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At least 19 recordsLinked to original sources
PubMed1987

Ultrastructural studies of the effects of amprolium and dinitolmide on Eimeria acervulina macrogametes.

Medication of chicks with 125 ppm amprolium or dinitolmide adversely affected oocyst sporulation of Eimeria acervulina (Weybridge strain). Dinitolmide delayed oocyst production and no oocyst wall formation was seen up to 168 h post infection. Both drugs caused large numbers of abnormally small wall-forming bodies to be produced in the macrogametes. In amprolium-fed chicks, abnormal oocyst wall formation was seen. It was concluded that the main drug action was against wall forming bodies of type 2.

Amprolium↗
PubMed1981

Effect of amprolium and dinitolmide on sporulation of oocysts of field isolates of Eimeria acervulina.

A laboratory strain of Eimeria acervulina and 9 field isolates consisting principally of E. acervulina were tested for sensitivity to amprolium (125 p.p.m.) or dinitolmide (125 p.p.m.) in the food and for effects of the drugs on sporulation of oocysts. Judged by weight gains and lesion scores, medicaments were only partially effective against the 9 field isolates, but were highly effective against the laboratory strain. Oocysts were produced in all the infections but the percentage sporulation of oocysts from field isolates was much higher than sporulation of oocysts of the "drug sensitive' laboratory strain. These results show that coccidia that are resistant to either amprolium or dinitolmide are able to cause lesions in the presence of the drugs and the oocysts that are produced will sporulate normally.

Amprolium↗
PubMed1984

Toxicity in utility pigeons caused by the coccidiostat dinitolmide.

Utility pigeons on 3 farms were affected by a severe neurological disturbance manifested by fine tremors, rolling gait and incoordination. Affected birds had necrosis of the Purkinje cells of the cerebellar cortex. The birds from the 3 farms had been fed a pelleted diet obtained from a single mix of feed prepared by a stockfeed manufacturer. When feed obtained from the farms was given to utility pigeons under controlled conditions at the laboratory, they suffered the same clinical signs and lesions as seen in birds from the farms. Cross-bred cockerels were not affected when given this feed from day-old to 6 weeks of age. Samples of the feed contained 185 to 226 ppm of the coccidiostat dinitolmide. Utility pigeons given a prepared diet containing a similar level (234 ppm) of dinitolmide developed an identical condition after 3 to 4 weeks feeding. Laying hens were not affected by this feed. Dimetridazole, which was also present in some of the original feed samples, did not exacerbate the condition when included in the diet at a rate of 233 ppm. Production of squabs from the affected farms was dramatically reduced, and many of the breeder had to be culled because of the long-standing neurological disease.

Animal Feed↗
PubMed1977

The anticoccidial effects of amprolium, dinitolmide and monensin against Eimeria maxima, E, brunetti and E. acervulina with particular reference to oocyst sporulation.

Chicks infected with the Weybridge strains of Eimeria maxima and E. acervulina were not protected by the normal levels of amprolium, but the sporulation of the oocysts was inhibited. With higher drug concentrations, fewer oocysts were produced. E brunetti was not so markedly affected, although oocyst sporulation was reduced by the higher dosage levels. The effects were not enhanced by the inclusion of ethopabate. With dinitolmide the phenomenon was not so marked, although oocysts of E. maxima and E. acervulina were reduced in numbers by the normal drug concentration and sporulation was reduced when this level was increased. Much higher drug levels were required to obtain these effects with E. brunetti. Monensin at 120 ppm affected neither oocyst numbers nor their sporulation in any of the species tested. The significance of the effects of anticoccidial drugs on gametogony and sporogony is discussed.

Amprolium↗
PubMed1981

Ultrastructural changes in the macrogamete and early oocyst of Eimeria maxima resulting from drug treatment.

