Experimental toxoplasmosis in Japanese quail.

Twenty-four 5-month-old battery-hatched Japanese quail were inoculated orally with 10(5) (ME 49 strain, group A, 6 birds), 10(3) (ME 49 strain, group B, 6 birds), 10(5) (GT-1 strain, group C, 6 birds), and 10(3) (GT-1 strain, group D, 6 birds) Toxoplasma gondii oocysts. All birds in group C died or were euthanized within 8 days after inoculation (DAI). Five of the 6 birds in group D died or were euthanized 8, 9, 15, 19, and 23 DAI. One of the 6 quail in group A died 9 DAI, and 1 of the 6 birds in group D died 16 DAI. The 11 quail (1 from group D and 10 from groups A and B) were euthanized 63 DAI; T. gondii was isolated by bioassays in mice from the brains of 10, hearts of 10, and skeletal muscles of all 11 quail. Quail that survived marked small intestinal and splenic toxoplasmosis lived long enough to develop severe protozoal pneumonia, myocarditis, or meningoencephalitis. The quail that survived only to be examined at 63 DAI had moderate multifocal nonpurulent encephalitis and myositis and had a hypertrophic spleen that contained hemosiderin-laden macrophages. Toxoplasma gondii antibodies were found in the sera of all quail examined 63 DAI. Antibody titers to T. gondii in the modified agglutination test were higher than in the indirect hemagglutination and latex agglutination tests. Antibodies were not detected in quail sera examined by the Sabin-Feldman dye test.

Experimental toxoplasmosis in pheasants (Phasianus colchicus).

Sixteen 6-mo-old battery-reared ring-necked pheasants (Phasianus colchicus) were inoculated orally with 10(5) (group A, ME 49 strain, five birds), 10(4) (group B, ME 49 strain, six birds) and 10(4) (group C, GT-1 strain, five birds) Toxoplasma gondii oocysts. The pheasants in groups A and B remained clinically normal. One of the pheasants in group C died 19 days after inoculation (DAI); T. gondii was found in histological sections of brain and heart and encephalitis, myocarditis and enteritis were the main lesions. Toxoplasma gondii was isolated by bioassays from pooled tissues of five of six pheasants in group B killed 36 DAI. Toxoplasma gondii was isolated from the brains, hearts and skeletal muscles of each of the four pheasants inoculated with the GT-1 strain (group C), and from the brains of four, hearts of three and skeletal muscles of four of five pheasants inoculated with the ME 49 strain (group A). All pheasants developed high (1: 1,600-1:25,600) antibody titers to T. gondii in the modified agglutination test (MAT) 36 to 68 DAI. Antibody titers detected with the MAT were higher than those detected in the indirect hemagglutination and latex agglutination tests. Antibodies were not detected in 1:4 dilution of pheasant sera with the Sabin-Feldman dye test.

Experimental toxoplasmosis in bobwhite quail (Colinus virginianus).

Twenty-four 3-5-mo-old battery-hatched bobwhite quail were inoculated orally with 10(5) (ME 49 strain, group A, 6 birds), 10(4) (ME 49 strain, group B, 6 birds), 10(5) (GT-1 strain, group C, 6 birds), and 10(4) (GT-1 strain, group D, 6 birds) Toxoplasma gondii oocysts. One quail in group B died 18 days after inoculation (DAI) due to undetermined etiology. Two quail from group C and 1 quail from group D given GT-1 oocysts died of acute toxoplasmosis 6, 7, and 8 DAI, respectively; numerous T. gondii tachyzoites were found in lesions in visceral tissues. The surviving quail in group A and B were killed 106 DAI and those in groups C and D were killed 60 DAI. Toxoplasma gondii was isolated from pooled tissues of 4 of 5 quail in group B. Brains, hearts, and skeletal muscles from quail in groups A, C, and D were bioassayed individually in mice; T. gondii was isolated from the brains of all 6, hearts of 3, and skeletal muscles of 2 of the 6 quail in group A; from the brains of all 4, hearts of 1, and skeletal muscles of 2 of the 4 quail in group C; and from the brains of all 5, hearts of 1, and skeletal muscles of 3 of the 5 quail in group D. Toxoplasma gondii antibodies were found in sera of all 20 quail killed 60 or 106 DAI. Antibody titers detected in the modified agglutination test using whole tachyzoites were higher than in latex agglutination and indirect hemagglutination tests that used soluble antigens. Antibodies were not detected in a 1:4 dilution of 19 of 20 quail sera in the Sabin-Feldman dye test.

