Diseases / List of Fungal / Algal Diseases / Disease description:

Aspergillosis in Birds (with special reference to Waterfowl and Cranes)

Click image for full page view with caption Aspergillosis granuloma. Click here for full-page view with caption.










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General and References

Disease Summary

Aspergillosis is an infectious but not contagious fungal infection (mycotic disease), primarily of the respiratory tract. Cases may occur as outbreaks or in individual birds. Disease in individuals is most commonly seen in stressed birds with decreased immune function, including birds which are in poor condition or have other disease problems, but may also result from overwhelming challenge, as is seen in outbreaks.

Aspergillosis is relatively common in captive waterfowl and in seabirds in captivity; also seen in wild birds.

  • This disease is seen frequently in association with Oiling, as a secondary disease during care and rehabilitation of oiled birds.

In Lagomorphs

  • Aspergillosis has been reported in domestic rabbits (Oryctolagus cuniculus domesticus) as a cause of granulomatous lesions that are usually confined to the lungs but may also affect the skin and reproductive tract. 

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Alternative Names (Synonyms)

  • Brooder pneumonia
  • Pseudotuberculosis
  • "Asper" mycosis
  • Mycotic pneumonia.

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Disease Type

 Fungal Infection

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Infectious/Non-Infectious Agent associated with the Disease

  • Aspergillus fumigatus, Aspergillus giganteus, Aspergillus flavus, possibly other Aspergillus spp.
  • Most commonly Aspergillus fumigatus. (B36.13.w13, P24.327.w4)
  • Aspergillus spores grow on the mucous membranes of the respiratory tract, and can also grow on wet skin and feathers. (B365.45.w45)
  • In cranes: Aspergillus spp. (B22.24.w16) Aspergillus fumigatus or Aspergillus flavus (P62.12.w1) Usually Aspergillus fumigatus. (B197.9.w9)


(B614.15.w15, J213.6.w1)

Further information on Disease Agents has only been incorporated for agents recorded in species for which a full Wildpro "Health and Management" module has been completed (i.e. for which a comprehensive literature review has been undertaken). Only those agents with further information available are linked below:

Infective "Taxa" in Waterfowl

Non-infective agents in Waterfowl


Physical agents in Waterfowl

Indirect / Secondary

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Disease Author

Dr Debra Bourne MA VetMB PhD MRCVS (V.w5); ; Nikki Fox BVSc MRCVS (V.w103)
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Major References / Reviews

Code and Title List

B9.6.w1:- The Swans.
B10.26.w10: Zoo and Wild Animal Medicine Second Edition
B11.35.w3, B11.37.w5, B11.40.w8, B11.18.w9:- BSAVA Manual of Raptors, Pigeons and Waterfowl.
B13.35.w2, B13.46.w1:- Avian Medicine: Principles and Application.
B15:- Diseases of Wild Waterfowl, Second Edition.
B16.19.w1:- Diseases of Exotic Animals Medical and Surgical Management
B18:- Diseases of Gamebirds and Wildfowl.
B22.23.w1:- Zoo and Wild Animal Medicine Current Therapy 3.
B32.16.w10:- Diseases of Poultry Tenth Edition.
B36.13.w13:- Field Manual of Wildlife Diseases
B37.x.w1:- Handbook of Avian Medicine
B48.16.w16:- Infectious and Parasitic Diseases of Wild Birds
J7.30.w2, J7.33.w3, J7.43.w1, J7.S1.w4:- Wildfowl
J8.17.w1:- Journal of Small Animal Practice

In cranes:
B22.24.w16, B115.5.w6, B197.9.w9, B214.3.28.w19, B336.20.w20, B702.19.w19, B703.10.w10
J2.36.w3, J4.183.w5, J54.32.w1, J311.21.w1, J436.25.w1
P1.1988.w6, P62.12.w1, P87.8.w9, P92.1.w5, P504.2001.w5

B600.16.w16, B608.21.w21, B613.6.w6, B614.15.w15

Other References

Code and Title List

J4.99.w1, J4.122.w1, J4.124.w1, J4.169.w2
J7.4.w1, J7.5.w1, J7.6.w1, J7.7.w1

.1986.w4, P87.7.w8

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Clinical Characteristics and Pathology

Detailed Clinical and Pathological Characteristics

Different forms of the disease have been described, acute and chronic, in individuals and as outbreaks.
  • Acute: Due to overwhelming challenge. This is the form usually seen in large-scale outbreaks in adult birds. It is also responsible for ‘brooder pneumonia’ in hatching birds.
  • Tracheal: Localised infection in the trachea, at or near to the syrinx. In swans, particularly the trumpeter swan Cygnus buccinator this form also occurs in the sharp curves of the coiled trachea (J7.S1.w4).
  • Chronic respiratory: An abscess or a series of granulomas in the air sacs and lungs.
  • Generalised invasive: Haematogenous (blood-borne) spread or spread via the air sac passages, to other parts of the body, e.g. eye, brain, liver, heart.

