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Impact of Heat Stress on Chicken Performance, Welfare, and Probable Mitigation Strategies



The poultry industry globally provides chicken meat and eggs, the most significant protein sources among animal foods. The industry is grappling with the effect of climate change which causes heat stress and harms the performance and welfare of the chicken. Heat stress has been the most significant environmental stress challenging the global poultry industry, as chickens only tolerate a narrow range of temperatures during heat stress. This review aims to assess the impact of heat stress on chicken performance, welfare, and probable mitigation strategies to ameliorate its hazard. The study reviewed research papers of different authors and revealed that heat stress affects the chicken's performance, nutrition, and health. Heat stress reduces feed efficiency, body weight, feed intake, and egg production, as well as an increase chicken mortality. Some mitigation strategies farmers have employed include modifying the environment by providing adequate ventilation and cooling systems and adjusting their nutrition to help lower the body's metabolic heat output and keep electrolyte levels stable under high-stress, high-temperature circumstances. Therefore, there is a pressing need to study the extent of the resilience of native chicken breeds to the effects of climate change. Moreover, it is necessary to develop newer varieties of chicken, especially heat-tolerant breed lines, in response to climate change and the diverse need of the farmers and consumers.
*Corresponding author: E-mail:,;
International Journal of Environment and Climate Change
12(11): 3120-3133, 2022; Article no.IJECC.92596
ISSN: 2581-8627
(Past name: British Journal of Environment & Climate Change, Past ISSN: 22314784)
Impact of Heat Stress on Chicken Performance,
Welfare, and Probable Mitigation Strategies
Abdul Rahman Sesay a*
a Department of Animal Science, Njala Campus, Njala University, Sierra Leone.
Author’s contribution
The sole author designed, analysed, interpreted and prepared the manuscript.
Article Information
DOI: 10.9734/IJECC/2022/v12i111360
Open Peer Review History:
This journal follows the Advanced Open Peer Review policy. Identity of the Reviewers, Editor(s) and additional Reviewers, peer
review comments, different versions of the manuscript, comments of the editors, etc are available here:
Received 03 August 2022
Accepted 07 October 2022
Published 14 October 2022
The poultry industry globally provides chicken meat and eggs, the most significant protein sources
among animal foods. The industry is grappling with the effect of climate change which causes heat
stress and harms the performance and welfare of the chicken. Heat stress has been the most
significant environmental stress challenging the global poultry industry, as chickens only tolerate a
narrow range of temperatures during heat stress. This review aims to assess the impact of heat
stress on chicken performance, welfare, and probable mitigation strategies to ameliorate its
hazard. The study reviewed research papers of different authors and revealed that heat stress
affects the chicken's performance, nutrition, and health. Heat stress reduces feed efficiency, body
weight, feed intake, and egg production, as well as an increase chicken mortality. Some mitigation
strategies farmers have employed include modifying the environment by providing adequate
ventilation and cooling systems and adjusting their nutrition to help lower the body's metabolic heat
output and keep electrolyte levels stable under high-stress, high-temperature circumstances.
Therefore, there is a pressing need to study the extent of the resilience of native chicken breeds to
the effects of climate change. Moreover, it is necessary to develop newer varieties of chicken,
especially heat-tolerant breed lines, in response to climate change and the diverse need of the
farmers and consumers.
Keywords: Climate change; heat stress; mitigation; poultry production; thermoneutral zone.
Review Article
Sesay; IJECC, 12(11): 3120-3133, 2022; Article no.IJECC.92596
The poultry industry globally provides chicken
meat and eggs, the most significant protein
sources among animal foods [1,2]. In some
areas of the world, poultry farming has a more
significant impact on the livestock industry than
other sectors [3,4]. Global chicken meat output
increased 1.3% in 2018 to 123.9 million tonnes,
while global poultry meat exports increased by
1.0% to 13.3 million tonnes in 2018 [5]. The
demand for more excellent chicken protein
sources around the globe is increasing due to the
fast growth of the global human population over
the past two decades, during which the poultry
industry has experienced significant growth [6,7].
Climate change is hurting chicken performance
and welfare, and the industry is struggling to
adapt [8,9]. Heat stress, in particular, appears to
be very dangerous for poultry in hot climates
[3,10]. Stress from the combination of high
temperature and high humidity is particularly
detrimental to birds and results in poor
performance [11,12].
Heat stress is the most significant environmental
stress impacting global poultry production
[11,13]. Due to the low heat tolerance of chicken
genotypes, heat stress significantly impacts
poultry birds' physiological, immunological, and
gastrointestinal health, resulting in substantial
economic losses [3,14]. Poultry production can
be negatively impacted by the birds' exposure to
high temperatures, as this can reduce egg
output, diminish egg quality, and reduce bird
weight [15,16]. Heat stress is responsible for
several alterations in the body's physiology, such
as oxidative stress, acid-base imbalance, and
diminished immune function [8,5,17]. These
changes contribute to a reduction in feed
efficiency, body weight, feed intake, and egg
production and an increase in chicken mortality
[7,18]. Heat stress can also affect the quality of
meat and eggs [19,7,1]. This makes climate
changes a significant threat to the chicken's
performance, health, and well-being, which may
lead to a high economic loss for the poultry
industry in the world [20,21]. Therefore, this
review aims to assess the impact of heat stress
on chicken performance, welfare, and probable
mitigation strategies to ameliorate its hazard.
