Weather fluctuations, particularly during seasonal transitions, create significant stress in poultry production systems. Sudden changes in temperature, humidity, ventilation patterns, and air quality weaken the birds’ immune defenses and predispose them to respiratory infections. Among these, Mycoplasmosis is one of the most economically important diseases affecting both commercial layers and breeder flocks.

The two major pathogenic species affecting poultry are:
– Mycoplasma gallisepticum infection (MG)
– Mycoplasma synoviae infection (MS)
These organisms are highly contagious and often become more problematic during changing weather conditions due to increased environmental stress and compromised flock immunity.

Why Changing Weather Increases Mycoplasma Problems
During weather transitions such as:
– Summer to monsoon
– Monsoon to winter
– Sudden cold or heat waves
birds experience physiological stress that suppresses their immune response. Several environmental factors contribute to Mycoplasma outbreaks:
1. Temperature Fluctuation
Rapid day-night temperature variation stresses birds and damages the respiratory mucosa, making it easier for Mycoplasma organisms to colonize the respiratory tract.
2. Poor Ventilation
Farmers often reduce ventilation during cold weather to conserve heat. This increases:
– Ammonia levels
– Dust accumulation
– Humidity
– Carbon dioxide concentration
Such conditions irritate the respiratory tract and favor Mycoplasma multiplication.
3. High Humidity and Wet Litter
During monsoon seasons, excessive moisture increases pathogen survival and worsens respiratory stress.
4. Secondary Infections
Changing weather also favors bacterial and viral co-infections such as:
– Newcastle disease
– Infectious bronchitis
– Escherichia coli infection

These infections intensify the severity of Mycoplasma disease.
Clinical Signs in Layers and Breeders
Affected birds may show:
– Coughing and sneezing
– Nasal discharge
– Rales and respiratory sounds
– Swollen sinuses
– Watery eyes
– Reduced feed intake
– Depression and poor growth
– Increased mortality in severe cases

In breeder flocks, fertility and hatchability may decline significantly.

Impact on Layer Performance
Mycoplasma infection severely affects commercial egg production.
1. Drop in Egg Production
Layers infected with MG or MS commonly show:
-Sudden reduction in egg production
– Irregular laying patterns
– Delayed peak production
Production losses may range from 5–20% depending on flock condition and secondary infections.
2. Poor Egg Quality
Infected layers may produce:
– Thin-shelled eggs
– Misshapen eggs
– Smaller eggs
– Poor shell strength
This increases breakage and market rejection.
3. Increased Feed Conversion Ratio (FCR)
Respiratory stress reduces feed efficiency, increasing production cost per egg.
4. Increased Culling and Mortality
Chronically affected birds become poor performers and require early culling.

Impact on Breeder Performance
The economic effect of Mycoplasma is even more serious in breeder operations.
1. Reduced Fertility
Mycoplasma infection negatively affects reproductive performance, lowering fertility percentage.
2. Poor Hatchability
Vertical transmission through eggs can infect embryos, causing:
– Embryonic mortality
– Weak chicks
– Poor hatchability
3. Transmission to Progeny
MG and MS can spread from infected breeders to chicks through eggs, creating long-term farm problems.
4. Reduced Chick Quality
Chicks from infected breeder flocks often show:
– Weakness
– Respiratory distress
– Poor growth potential
– Higher early mortality

Economic Losses
Mycoplasma outbreaks during changing weather can lead to major financial losses through:
– Reduced egg production
– Poor hatchability
– Increased medication costs
– Mortality and culling
– Lower chick quality
– Increased feed costs
– Trade restrictions in breeder operations

Diagnosis
Accurate diagnosis is essential for effective control. Common diagnostic methods include:
– Serological testing (ELISA, SPA)
– PCR testing
– Culture and isolation
– Postmortem examination

Typical lesions include:
– Air sacculitis
– Tracheitis
– Foamy air sacs
– Pneumonia

Prevention and Control Measures
1. Maintain Proper Ventilation
Ensure adequate airflow without creating drafts.
2. Reduce Environmental Stress
– Maintain uniform temperature
– Avoid sudden temperature changes
w Control humidity levels
3. Strengthen Biosecurity
– Restrict visitor movement
– Disinfect equipment
– Control wild birds and rodents
4. Vaccination
Vaccination programs against MG and MS should be followed according to veterinary recommendations.
5. Early Medication
Prompt treatment using appropriate antimicrobials under veterinary guidance can reduce severity.
6. Improve Litter and Air Quality
Regular litter management helps reduce ammonia and dust.
7. Nutritional Support
Provide vitamins, electrolytes, and immune boosters during stressful weather periods.

