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Sarcocystosis was diagnosed in 41 eighteen-month-old heifers and steers. Clinical signs included anorexia, severe weight loss, nervousness, hypersalivation, lameness, and hair loss on the extremities. Hair loss was noticed especially at the end of the tail, where there was complete loss of the switch, giving the animals a "rat-tail" appearance. Consistent gross changes observed at necropsy of four affected animals included generalized lymphadenopathy, erosions and ulcerations in the oral cavity and esophagus, and severe laminitis. Microscopically, young cysts of Sarcocystis sp were disseminated in the heart, skeletal muscle, and brain. Ultrastructural examination indicated that the cysts were young because they contained metrocytes. Affected animals had moderate to severe nonsuppurative myocarditis and myositis, with focal degeneration of myofibers and infiltration by macrophages, lymphocytes, and plasma cells. Indirect hemagglutination of sera from 19 animals revealed a mean antibody titer of 1:24,000 against Sarcocystis bovicanis antigen. Epidemiologic investigation incriminated resident farm dogs that had been housed in a farm hayloft as the source of infection. Hay contaminated with sporocysts in dog feces was thought to have been fed to the heifers and steers.

Activity of colostral whey, produced by a cow immunized with oocysts of Cryptosporidium parvum and found to provide prophylaxis against cryptosporidiosis in calves, was tested in 2 experiments. In one experiment BALB/c mice were given the immune whey (HW), whey from a nonimmunized cow (CW), or a balanced salt solution (HBSS) before, during, and after oral inoculation with oocysts of C. parvum. Significantly fewer (P less than 0.05) C. parvum were found in mice that received HW (undiluted, 1:20 or 1:50) than in those treated with similarly diluted CW or with HBSS. In the second experiment it was determined that protection was mediated by specific anti-sporozoite activity when significantly fewer (P less than 0.05) C. parvum were found in mice that received sporozoites treated with HW diluted 1:20 or 1:50 compared with mice that received sporozoites treated with similarly diluted CW or with HBSS.

Individual sporocysts containing 4 sporozoites were shed in the feces of dogs, foxes, and raccoons after ingestion of bovine tissue infected with Sarcocystis fusiformis bradyzoites. No sporocysts were shed by cats, monkeys, swine, skunks, ferrets, rats, guinea pigs, or rabbits after ingestion of similar bovine tissue. The shedding of sporocysts by dogs that had ingested tissue from a bovine experimentally infected with sporocysts from coyotes indicated that both canids were definitive hosts for the same species of Sarcocystis. After oral inoculation wtih sporocysts from dogs previously fed infected bovine heart, a calf became infected; but sheep, swine, rats, mice, rabbits, and monkeys did not. These results show the narrow specificity of the asexual stages of this parasite for the bovine intermediate host and the wider, though still restricted, host range of the sexual stages of this parasite for coyotes, dogs, foxes, and raccoons, the definitive hosts.

Lysate of Sarcocystis cruzi bradyzoites induced RAW 264.7 macrophages to release a factor that killed L 929 cells. Rabbit antibody to murine tumor necrosis factor (TNF) inhibited this killing effect, indicating that the factor causing cell death was similar to TNF (also called cachectin). Based on the present findings we hypothesize that TNF mediates, at least in part, the disease associated with this parasitic infection.

Muscles from tongue, heart, and limbs of 14 pigs inoculated orally with Toxoplasma gondii oocysts were irradiated with 10, 20, 25, and 30 krad of gamma (cesium-137 and cobalt-60) irradiation. Viability of T gondii cysts was assayed by feeding porcine muscles to T gondii-free cats and/or by inoculation of sediment from acid-pepsin digested porcine muscle into mice. Cats fed 500-g samples of muscles irradiated with up to 20 krad shed T gondii oocysts. Cats fed muscles irradiated with 25 or 30 krad did not shed oocysts. Mice were inoculated with 8 isolates of T gondii, and tissue cysts in their brains irradiated with up to 40 krad were infective to mice; however, there was a 10,000-fold reduction in the viability of organisms in tissue cysts irradiated with 40 krad, compared with that in nonirradiated cysts. At 50 krad of gamma irradiation, there were no detectable infective organisms in infected mouse brains.

