Effects of Monensin-Feeding Regimens on Flock Immunity to Coccidiosis

Effects of Monensin-Feeding Regimens on Flock Immunity to Coccidiosis W.

MALCOLM R E I D , JOHN D I C K , 1 JOHN R I C E 1 AND FARID STINO 2

Department of Poultry Science, University of Georgia, Athens, Georgia 30602 (Received for publication April 19, 1976)

POULTRY SCIENCE 56: 66-71,

A

1977

elude drug withdrawal. Two similarly designed floor-pen experiments were conducted at the University of Georgia with floor-reared replacement pullets. Different monensin levels, mild or severe oocyst exposure, and drug withdrawal were included in the experimental designs.

LTHOUGH new preventive anticoccidials are first introduced to protect meat strains of birds for short growing periods, the question inevitably arises as to effects the drug may have on development of immunity in layer or breeder replacements. Since any anticoccidial may affect cycling of the parasite, its use may retard development of flock immunity (Reid et al, 1960, 1968). Can monensin, which is now established as a broiler anticoccidial, provide protection for growing birds and yet permit immunity to develop before the drug is withdrawn or egg production is started? Callender and Shumard (1973) concluded that birds develop immunity earlier when lower levels of monensin (60 or 100 p.p.m.) were fed than with a higher level (120 p.p.m.). This immunity developed more rapidly as measured by severity of lesions after challenge if flocks were exposed to "direct" litter-seeding than if by "indirect" exposure (terminology of Callender and Tonkinson, 1971). Their experimental design did not in-

MATERIALS AND METHODS Leghorn-type pullets (Babcock) were started as day-old chicks on new pine shavings litter in floor-pens and reared to 20 weeks of age in two experiments. In both experiments six treatments were replicated in five pens with 50 pullets in each pen. Other groups of pullets were reared in sterilized wirefloored battery brooders. These susceptible controls were used to test the viability of the inoculum in challenge procedures. Experiment I. Monensin was included in the diet for 20 weeks at 120, 60 or 0 (control) p.p.m. Birds were either severely exposed ("direct seeding") or mildly exposed ("indirect seeding") to coccidiosis using techniques previously described (Reid et al., 1974, 1975; and Ruff et al., 1976). In both experiments direct seeding was initiated by placing 5 birds which had been inoculated with lOx Cocci-

1. Present address, Department of Poultry Science, Clemson University, Clemson, South Carolina 29631. 2. Present address, Faculty of Agriculture, Cairo University, Giza, Egypt.

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ABSTRACT Feed medication with monensin caused delays in development of immunity in two floor-pen experiments which simulated commercial broiler production. Development of immunity was retarded with the higher level of monensin (120 p.p.m.) but was progressively less delayed as the monensin level was decreased (100, 60 or 0 p.p.m.). Delay was greatest with Eimeria tenella, but also occured with intestinal species including E. acervulina, E. brunetti, E. maxima, E. mivati, and E. necatrix. Drug withdrawal permitted earlier development of immunity. Plans involving use of monensin on layer replacements which later will be maintained on the floor without medication should consider: 1) prevalence of infective oocyst exposure in the area, 2) the lowest possible level of drug required for protection, and 3) its use for the shortest possible period of time.

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MONENSIN AND F L O C K IMMUNITY

vac 3 in suspended cages above the principal birds when they were three weeks old.

Significant differences in degrees of immunity are recorded (Figs. 1 to 3) using the conventional lettering system (P < 0.05) for Duncan's multiple range test (1955). Since 3. Coccivac D® is produced by Sterwin Laboratories, Inc., Opelika, Alabama, and certified to include eight species of coccidia.

RESULTS Experiment 1. Immunity levels were significantly greater in birds being fed monensin at 60 than at 120 p.p.m. in all flock samples at 8, 14 and 20 weeks of age. These differences were consistent both in severe exposure ("direct seeding," Fig. 1) and mild exposure ("indirect seeding," Fig. 2). Similarly, immunity was stronger in unmedicated control groups in all four challenge studies than in groups fed 60 p.p.m. Immunity developed more rapidly from severe exposure at 5 and 8 weeks than from mild exposure. By 14 and 20 weeks differences due to severity of exposure had disappeared. At eight weeks birds being fed monensin at 120p.p.m. (Table 1) were still as susceptible to E. tenella as battery-reared controls. In this series of tests use of monensin did not significantly retard immunity development to E. acervulina, E. brunetti, E. maxima, and E. necatrix. However, delays in development of immunity to various intestinal species are obvious in the bar graphs at 5, 8 or 14 weeks (Figs. 1 and 2). Experiment 2. At eight weeks of age development of flock immunity was significantly slower in medicated than in unmedicated pens (Fig. 3). Differences were apparent both in directly (severe exposure) and indirectly (mild exposure) seeded pens. With the former, there was a more rapid development of immunity at 100 than at 120 p.p.m. of monensin. A satisfactory level of immunity was developed by 20 weeks after medication levels had been decreased by one-half from 8 to 12 weeks than withdrawn from 12 to 20 weeks. DISCUSSION Establishment of flock immunity occurred

