An Assessment of Effects of Vaccination on Genetic Resistance to Marek's Disease1 J. S. GAVORA, 1 A . A . GRUNDER, 1 J. L . SPENCER, 2 R. S. G O W E , 1 A . ROBERTSON 2 A N D G . W . SPECKMANN 2
Agriculture
Canada
(Received for publication July 3, 1973)
POULTRY SCIENCE 53: 889-897, 1974
AREK'S disease (MD) has been one of the most costly diseases to the poultry industry, but since 1971 effective vaccines have dramatically reduced losses from the disease. However, vaccinated chickens continue to shed the MD virus, therefore, it is not likely that the disease will be eradicated by vaccination programs (Purchase and Okazaki, 1971). Spencer et al. (1972) found that genetic resistance to MD plays a significant role in livability of populations vaccinated against MD. They reported that the ranking of strains for susceptibility to MD was not usually altered by vaccination, even though vaccination conferred significant protection to all the strains tested. Although the mechanisms of resistance to MD are not completely understood, it is usually considered to be inherited as a quan-
M
1 Animal Research Institute, Research Branch, Ottawa, Ont., Canada, K1A OC6. Contribution No. 502. 2 Animal Pathology Division, Health of Animals Branch, Animal Diseases Research Institute, P.O. Box 1400, Hull, Quebec, Canada, J8Y 1V9.
titative character. Early studies in this area dealt with the "leukosis complex" without differentiating between two of its components, MD and lymphoid leukosis, which are now recognized as two distinct diseases. Heritability of resistance against the "leukosis complex" was estimated at .08 by Lush et al. (1948) and at .05 by Robertson and Lerner (1949). From a short-term selection experiment with meat-type chickens, Friars et al. (1972) estimated realized heritability of resistance to MD at .67, for an index of full- and half-sib family means. Using mostly field data, Von Krosigk et al. (1972), estimated the average heritability of resistance to this disease at. 14 (adjusted to the 50 percent mortality level). Their estimate of hLD50 of resistance to MD was .10 or .20 when challenge with MD virus was by contact exposure or intraperitoneal inoculation, respectively. Relatively little is known about genetic relationship between resistance to MD and production traits. Hutt and Cole (1947) reported that during selection of one strain for resistance and one strain for susceptibility to the leukosis complex (largely MD) there
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ABSTRACT Relationship between resistance to Marek's disease (MD) and production traits in vaccinated and non-vaccinated birds was studied over two generations in two Leghorn strains under selection for high egg production and related characters. In two experiments female progeny of a total of 116 sires and 758 dams were injected with MD virus at 3 weeks and survivors examined for lesions of MD at 12 weeks of age. Full sisters of the challenged birds were placed on 497 day egg production tests in which they were adventitiously exposed to MD. In the second generation all birds on the egg production test were vaccinated for MD. Average heritability of resistance to MD among birds injected with MD virus was .61. Heritability of laying house livability which included mortality from MD and from other causes was .11. Correlations between resistance to MD and production traits indicate that birds genetically more resistant to MD tend to have lower body weight, to mature earlier and to lay smaller eggs. Positive genetic correlations observed between resistance to MD and the egg production rate in vaccinated birds would tend to maintain or increase the genetic resistance to MD in populations under selection for high egg production, even though vaccination would reduce the effects of natural selection for resistance.
