Coccidiostatic action of monensin fed to lambs: body weight gains and feed conversion efficacy.

Thirty crossbred ewe lambs weighing an average of 37.3 kg were allotted to 6 groups of 5 lambs each so that group weights were nearly equal. Lambs were fed dehydrated alfalfa pellets, initially at 1.14 kg/day and subsequently increased after experimental day 15 and 42. Each lamb was artificially infected with 18,000 sporulated oocysts of Eimeria ninakohlyakimovae. Groups 1, 2, 3, and 4 were given monensin in the form of medicated alfalfa pellets at dose levels of 5, 10, 20, and 30 g/metric ton, respectively. Groups 5 and 6 were infected controls (infected, nonmedicated). Lambs in groups 5 and 6 developed severe clinical coccidiosis, having diarrhea and losing weight rapidly. Group 1 lambs did not have diarrhea, but the lambs did not gain well. All other medicated lambs gained weight during the experimental period of 84 days. Feed conversion was good in medicated groups 2, 3, and 4 and was poor in control groups 5 and 6. Statistically significant differences in feed conversion and body weight gains (5 and 1% level of confidence) were observed between control and medicated groups.     

Control of bovine coccidiosis with monensin: in nonresistant newborn calves

Newborn Holstein male calves were purchased within 3 days after birth and were removed from the local farms to the Dixon Springs Agricultural Research Center. They were hand-fed for 7 weeks and then weaned to a prepared feed. Eight groups, each of 4 calves, were housed in separate pens. In each of 4 pens (pens 2 to 5), 1 calf was inoculated with sporulated oocysts of Eimeria bovis (and was not medicated); 1 calf was inoculated and given feed with added monensin at the dosage level of 10 g/906 kg of feed; and 2 calves were inoculated and given medicated feed with added monensin at the dosage level of 20 g/906 kg or 30 g/906 kg. In the 4 other pens (6 to 9), the calves were inoculated with E zuernii and otherwise were given feed without or with added monensin as in pens 2 through 5. Another group of 5 calves (all kept in 1 pen), served as noninoculated, nonmedicated controls. At 14 days after inoculations with E bovis, the single calves in each of the 4 pens that were given the nonmedicated feed began to show clinical signs of coccidiosis and discharged increasing numbers of oocysts. The other inoculated calves (given monensin) had fewer clinical signs and discharged fewer oocysts in the feces as the level of medication in the feed increased. The calves inoculated with E zuernii developed only moderately severe infections when compared with those inoculated with E bovis. Inoculated (with E bovis) nonmedicated calves had severe reductions in feed consumption and weight, and 3 of 4 died.(ABSTRACT TRUNCATED AT 250 WORDS)     

Evaluation of lasalocid as a coccidiostat in calves: titration, efficacy, and comparison with monensin and decoquinate

Two experiments were conducted to evaluate lasalocid as a coccidiostat in Holstein calves and to compare lasalocid with monensin and decoquinate. In experiment 1, calves in 3 groups (6 calves/group) were each inoculated with 500,000 sporulated oocysts, 88% of which were Eimeria bovis and 12% were E zuernii. Calves in each group were given lasalocid-medicated feed at 0.50 (group 3), 0.75 (group 4), or 1 mg/kg (group 5) of body weight/day for 45 days. Two control groups (6 calves/group) were also evaluated; calves in control group 2 were inoculated and nontreated, and calves in control group 1 were noninoculated and nontreated. At 0.50, 0.75, or 1 mg/kg/day, lasalocid was equally effective in preventing induced coccidiosis (E bovis and E zuernii) in calves. Compared with inoculated nontreated controls, treated calves had significantly (P less than 0.05) fewer oocysts in feces and had fewer clinical signs of coccidiosis from days 16 to 30 after inoculation. Experiment 2 was conducted to compare the effectiveness of monensin, lasalocid, and decoquinate for the prevention of experimentally induced coccidiosis. Calves (n = 48) were allotted into 4 groups (12 calves/group); each was inoculated orally with 275,000 sporulated oocysts, predominantly E bovis and E zuernii, and each was given nonmedicated feed (group 6) or feed medicated with 33 mg of lasalocid (group 7), decoquinate (group 8), or monensin (group 9)/kg of feed for 46 days. Calves given medicated rations had significantly (P less than 0.05) fewer oocysts in their feces and fewer clinical signs of coccidiosis than did calves given nonmedicated rations.(ABSTRACT TRUNCATED AT 250 WORDS)     

