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Acquired Immunity of Buquinolate-Medicated Chickens to Eimeria Tenella Infection
1492
M. KELLY AND C. E. HOLMES
SUMMARY
Diets containing 70 percent reconstituted high-moisture corn (25 percent total moisture) were fed to caged layers. There were no adverse effects of this corn when compared to normal corn (12.8 percent moisture) upon egg production, egg
weights or hatchability of fertile eggs. Feed consumption was greater for hens fed the diet containing reconstituted high-moisture corn but dry matter consumption was equal whether the hens were fed regular or highmoisture corn diets. The use of reconstituted high-moisture corn in these experiments resulted in lower feed ingredient cost per egg. REFERENCES Dixon, W. J., 1967. BMD Biomedical Computer Programs. University of California Press, Berkeley and Los Angeles, California. Giesler, F. L., 1960. Feed high-moisture corn? Hoards Dairyman, 105 : 1007. Perez, R., and T. R. Preston, 1970. Effect of ensiling high-moisture grain sorghum or maize on the performance of broilers. Abstracts of Scientific Communications of the XIV Convention of the World's Poultry Science Association; Madrid, Spain, p. 622. Stone, J. B., 1965. How to feed high-moisture corn. Hoards Dairyman, 110: 1103.
Acquired Immunity of Buquinolate-Medicated Chickens to Eimeria Tenella Infection WILLIAM D. LEATHEM AND ROBERT E. KOHLS Division of Veterinary Research, The Norwich Pharmacal Company, Norwich, New York 13815 (Received for publication March 18, 1971) INTRODUCTION
T
HE most widely used program for coccidiosis control in replacement flocks reared under floor pen conditions depends on accidental exposure of chickens to infective oocysts while using a coccidiostat in the feed (Reid et al., 1968). Ideally, the coccidiostat of choice permits a low level of infection to proceed, thus allowing the host to gradually acquire protective immunity to the coccidial species present without losing weight or showing clinical signs of disease. Studies in this laboratory (unpublished) show that, in the case of Eimeria tenella, buquinolate is an ideal coccidiostat for use in cage layer replacement pullets.
When chickens fed this coccidiostat are artifically infected with E. tenella they show no clinical signs of disease but still pass small numbers of oocysts (Brewer and Reid, 1967; Edgar and Flanagan, 1966). This observation suggests that the use of buquinolate does not interfere with the ability of the host to acquire immunity to subsequent infection with that coccidial species. Little information is available regarding the immune state of buquinolate-medicated chickens following drug withdrawal. Brewer and Reid (1967) in battery studies, and Womack (1968) in floor pen studies, found that buquinolate retarded the devel-
Downloaded from http://ps.oxfordjournals.org/ at Universitat Autonoma Barcelona on June 9, 2015
the regular corn diet. For commercial usage, it would seem logical to assume that high-moisture corn would have to be stored in air-tight silos and blended with concentrate at the farms. The storage costs of high-moisture corn varies considerably and would directly influence the economics of its use. The amount of feed blended should not exceed the daily consumption of the hens in order to reduce the chance of their feed becoming moldy. The addition of 0.25 percent calcium propionate could be used to help prevent molds from growing in the finished feed.
IMMUNITY TO EIMERIA
TENELLA
1493
Medicated feed was withdrawn from birds of Group 1 one week after the last immunizing inoculation. Two weeks subsequent to drug withdrawal, when the birds were 9 weeks of age, all immunized birds
RESULTS AND DISCUSSION Pierce et al. (1962) reported that an almost complete immunity, assessed by production of few oocysts in response to a
Downloaded from http://ps.oxfordjournals.org/ at Universitat Autonoma Barcelona on June 9, 2015
MATERIALS AND METHODS Oocysts used in this experiment were from a pure line culture, developed from a single oocyst, and maintained in this laboratory. Fresh oocyst suspensions were prepared routinely from the ceca of donor birds 7 days after an oral inoculation of 4,000 sporulated oocysts. Hubbard X White Mountain female chicks were obtained and housed as described by Leathern and Engle (1970). When the chicks were one week old they were divided into 4 groups of 10 birds each. Groups 1 and 2 constituted the experimental birds and Groups 3 and 4, the controls. Groups 1 and 2 were immediately removed to an isolation room where they were housed individually in wire-floored battery cages. Group 1 was fed a ration containing buquinolate 0.011%, and Group 2 a buquinolate-free ration. Three days after being placed on their respective diets, birds of both groups were inoculated per os with 500 E. tenella oocysts. The initial infection was followed by 3 immunizing inoculations of 5,000, 50,000 and 100,000 oocysts given when the birds were 3, 4, and 6 weeks of age, respectively.
