Electron microscope studies of the erythrocytic forms, including gametocytcs and asexual schizonts, of the protozoa Plasmodium fallax, P. lophurae, and P. cathemerium, have revealed a "cytostome," a specialized organclle of thc pcllicular membrane which is activc in the ingestion of host cell cytoplasm. In matcrial fixed in glutaraldehyde and postfixed in OsO~, thc cytostomc appears in face view as a pore limited by two dense circular membrancs and having an inside diameter of approximately 190 m/~. In cross-section, the cytostome is a cavity boundcd on each side by two dcnse scgments corresponding to the two dcnsc circles observed in facc view; its basc consists of a single unit mcmbranc. In the process of feeding, the cytostome cavity cnlarges by expansion of its membranc, permitting a large quantity of red ccll cytoplasm to come into contact with the cytostome wall. Subsequcnt digcstion of erythrocyte cytoplasm occurs exclusively in food vacuoles which emanatc from the cytostomc invagination. As digcstion progrcsscs, the food vacuoles initially stain more densely and thcrc is a marked build-up of hcmozoin granules. In the final stagc of digcstion, a single membrane surrounds a cluster of residual pigment particles and very little of the original host cell cytoplasm remains. The cytostome in exoerythrocytic stages of P. fallax has been observed only in merozoites and does not seem to play the same role in the feeding mechanism.
The fine structure of the exoerythrocytic cycle of an avian malarial parasite, Plasmodium fallax, has been analyzed using preparations grown in a tissue culture system derived from embryonic turkey brain cells which were fixed in glutaraldehyde-OsO4. The mature merozoite, an elongated cell 3-to 4-/~ long and l-to 2-# wide, is ensheathed in a complex doublelayered pellicle. The anterior end consists of a conoid, from which emanate two lobed paired organelles and several closely associated dense bodies. A nucleus is situated in the mid portion of the cell, while a single mitochondrion wrapped around a spherical body is found in the posterior end. On the pellicle of the merozoite near the nucleus a cytostomal cavity, 80 to 100 m/~ in diameter, is located. Based on changes in fine structure, the subsequent sequence of development is divided into three phases: first, the dedifferentiation phase, in which the merozoite loses many complex structures, i.e. the conoid, paired organelles, dense bodies, spherical body, and the thick inner layers of the pellicle, and transforms into a trophozoite; second, the growth phase, which consists of many nuclear divisions as well as parallel increases in mitochondria, endoplasmic reticulum, and ribosomes; and third, the redifferentiation and cytoplasmic schizogony phase, in which the specialized organelles reappear as the new merozoites bud off from the mother schizont.
SYNOPSIS. Cryptosporidium wrairi sp. n. is described from the laboratory guinea pig Cavia porcellus. The life cycle is given insofar as it is known. Two schizogonous generations are described; the 1st with 8 merozoites, the 2nd with 4 merozoites. The latter generation was previously referred to as the sporulated oocyst, but evidence is presented to show that it is a schizont. Micro‐ and macrogametogony are also described. No oocysts were found. Cross‐transmission to mice, chickens, turkeys and rabbits was unsuccessful. The generic character of oocysts with 4 naked sporozoites is discarded and the presence of endogenous stages in the striated border of epithelial cells is used as the emended generic character. A listing of valid and non‐valid species is given.
A disease resembling human typhoid fever has been induced by feeding live cultures of Salmonella typhosa to young chimpanzees, thus confirming the classical reports of Grünbaum and of Metchnikoff and Besredka.
Detailed clinical observations, results of stool and blood cultures, and serological studies have confirmed the impression that the disease produced in chimpanzees closely resembles the mild form of human typhoid fever frequently seen in childhood.
Gross and histologic examination of intestines, mesenteric lymph nodes, liver, spleen, and other organs of orally infected chimpanzees has demonstrated that the pathological findings are essentially indistinguishable from those seen in mild typhoid fever in man.
The clinical spectrum of disease seen in chimpanzees ranged from moderately severe illness, through transitory illness, to afebrile infection with or without bacteriemia (but invariably with an antibody response), occasionally leading to the development of persisting biliary infection and the carrier state. Thus the range of illness observed in chimpanzees resembled that seen in man, except that the severe and complicated forms of typhoid fever were not observed in the chimpanzee. A reason for this difference is proposed and discussed.
In contrast to the limitations imposed upon the interpretation of human epidemiologic observations, it has been possible to demonstrate in the chimpanzee that clinical variation in disease pattern from animal to animal may occur despite the administration of the same dose of the same bacterial strain simultaneously to an entire group of animals under study; in other words, variation in clinical pattern is dependent on inherent, non-specific host factors as well as on dose, strain or preceding state of immunity.
Variation in dose and in challenge strain of S. typhosa employed also appeared to have an effect upon the likelihood of producing febrile as against afebrile infection in chimpanzees. The dose required to produce clinical disease, even with the more virulent strain, was excessively large compared to what is believed to be the dose required to produce illness in man; the limitations of this assumption, and suggested explanations for the findings, are discussed.
The production of the spectrum of typhoid fever in the chimpanzee has made possible the study of basic problems in this disease which are not amenable to definitive study through the use of prevailing laboratory techniques.
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