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GAVORA, GRUNDER, SPENCER, GOWE, ROBERTSON AND SPECKMANN
Vaccination for MD could be expected to significantly reduce the effect of natural selection for genetic resistance. The main objective of this study was to determine if vaccination of populations under selection for high egg production and related characters would result in a decrease of their genetic resistance to MD. MATERIALS AND METHODS Strains. The origin and development of White Leghorn strains 4 and 5 have been described in previous publications (Gowe, 1970; Gowe et al., 1973). Briefly, strain 4
was formed in 1951 from seven commercial egg production stocks. Strain 5 is an unselected randomly bred control that has been maintained since 1950. Strain 8 was the only other strain used. It was derived in 1969 from the randombred control strain 7 (Gowe, 1970; Gowe et al., 1973), which had been synthesized in 1958 from 4 high egg production commercial stocks. Both strains 4 and 8 were selected for high egg number (hen-housed basis) to 273 days of age. A combination of individual records and full-sib and half-sib family records was used to evaluate females. Males were selected on the basis of performance of their fulland half-sisters. Selection at a lower level of intensity was directed at maintaining existing levels of fertility, hatchability and rearing and laying house livability (Gowe etal., 1973). In selecting breeders from the generation hatched in 1970, resistance to MD of fulland half-sib families based on the 1970 injection challenge test, was also considered. The chickens used in this study in 1970 and 1971 represented the selected generations 20 and 21 for strain 4, and generations 2 and 3 for strain 8. In both 1970 and 1971, two populations (hatches) of the above strains were tested. At the time of the first hatch, in both 1970 and 1971, the parents were one year old. In the second hatch, full-sibs of the chicks in the first hatch were produced when the surviving parents were 14 or 17 months old in 1970 or 1971 respectively. Egg Production Test and Vaccination Against MD. Pullets from the first hatch in both 1970 and 1971 were reared to 140 days of age in groups of 25 in a multiple-deck cage brooding and rearing house. The cages were assigned randomly to each strain, then progeny of each sire were randomized to each cage assigned to that strain. At 140 days of age, the pullets were housed in individual stair-step laying cages. Egg records were kept
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was an increase in egg production in the strain selected for resistance and a decrease in the strain selected for susceptibility to the disease. But the absence of a suitable control strain made it impossible to estimate the genetic changes in production independent of environmental changes. Friars etal. (1972) did not detect any large genetic correlations between resistance to MD and other economic traits. However, in their line selected for resistance to MD they observed a non-significant decrease in body weight when compared to the control. The findings of Han and Smyth (1972) also suggested that selection for rapid growth would result in increased susceptibility to MD. Von Krosigk et al. (1972) reported genetic correlations of - . 18 between MD mortality and rate of lay, .15 between MD mortality and age at sexual maturity and . 36 between total mortality in the laying house and MD mortality. In their data, body weight, shell thickness and egg weight were not significantly correlated with MD mortality. In a recent study, Grunder et al. (1974) found mostly negative rank correlations between egg production and incidence of MD, and positive correlations between MD incidence and age at sexual maturity or egg weight. However, almost none of these correlations between production traits of sires' sibs and incidence of MD in sires' progeny were significant.
MAREK'S DISEASE VACCINATION
MD Challenge Test. Pullets of strains 4 and 8 from the second hatch of each year were pedigree hatched while the control strain 5 pullets were simultaneously mass hatched. They were placed into a controlled environment house divided by wire partitions in 10 pens each measuring 3 x 3.7 m. (Grunder et al., 1972). All chickens in each test were randomly distributed throughout the 10 pens on the day of hatch. They were inoculated intra-abdominally at 22 days of age with blood from chickens infected with the BC-1 isolate of MD virus as described by Grunder et al. (1972). The challenge tests lasted 81 and 84 days in years 1970 and 1971 respectively. Post Mortem Examinations. Post mortem examinations in the MD challenge test were similar to those described by Grunder et al. (1972). MD mortality included all birds that died with gross lesions typical of MD in visceral organs, brachial and/or sciatic plexus or in muscles of breast or thighs. MD incidence included the MD mortality and birds with lesions of MD when killed at the termination of the experiment. Birds that died in the egg production tests were similarly examined for gross lesions. In 1971, all dead birds were necropsied, whereas in the previous year at least 84 percent of the birds of each strain that died between day 141 and 273 of age were examined. Estimates of MD mortality in the 1970
