Sarcocystis Idahoensis Sp. N. In Deer Mice Peromyscus Maniculatus (Wagner) and Geopher Snakes Pituophis Melanoleucus (Daudin)*,†

SYNOPSIS Deer mice Peromyscus maniculatus (Wagner) were trapped near Hammett, Idaho, as a possible source of Besnoitia jellisoni Frenkel and species of Sarcocystis to be used for life cycle studies. Forty-nine deer mice were necropsied; 20 (40.8%) were positive for sarcocysts structurally identical with those of Sarcocystis idahoensis sp. N. the source of S. idahoensis used for life cycle studies was a Great Basin gopher snake Pituophis melanoleucus deserticola Stejneger killed near Hammett, Idaho; 20 sporulated sporocysts measured 11.1 × 13.4 (11-12 × 13-14) μm. Structurally identical sporocysts were found in 7 of 14 Pacific gopher snakes P. m. catenifer (Blainville), and in 6 of 10 San Diego gopher snakes, P. m. annectens Baird & Girard. Totals of 148 deer mice and 17 gopher snakes were necropsied in the course of life cycle studies. Development of the first generation meronts took place within the hepatocytes of deer mice 2-10 days post-inoculation (PI) with sporulated sporocysts. Rosette-shaped meronts (6-8 days PI) contained tachyzoites attached by their posterior poles to a residual body. After release from the residual body, tachyzoites were initially retained in a meront wall and later released from the hot cells Within muscle cells a single tachyzoite-shaped structure was found 11 days PI and PAS-negative metrocyte-containing sarcocysts (2nd generation meronts) 13-34 days PI. PAS-positive material was first seen in sarcocysts 34 days II at which time bradyzoite formation became apparent. At 160 days PI, 10 sarcocysts measured 0.4 × 5.8 (0.2-0.9 × 1.8-9.9) μ and appeared to be mature and structurally identical with those from naturally infected deer mice. After ingestion of S. idahoensis-infected deer mice by gopher snakes, bradyzoites developed directly into microgamonts and macrogametes. These stages were first seen 5 days PI. Microgamonts were generally located above and macrogametes below the epithelial host cell nucleus. Seven to 11 days PI microgamonts were seen with mature microgametes, and oocysts which had not yet begun sporogony were found with oocyst walls. Clinical signs of illness were generally not observed in infected gopher snakes; however, one snake developed anorexia and cachexia, and became moribund after repeated ingestion of heavily infected deer mice. Acute hepatitis associated with developing meronts often was noted in deer mice given over 15,000 sporocysts each. Five to 6 days PI anorexia, weakness, ataxia, and dyspnea were observed: these clinical signs increased in severity until 6-8 days PI, when mice became recumbent and died, or were killed while moribund. Hepatosplenomegaly, petechial hemorrhage o the serosal and cut surfaces of the liver, and icterus were common. Diffuse coagulative necrosis with cellular infiltration (primarily neutrophils) was noted on microscopic examination.     

Sporocysts isolated from the southern copperhead (Agkistrodon contortrix contortrix) produce Sarcocystis montanaensis-like sarcocysts in prairie voles (Microtus ochrogaster)

Sporulated oocysts and free sporocysts of a Sarcocystis sp. were isolated from the feces of a southern copperhead (Agkistrodon contortrix contortrix) collected in Arkansas (USA). Twenty sporocysts measured 11.2 by 8.5 microns, lacked a Stieda body, and had four sporozoites and a granular sporocyst residuum. Sarcocysts similar to those of Sarcocystis montanaensis were present in the tongues of prairie voles (Microtus ochrogaster) inoculated orally with 800 sporocysts 128 days previously. Sarcocysts were thin-walled, divided into compartments by septa, and had electron dense projections (0.14 microns) on the primary cyst wall. Infection was not pathogenic for prairie voles under the conditions of this study. No infections were observed in ICR strain laboratory mice (Mus musculus) or white-footed mice (Peromyscus leucopus) following oral inoculation of 800 sporocysts.     