Conclusion
Changing weather conditions significantly increase the risk and severity of Mycoplasma infections in poultry farms. Layers suffer from reduced egg production and poor egg quality, while breeders face severe reproductive and hatchability losses. Because Mycoplasma infections often become chronic and difficult to eliminate, prevention through good management, ventilation, biosecurity, and stress reduction remains the most effective strategy.

Early detection and timely intervention are essential to maintain flock health, productivity, and profitability during seasonal

MS-associated EAA has a direct influence on income and biosecurity expenses because it increases cracked and degraded eggs, increases labour costs for sorting and cleanup and decreases hatchability through higher embryonic mortality when shell integrity is compromised. EAA manifests as irregularities at the egg’s apex, including thinning, increased translucency and susceptibility to cracks. These defects lead to increased egg breakage and spoilage, directly leading to degrading egg quality and marketability.

Etiology and Transmission:
Mycoplasma synoviae, belongs to the Mycoplasmataceae family and is fastidious about its culture conditions as it requires serum and NAD on modified Frey media. The pathogenicity of strains varies due to immune evasion, adhesins, sialidase activity, nitric oxide generation and antigenic diversity.

Fig. 1. Transmission of M. Synoviae
The host range of the MS infection includes chickens, turkeys, ducks, geese, guinea fowl, pheasants, quail and psittacines. Transmission occurs via both vertical and horizontal route. Vertical transmission takes place through transovarian infection, leading to early chick exposure, while horizontal transmission occurs via aerosol spread, respiratory secretions, fomites and human activity. Once introduced, the infection tends to persist, as infected flocks become lifelong carriers. Multi-age layer systems further support its persistence and contribute to episodic clinical outbreaks.

Pathogenesis:
M. synoviae primarily enters the host through the respiratory tract, with the upper respiratory mucosa serving as the initial site of colonization. With the help of specialized surface proteins and adhesions the organism attaches to the epithelial cells which help it to evade mucociliary clearance. From the respiratory tract, it can spread locally, causing tracheitis, airsacculitis and respiratory distress. In some birds, the pathogen disseminates via bacteraemia, reaching synovial membranes and joints, where it induces inflammation. This leads to synovitis, characterized by swelling, pain and lameness, often accompanied by exudation of yellowish synovial fluid. The organism may also localize in the tendon sheaths and bursae, producing tenosynovitis. Co-infections with other respiratory pathogens (e.g., E. coli, NDV and IBV) exacerbate disease severity. Chronic infections are common and affected birds may become carriers, serving as reservoirs for flock-to-flock transmission.

Clinical Signs:
Mycoplasma synoviae most commonly causes subclinical upper respiratory infections or infectious synovitis and tenosynovitis, while in layers it is also associated with eggshell apex abnormality (EAA) syndrome, characterized by thin, rough, translucent shell apices and intermittent production loss (Feberwee et al., 2009). The clinical expression of the disease is often expressed by stress and co-infections with pathogens such as infectious bronchitis virus (IBV), Newcastle disease virus (NDV) and Escherichia coli (Lockaby et al., 1998).

Fig.2. Dull, depressed hen, Inflammation of foot pad, hock joint and cavity filled with exudates
Affected birds may show mild respiratory involvement, including slight tracheal rales and sinusitis which are more evident under poor air quality or concurrent respiratory infections. The musculoskeletal form is marked by lameness, reluctance to walk, swelling of the hock joint, wing joints and footpads with exudative tenosynovitis of tendon sheaths and sternal bursitis. In systemic or severe cases, signs include depression, inappetence, ruffled feathers, weight loss and pale to cyanotic head parts, with occasional vasculitis and keel bursitis. Morbidity typically ranges from low to moderate, while mortality is generally low but may increase in the presence of secondary bacterial infections, wet litter, cold stress and immunosuppression.

Post Mortem Lesions:
– Respiratory tract:
– Mild to moderate airsacculitis with thickening, opacity and presence of turbid or caseous exudate.
– Mucoid tracheitis and sinusitis (especially when complicated by co-infections).
– Joints and musculoskeletal system:
– Synovitis: Swollen joints (particularly hock, wing and foot joints) with accumulation of yellow to serofibrinous exudate.
– Tenosynovitis: Inflamed tendon sheaths filled with exudate.
– Sternal bursitis (breast blisters) with fibrinous to caseous material.
– Systemic involvement:
– Generalized fibrinous polyserositis in some cases, especially with secondary E. coli infection.
– Emaciation and poor body condition due to chronic disease.
– Eggshell apex abnormality (in layers):
No specific gross lesion in reproductive tract, but post-mortem examination may reveal rough, thin and translucent apices of eggshells in affected flocks.