Oocyst Discharge, Rumen Metabolism and Performance of Early Weaned Lambs with Naturally Occurring Coccidiosis Fed Monensin

Ninety-six 9.5 kg early-weaned lambs with naturally occurring coccidiosis were fed monensin either at 0, 11, 22, or 33 mg/kg of feed for 105 days. Fecal oocyst discharge during the first three days was highest with monensin 22 mg, lowest with monensin 33 mg and averaged 149.6 × 10³ oocysts per gram feces for all lambs. Monensin at 22 mg/kg of feed reduced Eimeria ninakohlyakimovae and E. ahsata oocyst discharge.

Organic matter and crude protein digestibilities were highest (P ≤ 0.05) in lambs fed monensin 22 mg/kg of feed. Monensin increased (P ≤ 0.01) rumen ammonia and propionic acid and decreased (P ≤ 0.01) acetic acid. Feeding monensin 33 mg decreased (P ≤ 0.05) feed intake by 5% and had no effect on gain or feed efficiency. Optimal responses were observed with monensin at 11 mg, feed consumption was not affected, gains were 8% higher (P ≤ 0.05) and feed was utilized 9% more efficiently (P ≤ 0.05) than the controls. In conclusion, monensin was an effective therapeutic agent against naturally occurring coccidial infections in early weaned lambs. Performance responses were largest with monensin fed at the rate of 11 mg/kg of feed.

     

Effects of leucocyte extract, levamisole and sulphadimidine on natural coccidial infections (Eimeria spp.) in young lambs

The efficacy of leucocyte extract (LE) and sulphadimidine in preventing coccidiosis in naturally infected lambs on pasture was evaluated in 3 separate experiments, whereas the prophylactic effect of levamisole was studied in 1 of the experiments. LE prepared from ewes immune to coccidia (Eimeria spp.) was administered either intravenously or intraperitoneally to young lambs 7, 5, or 2 days before they were turned out on pastures contaminated with coccidia. In all experiments, LE failed to transfer protective immunity to the lambs against the first coccidial infection on pasture. The LE preparations used apparently had an immunosuppressive effect, which resulted in more severe clinical signs of coccidiosis in the recipients. The lambs given LE showed a higher incidence of diarrhoea, a poorer weight gain, a higher mortality, and a higher oocyst output than the untreated control lambs. In lambs treated with sulphadimidine at 200 mg/kg on days 12, 13, and 14 after turnout there was a reduced severity of the coccidial infections in all experiments. The sulphadimidine-treated lambs had better weight gains and passed fewer oocysts than the controls during the third and fourth week after turnout, but some of them developed diarrhoea. Lambs treated with levamisole at 2 mg/kg 2 days before turnout, at turnout, and 2 days after turnout were more severely affected by the first coccidial infection on pasture than the controls.To study the lambs’ immunity against a heavy challenge infection with coccidia as compared with their immunity against the natural reinfection on pasture, some of the lambs from the original groups (untreated, sulphadimidine-treated, LE-treated) were each inoculated with 2 mill. Eimeria spp. oocysts about 6 weeks after turnout. The oocyst counts of the challenged lambs, except the LE-treated lambs, increased to a new peak 19–20 days after challenge. The challenge infection caused a softening of the faeces and a marked depression in weight gain in all challenged groups of lambs, mainly between days 10 and 17 after challenge. The lambs were thus only partially immune to coccidia after the first coccidial infection on pasture. The lambs treated with either LE or sulphadimidine in connection with the first coccidial infection on pasture were not appreciably more susceptible to the challenge infection than the untreated lambs.     

Efficacy of maduramicin against ionophore-tolerant field isolates of coccidia in broilers

Maduramicin ammonium was given at 2.5-8 ppm in the feed to broilers experimentally infected with coccidia recently isolated from broiler farms where ionophores had been used for several years. Infection pressure varied from mild to severe in five trials: mortality in unmedicated controls ranged from 0 to 59%, intestinal lesion scores were high, and weight gain was depressed by the infections. The cultures of Eimeria were partly resistant to ionophores: birds medicated with monensin at 100-121 ppm had only modest reductions in lesion scores and incomplete protection against weight loss or mortality. Control of infections by maduramicin was significant at 4 ppm but best at 5-7 ppm. Maduramicin was more effective than monensin or narasin, but about the same as salinomycin, in reducing lesions and mortality and in protecting performance. Maduramicin was well tolerated within the dose range of 5-7 ppm.     