The ultrastructure of the macrogamete and developing oocyst of Eimeria maxima (Weybridge strain) was examined in the intestinal cells of chicks fed 3 different anticoccidial drugs. Amprolium at 125 p.p.m., arprinocid at 35 p.p.m. and dinitolmide at 250 p.p.m. caused considerable morphological abnormality and incomplete development of the wall-forming bodies of Type 2 (WFB II), which did not appear able to participate in oocyst wall formation. The wall-forming bodies of Type 1 (WFB I) were able in each case to participate in oocyst wall formation although amprolium and dinitolmide produced morphological abnormalities in them. In birds medicated with dinitolmide, the outer layer of the oocyst wall was formed initially at opposite poles of the macrogametes rather than as a uniform layer. Other abnormalities resulting from drug treatment are reported and some evidence that intravacuolar tubules may be formed by the parasite pellicle is presented.

Adenine↗
PubMed1975

The development of drug-resistant strains of Eimeria maxima in the laboratory.

The development of strains of Eimeria maxima resistant to buquinolate, methyl benzoquate, clopidol, sulphaquinoxaline and robenidine is described. It was not possible to standardize a schedule of inoculations and drug administration, which would enable the development of resistance to the different drugs to be compared directly. Resistance developed most readily to the quinolones. One robenidine-resistant strain proved to be drug-dependent. Dinitolmide showed unusual effects upon sporogony and three attempts to develop resistance against this activity failed. Chicks previously immunized with the parent strain were completely protected against infection with the drug-resistant strains.

Animals↗
PubMed1989

Eimeria tenella, E. acervulina and E. maxima: studies on the development of resistance to diclazuril and other anticoccidial drugs in the chicken.

Resistance to diclazuril was induced by 10 passages of the Houghton strains of Eimeria acervulina and E. tenella in chickens given progressively greater concentrations of the drug. This resistance was, however, not complete since the drug retained some efficacy against the drug-passaged lines. Attempts to passage the Houghton strain of E. maxima in birds medicated with concentrations of diclazuril greater than 0.016 parts per million (ppm) were unsuccessful and after 10 passages at this concentration resistance had not developed. Resistance to methyl benzoquate developed after 6 passages of E. tenella in medicated chickens but resistance to amprolium was only partial after 10 passages. The pathogenicity of diclazuril- and amprolium-resistant lines of E. tenella was lower than that of the parental line. Diclazuril was effective against lines of E. tenella resistant to amprolium, arprinocid, clopidol, dinitolmide, halofuginone, methyl benzoquate, monensin and robenidine.

Amprolium↗
PubMed1993

Toxoplasma gondii: susceptibility and development of resistance to anticoccidial drugs in vitro.

Anticoccidial drugs were evaluated for activity and for the development of resistance in a model of Toxoplasma gondii growing in human fibroblast cultures. Of 13 anticoccidial drugs tested, 9 had selective antitoxoplasma activity (50% inhibitory concentration, in micrograms per milliliter): decoquinate (0.005), arprinocid-N-oxide (0.015), robenidine (0.03), the aryl triazine CP-25,415 (0.2), toltrazuril (0.4), clopidol (1), dinitolmide (Zoalene; Dow) (10), and the carboxylic acid ionophores monensin (0.001) and salinomycin (0.04). Glycarbylamide, amprolium, nicarbazin, and the 6-(p-bromophenoxy)-7-chloro analog of halofuginone (Stenorol; Roussel-UCLAF) (CP-63,567) were toxic for the fibroblasts. Since Eimeria tenella has a similar drug susceptibility profile, anticoccidial drugs can be viewed as a potential source of new antitoxoplasma therapies. The development of resistance has limited the usefulness of most of these drugs as anticoccidial agents; in coccidia, resistance to all except the ionophores occurs readily in vivo. We explored the development of resistance in T. gondii by attempting to select mutants in vitro from parasites mutagenized with ethylnitrosourea. Mutants that had 20- to 50-fold-reduced susceptibility to decoquinate, arprinocid-N-oxide, and CP-25,415 were obtained. Ionophore-resistant T. gondii mutants were also selected in vitro; however, there was only a twofold difference in susceptibility between these mutants and the wild type. For three drugs (clopidol, robenidine, and toltrazuril), we were unable to select resistant mutants. For experimental anticoccidial drugs, there is currently no in vitro method for assessing the risk of development of resistance in Eimeria species. Our results suggest that T. gondii may offer a useful surrogate for this assessment.