– Diagnosis:
Diagnosis of MS relies on combination of clinical observation, serology, microbiology and molecular techniques. Observation of respiratory signs such as sneezing, coughing and nasal discharge, along with joint or tendon swelling indicative of synovitis or tenosynovitis and specially in layers, eggshell apex abnormalities like thin, rough or translucent apexes can be observed.
However, clinical signs alone are not definitive, as they can overlap with other infections like NDV, IBV or E. coli.

Serological tests, including ELISA, rapid plate agglutination (RPA) and hemagglutination inhibition (HI), are useful for flock-level monitoring, though maternal antibodies and past exposure can complicate interpretation. Microbiological isolation from choanal or tracheal swabs and synovial fluid using specialized media allows definitive identification of MS, but the process is slow and prone to contamination. Molecular methods such as PCR and real-time PCR offer rapid, sensitive and specific detection of MS DNA, even at low bacterial loads. For accurate diagnosis, a combination of clinical assessment, serology and molecular confirmation is recommended, especially in flocks showing respiratory disease, joint swelling, or eggshell defects.

Treatment
Along with careful use of antibiotics, proper management practices and vaccination strategies are very important in Mycoplasma synoviae management. Treatment typically relies on antimicrobials such as tylosin, tiamulin, doxycycline or enrofloxacin, which can reduce bacterial load and clinical signs, but complete eradication is difficult due to intracellular persistence. Widespread and indiscriminate antibiotic use has led to antimicrobial resistance (AMR) in MS strains because of these challenges, thus, vaccination plays a central role in flock protection, lower bacterial shedding and prevent eggshell apex abnormalities in layers.

Prevention and Control:
Prevention focuses on biosecurity measures, including sourcing MS-free breeders, controlling movement of personnel and equipment and minimizing stressors that predispose birds to infection. Integrated control combining vaccination, strict biosecurity, monitoring via serology or PCR and responsible antimicrobial use is essential to minimize economic losses, maintain flock health and reduce the risk of AMR development. Thus vaccination, combined with good biosecurity and management practices can control MS spread, minimizing antibiotic reliance and maintaining flock productivity.

Stallen South Asia Pvt Ltd is offering a unique inactivated vaccine MS-VAC particularly against Mycoplasma synoviae.
Key Features of MS-VAC:
– The Only Vaccine Made from highly immunogenic strains of Mycoplasma synoviae
– High titre (1010 CFU)
– Oil adjuvant
– High immunogenicity.
– High safety, effective protection and field compatibility

Duration of immunity in MS-VAC

Fig. 5 Duration of immunity in MS-VAC (3 weeks after challenging with virulent MS)
MS-VAC is a vaccine produced from highly immunogenic strains of Mycoplasma synoviae. The culture is inactivated and emulsified in light mineral oil, to ensure a high degree of protection after first vaccination, however the immunity is strongest and long lasting after second inoculation.
– Clinical observation of eggs laid, in vaccinated and non vaccinated commercial hens, after infection by field MS.

Field efficacy of MS-VAC against eggshell apex abnormalities (EAA):

A significantly lower (p=0,000) percentage of EAA affected eggs was observed in group 1 than in groups 2 and 3 (statistically significant difference for p<0.001).
Hence, MS-VAC proved to be effective in protecting commercial hens from EAA, significantly more than the competitiors, in farms infected with MS.

References are available on request

Dr. Nilay Deshpande1, Dr. Saurabh Mane2
1PhD Poultry Science, ICAR-Directorate of Poultry Research, Hyderabad
1MVSc Poultry Science, ICAR-Indian Veterinary Research Institute, Izzatnagar

Lipids represent one of poultry biology’s greatest paradoxes — simultaneously essential for optimal productivity and catastrophically dangerous when metabolism dysregulates. Modern chicken strains, refined through decades of genetic selection for explosive growth and extraordinary productivity, possess lipid metabolic machinery operating at remarkable efficiency. Yet this very efficiency, coupled with the metabolic stress of high-density production, creates a precarious system vulnerable to dysregulation. Understanding how chickens process dietary lipids—and critically, what happens when this process fails—is fundamental to contemporary poultry science. Lipids contribute over twice the energy per gram compared to proteins or carbohydrates, provide essential polyunsaturated fatty acids (omega-3 and omega-6) vital for immune competence and reproduction, and serve as carriers for fat-soluble vitamins A, D, E, and K. Yet when lipid metabolism spirals out of control, the consequences are severe: fatty liver syndrome, fatty liver haemorrhagic syndrome (FLHS), fatty liver kidney syndrome (FLKS), and hepatitis collectively represent one of the most significant challenges in modern poultry production.

