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Toxoplasma gondii infection in marine mammals is intriguing and indicative of contamination of the ocean environment with oocysts. T. gondii was identified in a Hawaiian monk seal (Monachus schauinslandi) that had visceral and cerebral lesions. Tachyzoites were found in the lymph nodes, spleen, diaphragm, heart, adrenal glands, and brain. A few tissue cysts were found in sections of the cerebrum. The diagnosis was confirmed serologically, by immunohistochemical staining with T. gondii-specific polyclonal rabbit serum, and by the detection of T. gondii DNA. The genotype was determined to be type III by restriction fragment length polymorphisms of the SAG2 gene. This is the first report of T. gondii infection in a Hawaiian monk seal.

The ultrastructural study of adrenal gland from mice experimentally infected with Trypanosoma evansi, in addition to intravascular and intracellular trypanosomes, showed different degrees of cortical cell alterations and capillary wall modifications. Beside its biological scope, these results suggest a role for the adrenal cortex to partake in Surra's etiopathogenesis and describe for the very first time a T. evansi intracellular stage.

The ultrastructural study of adrenal cortex from Plasmodium berghei infected mice showed different degrees of capillary wall alterations including disruption and widening of the fenestrae, capillaries packed with parasitized erythrocytes, necrosis of cortical cells, parasitized erythrocytes outside capillaries and in some instances inside cortical cell cytoplasm. Lymphocytes were also observed in degenerated cortical cells. Our results suggest that adrenal cortex lesions may be relevant in the etiopathogenesis of severe malaria.

A red fox (Vulpes vulpes) with signs of neurological disease was captured in Fairmount Park, Philadelphia, Pennsylvania (USA). The animal died in captivity and was examined because of suspected rabies. The liver had pale foci up to 4 mm in diameter. Foci of necrosis were associated with Toxoplasma gondii tachyzoites in several organs including liver, lungs and adrenal glands. Rabies antigen and distemper virus inclusions were not detected. The diagnosis of acute disseminated toxoplasmosis was confirmed by immunohistochemical staining.

The rat adrenal gland is poorly parasitized during the experimental infection with Y strain of Trypanosoma cruzi. In both cortical and medullary regions, the parasitism peaked at day 10 and was characterized by the predominance of single amastigotes over nests containing 2 or more parasites. After day 10 of infection, the tissue parasitism dropped rapidly to become practically null at day 32 of infection. In cortical tissue, the amastigotes occurred mainly inside the endocrine cells. In the medulla, they found mainly in glial cells and non-identified stromal cells. In both cortex and medulla, inflammatory processes were found till day 20 of infection. Our data do not support the hypothesis that a corticoid rich environment would favor T. cruzi parasitism in adrenal medulla.

Heavy renal infection in a pony with Klosiella equi resulted in moderate diffuse tubular nephrosis and tubular rupture. Multifocal non-suppurative interstitial nephritis was associated with ruptured tubules. Ultrastructural examination of sporoblasts demonstrated both the presence of a bilaminated membrane encasing organisms and nuclear budding. Endogenous corticosteroid production probably led to the development of an immune-compromized state and subsequent extensive parasitic replication.