Introduction

Climate change, in particular global warming, will affect the health and welfare of farm animals, both directly and indirectly. Effects of global warming include temperature-related illness and death, and also the effect on animals during extreme weather conditions. Indirect effects include pathways that include those, where organisms try to adapt to higher thermal environment. Animals try to adjust to higher ambient temperatures through various means to reduce metabolic heat production. Future climate changes will be variable according to the locations, some model climate projections suggest that precipitation will increase at high latitudes, and will decrease in the tropical and subtropical land regions (IPCC, 2007). Climate changes will also influence crop production, grain yields and further availability of grains as feed for livestock production systems. Heat stress reduces the reproductive performance of laying hens by interrupting egg production. This may be due not only by reduction in feed intake but also by disruption of hormones involved in reproduction (Donoghue et al., 1989). Abiotic and biotic factors contribute to environmental stress. When the extreme changes occur in the environment, it stimulates the body responses to counteract, failing which organism experiences stress (Bijlsma and Loeschcke, 2005; Ajakaiye et al., 2011). When environmental temperature exceeds the limits of thermoneutral zone, core body temperature of poultry/chicken increases. Prolonged heat stress results in dramatic physiological changes in chicken organs. These changes are used as indicators of heat stress (Melesse et al.,2011).

After China and USA, India is the third largest egg producer in the world (FAO, 2014). The poultry development in India has revealed 6-7% growth rate per annum in layers. Poultry inclusive of chicken contributes significantly as meat, for human consumption. Over the years poultry industry in India has contributed approximately US$229 million to the Gross National Product (GNP) (http://www.indianmirror.com/indian-industries/poultry.html, accessed on 12/12/2016).Grain yield is affected by global warming. It is stated that 2-4 Kg of cereals is required to produce 1 Kg of chicken meat. Hence poultry is the preferred species over other farm animals for protein food production. Population growth, rising incomes and urbanization are the driving forces behind poultry sector growth. Growing demand for livestock products will also have a negative impact on environment (FAO, 2006). Occurrence of poultry diseases due to heat stress should be of the prime concern in intensive poultry production. Poultry egg production is most environmentally efficient production system. It is felt that small farms of poultry are better able to adapt to warming (Seo and Mendelsohn, 2006). Poultry houses that do not have appropriate ventilation during extreme hot conditions, results in overheating of sheds, and thus causes heat stress to birds (Akyuz, 2009). Heat stress reduction in the layer sector reduces economic loss (St. Pierre et al., 2003).

To maintain normal body temperature chickens adapt to increased energy requirements or decreased energy requirements in the cold or hot environment, respectively. The nutrient composition of the diet determines the amount of heat produced during metabolism by the bird. This is referred to as heat increment of the diet. Poultry completely depends on dietary sources for all nutrients and the nutrients should be at optimal level in the diet. For each degree rise in temperature between 96-100^oF, a 2-3% loss of feed intake has been reported. As the temperature increases from 60^oF to 96^oF (ambient) the percentage of sensible heat loss decreases from 80% to 20% and evaporative heat loss increases from 20% to 80% (www.ces.ncsu.edu, accessed on October, 2016). In addition to high ambient temperature, relative humidity also plays an important role in bringing out stress in the chickens (Ajakaiye et al., 2011). The economic losses, as calculated in the layer sector are reported as $98.1 million, if the stress due to heat load is reduced, then it has been observed that loss is also reduced to $61million annually (St. Pierre et al., 2003).

The energy obtained from the feed is utilized for maintenance and productive functions. In the process of utilization of energy, heat generated should be dissipated. If the surrounding temperature is less, then the heat dissipation is more. The humidity in the atmosphere influences the heat dissipation process; higher the humidity lower is the heat dissipation. As the relative humidity increases, temperature of the bird’s body increases, which results in decrease in feed intake and less amount of heat is produced. With increase in temperature, production performance decreases (Czarick and Fairchild, 2009). The higher the air speed, the bird loses greater amount of heat. The air movement assists the bird to lose heat by respiratory moisture evaporation and at a lower speed, relative humidity also plays an important role. Under high humid conditions when air velocity is less, the bird suffers from heat stress even at lower day temperature (Simmons et al., 1993). Heat stress alone and in combination with humidity increases the stress on birds and affects performance.

