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Biomedical subjects

R Fayer

Publications and source records attributed to R Fayer.

At least 145 records · Page 8Linked to original sources

Disseminated visceral coccidiosis in sandhill cranes.

Disseminated visceral coccidiosis (DVC) caused by Eimeria spp was first recognized as a disease entity in captive sandhill cranes (Grus canadensis) and whooping cranes (G americana) at the Patuxent Wildlife Research Center. Because cranes produced at the Center are reintroduced to the wild to augment wild populations, studies involving both experimentally induced and natural infections were initiated to determine the potential or actual occurrence of DVC in wild Gruidae. Nine sandhill cranes dosed orally with eimerian oocysts of wild origin developed lesions characteristic of DVC. Extraintestinal granulomas associated with developing schizonts were found in 6 birds. Similar lesions were observed in wild sandhill cranes throughout parts of midwestern United States, Alaska, and Saskatchewan. These studies revealed the wide geographic distribution and the high frequency of occurrence of DVC in wild cranes.

Age Factors↗

Protective immunity against clinical sarcocystosis in cattle.

Five experiments involving 50 calves (Bos taurus) were conducted to determine if oral infection with sporocysts of the pathogen Sarcocystis cruzi or the non-pathogen Sarcocystis hirsuta would stimulate development of a protective immunity against illness or death from challenge infection with large numbers of S. cruzi sporocysts. Four experiments involved Holstein calves housed in individual pens in isolation buildings; one experiment involved Hereford calves on an open range. Calves infected with 50 000 to 100 000 S. cruzi sporocysts were protected from illness and death that would have resulted from challenge infections with 250 000 or 500 000 S. cruzi sporocysts given 70-252 days later. Calves treated with the anticoccidial drug amprolium from 21 to 35 days after being given an immunizing infection with S. cruzi to reduce clinical signs of the immunizing infection were also protected. Non-immunized calves and those given S. hirsuta sporocysts were not protected.

Amprolium↗

The effects of reducing conditions, medium, pH, temperature, and time on in vitro excystation of Cryptosporidium.

Whereas excystation of sporozoites from oocysts of most coccidian species requires exposure to reducing conditions followed by pancreatic enzymes and bile salts, sporozoites of a bovine isolate of a bovine isolate of Cryptosporidium excysted without exposure to either reducing conditions or to pancreatic enzymes and bile salts. Without prior exposure to reducing conditions, a high percent excysted after incubation in a mixture of trypsin and bile salts in Ringer's solution; fewer excysted after incubation in tap water, even fewer after incubation in salt solutions, and none after incubation in saliva. Excystation, generally greater at pH 7.6 than at pH 6.0 and at 37 degrees C than at 20 degrees C, was observed as early as 1 h after incubation in water or the trypsin-bile mixture. These findings provide circumstantial evidence that oocysts of Cryptosporidium can excyst in extraintestinal sites and liberate sporozoites that can initiate autoinfection.

Animals↗

Humoral and cellular immune responses in cattle and sheep inoculated with Sarcocystis.

Cattle inoculated with Sarcocystis bovicanis (= Sarcocystis cruzi) and sheep inoculated with Sarcocystis ovicanis were monitored for the appearance of Sarcocystis-specific antibodies and lymphocytes in the peripheral circulation. Anti-Sarcocystis antibody was identified by enzyme-linked immunosorbent assay, whereas antigen-reactive lymphocytes were discerned by an in vitro lymphocyte blastogenic assay. The antigens used were the soluble fraction recovered from disrupted bradyzoites of mature sarcocysts. Cattle developed anti-Sarcocystis immunoglobulin (Ig)M responses, beginning 3 to 4 weeks after inoculation, and IgG1 antibody responses, beginning 5 to 6 weeks after inoculation. The increase in IgM antibody was relatively brief, returning to near preinfection levels in 2 to 3 months. In contrast, IgG1 antibody levels remained high for at least 5 to 6 months. Neither IgG2 nor IgA antibody responses were demonstrable in cattle. In sheep, the IgG antibody levels followed a time course similar to that seen in cattle, except that the increase was slightly delayed (6 to 8 weeks after inoculation was done). Measurable IgM antibody response was not seen in sheep. Cellular immunoresponsiveness as judged by in vitro lymphocyte blastogenesis in cattle was different from that in sheep. Sarcocystis-specific lymphocytes were demonstrable in the circulation of cattle within 15 days after they were inoculated, but the activity decreased rapidly. In sheep, reactive cells were not evident until 3 to 4 weeks after inoculation were done, but peripheral blood lymphocytes taken from these sheep as long as 5 to 6 weeks after the inoculations remained capable of mounting strong blastogenic responses. Neither the enzyme-linked immunosorbent assay nor the blastogenic assay showed species specificity. Animals immunized with a given species of Sarcocystis gave similar in vitro responses to antigens from the immunizing species and to other species of Sarcocystis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Persistence of encysted Toxoplasma gondii in tissues of pigs fed oocysts.