egg production test were obtained by multiplying the total laying house mortality by the proportion of individuals with gross MD lesions among the birds necropsied. Statistical Analysis. Only data from families which had progeny in both the egg production and the MD challenge test were retained for analysis. Heritabilities of the all-or-none characters (MD incidence and total laying house mortality) were calculated by the x2-method of Robertson and Lerner (1949). The heritability on the binomial scale so obtained was transformed to heritability on the normal scale by the formula given by Lush et al. (1948). Estimates of heritability based on variation among sire families were calculated for each strain within each year. Pooled estimates over the two years for each strain were obtained only for heritability of MD incidence in the MD challenge tests. The estimates of heritability of the laying house mortality were not pooled because of the difference in MD vaccination between the 1970 and 1971 egg production tests. Estimates of correlations between MD resistance in the MD challenge tests and laying house mortality or hen-housed egg production in the egg production tests were calculated from data on all birds housed. For estimating the correlations between MD incidence in the MD challenge tests and the other traits measured in the egg production test (body size, age at maturity, egg production rate and egg quality traits) only data from survivors that laid at least 20% in each of three test periods (141-273,274-385 and 386-497 days) and had egg quality recorded at 240 days were used. The above restrictions are consistent with those used by Gowe et al. (1973) in their analysis of similar data. Dam family averages for characters expressed in percent were transformed by arcsin V % transformation. Sire components of variance and covariance were then estimated from analyses of variance and covariance of dam family
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for 5 consecutive days of each week throughout the test (141-497 days of age) and were adjusted to a 7-day week basis. The birds were weighed at 140 and 365 days of age and egg quality was measured at 240 days of age. An important difference between the populations in the egg production tests performed in 1970 and 1971 was that the 1971 population was vaccinated on the day of hatch with commercial turkey herpesvirus vaccine, whereas the 1970 population was not vaccinated.
891
856 (735)
827 (703)
165 (165)
161 (161)
27 (27)
26 (26)
4
8
1029 (856)
220 (216)
481 (349)
31 (31)
8
1008 (764)
560' (300) 2
212 (206)
Dams
5
32 (32)
Sires
4
5
Strain
657
632
139 80.9 83.8
55.9 55.6
76.4 76.3
248.8 240.6
155.8
1.46
84.5
52.7
149.7
69.8
1.53
1.50 188.8
86.3
55.5
76.4
198.8
158.5
1.50 173.3
81.3
56.0
76.9
229.9
151.2
1.56
851 787
85.4
53.1
73.4
153.5
174.1
1.53
Egg weight, (gm.)
245
7
(%)
a t
140d2 (kg.)
89
86
87
85
83
86
Egg quality at 240 days Specific gravity, (-1 Hau x 1000) un
I Total populations of birds housed. ^Restricted populations: survivors that laid at least 20% in each of three test periods (141-273, 274-385 and 386-497 days) and had egg q Populations on egg production test were vaccinated by the HVT vaccine on the day of hatch.
713
70
Year
Henday egg production 2
Henhoused egg production '
Body weight
Egg production tests (141-497 days)
Age at first egg, 2 (days)
Progeny tested MD Egg chall. prod. test test
Numbers of
TABLE 1.—Size and mean performance of populations in egg production tests and in MD
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M A R E K ' S DISEASE VACCINATION
averages within sires and used to calculate genetic correlations (Becker, 1964). Sire family averages were ranked from the highest to the lowest value and the ranks were used in calculations of Spearman's rank correlations corrected for rank tie-ups (Kendall, 1962). RESULTS AND DISCUSSION
the 1970 and 1971 challenge tests (Table 1) indicates that the control strain 5 was more resistant to MD in 1971 than in 1970 (x2 = 4.82; P :£ .05). Possible explanations may be environmental differences between the two tests, errors in sampling the strain for the tests, genetic changes in the strain or a combination of these factors. In the MD challenge tests an effort was made to keep the test conditions constant. Although errors in sampling the strain for the tests cannot be eliminated, it is possible that the heavy losses from MD which the control strain 5 experienced in 1970 may have resulted in an increase in its genetic resistance to MD. This change would have taken place despite the fact that in maintaining strain 5 in each generation each sire is represented by a son and each dam by a daughter. Thus, natural selection could act only on the variance within families which decreases its effectiveness by one half (Gowe et al, 1959). The assumption of a genetic change in strain 5 reduces its value as a control. Consequently, the incidence of MD in strains 4 and 8 would have to be evaluated without reference to the control strain 5. The results of the MD challenge tests (Table 1) would then indicate an increase in resistance of strain 8 in 1971 (x2 = 21.82; P s .01) and no change in strain 4 (x2 = .93). It should be noted that strain 4 was by 1970 under selection for high henhoused egg production for 20 generations and strain 8 for only 2 generations. Also, in the 1970 challenge test strain 8 was more susceptible to MD than strain 4 (Table 1). Therefore, the increase of MD resistance of strain 8 in 1971 and no change in resistance of strain 4 seem more likely than the decrease in resistance in 1971 of both strains 4 and 8 (Table 1) indicated when the incidence of MD is expressed as a deviation from the control strain 5. This is especially true because resistance to MD was included among criteria used in selection of strains 4 and 8 in 1970.
