Eimeria involved in a case of coccidiosis in farmed red-legged partridges (Alectoris rufa) in France: oocyst isolation and gross lesion description after experimental infection.

The aim of the present work was, after a coccidiosis outbreak in a farm rearing red-legged partridges (Alectoris rufa) in Brittany (France), to identify the Eimeria species and describe gross lesions induced by three of them (Eimeria kofoidi, Eimeria caucasica and Eimeria legionensis) after experimental infection. E. kofoidi oocysts measured 19.3 µm × 16.3 µm on average; neither micropyle nor oocyst residuum were present, but one, two or more small polar granules were visible. After inoculation of 300,000 oocysts per partridge, severe gross lesions were observed in the duodenum and jejunum, characterized by thickened oedematous mucosa and lumen filled with thick mucus, gas and sometimes false-membrane due to sloughed epithelium. E. caucasica oocysts were on average 29.8 µm × 19.5 µm in size; no oocyst residuum was observed, but a large granule was well visible. E. caucasica also invaded both the duodenum and jejunum, causing haemorrhagic points on the serosal surface, as well as mucoid duodenitis and catarrhal enteritis when 30,000 oocysts were inoculated per bird. E. legionensis oocysts measured 22.6 µm × 14.9 µm on average; they presented a clear micropyle beneath which one or two granulations were present. E. legionensis mainly invaded the caeca; low mortality was observed at the dosage of 200,000 oocysts per bird. Caecal walls were thickened and caseous material was condensed into off-white cheesy cores. For each species, oocyst shedding started 5 days post inoculation, peaked at 9, 8 and 6 days post inoculation for E. kofoidi, E. caucasica and E. legionensis, respectively, then decreased and persisted until 15 days post inoculation (end of examinations).

Immunological characterization of a 17-kDa antigen from Cryptosporidium parvum recognized early by mucosal IgA antibodies.

Cryptosporidium parvum antigens were characterized by immunoblot analysis of sera and intestinal secretions of BALB/c mice orally infected with 10(5) oocysts. A major band at 17 kDa under non-reduced conditions and at 18 kDa under reduced conditions was recognized by anti-C. parvum IgA and IgG in serum and intestinal secretions from day 15 post-infection. This recognition persisted throughout the experiment (day 30). Mouse-serum antibodies raised against the 17-kDa purified antigen (P17) showed no cross-reactivity with other C. parvum antigens. Immunofluorescence study revealed that this antigen is located on the sporozoite. It is suggested that this antigen could be a good candidate for studies of mucosal immune response to C. parvum and for vaccination.

Genotyping human and bovine isolates of Cryptosporidium parvum by polymerase chain reaction-restriction fragment length polymorphism analysis of a repetitive DNA sequence.

In order to define transmission routes of cryptosporidiosis and develop markers that distinguish Cryptosporidium parvum isolates, we have identified 2 polymorphic restriction enzyme sites in a C. parvum repetitive DNA sequence. The target sequence was amplified by polymerase chain reaction from 100 to 500 oocysts and the amplified product was subjected to restriction enzyme digestion. Typing of 23 isolates showed that 10/10 calf isolates had the same profile. In contrast, 2 patterns were observed among human isolates: 7/13 displayed the calf profile, and 6/13 presented another pattern. The PCR-RFLP assay described here is a sensitive tool to distinguish C. parvum isolates.

Use of Percoll for the infection of cells in vitro with Cryptosporidium parvum oocysts.

A method for the infection of non-adherent THP-1 cells and adherent MDBK cells with Cryptosporidium parvum oocysts using isotonic Percoll solutions was developed. Excystation was maximal after 2 h, but toxicity increased with the oocyst/cell ratio and the incubation time. The infection rates did not increase with the oocyst/cell ratio and both cell types were equally parasitized.

Effect of Cryptosporidium baileyi in specific pathogen free chickens vaccinated (CVI988/Rispens) and challenged with HPRS-16 strain of Marek's.

