Coccidiosis of ducks and geese.
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Animals↗
Biomedical subjects
S A Edgar
Publications and source records attributed to S A Edgar.
Ea-B and Ea-C cellular antigen genes in Leghorn lines resistant and susceptible to acute cecal coccidiosis.
Alloantigen genes B and C of respective loci Ea-B, the major histocompatibility complex (MHC) of chickens, and Ea-C were detected in Leghorn lines R and S selected from common ancestry for resistance and susceptibility to acute cecal coccidiosis, Eimeria tenella (ACC). The lines share genes B2 and C1; R line has B5, Br, and C4, and S line has B1, B3, B4, B6, C2, and C3. Haplotype Br is an apparent recombinant of B2 and B5, possibly F2G2-5. Expression of the F2G2- region of B2 and Br is strong in graft-vs.-host reactions but weak on erythrocytes; in contrast, that of F5G5- of B5 is reduced in graft-vs.-host reactions but strong on erythrocytes. Extinction of B4 in R line and B5 in S line occurred in the last stages of selection, and the frequency of B5 in R line increased as a result of intensification of selection pressure for resistance to coccidiosis. The respective C genes of highest frequency in lines R and S are C1 and C3. The latter is a probable recombinant of C1 and C2. Evidence of roles of the B and C systems in resistance and previous similar evidence for the AE system indicates that genes other than the chicken MHC have measurable effects on infectious diseases.
Alleles↗
Effect of mild infections with six species of Eimeria on skin pigmentation of broiler chickens.
Mild infections of Eimeria maxima, E. acervulina, E. mivati, E. brunetti, E. necatrix, or E. tenella that did not affect weight gain significantly (P greater than .05) caused significant (P less than .05) shank depigmentation in 6-week-old broilers fed a broiler diet. Infections of E. maxima, E. mivati, or E. acervulina caused numerically more depigmentation than did infections by E. tenella, E. brunetti, or E. necatrix. Significant depigmentation was first detected at 4 days postinoculation (pi) with some species, prior to other gross evidence of infection, and infected birds regained little lost pigment by 14 days pi. Pigmentation among the infections by different species from the time of innoculation to 14 days pi was not significantly different (P greater than .05) amongst the treatments.
Animals↗
Ea-A and Ea-E cellular antigen genes in Leghorn lines resistant and susceptible to acute cecal coccidiosis.
The purpose of the work was to explore the diversity and function of alloantigens in chickens differing in genetic resistance to acute cecal coccidiosis, Eimeria tenella (ACC). This paper describes A and E alloantigens, products of linked loci Ea-A and Ea-E, worked out in Leghorn lines R and S, previously selected for respective resistance and susceptibility to ACC. The R line possesses high frequency haplotypes A7E5 and A9E1 with very low frequencies of the recombinants. The S line possesses almost totally different haplotypes ranging from high to low frequency, respectively: A9E3, A9E5, A9E2, and A11E1. Alleles A7 and A11 were differentiated only by fortuitous production of an A reagent in other work on a commercial broiler line, suggesting that alloantigen variability in chickens is a continuum spanning varietal differences. The AE recombinants in both lines remained at very low frequencies for many generations after selection was suspended. Discussion is given for selection having been the most probable force producing nearly unique AE haplotypes in each of the two lines, largely from different cis-trans relations between similar A and E alleles. Thus, interactions of the A and E regions appeared to have been essential to the seeming action of AE on genetic resistance to ACC. The A and E antigens are shown to develop contemporaneously in ontogeny in the earliest generations of embryonic erythrocytes, further suggesting that AE is a coordinated functional complex.
Animals↗
Eimeria mitis invasion of the yolk sac diverticulum of chickens.
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Animals↗
Responses to prolonged selection for resistance and susceptibility to acute cecal coccidiosis in the auburn strain single comb white leghorn.
Selection in the parental Auburn Strain Leghorn (A line) for resistance (R line, 13 filial generations) and susceptibility (S line, 7 filial generations) to acute cecal coccidiosis (ACC) caused by Eimeria tenella resulted in a sixfold difference in the ACC mortality rates of the two lines. Relaxation of selection for resistance in line RR, derived entirely from R line, resulted in gradual regression of the ACC mortality rate toward that of the parental A line nonselected control. Progress of selection in R line based on the same low dose of oocysts employed in S line neared a plateau of low mortality after six generations. Average ACC mortality in the first four generations of S line was 50% greater than that in A line. Before infection, chicks of S line were smaller than those of lines A, R, and RR. After infection, growth of S line survivors was inferior to that of survivors of the other lines. Uninfected controls of S line and A line grew at similar rates; those of R line grew at a significantly lower rate. In R line, large doses of oocysts caused high mortality. The largest dose caused mortality approaching 90% in both sexes; at lower doses, males died at higher rates than females. Among the survivors, growth rates of females were inferior to those of males; the difference increased with increasing dose. Large doses of oocysts resulted in spreading of the infection beyond the typical site. In R line, severe infection occurred in the necks of the cecal pouches and rectum with comparatively mild infection in the bulbar portion of the pouches. In contrast, the chief focus of infection remained in the bulbar pouches in S line. Selection for resistance seemingly disrupted the typical host tissue specificity of E. tenella. Thus, genes mediating the response of the host to ACC are possibly identical or complementary to genes controlling tissue specificity.
