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PubMed1975

Remarks on the status of the genus Leucocytozoon Sambon, 1908.

Authorship of the genus Leucocytozoon has been variously assigned to several investigatiors, especially Danilewsky and Ziemann. Recently Hsu, Campbell & Levine (1973) have credited it to Berestneff. It is herein submitted that they erred in doing so and in relegating Akiba Bennett, Garnham & Fallis, 1965 and Saurocytozoon Lainson & Shaw, 1969 to synonymy with it. An attempt is made to clarify the confusion that has increasingly surrounded the genus Leucocytozoon, and it is recommended that the type species (by designation) should be Leucocytozoon majoris (Laveran, 1902), one of a mixture of organisms earlier lumped together under a name (Haemamoeba Grassi & Feletti, 1890) currently reserved for an avian subgenus of Plasmodium Marchiafava & Celli, 1885. We conclude that the generic name should be credited to Sambon, the 1st author to present an unequivocal description of the genus.

Animals↗
PubMed1975

Growth of Nosema algerae in pig kidney cell cultures.

Nosema algerae, a microsporidan parasite of mosquitoes, can infect pig kidney cell cultures. Sores germinated in the culture medium, infected the cells within 30 min of germination, multiplied, and produced spores. The early developmental stages in the N. algerae life cycle are discribed.

Animals↗
PubMed1975

Blood protozoa of imported birds.

Large numbers of birds, until recently, were brought into the United States each year. Countries of origin were varied, and included those of Australasia, Africa, South America, and the Caribbean islands, as well as other places. With them of course come their parasites, some of which may be potential pathogens to domestic avifauna. In part for this reason, a survey was undertaken of blood parasites of birds from pet shops and importers. So far a total of 1234 birds belonging to 186 species has been examined. Several new species and subspecies of avian Plasmodium have been found in the course of this study, including P. octamerium Manwell, 1968 in a Pintail Whydah, Vidua macoura, from Africa; P paranucleophilum Manwell & Sessler, 1971 in a South American tanager, Tachyphonus sp; and P. nucleophilum toucani Manwell & Sessler 1971 in a Swainson's Toucan, Ramphastos s. swainsonii. Plasmodium huffi Muniz, Soares & Battista is undoubtedly a synonym pro parte for the last. Plasmodium tenue Laveran & Maruliaz, long thought to be a synonym of Plasmodium vaughani Novy & MacNeal, was rediscovered and found to be a valid species. Plasmodium nucleophilum, infrequently seen in the New World, occurred in many Asian and African birds, and especially in starlings. Infections with other species of Plasmodium were common. Haemoproteus was the commonest blood parasite; Leucocytozoon was very rare as was Atoxoplasma (Lankesterella). The 2 families of birds best represented were the Fringillidae and the Psittacidae, but no blood parasites were seen in the latter. It is clear that imported birds are often infected with blood protozoa, some of which are unknown from native birds.

Animals↗
PubMed1975

Epizootic and enzootic aspects of Minchinia nelsoni (Haplosporida) disease in Maryland oysters.

Minichinia nelsoni disease in oysters (Crassostrea virginica) from Marumsco Bar, Pocomoke Sound, Maryland (an estuarine tributary of Chesapeake Bay) was studied for 8 years (1961-68) to determine epizootiologic relationships concerning life cycle of the parasite, pathologic effects on the host, and effects of physical factors on population density and recruitment of the host and parasite. The study period covered pre-epizootic, epizootic, and post-epizootic disease conditions. Data on the native oyster population as well as annual introductions of previously unexposed, susceptible populations of juvenile oysters from 1965-68 were included. Salinity, water temperature, mortality, prevalence, incidence, life cycle stages, gross pathology, and histopathologic relationships were observed. Mortality was high (45-55% per year) during the first 3 years of the study; however, M. nelsoni prevalences were low (less than 25%) and did not clearly imply a cause and effect relationship. Drought conditions that began in the summer of 1963 and continued through 1967 caused higher salinities, and apparently initiated epizootic disease in the native oyster populations. The epizootic peaked in May 1965 with a diagnosed prevalence in native oysters of 70%. Enzootic levels of annual mortality (40% in 1966, 30% in 1967, and 2% in 1968) and fall prevalence (16%, 24%, and 4%) developed after that time. Introduced populations had a typical epizootiologic pattern in 1965 55% annual mortality, 82% incidence) and 1966 (55% annual mortality, 66% incidence) which declined in 1967 (30% annual mortality, 44% incidence) followed by a disappearance of the disease in 1968. Epizootiologic differences noted between native oysters (adult and juvenile) and the introduced juvenile populations were also evident from the stages of the disease. Infections in native animals tended to be less serious, and in many cases were delayed or attentuated, while infections in introduced oysters progressed to advanced or terminal phases. Occult manifestations (mantle recession thought to be due to M. nelsoni in oysters not showing histologic evidence of infection) were absent in introduced populations and common in the native population. These differences are interpreted as evidence of resistance in surviving native oysters and their progency, and may indicate genetic resistance developed by natural selection and manifested by an increased ability to survive and overcome infection.

Animal Diseases↗
PubMed1975

Fine structure of Encephalitozoon cuniculi from rabbits, mice and hamsters.

Fine structure and development of Encephalitozoon cuniculi from rabbits were studied in rabbit choroid plexus (CP) cell cultures and were compared to hamster and mouse microsporida. Sporoplasms had a single limiting membrane and contained a large nucleus. Proliferative forms (schizonts) had double outer membranes, the outermost being associated with the formation of the limiting membrane of vacuoles formed within the host cell cytoplasm. These organisms were often binucleate and divided to form sporonts. Sporonts divided once to form 2 sporoblasts which developed into electron-dense spores. Spores had a thick, 3-layered wall and contained a polar filament. The developmental cycle of E. cuniculi in rabbit CP cultures progressed rapidly. Sporoplasms were observed in host cells at 3 hr postinoculation (PI). By 24 hr PI proliferative forms were associated with host cell cytoplasmic vacuoles which contained developing organisms. Mature spores were present in vacuoles by 2 days PI, indicating that the life cycle in the CP system is approximately 48 hr. The fine structure and the sequential developmental cycle of the mouse and hamster isolates were observed to be identical to those of the rabbit isolate and different from those of the genus Nosema. It is proposed, therefore, that the 3 organisms represent the same species, Encephalitozoon cuniculi.

Animals↗
PubMed1975

Encephalitozoon sp. in the blue-masked lovebird, Agapornis personata (Reichenow): first confirmed report of microsporidan infection in birds.

A microsporidan tentatively classified as Encephalitozoon sp. on the basis of structure and tinctorial qualities was identified in tissues from a group of blue-masked lovebirds. Agapornis personata (Reichenow). The organism was present in renal tubular epithelial cells, hepatocytes, bile duct epithelial cells, and intestinal epithelial cells. Focal hepatic necrosis occurred around clusters of the organisms but inflammation was minimal or absent in the other infected tissues. Attempts to infect laboratory mice with the organism were unsuccessful. Ultrastructural features were compared with those of E. cuniculi of mammals.

Animals↗