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Airsacculitis: Avian Respiratory Anatomy & Pathology

Scientific facts on Mycoplasma, E. coli respiratory lesions, and air sac bellows.

Scientific Overview

Airsacculitis is the inflammation of the avian air sacs, characterized by cloudiness, mucosal thickening, and caseous (cheesy) exudates. Lacking diaphragm muscles, birds rely on a healthy air sac bellows system for gaseous exchange; airsacculitis causes respiratory failure and ascites.

Avian Air Sac Anatomy & Bellows Physiology

Chickens possess nine air sacs (four paired and one single) that act as bellows to pump air through the rigid, non-expandable lungs. Because the air sacs are connected directly to the pneumatic bones (femur, humerus), respiratory infections can easily spread into the skeletal system. Healthy air sacs are crystal-clear, thin membranes.

Pathogenesis: Mycoplasma & E. coli

Airsacculitis is typically triggered by primary respiratory viruses (IBV, NDV) or Mycoplasma gallisepticum, which damage the tracheal cilia. Secondary opportunistic Escherichia coli bacteria then colonize the air sacs, causing acute fibrinous airsacculitis, perihepatitis (infected liver capsule), and pericarditis (infected heart sac). Necropsy reveals thick, yellow cheesy plaques in the thoracic cavity.

Environmental Control & Ventilation

Preventing airsacculitis requires keeping chicken farm ammonia levels below 15 ppm. Ammonia gas paralyses the tracheal cilia, allowing bacteria to migrate into the air sacs. Managing minimum ventilation fan cycle runtimes extracts evaporated moisture and keeps straw litter dry, preventing ammonia spikes.

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Airsacculitis: Avian Respiratory Anatomy & Pathology — Frequently Asked Questions

Can airsacculitis be treated? expand_more
Yes. Early-stage bacterial airsacculitis can be treated with antibiotics (Tylosin, Tilmicosin, or Enrofloxacin) under veterinary supervision. Late-stage cheesy lesions are irreversible.
Why is airsacculitis called a silent killer in broilers? expand_more
Birds display mild snicking (coughing) at start, but tissue damage progresses silently, leading to sudden cardiovascular failure (ascites or water-belly) at Week 5.
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