Eight Polled Dorset lambs were orally inoculated with Sarcocystis ovicanis sporocysts. Two lambs that received 100,000 or 200,000 sporocysts became clinically ill, recovered, and were killed 67 and 88 days after inoculation (DAI). Numerous intramuscular cysts were found in their skeletal and cardiac muscles. Three lambs received 100,000 sporocysts, three lambs received 1 million sporocysts, and three lambs received no sporocysts. After an acute clinical illness characterized by anemia, inappetence, weight loss, fever, and reduced serum protein, all lambs that received 100,000 sporocysts died 27 to 29 DAI and all that received 1 million sporocysts died 24 or 25 DAI. Hemorrhage involving the striated muscle and visceral organs was the most apparent gross lesion. The heart appeared most severely affected. Schizonts were found in vascular endothelial cells of all six inoculated lambs. Uninoculated lambs remained healthy, and neither lesions nor parasites were found in any tissues. Dogs fed tissues containing S. ovicanis cysts produced sporocytes 11 to 37 days after feeding; cats fed similar stages produced no sporocysts. Dogs fed tissues containing schizonts produced no sporocysts.

Five calves inoculated orally with 10(5)-10(6) sporocysts of Sarcocystis hominis from human feces were necropsied 10, 18, 24, 111, and 222 days postinoculation (DPI). Calves became febrile (greater than 40-41 C) between 10 and 24 DPI and developed mild anemia (packed cell volumes were reduced by 40% of initial values) between 29 and 57 DPI but otherwise remained clinically normal. Focal hepatitis, mesenteric lymphadenitis, and myocarditis were seen in calves at 10, 18, and 24 DPI. No stages of the parasite were found at any of these times except for a few merozoites in macrophages associated with myocardial lesions in the calf necropsied 24 DPI. Mature sarcocysts at 111 and 222 DPI were up to 950 microm long and their walls were up to 6 microm thick. They were found only in skeletal muscles. One immature sarcocyst was seen in the myocardium of the calf at 222 DPI.

Soluble antigen was prepared from Sarcocystis zoites obtained from heart muscle of a bovine inoculated with sporocysts from canine feces and killed 120 days after infection. The antigen was used in an indirect hemagglutination (IHA) test and an agar gel diffusion test to detect antibody to Sarcocystis in experimentally infected cattle. IHA serum titers began to rise 30 to 45 days after infection and reached levels up to 1:39,000 90 days after infection. Sera collected under field conditions from 21 dairy cows had IHA titers ranging from 1:54 to 1:486. Since all cows appeared in good health, titers of 1:486 or less can probably be considered nonsignificant with regard to diagnosis of clinical disease. No positive Sarcocystis IHA titers were obtained with human sera previously found to be IHA positive for toxoplasma, indicating a lack of cross reactivity between antigens. Precipitins in the agar gel diffusion test appeared 30 days postinoculation and became very pronounced at 65 to 90 days.

Between March and May 1983, tongues and esophagi of 355 adult ewes from Colorado and Idaho were examined for grossly visible sarcocysts. Sarcocysts of Sarcocystis gigantea were found in 35 sheep. Cats fed sarcocysts from these naturally infected sheep shed sporocysts in their feces. Two adult ewes and 12 lambs inoculated with 1,000 to 1,000,000 sporocysts were euthanatized at postinoculation days (PID) 146, 230, 265, 391, 721, and 882, and their tissues were fed to Sarcocystis-free cats. All inoculated sheep remained clinically normal except for mild pyrexia between PID 12 and 18. Sarcocysts first became grossly visible at PID 391 and sarcocysts from sheep first became infectious for cats at PID 230.

Sarcocystis cruzi forms cysts in striated muscle of the bovine host following schizogony. The fine structure of the immature cyst within muscle fibers of the ventricular myocardium was studied in relation to its development and to the multiplication of parasites within it. The young cyst is enclosed by a cyst wall containing numerous small protuberances. Metrocytes within the cyst are irregular in shape and are separated from each other and the cyst wall by a thin layer of ground substance. The parasite multiplies by endodyogeny within the metrocyte. As the cyst enlarges, the host muscle fiber is disrupted and large protrusions are present in the cyst wall.

Eighteen calves were orally inoculated with either 200,000 or 225,000 sporocysts of Sarcocystis cruzi. Eight goats were orally inoculated with 20,000 sporocysts of S capracanis. Calves and goats were euthanatized at various times after inoculation, and portions of their right and left biceps femoris, right and left longissimus dorsi, myocardium, and tongue were frozen at -150 C in precooled isopentane and stored at -70 C. Frozen sections of these muscles were stained with hematoxylin and eosin, modified Gomori's trichrome, nonspecific esterase, diphosphopyridine nucleotide tetrazolium reductase, and adenosinetriphosphatase at pH 10.4 and 4.6. Muscle from the same locations was fixed in 10% neutral buffered formalin, processed for paraffin embedding, sectioned, and stained with hematoxylin and eosin. Microscopic examination of both calf and goat tissue indicated that both type I and type II muscle fibers were equally infected and that infected myofibers showed no apparent damage other than displacement by sarcocysts. Occasionally, muscle fibers within the muscle spindles contained sarcocysts.