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Experiment 2. Monensin was fed at 120, 100 and 0 p.p.m. (controls), for 8 weeks to birds in pens which were directly or indirectly seeded. For the period between 8 and 12 weeks levels of monensin were reduced to 60 or 50 p.p.m., respectively, after which the drug was withdrawn during weeks 12 to 20. Flock immunity was tested by challenge of birds removed from each pen at 5, 8, 14 and 20 weeks of age in Experiment 1 and 8, 14, and 20 weeks in Experiment 2 (Reid et al, 1968; Dick et al., 1972). Four birds, two challenged and two as unchallenged controls, were selected at random for each test. An inoculum containing a mixture of oocysts of Eimeria acervulina, E. brunetti, E. maxima, E. tenella, E. necatrix and E. mivati was used for challenge. Lesion scores were recorded seven days post inoculation on the basis of 0 to +4 from four regions designated as "upper," "middle," "lower" intestine and "ceca" (Johnson and Reid, 1970). Single species challenges were also made with the first five of these species at 8 weeks in Experiment 2. Challenge dosages varied with species and inoculum, but were predetermined by assay to produce weight losses without heavy mortality. Parameters used to compare immunity were primarily total lesion scores or in some cases lesion scores of individual species. Mortality and weight gain data were also collected, but are considered useful in only occasional instances since there is considerable variability in these parameters in older birds which have ceased growing.

inoculum of different potency was used with different age groups, statistical comparisons are possible only within treatment groups of the same age.

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W. M. REID, J. DICK, J. RICE AND F. STINO

FIG. 1. Mean lesion scores of ten-bird samples (2 from each pen of the treatment group) from Experiment 1 subjected to direct seeding with 8 species of coccidia. Scores were assigned independently by region of the gut 7 days post inoculation. Statistical comparisons were made on total scores of 4 regions within the same age category (may also include groups of the same age shown in Fig. 2). Absence of common letters indicates significant differences in the degree of immunity (P < 0.05). most rapidly in unmedicated controls and was developed at progressively slower rates as levels of monensin were increased from 60 to 100 p.p.m. and from 100 to 121 p.p.m. Our experiments confirm the conclusion (Callender and Shumard, 1973) that immunity levels were unsatisfactory while birds remained on monensin at 100 or 121 p.p.m. More satisfactory levels of immunity occurred with both mold and severe exposure at 60 p.p.m. Mild exposure probably occurs more frequently in the field but immunity develops less rapidly with mild than with heavy exposure. Callender and Shumard (1973) reported rapid development of immunity to Eimeria maxima and E. brunetti while using monensin. Immunity development was intermediate with E. acervulina and E, mivati, but slower

with E. tenella and E. necatrix. Our results confirm these findings with the immunity to E. tenella being most retarded by use of higher levels of monensin. In heavily seeded pens birds fed on monensin were still as susceptible as unexposed controls at eight weeks. Even though monensin at higher levels retarded development of immunity in floorpens for 20 weeks, evidence of partial immunity could be drawn from lesion scores as well as from weight gain and mortality data (unreported) in medicated birds of 14 weeks or older. These latter findings have been confirmed in similar observations by Callender (personal communication). Immunity development in poultry flocks is dependent upon the presence of oocysts in the environment. This observation has been confirmed in both experiments where use of

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MONENSIN (ppm)q_ 60 120 AGE (Weeks) ^

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MONENSIN AND FLOCK IMMUNITY

INDIRECT SEEDING =

a

UPPER

=

•

MIDDLE

^

LOWER

m • CECA m

FIG. 2. Mean lesion scores of ten-bird samples (2 from each pen of the treatment group) from Experiment 1 subjected to indirect seeding (indirectly by such means as tracking). Scores were assigned independently for four regions of the gut 7 days post inoculation. Statistical comparisons were made on total scores of 4 regions within the same age category including the same age group shown in Fig. 1. Absence of common letters indicates differences in the degree of immunity (P s 0.05).

TABLE 1.—Immunity to 5 species of coccidia developed in pullets after 8 weeks in floor-pens on 120, 60 and 0 p.p.m. of monensin (Experiment 1) Monensin level (p.p.m.) 0 0 60 120

E. E. E. E. Direct E. tenella seeding acervulina maxima necatrix brunetti Treatment Unmedicated controls + 0a 1.2a 0.2a 0.5a* 0.4a 0.9a 0a 0.2a 2.3b 0a Unmedicated controls — 1.4a 1.2a 1.5b 1.7a 0a Monensin + 3.0b 2.3b 1.3a 1.5a 0a Monensin + Susceptible battery-reared 3.8b 2.7b 3.7b 3.1b 3.5c 0 Controls — *Average lesion scores within species with different letters from susceptible controls were significant (P s 0.05) indicating a partial or complete immunity.