Similar to mammals, poultry is homeothermic,
which means that their outer comfort zone
(thermoneutral zone) ranges between l8ºC and
36oC, but their interior environment (body
temperature) remains generally constant [22].
The optimal temperature for the health
and performance of chickens is within
their thermoneutral zone [23]. The term
"thermoneutral zone" describes the range of
temperatures where birds can maintain a steady
body temperature with the least effort [24]. The
chicken has the least stress when the ambient
temperature is within the thermoneutral zone
[25,23]. When kept in this temperature range,
birds don't have to work hard to maintain a
consistent body temperature [26]. Birds' normal
behavior varies when temperatures exceed their
comfort zone, causing them to pant and shift
their posture [27]. The lowest critical temperature
(LCT) is the coldest point in the thermoneutral
zone. Whenever the temperature drops below
that threshold, the bird will begin to use its food
as a heat source. The highest critical
temperature (HCT) is the highest temperature in
the thermoneutral zone. The birds will perish if
the temperature climbs above that point because
their bodies will overheat [28,29]. Between 36oC
and 37oC is the highest critical temperature for
broilers [30].
When the ambient temperature is within the
thermoneutral range, the chicken is most at ease
and operates at its best; if the temperature is
above or below their thermoneutral, they get
anxious [32]. The condition known as heat stress
occurs when an organism, whether it be a
person, a plant, or an animal, absorbs an
excessive amount of heat, which can lead to
anxiety, disease, or even death [33]. An animal
feels heat stress when the quantity of heat
energy it creates exceeds the amount of heat
energy it loses to its surroundings [11]. This
energy imbalance is affected by environmental
elements such as sunshine, thermal irradiation,
air temperature, humidity, and stocking density,
as well as animal-related parameters such as
body mass, feather distribution, dehydration
status, metabolic rate, and thermoregulatory
processes [11,34]. When the environment is
above the thermoneutral zone, animals employ
their thermoregulatory systems to release
heat through behavioral, biochemical, and
physiological responses [35,36]. Acute and
chronic heat stress are the two basic kinds of
heat stress. Acute heat stress refers to a brief
and rapid increase in environmental temperature
(a few hours), whereas chronic heat
stress is characterized by prolonged exposure to
high temperatures (several days) [37,26].
Sesay; IJECC, 12(11): 3120-3133, 2022; Article no.IJECC.92596
Fig. 1. Relationships between environment, body temperature, and metabolic rate. EET
combines air temperature, humidity, airflow, conduction, and radiant heat. When the EET
drops below the LCT, the animal shivers to create heat. When EET exceeds UCT, the animal
pants, which boosts its metabolism. The thermal neutral zone is between the LCT and UCT.
Above the UCT, panting can maintain body temperature until EET rises (a). At some point, EET
and body temperature rise too much, causing spiraling hyperthermia (b) and mortality if EET is
not decreased. Effective ambient temperature; lower critical temperature; upper critical
temperature [31]
Symptoms of heat stress include a high core
body temperature, lack of perspiration, and the
onset of neurological conditions like paralysis,
headache, vertigo, and unconsciousness [33].
During high ambient temperature of about 35.5oC
and relative humidity of 50-70%, the chicken
starts to develop a panting mechanism to
maintain homeothermy as this would allow a high
rate of cooling from the respiratory tract through
evaporation [30,22]. The animal dissipates
heat primarily through conduction, convection,
radiation, and evaporation [38]. The amount of
heat a birds loses by radiation is proportional to
its size [39]. When the external temperature
matches or exceeds the body temperature,
evaporation is the principal method by which
chickens can cool themselves [40]. When
moisture evaporates away from the respiratory
tract of chickens, evaporative cooling occurs
[40,39]. Evaporative cooling is required to
stabilize the chicken's body temperature for
efficient production [41].
Chicken is highly vulnerable to climate change
due to its low heat tolerance, affecting behavioral
and physiological activities [42]. Birds try to
dissipate heat during extreme heat and conserve
heat during freezing temperatures; however, in
both cases, birds need to expend much energy
to maintain their bodies within their comfort zone
[43]. To keep its internal temperature from rising
above its external temperature, a bird
experiencing heat stress will lower its food intake
[42,44]. Heat stress in the chickens leads to a
decrease in their feed intake due to the birds
being outside their comfort zone as the birds
tend to adjust to the changes in the environment
[45]. The most damaging consequences of heat
stress on chicken performance are likely to begin
with, lower feed intake, which then result in
decrease body weight, feed efficiency, egg
output and quality [46,43].