Experimental toxoplasmosis in turkeys.

Fourteen 2-3-wk-old turkeys were inoculated orally with 10(5) or 10(4) infective oocysts of the ME 49 strain of Toxoplasma gondii. Of the 8 turkeys given 10(5) oocysts in experiment 1, 3 died or were killed 12 or 14 days after inoculation (DAI) because of respiratory distress associated with a concomitant Aspergillus-like fungus infection. The remaining 5 turkeys remained normal and were killed 62 DAI. Toxoplasma gondii was isolated in mice from the heart of all 5, from the breast muscles of 2, leg muscles of 3, and from the brains and livers of none of the turkeys. All 6 turkeys fed 10(4) oocysts in experiment 2 remained clinically normal until necropsy on 41 DAI; T. gondii was isolated from pooled tissues from each turkey. All 14 turkeys developed high antibody titers to T. gondii in the modified agglutination test (MAT) using formalinized tachyzoites. The enzyme-linked immunosorbent assay (ELISA) was as sensitive as MAT for detecting T. gondii antibodies in turkey sera. The latex agglutination and indirect hemagglutination tests were less sensitive than the MAT and ELISA. No dye-test-measurable antibodies were found in sera of any turkey.

Characterization of the toxicity of the mycotoxins aflatoxin, ochratoxin, and T-2 toxin in game birds. III. Bobwhite and Japanese quail.

Bobwhite and Japanese quail were fed diets containing 1.25, 2.50, or 5.00 ppm aflatoxin; 1, 2, or 4 ppm ochratoxin A (OA); or 4, 8, or 16 ppm T-2 toxin. Aflatoxin induced mortality in bobwhites during the second and third week with 1.25 ppm (10%), 2.50 ppm (30%), and 5.00 ppm (40%), and during the same period with T-2 toxin at 8 ppm (20%) and 16 ppm (22.5%). Body weights of bobwhite quail were significantly decreased by the two higher levels of aflatoxin by 2 weeks of age, and by the two higher levels of T-2 toxin by 1 week of age. In Japanese quail, only the highest level of aflatoxin and T-2 toxin reduced body weight (by 3 weeks and by 1 week of age, respectively), and even then to a much lesser extent than in bobwhites (less than 10%). Aflatoxin did not affect feed-conversion ratio (FCR) in bobwhite quail, but the two higher levels of T-2 toxin increased FCR. None of the toxins induced mortality or increased the FCR in Japanese quail. Aflatoxin increased liver weight in both bobwhite and Japanese quail. OA increased kidney weight in 3-week-old Japanese quail but had no effect on the kidney weight of bobwhite quail. Mouth lesions were progressively more severe in bobwhite quail fed increasing levels of T-2 toxin, but lesions were far less severe in Japanese quail.

Prevention of coccidiosis in the chukar partridge (Alectoris chukar) by medication with sulfadimethoxine and ormetoprim (Rofenaid).

Rofenaid (a 5:3 mixture of sulfadimethoxine and ormetoprim) was effective in preventing coccidiosis of chukar partridges. Levels of .0100 or .0125% sulfadimethoxine, with the corresponding level of ormetoprim in the ration, gave the best results. These levels markedly reduced mortality in severe infections (over 75% mortality in unmedicated chukars) and eliminated mortality in medicated groups when infections produced 52% mortality or less in unmedicated controls. In the latter infections, Rofenaid also protected against the depression in weight gain seen 6 days postinoculation in unmedicated chukars. Studies in uninoculated chukars showed that Rofenaid has a wide safety margin and did not produce adverse effects even at levels of .0300% sulfadimethoxine. Rofenaid should, therefore, be an effective medication for the prevention of coccidiosis in chukars in the field. Data from the present studies are being submitted to the IR-4 Program of the Food and Drug Administration for consideration of approval for the use of Rofenaid in chukar partridges.

Characterization of the toxicity of the mycotoxins aflatoxin, ochratoxin, and T-2 toxin in game birds. I. Chukar partridge.

Chukar partridges were fed diets containing 1.25, 2.5, or 5 ppm aflatoxin; 1, 2, or 4 ppm ochratoxin A (OA); or 4, 8, or 16 ppm T-2 toxin. Toxin-induced mortality was seen during the third week with 4 ppm OA (12.5%) and 16 ppm T-2 toxin (15%), compared with the mortality in control chukars fed no toxin (2.5%). Body weights were significantly decreased by the highest level of aflatoxin at 3 weeks of age, by the highest level of OA by 2 weeks of age, and by 8 and 16 ppm T-2 toxin by 1 week of age. Aflatoxin did not affect liver weight and OA did not increase kidney weight in 3-week-old chukars. There was a slight decrease in kidney weight in chukars fed 4 ppm OA; however, the decrease was related to the decrease in body weight produced by the toxin. Mouth lesions were seen at all levels of T-2 toxin fed.

