K.E. Nestor*, Y.M. Saif +, J. Zhu+, and D.O. Noble*
*Department of Animal Sciences and +Food Animal Health Research Program
A line (F) of turkeys was developed from a randombred control population (RBC2) by selecting for increased 16-week body weight. The F line was more susceptible to Pasteurella multocida (the organism that causes fowl cholera) and Newcastle disease virus. The changes in disease resistance cannot be explained by changes in major histocompatibility (MHC) haplotypes of the F line although the MHC genotypes were shown to differ in resistance to both organisms. Two commercial sire lines of similar growth rate as the F line had similar mortality following challenge with P. multocida indicating that the genetic increase in body weight per se was associated with the increased susceptibility. A line selected long-term for increased egg production did not differ from its randombred control when challenged with washed P. multocida and Newcastle disease virus.
Genetic improvement in disease resistance of turkeys would be valuable to the commercial turkey industry. Measures are available for control, prevention, and treatment of a number of diseases. However, costs of treatments and vaccination and losses in performance of birds due to disease are substantial. Development of genetic resistance to diseases would allow vaccination with less virulent strains and would assist turkeys in overcoming pathogens.
Several experimental turkey lines were naturally exposed to fowl cholera (confirmed by isolations of P. multocida) and erysipelas (confirmed by isolations of Erysipelas rhusiopathiae). The experimental lines of turkeys included a line (E) selected long-term for increased egg production, a non-selected randombred control population (RBC1) which served as the base population for E, a line (F) selected long-term for increased 16-week body weight, and another randombred control (RBC2) which was the base population of F. The mortality occurring after the fowl cholera outbreak in males was 12, 25, 21, and 28% in the RBC1, E, RBC2, and F lines, respectively (Saif et al., 1984). In the erysipelas outbreak which occurred in females, the respective mortalities were 0, 0, 2, and 12%. Since natural outbreaks of diseases are usually a combination of several factors, a series of experiments were conducted to determine if the above lines differed in resistance to P. multocida under carefully controlled conditions and, if so, what physiological changes were responsible for the differences. In addition, the lines were challenged with a virulent virus (Newcastle disease virus) to determine whether the lines also differed in susceptibility to a virus.
Three preliminary challenge trials were run using a small number of birds to test the response of the E and RBC1 lines to unwashed P. multocida under carefully controlled conditions. In each trial, individuals were challenged with different doses and the age at challenge differed so the results of the trials could not be combined. In Trial 1, mortality following challenge with 1.2 X 107 bacteria at 6 weeks of age was 67% in the E line and 32% in the RBC1 line (P < .05) (Sharaf et al., 1988a). In Trials 2 and 3, the line differences were of similar magnitude but not significant. Sharaf et al. (1988b) observed that the RBC1 line had greater antibody response to P. multocida and Newcastle disease virus when vaccinated singularly or in combination. The above results suggest that the E line may be more susceptible to P. multocida. However, later trials using a larger number of birds indicated the E line was not more susceptible to P. multocida than the RBC1 line when the organism was washed to remove culture filtrates (Table 1; Sacco et al., 1991). It is possible that the E line is more susceptible than the RBC1 line to the cellular products and toxins produced by P. multocida. When the E and RBC1 lines were challenged with a virulent strain of Newcastle disease virus (Texas GB strain), mortality was not different between the lines (Table 2; Tsai et al. 1992), indicating that the lines did not differ in resistance to the organism. There was no sex difference in mortality after challenge with P. multocida (Table 1) or Newcastle disease virus (Table 2).
| Table 1. Mortality by genetic line and sex for turkeys challenged with Pasteurella multocida. | ||
| Type of turkeys1 | n | Mortality (%) |
| Line | ||
| E | 164 | 45.7a |
| RBC1 | 165 | 43.6a |
| F | 161 | 72.1b |
| RBC2 | 165 | 43.6a |
| Sex | ||
| Male | 346 | 54.3 |
| Female | 309 | 47.6 |
| 1 RBC1 = randombred control population 1; E =
subline of RBC1 selected for increased egg production;
RBC2 = randombred control population 2; F = subline of
RBC2 selected for increased 16-week body weight.