According to research by Lara and Rostagno
[11], feed consumption drops by 5% for every
1oC increase in temperature between 32oC and
38oC. When the ambient temperature increases
to 34oC, the mortality due to heat stress would be
very high in broilers by 8.4%, and the feed intake
of the chicken decreases from 108.3g/bird/day at
31.6oC to 68.9g/bird/day at 37.9oC, the egg
production would reduce by 6.4% [47]. Feed
intake in broilers is reduced by 16.4% when they
are subjected to chronic heat stress, and body
weight is lowered by 32.64% [48,47]. Laying
hens exposed to heat stress during 8-14 days,
30-42 days, and 43-56 days saw a decrease in
egg production of 13.2%, 26.4%, and 57%,
respectively [11]. Related research by Mashaly et
al. [49] shows that laying hens exposed
to chronic heat stress for five weeks have
Sesay; IJECC, 12(11): 3120-3133, 2022; Article no.IJECC.92596
significant drops in egg production (28.8%), feed
intake (34.7%), and body weight (19.3%). Deng
et al. [46] found that after 12 days of heat stress,
daily feed intake dropped by 28.58 g/bird, which
led to a 28.8% drop in egg production. Heat
stress in laying hens decreased feed conversion
by 31.6%, egg production by 36.4%, and egg
weight by 3.45%, as found by Star et al. [50].
According to a different set of researchers, Lin et
al. [51] found that heat stress led to poorer
production performance, thinner eggshells, and
more egg breaking. Ebeid et al. [52] also found a
drastic decrease in the egg weight (-3.24%),
eggshell thickness (-1.2%), eggshell weight (-
9.93%), and eggshell percent (-0.66%) when
birds are exposed to high temperatures. As
previously mentioned, Mack et al. [53] found that
heat stress caused a reduction in egg output,
egg weight, and eggshell thickness in laying
hens. Since chickens drink more water and eat
less feed when temperatures and sunshine are
high, heat stress can hurt the quantity and quality
of eggs and meat produced by chickens [54].
Thyroid hormones (3,5,30-triiodothyronine and
thyroxine) play an essential function in regulating
the metabolic rates of birds during the
development and egg-laying periods [55]. The
synchronization of thyroid gland activity is
essential for regulating body temperature and
maintaining homeostasis in poultry via energy
metabolism [56]. Due to heat stress, the thyroid
hormones of broiler chickens are negatively
impacted. The drop in thyroxine concentrations
leads to a decrease in protein synthesis, which
reduces body weight and daily growth [57]. Due
to a loss of appetite and a drop in feed
consumption, birds exposed to high ambient
temperatures have a decline in growth [58].
Corticosterone, the primary glucocorticoid
hormone in chickens, regulates appetite and
thermogenesis [59]. Increased amounts promote
brown tissue aggregation and white tissue
lipogenesis, impairing metabolism [59]. Under
heat stress conditions, an increase in blood
serum cortisol levels stimulates the
gluconeogenesis pathway, leading to a rise in
blood glucose concentration [60].
Beckford et al. [31] reported that heat stress
reduced feed intake, body weight, bicarbonate,
potassium, carbon dioxide, and triiodothyronine
while increasing mortality, glucose, pH,
plasma thyroxine, and corticosterone. In birds
experiencing heat stress, expression of
corticotropin-releasing hormone receptor 1 was
downregulated, but corticotropin-releasing
hormone receptor 2 mRNA levels were elevated.
Heat stress elevated the expression of thyroid
hormone receptor β (2.8-fold) and thyroid
stimulating hormone β (1.4-fold) [31]. Heat stress
generates unfavorable physiological reactions
and adverse effects on blood biochemical
parameters, the immune system, oxidative state,
thyroid hormones, mineral balance and
osmoregulation, and intestinal and ileal
microbiome [36]. According to Lin et al. [61],
acute heat exposure (32°C, 6h) produces
oxidative stress in 5-week-old broiler chicks.
Increased body temperature can generate
metabolic alterations associated with oxidative
stress [36,61]. Oxidative stress happens when
the number of reactive oxygen species (ROS) in
the body exceeds the antioxidant capacity of the
cells [26]. As a defense mechanism against
many stresses, oxidative stress has become a
significant factor in poultry production [26,36].
The efficiency with which cells generate energy
is decreased, and proteins, lipids, and DNA are
all damaged by oxidative stress [26]. Oxidative
stress causes an increased intestinal
permeability due to tissue damage in the
digestive tract causing toxins and infections to
enter more easily into the bloodstream from the
intestines [61]. The liver is more vulnerable
to oxidative stress than the heart in broiler
chickens [61].
Climate change alters the global disease
distribution and the emergence of poultry
diseases [54,62]. Typically, birds reduce feed
intake in hot environments to reduce heat
production from metabolism, but reduced feed
intake leads to watery droppings and diarrhea,
significantly reducing body weight [11]. Heat
stress affects the feed intake of the chicken and
lowers the immune system of the chicken, which
makes the chicken vulnerable to many
poultry diseases [63]. Heat stress increases
corticosterone release in hens, reducing the
birds' resistance to other diseases like coccidia
and putting them at risk for necrotic enteritis [64].
Both the quantity and activity of commensal
bacteria may be altered due to decreased feed
intake and weakened intestinal function [54].