Prevention of coccidiosis in bobwhites by medication.

The efficacy of amprolium, monensin, and salinomycin in preventing coccidiosis in bobwhite quail was studied using a mixed inoculum of equal numbers of Eimeria dispersa and E. lettyae. A total dosage per quail of 10(6) sporulated oocysts was chosen because this dosage gave a good (77%) depression of weight gain from Day 18 to Day 24. Levels of .008% monensin or .0055% salinomycin were the most effective for prevention of coccidiosis as evaluated by body weight gains. These levels significantly reduced parasite numbers in the duodenum with monensin administration and in both the duodenum and ileum with salinomycin administration. Monensin reduced parasite numbers in the illeum significantly in one experiment and in a second. Amprolium was ineffective for prevention of coccidiosis, as evaluated by body weight gains. Amprolium was also ineffective in consistently reducing parasite numbers in the duodenum and ileum. Both monensin and salinomycin had a reasonable safety margin in quail. Levels of monensin of .016%, twice the proposed level, significantly reduced body weight at 14 days of age compared with unmedicated controls or quail given .008% monensin. By 28 days, however, this effect was no longer significant. Levels of salinomycin at the proposed level of .0055% significantly reduced body weight at 14 days of age compared with unmedicated controls. By 28 days, however, this effect was no longer significant in quail given .0055% or .00825% salinomycin, although in quail fed .011% salinomycin body weights remained significantly lower (16.5%) at that date. There were no detectable monensin residues in the liver of quail fed a ration containing .008% monensin for 8 wk.(ABSTRACT TRUNCATED AT 250 WORDS)

Pathogenicity of Eimeria lettyae Ruff, 1985 in the northern bobwhite (Colinus virginianus L.).

Sporulated oocysts of Eimeria lettyae were administered orally to 5-day-old or 18-day-old northern bobwhites (Colinus virginianus, L.). Five-day-old bobwhites were more susceptible based on higher mortality and reduced weight gain. A dose of 5 X 10(5) oocysts produced 25-43% mortality in 5-day-old bobwhites, but none in 18-day-old bobwhites. A dose of 1 X 10(6) oocysts/bobwhite produced 83-100% mortality in 5-day-old bobwhites, and 17-83% mortality in 18-day-old bobwhites. Body weight gain was reduced significantly with a dose of 1 X 10(5) oocysts or greater in 5-day-old bobwhites and with a dose of 5 X 10(5) oocysts or greater in 18-day-old bobwhites. Infection in all age groups reduced concentrations of plasma pigment and plasma protein, but did not affect packed cell volumes. No grossly visible lesions were present in the intestine although there was a shortening of the villi in the duodenum. In mature bobwhites, infection with E. lettyae did not cause mortality, but did reduce egg production and fertility.

Intestinal absorption following challenge of immune chicks with Eimeria acervulina.

The absorption of glucose or L-methionine was measured in vitro in the intestine of broilers challenged with 1 x 10(6) sporulated oocysts of Eimeria acervulina. These broilers had various degrees of immunity resulting from previous inoculation with several dosages of oocysts given one to six times. Unimmunised broilers were also given the challenge inoculation of oocysts. The level of immunity had a marked effect on nutrient absorption post challenge (p.c.). Partially immune birds showed an enhanced absorption at 3 hours p.c. compared with absorption in unchallenged birds. With high levels of immunity, the enhanced absorption at 3 hours p.c. was not seen. A significant malabsorption was seen 6 hours p.c., but absorption returned to normal by 24 hours p.c. The absorption pattern during the first 24 hours in unimmunised control broilers was similar to that in partially immune birds. The degree of immunity was directly related to the protection against malabsorption at 6 days p.c. In solidly immune birds, absorption at 6 days p.c. was significantly greater than in immunised, unchallenged birds and equal to that in the unimmunised, unchallenged controls. The diffusion and mediated components of methionine absorption were, in general, both affected during malabsorption or stimulation of absorption. There was no evidence histologic-ally of epithelial loss in the 24 hours p.c. The pH in the duodenum was significantly decreased at 8 and 24 hours p.c. in immunised birds but was not affected by a primary inoculation given to unimmunised birds.

Effect of aging on survival and pathogenicity of Eimeria acervulina and Eimeria acervulina and Eimeria tenella.

