Heat stress: a major threat to ruminant reproduction and mitigating strategies.

Stress is an external event or condition that puts pressure on a biological system. Heat stress is defined as the combination of internal and external factors acting on an animal to cause an increase in body temperature and elicit a physiological response. Heat stress is a set of conditions caused by overexposure to or overexertion at excess ambient temperature and leads to the inability of animals to dissipate enough heat to sustain homeostasis. Heat exhaustion, heat stroke, and cramps are among the symptoms. For the majority of mammalian species, including ruminants, heat stress has a negative impact on physiological, reproductive, and nutritional requirements. Reproductive functions, including the male and female reproductive systems, are negatively affected by heat stress. It decreases libido and spermatogenic activity in males and negatively affects follicle development, oogenesis, oocyte maturation, fertilization, implantation, and embryo-fetal development in females. These effects lead to a decrease in the rate of reproduction and financial losses for the livestock industry. Understanding the impact of heat stress on reproductive tissues will aid in the development of strategies for preventing heat stress and improving reproductive functions. Modification of the microenvironment, nutritional control, genetic development of heat-tolerant breeds, hormonal treatment, estrous synchronization, timed artificial insemination, and embryo transfer are among the strategies used to reduce the detrimental effects of heat stress on reproduction. These strategies may also increase the likelihood of establishing pregnancy in farm animals.

The Impact of Heat Stress on Immune Status of Dairy Cattle and Strategies to Ameliorate the Negative Effects.

Heat stress (HS) is well known to influence animal health and livestock productivity negatively. Heat stress is a multi-billion-dollar global problem. It impairs animal performance during summer when animals are exposed to high ambient temperatures, direct and indirect solar radiations, and humidity. While significant developments have been achieved over the last few decades to mitigate the negative impact of HS, such as physical modification of the environment to protect the animals from direct heat, HS remains a significant challenge for the dairy industry compromising dairy cattle health and welfare. In such a scenario, it is essential to have a thorough understanding of how the immune system of dairy cattle responds to HS and identify the variable responses among the animals. This understanding could help to identify heat-resilient dairy animals for breeding and may lead to the development of climate resilient breeds in the future to support sustainable dairy cattle production. There are sufficient data demonstrating the impact of increased temperature and humidity on endocrine responses to HS in dairy cattle, especially changes in concentration of hormones like prolactin and cortisol, which also provide an indication of the likely im-pact on the immune system. In this paper, we review the recent research on the impact of HS on immunity of calves during early life to adult lactating and dry cows. Additionally, different strategies for amelioration of negative effects of HS have been presented.

Complete genome and phylogenetic analysis of bovine papillomavirus type 15 in Southern Xinjiang dairy cow.

BACKGROUND: Bovine papilloma is a neoplastic disease caused by bovine papillomaviruses (BPVs), which were recently divided into 5 genera and at least 24 genotypes. OBJECTIVES: The complete genome sequence of BPV type 15 (BPV Aks-02), a novel putative BPV type from skin samples from infected cows in Southern Xinjiang China, was determined by collecting warty lesions, followed by DNA extraction and amplicon sequencing. METHODS: DNA was analyzed initially by polymerase chain reaction (PCR) using the degenerate primers FAP59 and FAP64. The complete genome sequences of the BPV Aks-02 were amplified by PCR using the amplification primers and sequencing primers. Sequence analysis and phylogenetic analysis were performed using bio-informatic software. RESULTS: The nucleotide sequence of the L1 open reading frame (ORF) of BPV Aks-02 was 75% identity to the L1 ORF of BPV-9 reference strain from GenBank. The complete genome consisted of 7,189 base pairs (G + C content of 42.50%) that encoded 5 early (E8, E7, E1, E2, and E4) and 2 late (L1 and L2) genes. The E7 protein contained a consensus CX2CX29CX2C zinc-binding domain and a LxCxE motif. Among the different members of this group, the percentages of the complete genome and ORFs (including 5 early and 2 late ORFs) sequence identity of BPV Aks-02 were closer to the genus Xipapillomavirus 1 of the Xipapillomavirus genus. Phylogenetic analysis and sequence similarities based on the L1 ORF of BPV Aks-02 revealed the same cluster. CONCLUSIONS: The results suggest that BPV type (BPV Aks-02) clustered with members of the Xipapillomavirus genus as BPV 15 and were closely related to Xipapillomavirus 1.

A short-term supranutritional vitamin E supplementation alleviated respiratory alkalosis but did not reduce oxidative stress in heat stressed pigs.

OBJECTIVE: Heat stress (HS) triggers oxidative stress and respiratory alkalosis in pigs. The objective of this experiment was to study whether a short-term supranutritional amount of dietary vitamin E (VE) can mitigate oxidative stress and respiratory alkalosis in heat-stressed pigs. METHODS: A total of 24 pigs were given either a control diet (17 IU/kg VE) or a high VE (200 IU/kg VE; HiVE) diet for 14 d, then exposed to thermoneutral (TN; 20°C, 45% humidity) or HS (35°C, 35% to 45% humidity, 8 h daily) conditions for 7 d. Respiration rate and rectal temperature were measured three times daily during the thermal exposure. Blood gas variables and oxidative stress markers were studied in blood samples collected on d 7. RESULTS: Although HiVE diet did not affect the elevated rectal temperature or respiration rate observed during HS, it alleviated (all p<0.05 for diet×temperature) the loss of blood CO2 partial pressure and bicarbonate, as well as the increase in blood pH in the heat-stressed pigs. The HS reduced (p = 0.003) plasma biological antioxidant potential (BAP) and tended to increase (p = 0.067) advanced oxidized protein products (AOPP) in the heat-stressed pigs, suggesting HS triggers oxidative stress. The HiVE diet did not affect plasma BAP or AOPP. Only under TN conditions the HiVE diet reduced the plasma reactive oxygen metabolites (p<0.05 for diet× temperature). CONCLUSION: A short-term supplementation with 200 IU/kg VE partially alleviated respiratory alkalosis but did not reduce oxidative stress in heat-stressed pigs.