Animals↗
Reduced intestinal absorption in broilers during Eimeria mitis infection.
The absorption of glucose and L-methionine was as much as 52% less in the intestine of broilers inoculated with 2 strains of Eimeria mitis than in the intestine of noninoculated controls. This malabsorption was observed in the region of, and caudad to, the yolk sac diverticulum. Malabsorption was greater in birds given 500,000 sporulated oocysts than in those given 50,000 sporulated oocysts/bird. Depigmentation of the plasma was also considered an indication of malabsorption. Gross lesions were not evident in the intestine of these infected birds, even though histopathologic sections showed the presence of numerous parasites. Body weight was also less in inoculated birds, but PCV and plasma protein concentrations were not affected.
Animals↗
Influence of hormonal and chemical bursectomy on the development of acquired immunity to coccidia in broiler chickens.
The effect of bursectomy on the development of acquired immunity to coccidiosis in young broiler chickens was examined. Bursectomy was produced by a combination injection of testosterone at 12 days of embryonation and cyclophosphamide at 1 and 2 days after hatching. Immunity to coccidiosis developed in bursectomized chickens immunized with commercially prepared vaccine (CocciVac D) as were measured by resistance to challenge infection at either 6 or 10 weeks of age. Bursectomy had no marked effect on the development of cell-mediated immunity as measured by delayed type hypersensitivity to coccidial oocyst. Since the cell-mediated immune response was not inhibited in the bursectomized chickens, this response was necessary for the development of acquired immunity to coccidiosis.
Animals↗
Studies on infectious bursal disease in chickens. 2. Scoring microscopic lesions in the bursa of fabricius, thymus, spleen, and kidney in gnotobiotic and battery reared White Leghorns experimentally infected with infectious bursal disease virus.
During a 2 1/2 year study on the effect of experimentally-induced infectious bursal disease (IBD) in White Leghorns, a system for scoring microscopic lesions was developed. Microscopic changes in the bursa of Fabricius, thymus, spleen, and kidney were studied to create a lesion score for each organ. No changes occurred in the cecal tonsil and few, if any, changes occurred in the liver. The system was useful in evaluating the severity of pathologic and inflammatory changes in each organ during the course of the disease. Lesion scores for the bursa ranged from 0 for normal bursae to +4 for severely affected bursae. The lesion scores for the thymus, spleen, and kidney ranged from 0 to +3. The criteria for scoring lesions in the thymus were: 0 equaled no change; +1- cortex had a few empty spaces, pronounced hyperemia with some heterophil infiltration, especially in the medulla; +2- cortex had an increase in the number of empty spaces and increased heterophil infiltration, and the cortex and medulla had decreased hyperemia; +3- cortex had numerous round aggregations (12 to 16 mu in diameter) of cell debris and pyknotic nuclei, a definite decrease in the lymphocyte density in the cortex, and decreased hyperemia in cortex and medulla. This lesion scoring system was useful in determining the severity of IBD in different-aged progeny from IBD-immune and nonimmune dams.
Animals↗
Effects of lasalocid (.0125%) in combination with roxarsone on lesion reduction and oocyst suppression in chickens infected with Eimeria tenella field isolates.
Lasalocid (.0125%) alone and combined with roxarsone (.005%) was evaluated for its effect on lesion reduction and oocyst suppression in thirty-five controlled replicated battery experiments, using in excess of 6200 broiler chickens. The chickens were inoculated with field isolates containing predominantly Eimeria tenella species. Lasalocid (.0125%) used alone exhibited a high degree of anticoccidial activity. Lasalocid (.0125%) fed in combination with roxarsone (.005%) showed, in addition to high anticoccidial activity, a further reduction in gross lesion (P less than .01) and oocyst production (P less than .05) over lassalocid used alone.
Animals↗
Comparative susceptibility and effect of mild Aspergillus fumigatus infection on three strains of chickens.
A single Comb White Leghorn strain (Dryden X Auburn = DAX) was more susceptible to Aspergillus fumigatus infection and suffered significantly greater mortality than the Athens-Canadian or a Vantress X Arbor-Acres cross exposed soon after hatching. The unexposed controls of the three types weighed significantly more than the corresponding exposed survivors at 5 weeks of age.
Animals↗
Efficacy of Stenorol (halofuginone). I. Against recent field isolates of six species of chicken coccidia.