Chemoprophylaxis of coccidiosis in lambs with a single oral dose of toltrazuril

The prophylactic efficacy of a single oral dose of toltrazuril against coccidiosis (mixed Eimeria infections) in naturally infected lambs was evaluated in two experiments. Toltrazuril at 20 mg kg-1, given on Day 7 or Day 10 after turnout on pasture, proved to be highly efficacious in preventing clinical coccidiosis under Norwegian conditions. Toltrazuril reduced the oocyst output to very low levels, prevented the development of diarrhoea and improved weight gain during the first 4-5 weeks after treatment. Treatment on Day 7 was superior to treatment on Day 10 with respect to improving weight gain and preventing the development of soft faeces. Lambs treated with toltrazuril on Day 7 seemed to be as immune as untreated lambs to natural reinfections with coccidia later in the grazing season. In one of the experiments, natural infections with the nematode Nematodirus battus produced a coccidiosis-like disease in some lambs simultaneously with the outbreak of coccidiosis.     

Effect of monensin on experimental infections of Eimeria ninakohlyakimovae in lambs.

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.     

Interaction of T-2 fusariotoxin and monensin in broiler chickens infected with Coccidia

Field observations suggest that coccidiosis is a common cause of death in broiler chicken flocks fed diets containing sufficient amounts of ionophore antibiotics (monensin, narasin, etc.) and contaminated with mycotoxins, particularly with T-2 fusariotoxin. To study this phenomenon, broiler chickens fed diets containing different amounts of T-2 toxin and free from monensin, or containing a preventive dose (100 mg/kg of feed) of monensin, were infected experimentally with coccidian oocysts. In all groups fed a diet containing monensin plus T-2 toxin severe clinical symptoms of coccidiosis (blood-stained faeces etc). occurred. Deaths and retarded growth depended on the toxin dose and were considerable. The body mass gain of chicks fed a diet containing monensin and T-2 toxin but not infected with coccidia was inferior to that of groups fed diets which contained either monensin or T-2 toxin (experiment 2). On the basis of these findings a negative interaction of the two compounds is assumed. This seems to be supported by the results of experiment 3, i. e. the finding that the lethal dose of narasin, a compound closely related to monensin both in chemical structure and mechanism of action, proved to be much lower (LD50 = 102 mg/kg body mass) for chickens fed a diet supplemented with T-2 toxin than for the control chickens (LD50 = 176 mg/kg body mass). The present results suggest that the feeding of diets severely contaminated with T-2 toxin may alter the anticoccidial efficacy of monensin.     

Influence of monensin on the performance of cattle

Performance data on nearly 16,000 head of cattle that were used in trials to document effects of monensin on feedlot cattle were summarized. Cattle fed monensin-containing diets gained 1.6% faster, consumed 6.4% less feed and required 7.5% less feed/100 kg gain than cattle fed control diets. Monensin resulted in the greatest improvement in feed/gain at 2.9 Mcal metabolizable energy (ME)/kg diet dry matter (DM). Within the range of monensin concentrations used in the trials that were summarized (31.8 +/- 7.5 mg/kg DM), high monensin concentrations did not improve feed/gain over that obtained with lower concentrations. Carcass characteristics were not significantly influenced by monensin. Responses of cattle to monensin and implants were additive. Energy metabolism data suggested that monensin improved digestibility of DM, reduced fasting heat production and increased dietary net energy maintenance (NEm) values more than it increased net energy gain (NEg) values. Data showing the response of cattle to monensin when fed various dietary protein concentrations or sources of supplemental N suggested that monensin had a protein sparing effect. Monensin has also been shown to reduce lactic acid production, aid in the control of coccidia and bloat and to be toxic to face and horn fly larva in feces of monensin-fed cattle. In pasture trials, monensin improved daily gains. When fed to beef cows, monensin reduced amounts of feed required to maintain cow weight.     