Beneficial microbe populations can decrease
under the stress of heat [47]. It can also promote
the growth of latent pathogens and lead to
dysbiosis, augmented intestinal penetrability, and
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immune and metabolic disorders [65]. Clostridia,
Salmonella, and coliform bacteria populations
rise in heat-stressed chicken, whereas
Lactobacilli and Bifidobacterial populations
decrease [66,67]. Coccidiosis, hemorrhagic
syndrome, fowl pox, and bronchitis are only
some diseases that can spread rapidly in chicken
flocks due to changes in temperature and
humidity [68]. High winds can further disperse
airborne diseases in poultry flocks [69].
Oviedo-Rondón et al. [70] reported that
intestinal health significantly impacts poultry
productivity, animal welfare, and food safety.
Immunosuppression and damage to the gut
microbiota, intestinal integrity, and villus shape
are caused by heat stress, and consequently,
digestion and absorption of feed decrease
[71,35]. These variables enhance the likelihood
of epidemics of necrotic enteritis, which is one of
the most troublesome bacterial infections in
contemporary chicken farming [72]. In broilers
challenged with C. perfringens, researchers
Tsiouris et al. [73] discovered that cyclical acute
heat stress enhanced the incidence and severity
of necrotic enteritis and induced the disease in
birds not exposed to the bacteria. Heat stress
manifested itself in a variety of ways in the birds,
including delayed development and a drop in the
pH of the intestinal digesta [35,3]. Heat stress
increases the need for antibiotics because it
reduces feed digestibility, increases gut
permeability, and decreases immunity, all of
which increases the risk of gastrointestinal
diseases such as dysbacteriosis and nectrotic
enteritis in chickens [54,44,47].
Birds are homeothermic, meaning their internal
temperatures stay within a relatively constant
range [39]. High temperatures reduce the bird's
ability to disperse heat. It happens when heat is
brutal to evaporate quickly [74]. The optimum
temperature range differs significantly among
bird types and age ranges [75]. Observable
differences can be attributed to natural factors
and avian diversity [39,76]. The bird and its
surroundings can undergo radiant heat transfer if
its surface temperature differs from the surface it
is resting on or the ambient air temperature
[39,76,75]. The comb, wattles, face, legs, toes,
neck, torso, and wings produce convection by
radiating heat into the ambient air [39,75]. The
comb and wattles contribute 34% of the total
Sensible heat loss at 35°C [77]. Heat loss by
convection and radiation can also rise
dramatically with wind speed [39]. The increased
air velocity further exposes the skin, which may
enhance radiation losses [39,78]. Changes in
heat dissipation from non-evaporation to
increased evaporation occur as the surrounding
temperature rises [79]. To a large extent, birds
cool themselves by increasing their breath rate, a
process known as panting; in fact, this form of
enhanced respiration can account for as much as
60% of the total heat loss in some species
[78,77]. Dehydration can develop due to the loss
of water that occurs during the evaporation
process. Thermo-tolerance at greater ambient
temperatures is enhanced by drinking enough
water, which aids in heat loss [39,75].
When temperatures soar, birds attempt
thermoregulation by adjusting their behavior and
physiological balance [79,80]. When faced with
high environmental temperatures, animals
employ various strategies for thermoregulation
and homeostasis, including enhancing radiative,
convective, and evaporative heat loss through
vasodilation and perspiration [11]. Most bird
species respond equally to heat stress, while
there is some individual disparity in the severity
and length of responses [39,11]. Mack et al. [53]
stated that birds in heat stress eat less, drink and
pant more, stand still or rest with their wings
raised more often, and move or walk less
frequently. Air sacs are an additional means
through which birds facilitate heat exchange with
their surroundings [39]. During panting, air sacs
are helpful because they increase the surface
area exposed to air, which increases gas
exchanges with the air and, in turn, increases the
rate at which heat is lost by evaporation [81].
Local chickens displayed a behavioral coping
mechanism during heat stress by moving into the
shade [82,43]. Although this considerably
reduces radiant heat load, actively seeking
shade during the day may imply poor feed intake,
especially for rural poultry, which relies primarily
on scavenging around homesteads [82].
Since different species have different thermal
comfort zones, defining what constitutes a "high"
environment temperature is a matter of degree
[83]. An animal will feel heat stress if the
environmental temperature exceeds its thermo-
neutral zone [84,83]. When this occurs depends
not just on the relative humidity and air speed but
Sesay; IJECC, 12(11): 3120-3133, 2022; Article no.IJECC.92596
also the surrounding temperature [84]. As the
birds' thermal stress rises at higher
temperatures, their appetite and metabolism are
negatively impacted, limiting the temperature
range in which their output is at its peak [44].
Increased environmental heat causes changes in
hydration and nutrition intake, metabolic rate,
core temperature, heterophil/lymphocyte (H/L)
ratio, and gastrointestinal tract (GIT) maturation.
Some enzymes, for instance, wouldn't work as
effectively in hotter temperatures, limiting birds'
ability to eat and digest [54].
When the temperature increased from 32.2oC to
37.8oC, feed intake decreased by 9.9% per bird
per day compared to the intake at 21.1oC, and
the chicken will drink four times as much water at
38oC as it does at 21oC due to the higher
ambient temperature [85]. Chickens drink roughly
7% more water for every degree over 21°C [86].