were given a challenge inoculation of 5,000,000 oocysts. Groups 3 and 4 were held in a coccidiafree building and fed an unmedicated ration until 4 days prior to the time the immunized birds were challenged. At that time they were moved to the isolation building and housed in the same manner as the immunized birds. Group 3 was placed on a ration containing buquinolate 0.011%, and Group 4 on unmedicated ration. Simultaneously with the challenge inoculation of 5,000,000 oocysts given immunized birds, each control bird received an initial inoculation of the same magnitude. All chickens were weighed at the time of challenge (initial inoculation for controls), and on days 4 through 10 of the ensuing infection. Also, on those days, the pan under each bird was scored according to the number of bloody droppings observed: 0 = none, 1 = single bloody dropping, 2 = 2-4 bloody droppings, 3 = uniformly scattered bloody droppings, and 4 = confluent bloody droppings. The fecal material of each bird was collected every 24 hours, beginning on the 7th and terminating on the 11th day following challenge inoculation. The material from each bird was weighed and homogenized with an electric mixer; and a 5 gm. sample was taken. The sample was placed in a 250 ml. Erlenmeyer flask containing 100 ml. of 0.1N sodium hydroxide and some glass beads. The flask was allowed to sit for 10 minutes to dissolve the fecal material, and then was shaken to release the suspected oocysts. The number of oocysts in 1 ml. of this suspension, determined by counting with a hemacytometer, was used to calculate the total oocyst production for each bird.
opment of immunity to 6 species of poultry coccidia. Edgar and Flanagan (1967) reported that buquinolate acts to inhibit early asexual development of the parasite but also found that some parasites were able to complete their developmental cycle in the presence of the drug. Work in this laboratory based on both battery and floor pen trials suggests that, in the case of E. tenella, buquinolate does not interfere with the acquisition of immunity to reinfection. The present study was undertaken to confirm our findings.
1494
W. D. LEATHEM AND R. E. KOHLS
TABLE 1.—Effect of E. tenella infection in buqinolate-medicated and nonmedicated immune and nonimmune chickens in a 7-day period {days 4-10) following inoculation with 5,000,000 sporulated oocysts
Group
Treatment
$ £
No^irds
(weeks)
m
No.**
%weft
Pecal
SrouP
coccidiosis
9
10
0
(mean) \ / 7.45
(mean) \ / 0
per bird (mean) 0
0
0
v
Group l*1 Medicated, Immunized
^
Nonmedicated, Immunized
9
10
0
7.09
Group 3 2
Medicated, Nonimmunized
9
10
0
6.0
1.1
5,000,000
Group 42
Nonmedicated, Nonimmunized
9
10
1
-10.8
2.3
16,000,000
* = Received oral inoculations of 500, 5,000 and 100,000 E. tenella at 2, 3, 4 and 6 weeks of age, respectively. 1 =Buqinolate withdrawn from feed 2 weeks prior to challenge. 2 = Previously uninfected control chickens.
challenge infection, was developed in chickens which had previously received oral inoculations of 500, 5,000, and 50,000 E. tenella oocysts at weekly intervals. Leathem and Burns (1968) found that the immunity obtained was enhanced when each bird was given an additional inoculation of 100,000 oocysts. They reported that chickens immunized in this manner showed no clinical signs of disease when challenged 42 days after the last immunizing dose. Therefore, a similar immunizing schedule was employed in the present study. In order to assess accurately the degree of immunity obtained by buquinolate-medicated chickens (Group 1), unmedicated birds of the same hatch (Group 2) were given identical immunizing inoculations. Although no clinical signs of E. tenella infection were observed among chickens of Group 1 during the immunizing period, some characteristics of cecal coccidiosis, such as moderate hemorrhage, anorexia, and general inactivity were noted among birds of Group 2 on the 4th and 5 th days of the initial and 1st and 2nd immunizing infections. However, no clinical signs of coccidiosis were observed among birds of this group after the 3rd immunizing dose.
