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Experimental infection of marmoset monkeys (Callithrix jacchus) with Leptospira interrogans serovar Copenhageni showed microscopic patterns of tissue reactions comparable to those seen in the severe forms of human leptospirosis, including intra-alveolar hemorrhage. The most impressive microscopic changes were seen in the lung and kidney of animals killed at days 6 and 12 after inoculation. There were extensive and irregular areas of hemorrhage predominating around main bronchial branches or diffusely spread to the pulmonary parenchyma, as well as severe tubulointerstitial nephritis. Antibody response detected by the microscopic agglutination test was quantitatively similar to those seen in humans and paralleled severity of tissue lesions. The distribution of leptospires or antigenic debris in infected tissues was observed by immunofluorescence and confocal laser scanning microscopy. Large numbers of typical leptospires were seen in the lumen of proximal renal tubules. Positive reactions showing antigenic debris were closely associated with sites of tissue damage.

We report the comparative and sequential histologic analysis of lesions developed by Paracoccidioides brasiliensis-infected athymic and euthymic BALB/c mice, using conventional and specific stain to characterize the morphology of fungi and inflammatory cells as well as the extracellular matrix patterns. In both groups, neutrophils and macrophages were the predominant cells; macrophage transition to giant and epithelioid cells was observed. Degenerated fungi and fungal dust were associated with local neutropil infiltration and the presence of pseudoxantomatous macrophages. Paracoccidioides brasiliensis are always found within an extracellular matrix microenvironment. The main differences between lesions developed by nu/+ and nude (nu/nu) mice resided in the more pronounced encapsulating tendency in the former ones. In both groups of animals, lesions in several organs were associated with extensive hemopoiesis. At the first week of infection, there was evidence of fungal destruction and control of its proliferation in both mouse groups. At the fourth and seventh weeks, nu/+ mice maintained the control of the infection, as shown by the scarce numbers of budding yeast cells, while experimental nu/nu mice showed a tumor-like progression of the disease with a striking increase in fungal load in many organs (e.g., omental and mesenteric milky spots, lymph nodes, spleen), some of which present their structure replaced by granulomatous lesions.

The production of an antibody which reacts with endocardium, blood vessels, and cardiac interstitial tissue (EVI factor) was experimentally obtained in rabbits immunized either with heterologous heart crude antigen, Trypanosoma cruzi antigen, a mixture of heart and T. cruzi antigens, kidney antigen or lung antigen, and complete Freund's adjuvant. Immunization lasted 2 months, with multiple subcutaneous and foot pad injections being made every 15th day. Preimmunization serum from each animal was used as normal control serum. Rabbit sera were tested by indirect immunofluorescence against mouse heart and skeletal muscle unfixed cryostat sections and revealed by fluoresceinated anti-rabbit globulin diluted 1:80. The highest titers appeared with anti-heart sera (1:192) and with anti-heart/T. cruzi sera (1:96). Incorporation of T. cruzi antigen in heart extract did not increase EVI antibody titers. It is suggested that the EVI factor is an antibody to many antigenic determinants, the majority of which are present in the heart and some of which cross-react with T. cruzi.