Increasing the bird's water intake may help it by
increasing the efficiency of its cooling system,
which relies on evaporation [77]. Thus, water
plays a vital role in the metabolism of chickens
by helping regulate body temperature, digestion,
feed absorption, and nutrient delivery [87]. Heat
stress is associated with decreased feed intake,
which may lead to less overall body weight gain if
water intake is also reduced [88]. Gains in weight
were lower in the high-temperature group of
chickens compared to the average-temperature
group [88,87]. Heat stress negatively impacts the
nutrition of chicken which is a severe problem for
the poultry industry as optimal nutrition intake
and use are crucial to weight gain and egg
production, which drive poultry enterprise
productivity and profitability [89].
7.1 Feeding Approaches
Climate change's impact on chicken production
is just one more difficulty that poultry farmers
face in an already challenging sector [90]. Heat
stress can be reduced through several measures
related to environmental control, dietary
modification, feed additive use, and electrolyte
additions to drinking water [11,90]. In high-
temperature stressful settings, it may be possible
to lower metabolic heat generation and maintain
electrolyte balance by modifying the chickens'
surroundings with the addition of ventilation,
cooling devices, and dietary changes [11]. In
contrast, chicks can improve their thermo-
tolerance and thus their survival rate under heat
stress through early-age heat conditioning and
regulated fasting in the first few days of life [3].
Changes in energy-to-protein ratio, wet feeding,
electrolyte supplementation, feeding time, drinker
type, and height are only some feeding
management methods shown to boost
performance in the face of heat stress [91].
Based on their findings that heat stress can
cause hyperthermia in poultry, Syafwan et al.
[77] advise free-choice feeding with high-protein
or high-energy diet options. The bird's free-
choice food must contain a variety of particle
sizes or shapes. A big particle size aids in the
maturation of the GIT, particularly the gizzard
and the caeca. The amount of heat generated by
digestion could be reduced if birds had large
gizzards, as this would allow for more efficient
grinding and possibly better digestion further
down the GIT [77,3]. The chicken may be able to
self-select its diet in such a way that it optimizes
the heat load associated with the metabolism of
the nutrients it consumes [92,77].
The local poultry farmers employ traditional
procedures, such as early stocking of birds,
increased litter changes during the hot period,
and the maintenance of native bird breeds
[93,94]. Rajkumar et al. [94] suggested that the
naked neck birds fared much better in terms of
growth, carcass, and metabolic markers at high
ambient temperatures. The lower feather bulk of
the naked-necked birds allows for more efficient
heat dissipation, making them more resistant to
the effects of heat stress. Nyoni et al. [82] also
stated that using genetics and adaptation, and
native breeds may do better than foreign ones in
a warmer world.
7.2 Supplementation of Vitamins,
Minerals, and Electrolytes in the
Chicken Diet
Nutritional solutions have been extensively
examined and proven to mitigate the adverse
effects of heat stress. These include limiting feed
intake, wet or dual feeding, increasing fat intake,
and supplementing with vitamins, minerals,
osmolytes, and phytochemicals [89]. Alpha-
tocopherol, often known as vitamin E, is a fat-
soluble vitamin with antioxidant characteristics
that aid in the detoxification of harmful free
radicals produced inside cells [95]. Adding
vitamin E to the diets of laying hens under heat
stress increases egg production, eggshell
thickness, egg-specific gravity, and the Haugh
unit [96]. As it aids in creating and releasing
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protein-vitellogenin, the liver is a crucial organ for
egg development [97]. In heat stress
circumstances, supplementation with vitamin E
(250 mg/kg of feed) decreases liver and serum
malondialdehyde (MDA) concentration and
increases serum and liver vitamin E and A
concentration [98]. At low oxygen pressures,
vitamin A is the most efficient antioxidant,
quenching singlet oxygen and neutralizing thiyl
radicals [99]. Treatment with vitamin A (IU/kg of
feed) in heat-stressed broilers increased live
weight growth, improved feed efficiency, and
decreased blood MDA levels [89].
Vitamin C, an antioxidant, prevents damage to
cells caused by oxidative stress by scavenging
reactive oxygen species (ROS), neutralizing
hydroperoxyl radicals that are vitamin E
dependent, and protecting proteins from
alkylation and electrophilic lipid peroxidation
products [100]. Vitamin C (250 mg/kg of feed)
improved growth rate, food utilization, egg
production and quality, immune response, and
antioxidant status in birds exposed to heat stress
[101]. Supplementing broiler feed with 200 mg of
ascorbic acid per kg boosted growth and FCR
[102]. According to Sahin et al. [103],
supplementing with either vitamin C or chromium
led to better live weight gain, feed efficiency, and
carcass traits and reduced blood corticosterone
and MDA concentrations. According to Mahmoud
et al. [104], supplementing broilers' diets with
250 mg/kg of propolis, vitamin E, or vitamin C
helps mitigate the oxidative damage caused by
heat stress. Sujatha et al. [105] found that
oxidative stress in broilers might be alleviated
throughout the summer by employing antioxidant
synthetic vitamin C and the polyherbal anti-
stressor, immunomodulator, and adaptogenic
feed premix. According to Selvam et al. [106],
Phytocee supplementation has an anti-stress
impact on hens by bringing their serum
corticosterone levels and thermoregulatory
systems back to normal.