The striped skunk (Mephitis mephitis) is an intermediate host for Sarcocystis neurona

Striped skunks, initially negative for antibodies to Sarcocystis neurona, formed sarcocysts in skeletal muscles after inoculation with S. neurona sporocysts collected from a naturally infected Virginia opossum (Didelphis virginiana). Skunks developed antibodies to S. neurona by immunoblot and muscles containing sarcocysts were fed to laboratory-reared opossums which then shed sporulated Sarcocystis sporocysts in their faeces. Mean dimensions for sporocysts were 11.0 x 7.5 microm and each contained four sporozoites and a residuum. Sarcocysts from skunks and sporocysts from opossums fed infected skunk muscle were identified as S. neurona using PCR and DNA sequence analysis. A 2-month-old, S. neurona-naive pony foal was orally inoculated with 5 x 10(5) sporocysts. Commercial immunoblot for antibodies to S. neurona performed using CSF collected from the inoculated pony was low positive at 4 weeks p.i., positive at 6 weeks p.i., and strong positive at 8 weeks p.i. Gamma-interferon gene knockout mice inoculated with skunk/opossum derived sporocysts developed serum antibodies to S. neurona and clinical neurologic disease. Merozoites of S. neurona present in the lung, cerebrum, and cerebellum of mice were detected by immunohistochemistry using polyclonal antibodies to S. neurona. Based on the results of this study, the striped skunk is an intermediate host of S. neurona.     

Sarcocystis hemionilatrantis (Sp. N.) life cycle in mule deer and coyotes.

Fifteen coyotes (Canis latrans) shed sporulated sporocysts in their feces after eating freshly ground skeletal muscles from a mule deer (Odocoileus hemionus hemionus) infected with microscopic-sized cysts of Sarcocystis. Sporocysts were shed intermittently from 12 to 36 days after ingestion of the infected meat. Sporocyst size averaged 14.4 X 9.3 mum. Eleven mule deer fawns orally inoculated with these sporocysts became infected and 9 of 11 died between post-inoculation days (PID) 27 and 63. Clinical signs of anorexia, weight loss, pyrexia and weakness were evident prior to death. A calf (Bos taurus) and two lambs (Ovis aries) orally inoculated with these sporocysts did not become infected and remained healthy throughout the experiments. Similarly, uninoculated control animals consisting of three mule deer fawns, two lambs and one calf remained healthy during the experiment. Preliminary histologic examinations conducted on selected tissues from all animals revealed microscopic-sized schizogonous stages in macrophages, between muscle fibers and near blood vessels in the esophagus, heart, biceps femoris, semi-membranosus, diaphragm and tongue from seven of eight fawns which died between PID 27 and 39. Developing or mature muscle cysts were not found in fawn tissue until PID 60. Sarcocysts were found in the three infected fawns examined after this time. Muscle cysts or earlier schizont stages were not found in tissues from the inoculated or uninoculated calves and lambs. A single muscle cyst was found in one control fawn; the other two control fawns were negative for both muscle cysts and other schizogonous stages. These results established that the life cycle of this species of Sarcocystis can be completed with coyotes as the definitive host and mule deer as the intermediate host. Based on the demonstrated host specificity and earlier findings, the name Sarcocystis hemionilatrantis is proposed for this parasite of mule deer and coyotes.     

Experimental infection of nontarget species of rodents and birds with Brucella abortus strain RB51 vaccine

The Brucella abortus vaccine strain RB51 (SRB51) is being considered for use in the management of bnucellosis in wild bison (Bison bison) and elk (Cervus elaphus) populations in the Greater Yellowstone Area (USA). Evaluation of the vaccines safety in non-target species was considered necessary prior to field use. Between June 1998 and December 1999, ground squirrels (Spermophilus richardsonii, n = 21), deer mice (Peromyscus maniculatus, n = 14), prairie voles (Microtus ochrogaster, n = 21), and ravens (Corvus corax, n = 13) were orally inoculated with SRB51 or physiologic saline. Oral and rectal swabs and blood samples were collected for bacteriologic evaluation. Rodents were necropsied at 8 to 10 wk and 12 to 21 wk post inoculation (PI), and ravens at 7 and 11 wk PI. Spleen, liver and reproductive tissues were collected for bacteriologic and histopathologic evaluation. No differences in clinical signs, appetite, weight loss or gain, or activity were observed between saline- and SRB51-inoculated animals in all four species. Oral and rectal swabs from all species were negative throughout the study. In tissues obtained from SRB51-inoculated animals, the organism was isolated from six of seven (86%) ground squirrels, one of six (17%) deer mice, none of seven voles, and one of five (20%) ravens necropsied at 8, 8, 10, and 7 wk PI, respectively. Tissues from four of seven (57%) SRB51-inoculated ground squirrels were culture positive for the organism 12 wk PI; SRB51 was not recovered from deer mice, voles. or ravens necropsied 12, 21, or 11 wk, respectively, PI. SRB51 was not recovered from saline-inoculated ground squirrels, deer mice, or voles at any time but was recovered from one saline-inoculated raven at necropsy, 7 wk PI, likely attributable to contact with SRB51-inoculated ravens in an adjacent aviary room. Spleen was time primary tissue site of colonization in ground squirrels, followed by the liver and reproductive organs. The results indicate oral exposure to SRB51 does not produce morbidity or mortality in ravens, ground squirrels, deer mice, or prairie voles.     