a,b Line means within a column followed by different lower-case superscripts are significantly different (P < 0.01). Differences due to sex were not significant. | ||
| Table 2. Mortality by genetic line and sex for turkeys infected with Newcastle disease virus. | ||
| Type of turkey1 | n | Mortality (%) |
| Line | ||
| E | 194 | 17.5a |
| RBC1 | 196 | 18.4a |
| F | 194 | 32.5b |
| RBC2 | 196 | 15.8a |
| Sex | ||
| Male | 376 | 20.7 |
| Female | 404 | 23.8 |
| Total | 780 | 22.3 |
| 1 RBC1 = randombred control population 1; E =
subline of RBC1 selected for increased egg production;
RBC2 = randombred control population 2; F = subline of
RBC2 selected for increased 16-week body weight.
a,b Values followed by different lower-case superscripts are significantly different (P < 0.01). Difference due to sex was not significant. | ||
The F line was more susceptible to P. multocida (1.2 X 107 washed bacteria per bird at 6 weeks of age) than the RBC2 line (Table 1; Sacco et al., 1991). The line difference in mortality (72 vs 44%) was highly significant. The secondary antibody response to P. multocida was lower in the F line than in the RBC2 line but there was no line difference in primary antibody response (Sacco et al., 1994), again suggesting a line difference in susceptibility.
The F line is similar in growth rate to commercial sire lines. In order to determine whether the susceptibility to P. multocida is associated with to genetic increases in body weight per se, samples of the F, RBC2, and sire lines from two commercial turkey breeders were challenged with washed P. multocida. Mortality was similar among the three large-bodied lines (F and two commercial sire lines) and higher than that of the RBC2 line (Table 3). These results suggest that selection for growth rate may increase the susceptibility to P. multocida.
| Table 3. Percentage mortality of turkeys following challenge with Pasteurella multocida at 6 weeks of age.1 | ||||
| Line2 | ||||
| Trial | RBC2 | F | A | B |
| 1 | 28.0 (253)b | 53.8 (26)a | 54.2 (24)a | 51.9 (27)a |
| 2 | 23.0 (26)b | 76.9 (26)a | 61.5 (26)a | 56.0 (25)a |
| Both | 25.5 (51)b | 65.3 (52)a | 58.0 (50)a | 53.8 (52)a |
| 1 Birds were injected subcutaneously in the back of the
neck with 1.2 X 107 bacteria of a field isolate (capsular
serotype A, somatic serotype 3,4) of P. multocida.
2 RBC2 = randombred control population; F = subline of RBC2 selected 28 generations for increased 16-week BW; A = primary breeding sire line from Breeder A; and B = primary breeding sire line from Breeder B. 3 Number of birds. a,b Means within a row with no common superscript are different (P < 0.05). | ||||
The F line was more susceptible to challenge with Newcastle disease virus than the RBC2 line (Table 2; Tsai et al., 1992). Mortality of the F line was twice that of the RBC2 line when challenged with the virulent Texas GB strain of the Newcastle disease virus.
The major histocompatibility complex (MHC) has been shown to be involved in resistance or susceptibility to several diseases in chickens, including Newcastle disease virus (Dunnington et al. 1992) and P. multocida (Lamont et al., 1987). The MHC is a gene family encoding a group of glycoproteins involved in some important aspects of the immune response.