This study was performed to examine the effect of Marek's disease virus (MDV) serotype 1 vaccine (CVI988/Rispens) on the pathogenicity of Cryptosporidium baileyi , and to determine whether C. baileyi infection could prevent the development of vaccinal Marek's disease (MD) immunity in specific pathogen free (SPF) chickens. Sixty-eight SPF homozygous B13 White Leghorn chickens were divided into seven groups. C. baileyi was orally administered at 5 days of age (day 4) in chickens infected with Rispens vaccine at day 0 or at day 8 and challenged with HPRS-16 strain of oncogenic MDV at day 15. Relevant control groups were constituted. The chickens were kept in isolators until the end of the experiment at day 62. The parameters evaluated were clinical signs, kinetics of oocyst shedding, mortality, macroscopic and microscopic lesions, cryptosporidia location in various organs and serum anti- C. baileyi antibodies at days 42 and 62. Our results show that C. baileyi , which is considered to be non-pathogenic when inoculated orally, may become highly pathogenic. It induced severe mortality and developed in organs other than classical target sites when chickens were vaccinated with Rispens vaccine and challenged with the HPRS-16 strain of MDV.However,parasite infection does not prevent the induction of vaccinal immunity for MD. Our results also show that vaccination of B13 chickens at hatching induces higher protection against challenge with HPRS-16 MDV at day 15 than vaccination at day 8.

Evaluation of decoquinate to treat experimental cryptosporidiosis in kids.

The purpose of this trial was to evaluate the effects of decoquinate at 2.5 mg/kg/day for 21 days to prevent an experimental cryptosporidiosis in kids. Twenty 1-day-old male kids (French Alpin), fed initially goat colostrum heated 1 h at 56 degrees C and fed twice daily with nonmedicated milk replacer, were assigned into 2 groups. Kids of both groups were orally inoculated with 10(6) Cryptosporidium parvum (D0 = inoculation day). Group A kids were kept as nonmedicated controls and group B kids were orally medicated with 2.5 mg/kg/day of decoquinate (Deccox L. Rhône Poulenc Animal Nutrition) for 21 days from D-3 to D17. The studied criteria were body weight gain, oocyst shedding and specific anti-C. parvum immune response. In group A, the inoculation was not followed by mortality; but only by diarrhea and high oocyst shedding. Decoquinate reduced the severity of cryptosporidiosis in group B kids. The treatment prevented episodes of diarrhea and weight gain decrease for the D0-D7 and D0-D14 disease periods but did not allow a better final weight gain. The oocyst shedding was decreased in number and in duration. This parasitic development has induced a specific anti-C. parvum immune response. This drug is well-tolerated by animals and may be recommended in the prevention of ruminant cryptosporidiosis, a disease which has very limited treatment options.

Prevalence of Cryptosporidium infection in calves in France.

Two multicentre surveys were conducted in France to estimate the prevalence of Cryptosporidium infection in calves using qualitative ELISA for detection of Cryptosporidium coproantigens and oocysts. The first survey involved 4-12-day-old calves in six dairy-calf distribution centres, collecting calves from seven Administrative Regions (Aquitaine, Bretagne, Franche-Comté, Lorraine, Normandie, Nord, Pays de Loire). For each region, 20 calves were selected every month for 12 consecutive months (October 1995-September 1996). Prevalence of Cryptosporidium infection was 17.9% (Confidence Intervals (C.I.) 95%=[16.1%; 19.8%]) among the 1628 selected calves, of which only 5.3% had diarrhoea. The second survey conducted between November 1995 and May 1996 involved 4-21-day-old calves examined by veterinary practitioners who selected 189 livestock farms of dairy- or suckler-type in ten Administrative Departments (Allier, Cantal, Creuse, Doubs, Ille-et-Vilaine, Maine-et-Loire, Manche, Pas-de-Calais, Saône-et-Loire, Vendée). Cryptosporidia were detected in 105 (55.6%) of the farms. Among the 440 calves examined, of which 398 (90.5%) presented diarrhoea, cryptosporidia were found in 191 animals, i.e. a prevalence of 43.4% (C.I. 95%=[38. 8%; 48.0%]). Breed of calves and type of housing had very little impact on prevalence in this survey. Some regional variations could be noticed, even if cryptosporidia infection is widespread. Monthly variations could be related to seasonal peaks in calving with a lower infection rate during summer.

The effect of halofuginone lactate on experimental Cryptosporidium parvum infections in calves.