Isolation of Sarcocystis speeri Dubey and Lindsay, 1999 parasite from the South American opossum (Didelphis albiventris) from Argentina

Sarcocystis sporocysts from the intestines of 2 opossums (Didelphis albiventris) from Argentina were fed to gamma-interferon knockout (KO) and nude mice. Protozoal schizonts were seen in brain, liver, spleen, and adrenal glands of mice examined 33-64 days after feeding sporocysts. Sarcocysts were seen in skeletal muscles of KO mice 34-71 days after feeding sporocysts. Schizonts and sarcocysts were structurally similar to Sarcocystis speeri Dubey and Lindsay, 1999 seen in mice fed sporocysts from the North American opossum Didelphis virginiana from the United States.     

Pathogenesis of Sarcocystis falcatula (Apicomplexa: Sarcocystidae) in the budgerigar (Melopsittacus undulatus). III. Pathologic and quantitative parasitologic analysis of extrapulmonary disease

Forty-four budgerigars (Melopsittacus undulatus) were administered sporocysts of Sarcocystis falcatula orally and were examined at necropsy intervals from less than 12 hr to 168 days. Tissue were examined by touch preparations (of organ cut surfaces), light microscopy, and electron microscopy. Meront and cyst burdens were determined in various organs and correlated with duration of infection, inoculum, and the meront or cyst burdens of other organs. Host inflammatory tissue reactions were quantitated and correlated with meront and cyst burdens. Quantitation of meronts was more accurate in tissue sections than in touch preparations, but quantitation of merozoites was better in touch preparations. More than 97% of meronts were found in capillary, venular, and venous endothelial cells. Cysts were found only in cardiac and skeletal myocytes. Merogony began in the lamina propria of the small intestine less than 12 hr postinoculation (PI). Meronts were in liver and lung by the second day PI and in other organs by 3-7 days PI. Mean meront burdens were highest in lung (33 meronts/mm2), lower in liver and kidney (1-3 meronts/mm2), and infrequent in other organs (less than 0.9 meronts/mm2). Cysts were first seen in cardiac myocytes 7 days PI. They developed through the metrocyte stage and then degenerated, rarely reaching maturity. Cysts were first noted in skeletal muscle at 8 days PI. In leg, upper esophagus, and tongue, cysts matured between 44 and 77 days PI. In pectoral muscles, the majority of cysts degenerated during the late metrocyte and early intermediate stages (28-42 days PI). In addition to a previously reported and often fatal acute interstitial pneumonitis, S. falcatula-infected budgerigars also sustained a chronic active hepatitis, interstitial myocarditis, myositis, nephritis, splenitis, and encephalitis. These lesions weakly correlated with meront burdens in most sites during early infection (up to 50 days PI).     

Extraintestinal development of Caryospora simplex (Apicomplexa: Eimeriidae) in experimentally infected mice, Mus musculus

Developmental stages of Caryospora simplex were found in connective tissue of the cheek, tongue, and nose of Swiss-Webster and C57 BL/6 mice (Mus musculus) from 8 through 70 days after oral inoculation with 50,000 or 250,000 oocysts, or 60,000 free sporocysts of the same species obtained from an Ottoman viper, Vipera xanthina xanthina. The earliest developmental stages were seen on day 8 post-inoculation (PI) and consisted of two types of meronts and gamonts (undifferentiated sexual stages). Gamonts, microgametocytes, macrogametes, and unsporulated oocysts were found on days 10 and 12 PI. Fully sporulated, thin-walled oocysts containing eight sporozoites surrounded by a thin sporocyst membrane were first seen 12 days PI. Monozoic cysts (caryocysts) were first seen 12 days PI and appeared fully viable throughout the duration of the study, 70 days PI. Four mice injected intra-peritoneally with 150,000 free sporozoites and killed 12 days PI contained unsporulated and sporulated oocysts in connective tissues of the cheek, tongue, and nose, suggesting that sporozoites may be carried to the site of infection via the lymphatic/circulatory system. Four cotton rats, Sigmodon hispidus, inoculated orally with 250,000 oocysts all had unsporulated and sporulated oocysts of C. simplex in connective tissue of the cheek, tongue, and nose when killed on day 12 PI, indicating extraintestinal development in the secondary host is not species specific. This is the first report of a heteroxenous coccidium with both asexual and sexual development in the primary (predator) and secondary (prey) hosts.     