(B15, B22.23.w1, B36.13.w13)

Clinical Characteristics Duration:
  • Usually a chronic disease, although an acute course can occur in some circumstances with overwhelming infection. (B36.13.w13, D48)
  • In the acute disease the clinical course is only a few days. (B365.45.w45)
  • In chronic disease the time course is usually longer than three weeks. (B365.45.w45)

Acute disease (including "brooder pneumonia"):

  • Sudden death.
  • Acute respiratory distress (dyspnoea) and open-mouth breathing/gasping
  • Inappetance
  • Weakness.
  • Nervous signs have been seen in chicks with "brooder pneumonia" (J4.124.w1)
  • Diarrhoea may be present. 
(B36.13.w13, B197.15.w15, B365.45.w45, J4.122.w1, J4.124.w1)

Chronic disease:

  • Insidious, non-specific subtle signs. (B22.23.w1, P24.327.w4)
  • Changes in behaviour. (B22.23.w1, P24.327.w4)
  • Initial slight loss of vigour (B22.23.w1) later more obvious weakness; (B36.13.w13, P24.327.w4)
    • Wild birds may not try to escape. (B36.13.w13)
  • Gradual loss of weight and body condition, eventual emaciation. (B22.23.w1, , B36.13.w13, B365.45.w45, D48, P14.4.w28)
  • Depression (B365.45.w45, P14.4.w28); general malaise (reduced appetite, weakness, lethargy, reduced exercise tolerance, fluffed-up plumage). (D48)
  • Wings may droop. (B36.13.w13)
  • Birds may sit lower than normal in the water. (P24.327.w26)
  • Respiratory signs: progressive breathing difficulties. Laboured noisy breathing, tail bobbing (the tail moves up and down with each breath), gaping or rapid opening and closing of the bill. (B36.13.w13, D48)
    • Respiratory signs are usually notable only in the final stages. (B365.45.w45)
    • A white discharge from the glottis may be noted. (P14.4.w28)
  • Change in voice sometimes; particularly when a lesion is developing in the trachea. (B22.23.w1, P24.327.w4)
  • Pallor of mucous membranes and/or legs due to anaemia. (P24.327.w26)
  • Polyuria and polydipsia may be seen. (B365.45.w45)
  • Neurological signs: Loss of co-ordination, twisting of the head and neck or head tilt and posterior paresis may be seen if the infection reaches the CNS. (B36.13.w13, B365.45.w45)
    • Posterior paresis may result from involvement of the spinal cord. (P14.4.w28)
  • Advanced infection: depression, weight loss, emaciation, weakness, oculonasal discharge, facial swelling, sneezing, respiratory noise, dyspnoea. (P24.327.w4)
  • With hepatic involvement, biliverdinuria may be seen. (P14.4.w28)
  • Retrobulbar masses may occur if the fungus infiltrates the eye. (P14.4.w28)
  • Localised tracheal/syrinx lesion: 
    • Change in voice, loss of voice, progressing to severe dyspnoea, open-mouth breathing, tail bobbing, head-shaking, pronounced movements of the sternum and neck stretching. (B365.45.w45)

(B36.13.w13, D48, P24.327.w4, P24.327.w26).

Clinical pathology:

  • Increased white blood cell count indicating an acute infection; increased heterophil and monocyte counts, decreased lymphocytes. (P14.4.w28)

  • Nonregenerative anaemia may be present. (P14.4.w28)
  • Increases in total protein, uric acid (if there is renal involvement), SGPT, SGOT, alkaline phosphatase and bile acids (if the liver is involved). (P14.4.w28)
WATERFOWL Dyspnoea is a typical major clinical sign.

Acute disease:

  • May be found dead with few or no signs (particularly juveniles), or show acute respiratory distress, with e.g. increased respiratory rate, open-mouth gasping. May be gurgling or crackling noises on auscultation.