The response of cells or a whole organism to heat shock is extremely rapid, but it takes place slowly. This process involves the synthesis and participation of preformed heat-shock proteins within the cell as well as immediate translation of preformed messenger RNA (mRNA) into heat-shock proteins and immediate transcription of genes encoding heat-shock proteins (Yost et al.,1990). In warm tropical and subtropical regions, poultry when maintained at natural environmental temperatures which bring out changes in molecular, physiological and behavioural aspects that enable chickens to cope with the flux of energy into and out of their tissues at high ambient temperatures (Pawar et al., 2016).

Heat Stress and Laying Performance

Reduction in egg number, egg weight and shell thickness has been reported during heat stress. An interesting finding by Wolfenson et al. (2001) was that the productivity decreases only when hens experienced nocturnal heat stress but not experienced during day time. Hen-day egg production was significantly decreased through all 13 weeks for hens exposed to the constant hot temperature compared with those in the control group (Allahverdi et al., 2013). India’s per capita consumption of chicken meat is 4.2 kg per person and eggs is 60 per person. Poultry and egg proteins are easy to digest, cheaper and easily accessible (poulvet.com/inc/poultry India 2014.pdf, accessed on October, 2016). As the ambient temperature rises above 30^oC, heat stress begins, birds start to pant. Birds reared in cages are more susceptible to heat stress than those reared using deep litter systems. In layers peak production may not be achieved and the eggs produced will be soft shelled and weigh less with poor egg size quality and shell strength (Faria et al., 2001). Chronic heat stress is either categorized as cyclic chronic heat stress which refers to a limited period of heat stress exposure followed by comfortable temperature for the rest of the day or constant chronic heat stress where by the bird is continuously confronted with high ambient temperature.

The physiological, endocrine and productive responses are adversely affected by heat stress (Khan et al., 2012). There is acid-base (Imik et al., 2013), electrolytes imbalance (Borges et al.,2004) and these disturbances are due to increased respiration rate (Renaudeau et al., 2011). When such physiological disturbances take place, it even leads to increased mortality (Sandhu et al.,2012). Increased panting under heat stress conditions leads to decreased blood carbon dioxide levels and higher blood pH (alkalosis) that in turn hampers blood bicarbonate availability for egg shell mineralization. Osmotic change and dehydration are due to the result of water imbalance which in turn affects the cell performance negatively (Sahin et al., 2002).

Heat Stress and Immune Functions

The response to stress is exhibited in many ways and the effect on immune system is dependent on the extent to which one is able to cope up with changes associated with stress. Usually, farm animals under stress adapt themselves to maintain homeostasis of the functions of the body (McEwen and Seeman, 1999). The neuroendocrine system gets stimulated under the effect of stress. The hypothalamic neurons perceive the increases in body temperature and exert an inhibiting influence on cells that are responsible for controlling feed intake. The two major systems are hypothalamic pituitary axis and the sympathetic nervous system. The hormones corticosterone, catecholamines like epinephrine and norepinephrine secreted by the above mentioned systems, act on the immune cells. It is well known that immune cells have receptors for these hormones (El-Lethay et al., 2003). The down regulation of immune response to stress reduces resistance of the body to microbes (Dohms and Metz, 1991). Studies by El-Lethey et al.(2003) in White Leghorns revealed that there are stress resistant and stress susceptible antibody responses. Heterophils, granulocytes in chicken exhibit different functions when stimulated such as phagocytosis (Genovese et al., 2013; 2006), degranulation (He et al., 2005) and produce extracellular traps (Chuammitri et al., 2009). The extracellular traps are formed by decondensed chromatin fibres, contain antimicrobial peptides released by granules of neutrophils (Donis-Maturano et al., 2015) which trap and kill microorganisms. But if this process continues it kills antigen presenting cells such as macrophages and dendritic cells. This is for controlling the inflammatory process (Donis-Maturano et al., 2015).

