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Fungal Pneumonia, Mycosis

Aspergillosis is a common, non-contagious fungal infection of ducks caused by members of the fungal genus Aspergillus. A. fumigatus is the most common species isolated from infected ducks. Aspergillus spp. are widespread in nature. Healthy ducks are regularly exposed to fungal spores on a daily basis, sometimes even carrying them in their lungs and air sacs without causing a problem. However, Aspergillus spp. are quite opportunistic, so if a vulnerable duck is exposed (usually the result of a concurrent infection or injury that has worn down their immune defenses), than it takes the opportunity to cause infection. Clinical signs vary widely, depending on what organs are affected. Aspergillosis can be either localized or diffuse, and often results in a progressive, debilitating illness. Aspergillosis usually affects the duck's upper and lower respiratory tract, although any organ systems can become infected.

Ducks are most susceptible to becoming infected with Aspergillus spp. during the following situations:
  • They have been receiving antibiotics and/or steroids for longer than a week in duration.
  • They are regularly exposed to damp bedding that is rarely changed
  • They are living in a warm, humid environment with poor air circulation or ventilation.
  • They are regularly exposed to large accumulations of dust; on the walls, bedding, and/or surrounding objects, especially at those surfaces that at their same level.
  • They have a concurrent or chronic disease, resulting in pain and/or impairment of the immune system.
  • They are living in overcrowded conditions
  • They are kept in a poor sanitary environment that is rarely cleaned, with a buildup of feces.
  • They are given moldy feed to eat, or exposed regularly to mold accumulation on old damp bedding, straw, hay, leftover food substances, etc.
Aspergillus spp. are opportunistic fungi commonly found in nature in the environment (bedding litter, hay, straw, dust, air), soil and feed grains. They are distributed worldwide and tend to multiply rapidly with high humidity and warm (> 77°F (25°C)) temperatures. Aspergillosis can manifest in both acute and chronic form.
  • Acute disease: Acute aspergillosis is a fatal respiratory disease that most commonly occurs in young, highly stressed or immunocompromised, newly captive ducks that are exposed to large amounts of Aspergillus spores in their captive environment. Clinical signs have a rapid onset, resulting in death in a matter of days. Most commonly observed signs include depression, difficulty breathing, lethargy, loss of appetite, increased thirst, cyanosis, abdominal enlargement, and sometimes sudden death.
  • Chronic aspergillosis: Chronic aspergillosis is usually the most frequent form of aspergillosis in ducks, and is most common in mature, adult ducks. These ducks usually have a recent history of receiving antibiotics or corticosteroids, previous disease, stressful event (relocation to a new location, predator attack, etc.), or suffering from a chronic disease such as bumblefoot. Clinical signs develop slowly, and often non-specific, such as reduced activity level, loss of appetite, change in behavior, or weight loss while maintaining a good appetite. When air sacculitis is involved, caused by infection of the air sacs with the fungus, clinical signs include increased respiratory effort, vocalization changes, tail-bobbing, open-mouthed breathing, and audible respiratory sounds.
Aspergillosis is not a transmittable disease, ducks are infected through inhaling Aspergillus spores in the environment. Since multiple flock members live in the same environment, multiple birds may become affected.

Aspergillosis treatment requires long-term antifungal therapy, often required for a minimum of 8 weeks.


Loss of appetite
Open-mouthed breathing
Tail bobs
Voice change
Rapid weight loss


  • History
  • Clinical signs
  • Physical exam
  • Fungal culture
  • Radiographs of lungs
  • Necropsy -Presence of yellowish white nodular growths of various sizes in lungs, abdominal cavity and intercostals areas with thickened air sacs.
  • Histopathology - lungs display multiple foci of g


MethodMethod Summary
Supportive careIsolate the bird from the flock and place in a safe, comfortable, warm location (your own duck "intensive care unit") with easy access to water and food. Limit stress. Call your veterinarian.
Antifungal medications

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


  • Minimizing use of antibiotics and corticosteroids
  • Sporadic or repeated antifungal treatment by spraying fungistatic agents such as thiabendazole, nystatin, or copper sulphate on bedding litter
  • Maximizing ventilation
  • Provide balanced nutrients
  • Do not overcrowd
  • Eliminate moldy feed from the bird's diet and environment
  • Line areas exposed to slow drainage with a coarse material such as pea gravel.
  • Old food, decaying vegetable matter, and dried fecal matter should be regularly cleaned from the bird's pen
  • Frequently move feed troughs and water dispensers
  • Place feeders and waterers on elevated platforms
  • Conduct regular air quality tests


Risk Factors

  • Inadequate ventilation
  • Poor quality feed
  • Poor bedding litter quality, storage or management
  • Improper storage of feed
  • High humidity levels
  • Vitamin A deficiency
  • Stress
  • Repeated or prolonged use of antibiotics or steroids
  • Exposure to large number of spores
  • Concurrent illness or infection



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