The chemoprophylactic effects of halofuginone lactate were tested against calf experimental cryptosporidiosis. Twenty 2-day-old calves, divided into four groups, were orally inoculated with 1 x 10(6) oocysts of Cryptosporidium parvum. The infected control group was unmedicated whereas the three other groups were medicated with the drug at 30, 60 and 120 micrograms kg-1 day-1, respectively, for 7 days, from Day (D) 2 to D8 post-inoculation (D 0 was inoculation day). The calves were weighed twice weekly and disease development and drug efficacy were assessed daily from D0 to D30 from consistency of feces, shedding of oocysts and mortality. Experimental C. parvum infection caused a severe clinical disease with profuse watery diarrhea, high oocyst shedding and mortality (3 out of 5) in the unmedicated group. The results clearly demonstrated the efficacy of halofuginone lactate in reducing the severity of clinical cryptosporidiosis. This efficacy was dose-dependent. The lowest dose (30 micrograms kg-1 day-1) was not able to prevent clinical disease and mortality (3 out of 5). No clinical signs were observed with the 60 and 120 micrograms kg-1 day-1 doses, but the animals shed oocysts after drug withdrawal. This shedding was more delayed the higher the dose of drug administered, but the delayed shedding had no effect on the growth of the animals.

Inhibition of Eimeria tenella replication after recombinant IFN-gamma activation in chicken macrophages, fibroblasts and epithelial cells.

We have previously shown that activation of primary cultures of chicken bone-marrow macrophages and embryo fibroblasts with supernatants of concanavaline A-stimulated or reticuloendotheliosis virus (REV)-transformed chicken spleen cells as source of IFN-gamma significantly decreases Eimeria tenella growth in vitro. In the present study, we used various chicken cell lines, HD11 macrophages and DU24 fibroblasts, both virally transformed, CHCC-OU2 fibroblasts and LMH hepatic epithelial cells, both chemically transformed, to replicate E. tenella in vitro. We confirmed the previous results by showing that HD11 macrophages pre-treated for 24h with recombinant chicken IFN-gamma (either produced in E. coli or by transfected COS cells), at doses ranging from 1000 to 10U/ml, drastically inhibited E. tenella replication as measured by [3H] uracil uptake after a further 70h of culture, as when treated with REV supernatant. Likewise the fibroblast and epithelial cell lines exhibited significant inhibitory activity on E. tenella replication after pre-treatment with recombinant chicken IFN-gamma, but were less sensitive (1000-100U/ml) than when treated with REV supernatant. Recombinant chicken IFN-alpha pre-treatment of all cell lines had no inhibitory effect on parasite development.

Role of Cryptosporidium parvum as a pathogen in neonatal diarrhoea complex in suckling and dairy calves in France.

This study was carried out to find the importance of Cryptosporidium parvum in diarrhoea of neonatal calves in two types of breeding - suckling and dairy calves - in France. Different agents causing neonatal diarrhoea, E. coli, rotavirus, coronavirus, Salmonella and Cryptosporidium were systematically researched in faeces. 1. Suckling calves: In 40 livestock farms selected for diarrhoea, 311 calves 4 to 10 days old which had diarrhoea for less than 24h or no diarrhoea, were included in the study. A prophylaxis of neonatal diarrhoea had been carried out in 21 of the 40 livestock farms. On D0 (inclusion day), the mean age was 6 days, 82% presented a good initial general condition and 76.2% had a good appetite; 48.6% were diarrhoeic but 91.3% presented no sign of dehydration. Only 6.1% were infected by E. coli K99, 14.3% by rotavirus, 6.8% by coronavirus, 0.3% by Salmonella but 50% excreted C. parvum oocysts. This later percentage increases up to 84% and 86% by D3 and D7, respectively . We note that 16% of the 4-day-old calves on D0 are excreting oocysts and this percentage increases as a function of the age of the calf on D0 to reach 90% to 95% by the age of 8 days. 10 out of 12 dead calves excreted C. parvum oocysts. From D0 to D14 the other pathogen agents show a relative or a decreasing stability. 2. Dairy calves: 382 calves which had diarrhoea for less than 24 h or no diarrhoea, aged 8 to 15 days coming from six industrial livestock farms were included in the study. On D0, 99% of the calves presented a good initial general condition, 99.7% had a good appetite and no calf was dehydrated. At this date (D0), 16.8% of the calves excreted cryptosporidia. This percentage increases up to 23% and 51.8% on D3 and D8, respectively, then decreases to 31.9% on D14. The pressure of the other pathogenicagents remains relatively stable, excepted for rotavirus on D7 (from 9.9% on D0 to 27.2% on D7, then 12.6% on D14) which does not explain the concomitantpeak in diarrhoea because the infection by rotavirus on D7 is more frequent in non-diarrhoeic calves than in diarrhoeic calves. Our results show that Cryptosporidium prevalence is higher in suckling than in dairy calves and C. parvum constitutes actually in both cases the major aetiological agent of neonatal diarrhoea.