Corticosterone concentration is responsible for quantitative and qualitative changes in immune functions. The most reported effect of stress is the suppression of immune organs and immune cells (Shini, 2004; Shini et al., 2008a). The hormone whose concentration gets elevated in plasma due to stress is corticosterone, is well documented in birds resulting in increase in the number of heterophils and decrease in the number of lymphocytes thus, favoring higher ratio for heterophils which has been well studied by Shini et al. (2008 a, b; 2009). It is also reported that acute heat stress may enhance immune system (Dhabhar, 2009) function and prepare the immune system for subsequent challenges. The immediate response to stress or stressor is to increase the circulatory level of glucose (Assenmacher, 1973). Elevation in blood glucose level may be attributed to increase in glucocorticoids secretion which plays a major role in glucose metabolism. The decline in blood glucose concentration during heat stress may be due to a decrease in concentration of thyroxine, which is closely associated with energy metabolism during heat stress. Reduction in serum thyroxine is probably due to lower metabolic rate for thermoregulation and to prevent hyperthermia. Chronic stress system may cause immune suppression by involution of immune organs (Bursa of Fabricius, thymus and spleen) (Puvadolpirod and Thaxton, 2000; Shini, 2004; Shini et al., 2008 a, b). Stress with respect to elevated level of corticosterone brings about up regulation of proinflammatory chemokines of both heterophils and lymphocytes. It also significantly up regulates proinflammatory cytokines IL-6 and IL-18. This was due to acute stress experience. Similar results were observed by Shini et al. (2010) as early as 3 h post exposure to stress. Chronic heat stress in 26 week old layer hens resulted in a decrease in antibody titer to sheep red blood cells (Mashalay et al., 2004). Macrophages and heterophils in addition to phagocytic function produce derivatives of oxygen, reactive oxygen species which attack targets along with NADPH oxidase by respiratory burst and kill micro organisms (Lin et al., 1992). Studies by Muir and Craig (1998), Cheng and Jefferson (2008) revealed that laying hens of selected breeds, through genetic selection for egg production or productivity parameters has led to the development of successful technology, resulting in the improved response of the animal to stress. Berthelot-Herault et al. (2003) reported that IgG and IgA levels were higher in layer line (B13) and Leghorn line (L2) compared to another Leghorn line (PAI2) and meat type line (YII) when subjected to infections. It was observed that immune response is different in different layer lines or breeds.

The suppression or decrease in the weight of spleen is contributed to the decrease in the physiological functions of leucocytes. It acts as an important organ for assessing immune suppression (Dietert et al., 1994). Not only the number of immune cells, but their products like cytokines and chemokine’s expression is also affected. Redmond et al. (2011) reported that heterophils from Leghorns expressed higher level of CXCLi2 mRNA than those from Fayoumis. Felver and Gant (2012) reported higher level of heat shock protein HSP70 in the liver of White Leghorn hens (KGB) selected for productivity than the White Leghorn hens selected for higher egg production (DXL).

Heat Stress and Enzyme Activity

Melesse et al. (2011) studied levels of different metabolic enzymes like Lactate dehydrogenase, Creatine kinase, Glutamic pyruvic transaminase etc. in different breeds and he observed that WL-dw (dwarf White Leghorn) was the most heat tolerant one. From all these studies it was inferred that distinct genetic lines respond differently to stressors. Heat stress has detrimental effect on egg production parameters (Rozenbiom et al., 2007; Faria et al., 2001), which has been shown to be not related to feed intake (Smith and Oliver, 1972). All studies indicate that high temperatures reduce the efficiency of feed energy utilization for productive purposes. Layers not only eat less, even their production is less at high temperatures, but also produce less heat per unit of intake, especially at temperatures above 30°C even when exposed to three days (Attia et al., 2016).