This observation offered indirect evidence that birds of Group 2, as judged by the absence of clinical signs of coccidiosis, were immune to reinfection with E. tenella following the 3rd inoculation (50,000 oocysts). Similarly, no evidence of a latent coccidial infection was observed among birds of Group 1 after the drug was withdrawn 7 days following the 4th inoculation (100,000 oocysts). Workers have shown that when buquinolate is removed from the ration of infected chickens the parasites, whose life cycle is inhibited in the presence of the drug, continue their development and the birds pass oocysts as though they were inoculated at the time of drug withdrawal (Edgar and Flanagan, 1967). Therefore, it appears that the buquinolatemedicated chickens were also immune subsequent to the 3rd inoculation. These findings are in agreement with those of Mukkur and Bradley (1969) who found that pre-exposure to at least 50,000 E. tenella oocysts was required to afford complete protection against a challenge dose of 100,000 oocysts. A challenge inoculation of 5,000,000 oocysts given 3 weeks after the last immunizing dose caused no adverse effects to birds
Downloaded from http://ps.oxfordjournals.org/ at Universitat Autonoma Barcelona on June 9, 2015
Group 2*
IMMUNITY TO EIMERU
SUMMARY
These findings offer direct evidence that buquinolate-medicated chickens immunized by multiple doses of E. tenella oocysts, acquire an immunity identical to that observed in unmedicated chickens immunized in a like manner. They also suggest that in environments such as those encountered in replacement flocks reared under floor-pen conditions the use of buquinolate as a coccidiostat will not interfere with the development of host immunity to reinfection with that coccidial species. REFERENCES Brewer, R. N., and W. M. Reid, 1967. Efficacy of buquinolate against six species of coccidia. Poultry Sci. 46: 642-646. Edgar, S. A., and C. Flanagan, 1966. Coccidiosis and other effects of buquinolate in poultry. Poultry Sci. 45: 1081-1082. Edgar, S. A., and C. Flanagan, 1967. A new drug for control of coccidiosis in chickens. Highlights of Agricultural Research 14(2): 5, Summer. Leathern, W. D., and W. C. Burns, 1968. Duration of acquired immunity of the chicken to Eimeria tenella infection. J. Parasitol. S4: 227-232. Leathern, W. D., and A. T. Engle, 1970. Effect of two levels of buquinolate on the endogenous development and oocyst suppression of Eimeria tenella. Poultry Sci. 49: 1109-1113. Mukkur, T. K. S., and R. E. Bradley, 1969. Eimeria tenella: Packed blood cell volume, hemoglobin, and serum proteins of chickens correlated with the immune state. Experimental Parasitol. 26: 1-16. Pierce, A. E., P. L. Long and C. Horton-Smith, 1962. Immunity to Eimeria tenella in young fowls {Gallus domesticus). Immunology, 5: 129-1S2. Reid, W. M., H. E. Womack and J. Johnson, 1968. Coccidiosis susceptibility in layer flock replacement programs. Poultry Sci. 47: 892-899. Womack, H. E., 1968. The use of coccidiostats and their effect on immunity. Masters degree thesis, Univ. Georgia, Athens, Georgia. 44 p.
MARCH 23-25, 1972. SUPER SHOW, THE PACIFIC EGG AND POULTRY ASSOCIATIONS, TOWN AND COUNTRY HOTEL, SAN DIEGO, CALIFORNIA
Downloaded from http://ps.oxfordjournals.org/ at Universitat Autonoma Barcelona on June 9, 2015
of Groups 1 and 2, the birds continued to show good weight gains and no oocysts were recovered from their fecal material (Table 1). Simultaneous with the challenge of immune birds control birds were given an initial inoculation of 5,000,000 oocysts. Subsequently, none of the Group 3 birds, which received buquinolate 0.011% in their feed, died as a result of the massive inoculation, and percentage weight gain was only slightly lower than that of either immune group. However, all birds of Group 3 experienced moderate hemorrhage and passed an average of 5,000,000 oocysts per bird from the 6th through 10th day of infection (Table 1). In contrast, birds of Group 4, which received unmedicated ration, were affected severely. One bird died of cecal coccidiosis, and the survivors all showed a marked decrease in weight, hemorrhaged extensively, and passed an average of 16,000,000 oocysts during the same period of infection (Table 1). The low mortality among unmedicated birds does not reflect the virulence of the inoculum, rather, it supports previous work (Leathern and Burns, 1968) which suggested that the age of the host is a factor in E. tenella infections. Brewer and Reid (1967) in battery studies and Womack (1968) in floor-pen studies found that buquinolate interfered with the development of immunity to several species of poultry coccidia. Though in the case of E. tenella, the results of the present study are in contrast to the findings of these investigators, it is evident that the immune status of the birds of Groups 1 and 2 depended on the number of oocysts the birds had previously received.