Ovine coccidiosis: comparison of the effects of monensin and aureomycin on lambs infected with coccidia

Lambs naturally infected with mixed species of Eimeria were fed monensin (30 mg/kg of feed) and aureomycin (10 mg/kg of feed) separately and in combination. An evaluation was made of the efficacy of the treatments in the suppression of oocyst production. Comparisons were made of the parasitic damage to the intestinal surface. Performance of the lambs was measured by weight gains and feed efficiency. Monensin given separately or in combination with aureomycin produced decreases in oocyst counts that were not significantly different from those in the lambs given only aureomycin. Body weight gains and feed efficiency were best in the aureomycin-treated group, and less so in the monensin-treated and the control groups. Animals fed the monensin-aureomycin combination had the poorest weight gains and feed efficiency. Scanning electron microscopy indicated that the groups fed monensin or aureomycin separately had morphologically normal intestinal surfaces. This was in contrast to the control group and the group fed the monensin-aureomycin combination, wherein there was disrupted intestinal surface morphology.     

Effects of intermittent and continuous administration of decoquinate on bovine coccidiosis in male calves

Male Holstein calves were each inoculated with 350,000 sporulated oocysts of Eimeria bovis. Two calves were given decoquinate (0.5 mg/kg of body weight) continuously in dry feed for 29 days, and 2 calves each were given 0.5, 1, or 1.5 mg of decoquinate/kg on an every 2nd-or 3rd-day schedule for 29 days. Calves given decoquinate continuously did not discharge oocysts but had slightly loose feces. In general, the number of oocysts discharged increased and fecal consistency decreased as the time between feeding of medicated feed increased. Calves given 0.5 or 1.5 mg of decoquinate/kg every 3rd day discharged more oocysts and had more diarrhea than did calves given 1 mg of decoquinate/kg every 3rd day. At postinoculation day 29, calves were euthanatized. At necropsy, intestinal tissues of calves given decoquinate were mostly normal. Apparently, reduced infections along with the elapsed time were sufficient to resolve most intestinal lesions caused by the coccidia. Decoquinate was most effective when fed continuously at 0.5 mg/kg. However, when fed at 1 or 1.5 mg of decoquinate/kg every 2nd day or 1.5 mg of decoquinate/kg every 3rd day, oocyst production was reduced and clinical coccidiosis was prevented.     

The efficacy of anticoccidial products against Eimeria spp. in northern bobwhites

To determine whether chemotherapeutic compounds available for use in domestic poultry are effective at controlling coccidiosis in northern bobwhites (Colinus virginianus), we tested 13 chemotherapeutic anticoccidials including amprolium (250 parts per million [ppm]), clopidol (125 ppm), diclazuril (1 ppm and 2 ppm), decoquinate (30 ppm), lasalocid (120 ppm), monensin (90 ppm), narasin/nicarbazin (36/36 ppm), robenidine (33 ppm), roxarsone (50 ppm), sulfadimethoxine/ ormetoprin (125/75 ppm), salinomycin (60 ppm), semduramicin (25 ppm), and zoalene (125 ppm and 150 ppm). Three tests were conducted using two replicates of 10 birds each: Infected, unmedicated controls and medicated birds were challenged with 1 x 10(6) oocysts of a field isolate consisting primarily of Eimeria lettyae. Subsequently, we tested clopidol, lasalocid, salinomycin, diclazuril (1 ppm), and monensin against mixed-species field isolates containing E. lettyae, E. dispersa, E. colini, or all. Weight gain, gross intestinal lesions, severity of diarrhea, and feed conversion ratio (FCR) 6 days postinfection were recorded. Lesion score, as previously reported, was unreliable as a measure of severity of infection in comparison with weight gain, fecal scores, and FCR. Excellent to good efficacy was found in clopidol, decoquinate, diclazuril (1 ppm and 2 ppm), and in lasalocid, narasin and nicarbazin, robenidine, sulfadimethoxine/ormetoprin, and zoalene (150 ppm). Marginal protection was found using monensin, salinomycin, semduramicin, or a roxarsone/semduramicin combination. Amprolium, roxarsone, and zoalene (125 ppm) were ineffective at controlling coccidia. Two of the six isolates tested against diclazuril 1 ppm and clopidol demonstrated a high degree of resistance, but none of the six isolates was resistant to lasalocid. Four of the eight isolates showed mild to moderate, and moderate to high, resistance against monensin and salinomycin, respectively. These findings indicate that several available compounds are effective at controlling coccidiosis in bobwhites.     