There are around 300 enzymes that can't
function without zinc. Antioxidant defense,
immune system health, and proper skeletal
growth are all bolstered by zinc's presence in the
body [107]. Zinc is necessary for synthesizing the
free radical scavenger metallothionein [108]. Zinc
supplementation helps to reduce free radical
formation since it is a component of antioxidant
enzymes such as superoxide dismutase,
glutathione, glutathione S-transferase, and
hemeoxygenase-1 [109]. Heat-stressed quails
given zinc and magnesium significantly
increased live weight, feed intake, and hot and
chilled dressing percentage [110]. Zinc
supplementation in the form of Zn-methionine
(80-100 mg/kg of diet) increased eggshell
thickness and decreased defects in laying hens
Chromium is a vital mineral because it is a
constituent of chromodulin and helps insulin work
properly [113]. Adding 0.4-2 mg of chromium/kg
of feed as CrPic to a laying hen's diet improved
her immune response, egg quality, and Haugh
unit while lowering her blood sugar, cholesterol,
and triglyceride levels [114,115]. Selenium is a
component of at least 25 selenoproteins,
including glutathione peroxidase and thioredoxin
reductases [116]. Inorganic and organic selenium
is used as poultry supplements [117]. The
organic versions are more absorbable than their
inorganic counterparts [118]. Selenium improves
laying hens' and quails' fertility [119]. Under
heat stress, selenium supplementation (0.15-
0.30 mg/kg of feed sodium selenite or
selenomethionine) increased feed intake, body
weight, and egg production in laying quails [120].
Organic and inorganic selenium increased
Haugh units and eggshell weights [89].
When birds are under extreme heat stress, they
pant, which alters their blood's acid-base balance
and causes them to develop respiratory
alkalosis. This can be restored using electrolytes
like NH4Cl, NaHCO3, and KCl [121]. It has been
found that heat stress in chickens can be
reduced by providing a more variable dietary
electrolyte balance (DEB) [122]. Under high
temperatures, sodium bicarbonate (NaHCO3) is
the salt of choice [123]. Incorporating this salt
into the diets of heat-stressed broiler chickens
improved their performance [124]. Ingestion of
1.52.0% K from KCl improved FCR under
conditions of chronic heat stress. In addition to
including these salts in the diet, supplementing
drinking water with 0.2% NH4Cl, 0.150% KCl,
and carbonated water enhanced chicken
performance [61].
The diet helps alleviate heat stress. Diets are
supplemented with feed additives to reduce heat
stress in poultry [11]. Poultry nutritionists are
becoming increasingly interested in probiotics
because they can improve the health and
productivity of heat-stressed chicken by
influencing its physiology, gut shape and
structure, and immune function [125]. By
supplementing the broiler diet with probiotics,
researchers saw dramatic increases in feed
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consumption, daily growth, total body weight,
intestinal absorption, and immunity [46]. By
controlling corticosterone levels and the
overproduction of pro-inflammatory chemicals
that cause intestinal tissue damage and
increased tissue permeability in heat-stressed
birds, probiotics can aid in repairing villus-crypt
structures [126]. Birds grown in high-temperature
environments benefit from probiotics because
they improve gut microbial ecology
and morphology, physiological conditions, the
immune system, and overall performance [46].
Heat stress is responsible for many physiological
changes, including oxidative stress, acid-base
imbalance, and suppressed immunocompetence.
These changes contribute to an increase in
mortality and a reduction in feed efficiency, body
weight, feed intake, and egg production. Heat
stress also has an impact on the quality of meat
and eggs.
Therefore, rural poultry may have a higher level
of heat tolerance than commercial breeds, but
the extent of their tolerance threshold to
temperature variation is unknown and requires
urgent attention. Breeding projects to improve
the climate resilience of native birds should also
be promoted. Moreover, it is necessary
to develop newer varieties of chicken, especially
heat-tolerant breed lines, in response to
climate change and the diverse need of the
farmers and consumers. Finally, a well-planned
and carried-out adaptation response system for
the poultry industry will raise enough awareness
and adaption to extreme climate circumstances.
Author has declared that no competing interests
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Heat stress has emerged as a serious threat to the global poultry industry due to climate change. Heat stress can negatively impact the growth, gut health, immune function, and production and reproductive performances of poultry. Different strategies have been explored to mitigate heat stress in poultry; however, only a few have shown potential. Probiotics are gaining the attention of poultry nutritionists, as they are capable of improving the physiology, gut health, and immune system of poultry under heat stress. Therefore, application of probiotics along with proper management are considered to potentially help negate some of the negative impacts of heat stress on poultry. This review presents scientific insight into the impact of heat stress on poultry health and growth performance as well as the application of probiotics as a promising approach to alleviate the negative effects of heat stress in poultry.