Chronic forms:

  • Slow loss of weight, slight decrease in activity and (particularly with tracheal lesions) a change in voice may be noted in advance of obvious respiratory signs, with depression and emaciation later in the disease. Obvious weakness, wing-droop, cachexia, and diarrhoea may be seen at a late stage.
  • Unilateral wing droop may be seen with infection of the clavicular air sac.
  • Ataxia (loss of muscular coordination) or torticollis (twisting of the neck) may be seen with nervous system involvement.

Tracheal/syrinx form: 

  • A change in voice is common. (B197.11.w11)

(J8.17.w1, B10.26.w10, B11.37.w5, B13.35.w2, B13.46.w1, B15, B16.19.w1, B36.13.w13, B197.11.w11)

  • Respiratory signs, e.g. open-mouth breathing with the head and neck extended, rasping breathing, respiratory click, auscultatable harsh sounds. (B115.5.w6, P62.12.w1)
  • General debility - weight loss and poor appetite, plus minimal respiratory signs. (P62.12.w1)
  • Lethargy. (B115.5.w6)
  • Mucous membranes pale or cyanotic (blue). (B115.5.w6)

In chicks with "brooder pneumonia"

  • General signs of pneumonia. (J311.21.w1)

In a four-month-old Grus japonensis - Red-crowned crane crane chick: (J436.25.w1)

  • Problems walking progressing to inability to stand; depression, inappetance, anaemia. Death after 37 days of illness. (J436.25.w1)

In a 42-day-old Grus japonensis - Red-crowned crane chick: (J4.183.w5)

  • Respiratory signs - wheezing, laboured, rasping breathing;
  • Anorexia. 
  • Death during restraint and treatment with antibiotics. (J4.183.w5)

This is commonly a chronic disease with a gradual onset of dyspnoea and cachexia as the main clinical signs. (B614.15.w15) However, pulmonary aspergillosis may also occur subclinically in apparently healthy rabbits. (J213.6.w1)

Other clinical signs reported include:


  • A short incubation period and sudden death is a feature of overwhelming infection as seen in epizootic aspergillosis and brooder pneumonia. (B36.13.w13, B365.45.w45)
    • Brooder pneumonia may be seen within a day of hatching. (J4.122.w1, J4.124.w1)
  • Other forms of aspergillosis are usually chronic. (B36.13.w13)
  • May die acutely from blockage of the trachea with fungal plaque. 
WATERFOWL Variable. May be only a few days in 'brooder pneumonia' but weeks to months in the chronic form (B13.35.w2).
CRANES Can be only days, since fatal infection has occurred in chicks as young as nine days old. (B12.56.w14, B197.9.w9)

Mortality / Morbidity

  • Aspergillosis is usually a sporadic disease. (B36.13.w13, D48)
  • High-mortality outbreaks also occur.
  • There can be high mortality in casualty seabirds, particularly oiled seabirds. (B197.15.w15, B284.18.w18)

Mortality / Morbidity

WATERFOWL Fairly common in captive birds. Occurs both as high mortality outbreaks and sporadic mortality (J1.14.w1, J8.17.w1, B10.26.w10, B15, B36.13.w13).
  • Fairly common in captive cranes. (B197.9.w9, B214.3.28.w19)
  • A common cause of respiratory disease in crane chicks, particularly after two weeks of age; also occurs in adults. (B12.56.w14)
  • Seen occasionally in wild cranes. (B22.24.w16)
  • Very severe, fatal, aspergillosis was seen in two Grus americana - Whooping cranes in Florida. (B702.19.w19)
  • Relatively common in chicks; can be seen as early as nine days of age. (B336.20.w20)
  • Once disease is severe, generally fatal even with aggressive treatment. (B336.20.w20)
LAGOMORPHS Aspergillosis is not a commonly reported disease of rabbits.


Lesions present depend on the time span of infection, the affected organ system and the number of spores to which the bird was exposed. (B365.45.w45)


  • General body condition: normal or good. (B36.13.w13)
  • Respiratory tract:
    • Lung firm, dark red, studded with 1-2 mm diameter white or yellow nodules. (B36.13.w13, B365.45.w45)
      • Foci may be described as seed-like (J4.122.w1) or miliary. (B365.45.w45)
    • Small irregular dark foci may be present in the lung tissue. (B197.15.w15)
    • Air sacs are usually thickened. (B36.13.w13)
    • Trachea may be blocked by fungal plaque.
    • In brooder pneumonia: white bronchial plugs may be the only gross lesions in very young chicks (e.g. day-old), with bronchial plugs being more yellow and seen together with nodules in the air sacs and lungs in birds several days (five days or more) old. (J4.124.w1)