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From Ingestion to Hepatic Processing: The Initial Lipid Journey
The lipid metabolic odyssey begins in the gastrointestinal tract. Dietary triglycerides, the predominant lipid form in poultry feeds, undergo enzymatic hydrolysis by pancreatic lipase in the small intestine, yielding monoglycerides and free fatty acids. Bile acids emulsify these hydrophobic molecules, facilitating their incorporation into micelles that traverse the intestinal epithelium with impressive efficiency—typically 85-90% digestibility. Once absorbed, enterocytes re-esterify these components into triglycerides and package them into protomicrons— lipoprotein particles analogous to mammalian chylomicrons. These protomicrons enter the portal circulation, delivering absorbed lipids directly to the hepatocyte, establishing the liver as the metabolic epicentre determining the fate of dietary lipids: oxidation for energy, incorporation into structural membranes, or re-export to peripheral tissues. The composition of dietary lipid sources profoundly influences downstream metabolic consequences. Plant oils (soybean, sunflower, canola) provide predominantly linoleic acid (omega-6 PUFA) and oleic acid (MUFA), while animal fats contribute greater quantities of saturated and monounsaturated fatty acids.

The omega-3 to omega-6 ratio fundamentally shapes the lipid mediator profile—excessive omega-6 without compensatory omega-3 supplementation shifts the lipid-derived inflammatory mediator balance toward pro-inflammatory species, predisposing to metabolic dysfunction. Critically, chickens cannot synthesize linolenic acid, creating an absolute dietary requirement for this omega-3 PUFA.

Hepatic Synthesis and Export: The Metabolic Bottleneck
The liver functions simultaneously as processor of absorbed lipids and de novo fatty acid synthetic factory. In laying hens, the hepatic lipogenic capacity is extraordinary— synthesizing sufficient triglycerides to support daily yolk deposition, where lipids constitute approximately 33% of yolk mass by weight. This synthetic machinery operates through acetyl-CoA carboxylase and fatty acid synthase, generating novel fatty acids from carbon skeletons derived from dietary carbohydrates or amino acids. These newly synthesized lipids, together with absorbed dietary fatty acids, must be exported from hepatocytes to peripheral tissues —predominantly through very low-density lipoprotein (VLDL) particles and, in laying hens, through vitellogenin-mediated transport to the ovary.