The life cycle of Cryptosporidium baileyi n. sp. (Apicomplexa, Cryptosporidiidae) infecting chickens

The life cycle and morphology of a previously undescribed species of Cryptosporidium isolated from commercial broiler chickens is described. The prepatent period for Cryptosporidium baileyi n. sp. was three days post oral inoculation (PI) of oocysts, and the patent period was days 4-24 PI for chickens inoculated at two days of age and days 4-14 for chickens inoculated at one and six months of age. During the first three days PI, most developmental stages of C. baileyi were found in the microvillous region of enterocytes of the ileum and large intestine. By day 4 PI, most parasites occurred in enterocytes of the cloaca and bursa of Fabricius (BF). Mature Type I meronts with eight merozoites first appeared 12 h PI and measured 5.0 x 4.9 micrometers. Mature Type II meronts with four merozoites and a large granular residuum first appeared 48 h PI and measured 5.1 x 5.1 micrometers. Type III meronts with eight short merozoites and a large homogeneous residuum first appeared 72 h PI and measured 5.2 x 5.1 micrometers. Microgamonts (4.0 x 4.0 micrometers) produced approximately 16 microgametes that penetrated into macrogametes (4.7 x 4.7 micrometers). Macrogametes gave rise to two types of oocysts that sporulated within the host cells. Most were thick-walled oocysts (6.3 x 5.2 micrometers), the resistant forms that passed unaltered in the feces. Some were thin-walled oocysts whose wall (membrane) readily ruptured upon release from the host cell. Sporozoites from thin-walled oocysts were observed penetrating enterocytes in mucosal smears. The presence of thin-walled, autoinfective oocysts and the recycling of Type I meronts may explain why chickens develop heavy intestinal infections lasting up to 21 days. Oocysts of C. baileyi were inoculated orally into several animals to determine its host specificity. Cryptosporidium baileyi did not produce infections in suckling mice and goats or in two-day-old or two-week-old quail. One of six 10-day-old turkeys had small numbers of asexual stages only in the BF. Four of six one-day-old turkeys developed mild infections only in the BF, and sexual stages of the parasite were observed in only one of the four. All seven one-day-old ducks and seven two-day-old geese developed heavy infections only in the BF with all known developmental stages present.     

Extraintestinal Development of Caryospora simplex (Apicomplexa: Eimeriidae) in Experimentally Infected Mice,Mus musculus1

Developmental stages of Caryospora simplex were found in connective tissue of the cheek, tongue, and nose of Swiss-Webster and C57 BL/6 mice (Mus musculus) from 8 through 70 days after oral inoculation with 50,000 or 250,000 oocysts, or 60,000 free sporocysts of the same species obtained from an Ottoman viper, Vipera xanthina xanthina. The earliest developmental stages were seen on day 8 post-inoculation (PI) and consisted of two types of meronts and gamonts (undifferentiated sexual stages). Gamonts, microgametocytes, macrogametes, and unsporulated oocysts were found on days 10 and 12 PI. Fully sporulated, thin-walled oocysts containing eight sporozoites surrounded by a thin sporocyst membrane were first seen 12 days PI. Monozoic cysts (caryocysts) were first seen 12 days PI and appeared fully viable throughout the duration of the study, 70 days PI. Four mice injected intra-peritoneally with 150,000 free sporozoites and killed 12 days PI contained unsporulated and sporulated oocysts in connective tissues of the cheek, tongue, and nose, suggesting that sporozoites may be carried to the site of infection via the lymphatic/circulatory system. Four cotton rats, Sigmodon hispidus, inoculated orally with 250,000 oocysts all had unsporulated and sporulated oocysts of C. simplex in connective tissue of the cheek, tongue, and nose when killed on day 12 PI, indicating extraintestinal development in the secondary host is not species specific. This is the first report of a heteroxenous coccidium with both asexual and sexual development in the primary (predator) and secondary (prey) hosts.     