Immunization of chukar partridges against coccidia (Eimeria kofoidi and Eimeria legionensis) with low doses of live oocysts

Experiments were conducted to determine whether chukar partridge (Alectoris chukar) chicks would develop protective immunity after inoculation with coccidia. Young chukar chicks in battery cages inoculated with 100 or more oocysts of Eimeria kofoidi or Eimeria legionensis had significant protection at challenge 4 wk later, as measured by greatly reduced oocyst shedding and improved weight gain as compared with unvaccinated, challenged controls. However, when birds were housed in litter pens and vaccinated by various regimens (including two species of chukar coccidia at 100/dose), coccidiosis rapidly spread through all treatments and caused significant mortality. Vaccination with Coccivac-T or with 100 oocysts of Eimeria dispersa did not prevent mortality resulting from accidental contamination, and feed treatment with a Lactobacillus competitive-exclusion product had no benefit. Most if not all of the mortality was from E. kofoidi. This study illustrated the natural fecundity of chukar coccidia in a floor-pen environment where multiplication rate and reinfection combine to produce clinical disease from a small original exposure. Further, these results cast doubt on the potential use of low doses of live oocysts as a vaccine in the chukar partridge.     

饲粮中添加不同生物制剂对杜寒杂交肉羊生产性能和屠宰性能的影响

本试验旨在比较饲粮添加不同生物制剂对杜寒杂交肉羊生产性能、屠宰性能、组织器官发育及肉品质的影响。采用单因素试验设计,选取平均体重约为32 kg的杜寒杂交F1代肉羊160只,随机分为5组,每组4个重复,每个重复8只。对照组采用基础饲粮,试验组分别添加21 mg/kg莫能菌素、4×109CFU/kg地衣芽孢杆菌、3.2×109CFU/kg酿酒酵母菌、1.1 g/kg复合生物制剂(地衣芽孢杆菌≥6×109CFU/g、酿酒酵母菌≥4×109CFU/g、碱性蛋白酶≥1 000 U/g)。预试期10 d,正试期56 d,每2 d记录1次采食量,每20 d进行1次称重,当复合生物制剂组羊只的平均体重达到约50 kg时,每组选取10只羊进行屠宰,测定其屠宰性能、组织器官重量和肉品质指标。结果表明:1)复合生物制剂组平均日增重、屠宰率显著高于对照组(P0.05);地衣芽孢杆菌组和复合生物制剂组料重比显著低于对照组(P0.05)。2)地衣芽孢杆菌组、酿酒酵母菌组、复合生物制剂组复胃重量均显著高于对照组(P0.05),复合生物制剂组复胃重量占宰前活重比例显著高于对照组和莫能菌素组(P0.05);地衣芽孢杆菌组、酿酒酵母菌组、复合生物制剂组小肠重量及其占宰前活重比例均显著高于对照组、莫能菌素组(P0.05)。3)酿酒酵母菌组肾脏重量占宰前活重比例显著高于对照组(P0.05),其他内脏器官重量占宰前活重比例在各组间无显著差异(P0.05)。4)各组肉品质指标差异不显著(P0.05)。综合得出,从作为饲料添加剂对肉羊生产性能作用效果来看,地衣芽孢杆菌、酿酒酵母菌、复合生物制剂可以替代莫能菌素,地衣芽孢杆菌好于酿酒酵母菌,复合生物制剂最佳。     

复方球虫散对人工感染鸡球虫病治疗效果的临床试验

为科学、客观地评价复方球虫散对实验性鸡球虫病的防治效果,采用人工接种柔嫩艾美耳球虫孢子化卵囊的方法复制鸡球虫病,使用纯中药组方复方球虫散进行鸡球虫病的临床疗效试验,观察并计算复方球虫散对试验鸡的死亡率、相对增重率、病变值和卵囊值的影响,并求出复方球虫散的抗球虫指数(ACI).试验结果表明:复方球虫散按1.0%拌料混饲,对鸡球虫病有较好的治疗效果.     

Prevention and control of coccidiosis in goats with decoquinate

Decoquinate was evaluated as a coccidiostat in domestic goats. Fifty goats less than 4 months of age were assigned to 5 groups (pens) of 10 goats each and were treated for 87 days with 0 (control), 0.3, 0.5, 1.0, or 4.0 mg of decoquinate in feed/kg of body weight. Goats were inoculated orally weight. Goats were inoculated orally with 30,000 oocysts, mainly Eimeria christenseni (74%) and E ninakohlyakimovae (20%) on day 19. Nontreated goats developed profuse watery diarrhea and tenesmus and gained weight poorly; 2 died. Treated goats did not develop clinical coccidiosis and gained significantly more weight (P less than 0.05), regardless of the dose used. Treated goats also had significantly fewer (P less than 0.05) oocysts in feces than did nontreated controls. Oocyst numbers were inversely related to dose; a more rapid decrease in oocyst numbers occurred as the dose was increased. At the doses used, decoquinate was safe in goats and was an effective drug for the prevention of clinical coccidiosis.     