The efficiency of hepatic lipid export fundamentally depends upon apolipoprotein synthesis, particularly apolipoprotein B (apoB), which serves as the structural scaffold of VLDL particles. This apoB synthesis, in turn, requires abundant phospholipid availability, which depends on choline—a nutrient that must be provided dietarily or synthesized through dietary methionine via methylation reactions. The lipotropic hypothesis elegantly explains why supplemental choline, methionine, and betaine mitigate fatty liver development: these nutrients are not direct energy sources but rather essential cofactors enabling the synthetic machinery supporting VLDL assembly and hepatic lipid export. When lipotropic substances become limiting, the hepatocyte becomes an anatomical traffic jam: lipids accumulate internally faster than export machinery can mobilize them peripherally, creating the pathological lipid accumulation characteristic of fatty liver.
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When Export Fails: Pathophysiology of Fatty Liver and FLHS
Hepatic steatosis—excessive hepatic triglyceride accumulation—arises when hepatocyte lipid uptake and synthesis exceed oxidation and export capacity. In laying hens, this dysregulation commonly emerges from the synergistic dysfunction of multiple regulatory pathways. High-energy or high-fat diets, particularly those rich in saturated animal fats, overwhelm export capacity through sheer substrate excess. Simultaneously, inadequate lipotropic nutrient provision cripples VLDL assembly. The gene regulatory landscape becomes progressively dysregulated: the peroxisome proliferator-activated receptors (PPARα and PPARγ), which normally enhance fatty acid oxidation and promote metabolic flexibility, show reduced hepatic expression, while sterol regulatory element-binding protein 1 (SREBP1), a master transcription factor governing lipogenic enzyme expression, becomes hyperactivated. The consequence is a metabolic phenotype characterized by relentless lipogenesis coupled with suppressed lipolysis.
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Fatty liver hemorrhagic syndrome represents the catastrophic progression of unchecked hepatic steatosis. Beyond simple triglyceride accumulation, FLHS involves severe impairment of VLDL secretion accompanied by oxidative stress, hepatocellular ballooning, and inflammatory cell infiltration. The accumulated lipids generate reactive oxygen species (ROS) as mitochondria become overwhelmed processing fatty acid substrates through β-oxidation. The hepatocellular accumulation of lipid droplets physically displaces functional hepatocytes, reducing synthetic capacity for essential proteins (albumin, clotting factors, cytochromes P450) and impairing detoxification function. Bile acid synthesis and signaling become dysregulated, further compromising lipid export. Ultimately, hepatic capillary rupture causes hemorrhage, often precipitating sudden mortality during capture or handling.
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FLHS epidemiology reveals particularly severe disease manifestations in caged laying hens during peak productivity—the combination of extreme hepatic lipogenic demand, minimal physical activity reducing fatty acid oxidation, and often suboptimal nutritional management creates a metabolic catastrophe. Prevention requires aggressive intervention: dietary fat restriction to 3-5%, polyunsaturated fat emphasis (soybean oil 2-3%), omega-3 supplementation (flaxseed or fish oil 0.5-1%), and robust lipotropic provision (choline 1200-1500 ppm, methionine and betaine at NRC-recommended levels). Antioxidant fortification with vitamin E (100+ IU/kg) and selenium (0.3-0.5 ppm) protects hepatocytes from oxidative damage.
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FLKS: The Young Broiler’s Metabolic Crisis
Fatty liver kidney syndrome predominantly affects rapidly-growing broiler chicks (2-6 weeks age), representing a distinct but equally severe lipid metabolism dysregulation. FLKS manifests as simultaneous pathological lipid accumulation in both liver and kidneys, precipitating growth depression, poor feed efficiency, and substantial mortality.
The pathophysiological substrate differs from FLHS: young broilers experience extraordinary anabolic demand for lipids required for cell membrane synthesis and organ development during rapid tissue accretion. The hepatic export system, dependent on lipotropic nutrient availability and coordinated gene expression, becomes rate-limiting under this intense metabolic stress.
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Choline emerges as the critical intervention point. Deficiency impairs both phospholipid synthesis (necessary for VLDL assembly) and apoB expression, directly constraining VLDL particle formation. The resulting lipid entrapment in hepatocytes, combined with dysregulated lipid transport to peripheral tissues, precipitates renal lipid accumulation through mechanisms not yet fully elucidated—potentially involving impaired renal lipid oxidation capacity or inflammatory responses to elevated circulating lipid levels. Management requires elevated choline provision (800-1200 ppm), particularly in starter diets, combined with polyunsaturated fat inclusion (soybean, sunflower oils 3-5%) and comprehensive antioxidant protection. Notably, excessive dietary energy density paradoxically increases FLKS risk—high carbohydrate-based energy triggers amplified de novo hepatic lipogenesis, overwhelming export capacity.
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Hepatitis and Metabolic Dysfunction: Inflammation Disrupts Lipid Homeostasis
Hepatitis—whether triggered virally, bacterially, toxically, or metabolically—fundamentally disrupts lipid homeostasis through multiple mechanisms. Hepatocellular inflammation directly impairs VLDL synthesis capacity, causing triglyceride and non-esterified fatty acid accumulation. Oxidative stress accompanying inflammation damages lipid membranes through peroxidation, generating lipid peroxides that perpetuate cellular damage. Heat stress-associated hepatitis particularly dysregulates lipid-related gene expression, specifically reducing PPARα and fatty acid oxidation capacity while maintaining or elevating lipogenic gene expression. The net result is secondary steatosis superimposed upon acute inflammation.
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Dietary management during hepatitis requires omega-3 enrichment (fish oil 1-2%) to support synthesis of pro-resolving lipid mediators (lipoxins, resolvins, protectins) that actively terminate inflammation. Saturated fat restriction minimizes pro-inflammatory lipid mediator generation. Comprehensive antioxidant support—emphasizing natural vitamin E (80-100 IU/kg), selenium (0.3+ ppm), and potentially additional antioxidants—counters oxidative stress. Identification and elimination of the hepatitis trigger (viral vaccination, bacterial antimicrobials or probiotics, mycotoxin removal) remains paramount.
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Integrated Prevention: Synthesizing Metabolic Knowledge into Practice
Effective prevention of lipid metabolism disorders requires systematic integration of nutritional, environmental, and managerial strategies. Dietary fat inclusion must balance energy requirements against metabolic risk—typically 3-5% for layers, 4-6% for broilers—with stringent prioritization of polyunsaturated plant oils over saturated animal fats. Lipotropic nutrient provision should exceed minimum requirements during stress periods: choline 1200-1500 ppm, methionine and betaine at NRC recommendations or above. Micronutrient fortification with vitamin E (50-100 IU/kg) and selenium (0.3+ ppm) protects against oxidative stress inherent to lipid-intensive metabolism.​
Environmental management—heat stress mitigation through ventilation, optimal stocking densities permitting normal activity, biosecurity preventing stress-inducing pathogens—directly supports metabolic resilience. Feed quality monitoring ensuring absence of rancid fats and mycotoxins prevents additional hepatic burden. Strain-specific considerations recognize that modern high-productivity genetics carry metabolic vulnerabilities requiring targeted nutritional support; consultation with poultry nutritionists familiar with your specific genetic line optimizes intervention strategies.
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Conclusion: Metabolic Excellence Through Informed Management
Lipid metabolism in chickens exemplifies the exquisite complexity underlying productive physiology—a system of extraordinary sophistication vulnerable to dysregulation under contemporary production stresses. The disorders arising from lipid metabolic failure—fatty liver, FLHS, FLKS, hepatitis—represent not arbitrary diseases but rather predictable consequences of pushing metabolism to or beyond biological limits. These conditions remain largely preventable through evidence-based nutritional and management practices informed by mechanistic understanding of underlying pathophysiology. By maintaining optimal dietary lipid balance emphasizing unsaturated sources, providing robust lipotropic and micronutrient support, managing environmental stressors, and employing strain-appropriate protocols, producers can sustain the metabolic machinery enabling both productivity and welfare. The lipid paradox—that lipids are simultaneously essential and potentially catastrophic—demands perpetual vigilance and informed decision-making; the reward is flocks maintaining both exceptional productivity and robust metabolic health.

