Chronic effects of agar, guar gum, gum arabic, locust-bean gum, or tara gum in F344 rats and B6C3F1 mice.

Diets containing 25,000 (2.5%) or 50,000 ppm (5.0%) agar, guar gum, gum arabic, locust-bean gum or tara gum were fed to groups of 50 male and 50 female F344 rats and B6C3F1 mice for 103 wk. Separate groups of 50 rats and 50 mice of each sex served as controls for each study. There were no significant differences in survival between any of the dosed groups of rats or mice and their respective control groups. Depressions in body-weight gain greater than 10% for dosed groups relative to their respective control groups were observed for male (low dose only) and female mice fed diets containing agar, female mice fed diets containing guar gum (high dose only), male mice fed diets containing locust-bean gum (high dose only) and male and female mice fed diets containing tara gum (high dose only). Depressions in body-weight gain greater than 5% were observed for female rats fed diets containing agar, guar gum or gum arabic. There were no histopathological effects associated with the administration of the test materials. Under the conditions of these bioassays, none of the five polysaccharides was carcinogenic for F344 rats or B6C3F1 mice of either sex.

Experimentally induced cerebrospinal nematodiasis in rabbits (Oryctolagus cuniculus).

To determine if the rabbit can act as an intermediate host for ascarids from certain carnivorous animals (skunks, pigs, dogs), 12 rabbits were infected with Ascaris columnaris, Ascaris suum, or Toxocara canis. Clinical signs, microscopic lesions, and morphologic features of ascarids with naturally occurring and experimentally induced A columnaris infections were identical. Of the 3 induced parasitic infections, A columnaris caused the most severe lesions in the central nervous system (CNS). It appears that rabbits may potentially act as intermediate hosts for A columnaris.

Transmission of marble spleen disease in turkeys and pheasants.

Marble spleen disease (MSD) of ring-necked pheasants (Phasianus colchicus L.) was transmitted in the laboratory to pheasants and turkeys (Meleagris gallopavo L.) by oral, colonic, and intravenous routes of inoculation, using cell-free supernatant fluids of splenic suspension from birds with naturally occurring MSD. Gross lesions consisted of large mottled spleens, a lesion more prominent in infected pheasants than in turkeys. The only microscopic lesion and also the criterion of infection were the presence of typical intranuclear inclusions of MSD. Similar to microscopic observations in naturally infected birds was the presence of inclusions in cells of spleen, bone marrow, liver, lung, bursa of Fabricius, and intestine-associated lymphoid tisse (IALT) OF EXPERIMENTALLY INFECTED BIRDS. Ultrastructural examination of splenic cells with intranuclear inclusions from turkey and pheasant with experimentally transmitted disease revealed viral particles and inclusions morphologically indistinguishable from those observed in naturally infected birds. Results of viral isolation procedures in turkey embryo chorioallantoic membrane (CAM) and yolk sac, as well as in turkey embryo fibroblast (TEF) and turkey kidney cell (TKC) cultures, were negative. Serologic assay by agar gel immunodiffusion tests indicated cross-reactivity between splenic MSD antigen and spleinic hemorrhagic enteritis (HE) of turkey antigen. Lines of fusion were formed between the splenic antigen from naturally occurring MSD in pheasants, experimentally transmitted MSD in turkeys, and HE of turkeys, using the homologous serum antibody to each of the 3 antigens.

Demonstration of an avian adenovirus as the causative agent of marble spleen disease.

A purification procedure, using chloroform or fluorocarbon extraction and centrifugation on a cushion of cesium chloride (CsCL), was designed to isolate the causative virus of marble spleen disease. Virus was purified, inoculated into turkeys, and subsequently reisolated by purification from the spleen of inoculated turkeys, thus fulfilling Koch's postulates. Splenic antigen was detected by the agar gel precipitin test, and viral inclusions with viral particles were observed by light and electron microscopy. Results of further studies indicated splenic lymphoreticulum cell hyperplasia was a sensitive indicator of marble spleen disease virus (MSDV) infection. Direct fluorescent antibody staining revealed nuclear fluorescence in virus-infected splenic cells from turkeys inoculated with purified MSDV. With negative stain electron microscopy, MSDV was observed to be 90 nm across with an icosahedral capsid composed of 252 capsomeres. This morphologic feature was consistent with that of an avian adenovirus. Serologic evidence for classification of MSDV as an adenovirus was the cross reaction of MSDV antigen with antiserum to turkey adenovirus serotypes TA-1 and TA-2 in the agar gel precipitin test.

A Hammondia-like coccidian with a mink-muskrat life cycle.

A tissue cyst-forming coccidian morphologically resembling the known species Hammondia has a mink-muskrat life cycle. Cysts are found in skeletal muscle of muskrats (Ondatra zibetheca). Mink (Mustela vison) fed infected muskrat carcasses shed oocysts for 4 to 6 days after a prepatent period of 6 to 8 days. The oocysts, 99% of which are unsporulated in mink feces, measure 11.5 to 12 microns X 10 to 11 microns. Sporulated oocysts have 2 sporocysts, each with 4 sporozoites. The present work was insufficient to establish whether this Hammondia-like parasite is identical to the known Hammondia spp. or is a new parasite, although the evidence gathered supports the hypothesis that this parasite is a new member of the genus Hammondia.

Experimentally transmitted marble spleen disease in pen-raised wild turkeys.

Pen-raised North American wild turkeys (Meleagris gallopavo L.) were experimentally infected with marble spleen disease (MSD) to determine their susceptibility to this disease. Gross and microscopic lesions were consistent with experimental MSD in pheasants and domestic turkeys: an enlarged mottled spleen, intranuclear inclusion bodies, and absence of pulmonary edema and hemorrhage. Detectable levels of viral antigen were not demonstrable in sera of turkeys using the agar gell precipitin test.