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The size of populations tested, the means for egg production and other traits in the egg production test, as well as the data from the MD challenge tests, are shown in Table 1. The effect of vaccination on mortality is apparent when the egg production test of 1971 is compared with that of 1970. The 1970 laying house mortality (141-273 days) due to MD was approximately 21 percent in the control strain 5 and 6 and 11 percent in the selected strains 4 and 8 respectively (estimated from the total laying house mortality and the proportion of MD positive birds among birds necropsied). The relative resistance of strains 5 and 4 to MD agrees well with other tests (Grunder et at, 1972). In 1971, when there was generally lower total laying house mortality, the MD mortality was negligible. It should be noted that in 1970 losses from MD on the premises were higher than in previous years. The high losses are reflected in the high mortality in the control strain 5 in the egg production test (Table 1). The two strains 4 and 8 selected for high egg production were, however, relatively more resistant to MD than the control strain 5. This was also apparent from the results of the MD challenge tests. The relatively low incidence of MD in challenge tests may not be advantageous for obtaining estimates of genetic parameters but it probably represents the situation in breeding stocks in the poultry industry. The increased livability attributed to vaccination in 1971 is apparent also in hen-housed egg production which indirectly involves mortality. Comparison of incidence of MD between
893
894
GAVORA, GRUNDER, SPENCER, G O W E , ROBERTSON AND SPECKMANN
TABLE 2.—Heritability estimates of MD incidence in MD challenge tests and of total mortality in egg production tests
TABLE 3.—Relationship between MD resistance (MD challenge test) and production traits (egg production test). Rank correlations between sire family means (RANK) and correlations based on analysis of variance and covariance of dam family means within sires (ANCOVA) 1970 Traits MD resistance and 140d body weight 2
Strain
365d body weight 2 Age at first egg2 Total laying house livability1 Hen-housed egg production 1
141-273d
Hen-day percent production
2
Total laying house livability1 141-497d ' Hen-housed egg production 1 Hen-day percent production 2 Egg weight 2
1
240d j Egg specific gravity 2
<
J Haugh units 2
\ Blood spots 2
4 8 4 8 4 8 4 8 4 8 4 8 4 8 4 8 4 8 4 8 4 8 4 8 4 8
RANK .06 -.01 -.14 -.06 .13 -.10 .13 ^Q***
.00 5j#*#
-.26 .30* .04
«*** .06 58*** -.20 .25 .06 .02 .20 -.16 .12 .15 .22 -.16
ANCOVA -.08 .02 .35 -.29 .57 -.23 .58 1.13
t
1.06 -.15 .69 .20 1.17 .48 .37 .14 .34 .16 .12 .20 -.19 .14 -.12 .39 -1.76
19713 ANCOVA RANK -.29 -.09 — 43*** -.37* -.08 -.35* .03 5Q***
.10 .40** .30 .26 -.03 .39 .23 .41** .31 .36* — 53*** -.24 -.05 .18 .09 -.14 .05 -.30
-.22 .03 -.27 -.55 -.12 -.46 .69 2.62 .98 .46 .75 .17 1.48 .61 .16 .69 .60 .42 -.80 -.40 -.04 .27 .12 -.44 .16 -.42
Total populations of birds housed. Restricted populations: survivors that laid at least 20% in each of three test periods (141-273, 274-385 and 386-497 days of age) and had egg quality recorded at 240 days. Populations on egg production test were vaccinated for MD on the day of hatch. *P fi .10; ** P =s .05; *** P s .01 fEstimate not available because of a negative variance component.