Treatment of experimental ovine cryptosporidiosis with ovine or bovine hyperimmune colostrum.

Ovine or bovine colostrums with different antibody titers were tested for their ability to prevent cryptosporidiosis in five groups of neonatal lambs experimentally infected with 10(6) Cryptosporidium parvum oocysts 2 days after birth (Day 0). In a control group (Group 1), six lambs were deprived of ewe colostrum and exclusively fed with milk replacer. Two groups of six lambs were allowed to suckle their non-hyperimmunized (Group 2) or hyperimmunized (Group 3) dams throughout the experiment. Two groups of seven lambs were separated from their dams at birth before suckling and fed with non-hyperimmune (Group 4) or hyperimmune (Group 5) bovine colostrum; for 7 days they received 50 ml of colostrum completed by milk replacer twice a day, then they were fed with milk replacer exclusively. Control lambs became infected and developed clinical cryptosporidiosis with diarrhea on Days 4-9 post inoculation, oocyst shedding and mortality (2/6). In all the treated groups, the colostrum prevented mortality and clinical cryptosporidiosis. The mortality (5/7) observed in Group 5 was not due to cryptosporidiosis but anemia. In treated groups, specific antibodies were detected on Day 0 after 2 days of colostrum intake and varied little in time for IgM and IgG in spite of the parasite development, whereas they appeared later in the control group, on Day 4 for IgM, Day 11 for IgA and Day 14 for IgG. In all groups, the response which was the most consistent was the IgA response which evolved from Days 11 to 18 in association with the decline of oocyst shedding. Our results show that whatever the serum antibody titers were, the specific C. parvum circulating antibodies have no influence on the control of cryptosporidiosis. The prophylaxis or the treatment of cryptosporidiosis require high titers of specific C. parvum antibodies in the gut lumen during a sufficiently long period.

Major antigens of Cryptosporidium parvum recognised by serum antibodies from different infected animal species and man.

Serum humoral immune response to Cryptosporidium parvum was evaluated in six species: mouse, rabbit, lamb, calf, pig and man. Electrophoretic and immunoblot analysis showed that specific animal antibody response appeared between Day 4 and Day 15 post inoculation. The two main target antigens had apparent molecular weights of 15-17 and 23 kDa. They were recognised by each species studied. Serum IgA intensively recognised the 15-17 kDa antigen, except in rabbit. This study demonstrates that these two antigens are consistent targets of humoral immune response and can therefore be of great interest in studies of therapy/prophylaxis.

Interaction of Marek's disease virus and Cryptosporidium baileyi in experimentally infected chickens.

Histocompatible B13/B13 white specific-pathogen-free leghorn chickens were used to investigate the effect of coinfection with Cryptosporidium baileyi and the HPRS 16 strain of Marek's disease virus (MDV) in chickens and to assess the pathogenicity of C. baileyi when MDV is given before or after the parasite. Groups of chickens concurrently infected with C. baileyi orally inoculated at day (D)4 and MDV inoculated at hatching (C4M0 group) or at D8 (C4M8 group) were compared with relevant control groups inoculated with only C. baileyi at D4 (C4 group), only MDV at hatching (M0 group) or at D8 (M8 group), and an uninoculated control group (UC group). The chickens were kept in isolator units until the end of the experiment at D62. Our results showed a considerable synergistic effect in concurrently infected chickens and more severe consequences when chickens received MDV before C. baileyi infection. In fact, except for a slight transitory weakness, the chickens in C4 group remained free of overt clinical signs and there was no mortality. However, coinfection with both pathogens induced more lasting or permanent oocyst shedding. Severe clinical cryptosporidiosis with weakness, anorexia, depression, growth retardation, and chronic and severe respiratory disease causing death occurred in all chickens in the C4M0 group between D12 and D43 and in 67% of the chickens in the C4M8 group between D17 and D57. Eighty-two percent and 33%, respectively, died before the development of specific Marek's disease lesions. Mortality rates were 27% and 33% in the M0 and M8 groups, respectively. The presence of MDV enhanced the establishment of more lasting cryptosporidial infection in the respiratory tract, esophagus, crop, proventriculus, and kidneys (only in C4M0 group) as well as in bursa of Fabricius, ceca, and cloaca. Serologic analysis showed that chickens with chronic cryptosporidiosis in the C4M8 group had an increased level of C. baileyi-specific immunoglobulin A. Our results may explain some cases of mortality in chickens naturally infected with MDV and Cryptosporidium.