Effect of coccidiosis on reproductive maturation of male Japanese quail

The effects of coccidiosis on reproductive development of male Japanese quail were examined. Male Japanese quail were exposed to high (5 x 10(5) sporulated oocysts/quail) or low (5 x 10(3) sporulated oocysts/quail) doses of Eimeria uzura at 16 or 30 days of age and sampled at 37 days. Quail given high doses of coccidia had reduced testes weight and lowered circulating concentrations of androgen compared with control males. Low doses of coccidia did not affect testes weight but did result in elevated plasma androgen levels. There were no differences in average testes weights by 51 days; however, plasma androgen was still reduced in most groups. To study the effects of coccidiosis on egg production, males exposed to high doses of coccidia at 16 (16H) or 30 (30H) days of age were mated with control females, and control males were mated with control or 16H females. The onset of laying was delayed for 5 days in the control male: 16H female group. During the first week of production, eggs from females bred to 30H males had lower fertility and hatchability than those bred to control or 16H males. By the third week of production, levels of fertility were similar. Apparently, exposure of quails to coccidiosis before sexual maturation might result in long-term effects on later reproductive capability.     

Efficacy of arprinocid against coccidiosis of broilers in battery and floor-pen trials

Medication of broilers with arprinocid [9-(2-chloro-6-fluorophenylmethyl)-9H-purine-6-amine] gave protection against the effects of coccidiosis in both battery and floor-pen trials. In battery trials, efficacy was tested on single-species inoculations of Eimeria acervulina, E. mivati, E. necatrix, E. maxima, E. Brunetti, and E. tenella. Two strains of each species recently recovered from the field, were tested separately. In floor-pen trials, all six species, both field and laboratory strains, were used as a mixed infection. In batteries, 60 and 70 ppm essentially eliminated coccidiosis-induced mortality and weight depression. Effects of 50 ppm on weight gain were variable. The effectiveness of different medication levels varied between strains within a species. In floor-pen trials, 40, 60, or 80 ppm was effective in controlling mortality and weight depression, and increasing feel-conversion ratios. All levels were significantly as effective as monensin in protecting against coccidiosis. With severe exposure to coccidia, 60 and 80 ppm gave significantly lower lesion socres than did 40 ppm of arprinocid or 120 ppm monensin.     

Higher incidence of Eimeria spp. field isolates sensitive for diclazuril and monensin associated with the use of live coccidiosis vaccination with paracox-5 in broiler farms

Twenty European Eimeria spp. field isolates were subjected to an anticoccidial sensitivity test (AST). The anticoccidial drugs tested were diclazuril (Clinacox) and monensin (Elancoban). The assay was performed in a battery cage trial. Infected medicated birds were compared with an unmedicated control group. Coccidial lesion scores and oocyst shedding were used as parameters. The results of the AST show that resistance is common amongst coccidiosis field isolates, especially Eimeria acervulina (68% and 53% resistance for diclazuril and monensin, respectively). Resistance is less frequent amongst Eimeria maxima (38% and 50% resistance for diclazuril and monensin, respectively) and Eimeria tenella isolates (23% and 38% resistance for diclazuril and monensin, respectively). A highly significant influence of the coccidiosis prevention program (live coccidiosis vaccination with Paracox-5 vs. anticoccidial drugs in feed) on the sensitivity patterns of Eimeria spp. field isolates for both diclazuril (P= 0.000) and monensin (P= 0.001) was found. Further, when looking at the single species and each anticoccidial drug level, significantly more sensitivity of E. acervulina for monensin (P= 0.018), E. maxima for diclazuril (P = 0.009), and E. tenella for diclazuril (P = 0.007) was found in isolates originating from vaccinated flocks. Moreover, for E. acervulina and diclazuril, E. maxima and monensin, and E. tenella and monensin a trend toward higher sensitivity of isolates for these products was found when live coccidiosis vaccination was applied. The present study shows that sensitivity for the anticoccidial drugs diclazuril and monensin is more frequent in Eimeria spp. field isolates originating from broiler farms where a coccidiosis vaccination policy is followed.