The Life Cycle of Cryptosporidium baileyi n. sp. (Apicomplexa, Cryptosporidiidae) Infecting Chickens

ABSTRACT. The life cycle and morphology of a previously undescribed species of Cryptosporidium isolated from commercial broiler chickens is described. The prepatent period for Cryptosporidium baileyi n. sp. was three days post oral inoculation (PI) of oocysts, and the patent period was days 4–24 PI for chickens inoculated at two days of age and days 4–14 for chickens inoculated at one and six months of age. During the first three days PI, most developmental stages of C. baileyi were found in the microvillous region of enterocytes of the ileum and large intestine. By day 4 PI, most parasites occurred in enterocytes of the cloaca and bursa of Fabricius (BF). Mature Type I meronts with eight merozoites first appeared 12 h PI and measured 5.0 × 4.9 μm. Mature Type II meronts with four merozoites and a large granular residuum first appeared 48 h PI and measured 5.1 × 5.1 μm. Type I meronts with eight short merozoites and a large homogeneous residuum first appeared 72 h PI and measured 5.2 × 5.1 μm. Microgamonts (4.0 × 4.0 μm) produced 16 micro-gametes that penetrated into macrogametes (4.7 × 4.7 μm). Macrogametes gave rise to two types of oocysts that sporulated within the host cells. Most were thick-walled oocysts (6.3 × 5.2 μm), the resistant forms that passed unaltered in the feces. Some were thin-walled oocysts whose wall (membrane) readily ruptured upon release from the host cell. Sporozoites from thin-walled oocysts were observed penetrating enterocytes in mucosal smears. The presence of thin-walled, autoinfective oocysts and the recycling of Type I meronts may explain why chickens develop heavy intestinal infections lasting up to 21 days. Oocysts of C. baileyi were inoculated orally into several animals to determine its host specificity. Cryptosporidium baileyi did not produce infections in suckling mice and goats or in two-dayold or two-week-old quail. One of six 10-day-old turkeys had small numbers of asexual stages only in the BF. Four of six one-day-old turkeys developed mild infections only in the BF, and sexual stages of the parasite were observed in only one of the four. All seven one-day-old ducks and seven two-day-old geese developed heavy infections only in the BF with all known developmental stages present.     

Life cycle of Isospora rivolta (Grassi, 1879) in cats and mice

The endogenous development of Isospora rivolta (Grassi) was studied in cats fed oocysts, and was compared with the endogenous cycle after feeding them mice infected with I. rivolta. For the mouse-induced cycle, 14 newborn cats were killed 12 to 240 h after having been fed mesenteric lymph nodes and spleens ofmice. Asexual and sexual development occurred throughout the small intestine, in epithelial cells of the villi and glands of Lieberkühn. The number of asexual generations was not determined with certainty, but there were at least 3 structurally different meronts. Type I meronts appeared at 12-48 h postinoculation (HPT). They were 8.5(6-13) x 5.1(3-6) micrometer, contained 2-8 merozoites, and divide by binary division or endodyogeny. Type II meronts were multinucleate merozoite-shaped meronts within a single parasitophorous vacuole. They were found at 48-172 HPI and measured 12.6(9-18) x 9.8(9-13) micrometer. Individual multinucleate merozoite-shaped meronts were 7-13 x 3-5 micrometer in sections and contained 2-30 slender (5.5 x 1.0 micrometer) merozoites. Type III meronts occurred at 72-192 HPI and gamonts at 72-96 HPI. Mature microgamonts measured 11.3(9-15) x 8.0(6-9) micrometer in sections and up to 21.5 x 14 micrometer in smears, and contained up to 70 microgametes. Macrogamonts measured 13.3(11-18) x 9.0(5-13) micrometer in sections and 18 x 16 micrometer in smears, and contained up to 70 microgametes. Macrogamonts measured 13.3(11-18) x 9.0(5-13) micrometer. Sporulation was completed within 24 h at 22-26 C. For the study of the oocyst-induced cycle in cats, 18 newborn cats were killed between 6 and 192 HPI. The endogenous development was essentially similar to the mouse-induced cycle, but merogony and gametogony occurred 12-48 h later than in the latter cycle. Isospora rivolta was pathogenic for newborn but not for weaned cats. Newborn cats fed 10(6) sporocysts or infected mice usually developed diarrhea 3-4 days after inoculation. Microscopically, desquamation of the tips of the villi and cryptitis were seen in the ilium and cecum in association with meronts and gamonts. For the study of the development of I. rivolta in mice, mice were killed from day 1 to 23 months after having been fed 10(5)-10(6) sporocysts, and their tissues were examined for the parasites microscopically, and by feeding to cats. The following conclusions were drawn. (A) Isospora rivolta most freqeuntly invaded the mesenteric lymph nodes ofmice and remained there for 23 months at least. Ii also invaded the spleen, liver, and skeletal muscles of mice. This species could not be passed from mouse to mouse. Sporozoites increased in size from approximately 6.8 x 4.9 micrometer on day 1 to approximately 13.4 x 6.9 micrometer on day 31 postinoculation. Division was not seen. Prepatent period was 4-7 days and patent periods ranged from 2 to several weeks.     

