Mycoplasma gallisepticum Infections in Chickens: Transmission and Control

Introduction

Mycoplasma gallisepticum is a pathogenic bacterium belonging to the class Mollicutes, characterized by the absence of a cell wall and a minimal genome [1]. It is the primary etiological agent of chronic respiratory disease (CRD) in chickens and infectious sinusitis in turkeys [2]. The organism colonizes the respiratory epithelium, causing a persistent, often subclinical infection that can exacerbate under stress or co-infection with other respiratory pathogens [1, 2]. This review provides a detailed examination of M. gallisepticum infections in chickens, with emphasis on transmission pathways and integrated control measures. For complementary information on laboratory diagnostics and vaccination, readers are directed to the companion article Mycoplasma gallisepticum and Mycoplasma synoviae Infections in Chickens: Laboratory Diagnosis and Control Strategies and Avian Mycoplasmosis: Mycoplasma gallisepticum and Other Species, Vaccination and Control in Poultry.

Etiology

M. gallisepticum is a pleomorphic, non-motile bacterium that requires a sterol-supplemented medium for growth [1]. Its small genome (approximately 1.0 Mb) limits biosynthetic capacity, making it an obligate parasite dependent on host cells for nutrients [1, 2]. The organism possesses a specialized tip structure, the bleb, which mediates adhesion to sialic acid receptors on ciliated respiratory epithelial cells [2]. Adhesion is a critical virulence factor; strains lacking the ability to adhere are attenuated [1]. M. gallisepticum also exhibits antigenic variation through phase and size variation of surface lipoproteins, enabling immune evasion [2]. The organism is sensitive to heat, drying, and common disinfectants but can survive for days in organic material such as nasal exudate and feather dust [1].

Epidemiology and Host Range

M. gallisepticum infects chickens, turkeys, and other galliform birds, with occasional reports in passerines and game birds [1, 2]. In chickens, the infection is distributed worldwide, with higher prevalence in multi-age and backyard flocks compared to single-age commercial operations [2]. The infection can be vertically transmitted through the egg, leading to infected progeny that may remain subclinical for weeks [1]. Horizontal transmission occurs rapidly among susceptible birds housed in close contact [2]. The expression of clinical disease is influenced by concurrent infections with infectious bronchitis virus, Newcastle disease virus, Escherichia coli, or Mycoplasma synoviae, as well as environmental stressors such as ammonia, dust, and poor ventilation [1, 2]. Co-infection with E. coli is common; refer to Colibacillosis in Poultry: Escherichia coli Infections in Chickens for details on this interaction.

Transmission: How Is Mycoplasma Spread in Chickens?

Understanding how mycoplasma is spread in chickens is fundamental to designing effective control programs. M. gallisepticum transmission occurs via two primary routes: vertical (transovarian) and horizontal (direct and indirect) [1, 2].

Vertical transmission
Infected breeder hens shed M. gallisepticum into the reproductive tract, and the organism can enter the developing egg before shell deposition [1]. This leads to infected chicks at hatch, which may appear normal but carry the pathogen [2]. Vertical transmission is the main mechanism by which the infection is perpetuated in commercial broiler and layer flocks if breeder flocks are not monitored [1].

Horizontal transmission
Direct bird-to-bird transmission occurs through aerosolized respiratory droplets, especially during coughing and sneezing [2]. The organism can also be spread via contaminated dust, feathers, and fomites (e.g., egg trays, transport crates, human clothing) [1]. Airborne transmission over short distances (up to several meters) is documented [1]. In crowded, poorly ventilated housing, transmission is amplified [2]. The following table summarizes transmission routes:

For a more focused discussion on transmission dynamics, see How Mycoplasma gallisepticum Spreads in Chicken Flocks: Transmission Dynamics and Control.

Clinical Signs

The incubation period in chickens is typically 10 to 14 days [1]. In uncomplicated infections, clinical signs are often mild or inapparent, especially in adult birds [2]. When clinical disease occurs, it manifests as chronic respiratory disease characterized by rales, coughing, sneezing, nasal discharge, and conjunctivitis [1, 2]. Infected birds may show decreased feed intake, reduced growth rate, and lower egg production [2]. In layers, egg quality may decline with shell thinning and reduced interior quality [1]. Secondary bacterial infections, particularly with avian pathogenic E. coli, can lead to severe airsacculitis, pericarditis, and perihepatitis, increasing mortality [2]. Ocular infections with frothy ocular discharge are common in young birds, especially in M. gallisepticum outbreaks among backyard flocks [1]. For a broader overview of ocular signs and treatment, see Mycoplasma in Poultry: Clinical Signs, Eye Infections, Treatment, and Control.

Pathology

Gross lesions are primarily confined to the respiratory tract. Serous to catarrhal exudate is present in the nasal passages, infraorbital sinuses, trachea, and bronchi [1]. The air sacs may appear thickened, cloudy, or filled with caseous exudate, particularly when airsacculitis develops [2]. In severe cases with E. coli co-infection, fibrinous pericarditis and perihepatitis are common [2]. Histologically, M. gallisepticum causes hyperplasia and loss of cilia in the tracheal epithelium, infiltration of lymphocytes and plasma cells into the lamina propria, and lymphoid follicle formation [1]. Air sac lesions consist of granulomatous inflammation with macrophages and multinucleated giant cells [1]. The organism persists intracellularly within epithelial cells and macrophages, contributing to chronicity [2].

Diagnostics

Laboratory confirmation is essential because clinical signs are not pathognomonic [1]. Diagnostic approaches are detailed in the companion article Mycoplasma gallisepticum and Mycoplasma synoviae Infections in Chickens: Laboratory Diagnosis and Control Strategies. A brief summary is provided here.

