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Other Names: Mycotic Infection, Bronchomycosis, Pneumomycosis, Pulmonary Aspergillosis

Aspergillosis is a noncontagious, opportunistic fungal (mycotic) infection caused by Aspergillus spores. The disease is common in chickens and other captive birds. Birds are particularly susceptible due to their unique respiratory system. A. fumigatus is the most common causative species, followed by A. flavus. Aspergillus spores are ubiquitous in the environment, and grow anywhere there is organic matter and moisture, especially in warm, humid weather.

Aspergillosis can present in acute or chronic form.
  • Acute form: The acute form, often referred to as brooder pneumonia, is usually seen in young chicks, resulting from exposure to an overwhelmingly high concentration of fungal spores.
  • Chronic form: The chronic form is typically seen in adult chickens with compromised immune systems.
Besides the two forms of aspergillosis, there are also several manifestations of the disease, depending on which body systems or organs are infected. Pulmonary aspergillosis is the form most common in chickens, manifesting as respiratory disease. Other less common forms involve infections of the eye (ophthalmitis), brain (encephalitis), skin (dermatitis), joints (osteomycosis), and viscera (systemic).
Types of Aspergillosis in chickens


Chickens become infected with Aspergillus spores through exposure in their environment. Any disturbances which generate large amounts of dust particles, usually contain Aspergillus spores.
Aspergillus transmission to chickens
If a chicken inhales significant quantities, it can cause disease. However, the inhaled spores may not cause disease right away, and instead remain dormant in the bird's air sacs and lungs, until a stressful event or illness triggers Aspergillus to begin to cause damage.


Early diagnosis and treatment of Aspergillosis can be difficult since obvious clinical signs often do not develop until the disease is advanced. Diagnostic testing includes blood work (complete blood count (CBC), biochemistry), fungal culture, serology, radiographs, endoscopy, and histopathology.
  • Blood work: The following characteristics may be indicative of aspergillosis:
    • Elevated liver values (aspartate aminotransferase and lactate dehydrogenase)
    • Elevated creatine kinase
    • Increased uric acid
    • Electrolyte abnormalities
    • Decreased albumin: globulin ratio (<0.5)
    • Moderate to severe leukocytosis with heterophilia (25,000–100,000 cells/mcL)
    • Hyperglobulinemia (beta and gamma)
    • Hypoalbuminemia
    • Hypoglycemia
    Repeated blood work can be used to evaluate disease progression and treatment success.
  • Radiographs: May be helpful for finding general cloudiness to air sac or lung fields, and pulmonary or air sac granulomas. Although, these lesions will only be seen during the later stages of the infection.
  • Cytology and fungal culture: Using samples taken from the trachea, air sacs, or throat. Can be useful for detecting fungal spores. Cytology may show septate, 5- to 10-mcm-thick hyphae with straight parallel sides, ball-shaped terminal ends, and 45° branching.
  • Necropsy exam: Lesions typically involve the respiratory system; chronic lesions usually involve the entire respiratory system, but acute cases can have lesions in the lungs and air sacs. Chickens with aspergillosis typically have white or yellow plaques or nodules/granulomas and a mold-like lesion, or a general cloudiness, in the air sacs and lungs of affected birds.


Aspergillosis treatment is difficult and lengthy. Therapy generally consists of 4 to 6 months of systemic antifungal agents, such as itraconazole, topical application of antifungal agents to granulomas using endoscopy, or nebulization with antifungal agents. It also requires modification of the bird's environment, and supportive care.

Clinical Signs

Loss or change in voice pitch
Reduced crowing
Difficulty breathing
Tail bobbing
Increased thirst
Respiratory abnormalities (dyspnea, tachypnea, cyanosis)
Reduced appetite
Weight loss
Enlarged nares
Green urates in droppings
Cloudy cornea
Eye discharge
Conjunctival yellow exudate


  • History
  • Clinical signs
  • Physical exam
  • Complete blood count (CBC)
  • Fungal culture - taken of the throat, trachea or air sacs
  • Cytology
  • Endoscopy
  • Radiography
  • Necropsy and histopathology

Reported Cases

  • Case 1: Tracheal aspergillosis in a Chickens Tracheal aspergillosis was diagnosed in a flock of 3-week-old replacement pullets. The flock showed an increase in mortality after a windy weekend. At necropsy, the birds exhibited cyanotic beaks, small, yellowish, raised nodules on the tracheal mucosa (which was also hemorrhagic), and congested lungs, kidneys and liver. Microscopically there was brinonecrotic tracheitis associated with large numbers of septate fungal hyphae. Aspergillus fumigatus was isolated from several tracheas. Ref

  • Case 2: Tracheal aspergillosis in a Chickens Focal mycotic tracheitis resulting in obstruction of the syrinx was the cause of death in three chickens from three different premises with a history of unexplained, sudden death. Postmortem examination revealed a caseous plug formed from focal fungal infection obstructing the syrinx. Ref