Prevalence of Borrelia burgdorferi and Babesia microti in mice on islands inhabited by white-tailed deer.

Borrelia burgdorferi and Babesia microti were isolated from 35 of 51 white-footed mice (Peromyscus leucopus) and meadow voles (Microtus pennsylvanicus) captured on two Narragansett Bay, R.I., islands inhabited by deer, the principal host for the adult stages of the vector tick, Ixodes dammini. Immature ticks parasitized mice from both islands. From 105 mice captured on four other islands not inhabited by deer neither pathogen was isolated, nor were I. dammini found.     

Prevalence of Borrelia burgdorferi and Babesia microti in mice on islands inhabited by white-tailed deer

Borrelia burgdorferi and Babesia microti were isolated from 35 of 51 white-footed mice (Peromyscus leucopus) and meadow voles (Microtus pennsylvanicus) captured on two Narragansett Bay, R.I., islands inhabited by deer, the principal host for the adult stages of the vector tick, Ixodes dammini. Immature ticks parasitized mice from both islands. From 105 mice captured on four other islands not inhabited by deer neither pathogen was isolated, nor were I. dammini found.     

Life Cycle of Cystoisospora felis (Coccidia: Apicomplexa) in Cats and Mice

Cystoisospora felis is a ubiquitous apicomplexan protozoon of cats. The endogenous development of C. felis was studied in cats after feeding them infected mice. For this, five newborn cats were killed at 24, 48, 72, 96, and 120 h after having been fed mesenteric lymph nodes and spleens of mice that were inoculated with C. felis sporulated sporocysts. Asexual and sexual development occurred in enterocytes throughout the villi of the small intestine. The number of asexual generations was not determined with certainty, but there were different sized merozoites. At 24 h, merogony was seen only in the duodenum and the jejunum. Beginning at 48 h, the entire small intestine was parasitized. At 24 h, meronts contained 1–4 zoites, and at 48 h up to 12 zoites. Beginning with 72 h, the ileum was more heavily parasitized than the jejunum. At 96 and 120 h, meronts contained many zoites in various stages of development; some divided by endodyogeny. The multiplication was asynchronous, thus both immature multinucleated meronts and mature merozoites were seen in the same parasitophorous vacuole. Gametogony occurred between 96 and 120 h, and oocysts were present at 120 h. For the study of the development of C. felis in murine tissues, mice were killed from day 1 to 720 d after having been fed 10⁵ sporocysts, and their tissues were examined for the parasites microscopically, and by bioassay in cats. The following conclusions were drawn. (1) Cystoisospora felis most frequently invaded the mesenteric lymph nodes of mice and remained there for at least 23 mo. (2) It also invaded the spleen, liver, brain, lung, and skeletal muscle of mice, but division was not seen based on microscopical examination. (3) This species could not be passed from mouse to mouse.     