1495
TENELLA
M. KELLY AND C. E. HOLMES
SUMMARY
Diets containing 70 percent reconstituted high-moisture corn (25 percent total moisture) were fed to caged layers. There were no adverse effects of this corn when compared to normal corn (12.8 percent moisture) upon egg production, egg
weights or hatchability of fertile eggs. Feed consumption was greater for hens fed the diet containing reconstituted high-moisture corn but dry matter consumption was equal whether the hens were fed regular or highmoisture corn diets. The use of reconstituted high-moisture corn in these experiments resulted in lower feed ingredient cost per egg. REFERENCES Dixon, W. J., 1967. BMD Biomedical Computer Programs. University of California Press, Berkeley and Los Angeles, California. Giesler, F. L., 1960. Feed high-moisture corn? Hoards Dairyman, 105 : 1007. Perez, R., and T. R. Preston, 1970. Effect of ensiling high-moisture grain sorghum or maize on the performance of broilers. Abstracts of Scientific Communications of the XIV Convention of the World's Poultry Science Association; Madrid, Spain, p. 622. Stone, J. B., 1965. How to feed high-moisture corn. Hoards Dairyman, 110: 1103.
Acquired Immunity of Buquinolate-Medicated Chickens to Eimeria Tenella Infection WILLIAM D. LEATHEM AND ROBERT E. KOHLS Division of Veterinary Research, The Norwich Pharmacal Company, Norwich, New York 13815 (Received for publication March 18, 1971) INTRODUCTION
T
HE most widely used program for coccidiosis control in replacement flocks reared under floor pen conditions depends on accidental exposure of chickens to infective oocysts while using a coccidiostat in the feed (Reid et al., 1968). Ideally, the coccidiostat of choice permits a low level of infection to proceed, thus allowing the host to gradually acquire protective immunity to the coccidial species present without losing weight or showing clinical signs of disease. Studies in this laboratory (unpublished) show that, in the case of Eimeria tenella, buquinolate is an ideal coccidiostat for use in cage layer replacement pullets.
When chickens fed this coccidiostat are artifically infected with E. tenella they show no clinical signs of disease but still pass small numbers of oocysts (Brewer and Reid, 1967; Edgar and Flanagan, 1966). This observation suggests that the use of buquinolate does not interfere with the ability of the host to acquire immunity to subsequent infection with that coccidial species. Little information is available regarding the immune state of buquinolate-medicated chickens following drug withdrawal. Brewer and Reid (1967) in battery studies, and Womack (1968) in floor pen studies, found that buquinolate retarded the devel-
Downloaded from http://ps.oxfordjournals.org/ at Universitat Autonoma Barcelona on June 9, 2015
the regular corn diet. For commercial usage, it would seem logical to assume that high-moisture corn would have to be stored in air-tight silos and blended with concentrate at the farms. The storage costs of high-moisture corn varies considerably and would directly influence the economics of its use. The amount of feed blended should not exceed the daily consumption of the hens in order to reduce the chance of their feed becoming moldy. The addition of 0.25 percent calcium propionate could be used to help prevent molds from growing in the finished feed.
IMMUNITY TO EIMERIA
TENELLA
1493
Medicated feed was withdrawn from birds of Group 1 one week after the last immunizing inoculation. Two weeks subsequent to drug withdrawal, when the birds were 9 weeks of age, all immunized birds
RESULTS AND DISCUSSION Pierce et al. (1962) reported that an almost complete immunity, assessed by production of few oocysts in response to a
Downloaded from http://ps.oxfordjournals.org/ at Universitat Autonoma Barcelona on June 9, 2015
MATERIALS AND METHODS Oocysts used in this experiment were from a pure line culture, developed from a single oocyst, and maintained in this laboratory. Fresh oocyst suspensions were prepared routinely from the ceca of donor birds 7 days after an oral inoculation of 4,000 sporulated oocysts. Hubbard X White Mountain female chicks were obtained and housed as described by Leathern and Engle (1970). When the chicks were one week old they were divided into 4 groups of 10 birds each. Groups 1 and 2 constituted the experimental birds and Groups 3 and 4, the controls. Groups 1 and 2 were immediately removed to an isolation room where they were housed individually in wire-floored battery cages. Group 1 was fed a ration containing buquinolate 0.011%, and Group 2 a buquinolate-free ration. Three days after being placed on their respective diets, birds of both groups were inoculated per os with 500 E. tenella oocysts. The initial infection was followed by 3 immunizing inoculations of 5,000, 50,000 and 100,000 oocysts given when the birds were 3, 4, and 6 weeks of age, respectively.