  • General body condition: emaciated.
  • Air sacs .
    • The caudal thoracic and abdominal air sacs are often involved. (B365.45.w45)
    • Typically, flattened, yellow plaques with a cheesy appearance and consistency; may completely line the air sac.  (B36.13.w13)
      • Air sacs may be thickened, with or without a caseous exudate. (B365.45.w45)
    • May be extensive fungal growth with velvety, blue-green or grey fungal mat on tissues and on the air sac surfaces, similar in appearance to bread mould. (B36.13.w13)
    • Yellow focal lesions on the surfaces of the air sacs, sometimes with fluffy white fungal hyphae. (B197.15.w15)
  • Lungs: 
    • Nodules within the parenchyma; the centre of the nodule may be caseous, consolidated or necrotic. (B365.45.w45)
    • Large granulomas may be found. (B365.45.w45)
  • Ocular: Less commonly cheesy lesions may be seen beneath the nictitating membrane (third eyelid). (B36.13.w13)
  • Other organs: caseous nodules within the parenchyma. (B365.45.w45)
    • Disseminated (from the air sacs) infection may occur with sites of infection such as the coelomic cavity, CNS, liver, intestines, kidneys, pneumatic bones, adrenals and spinal column. (B365.45.w45)
  • In chickens and pigeons, necrotic skin granulomas have been described. (B36.13.w13)
  • In wild herring gulls and a jackdaw, typical plaques were found throughout the thoracic and abdominal viscera. (J42.65.w1)
  • In wild woodpigeons, while some typical concentric plaques were notes, large irregular necrotic nodules also occurs, sometimes particularly marked in the liver; lesions were mainly in the peritoneal cavity, with relatively little involvement of the respiratory tract. (J42.65.w1)

(B36.13.w13, D48)

Localised lesions :

  • Trachea/bronchi/syrinx: white to yellow plaques or caseous mass or masses. (B365.45.w45)
  • Other organs: granulomas, cavitating masses and nodular masses have been described. (B365.45.w45)


  • Keratitis and uveitis (mixed Aspergillus and Candida infection) has been described. (B365.45.w45)


  • Granulomatous inflammation, presence of hyphae. (B336.75.w75)
  • Granulomatous lesion(s) of the sinuses, nasal cavity, trachea, bronchi, internal organs or body cavities. (B365.45.w45)
  • Localised lesion of the trachea/bronchi/syrinx:
    • Caseous granulomatous nodules formed from a combination of fungal mycelia and inflammatory cells. (B365.45.w45)
  • In subacute infection: nodules of necrosis with plasma proteins and granulocytes but otherwise little sign of reaction, in the air sacs, lungs and intestinal serosa of affected Larus argentatus - Herring gull. Typical mycotic structures were present in affected tissues. (J1.5.w2)


  • Lung congested and consolidated (red and firm), with multiple small yellow foci. Haemorrhage, necrosis and oedema in the lungs, with radiating septate fungal hyphae and minimal leucocyte response. Air passages are filled with numerous hyphae, fibrin, necrotic debris, mucus and some lymphocytes. Air sacs usually thickened (B10.26.w10, B15, B16.19.w1B36.13.w13).


