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By means of light and electron microscopy, the structural pattern of muscle cysts (sarcocysts) was examined for the four species of the genus Sarcocystis: S. muris (from murine skeletal muscles), Sarcocystis sp. and S. fusiformis (from, respectively, heart and skeletal muscles of buffalo), and S. ovifelis (from ovine tong muscles). The orderly fashion of the interior of the cyst is attained by partitition of its space into numerous compartments with the involvement of the intermediate filaments. These, in their turn, are bound to each other by thin filaments to make eventually a common filamentous net. The net limits separate groups of cells referred to as cyst zoites. The common net of filaments and microtubules (when present) may be regarded not only as the organizer of the cyst interior cytoskeleton, but also as the main mechanism of substance transportation in various directions: from the host cell to the sarcocyst, and within or outside the cyst. The role of dedifferentiation, proliferation and differentiation processes is suggested in the establishment of the fixed sequence of events throughout the unidirectional development of cyst cells and their interaction, from precystic meronts to cyst merozoites (gamonts). Special attention is paid to metrocyte morphogenesis and functioning. In the present work, metrocytes subjected to apoptosis were recognized. It is suggested that phenomenon of programmed cell death in metrocytes may be associated with the control of cell number in mature and ageing sarcocysts.

The participation of the sarcocyst surface apparatus (SSA) of two sarcosporidian species, Sarcocystis muris and S. ovifelis (Coccidia, Sporozoa, Apicomplexa), in degradation of disrupted host cell substances was investigated. After degradation, these substances are transported through the membrane of the SSA to the sarcocyst ground substance (GS), but this process cannot be regarded as endocytosis. At first, the transported substances were found in SSA pits in the form of fibrillar structures. Later on, these were seen as twisted up granules. In some cases, such granules restore their fibrillar shape, penetrate through the SSA membrane and appear in the sarcocyst GS. In other cases, the small granules may be released from SSA pits directly to the sarcocyst GS. Besides, two SSA primembrane layers were seen to disappear during the transportation of host cell substances. In addition, multimembrane structures (membranous whorls) were first demonstrated between the plasmalemma and inner membrane complex of the zoite pellicle. Multimembrane structures were found, in addition, in the zoite cytoplasm in connection with micronemes. These structures resembling chloroplast granae of thylakoids may presumably fill the gap in membrane pool of the SSA contributing to its renewal.

The structure of the sarcocyst surface apparatus (SSA) was investigated for two sarcosporidian species: Sarcocystis muris (non-pathogenic) and S. fusiformis (pathogenic). The surface membrane, being the main SSA subsystem, makes numerous vesicle-like protrusions with different ultrastructural patterns. This made it possible to distinguish between four and three types of these protrusions in S. fusiformis and S. muris, respectively. Vesicles of similar structure, pinched off from the fully formed protrusions, were classified, correspondingly, in the same four and three different types. A presumable functional role of both protrusions and membrane-coated vesicles in pathogenicity of different sarcosporidian species is proposed. The vesicles pinched off from corresponding protrusions may be involved in transporting certain substance complexes from the sarcocyst to the harbouring host cell. In addition, another way of substance transporting was observed, when the cystic substances, not surrounded with any membrane coating, are thrown from open protrusions directly into the immediate cytoplasm of the host cell.

The obligatory heterogenous tissue cyst-forming coccidia of the genus Sarcystosis are regarded as an excellent example of specific coexistence of two organisms, i.e., the host and parasite. These parasitic protozoans are known as causative agents of the chronic, often life-threatening disease, sarcocystosis, which still cannot be effectively controlled. In Sarcocystis, the entire phase of asexual multiplication was transferred to the intermediate host. Of special interest is the parasite's ability to persist in this host at the stage of tissue cyst or sarcocyst. This is a giant meront, in which unidirectional development proceeds starting from a little differentiated metrocyte, through intermediate cells, and towards highly differentiated cyst merozoites (gamonts) unable to further divide. The life span of the sarcocyst depends, to a great extent, on self-regulation within the cyst itself and on relations between the cyst and its immediate environment. A totally new field of research into Sarcocystis was initiated by the discovery that the intracellular parasite damages both cyst harboring and intact muscle cells, apart from the adjacent connective and nervous tissue. The previously unknown cytopathological effects of sarcocysts have been described and characterized. The changes observed within and outside the sarcocysts have been analyzed in terms of general biological processes: proliferation, differentiation, and programmed cell death.

20 laboratory mice (Mus musculus) were fed each a single dose of 20,000 Sarcocystis muris sporocysts to be then sacrificed 1, 2.5, 4, 6 and 10 months following infection (p.i.). A visual infection of the murine corps demonstrated that the number of sarcocysts per animal increased regularly as the time of infection was progressing, being eventually higher after 6 and 10 months p.i. than within 1-4 months p.i. This phenomenon was poorly understood from the knowledge that the tissue cysts (sarcocysts) are able to increase in size, rather than in number, and that the original number of sarcocysts largely depends on the number of precystic merozoites available. In our experiments, each of 20 mice was fed an equal number of sporocysts, and thus the number of precystic merozoites ought to be expected also more or less equal. EM investigation of murine skeletal muscles 6 and 10 months p.i. revealed, along with numerous normal sarcocysts, the presence of some separate, individual zoites, both within and outside the muscle fibre, in the endomysium. Besides, a colony of zoites, living freely without any visible common wall, was detected within a muscle fibre adjacent to another one, containing a sarcocyst of normal structure. These zoites may have originated from one or more sarcocysts, whose cyst walls were spontaneously broken, time after another, and thus led the cyst cells go out. These discharged zoites could either perish, being enzymatically degraded, or penetrate the neighbouring muscle fibres to proceed their further development. The colony making zoites were confined to two cell types only: the intermediate cells and the merozoites (gamonts). No metrocytes were recognized due, presumably, to inability of these little differentiated cells, devoid of penetrative organelles, to invade the host muscle cell. The colony of zoites turned out to be a developing population of live cells, able to destroy progressively the harbouring muscle fibre, except its basal membrane and sarcolemma. It does not seem unlikely that the outer coverings of the infected cell could be transformed eventually into a cyst wall to make, thus, a new sarcocyst. The above phenomena have never been found in murine muscles earlier than 6 months p.i. Although these facts are few and far between, they may prompt a possible mechanism of sarcocyst increase in number, in the intermediate host with age, even without any additional sporocyst contamination.