Introduction
Inclusion Body Hepatitis (IBH) is an economically important viral disease of broiler chickens characterized by sudden mortality, hepatitis, and the presence of intranuclear inclusion bodies in liver cells. The disease is primarily caused by Fowl Adenoviruses (FAdVs), particularly serotypes belonging to species D and E. IBH has become increasingly significant worldwide due to its impact on broiler performance, increased mortality, poor feed conversion, and substantial economic losses. The disease mainly affects young broiler chickens between 3 and 7 weeks of age, although birds of other ages may also be affected. Vertical transmission from breeder flocks and horizontal spread through contaminated litter, water, equipment, and personnel play major roles in disease dissemination.

Etiology
IBH is caused by Fowl Adenoviruses (FAdVs), non-enveloped double-stranded DNA viruses belonging to the genus Aviadenovirus within the family Adenoviridae. Several serotypes have been associated with disease outbreaks, including FAdV-2, FAdV-8a, FAdV-8b, and FAdV-11.
Predisposing factors include:
– Immunosuppression caused by Infectious Bursal Disease (IBD)
– Chicken Infectious Anemia (CIA)
– Mycotoxicosis (Poor quality of feed ingredients contaminated with fungus and Mycotoxins).
– Poor Biosecurity and Management
– High stocking density

Clinical Signs
Affected broiler flocks may exhibit:
– Sudden increase in mortality
– Depression and lethargy
– Huddling with Ruffled feathers
– Reduced feed and water consumption
– Usually affects birds of 3 to 5 weeks age, but can be seen in the chicks aging from 4-5 day old.
– Pale comb and wattles
– Poor weight gain
– Diarrhoea with mucoid droppings or green droppings
– Anemia in severe cases
Mortality rates generally range from 5–15%, but outbreaks may occasionally result in mortality exceeding 30%.

Post-Mortem Lesions
The most characteristic lesions are observed in the liver.
Gross Lesions
Liver
– Enlarged, swollen, and pale liver
– Yellowish discoloration
– Multifocal necrotic foci
– Petechial and ecchymotic hemorrhages
– Friable consistency
Kidneys
– Enlarged and pale kidneys
– Congestion
Heart
– Hydropericardium may occasionally be present
– Pale myocardium
Spleen
– Enlargement and congestion
Histopathological Lesions
Microscopic examination reveals:
– Severe hepatic necrosis
– Basophilic intranuclear inclusion bodies in hepatocytes
– Degeneration and destruction of liver cells
– Mononuclear cell infiltration
The presence of characteristic intranuclear inclusion bodies is considered pathognomonic for IBH.

Serology
Serological testing is useful for monitoring flock exposure and breeder immunity.
Common serological methods include:
ELISA (Enzyme-Linked Immunosorbent Assay)
– Detects antibodies against Fowl Adenovirus
– Useful for flock monitoring
– Evaluates maternal antibody levels
Virus Neutralization Test (VNT)
– Determines serotype-specific antibodies
– Primarily used in research and epidemiological investigations
Interpretation
– High antibody titers in breeders provide maternal protection to progeny.
– Seroconversion in broilers indicates field exposure.
– Paired serum samples can help determine recent infection.
Diagnosis
Diagnosis should be based on a combination of clinical history, post-mortem findings, histopathology, and laboratory confirmation.
Field Diagnosis
Suspect IBH when:
– Sudden mortality occurs in 3–7 week-old broilers.
– Enlarged, pale, hemorrhagic liver is observed.
– There is a history of immunosuppressive diseases.
Laboratory Diagnosis
Histopathology
– Demonstration of intranuclear inclusion bodies in hepatocytes.
Polymerase Chain Reaction (PCR)
– Highly sensitive and specific.
– Detects and identifies FAdV serotypes.
Virus Isolation
– Performed in chicken embryo liver cells or embryonated eggs.
Immunohistochemistry
– Detects adenoviral antigen within tissues.
Sequencing
– Used for epidemiological studies and strain characterization.

Treatment
There is no specific antiviral treatment for Inclusion Body Hepatitis.

Management is mainly supportive:
Supportive Therapy
– Multivitamin supplementation
– Vitamin E and Selenium administration
– Use D’Bio-Mix 20-25 mL per 100 birds and ABES-URZZA 20 ml for 100 birds.
– Ionic electrolyte (ABESTRAL) supplementation and probiotic prebiotic supplementation
— Adequate hydration
Control of Secondary Infections
– Antibiotics may be administered under veterinary supervision to control secondary bacterial infections.
Management Measures
– Reduce stress factors
– Improve ventilation
– Maintain litter quality
– Ensure proper nutrition

Prevention and Control
Effective prevention relies on biosecurity and breeder vaccination.

Biosecurity Measures
– All-in/all-out management
– Thorough cleaning and disinfection
– Restriction of farm visitors
– Proper disposal of dead birds
– Control of rodents and insects
– Sanitation of equipment and vehicles
Breeder Flock Management
– Monitor antibody levels regularly.
– Vaccinate breeders to ensure maternal antibody transfer.
– Prevent immunosuppressive diseases such as IBD and CIA.
Control of Vertical Transmission
– Maintain healthy breeder flocks.
– Conduct routine serological surveillance.
– Implement strict hatchery hygiene.

Vaccination Schedule
Vaccination strategies vary according to local epidemiology and circulating serotypes.
Breeder Vaccination Program
Age Vaccine
8–10 weeks Killed IBH (primary dose)
14–16 weeks Booster dose
18–20 weeks (before lay) Optional booster in high-risk areas
Broiler Vaccination
Routine vaccination of broilers is generally not practiced in many regions because protection is primarily achieved through maternal antibodies. However, live or inactivated vaccines may be considered in endemic areas under veterinary guidance.
Objectives of Vaccination
– Prevent vertical transmission
– Enhance maternal antibody levels
– Reduce mortality and production losses
– Improve flock uniformity

Economic Impact
IBH can result in:
– Increased mortality
– Poor growth performance
– Reduced feed efficiency
– Higher medication costs
– Increased carcass condemnation
– Significant financial losses to poultry producers

Conclusion
Inclusion Body Hepatitis remains an important viral disease of modern broiler production. Early diagnosis, strict biosecurity, breeder vaccination, and effective management practices are essential for disease prevention and control. Maintaining strong maternal immunity through breeder vaccination and minimizing immunosuppressive conditions can significantly reduce the impact of IBH on commercial poultry operations.

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