were given a challenge inoculation of 5,000,000 oocysts. Groups 3 and 4 were held in a coccidiafree building and fed an unmedicated ration until 4 days prior to the time the immunized birds were challenged. At that time they were moved to the isolation building and housed in the same manner as the immunized birds. Group 3 was placed on a ration containing buquinolate 0.011%, and Group 4 on unmedicated ration. Simultaneously with the challenge inoculation of 5,000,000 oocysts given immunized birds, each control bird received an initial inoculation of the same magnitude. All chickens were weighed at the time of challenge (initial inoculation for controls), and on days 4 through 10 of the ensuing infection. Also, on those days, the pan under each bird was scored according to the number of bloody droppings observed: 0 = none, 1 = single bloody dropping, 2 = 2-4 bloody droppings, 3 = uniformly scattered bloody droppings, and 4 = confluent bloody droppings. The fecal material of each bird was collected every 24 hours, beginning on the 7th and terminating on the 11th day following challenge inoculation. The material from each bird was weighed and homogenized with an electric mixer; and a 5 gm. sample was taken. The sample was placed in a 250 ml. Erlenmeyer flask containing 100 ml. of 0.1N sodium hydroxide and some glass beads. The flask was allowed to sit for 10 minutes to dissolve the fecal material, and then was shaken to release the suspected oocysts. The number of oocysts in 1 ml. of this suspension, determined by counting with a hemacytometer, was used to calculate the total oocyst production for each bird.
opment of immunity to 6 species of poultry coccidia. Edgar and Flanagan (1967) reported that buquinolate acts to inhibit early asexual development of the parasite but also found that some parasites were able to complete their developmental cycle in the presence of the drug. Work in this laboratory based on both battery and floor pen trials suggests that, in the case of E. tenella, buquinolate does not interfere with the acquisition of immunity to reinfection. The present study was undertaken to confirm our findings.
1494
W. D. LEATHEM AND R. E. KOHLS
TABLE 1.—Effect of E. tenella infection in buqinolate-medicated and nonmedicated immune and nonimmune chickens in a 7-day period {days 4-10) following inoculation with 5,000,000 sporulated oocysts
Group
Treatment
$ £
No^irds
(weeks)
m
No.**
%weft
Pecal
SrouP
coccidiosis
9
10
0
(mean) \ / 7.45
(mean) \ / 0
per bird (mean) 0
0
0
v
Group l*1 Medicated, Immunized
^
Nonmedicated, Immunized
9
10
0
7.09
Group 3 2
Medicated, Nonimmunized
9
10
0
6.0
1.1
5,000,000
Group 42
Nonmedicated, Nonimmunized
9
10
1
-10.8
2.3
16,000,000
* = Received oral inoculations of 500, 5,000 and 100,000 E. tenella at 2, 3, 4 and 6 weeks of age, respectively. 1 =Buqinolate withdrawn from feed 2 weeks prior to challenge. 2 = Previously uninfected control chickens.
challenge infection, was developed in chickens which had previously received oral inoculations of 500, 5,000, and 50,000 E. tenella oocysts at weekly intervals. Leathem and Burns (1968) found that the immunity obtained was enhanced when each bird was given an additional inoculation of 100,000 oocysts. They reported that chickens immunized in this manner showed no clinical signs of disease when challenged 42 days after the last immunizing dose. Therefore, a similar immunizing schedule was employed in the present study. In order to assess accurately the degree of immunity obtained by buquinolate-medicated chickens (Group 1), unmedicated birds of the same hatch (Group 2) were given identical immunizing inoculations. Although no clinical signs of E. tenella infection were observed among chickens of Group 1 during the immunizing period, some characteristics of cecal coccidiosis, such as moderate hemorrhage, anorexia, and general inactivity were noted among birds of Group 2 on the 4th and 5 th days of the initial and 1st and 2nd immunizing infections. However, no clinical signs of coccidiosis were observed among birds of this group after the 3rd immunizing dose.