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Total mortality MD incidence in egg production tests in MD challenge 141-497 days of age 141-273 days of age tests Normal Binomial Binomial Normal Normal Binomial scale scale scale scale scale Year Strain scale .10 ± .09 .05 ± .04 .17 ± .14 .05 ± .04 .98 ± .31 .37 ± .12 1970 4 .27 ± .12 .15 ± .06 .15 ± .10 .07 ± .05 .23 ± .13 .11 ± .06 8 .03 ± .13 .01 ± .03 .38 ± .36 .05 ± .04 .85 ± .33 .30 ± .11 4 1971 .00 ± .11 .00 ± .03 .45 ± .24 .15 ± .08 8 .00 ± .21 .00 ± .03 .92 ± .22 .33 ± .08 4 1970, 1971 * * * * .30 ± .12 .12 ± .05 8 * * * * *Heritability estimates for the two years were not combined because the birds in the egg production test were not vaccinated against MD in 1970 but were vaccinated in 1971.
M A K E R ' S DISEASE VACCINATION
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The average genetic relationship within sire the birds more resistant against MD also have families (each family being a mixture of full better general livability in the laying house. and half sisters) used in the calculation of This relationship was more strongly exthe between sires heritability varied in the pressed in strain 8 than in strain 4 and does tested populations from .268, for strain 8 in not seem to have been changed by MD the 1970 challenge test, to .296 for strain 4 vaccination of the 1971 populations on the in the 1971 challenge test. The binomial and egg production test. In the strains tested, MD normal scale heritabilities of MD incidence resistance was generally positively correlated in the injection challenge tests and of the with the population index (hen-housed egg total laying house mortality in the egg pro- production) which indirectly includes livduction tests are shown in Table 2. In the ability. challenge tests, the average normal scale For the rest of the production characters heritability (strains and years combined) of studied, the correlation coefficients estimated MD incidence was .61. This heritability is from the 1970 data (Table 3), in which the similar to the estimate of realized family pullets on the egg production test were not heritability of MD resistance reported by vaccinated against MD, are rather erratic and Friars et al. (1972) but it is higher than there is little consistency between correlaestimates obtained by other authors (Lush tions obtained for the same characters by et al., 1948; Robertson and Lerner, 1949; Von the two methods used or between correlations Krosigk et al., 1972). The estimates of heri- estimated for the two strains. On the other tability for the laying house mortality ranged hand, the estimates obtained in the next year, between 0 and .38 (average .11) and are using data on MD resistance from the 1971 comparable to estimates compiled by Kinney MD challenge test and data on production (1969). Three out of four estimates of heri- traits from birds vaccinated against MD, show tability of laying house mortality in the 1971 a more consistent picture (Table 3). They vaccinated populations are lower than the indicate that birds genetically resistant against comparable estimates in the 1970 non-vacci- MD have a lower body weight, have the nated populations. However, the magnitude genetic potential to mature sexually earlier of standard errors of these estimates does and to lay eggs at a higher rate. There seems not permit definite conclusions about these to be a negative genetic correlation between differences. MD resistance and early egg weight of vacCorrelations between resistance to MD (the cinated birds (the higher the MD resistance proportion of birds which did not develop the lower the egg weight). Little genetic gross lesions typical of MD in the challenge relationship, if any, is indicated by the results test) and production characters (measured in between the ability of birds to resist challenge the egg production tests) are given in Table by the MD virus and any of the other three 3. Both the rank correlations of sire family egg quality characters measured. means and the correlations estimated from The results suggest that vaccination against analysis of variance and covariance of dam MD may have influenced the magnitude and family averages within sires shown in the the direction of some genetic correlations table, express genetic relationship between between MD resistance and production charMD resistance and the production characters acters. However, since the effects of MD measured. The correlations describing the vaccination of the birds in the egg production part-whole relationship between MD resis- test were confounded with the effects of year tance and short-term as well as long-term and generation it is only possible to suggest laying house livability indicate that in general that the effect of vaccination on genetic