Ten pigs were fed 100 to 10,000 Toxoplasma gondii oocysts. Two pigs died 7 and 11 days later, and 8 pigs were euthanatized at days 38, 38, 91, 126, 168, 169, 170, and 171. From the euthanatized pigs, portions of 15 organs digested in pepsin-HCl solution were inoculated into mice, as a bioassay for viable T gondii. Such organisms were isolated from the brain and heart of these 8 pigs, from the tongue of 7, from thigh muscles of 5, from the diaphragm of 4, from kidneys, liver, and small intestines of 2, and from salivary glands and eyes of 1 pig; but not from lungs, spleen, spinal cord, mesenteric and prescapular lymph nodes of any pig. Results indicate that T gondii can persist in edible tissues of living pigs for at least 171 days and that heart and brain may be the most suitable porcine tissues for epizootiologic surveys.

Animals↗

Effects of sarcocystosis on milk production of dairy cows.

Sixteen multiparous Holstein cows were allotted randomly to four groups of four cows each. Cows in 1 and 2 were uninfected. Those in 3 received 60,000 and those in 4 received 120,000 Sarcocystis bovicanis sporocysts per os approximately 30 days before the expected onset of lactation to produce nonclinical and clinical infections in 3 and 4, respectively. Combined stresses of infection, parturition, lactation, and high ambient temperatures caused all infected cows to develop clinical illness. Clinical signs included fever, anemia, glossitis, myositis, nasal discharge, hypersalivation, anorexia, and hind limb weakness; two cows died and two others were killed in extremis. Six cows in 3 and 4 developed high Sarcocystis-specific immunoglobulin G1 antibody. Uninfected control cows had no clinical signs and no rising concentrations of antibody against Sarcocystis antigen. When lactation began, cows were milked twice daily, and milk production was recorded for 70 consecutive days. All sarcocystis-infected cows (3 and 4) decreased feed intake and milk production compared with uninfected controls. The Wisconsin Mastitis Test on milk production compared with uninfected controls. The Wisconsin Mastitis Test on milk samples at 1, 2, 4, 8, and 12 wk of lactation did not differ among groups.

Animals↗

Experimental Sarcocystis ovicanis infection in lambs: salinomycin chemoprophylaxis and protective immunity.

Salinomycin, administered prophylactically, was effective in controlling clinical sarcocystosis resulting from infection with Sarcocystis ovicanis in two experiments involving a total of 50 lambs. In each experiment, five lambs were used in each of five test groups--uninoculated and unmedicated, inoculated and unmedicated, uninoculated and medicated (2 mg/kg), inoculated and medicated (2 mg/kg), and inoculated and medicated (1 mg/kg). Salinomycin was included in the feed of each medicated group for 30 days beginning on the day of oral inoculation with 10(6) S. ovicanis sporocysts. Lambs were challenged with 10(6) sporocysts 9 wk PI and the experiment was terminated 7 wk later. Data from deaths, weight gains, body temperatures, packed cell volumes, hemoglobin values, serum protein levels, and postmortem and histological examinations indicated that salinomycin at both doses tested reduced the number of deaths and severity of signs of sarcocystosis in infected lambs as compared with unmedicated controls. Infected, medicated lambs developed a protective immunity as determined by challenge inoculation. An additional group of five lambs, each inoculated orally with 10(6) sporocysts, were treated therapeutically with 2 mg/kg per day beginning 21 days after inoculation. All five died from acute sarcocystosis.

Animals↗

Sarcocystosis in an aborted bovine fetus.

Sarcocystosis was diagnosed in an aborted bovine fetus. Immature and mature schizonts of Sarcocystis were disseminated in the vascular endothelium of all organs, but especially the brain. Microscopic granulomas, focal gliosis, and petechial hemorrhages in the neuropil were scattered in the brain. Multifocal collections of mononuclear cells were observed in the kidney, liver and heart. Organisms in sections of frozen tissues were demonstrated by immunofluorescent techniques to be Sarcocystis.