Analysis of humoral immune response in chickens after inoculation with Cryptosporidium baileyi or Cryptosporidium parvum.

White leghorn chickens aged 14 days were orally inoculated with 1 x 10(6) oocysts of Cryptosporidium baileyi or C. parvum to compare the specific immune responses. Cross-reactions were evaluated using homologous or heterologous antigens in enzyme-linked immunosorbent assay (ELISA) and Western blot to determine the occurrence of an antigenic homology between these two species. Blood, bile, whole intestine, bursa of Fabricius, and feces were collected daily from the day of inoculation (day 0) to day 22 postinoculation (PI). Eight control chickens remained negative up to day 22 PI. Chickens inoculated with C. baileyi did not express clinical symptoms but shed oocysts from days 6 to 21 PI. Chickens inoculated with C. parvum exhibited no clinical signs, no oocysts in feces, and no developmental stages of the parasite. However, a specific immune response to both antigens appeared on day 9 PI. ELISA using homologous or heterologous antigens showed that anti-C. baileyi and anti-C. parvum antibodies in serum or bile were detectable using C. baileyi or C. parvum oocysts as antigen, but the intensity of the response was significantly higher when C. baileyi was used. Cross-reactions in immunoblot analysis confirmed ELISA results, revealing a greater number of bands using C. baileyi as antigen but showing that epitopes recognized on the protein with a molecular weight of 15,000-17,000 were different.

Inhibition of Eimeria tenella development in vitro mediated by chicken macrophages and fibroblasts treated with chicken cell supernatants with IFN-gamma activity.

Pretreatment of chicken macrophages or fibroblasts with supernatants from concanavalin A-stimulated spleen cells or from the virus-transformed cell line reticuloendotheliovirus as source of interferon gamma (IFN-gamma) slows down subsequent sporozoite replication in the cells. To identify the presence of IFN-gamma, we combined four typical activities of IFN-gamma: inhibition of cytopathic effect of vesicular stomatitis virus on IFN-gamma-treated fibroblasts, cytostatic activity of IFN-gamma-activated macrophages, induction of major histocompatibility complex II antigen expression on IFN-gamma-activated fibroblasts and macrophages, and induction of nitrite production in macrophages. We have shown that chicken fibroblasts and macrophages possess a microbiostatic capacity once they are able to prevent the otherwise unchecked intracellular replication of Eimeria tenella following activation with culture supernatants identified as containing a strong IFN-gamma activity.

Mechanisms of the Eimeria tenella growth inhibitory activity induced by concanavalin A and reticuloendotheliosis virus supernatants with interferon gamma activity in chicken macrophages and fibroblasts.

Pretreatment of chicken bone marrow macrophages and embryo fibroblasts with supernatants containing chicken interferon gamma (IFN-gamma) for 24 hr prior to inoculation inhibited intracellular Eimeria tenella replication, measured by [3H] uracil incorporation. The supernatants (Sns) were obtained from culture of lymphoblastoid cells transformed by a reticuloendotheliosis virus (REV) and chicken splenocytes stimulated with concanavalin A (Con A). The mechanisms of the E. tenella growth inhibitory activity induced by Sn REV and Sn Con A in chicken macrophages and fibroblasts were studied. Addition of oxygen scavengers (superoxide dismutase, D-mannitol, DABCO, benzoic acid, L-histidine hydrochloride) was able to overcome the inhibition of E. tenella replication after pretreatment with Sn REV or Sn Con A in macrophage cultures but not in fibroblast cultures. Nitric oxide (NO) synthesis was induced in macrophage culture treated with Sn REV or Sn Con A but not in fibroblast culture. Addition of NG monomethyl-L-arginine, an NO synthase inhibitor together with the supernatants was also able to overcome inhibition of E. tenella replication in macrophage culture. On the other hand, addition of L-tryptophan to Sn REV- or Sn Con A-treated fibroblasts was able to reverse the inhibitory effect on E. tenella replication. In conclusion, production of inorganic NO or toxic oxygen intermediates may be involved in the E. tenella growth inhibitory activity of chicken macrophages pretreated with supernatants containing an IFN-gamma activity, and cellular tryptophan depletion may be involved for chicken fibroblasts, thus matching the mechanisms of the IFN-gamma-induced growth inhibitory activity for protozoans in mammals.