  • Case 3: Disseminated aspergillosis in a Broiler breeders Increased morbidity and mortality occurred in a 5-wk-old broiler breeder replacement pullet flock. The affected broiler pullet flock was housed on the first floor of a two-story confinement building. Mortality increased to 0.1%/day compared to the flock on the second floor, which had mortality levels of less than 0.01%/day. Clinical signs in the affected chickens included inactivity, decreased response to stimuli, and anorexia. No respiratory or neurologic signs were observed. On necropsy, affected pullets were dehydrated and emaciated and had disseminated variably sized single or multiple heterophilic granulomas that contained intralesional septate and branching fungal hyphae. Lesions were extensive around the base of the heart in the thoracic inlet and in the kidneys. Other affected organs included eyelid, muscle, proventriculus, ventriculus, intestine, liver, spleen, lung, and heart. Aspergillus flavus was cultured from the visceral granulomas. The source of flock exposure to the organism was not determined. Ref

  • Case 4: Aspergillosis in a Chickens Two flocks of broiler chickens aged 15 to 30 days presented respiratory signs such as dyspnea and up to 25% mortality. These were the only two flocks in the farm where a bed of sunflower shells was used instead of the rice-hull bedding used in other flocks. At necropsy, severe ascites, right heart hypertrophy, pulmonary congestion, and extensive multifocal granulomatous pneumonia were recorded. Histopathologic examination revealed chronic multifocal mycotic granulomatous pneumonia. Aspergillus fumigatus was identified by microbiologic study from pulmonary specimens. After disinfecting the floor and changing the bedding, no clinical signs were recorded in the farm. Severe chronic granulomatous pneumonia caused by A. fumigatus in the chickens of the present study may have caused hypoxia, leading to pulmonary hypertension, heart failure, and ascites. Ref

  • Case 5: Aspergillosis in a Chickens Between the fifth and tenth day of life, 360 chicks from a flock of 4000 developed unspecific clinical signs and died. The birds were housed in a reused aviary litter, without previous treatment. In 11 six-day-old female ISA Brown chicks, necropsy revealed firm, yellowish-white, multinodular lesions extending from the pleura to the lung parenchyma. Histologically, a granulomatous, multifocal to coalescent pneumonia was observed. Granulomas were characterized by central necrosis, with heterophil and epithelioid macrophage infiltration and presence of countless Y-shaped intralesional septate hyphae morphologically compatible with Aspergillus spp. The diagnosis through isolation confirmed Aspergillus fumigatus. Ref

  • Case 6: Aspergillosis in a Kingfisher A 4-yr-old male Micronesian kingfisher was suspected of having an aspergillus infection. The infection was thought to be related to stress associated with movement to a new enclosure/exhibit and cage-mate aggression. The diagnosis was based on an elevated white cell count, positive antibody and antigen aspergillus titers, and abnormal plasma protein electrophoresis characterized by a moderate elevation of 2 and severe elevation on the protein fractions. The bird was treated with antifungal medication administered systemically and by nebulization for 10 wk. Response to treatment was monitored by serial white cell counts and plasma electrophoresis. Clinical improvement in this bird was correlated with a return of the white blood cell count to normal levels and what was considered a normal protein electrophoresis distribution. Ref

  • Case 7: Aspergillosis in a Pacific eider A four-year-old Pacific eider (sea duck) was reported to have a history of open-mouth breathing. They had been treated for suspected aspergillosis prior to death and was submitted to Texas A&M Veterinary Medical Diagnostic Laboratory (TVMDL) for necropsy. At necropsy, the clinical suspicion of aspergillosis was confirmed. All air sacs were coated by green, velvety, fungal colonies that released spores upon manipulation. Some air sacs were also covered by thick layers of fibrin, and inflammatory exudate extended into the lungs. Histopathology showed abundant fungal hyphae coated by layers of conidia. Ref

  • Case 8: Aspergillosis in a Chickens Aspergillosis was diagnosed in two flocks of 9-day-old chicken broilers. The birds presented for gasping and elevated mortality. On necropsy, most birds had yellow, mucoid plugs partially occluding the trachea, in the region of the syrinx. Aspergillus favus, Aspergillus fumigatus and Zygomyces fungi were isolated from the lungs. The source of infection was most likely contaminated bedding material Ref

  • Case 9: Aspergillosis in a Hen A 5-month-old female chicken with a history of dyspnea was presented to the Texas A&M Veterinary Medical Diagnostic Laboratory (TVMDL) in Gonzales for necropsy. Duration of illness was approximately one week. This bird was the only one that had died out of a flock of four. Upon examination, the bird weighed 692 grams and had moderate breast muscle atrophy. Numerous 1-3 mm, round, cream-colored nodules were present in the anterior and posterior air sacs and were scattered throughout the parenchyma of both lungs. The right primary bronchus, immediately distal to the syrinx, was completely occluded by caseous inflammatory exudate. Gross lesions consist of small, white, caseous nodules scattered throughout the lung tissue, usually accompanied by similar-sized caseous plaques on thickened air sac membranes. Caseous exudate can also be observed at the level of the syrinx and within the bronchi. Ref