Isolation and identification
M. gallisepticum can be cultured from tracheal swabs, sinus exudate, or air sac lesions using specialized media (e.g., Frey's medium supplemented with swine serum and nicotinamide adenine dinucleotide) [1]. Colonies on agar exhibit the typical "fried egg" appearance with a central dense core [2]. Growth is slow, requiring 3 to 10 days [1]. Identification is confirmed by growth inhibition tests or immunofluorescence using specific antisera [2].

Serology
Serum plate agglutination (SPA), hemagglutination inhibition (HI), and enzyme-linked immunosorbent assays (ELISA) are used for flock screening [1, 2]. SPA is sensitive but can yield false positives due to cross-reactions with other mycoplasma species [1]. HI and ELISA are more specific [2].

Molecular detection
Polymerase chain reaction (PCR) targeting the 16S rRNA gene or the mgc2 adhesion gene is now the method of choice for rapid, sensitive detection [2]. Real-time PCR allows quantification and differentiation from M. synoviae [1]. These molecular assays are widely available in diagnostic laboratories and can be applied to tracheal swabs, air sac samples, and even egg contents [2].

A diagnostic decision tree integrating these methods is presented below.

flowchart TD
    A[Clinical suspicion in chickens], > B[Collect tracheal swab / sinus exudate]
    B, > C{Initial testing}
    C, > D[Apply PCR for M. gallisepticum]
    D, > E{Result}
    E, >|Positive| F[Confirm with culture or serology]
    E, >|Negative| G[Rule out or test for other pathogens]
    F, > H[Flock diagnosis established]
    H, > I[Implement control measures]
    G, > J[Consider M. synoviae / bacterial co-infections]
    J, > K[Refer to companion articles]

Treatment

Antibiotic therapy can reduce clinical signs and shedding but rarely eliminates the organism from a flock [1, 2]. M. gallisepticum lacks a cell wall, so beta-lactam antibiotics are ineffective [1]. Effective classes include macrolides (tylosin, tilmicosin, tulathromycin), pleuromutilins (tiamulin), tetracyclines (chlortetracycline, doxycycline), fluoroquinolones (enrofloxacin), and aminoglycosides (gentamicin) [2]. However, resistance to tylosin and tetracyclines has been reported [1]. Treatment via drinking water or feed is common, but individual injection may be used for valuable breeding stock [2]. The decision to treat should be guided by in vitro susceptibility testing if possible [1]. Importantly, treated birds remain carriers, and treated eggs may still transmit infection [2]. Vaccination is a more sustainable long-term strategy; see Mycoplasma gallisepticum Vaccine in Poultry: Protocols and Efficacy and Avian Mycoplasma Vaccine: Principles, Efficacy, and Application in Poultry.

Control Strategies

Control of M. gallisepticum in chickens relies on an integrated approach combining biosecurity, surveillance, eradication in breeding stock, and vaccination [1, 2].

Biosecurity and management
Preventing introduction of infected birds is paramount. Replacement stock should originate from M. gallisepticum-free sources. Strict all-in/all-out management with thorough cleaning and disinfection between flocks is recommended [2]. Rodent control and limiting visitor access reduce fomite transmission [1]. M. gallisepticum is inactivated by common disinfectants such as quaternary ammonium compounds, chlorhexidine, and formaldehyde [2].

Surveillance and eradication
In primary breeding flocks, regular serological testing (e.g., monthly SPA and HI) is used to detect infection [1]. Positive flocks are culled to maintain pathogen-free status (mycoplasma-free certification) [2]. In commercial layers and broilers, eradication is often not economically feasible, so management aims to minimize clinical disease [1].

Vaccination
Live attenuated vaccines (e.g., strain ts-11 or 6/85) and inactivated bacterins are available [1, 2]. Live vaccines are administered via eye drop or spray to pullets before lay. They reduce respiratory lesions, egg transmission, and clinical signs [2]. However, they do not prevent infection; they limit shedding and disease expression [1]. The Mycoplasma in Poultry: Causes, Clinical Signs in Chicken Poop, and Control Strategies article provides additional management context.

Antimicrobial metaphylaxis
In high-risk situations, in-feed tylosin or chlortetracycline may be used prophylactically, but this practice is discouraged due to resistance development [1, 2].

The following table outlines key control measures by production type:

For vaccination strategies in detail, see Mycoplasma Infections in Poultry: Vaccination Strategies and Control Programs.

Conclusions

Mycoplasma gallisepticum remains a significant pathogen in chicken flocks worldwide, causing chronic respiratory disease and economic losses through reduced performance. Its ability to transmit both vertically and horizontally necessitates stringent control measures in breeding pyramids. Modern diagnostics, including PCR and serology, enable early detection, while vaccination and biosecurity form the backbone of sustainable control. Understanding how mycoplasma is spread in chickens is the first step in breaking the transmission cycle. Continued vigilance and adherence to quality assurance programs are essential to maintain flock health.

References

[1] Swayne, D. E., Boulianne, M., Logue, C. M., McDougald, L. R., Nair, V., & Suarez, D. L. (Eds.). (2020). Diseases of Poultry (14th ed.). Wiley-Blackwell.

[2] Aiello, S. E., & Moses, M. A. (Eds.). (2025). The Merck Veterinary Manual (11th ed.). Merck & Co., Inc. *** Disclaimer: This article is for educational and informational purposes only. It is not intended to substitute for professional veterinary advice, diagnosis, treatment, or regulatory guidance. Always consult a licensed veterinarian or qualified specialist regarding animal health, disease diagnosis, and therapeutic decisions.