Experimental infection and horizontal transmission of Modoc virus in deer mice (Peromyscus maniculatus)

Deer mice (Peromyscus maniculatus) were inoculated with a sublethal dose of a field strain of Modoc virus to determine patterns of viral persistence, shedding, and transmission. Blood, serum, urine, fecal, and oral swab samples were collected at selected intervals until 63 days postinoculation (PI) after which lung, liver, spleen, kidney, and salivary glands were explanted. Viral assays were conducted by intracranial inoculations of suckling mice and antibody titers were determined by the micro-complement-fixation test. Viremias lasted for up to 4 days PI. Antibody titers were present by day 8 PI, peaked at day 13-20 PI, and persisted until day 63 PI. There was no evidence of viral shedding in urine, fecal, or oral swab samples. Virus was detected in explanted lungs only. In a separate experiment, deer mice were inoculated with virus and lungs were removed from five mice per wk for 10 wk. Indirect fluorescent antibody (IFA) techniques were used to determine the location of virus in lung tissue and to examine fixed tissue for lesions. IFA showed virus in lung parenchymal cells beginning 42 days PI and persisting at least 70 days PI. No histopathologic changes were seen. Horizontal transmission of the virus was studied by placing uninoculated mice with inoculated mice for 42 days and determining if the test animals developed antibodies or had virus in their lungs. Fifty-percent of the uninoculated mice developed antibody. One of these animals had virus in its lungs. Therefore, Modoc virus may be transmitted by direct contact.     

Electron microscope study of merogony preceding cyst formation of Sarcocystis sp. in roe deer (Capreolus capreolus)

Precystic merogony of Sarcocystis sp. was studied in roe deer fawns 33, 45, and 49 days postinoculation (pi) with 2 X 10(4)-10(5) sporocysts recovered from dogs. Single merozoites, but no meronts, were found 33 days pi in liver, spleen, and lymph nodes. Transforming merozoites and meronts were found in myofibroblasts, satellite cells, and endothelial cells of muscle tissue on 45 and 49 days pi; they were surrounded by two membranes. Typical coccidian merozoites differentiated simultaneously around an enlarged, lobed nucleus.     

Isospora peromysci Davis, 1967 (Apicomplexa: Eimeriidae) in Peromyscus leucopus and P. maniculatus (Rodentia: Cricetidae) from Texas

Oocysts of Isospora peromysci (Davis, 1967) (Apicomplexa: Eimeriidae) were recovered from the feces of 1/30 (3.3%) white-footed mice, Peromyscus leucopus , in Johnson County, Texas. This report represents a new host and geographic record for the parasite. The coccidium was also found in 1/20 (5.0%) deer mice, P. maniculatus , from the same locale. Morphological data are provided on the sporulated oocyst of I. peromysci and comparisons are made with previously published information on the species from other geographic localities.     

Isospora peromysci Davis, 1967 (Apicomplexa: Eimeriidae) in Peromyscus leucopus and P. maniculatus (Rodentia: Cricetidae) from Texas

Oocysts of Isospora peromysci (Davis, 1967) (Apicomplexa: Eimeriidae) were recovered from the feces of 1/30 (3.3%) white-footed mice, Peromyscus leucopus, in Johnson County, Texas. This report represents a new host and geographic record for the parasite. The coccidium was also found in 1/20 (5.0%) deer mice, P. maniculatus, from the same locale. Morphological data are provided on the sporulated oocyst of I. peromysci and comparisons are made with previously published information on the species from other geographic localities.     

Experimental infections of Sarcocystis cruzi, Sarcocystis tenella, Sarcocystis capracanis and Toxoplasma gondii in red foxes (Vulpes vulpes)

Four littermate 6-wk-old red foxes (Nos. 1-4) were fed Toxoplasma gondii, Sarcocystis cruzi, S. tenella and S. capracanis. One littermate fox (No. 5) served as the control. Two foxes (Nos. 1, 2) were fed tissue cysts of T. gondii and two foxes (Nos. 3, 4) were fed oocysts of T. gondii. Twenty-one to 42 days later, the same five foxes were used to test the infectivity of meat of goat, sheep, and ox experimentally inoculated with Sarcocystis. Fox 2 was fed goat meat and shed S. capracanis-like sporocysts 10 days later. Foxes 3 and 4 were fed beef, and they shed S. cruzi-like sporocysts 9 days later. Fox 5 was fed sheep meat and shed S. tenella-like sporocysts 8 days later. Foxes were killed between 36 and 55 days of the experiment and their tissues were inoculated into mice to recover T. gondii. All foxes remained clinically normal and T. gondii was recovered from all inoculated foxes and not from the control. Sarcocystis sporocysts from foxes induced lethal infections in goats, sheep, and ox. The sporocysts, meronts, merozoites, and sarcocysts of fox-derived parasites were similar to those derived from coyotes or dogs. It was concluded that the red fox can act as a final host for the three pathogenic species of Sarcocystis in cattle, sheep, and goats.