There are many unanswered questions and observations that appear contradictory within the subject of how sarcocystosis affects fetal health. Some fetuses are infected and have lesions, others are unaffected. Some fetal placentas are infected and have lesions, others are unaffected. Some maternal placentomes are infected and have lesions, others are unaffected. Most pregnant animals have overt clinical illness at the time the fetus is affected, others do not. Several possible mechanisms have been hypothesized by which sarcocystosis may directly or indirectly affect fetal health.

Distribution of Toxoplasma gondii cysts in tissues used for human consumption was studied in 4 naturally infected pigs (acquired infections) and in 2 experimentally infected pigs. On the day of euthanasia, pigs with acquired toxoplasmosis had serum antibody titers of 160 to 1,280 against T gondii (modified agglutination test). Experimentally infected pigs were inoculated with 10,000 oocysts of the GT-1 strain of T gondii and were euthanatized 267 or 357 days after inoculation. On the day of euthanasia, the experimentally infected pigs had serum antibody titers of 16 and 32 against T gondii. Fifty- to 100-g specimens from each of 6 cuts of meat commercially used to prepare Boston butt, arm picnic, ham, tenderloin, spareribs, and bacon and from the tongue, heart, brain, liver, kidneys, and diaphragm were collected from each pig and were digested in acid pepsin solution. Washed sediment from the digest of each specimen was inoculated SC into mice (6 mice/organ). Toxoplasma gondii was isolated from tissues of the 4 pigs with acquired toxoplasmosis; T gondii was isolated from the arm picnic, Boston butt, and tongue of 3 pigs, from the ham, tenderloin, spareribs, diaphragm and heart of 2 pigs, and from the bacon and brain of 1 pig. Toxoplasma gondii was not isolated from the kidneys of the 4 pigs with acquired toxoplasmosis. Toxoplasma gondii was isolated from the arm picnic, Boston butt, ham, spareribs, bacon, tongue, diaphragm, heart, and brain of the 2 experimentally infected pigs, and from the kidneys of one of the experimentally infected pigs.(ABSTRACT TRUNCATED AT 250 WORDS)

A large, heavily populated area regionalized the care of critical trauma in 1980. To evaluate the system, we reviewed patient outcome for thoracic aortic transection due to blunt injury for the first 18 months of trauma system operation. Of the total of 86 patients, 43 were transferred to trauma centers, 8 to nontrauma centers, and 35 were either directly transported to the coroner or dead on arrival at the hospital. Of the eight patients transported to non-trauma centers, seven were in cardiopulmonary arrest during transport and the eighth was pronounced dead shortly after admission to the emergency department. Twenty-seven of the 43 patients transferred to trauma centers were dead within 24 minutes of admission. The cause of death was rupture of a transected aorta in 22 patients and other multiple injuries in the remaining 5. Sixteen were alive long enough in the emergency department for evaluation. Nine of these patients underwent correction of aortic transection as well as other injuries and all survived. Two of the nine survivors sustained partial or complete spinal cord damage. The remaining seven patients died, but in only one patient did the undiagnosed aortic injury contribute to the cause of death. This patient had a normal cineangiogram and the diagnosis was made at autopsy. He was considered potentially salvageable, so 9 of 10 potentially salvageable patients survived (90 percent). Of the total of 86 patients with aortic transection, 77 died (90 percent). This study shows that regionalization of trauma care offers an excellent chance for survival of patients with thoracic aortic transection.

Two nearly identical experiments were conducted to determine the effects of the coccidiostatic compound monensin on Polled Dorset lambs experimentally infected with oocysts of Eimeria ninakohlyakimovae. Prophylactic medication at a dose level of 1 mg/kg of body weight was started 2 days before inoculation and prevented diarrhea and reduced oocyst production. Therapeutic medication at a dose level of 2 mg/kg, started with the appearance of signs of infection, reduced oocyst production below that of nonmedicated controls but did not eliminate diarrhea. Weight gains of medicated lambs were less than those of noninoculated, nonmedicated controls in both experiments. Apparently monensin, at the dose levels used, reduced oocyst production but also prevented weight gains as high as those in inoculated nonmedicated controls.

Sarcocystis, a protozoan that parasitizes muscle tissue of reptiles, birds, and mammals, including man, developed in avian and mammalian cell cultlures. Mctile banana-shaped organisms, released from cysts in grackle muscle, entered cells and transformed into enlarged ellipsoid or oblong stages, which developed into either multinucleate or cyst-like stages, or both.