  • General: emaciation.
  • Respiratory tract lesions:
    Air sacs- Thickened, cloudy air sacs, with fungal plaques (discoid or coalescing, yellowish cheesy lesions or a green-blue velvety fungal mat – indicating formation of spore-bearing conidia) on the walls of the air sacs. Histopathology: plaques consist of fibrinonecrotic debris and fungal hyphae, with a cellular response of multinucleated giant cells, macrophages, heterophils, and fewer lymphocytes and plasma cells.
    Trachea - Fungal plaques in the trachea can be large and may block the trachea.
    Lungs - (particularly in acute aspergillosis): Congested or consolidated with numerous small yellow, creamy or greenish white small firm nodules (e.g. 1-2mm). Fewer, larger lesions may be seen in less acute cases. Thick-walled yellow granulomas may form in chronic cases. Histopathology: haemorrhagic pneumonia and lymphocyte infiltration. Granulomas, containing hyphae, sometimes with necrotic centres, surrounded by epithelioid cells, lymphocytes and occasional giant cells. Fungal hyphae may also be seen in the air capillaries (J1.5.w1, J1.14.w2, J8.17.w1, B10.26.w10, B15, B16.19.w1, B36.13.w13, J37.13.w1).
  • Syrinx - Complete occlusion of the syrinx was recorded in three wild Branta canadensis - Canada goose. The lesion was described as ‘a white to cream-coloured fibrino-caseous plug’ adherent to the wall of the syrinx. Histologically the plug was composed of fungal hyphae, fibrin, necrotic debris and inflammatory cells, with erosion of the tracheal epithelium and in some areas invasion of fungal hyphae into the submucosa. (J4.181.w1).
  • Brain: Small (2-8mm) pink necrotic foci in the cerebrum. Histologically: necrotic area with numerous engorged capillaries and arterioles centrally. At the periphery, gliosis and perivascular cuffing by monocytes. Also monocytes clustered loosely around mycelia and some vessels thrombosed. Meningeal infiltration by lymphocytes was also noted (J5.2.w1).
  • Liver: necrotic areas. Granulomatous appearance: necrotic centres with mycelia, surrounded by epithelial cells with numerous lymphocytes around the periphery and extending to surrounding areas (J5.2.w1).
  • Other organs: plaques have also been seen occasionally on the kidneys and other abdominal organs, and in the proventriculus and small intestine (J1.14.w2, J1.5.w1).
  • Amyloidosis may also be seen secondary to chronic infection (B39.w1).
  • Unusual manifestations : Multiple nodular lesions throughout the body cavity were noted in a wild Anas platyrhynchos - Mallard, initially appearing similar to avian tuberculosis. Histologically, hyphae were visible and Aspergillus fumigatus was cultured on Sabouraud’s dextrose agar (J5.5.w1).
CRANES Gross pathology
  • Respiratory: 
    • The trachea may contain a plug of thick, tan-yellow material. (P62.12.w1)
      • A granuloma may form at the tracheal bifurcation. (B703.10.w10)
    • Lungs, air sacs and airways containing small white nodules (granulomas). (P62.12.w1)
    • Air sacs and pulmonary airways may contain dry, fuzzy "bread mould" type blue-green fungal colonies. (P62.12.w1)
      • Not usually present in "brooder pneumonia". (J311.21.w1)
    • Occasionally, adherent to the air sacs are thick, caseated plaques surrounded by translucent yellow fluid. (P62.12.w1)
  • In a four-month-old Grus japonensis - Red-crowned crane crane chick: (J436.25.w1)
    • "Markedly undernourished." 
    • In the lungs, air sacs, liver, adrenals, posterior thoracic vertebrae, many millet-seed to soybean-size nodules/necrotic lesions. (J436.25.w1)
  • In a 1.5 month old Grus japonensis - Red-crowned crane chick: (J4.183.w5)
    • Respiratory: Left lung collapsed. In the ventral surface of the left lung, a 60-70 mm diameter approximately spherical nodular firm mass, creamy colorued, bounded by a thin fibrous capsule, with a central cavity about 20 mm diameter containing serous, straw-coloued fluid, and made up of discrete, firm, irregular nodules, each 2-3 mm diameter. 
    • GIT: Oesophagus deviated to the rightside of the thorax. On the serosal surfaces of the duodenum and jejunum, two 3-4 mm diameter granulomas.
    • Spleen: 20 mm diameter, with nodular consistency suggesting lymphoid hyperplasia.
    • Bursa of Fabricius: 15 mm diameter (normal for a 1.5-month-old crane chick).
    • Hepatic: Liver 165g, appeared large.
    • Renal: Kidneys congested, moderately swollen.
    • Cardiac: On the epicardium, a few petechiae, serous atrophy of coronary fat, and excess pericardial fluid, serous and stained with haemogobin.


  • PAS or silver stains will show fungal elements. (P62.12.w1)
  • In a 1.5 month old Grus japonensis - Red-crowned crane chick: (J4.183.w5)
    • Masses: multiple discrete granulomata, consisting of a core of necrotic debris, surrounded by a zone of multinuclete giant cells and successive zones of macrophages, fibrocytic-type cells and inflammatory cells.With silver-impregnated stains, septate branching hyphae were visible associated wit the centres of the granulomata. Acid-fast stains did not reveal any bacteria.
    • Lungs: in the air pasages, cellular debris and occasional inflammatory cells.
    • Lymphoid follicles depleted
    • Bursa of Fabricius: granuulocytes in the cortical regions.
    • Spleen: deposition of homogenous eosinophilic material.
    • Liver: mild perivascular infiltrate of inflammatory cells.
    • Kidneys: in the glomeruli, dark brown pigment (unknown source).