Renal Cryptosporidiosis (Cryptosporidium baileyi) in specific-pathogen-free chickens experimentally coinfected with Marek's disease virus.

Renal Cryptosporidiosis was experimentally induced during a study to investigate the pathogenicity of Cryptosporidium baileyi in specific-pathogen-free (SPF) chickens coinfected with Marek's disease virus (MDV). Cryptosporidium baileyi was administered orally at 4 days of age to chickens previously infected at hatching (day 0) with the HPRS 16 strain of oncogenic MDV. Three control groups received MDV at hatching, C. baileyi on day 4, or placebo consisting of distilled water. Renal cryptosporidiosis lesions were induced in the group coinfected with MDV and C. baileyi. The kidneys were markedly swollen and pale, with visible urate crystals in the ureters and surface tubules. Oocysts of C. baileyi were demonstrated in six of seven cases tested by a scoring method with modified Sheather's sugar solution on renal tissue scrapings and were confirmed in three cases by histologic examination of paraffin-embedded kidney sections. Histologic study also revealed subacute interstitial nephritis, acute ureteritis, and attachment of cryptosporidia on the epithelial cell surface of the ureters and collecting ducts, collecting tubules, and distal convoluted tubules. Various developmental stages of the parasite were present in the kidney sections. To our knowledge, this is the first report of experimentally induced renal cryptosporidiosis in SPF chickens coinfected with MDV.

Influence of digestive microflora on parasite development and the pathogenic effect of Eimeria ovinoidalis in the axenic, gnotoxenic and conventional lamb.

The interaction between the digestive microflora and the development and pathogenic effect of Eimeria ovinoidalis was studied in lambs. All animals were reared and fed in the same conditions and were infected on the second day after birth with 150,000 sterilised oocysts. Two conventional lambs that had absorbed colostrum had haemorrhagic diarrhoea for several days and excreted 10(5) to 10(6) oocysts g-1 faeces. One lamb died. Similar results were recorded in two gnotoxenic lambs inoculated with 63 pure bacterial strains representative of the dominant digestive microflora and free of all pathogenic organisms. By contrast, no clinical signs and, in particular, no diarrhoea were observed in nine axenic lambs. OOcyst excretion in these only started on the 16th day, and the number of oocysts was between 10(2) and 10(3) g-1. The presence of digestive microflora is thus essential to the development of the parasite's pathogenic expression.

Experimental study of some factors limiting 'competitive exclusion' of salmonella in chickens.

Some factors affecting the efficiency of competitive exclusion of Salmonella typhimurium var copenhagen in chicks were studied experimentally under gnotobiotic conditions. Axenic chickens were given dilute suspensions of adult faeces and exposed to the salmonellae. Prevention of colonisation of the gut by salmonellae ('competitive exclusion') was variable and depended possibly in part on the source of the adult faeces used to protect the chicks. Exclusion was also dose-dependent, a large inoculum of the salmonellae (10(7) viable organisms per animal) leading to colonisation in treated chicks. An inapparent carrier state was sometimes produced by lower doses of the salmonellae (10(2) viable organisms per animal), but bursts of excretion still appeared after inoculation of the salmonellae. In inapparent healthy carriers, the inoculation of a dose of Eimeria tenella oocysts that was known to produce subclinical caecal coccidiosis led to the shedding of large numbers of salmonellae for over two weeks, and the use of 'competitive exclusion' in poultry as a preventive measure for salmonella infections might thus be limited by the frequent occurrence of subclinical coccidiosis in the field.

Evaluation of the efficacy of salinomycin in the control of coccidiosis in chicks.

Salinomycin (Coxistac) was tested for efficacy in broilers reared in floor pens at 60 and 80 ppm fed continuously from 1 to 56 days of age. One trial was conducted. Comparisons were made with unmedicated, infected and medicated, noninfected treatments (controls) in addition to infected treatments given either monensin at 100 ppm or halofuginone at 3 ppm continuously (days 1 to 56) in the feed. Coccidia exposure was obtained by infection via the feed. Salinomycin was highly efficacious at 60 ppm based upon improved performance, lesion score, hematocrit, and serum optical density compared with the unmedicated, infected group. Statistical analysis of main effects on weight gain, feed conversion ratio, hematocrit value, and serum optical density showed no significant differences between salinomycin, monensin, or halofuginone. The weight gain of birds given salinomycin at 80 ppm was depressed significantly (P less than .01) at 56 days as a result of decreased feed consumption.