References are available on request.

What is Stress?
• Stress is a state of worry caused by a difficult situation, a natural response to address challenges & threats in life. Stress is a situation just opposite to Comfort
• Chicken has a limited amount of stored up resources to help adapt to unstable conditions, a challenge or a threat. As long as the challenges are within tolerable limits, chicken manages through its reserves, adjust to the situation & come out with little/no damage
• Stress is the situation when these challenges are more intense or greater numbers, resulting a serious chemical, physical & psychological changes in chicken with harmful consequence

Picture 1
Development stages of Stress in Chicken
– The 3 stages of Stress are ALARM, ADAPTATION & EXHAUSTION
– The first stage is Alarm, a short neurological stage. It is the ‘fright or flight’ reaction based on adrenalin release which triggers the release of glucose into the blood & helps the bird prepare to power to escape
– Adaption is next, where hormones are released to control the long-term effects of stress as they adjust to the new changes in their environment. There may be elevated cortisone levels in the blood, which arrange release of glucose from the body’s reserves of carbohydrates, proteins & fats to help the bird to adjust to the stressor. Diseases associated with long term stress, like diseases of heart, digestive system, metabolic imbalances and susceptibility to disease, are all attributed to high corticosteroid production in managing long term stress.
– The third stage, Exhaustion occurs when chicken does not recover from the stressor, its body reserves depleted, and the normal metabolic function fails with death of the bird.

Once chicken is exposed to stress, it results in immunological or metabolic consequences as below:
– Regression of immune organs/systems leads to Suppressed immune function & increased disease susceptibility
– Reduction of the oxidative metabolic capacity of mitochondria
– Deficit of antioxidant reserves
– Changes in the activity of antioxidant enzymes

Types of Stress in Chicken
– Noticeable Stress
– Disease
– Environment; Heat Stress, Winter Chilling, High Speed Wind (Cyclone), Poor Ventilation
– Starvation or Drinking Water shortage
– Debeaking

– Non-Noticeable Stress
• High performance; rapid growth and peak egg production
• Overcrowding
• Mycotoxin
• Endotoxin
• Wet Litter
• Litter Ammonia
• Poor Quality Feed
• Change of Feed
• Handling
• Transportation
• Vaccination
• Transfer/Mixing/Isolation

Factors responsible for Stress in Chicken:
A. Physiological
1. High Body Weight Gain in Broiler
2. Egg Laying, especially Peak period in Layer & Breeder

B. Nutritional
1. Feed Starvation due to poor supply or inefficient feeding system
2. Drinking Water scarcity
3. Deficiency of Protein, Carbohydrate, fats, Minerals, & Vitamins.
4. Poor quality like Dusty, too Hard or too Big Particle size or old damage feed

C. Environmental
1. Heat Stress
2. Winter Chilling
3. High Humidity
4. Cyclonic Wind
5. Lightening
6. Splash of Rain water
7. Earthquake

D. Operational
1. Debeaking or Beak Trimming
2. House/Cage Transfer, Mixing & Isolation
3. Transportation from one farm to another (Chick to Grower and to Laying farm)
4. Vaccination
5. Handling for Insemination, medication & vaccination
6. Management issues like poor Space (overcrowding), Ventilation, Wet litter, Litter Ammonia
7. Change in Feed
8. Change of attendant

E. Pathological
1. Infections; bacterial, viral, fungal, protozoan, etc
2. Metabolic Disorder like gout, ascites, etc.
3. Endotoxins
4. Mycotoxins
Out of all above, the important & dreaded stresses are all Pathological stress like Infections, Mycotoxins, Endotoxins, Metabolic disorders and 2 environmental stresss, viz. Heat Stress & Cold Stress or Chilling. Please remember when one stress comes after another, then 1 + 1 is not 2 but become 11, means combined stresses are dreaded to chicken.