Increase in plasma concentration of enzymes lactate dehydrogenase, glutamic oxaloacetic transaminase and creatine kinase reflect tissue damage, in liver (Mikami et al., 2004) and muscle (Sandercock et al., 2006). In layers, it is reported that acute heat stress does not lead to tissue damage (Lin et al., 2006). The damage is caused by oxidative injuries. The same author reported an increase in plasma MDA level as an indicator of lipid peroxidation. Oxidative damage may be minimised by antioxidant defence mechanisms that protect the cell against cellular oxidants and repair systems that prevent the accumulation of oxidatively damaged molecules. Antioxidant enzymes (CAT, SOD, GPx) play a vital role in protecting cells or tissues from harmful effects of Reactive Oxygen Species. Activities of different enzymes in plasma like glutamic pyruvic transaminase (GPT), glutamic oxalo acetate transaminase (GOT), creatine kinase (CK) and lactate dehydrogenase (LDH) when estimated in chickens (layers) belonging to four different genotypes mainly dwarf White Leghorn, White Leghorn with improved feed efficiency, New Hampshire Lohmann White and Lohmann Brown; (the control group was maintained at 18-20^oC and experimental groups were maintained at 30-32^oC), control groups of the respective genotypes did not exhibit any significant difference with respect to activity of enzymes when compared between the groups. However, under high temperature conditions, the activities of the different enzymes were significantly different from their respective control groups of chicken. In experiments conducted by Khan and Sardar (2005) in Layers, namely Desi Fayoumi and Commercial White Leghorn revealed that when these birds were reared under high ambient temperatures, egg production, feed consumption, egg weight and egg shell thickness decreased. The blood levels of enzymes alkaline phosphatase, glutamate pyruvate transaminase and glutamate oxalate transaminases increased. In contrast, the ascorbic acid levels decreased. It has been reported by Cheng et al. (1990), Chakraborty and Sadhu (1983), Takeda and Hare (1985), the increase in the level/activities of the enzymes is due to leakage of enzymes under stressful conditions (Bhatti et al., 2003; Bhatti and Dil, 2005).

Heat Stress and Gut

When subjected to heat stress the tight junctions between epithelial cells of the intestine become leaky, which has an effect on absorption of nutrients and pathological bacteria can go in to systemic circulation leading to inflammatory response. One of the main toxin is the lipo-polysaccharide which acts as an endotoxin and elicits immune response after heat stress (Slawinska et al., 2016).It has been observed that expression of ghrelin gene in hypothalamus of HY-line layers was upregulated whereas, those of orexigenic genes was not affected. Central (hypothalamus) and peripheral (duodenum and jejunum) CCK mRNA levels in heat-exposed laying hens decreased intestine mobility and, hence, a lower passage rate, which allowed intestine enzymes more time to digest nutrients (Song et al., 2012). Results of the studies of the same authors indicated that some hypothalamic and gastrointestinal tract peptides were involved in the appetite regulation in heat-exposed laying hens. In addition to this, heat exposure resulted in a significant decrease in body weight gain, feed intake, laying rate, average egg mass, egg production and shell thickness. Similar results were reported by Anjum et al. (2014).

