Heat stress (
HS
) is a major problem in poultry business which affects chickens' performance and may trigger large economic losses. This study intends to analyze the impact of HS on broiler chickens' performance compared with those under normal condition. A literature search was performed on PubMed, Web of Science, and Cochrane Library for studies published in English up to January 17, 2020. Outcomes of body weight gain (
BWG
), feed intake (
FI
), feed conversion ratio (
FCR
), and mortality were calculated by weighted difference (
WMD
) or odds ratio (
OR
) with 95% confidence interval (
CI
). A total of 12 studies with 470 broiler chickens were included. HS significantly decreased FI (11 trials: WMD = −97.95, 95% CI: −141.70, −54.20) and BWG (7 trials: WMD = −151.40, 95% CI: −198.59, −104.21) and significantly increased FCR (9 trials: WMD = 0.17, 95% CI: 0.04, 0.29) and mortality (8 trials: OR = 3.74, 95% CI: 1.39, 10.12) compared with the control. In conclusion, HS significantly affected broiler chickens' BWG, FI, FCR, and mortality, indicating the importance to control housing temperature to avoid unnecessary costs.
A semi‐nested polymerase chain reaction (snPCR) assay was developed for the rapid detection of resistant/susceptible BF haplotypes to Marek’s disease (MD) using the cDNA samples from peripheral blood leucocytes, liver, spleen and heart from Xiayan homozygous chickens: A11, C23, D8 and D12 (resistant to MD), A5 and B21 (susceptible to MD). The snPCR was utilized to span alternative splicing‐out of the sequence encoding the second segment of the cytoplasmic part of the mature BF molecules (exon 7). This alternative exon 7 splice variant was detected in BF*A5 and BF*B21 (susceptible to MD), but not in the MD‐resistant BF*A11, BF*C23, BF*D8 and BF*D12 haplotypes, suggesting a potential role of exon 7 for the detection of resistant/susceptible BF haplotypes to MD.
1. The aim was to analyse the variability of the BLB2/BF2 genes of Xiayan chickens to identify homozygous birds with resistance or susceptibility to Marek's disease (MD). 2. The experiment used two lines: birds from a common line were divided into Group A (unvaccinated) and Group B (vaccinated with herpesvirus of turkeys (HVT)); and birds from an MD-resistant line were divided into Group C (unvaccinated) and Group D (vaccinated with HVT). They were challenged intra-abdominally with Marek's disease virus (MDV) and genomic DNA extracted from peripheral blood lymphocytes so that polymorphism of the BLB2/BF2 genes could be analysed using polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP) and nucleotide sequence analysis. 3. A 374-bp fragment of the BLB2 gene was amplified from the samples and, after digesting with restriction enzymes Alu I, Cai I, Cfr I, Hin1 I, Hinf I and Rsa I for RFLP analysis, the 6 electrophoretic patterns were analysed. Seven homozygous genotypes were found and used tentatively to identify alleles of the BLB2 gene. 4. A 765-bp fragment of the BF2 gene was amplified from the 7 samples for cloning and sequencing. 5. Six homozygous birds were confirmed from the sequenced BLB2/BF2 gene. Four birds were resistant to MD. Three birds had identical nucleotide sequences and were highly homologous with MHC haplotype B⁶, which is MD resistant. One bird had high homology with the highly MD-resistant B²¹ haplotype, and two birds were susceptible and highly homologous to the B¹⁹ haplotype, which is highly MD susceptible.
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