Heat Stress:
– Heat Stress is a situation when chicken faces difficulty in achieving balance between body heat production & body heat loss
– Chickens lack sweat glands to facilitate latent heat loss by evaporation (perspiration), and have limited un-feathered body surface areas for loss of sensible heat through conduction, radiation, & convection
– Genetics, Feather cover, Age, Body Weight, Egg Production stage & flock maintenance all affect a chicken’s heat tolerance
– Chickens are homeotherms & regulate their body Temperature across a wide range of external Temperature.
– But continuous high climate Temp overwhelm the thermoregulatory mechanisms, resulting imbalance between the amount of metabolic heat produced & their capacity to dissipate body heat in the environment

Picture 2

Picture 3

Physiological response of Chicken to elevated temperature and the Loss in Poultry?
– With Increase in Climate Temp, the Thermal gradient between the Body surface & the surrounding environment lessens with Dissipation of Heat decreasing, resulting Chicken suffering from environment-induced Hyperthermia.
– This increases Respiratory rate (Thermal Polypnea or Panting) to increase Latent Heat Loss via Evaporation of water from the Respiratory tract
– Dehydration is the most harmful effect of panting, which causes Respiratory Alkalosis, acid base imbalance leading to permanent physiological damages
– Alkalosis reduces blood ionized Calcium and ultimately Eggshell mineralization resulting Reduced Egg production, Pale Egg, Soft Shell Eggs, Thin Shell Egg, Increased Broken egg % in Layer & Breeder
– Panting causes Oxidative Stress leading to Immunosuppression, damage of Gut mucosa leading to poor digestion, Dysbacteriosis, Enteritis and increase incidence of secondary infections (Viral like LPAI & ND, Mycoplasma & Bacterial) because of immunosuppression & leaky gut situation.
– Heat Stress reduces feed consumption resulting Poor Body Weight gain in Broiler and reduced Egg production in layer & breeder.
– Heat Stress has Permanent damaging effect; damages the muscles affecting Meat Quality and Lowering Breast Muscle Yield
– Reduces Protein content of the muscles, reduction of muscle pH & Water Holding Capacity and ultimately affecting Juiciness of Chicken Meat
– Disturbs Lipid metabolism by affecting enzyme function in lipid breakdown causing Excess Fat deposition instead of converting to meat
– Heat Stress reduces Male fertility in breeder and affects hatchability severely.
– Heat Stress impact the Expression of Gene related to Growth, Production Performance & Resistance to disease
– Heat stress impairs chicken’s immune system, leading to a reduced response to vaccines, suppressing the production of antibodies and affecting the function of immune cells, particularly lymphocytes, due to the atrophy of immune organs like thymus under high temperatures; heat stress makes it harder for chicken to fight against infections after vaccination and increases their vulnerability to disease
– Heat stress lowers the level of circulating antibodies (IgM & IgG) produced after vaccination, resulting in a weaker immune response against pathogens
– High Temp cause atrophy of thymus, leading to decreased T-cell production and impaired cell-mediated immunity
– Heat stress increases release of corticosteroid and further suppress the immune system.
– Heat stress disrupts the function of immune cells; macrophages & lymphocytes, affecting their ability to recognize and fight pathogens.
– Heat stress damage the intestinal lining, allowing entry of harmful & resident microorganisms into the body system to produce infections.

How to reduce the effect of heat stress in Chicken?
– Poultry House Environment need to made near comfort zone in terms of Temperature, Humidity & Ventilation. Closed Environment Control poultry house is the perfect answer.
– Plantation of Tress on both side of each shed
– Farm construction near forest or under Coconut or Mango Garden
– Reduce Stocking Density in summer to provide more space & more ventilation
– In open house system action must be taken to REDUCE TEMPERATURE at Birds level through