Heat Stress and Egg Shell Quality

Heat stress affects biological defence mechanisms including immunological and metabolic functions. Higher ambient temperature can have negative impact on the productivity of birds. It has been reported in heat stressed commercial layers that when they have been exposed to high temperature at 36^oC, plasma calcium concentration decreased and pH increased. Layers exposed to high ambient temperature results in decreased egg production and quality (Allahverdi et al.,2013; Aberra et al., 2010). The calcium binding protein calbindin localization in intestinal segments and egg shell gland is decreased when exposed to high temperature (Ebeid et al., 2012). During summer, stress can result in smaller eggs and reduced shell quality via a number of physiological processes occurring within the bird (Usayran et al., 2001; Allahverdi et al., 2009). Heat stress also reduces the activity of carbonic anhydrase, an enzyme which results in the formation of bicarbonate which contributes carbonate to the formation of egg shell (Balnave and Muherreza, 1997). Albumen height and Haugh units decrease with storage time and this decrease occurs more quickly at higher temperatures.

Heat Stress Hormones and Reproduction

It is suggested that reduced feed consumption may account for impairment in reproduction. It has been suggested that heat stress may modulate the activity of hypothalamus and pituitary (Braganza and Wilson, 1978; Jeronen et al., 1978). It has been reported by Johnson (1981) in laying hens, that heat stress decreased circulatory prolactin and gonadotropins, which affect the reproductive function. Studies in White Leg Horn, layers revealed that when birds were subjected to heat stress 42±3^oC for 15d, egg production dropped by 20% and there was a decrease in egg weight and follicles with a concomitant decrease in the expression level of cytochrome P 450, 17α hydroxylase enzymes. Further, non significant decrease in the expression level of cytochrome P 450 aromatase and plasma estradiol level has also been reported (Rozenboim et al., 2007). But, the high ambient temperature did not affect yolk or plasma concentration of corticosterone. Similarly Hester et al. (1996) reported difference in concentration of plasma corticosterone between control and heat stress treated groups. Heat stress reduces luteinizing hormone and hypothalamic gonadotropin – releasing hormone levels in Leghorns due to increased prolactin levels, which in turn causes ovarian regression (Donoghue et al., 1989; Rozenboim et al., 1993; You et al., 1995).

Thyroid hormones play an important role in regulating metabolic and thermogenesis functions in chicken (Lam and Harvey, 1990; He et al., 2000; Tao et al., 2006).The level of thyroxine (T₃) in blood plasma was reduced in all the heat stressed different layer genotypes. Similar results have been observed in layers (Decuypere and Kahn, 1988; Maak et al., 2003; Tao et al., 2006; Melesse et al., 2011). Circulatory levels of T₃ have been linked to the size of the bird. Small size chickens produce less T₃ (Tixier-Boichard et al., 1990; Zeman et al., 1996). Higher level of plasma T₃ has been attributed to decreased ability to lose heat or increased heat production. Thyroid hormones viz. thyroxin and triodothyronine provide a major mechanism of acclimatization. The role of thyroid gland hormone in adaptation to heat stress is related to the role of hormones in regulation of metabolic rate of birds (Mc Naff, 1988). Corticotrophin Releasing Hormone from the hypothalamus influences the decreased production of T₄ and T₃ and it has been used as an indicator of stress in laying birds (Melesse et al., 2011).

A decrease in egg production may also be due to decrease in uptake of gut calcium or enzyme production related to maintenance of calcium homeostasis (Franco-Jimenez et al., 2007). The level of circulatory T₃ denotes or is related to egg productivity and they are directly related to each other (Elnagar et al., 2010). Klandorf and Harvey (1985) reported that reduced feed intake reduces circulatory T₃ concentrations, but, reports of Mack et al. (2013) stated that, the decrease in T₃ concentration was irrespective of feed intake.

The effect of hot environment has been found to vary among different breeds of chicken (Deeb and Cahaner, 2002; Melesse et al., 2011; Mashaly et al., 2004). Some have reported that acute heat stress does not have effect on plasma T₃ or T₄ concentration (Bowen and Washburn, 1985; May et al., 1986). The higher level of circulatory T₃ causes increased metabolic rate and reduced thermotolerance (Bowen and Washburn, 1985). This is associated with changes in sizes of thyroid gland and its secretion. Heat stress caused hypothyroid effect, decreased plasma progesterone concentration and increased plasma prolactin concentration in Hy-Line laying hens (Elnagar et al., 2010). Estrogen, T₃ and T₃/T₄ ratio was observed to decrease under heat stressed conditions. Decrease in thyroid hormone activity has been reported under heat stress conditions (Sinurat et al., 1987).