  • Case 10: Aspergillosis in a Indian runner duck Aspergillosis was the cause of death of a 3-month-old, Indian runner duck, submitted with a clinical history of marked difficulty breathing. At necropsy, the bird had a localized accumulation of a yellowish exudate at the bifurcation of the trachea and syrinx, from which A. fumigatus was isolated. Histologically, severe inflammation and large numbers of fungal hyphae obstructed the tracheal lumen and infiltrated the cartilage rings. The litter material covered by a blackish mold in the coop of this bird was likely the source of infection. Ref

  • Case 11: Fungal ophthalmitis in a Chicks A flock of 15-day-old chicks from a breeder farm started developing unilateral periorbital swelling and turbid discharge from the eye, eyelids swollen shut and adhered together, with a cloudy cornea and cheesy yellow exudate within the conjunctival sac. Ref

  • Case 12: Mycotic keratitis in a Duck A 1.5-year-old female khaki Campbell duck was evaluated for lethargy and a swollen left eye (OS). Mucoid discharge, chemosis, and conjunctival hyperemia with trace aqueous flare, indicating anterior uveitis, in the anterior chamber were evident on ophthalmic examination. There was no fluorescein stain uptake by the cornea. Initial topical antibiotic therapy and systemic anti-inflammatory treatments were unsuccessful, and the lesion progressed to a diffuse, yellow-white plaque, which covered 90%–95% of the cornea 4 days later. There was moderate blepharospasm, mild blepharedema, and epiphora OS. The mobility of the nictitating membrane was impaired because of the presence of the plaque over the cornea. Cytologic examination of a corneal scraping revealed fungal hyphae, and aerobic culture confirmed Aspergillus species. Treatment with topical voriconazole (1 drop OS q4h–q6h) was initiated and was switched to oral voriconazole (20 mg/kg PO q12h) 6 days after initiating treatment. The ocular disease improved during the antifungal treatment period. Eighty-four days after initial presentation (9 days after discontinuation of treatment), there was no clinical evidence of mycotic keratitis on ophthalmic examination. Ref


Supportive careIsolate the bird from the flock and place in a safe, comfortable, warm location (your own chicken "intensive care unit") with easy access to water and food. Limit stress. Call your veterinarian.
Amphotericin B1.5 mg/kg every 8 hours for 3-5 days (given IV), 1 mg/kg every 8 to 12 hours, diluted with 1 mL of sterile water (given intratracheal via nasal flush), or 7 mg/mL administered with 1 mg/mL sterile water/saline for 15 minutes, every 12 hours (if given via nebulization).
Clotrimazole1% aqueous solution used for nasal flush or nebulization for 30-60 minutes. Can also be applied topically (10 mg/kg) directly into the tracheal lesion.
Itraconazole5-10 mg/kg administered orally, every 12 hours for 5 days, than once a day for 16 days. Usually given in combination with amphotericin B IV route.
Ketoconazole10-30 mg/kg administered orally, every 12 hours for 21 days.
Terbinafine hydrochloride15-30 mg/kg administered orally, every 12 hours, in conjunction with itraconazole. Can also be nebulized as 1 mg/mL of aqueous solution for 20 minutes, every 8 hours.
Voriconazole10 mg/kg every 12 hours, administered orally.
Fluconazole5-15 mg/kg PO every 12 hours.



  • Minimizing use of antibiotics and corticosteroids
  • Design coops with good ventilation to ensure regular air flow. Dry and dusty environments favor spore formation.
  • Remove moldy straw or hay
  • Frequently move feeders and water dispensers to different areas to prevent growth of mold
  • Conduct regular air quality tests
  • Reduce the potential for condensation on cold surfaces by adding insulation.
  • Design run floor for proper drainage to eliminate standing water after rains.


Treatment is usually long-term, frustrating, and often unrewarding if the disease is not recognized until the later stages of the infection. Early treatment is essential for a postive outcome.

Scientific References

Good Overviews

Risk Factors

  • Immunosuppression
  • Stress
  • Poor ventilation or air quality
  • Exposure to moldy litter, hay, stray, bedding, or feed.
  • Using corncob, saw dust, or walnut shells for bedding
  • Preexisting disease condition
  • Corticosteroid use
  • Long-term antibiotic use
  • Nutritional deficiencies (especially vitamin A)
  • Exposure to respiratory irritants (disinfectant fumes, aerosol sprays, air freshers, etc.)