I) Elevated Roof, higher centre height
ii) Coated Roofing materials
iii) Extended side roof overhang to prevent entry of direct Sunlight
iv) Thatching of Roof by Agricultural waste (Paddy & wheat straw, Jute stick, Mustard/seasame harvested dry plant) and Ceiling by Thermostat Aluminium foil
v) Constructing Side Pandals (Leaned Roof Over-hang 1 meter)
vi) Hanging of Gunny with Dipper on both side (2 layers is best)
vii) Ceiling fans in case of Broiler and Circulatory fans in Layer or breeder to improve ventilation
viii) Springler on Rooftop to cool the roof
ix) Fogger inside the shed to reduce inside temperature

Disease Stress:
– Dis ease (Not fine) or Disease is No 1 stress factor in chicken like all other living being. Even unnoticed infection cause stress to force chicken to sit without movement and stay away from feed & water.
– Stress due to Diseases is the most neglected chapter in poultry farming, especially the subclinical or asymptomatic diseases.
– Global Animal Productivity loss due to clinical & subclinical diseases is 20%. Hence, we need to understand the disease stress on chicken and must act to minimize the same.
– Every disease has some specific symptoms but there are some common manifestations to every disease as below:
1. Anorexia or off-feed
2. Dullness, lack of movement or inactive
3. Poor eye reflection
4. Huddling
5. Poor body Weight Growth and poor Egg production
6. Death

Picture 4

Picture 5

Disease Stress produces:
– Uneasy physical status beyond comfort level
– Many physiological changes in the body resulting different symptoms
– Loss of appetite, poor growth & poor production
– Direct or indirect Immunosuppression inviting many other diseases
– Death due to system failure or lack of food for long time anorexia

Mitigation of Disease:
– Practical & 100% Biosecurity to avoid disease entry in to the poultry area.
– Welfare of chicken with respect to space, ventilation, temperature, drinking water & nutrition
– Daily Health monitoring
– Monitoring of Bird’s activity & Feed Intake everyday
– Immediate identification of any deviation in health & production parameter
– Immediate diagnosis at farm & confirmatory from laboratory
– Immediate treatment or necessary action to protect the health & life of chicken

How to Recognize Stress in Chicken
– Vocalization: Chickens have alarm sounds to alert other chickens, like repetitive chirps or screaming.
– Loss of Appetite; poor feed consumption, eating little sometime & stay away from feed in almost all stresses including Heat or Cold stress and disease stress.
– Abnormal Posture: In Heat Stress Birds sits on its belly & breast touching the floor and wings spread apart to lose heat through conduction, convection & radiation. In case of Disease Stress, birds are usually inactive & huddle together near to corner or at areas of Sunlight in open shed.
– Abnormal Behavior: In Heat Stress, there will be too much Panting to lose body heat through evaporation. During disease stress, the birds remain inactive and lying with head down & beak inside litter. Deep breathing is seen in respiratory diseases.
– Water Intake: Heavy increase in case of Heat Stress but reduced in Cold stress and in most diseases.
– Repetitive Behavior: include packing, constant rocking back & forth, head swinging or toe-taping

Effect of Stress in Chicken
– Uneasy state of life, abnormal posture & abnormal activity
– Stressed chickens usually extremely anxious, pick feather & self-mutilate, may cause permanent damage of feather follicles and scar develop on their skin
– Reduced Feed intake & reduced water (except Heat Stress) intake
– Immuno-suppression leading to many diseases from already existing microorganism in the house environment or in the intestine as commensal
– Oxidative stress leading to damage of gut mucosa, poor digestion, dysbacteriosis and enteritis
– Panting & Dehydration
– Excess release of Stress hormone (corticosteroid) leading to further immunosuppression & loss of body condition
– Poor commercial performance like, poor body weight gain & high FCR in broiler and reduced egg production with poor egg shell quality in layer & breeder
– Mortality

Mitigation of Stress in Chicken
– Maintain clean, calm & disease-free poultry house environment
– Noise-free environment; chicken don’t like unusual circumstances
– Avoid environmental stress like winter chilling, summer heat stress, monsoon high humidity inside poultry house through modification of infrastructure & husbandry practice.
– Need conceptual, infrastructural & operational changes to avoid environmental stress with climate change induced global worming situation.
– Avoid compromised ventilation, especially during winter & rainy days in open system farming. Avoid poor ventilation during high humid monsoon & chilly winter months in EC shed especially with compromised structure
– Avoid overcrowding; welfare is most unattended issue creating stress in poultry
– Avoid litter ammonia, wet litter & dust in poultry house
– Follow SOP & behave gently while handling, transfer, mixing, transportation, vaccination and insemination.
– Implement 100% Biosecurity, arrange regular health monitoring & health management. Educate your team about importance of biosecurity in poultry.
– Making sure your flocks have access to safe drinking water and regular supply of recommended fresh nutritious feed during the whole production cycle.