Abortion, Veterinary↗

Infectivity of sarcocystis spp. from bison, elk, moose, and cattle for cattle via sporocysts from coyotes.

Bison bison (bison), Cervus canadensis (elk), Alces alces (moose), and Bos taurus (cattle) musculature containing Sarcocystis spp. cysts was fed to laboratory raised Canis latrans (coyotes), Sporocysts collected from the feces of coyotes fed musculature of each of the ruminant species were fed to four groups of three laboratory-raised domestic calves, respectively, to determine if Sarcocystis spp. was transmissible from wild to domestic ruminants and if so, to compare clinical signs of infection and morphologic features of cysts with those resulting from infection with Sarcocystis bovicanis. All calves fed sporocysts of Sarcocystis from coyotes that ate bison or cattle muscle had similar clinical signs and harbored morphologically similar parasites, suggesting that both bison and cattle are intermediate hosts for S. bovicanis and that this species is transmissible between the two ruminant species. All calves fed sporocysts from coyotes that ate elk muscle or moose muscle remained asymptomatic but one calf in each group had intramuscular cysts. The finding of relatively large numbers of intramuscular cysts in one calf fed sporocysts of elk origin and smaller numbers in one calf fed sporocysts of moose origin could represent either spurious natural infections or indicate low infectivity of Sarcocystis spp. from elk and moose to cattle.

Animal Population Groups↗

Development of Sarcocystis fayeri in the equine.

Eight ponies and a horse were inoculated orally with sporocysts of Sarcocystis fayeri from dogs. They were examined for clinical signs of infection and killed 10, 15, 20, 25, 30, 50 (horse), 77, 101, and 156 days after inoculation (DAI). Elevated temperature was observed in three ponies 20 and 26 DAI and anemia was observed in three ponies and the horse 15 to 69 DAI. Schizonts were found in or near cells lining capillaries or arteries of the heart, brain, and kidney 10, 20, and 25 DAI. Immature cysts containing only metrocytes were first found in muscles 50 DAI. Mature intramuscular cysts containing metrocytes and zoites or zoites alone were found 77, 101, and 156 DAI and produced patent infections in dogs fed infected meat.

Animals↗

Attempted transmission of Sarcocystis bovicanis from cows to calves via colostrum.

Sixteen pregnant cows were divided into four equal groups. Groups 1 and 2 were uninoculated controls; Groups 3 and 4 received 60,000 and 120,000 S. bovicanis sporocysts per os, respectively, about 30 days before expected parturition. Stained smears of colostrum from each quarter of the udder of each cow were examined microscopically for zoites. As a bioassay for infectious zoites in colostrum of acutely infected cows, colostrum from infected Group 4 cows was fed to calves from control Group 1 cows. Calves in Groups 2 and 3 received colostrum from their dams. Calves in Group 1 received colostrum from uninoculated normal cows. All calves were killed at 61 to 68 days of age and their tissues examined microscopically for Sarcocystis cysts. Because zoites were not found in colostrum smears and cysts were not found in calf tissues, it was concluded that lactogenic transmission of S. bovicanis did not occur.

Animals↗

Hematology of experimental acute Sarcocystis bovicanis infection in calves. I. Cellular and serologic changes.

Of four Holstein-Friesian calves infected with 200,000 sporocysts of Sarcocystis bovicanis, three became ill and died on days 35, 55, and 59 of a 63-day experiment. No control calves became ill or died. Three of the four infected calves developed normocytic normochromic anemia with about a 50% decrease in hemoglobin concentration on days 25 through 35, and had hyperbilirubinemia from day 25 or 26 to death (day 35); this disappeared when the anemia stabilized in surviving calves. Packed cell volume increased slowly after day 35 in the surviving anemic calves. Indirect and direct Coombs' tests were negative throughout the experiment in the control and infected calves. A reduction in numbers of neutrophils and lymphocytes paralleled the crisis of anemia in the infected calves. Serum antibody titers to S. bovicanis antigen were increased substantially in all infected calves 35 days or more after inoculation.

Animals↗

Hematology of experimental acute Sarcocystis bovicanis infection in calves. II. Serum biochemistry and hemostasis studies.