Animals↗
PubMedDate not supplied

Investigations of toxicity episodes involving chemotherapeutic agents in Victorian poultry and pigeons.

This series of case reports details observations on toxicity episodes in poultry due to a variety of chemotherapeutic agents. These problems arose owing to overdosage, variation in species susceptibility, potentiation of the toxic effects of one substance by the presence of another substance, and particular disease or other on-farm factors. Ignorance and accident were responsible for some of these situations. The episodes involved monensin, salinomycin, nicarbazin, sulphaquinoxaline, dinitolmide, dimetridazole, nitrofurans, streptomycin, and 3-nitro-4-hydroxyphenylarsonic acid.

Animals↗
PubMed1980

Mutagenicity screening of feed additives in the microbial system.

18 feed additives were tested for DNA-modifying effects by the repair test named "rec-assay" with Bacillus subtillis H17 (rec+) and M45 (rec-), and for mutagenicity with Escherichia coli WP2 hcr and 5 Salmonella typhimurium tester strains with the use of a top-agar overlay method. Carbadox, furazolidone, panazon and zoalene were positive in both assays. The former 3 were mutagenic for TA100, TA98 and WP2 hcr, while zoalene was mutagenic for all strains. These 4 compounds did not require a metabolic activation for their mutagenic activities. Nicarbazin was weakly mutagenic for TA1538 and TA98 with and without S9 mix. Amprolium and caprylohydroxamic acid also showed very weak mutagenicities only for TA100 with S9 mix and for WP2 hcr with and without S9 mix, resp. The mutagenic activities of carbadox, furazolidone and panazon for TA100 were reduced only by the addition of S9 mix, but not by S9 fraction or blood, whereas that of zoalene was decreased by any of the 3 factors.

Animal Feed↗
PubMed1976

Laboratory studies with some older anticoccidials.

Features of the anticoccidial activity of nicarbazin, amprolium, zoalene, sulphadimidine, diaveridine, Darvisul, spiramycin, chloramphenicol and oxytetracycline have been re-investigated both in vivo and in cell culture using Eimeria tenella. Of the drugs studied, only spiramycin was appreciably coccidiocidal, although nicarbazin and amprolium showed possibly slower coccidiocidal activity. In order to show activity against a particular stage in the life-cycle, higher concentrations of drug than those usually recommended for field usage had in most cases to be used. Under these conditions, parasites were usually inhibited as multinucleate 1st generation schizonts. With delayed medication, effects against 2nd generation parasites were in most cases found, and in many cases, although the parasites never matured to give viable merozoites, the large degenerating forms produced were able to cause extensive tissue destruction and haemorrhage. Methodology in this type of study is discussed in relation to more active and more recent anticoccidials, and some further experiments with robenidine reported.

Amprolium↗
PubMed1979

Efficacy and cross-resistance studies on N, N'-bis (3,4 ditrifluoromethylphenyl) methylmalonamide, a novel anticoccidial agent.

N,N'-bis (3,4 ditrifluoromethylphenyl) methylmalonamide (Sch 18545) completely controlled a mild Eimeria necatrix infection at 50, 40 or 30 p.p.m. in the diet, and controlled E. tenella infections at 50 and 40 p.p.m. Slight oocyst passage was observed at each E. tenella treatment level with a marked increase at the 30 p.p.m. treatment level. Fifty p.p.m. were necessary to control E. acervulina infections; levels of 40 p.p.m. reduced E. acervulina oocyst production while 30 p.p.m. were ineffective. Evaluations of Sch 18545 using a mixed infection (Coccivac D) further suggested that activity with this compound was weakest against E. acervulina. Weight gains decreased with increasing concentration of drug in the diet of treated, infected birds and thus the compound showed an insufficient safety margin to be of practical value. Such 18545 administered at 35 p.p.m. in the diet was effective against amprolium, zoalene, aklomide or nicarbazin-resistant strains of E. tenella.

Amprolium↗