Four haplotypes of the turkey MHC Class II genes were discovered in the RBC1 and RBC2 lines by Emara et al. (1992) using molecular biology methods. The haplotypes were characterized to have allelic specificities by Emara et al. (1993). Zhu et al. (1995) estimated the allelic frequencies of MHC haplotypes in the RBC1, RBC2, E, and F lines (Table 4). In addition to the four haplotypes (A, B, C, and D)
| Table 4. Haplotype frequencies of the MHC Class II in the four turkey lines. | ||||
| Lines1,2 | ||||
| Haplotypes | RBC1 | E | RBC2 | F |
| (%) | ||||
| A | 13.9 | 29.9 | 34.0 | 29.6 |
| B | 31.3 | 47.9 | 24.3 | 10.2 |
| C | 9.0 | 0 | 1.4 | 8.8 |
| D | 31.9 | 0.4 | 10.4 | 46.8 |
| X | 1.4 | 20.8 | 0 | 0.9 |
| Y | 9.7 | 0 | 0 | 0 |
| Z | 2.8 | 0 | 24.3 | 2.8 |
| R3 | 0 | 1.0 | 5.6 | 0.9 |
| 1 RBC1 = randombred control population (36 males,
36
females); E = subline of RBC1 selected for egg production (72 males, 72 females); RBC2 = random- bred control population (36 males, 36 females); and F = subline of RBC2 selected for 16-week body weight (36 males, 72 females). 2 Haplotype frequencies between four lines (RBC1 vs RBC2, RBC1 vs E, RBC2 vs F, and E vs F) were significantly different (P < 0.01). 3 R = pooled rare haplotypes. | ||||
found by Emara et al. (1992), three additional MHC haplotypes in relative high frequencies (X, Y, and Z) and some rare haplotypes were found. Selection for increased egg production in the E line and increased 16-week body weight in the F line resulted in changes in frequencies of MHC haplotypes, and the changes were generally in opposite directions. Haplotypes A, B, and X increased, whereas Haplotypes C, D, and Y decreased in the E line. In the F line, Haplotypes C and D increased and Haplotypes A, B, and Z decreased.
Four highly inbred, but not congenic, lines carrying Haplotypes A, B, C, or D in homozygous form were developed. The lines were challenged with P. multocida and Newcastle disease virus. The MHC genotypes differed in mortality following challenge with P. multocida (Table 5; Nestor et al., 1996). The BB and DD genotypes had similar and higher mortality than the AA and CC genotypes which had similar mortality. Genotype CC had the highest mortality following challenge with Newcastle disease virus (Table 6; Nestor et al., 1996). Genotype BB had the next highest mortality followed by Genotypes AA and DD which were similar. These results suggest that the MHC influences resistance to P. multocida and Newcastle disease virus. However, the rankings of the genotypes were not the same for both organisms.
The increased susceptibility of the F line to P. multocida and Newcastle disease virus cannot be explained by the observed changes in the frequency of MHC haplotypes in the F line. For P. multocida, one susceptible haplotype (B) decreased while another susceptible haplotype (D) increased in frequency in the F line. One resistant haplotype (A) decreased while the other resistant haplotype (C) increased in frequency in the F line. Likewise, the increased susceptibility of the F line to Newcastle disease virus can not be explained by the observed changes in frequencies of MHC haplotypes.
| Table 5. Mortality of turkeys with different MHC genotypes following challenge with Pasteurella multocida. | |||||||
| MHC genotype | |||||||
| Trials | Variable | AA | BB | CC | DD | RBC21 | F2 |
| 1992 | No. birds | 77 | 76 | 70 | 64 | . . . | 8 |
| % mortality | 3.9y | 11.8x | 8.6xy | 12.5x | . . . | 62.8 | |
| 1993 | No. birds | 38 | 39 | 41 | 38 | 39 | 40 |
| % mortality3 | 31.6cy | 48.7bx | 31.7cy | 52.6bx | 38.5c | 67.5a | |
| Weighted average | % mortality | 13.6y | 24.7x | 16.6y | 26.4x | . . . | 64.2 |
| 1 RBC2 = randombred control line.
2 F = subline of RBC2 selected for increased 16-week BW. 3 Differences among genetic groups were significant (P < 0.004). a-c Means within a row with no common superscript differ significantly (P < 0.05). x,y MHC genotype means within a row with no common superscript differ significantly (P < 0.05). | |||||||
| Table 6. Mortality of turkeys of different MHC genotypes following challenge with Newcastle disease virus. | ||||||
| MHC genotype | ||||||
| Variable | AA | BB | CC | DD | RBC21 | F2 |
| No. birds | 107 | 106 | 71 | 110 | 58 | 60 |
| % mortality | 0.9d | 4.7c | 9.9ab | 0d | 6.9bc | 11.7a |
| 1 RBC2 = randombred control line.
2 F = subline of RBC2 selected for increased 16-week BW. a-d Means within a row with no common superscript differ significantly (P < 0.05). | ||||||
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