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GAVORA, GRUNDER, SPENCER, GOWE, ROBERTSON AND SPECKMANN
be advisable to vaccinate commercial populations under selection for high growth rate. On the other hand, the results of this study indicate that existence of positive genetic correlations between resistance to MD and egg production rate of vaccinated birds can be expected to prevent a decrease in MD resistance of vaccinated populations under continuous selection for high egg production. Hence, in such populations a deterioration of the effectiveness of vaccination, due to a decrease in genetic resistance, should not be anticipated. ACKNOWLEDGEMENTS The authors are indebted to Messrs. R. A. Lacroix, P. Apedaile, J. Dickie and E. Moreau and to Mrs. D. Croswell for their technical assistance and to Mr. M. Zawalsky for his help in processing the experimental data. REFERENCES Becker, W. A., 1964. Heritability of a response to an environmental change in chickens. Genetics, 50: 783-788. Friars, G. W., J. R. Chambers, A. Kennedy and A. D. Smith, 1972. Selection for resistance to Marek's disease in conjunction with other economic traits in chickens. Avian Diseases, 16: 2-10. Gowe, R. S., 1970. Long term selection for egg production in two strains of chickens. 19th Annual Breeders Roundtable, KansasCity, Missouri, U.S.A. Gowe, R. S., A. Robertson and B. D. H. Latter, 1959. Environment and poultry breeding problems 5. The design of poultry control strains. Poultry Sci. 38:462-471. Gowe, R. S., W. E. Lentz and J. H. Strain, 1973. Long-term selection for egg production in several strains of White Leghorns: Performance of selected and control strains including genetic parameters of two control strains. 4th European Poultry Conference, London, England: 225-245. Grunder, A. A., T. K. Jeffers, J. L. Spencer, A. Robertson and G. W. Speckmann, 1972. Resistance of strains of chickens to Marek's disease. Can. J. Animal Sci. 52: 1-10. Grunder, A. A., J. L. Spencer, A. Robertson, G. W. Speckmann and R. S. Gowe, 1974. Resistance to Marek's disease observed among sire families
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variance should be tested further. The genetic correlations estimated in MD vaccinated populations are in general agreement with those reported by Von Krosigk et al. (1972), who used MD susceptibility rather than MD resistance in their studies and found it to be positively correlated with age at sexual maturity and with total laying house mortality, and negatively correlated with egg production. The observed tendency of the birds with lower body weight to be more resistant to MD agrees with the findings of Han and Smyth (1972), and Friars et al. (1972). There is also general agreement between the results of the present study and correlations between incidence of MD and production traits found by Grunder et al. (1974), who analyzed other data from the same strains. The negative genetic correlation between MD resistance and egg weight suggested by the results may lead to a decrease in genetic resistance of vaccinated populations. This would occur if in a multitrait selection program, selection for high egg weight was emphasized. However, in practice the selection for egg weight is usually not emphasized but is restricted and is aimed mainly towards maintaining a desired egg size. As mentioned earlier, genetic resistance plays a significant role in livability of populations vaccinated for MD (Spencer et al., 1972). On the other hand, vaccination can be expected to reduce the effects of natural selection for resistance to MD. Thus, the fate of genetic resistance to MD in vaccinated populations would largely depend on the genetic correlation between resistance to MD and the trait (traits) under selection. For example, resistance to MD in populations under selection for rapid growth may decrease because of a negative genetic correlation between resistance to MD and body weight as observed in this and other studies (Han and Smyth, 1972; Friars et al, 1972). This may lead to a decrease in the effectiveness of vaccination. Therefore, it may not
M A R E K ' S DISEASE VACCINATION
vaccination with herpesvirus of turkeys (HVT) on horizontal spread of Marek's disease herpesvirus. Avian Diseases, 15: 391-397. Robertson, A., and I. M. Lerner, 1949. The heritability of all-or-none traits: viability in poultry. Genetics, 34: 395-411. Spencer, J. L., A. A. Grunder, A. Robertson and G. W. Speckmann, 1972. Attenuated Marek's disease herpesvirus: Protection conferred on strains of chickens varying in genetic resistance. Avian Diseases, 16: 94-107. Von Krosigk, C. M., C. F. McClary, E. Vielitz and D. V. Zander, 1972. Selection for resistance to Marek's disease and its expected effects on other important traits in White Leghorn strain crosses. Avian Diseases, 16: 11-19.