This observation offered indirect evidence that birds of Group 2, as judged by the absence of clinical signs of coccidiosis, were immune to reinfection with E. tenella following the 3rd inoculation (50,000 oocysts). Similarly, no evidence of a latent coccidial infection was observed among birds of Group 1 after the drug was withdrawn 7 days following the 4th inoculation (100,000 oocysts). Workers have shown that when buquinolate is removed from the ration of infected chickens the parasites, whose life cycle is inhibited in the presence of the drug, continue their development and the birds pass oocysts as though they were inoculated at the time of drug withdrawal (Edgar and Flanagan, 1967). Therefore, it appears that the buquinolatemedicated chickens were also immune subsequent to the 3rd inoculation. These findings are in agreement with those of Mukkur and Bradley (1969) who found that pre-exposure to at least 50,000 E. tenella oocysts was required to afford complete protection against a challenge dose of 100,000 oocysts. A challenge inoculation of 5,000,000 oocysts given 3 weeks after the last immunizing dose caused no adverse effects to birds
Downloaded from http://ps.oxfordjournals.org/ at Universitat Autonoma Barcelona on June 9, 2015
Group 2*
IMMUNITY TO EIMERU
SUMMARY
These findings offer direct evidence that buquinolate-medicated chickens immunized by multiple doses of E. tenella oocysts, acquire an immunity identical to that observed in unmedicated chickens immunized in a like manner. They also suggest that in environments such as those encountered in replacement flocks reared under floor-pen conditions the use of buquinolate as a coccidiostat will not interfere with the development of host immunity to reinfection with that coccidial species. REFERENCES Brewer, R. N., and W. M. Reid, 1967. Efficacy of buquinolate against six species of coccidia. Poultry Sci. 46: 642-646. Edgar, S. A., and C. Flanagan, 1966. Coccidiosis and other effects of buquinolate in poultry. Poultry Sci. 45: 1081-1082. Edgar, S. A., and C. Flanagan, 1967. A new drug for control of coccidiosis in chickens. Highlights of Agricultural Research 14(2): 5, Summer. Leathern, W. D., and W. C. Burns, 1968. Duration of acquired immunity of the chicken to Eimeria tenella infection. J. Parasitol. S4: 227-232. Leathern, W. D., and A. T. Engle, 1970. Effect of two levels of buquinolate on the endogenous development and oocyst suppression of Eimeria tenella. Poultry Sci. 49: 1109-1113. Mukkur, T. K. S., and R. E. Bradley, 1969. Eimeria tenella: Packed blood cell volume, hemoglobin, and serum proteins of chickens correlated with the immune state. Experimental Parasitol. 26: 1-16. Pierce, A. E., P. L. Long and C. Horton-Smith, 1962. Immunity to Eimeria tenella in young fowls {Gallus domesticus). Immunology, 5: 129-1S2. Reid, W. M., H. E. Womack and J. Johnson, 1968. Coccidiosis susceptibility in layer flock replacement programs. Poultry Sci. 47: 892-899. Womack, H. E., 1968. The use of coccidiostats and their effect on immunity. Masters degree thesis, Univ. Georgia, Athens, Georgia. 44 p.
MARCH 23-25, 1972. SUPER SHOW, THE PACIFIC EGG AND POULTRY ASSOCIATIONS, TOWN AND COUNTRY HOTEL, SAN DIEGO, CALIFORNIA
Downloaded from http://ps.oxfordjournals.org/ at Universitat Autonoma Barcelona on June 9, 2015
of Groups 1 and 2, the birds continued to show good weight gains and no oocysts were recovered from their fecal material (Table 1). Simultaneous with the challenge of immune birds control birds were given an initial inoculation of 5,000,000 oocysts. Subsequently, none of the Group 3 birds, which received buquinolate 0.011% in their feed, died as a result of the massive inoculation, and percentage weight gain was only slightly lower than that of either immune group. However, all birds of Group 3 experienced moderate hemorrhage and passed an average of 5,000,000 oocysts per bird from the 6th through 10th day of infection (Table 1). In contrast, birds of Group 4, which received unmedicated ration, were affected severely. One bird died of cecal coccidiosis, and the survivors all showed a marked decrease in weight, hemorrhaged extensively, and passed an average of 16,000,000 oocysts during the same period of infection (Table 1). The low mortality among unmedicated birds does not reflect the virulence of the inoculum, rather, it supports previous work (Leathern and Burns, 1968) which suggested that the age of the host is a factor in E. tenella infections. Brewer and Reid (1967) in battery studies and Womack (1968) in floor-pen studies found that buquinolate interfered with the development of immunity to several species of poultry coccidia. Though in the case of E. tenella, the results of the present study are in contrast to the findings of these investigators, it is evident that the immune status of the birds of Groups 1 and 2 depended on the number of oocysts the birds had previously received.
1495
TENELLA