After 6 to 8 months of storage, cultures of sporulated Eimeria acervulina and E. tenella oocysts ahd a marked drop in the number of sporocysts that survived grinding, sporozoites that survived after excystation, and sporozoites that penetrated chick kidney cells in vitro. The rate of excystation was unaffected by storage of up to one year. In vivo pathogenicity, based on weight gain, lesion score, and plasma pigment, declined after 5 months of oocyst storage. The reduction in pathogenicity in vivo could be compensated for by adjusting the inoculation dosage to reflect the loss of infectivity seen in the in vitro test.

Total intestinal absorption of glucose and L-methionine in broilers infected with Eimeria acervulina, E. mivati, E. maxima or E. brunetti.

The in vitro absorption of glucose and L-methionine in the intestine of broiler chickens was measured 7, 14 and 21 days post-inoculation (p.i.) with sporulated oocysts of Eimeria acervulina, E. mivati, E. maxima or E. brunetti. The small intestine of each bird was divided into 8 regions of equal length and absorption was measured on 3 tissue disks of equal size from each region. The absorption rate of each substrate with each coccidial species was measured based on (1) an equal area from each region, (2) an equal weight from each region, (3) the total absorption in each region, and (4) the total potential absorption in the intestine. Comparisons of absorption rate of equal areas in each intestinal region demonstrated that infected birds at 7 days p.i. absorbed significantly less substrate per unit area in the regions of maximum infection than uninfected controls. Malabsorption was less apparent when the weight of the region was used as the unit of measurement. Compensatory absorption was seen in some uninfected regions with E. acervulina. The total potential intestinal absorption at 7 days p.i. was reduced with E. mivati, E. maxima and E. brunetti but not with E. acervulina. At 14 days p.i., total L-methionine and glucose absorption in some regions of the intestine was significantly increased with E. acervulina but not with E. mivati, E. maxima or E. brunetti. No absorption differences were seen at 21 days p.i. with any species.

Effect of dimetridazole on transmission of Histomonas meleagridis by Heterakis gallinarum.

The administration of an antihistomonal drug, dimetridazole, at a dose of 0.08% in feed, controlled experimental infections with Histomonas meleagridis in chickens. The treated birds developed no lesions and the duration of infection with H. meleagridis was reduced. This drug regimen, however, did not always prevent incorporation of H. meleagridis into eggs of Heterakis gallinarium; heterakid eggs pooled from medicated chickens in which H. meleagridis had never been detected transmitted the protozoan to 1 of 10 turkeys fed the eggs. Thus, therapeutic treatment of chickens with dimetridazole may reduce, but not eliminate, transmission of H. meleagridis by eggs of H. gallinarum from medicated birds.

Comparative responses of White Leghorn and New Hampshire chickens to experimental infections with Histomonas meleagridis and Heterakis gallinarium.

Experimental infections with Histomonas melegridis and Heterakis gallinarum were produced in young White Leghorn (W.L.) and New Hampshire (N.H.) chickens and Beltsville Small White turkeys (B.S.W.T.). Although the histomonads caused liver lesions and high mortality in B.S.W.T., infections in chickens were not fatal and were confined to the ceca. Cecal involvement in the W.L. was slightly more severe, but also more transitory, than in the N.H. With regard to length, survival, and reproductive capacity, the heterakids thrived best in the W.L. Furthermore, the W.L. had the greatest potential for disseminating Histomonas-bearing heterakid eggs. These findings are similar to those of a previous study with the same breeds of birds but with a different strain of W.L. Thus, the differences in responses according to breed were quite consistent, whereas any difference according to strain was insignificantly by comparison.

The wild turkey as a host for Heterakis gallinarum and Histomonas meleagridis.

Freshly embryonated eggs of Heterakis gallinarum gathered from naturally infected domestic turkeys and chickens developed the first 4 weeks essentially as well in young wild turkeys as in domestic poults, but then became progressively retarded and failed in most birds to result in females with fertile eggs. There was no significant difference in the prevalence or progress of infections with Histomonas meleagridis in the two kinds of turkeys, both of which differed from chickens only in that the latter had neither liver involvement nor mortality. In a second test, heterakids hatched from eggs stored 5-6 months at 4 C (comparable to overwintering) sustained very heavy losses in all birds, with greatly accelerated liberations of H. meleagridis, Few worms reached maturity and still fewer produced fertile eggs. In turkeys, and especially in wild turkeys, replacement of infective stages was so poor, that these birds were of no importance in contaminating the soil.