Studies on the pathogenesis of actinomycotic mycetoma in animals injected with fractions isolated from Nocardia brasiliensis.

In the present study the participation was evaluated of isolated fractions of Nocardia brasiliensis in the genesis of the inflammatory response observed in actinomycotic mycetoma. Subcutaneous injection in mice of a suspension containing a polysaccharide fraction F1 obtained by treating cell walls with sodium hydroxide induced an inflammatory response at the inoculation site which was characterized by a large influx of polymorphonuclear (PMN) and mononuclear (MN) leucocytes between the 2nd and 4th days. On the 8th day, a typical granulomatous reaction was observed involving large numbers of epithelioid cells. Intravenous injection of the lipid extract adsorbed to charcoal particles into mice induced an inflammatory reaction around the particles embolized in the pulmonary microcirculation which was similar to that described above. The kinetics of the inflammatory cell migration was studied by total and differential counts of leukocytes that migrated to the peritoneal cavity of rats inoculated intraperitoneally with the F1 and lipid fractions. Both fractions initially induced intense PMN migration, which was later reduced, with a simultaneous increase in mononuclear cells. The present results demonstrate that a polysaccharide fraction (F1) and the lipid fraction reproduce the fundamental lesion of actinomycotic mycetoma.

Mouse toxicity induced by lipids and cell walls isolated from actinomycetes.

The possibility was examined that the toxicity induced in mice by Actinomadura madurae, 'Streptomyces pelletieri' and Nocardia brasiliensis was due to lipid and cell-wall constituents. Mice were inoculated intraperitoneally with heat-killed bacteria, lipid extracts and cell-wall preparations emulsified in mineral oil: toxicity was evaluated by recording weight loss and deaths. Killed cells and cell-wall preparations of all three actinomycetes produced a pronounced loss of body weight, tissue necrosis, splenomegaly, a granulomatous inflammation and sometimes death. Mice inoculated with lipid extracts from A. madurae and 'S. pelletieri' neither died nor showed toxic effects, but mice injected with lipids isolated from N. brasiliensis did suffer toxic effects. They showed more marked wasting symptoms than observed after inoculation of heat-killed bacteria or of the cell-wall preparation.

Role of cord factor in the modulation of infection caused by mycobacteria.

The subcutaneous, intradermal, and pulmonary inflammatory lesions induced in mice by viable Mycobacterium bovis (BCG) with no glycolipid cord factor (CF) on the outer cell wall (delipidated BCG, dBCG) was drastically different from that induced by inoculation with intact bacteria. The reaction caused by dBCG was of an acute nature: the cells making up the inflammatory infiltrate exhibited polymorphonuclear-like (PMNs) morphologic characteristics, there was a decrease on delayed hypersensitivity response, and the lesion was resolved around the 16th day after inoculation. Complete disappearance of viable organisms from the lungs, liver, and spleen of these animals occurred in parallel with the dissipation of the dBCG-induced inflammatory infiltrate, showing that CF plays an important role in the host-parasite relationship that takes place in infections caused by mycobacteria. In addition, when deprived of this glycolipid component, bacilli lose their immunostimulant ability.

Granulomatous reactions induced by lipids extracted from Fonsecaea pedrosoi, Fonsecaea compactum, Cladosporium carrionii and Phialophora verrucosum.

Granulomatous reactions induced by lipid extracts from the dermatophyte fungi Fonsecaea pedrosoi, Fonsecaea compactum, Cladosporium carrionii and Phialophora verrucosum, the causal organisms of chromoblastomycosis, were studied. Charcoal particles coated with the lipid extracts were prepared and injected intravenously into mice. Inflammation was characterized by an intense mononuclear cell infiltrate that lodged in the lung from 4 to 8 d after inoculation.