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Heat stress is one of the major environmental stressors in the poultry industry resulting in substantial economic loss. Heat stress causes several physiological changes, such as oxidative stress, acid-base imbalance, and suppressed immunocompetence, which leads to increased mortality and reduced feed efficiency, body weight, feed intake, and egg production, and also affects meat and egg quality. Several strategies, with a variable degree of effectiveness, have been implemented to attenuate heat stress in poultry. Nutritional strategies, such as restricting the feed, wet or dual feeding, adding fat in diets, supplementing vitamins, minerals, osmolytes, and phytochemicals, have been widely studied and found to reduce the deleterious effects of heat stress. Furthermore, the use of naked neck (Na) and frizzle (F) genes in certain breed lines have also gained massive attention in recent times. However, only a few of these strategies have been widely used in the poultry industry. Therefore, developing heat-tolerant breed lines along with proper management and nutritional approach needs to be considered for solving this problem. Thus, this review highlights the scientific evidence regarding the effects of heat stress on poultry health and performances, and potential mitigation strategies against heat stress in broiler chickens and laying hens.
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The current climate changes have increased the prevalence and intensity of heat stress (HS) conditions. One of the initial consequences of HS is the impairment of the intestinal epithelial barrier integrity due to hyperthermia and hypoxia following blood repartition, which often results in a leaky gut followed by penetration and transfer of luminal antigens, endotoxins, and pathogenic bacteria. Under extreme conditions, HS may culminate in the onset of “heat stroke”, a potential lethal condition if remaining untreated. HS-induced alterations of the gastrointestinal epithelium, which is associated with a leaky gut, are due to cellular oxidative stress, disruption of intestinal integrity, and increased production of pro-inflammatory cytokines. This review summarizes the possible resilience mechanisms based on in vitro and in vivo data and the potential interventions with a group of nutritional supplements, which may increase the resilience to HS-induced intestinal integrity disruption and maintain intestinal homeostasis.
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Though climate events pose increasing challenges for crop and animal production in Africa, most climate adaptation studies focus on staple food crops. Few studies have examined climate adaptation for livestock with even fewer looking at small animals such as poultry. Heat stress associated with climate change is a severe challenge to poultry farmers due to its negative effect on chicken growth and productivity. As poultry plays an important food security role across Africa (being a source of livelihood and an important source of animal protein), understanding how farmers deal with the realities of poultry production due to climate change is critical. This study explores the level and determinants of the adoption of climate change adaptation strategies among poultry farmers in Nigeria. A multivariate probit analysis (which allows for the possibility that the decision to adopt various practices are jointly made) reveals that while poultry farmers are adapting to climate change, there is a clear heterogeneity of adaptation strategies at different production scales. Small farms tend to invest in traditional strategies such as the stocking of local breeds while medium and large farms adopt modern technologies such as air and water ventilation as well as the use of low energy bulbs that emit less heat. Our study finds that farmers who have experienced heat-related losses are more likely to adopt modern practices and more likely to adopt multiple adaptation strategies concurrently.
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This study examined effect of a dietary synbiotic supplement on the concentrations of plasma thyroid hormones, expressions of heat shock protein 70 (HSP70), and intestinal histomorphology in broiler chickens exposed to cyclic heat stress (HS). Three hundred and sixty day old male Ross 708 broiler chicks were randomly distributed among 3 dietary treatments containing a synbiotic (PoultryStar meUS) at 0 (control), 0.5 (0.5×), and 1.0 (1.0×) g/kg. Each treatment contained 8 replicates of 15 birds each housed in floor pens in a temperature and lighting controlled room. Heat stimulation was established from days 15 to 42 at 32°C for 9 h daily. The results indicated that under the HS condition, both synbiotic fed groups had lower liver and hypothalamus HSP70 levels (P < 0.001) compared to control group; however, HSP70 mRNA expression was not different among treatments (P > 0.05). There were no treatment effects on the levels of triiodothyronine (T3) and thyroxine (T4) as well as T3/T4 ratio (P > 0.05). Compared to controls, 1.0× HS broilers had greater villus height in the duodenum (P < 0.01), and greater villus height and villus height:crypt depth ratios in the ileum (P < 0.01). There were no differences among treatments on the measured intestinal parameters in the jejunum (P > 0.05). The results suggest that the synbiotic may ameliorate the negative effects of HS on chicken health as indicated by the changes in the intestinal architecture and the levels of HSP70. Dietary synbiotic supplement could be a feasible nutritive strategy for the poultry industry to improve the health and welfare of chickens when exposed to hot environmental temperature.
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A reduction in the thermogenic activity of brown adipose tissue (BAT) is presently discussed as a possible determinant for the development of obesity in humans. One group of endogenous factors that could potentially affect BAT activity is the glucocorticoids (e.g. cortisol). We analyse here studies examining the effects of alterations in glucocorticoid signaling on BAT recruitment and thermogenic capacity. We find that irrespective of which manipulation of glucocorticoid signaling is examined, a seemingly homogeneous picture of lowered thermogenic capacity due to glucocorticoid stimulation is apparently obtained: e.g. lowered uncoupling protein 1 (UCP1) protein levels per mg protein, and an increased lipid accumulation in BAT. However, further analyses generally indicate that these effects result from a dilution effect rather than a true decrease in total capacity; the tissue may thus be said to be in a state of pseudo-atrophy. However, under conditions of very low physiological stimulation of BAT, glucocorticoids may truly inhibit Ucp1 gene expression and consequently lower total UCP1 protein levels, but the metabolic effects of this reduction are probably minor. It is thus unlikely that glucocorticoids affect organismal metabolism and induce the development of obesity through alterations of BAT activity.