NEWS AND NOTES (Continued from page 885) Assembly of the Nova Scotia Agricultural College. The scholarship is given each year to a student with a "specific interest in poultry." Miss Butler completed the first year of the Technician Course in Animal Science, and has been accepted for the first year of the Biology Laboratory Technology Course.
ment, Hubbard Farms is the first poultry breeder to receive this highest presidential export award. In making the presentation, Secretary of Agriculture Earl Butz noted the award was given for excellent achievement in export sales. Butz said Hubbard's creativity in opening new markets and consolidating its position in others, enabled it to capture an estimated 21 percent of the world market for poultry meat breeding stock.
OIL CHEMISTS' CONFERENCE The 1974 Summer Conference on the Analysis of Lipids and Lipoproteins, sponsored by the American Oil Chemists' Society will be held June 12-15, at the Sheraton Park Hotel, Washington, D.C. Dr. E. G. Perkins, Department of Food Science, Burnsides Research Laboratory, University of Illinois, Urbana, is Conference Chairman. The fees are: A.O.C.S. members—$125.00 ($100.00 if prepaid), Nonmembers—$155.00 ($130.00 if prepaid), and Students—$70.00 ($50.00 if prepaid). For further information contact: 1974 A.O.C.S. Lipids Conference, American Oil Chemists' Society, 508 South Sixth Street, Champaign, Illinois 61820. HUBBARD NOTES Hubbard Farms, international poultry breeding firm, was the recipient of the Presidential "E Star" award. In recognition of continued superior export achieve-
CAMPBELL SOUP NOTES Dr. Richard H. Forsythe has joined The Institute for Food Research, Campbell Soup Company, as Vice President—Basic Research. He succeeds Dr. E. J. Briskey who recently was elected Vice President— Technical Administration. In his new post Dr. Forsythe will direct the Company's overall basic research program including the physiochemical, microbiological, biochemical, and nutritional characteristics of foods and their ingredients. Other investigations conducted by the Institute, which was established in 1966, deal with research techniques, and improvements in manufacturing processes and food products. The Campbell Institute for Food Research is headed by Dr. Carl H. Krieger, who also is Vice President— Product Research of the parent Campbell Soup Company. Dr. Forsythe, a native of Cass County, Iowa,
(Continued on page 926)
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and inbred lines. British Poultry Sci. (in press) Han, P. F.-S., and J. R. Smyth, Jr., 1972. The influence of growth rate on the development of Marek's disease in chickens. Poultry Sci. 51: 975-985. Hutt, F. B., and R. K. Cole, 1947. Genetic control of lymphomatosis in the fowl. Science, 106: 379-384. Kendall, M. G., 1962. Rank Correlation Methods. Hafner Publ. Co., New York. Kinney,T.B., 1969. A summary of reported estimates of heritabilities and of genetic and phenotypic correlations for traits of chickens. Agriculture Handbook No. 363, Agricultural Research Service, U.S.D.A., Washington, D.C., U.S.A. Lush, J. L., W. F. Lamoreaux and L. N. Hazel, 1948. The heritability of resistance to death in the fowl. Poultry Sci. 27: 375-388. Purchase, H. G., and W. Okazaki, 1971. Effects of
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