The efficacy of Stenorol (halofunginone) was tested against six species of chicken Eimeria in a series of four battery experiments utilizing 3- to 4 1/2-week-old Cobb color-sexed broiler chickens. There were five replicates of eight chickens per replicate for each treatment of an experiment or a total of 1080 birds used in the study. The isolates were predominantly E. tenella, E. maxima, E. acevulina, E. necatrix, E. brunetti, or E. mivati and had previously been proven partially to totally resistant to several commercially available anticoccidial drugs. Halofunginone, at 3 ppm in the ration, was highly effective (P less than .01) against all six isolates as measured by weight gain at D+6 or +7and D+12 or +14 postinoculation; feed efficiency at D-2 to D+12 or +14; morbidity; mortality; dropping score; lesion score (D+6 or +7); and oocyst production during 4 or 5 days postinoculation (D = day of inoculation). The drug was not as effective against E. acervulina as against the other species, and increasing halofuginone to 4 ppm failed to improve activity of the drug signif;cantly against this isolate. However, 3 ppm of drug was effective against two other isolates of E. acervulina (from Alabama and Mississippi); 4 ppm was quite effective (P less than .01) in reducing dropping and lesion scores, but not significantly better than 3 ppm as measureed by other parameters. No relapse occurred after drug withdrawal and halofuginone was found to be cidal rather than static.
Animals↗
Efficacy of Stenorol (halofuginone). II. Plus roxarsone or bacitracin MD against selected strains of chicken Eimeria.
A total of 879 broiler strain chickens ranging from 2 1/2- to 7 1/2 weeks of age was utilized in four battery experiments to determine whether Roxarsone and/or bacitracin MD added to halofuginone were compatible and beneficial in reducing the effects of coccidial infections. The additives were generally beneficial as measured by weight gain and feed efficiency but not as measured by other parameters such as dropping score, lesion score, or oocyst production. The addition of 200 g of bacitracin/ton of feed did not give an additional response above that from 50 g/ton. Roxarsone in the ration was more effective in younger chickens (2 1/2 week old) than older ones (6 weeks, 2 days and 7 weeks, 3 days).
Animals↗
Efficacy of Stenorol (halofuginone). III. for the control of coccidiosis in turkeys.
Halofuginone at 3 ppm in the ration was tested against turkey coccidial infections caused by four species, in a series of eight battery trials of 16 days duration. The drug was evaluated against infections caused by Eimeria meleagrimitis, E. adenoeides, E. gallopavonis, and E. dispersa. As measured by livability, weight gain, feed efficiency, morbidity, dropping score, lesion score, and oocyst production the drug was highly effective in Beltsville Small White turkeys. The drug at 3 ppm appeared to be about equally effective against all four species and almost completely prevented infection or the effects of infection in some experiments, except when the challenge was too severe.
Animals↗
Possible secretory function of the rhoptries of Eimeria magna during penetration of cultured cells.
Ultrastructure of the penetration of Eimeria magna sporozoites into embryonic bovine trachea cells demonstrated that the host cell membrane was not broken during entry of the parasite. This membrane did, however, undergo alterations characterized by blebbing of vesicles, thickening, and eventual disorganization once penetration was completed. Concurrent with the entrance of the parasite into the cell, and the subsequent membrane alterations, was the appearance of empty membrane saccules, probably rhoptries, in the apical region of the sporozoite. It was proposed that rhoptry secretions aided penetration by changing cell surface characteristics which produced an eventual breakdown of the invaginated protion of the host cell membrane.
Animals↗
Effects of antiphagocytic agents on penetration of Eimeria magna sporozoites into cultured cells.
Madin-Darby Bovine Kidney cells were treated with sodium flouride, iodoacetate, and 2-deosyglucose, reagents that block glycolysis, and thus reduce phagocytosis. Sporozoites readily entered cells whose ATP stores were largely depleted. They also entered cells treated with colchicine, colcemid, and vinblastine. These latter agents did not inhibit sporozite motility after 6 hr incubation. Cytochalasin B prevented penetration of cells by inhibiting the motility of sporozoites. This effect was reversible. Warm sporozoites entered cold cells 4 times more radily than cold sporozoites into warm cells. The above findings suggest that phagocytosis is not the mechanism for entry of E. magna sporozoites into cultured cells, but that sporozoite motility is of primary importance.
Animals↗
The epizootiology of infectious bursal disease and prevention of it by immunization.
Transport of leftover feed from infectious disease (IBD) farms to susceptible flocks on clean premises is believed to have played an important role in the transmission of this disease to new farms and to new areas. Servicemen, caretakers, contaminated equipment and air were suspected in the spread of the disease, but these modes were not demonstrated. Litter, drinking water and samples of feed from feeders of IBD flocks were found to be infectious when added to rations of susceptible chickens but were not when added to drinking water. Infectious bursal agent (IBA) remained viable for at least 6 months in dry litter and in unused dry chicken houses for more than 1 year. IBA was found in circulating blood of infected chickens 36 hours after inoculation, but not after 72 hours. Liver, spleen, thymus, kidney, pancreas and intestines were infectious at 72 hours. Bursa and feces were infectious from 48 hours through 7 days after inoculation. Tests on 4 1/2 to 6-week-old birds from 10-12 farms of each of several broiler complexes in three southeastern states of the U.S. revealed IBA present on a high percentage of farms even though none had used vaccine. Vaccination with modified or unmodified IBA administered to millions of 4-10-day-old chicks gave good protection for the life of broilers and laying birds. Effect of IBD on development of immunity to other diseases will be discussed.
Animals↗
Immunization of chickens for the control of infectious bursal disease.
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Administration, Oral↗