by an association of Pasteurella granulomatis (syn: Mannheimia granutomatis) and Dermatobia hominis.