Of four Holstein-Friesian calves infected with 200,000 sporocysts of Sarcocystis bovicanis, three become ill and died on days 35, 55, and 59 of a 63-day experiment. No control calves became ill or died. Serum biochemicals and hematologic indicators of hemostasis from both groups were measured throughout the experiment. Creatine phosphokinase values for both groups increased markedly during acute infection. Lactic dehydrogenase and aspartate aminotransferase values were high in infected calves on days 25 to 35 and days 24 to 63, respectively, indicating injury of muscle, liver, or other tissues. Sorbitol dehydrogenase values were significantly higher for infected than for control calves on days 25 and 35, indicating liver injury. Serum bilirubin and blood urea nitrogen values were significantly increased in three anemic infected calves from day 25 or 26 to day 35, probably reflecting destruction of erythrocytes. The fourth infected calf was not anemic and had no hyperbilirubinemia and only minimal azotemia. Serum protein and albumin values decreased in infected calves on days 21 to 30 or 35, when, although hypoalbuminemia persisted, total protein concentration increased. Glucose, calcium, sodium, and chloride values decreased in infected calves slightly before onset of illness and remained low throughout the experiment. Potassium, magnesium, and phosphorus values did not differ between infected and control calves. Activated partial thromboplastin time and Russell's viper venom time were normal; prothrombin time was significantly higher from day 27 to day 49 in infected calves. This pattern was interpreted as evidence for acquired factor VII deficiency. Abnormal retraction of blood clots and enlarged platelets in blood smears, which indicate platelet dysfunction and increased platelet turnover, respectively, were seen on days 27 through 35 in anemic infected calves. Values for thrombin time (three calves) and fibrin degradation product concentration (one calf) increased just before death of the infected calves.

Animals↗

Sarcocystis spp. in white-tailed deer. I. Definitive and intermediate host spectrum with a description of Sarcocystis odocoileocanis n. sp.

Sporocysts containing four sporozoites and measuring (avg.) 15.2 micrometers X 10.7 micrometers (N = 195) were shed in the feces of dogs (Canis familiaris) 8 to 16 days (avg. 11.6 days) after the first feeding of venison infected with Sarcocystis sp. Sporocysts containing four sporozoites and measuring (avg.) 11.5 micrometers X 8.1 micrometers (N = 35) were shed by a cat (Felis catus) 14 days after ingesting Sarcocystis-infected venison. Statistical (pooled t-test) comparison of the mean measurements of the sporocysts passed by the dog and cat demonstrated a significant difference (P less than .01). The raccoon (Procyon lotor) and opossum (Didelphis virginiana) could not be infected with Sarcocystis from white-tailed deer (Odocoileus virginianus). The name, Sarcocystis odocoileocanis, is proposed for the species transmitted from white-tailed deer to dogs. Sarcocystis odocoileocanis is differentiated from S. hemionilatrantis Hudkins and Kistner, 1977 of mule deer (Odocoileus hemionus), S. ovicanis Heydorn, Gestrich, Mehlhorn and Rommel, 1975 of sheep (Ovis aries) and S. cruzi Hasselmann, 1926 (=S. bovicanis Heydorn, Gestrich, Mehlhorn and Rommel, 1975) of cattle (Bos taurus) because S. odocoileocanis has (1) low infectivity for calves and sheep and (2) apparent insignificant pathogenicity for its intermediate host.

Animals↗

Toxoplasmosis update and public health implications.

Toxoplasma gondii has a coccidian life cycle in the intestine of domestic and wild felids that includes a series of asexual and sexual stages and an oocyst stage that is shed in the feces. Oocysts complete their development outside the body, eventually becoming infective for about 350 species of vertebrates including cats and man. The effects of climate on oocyst survival and the physical and biological means of oocyst dispersal are discussed. Infectivity and pathogenicity for livestock species vary. Acute disease results from rapidly multiplying tachyzoites that may be transmitted by carnivorism, transfusion, vertical transmission and other routes. Patent infections may persist for the life of a host as bradyzoites within tissue cysts. Bradyzoites initiate acute infection in other hosts after carnivorism or organ transplantation or in the same host after immunosuppression. Also discussed are: (a) prevalence of T. gondii in livestock as determined by digestion and serological techniques, (b) identification in humans as accomplished by isolation, serological and skin test techniques and (c) identification in cats as accomplished primarily by fecal examinations for oocysts infective for mice. Source of human infections, major outbreaks, treatment, effects on mental health and methods for preventing toxoplasmosis in man and livestock are listed.

Animals↗