The regulatory mechanisms for the reduced reproductive efficiency in the hens when subjected to high ambient temperature is modulated at the level of hypothalamus and pituitary (Braganza and Wilson, 1978 a,b; Jeronen et al., 1978). When ovaries are affected by heat stress, functions of granulosa and theca cells are delayed and hence steroidogenesis. When reproductive hormones are affected, it leads to decrease in reproductive efficiency (Rozenboim, 2007). In Vitro study by Hrabia et al. (2004) indicated that prolactin affects steriodogenesis by ovarian follicle and type of follicular layer. The change in ovarian steroid production is due to heat stress which is due to decreased ovarian blood flow in laying hens (Wolfenson et al., 1981). Stress has been shown to affect the pathway for PRL, FSH and LH in laying hens. Circulatory plasma prolactin and gonadotropin levels decline (Johnson, 1981). Hens subjected to acute thermal stress had decreased circulating LH levels and was attributed to reduced LH releasing ability of the hypothalamus (Donoghue et al., 1989).

The layer hens, 16 week old Ross Brown, when subjected to high ambient temperature ranging between 25 to 35^oC, it was observed that T₃, T₄ and TSH concentrations in the serum was less and serum ACTH concentration was higher (Sahin and Kacuk, 2001). Further, under heat stress, albumin, triglycerides and cholesterol concentration in serum decreased. In the same species/breed effect of high ambient temperature (30-40^oC) on sixteen week old hens for sixteen weeks was studied, it was observed that level of Vitamin A and E in serum and liver was less when compared with the control counterparts. Similarly, activity of glutathione peroxidase and reduced glutathione in serum, liver and muscle had decreased; whereas the TBARS level in liver and muscle had increased significantly (Naziroglu et al., 2000).

Heat Stress and Oxidative Stress

In layers metabolic heat production is high as a result of high rate of egg production (Blem, 2000). Heat stress causes effects on mineral balance, plasma electrolyte concentrations (Deyhim and Teeter, 1990; Belay and Teeter, 1993) and has an impact on disease resistance vis a vis with an effect on immune system. Studies by Kutlu and Forber (1993) and Berrong and Washburn (1998), indicated that heat stress also affects, plasma protein concentration. Further, decrease in concentration of plasma minerals like calcium and phosphorus has also been reported (Usayran et al., 2001). When there is prolonged heat stress, it leads to decreased ATP synthesis, cellular calcium homeostasis and cell permeability which predispose cells to apoptosis. Mujahid et al.(2007) reported that when chickens were exposed to acute heat conditions, concentration of plasma and mitochondrial MDA increased significantly. When stress is experienced during hot conditions, ROS when generated, they trigger and modulate cell signalling activities. The activation of transcription factors AP-I, NF-KB and Nrf2 have been shown to take place in heat stressed chickens. AP-I is a modulator of genes which gets stimulated by environmental stimuli. NF- kB expression regulates pro-inflammatory responses. When the heat stress is severe or prolonged, over production of ROS in mitochondria damages proteins, lipids and DNA , which in turn leads to decreased ATP synthesis and calcium dyshomeostasis. Finally it leads to cell apoptosis and necrosis (Akbarian et al., 2016, review).