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MONENSIN (ppm AGE (Weeks)

W. M. REID, J. DICK, J. RICE AND F. STINO

70

WEEKS

°

8 20 SUSC. l _ CONTROLS

100 120

100 120

100 120

14

20

DIRECT SEEDING

100 120

100 120

100 120

14

20

INDIRECT SEEDING

FIG. 3. Mean lesion scores of ten-bird samples (2 from each pen of the treatment group) in Experiment 2. Lines above bars indicate standard error of total mean scores. Scores were assigned independently by region of the intestine 7 days post inoculation. Statistical comparisons were made of total lesion scores among different treatments in the same age category only and indicate significant differences in the degree of immunity (P r< 0.05) if common letters do not occur.

monensin appears to delay the cycling of coccidia. Whether monensin will retard development of immunity in commercial replacement operations depends upon frequency of exposure to oocysts of each species. In Georgia high exposure rates to four species (Eimeria acervulina, E. necatrix, E. brunetti and E. tenella) has been demonstrated in immunity tests of 17 field flocks ranging in age between 12 and 76 weeks (Karlsson et al., 1976). Poultrymen more concerned with early protection against coccidiosis than with the early development of flock immunity of floor-reared replacements may be able to devise a program using

monensin. They may need to risk using lower levels of anticoccidial than recommended for broilers and confine the time of use to 8 or at most 12 weeks. ACKNOWLEDGEMENTS Technical assistance of Mrs. Joyce Johnson in lesion scoring is gratefully acknowledged. Inoculum including species originally isolated by Dr. S. A. Edgar was provided by Sterwin Laboratories, Inc. REFERENCES Callender, M. E., and R. F. Shumard, 1973. Effects

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MONENSIN (ppm)°

MONENSIN AND FLOCK IMMUNITY

different management conditions. Poultry Sci. 55: 2051. Reid, W. M., J. W. Dick and F. K. R. Stino, 1974. Preventing coccidiosis by continuous medication. Georgia Agric. Res. 16: 4-10. Reid, W. M., J. Johnson and J. Dick, 1975. Anticoccidial activity of lasalocid in control of moderate and severe coccidiosis. Avian Dis. 19: 12-18. Reid, W. M., A. G. Kemler and M. R. Raja, 1960. Prevalence of various species of coccidia in Georgia. Poultry Sci. 39: 1287. Reid, W. M., H. E. Womack and J. Johnson, 1968. Coccidiosis susceptibility in layer flock replacement programs. Poultry Sci. 47: 892-899. Ruff, M. D., W. M. Reid and A. P. Rahn, 1976. Efficacy of different feeding levels of monensin in the control of coccidiosis in broilers. Amer. J. Vet. Res. 37: 963-967.

NEWS AND NOTES (Continued from page 65) S.P. & E.A. NOTES The Directors of the Southeastern Poultry & Egg Association have voted to finance further research in the fields of cholesterol and finding new ways to utilize the protein content of eggs. Southeastern will make a grant of $5,000 to the Harlan E. Moore Heart Research Foundation, Champaign, Illinois, to further the work already underway dealing with the extent cholesterol plays in relation to coronary heart disease. Researchers there are working on the basis that if the metabolic cause of the disease can be found, eggs will be no longer considered a risk factor in heart disease. A second grant of $5,000 will be made for researching ways to make available the high protein in eggs for use in convenience foods, such as soft drinks, potato chips, catsup, and other snack foods. Universities with food research facilities are being asked to submit applications and proposals to Southeastern. BREEDERS' ROUNDTABLE Dr. George Farnsworth, Nicholas Turkey Breeding

Farms, Inc., Sonoma, California, has been named Chariman for the 1977 Breeders' Roundtable. Editor for the 1976 Proceedings will be Dr. Paul Marini, Decatur, Arkansas, and Editor for the 1977 Proceedings will be Dr. Howard L. French, Shaver Poultry Breeding Farms, Ltd., Cambridge, Ontario, Canada. Copies of the 1976 Roundtable Proceedings will be available before December 31, 1976, at $7.50 plus postage, per copy, and orders should be sent to Poultry Breeders of America, 521 E. 63rd St., Kansas City, Missouri 64110. WAMPLER SCHOLARSHIP A Charles W. Wampler Sr. Memorial Scholarship Fund has been established by the Virginia Poultry Federation. The organization will set up a permanent endowment honoring the "father of the commercial turkey industry" to provide college scholarships for young people in the poultry field. Wampler, founder and first President of the National Turkey Federation, and President of the Virginia Poultry Federation from 1934-1939, died May 26, at the age of 91.

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of monensin on development of immunity to coccidia. Poultry Sci. 52: 2007. Callender.M. E.,andL. V.Tonkinson, 1971. Coccidial infections in chickens resulting from the direct and indirect seeding of litter with oocysts. Poultry Sci. 50: 1560. Dick, J. W., J. Johnson and W. M. Reid, 1972. Coccidiosis: parameters used in evaluation of immunity challenge tests. Poultry Sci. 51: 1801. Duncan, D. B., 1955. Multiple range and multiple F tests. Biometrics. 11: 1-42. Johnson, J., and W. M. Reid, 1970. Anticoccidial drugs: lesion scoring techniques in battery and floor-pen experiments with chickens. Exp. Parasitol. 28: 30-36. Karlsson, T., W. M. Reid and J. Johnson, 1976. Prevalence of four species of coccidia (E. acervulina, E. necatrix, E. brunetti, and E. tenella) under

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