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Gut microbiota** play important roles in the health and disease status of both humans and animals. Little is known about whether heat stress changes the composition of the gut microbiota in chicken. The aim of this study was to investigate the effects of heat stress on changes in caecal microbiota, including changes in growth performance as well as HSP70 and cortisol levels. Sixty 14-day-old female broilers were equally divided into 2 treatment groups with different housing temperatures for 28 D: a control group (C) at 24 to 26°C and a heat stress (HS) group at 34 to 38°C. The caecal contents of the broiler chicken were then extracted on days 1, 3, 7, 14, and 28. Genomic DNA was extracted and amplified based on the V3∼V4 hypervariable region of 16S rRNA high-throughput sequence analyses. The results showed that the average daily gain and average daily feed intake were significantly decreased and that the feed conversion ratio was increased by heat stress. The concentrations of HSP70 and cortisol in the serum were significantly increased. The composition of gut microbiota was influenced by heat stress** through beta diversity analysis and taxon-based analysis. In particular, at the phylum level the composition of Firmicutes, Tenericutes, and Proteobacteria in HS group was increased than that of C group, and Bacteroidetes and Cyanobacteria in HS group were reduced than that of C group. In addition, the composition of Anaeroplasma and Lactobacillus phyla in HS group were increased than that of C group, whereas the Bacteroides, Oscillospira, Faecalibacterium, and Dorea genera in HS group were decreased than that of C group. In conclusion, the gut microbiota in broilers were changed by heat stress. And the changes of the gut microbiota could provide the basis for further research on the heat stress.
As global temperatures reach record highs, threats posed by climate change to biodiversity become ever more severe. For endotherms, maintaining body temperature within safe bounds is fundamental for performance and survival. Animals routinely modify their behavior to buffer physiological impacts of high temperatures (eg ceasing activity, seeking shade). However, this can impose substantial costs related to missed opportunities to engage in other important activities, with potentially large but often overlooked consequences for survival and reproduction. Here, we outline behavioral trade‐offs birds and mammals face in navigating thermal landscapes and associated challenges of balancing energy, water, and time budgets; review the rapidly expanding knowledge in this field; and summarize examples – across taxa – of fitness costs during hot weather. We argue that a shift is needed in evaluating the impacts of heat on birds and mammals, and that fitness costs of missed opportunities must be explicitly integrated into climate‐change vulnerability frameworks.
Stress is a biological adaptive response to restore homeostasis, and occurs in every animal production system, due to the multitude of stressors present in every farm. Heat stress is one of the most common environmental challenges to poultry worldwide. It has been extensively demonstrated that heat stress negatively impacts the health, welfare and productivity of broilers and laying hens. However, basic mechanisms associated with the reported effects of heat stress are still not fully understood. The adaptive response of poultry to a heat stress situation is complex and intricate in nature, and it includes effects on the intestinal tract. This review offers an objective overview of the scientific evidence available on the effects of the heat stress response on different facets of the intestinal tract of poultry, including its physiology, integrity, immunology and microbiota. Although a lot of knowledge has been generated, many gaps persist. The development of standardized models is crucial to be able to better compare and extrapolate results. By better understanding how the intestinal tract is affected in birds subjected to heat stress conditions, more targeted interventions can be developed and applied.
Ever since the European ban on use of in‐feed antibiotics in food animals, the search for alternate antibiotic‐free growth promoter is undertaken worldwide. There are few alternatives such as probiotics, pre‐biotics, phytochemicals, enzymes and organic acids. Among these alternatives, the organic acids or simply acidifiers play an important role in gut health in animals. The acidifiers could be used to favourably manipulate the intestinal microbial populations and improve the immune response, hence perform an activity similar to antibiotics in food animals in countering pathogenic bacteria. Acidifiers also improve the digestibility of nutrients and increase the absorption of minerals. The incorporation of organic acids also leads to thinning of the intestinal lining which facilitates better absorption of nutrients and its efficient utilization. However, their effect will not be similar among all types of organic acids as their mechanism of activity is based on its pKa value. Moreover, there are claims about the neutralization of acids by the secretion of bicarbonates in the initial part of intestine, reactivity with metallic items in feed mills and reduced palatability due its bitter taste demands non‐reactive and targeted delivery for better performance. Currently, coated salts of acidifiers are available commercially for use in food animals especially pigs and poultry. The present review highlights the role of different acidifiers in livestock nutrition with their potent applications in improving nutrient digestibility, mineral utilization, meat quality, enhancing immunity, antimicrobial effects in countering pathogenic bacteria, boosting performance and production, and thus safeguarding health of livestock animals and poultry.