Heat Stress and Osmoregulation

The monovalent minerals Na⁺, K⁺ and Cl^– exert characteristic effects on hen’s acid-base homeostasis, regulation of osmotic pressure and absorption of amino acids. The Na⁺ and K⁺ are mainly alkalogenic causing shift towards alkaline pH of the body fluids (Borges et al., 2003). Minerals such as copper and magnesium affect the structural composition of the egg shell (Roberts, 2004; Balnave, 2004; Vecerek et al., 2002). High ambient temperature conditions cause decrease in concentration of blood serum electrolytes (Franco-Jimenez and Beck, 2007; Pavlik et al., 2009). The physiological mechanisms that are invoked by birds exposed to high temperatures must meet the opposing demands of thermoregulation and respiratory alkalosis. Dissipation of heat by evaporative cooling causes an increase in respiration, while respiratory alkalosis causes decrease in respiration. Laying hens within the thermoneutral zone consume approximately 200 ml of water per day, whereas hens maintained at 40°C will consume approximately 500 ml per day (North and Bell, 1990). Arad et al. (1983) observed that even without subjecting birds to heat stress, water deprivation for 48 h, which included 24 h without food, of fowls maintained at 25°C was associated with an increase in serum concentrations of sodium and in serum osmolality.

Heat Stress and Different Genotypes

Study by Mack et al. (2013) revealed that heat stress caused reduction in productivity and different behavioral changes were observed in laying hens, but it was observed that the response was varying depending on the genotype of the bird. The two strains of the White Leghorn hens used were Dekalb XL and Kind gentle bird. In these breeds heat stress did not affect body weight of the birds. Results of Fox (1951) and Gowe et al. (2008) revealed that differences in genetic background, may contribute to difference in responses. The differences in egg quality have been observed in hens under heat stress whose response varied with respect to difference in strains (Melesse et al., 2010). Reason given by Zhang et al. (2005), Wright et al. (2006) and Goraga et al. (2010) was that the difference in genotypes may result in affecting physiological functions differently, which in turn might influence quality of the egg differently. The behavioural changes associated with heat stress, has been reported as reduced time spent in walking and spent more time in walking and also in keeping the wings elevated. All these behavioral adaptations have been attributed for causing reduction in body temperature (Gowe et al., 2008; Gerken et al.,2006). Reports of Mack et al. (2013) stated that panting was the only response observed in hens, subjected to heat stress. Photoperiod length and light intensity have been also reported as factors affecting sexual maturity and behavioural responses (Koelkebeck, 2001). Studies by Koelkebeck et al. (1992, 1993) revealed that under heat stress, layer’s bone characteristics were affected in commercial caged layer flocks. Koelkebeck et al. (1993), in an experiment on heat-stressed laying hens, found that when birds were provided with carbonated drinking water it improved tibia breaking strength. They suggested that carbonated drinking water during heat stress may reduce bone breakage during the processing of spent hens. Mortality due to osteoporosis is less, but accounts up to one third of mortality. It has been indicated that it is due to deficiency of calcium, phosphorus and Vitamin D (Webster, 2003).Cross bred naked neck and frizzle phenotypes produced more eggs when compared with their normal feathered sibs. Similar were the results obtained with the other production parameters. It showed that the cross bred strains mentioned had better tolerance to hot and humid environments (Hagan et al., 2011, 2013, 2014). These studies clearly indicated that by introducing heat tolerant genes, some of the cross breeds obtained had better capacity to withstand the higher ambient temperatures (Aberra et al., 2013). Studies by Mahrous et al. (2008) suggested that selection of genotypes with naked neck and frizzle genes, had better disease resistance ability and breeds may be more suitable for rearing under unfavourable conditions. In recent times, newer methods like genetic marker assisted selection of poultry breeds are being explored, for increased heat tolerance and disease resistance. Application of modern molecular techniques in poultry breeding has great potential to improve poultry productivity through understanding various cellular and molecular mechanisms involved in production, physiological and immunological aspects of the poultry birds.

Conclusion

In conclusion, scientists in different fields, must work together to combat difficulties arising from heat stress by developing new methods of cooling systems, newer indices to evaluate climate change effects, selection of better genotypes getting adapted to higher temperature effects and above all conservation of natural resources for alleviating heat stress in future.

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