  • In a five-month-old Grus americana - Whooping crane which died from exertional myopathy (Capture Myopathy): (J2.36.w3)
    • Respiratory: In the trachea, one primary bronchus and lung, small pyogranulomatous plaques. Aspergillus fumigatus confirmed by culture. (J2.36.w3)
LAGOMORPHS Granulomas: central necrosis surrounded by an inflammatory response (mononuclear). Typical septate fungal hyphae present. Hyphae are more visible with PAS or methenamine silver. (B613.6.w6)
  • Skin:
    • Papules: cystic follicles distended with dichotomously branching hyphae and necrotic debris. (B608.21.w21)
  • Lungs:
    • Pulmonary granulomas. (J10.36.w1)
    • Gross pathology: 1 mm to 3 mm granulomatous lesions. (J213.6.w1)
    • Histopathology: fungal hyphae with "asteroid" bodies present. (J213.6.w1)

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Human Health Considerations

  • Minimal zoonotic importance. 
  • Although aspergillosis is not contagious, it should be remembered that humans, particularly if immunosuppressed, may be susceptible to infection from the same sources as those which may infect birds. 
  • People could become exposed to spores while undertaking post mortem examination of birds. 
  • People who work with the fungus can also develop an allergy to it, which can be life-threatening. 

(B10.26.w10, B36.13.w13, B197.11.w11, D48)

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Susceptibility / Transmission

General information on Susceptibility / Transmission

  • Probably all birds are susceptible.
  • Immunocompromised birds exposed to spores persistently at low level are likely to develop chronic infection. (B365.45.w45)
  • Chicks may show higher susceptibility than adults. (B365.45.w45)
  • In wild birds this disease is generally seen as a secondary infection. (P24.327.w4)
  • Debilitated birds are more susceptible. (P3.1961-1970.w1)
  • Stress and immunosuppression, due to shot wounds, oiling, malnutrition (particularly vitamin A deficiency), recent capture, injury, other diseases (such as lead poisoning, as well as viral, bacterial or parasitic disease), transportation etc., increases susceptibility. (B36.13.w13, B365.45.w45, P24.327.w4)
    • Stress associated with capture, transportation, confinement and thiamine deficiency were considered to have allowed the development of clinical disease in recently captured Larus argentatus - Herring gull which appeared healthy at the time of capture. (J1.5.w2)
  • Prolonged use of antibiotics may predispose. (B365.45.w45)
  • Seabirds and loons are very susceptible while in care for other problems, including oiling; this susceptibility is probably associated with stress due to capture, and to emaciation and weakness of such casualties. (P24.327.w26, B36.13.w13, B197.15.w15, B363.9.w9, D48)
    • Increased susceptibility of aquatic birds may also be related to lower levels of Aspergillus spores normally present in the aquatic environment than on land. (P24.327.w26)
  • This condition is occasionally present in wild birds, including corvids, aquatic birds, raptors and small passerines, at the time of presentation; these individuals may have been under stress in the wild, for example in poor body condition, or otherwise in suboptimal health. (D48, P24.327.w4)
  • Typical aspergillosis has been described in both oiled and non-oiled loons (Gavia immer) during a winter die-off of these birds. (J4.169.w2)
  • Raptors, loons (divers - Gaviidae - Loons (Family)) and alcids as well as waterfowl may be considered susceptible species. (B365.45.w45)
    • Susceptible species in which prophylaxis has been recommended under conditions of stress, management changes, oiling and lead poisoning (see: Lead Poisoning in Waterfowl) include loons (divers), trumpeter swans, eider ducks, some psittacines (blue-fronted Amazon Amazona aestiva aestiva, African gray parrot Psittacus erithacus), hill mynah Gracula religiosa and several raptors (gyr falcon Falco rusticolus, northern goshawk Accipiter gntilis, immature red-tailed hawks Buteo jamaicensis, great sparrow hawk, golden eagle Aquila chrysetos, bald eagles Haliaeetus leucocephalus (with lead poisoning), snowy owl and rough-legged buzzard). (B11.3.w28, B11.18.w29, B365.45.w45)
    • Penguins are recognised as being highly susceptible to aspergillosis. (P14.4.w28)
  • Note: Aspergillosis is an important cause of death in oiled birds. Poorly-ventilated facilities used for rehabilitation of oiled birds following an oil spill (see: Oiling) play a significant part in development of aspergillosis in birds being treated. (P14.4.w28)
  • Aspergillus fumigatus is common in damp soils, decaying vegetation etc.
  • Spores may be present in hay or straw provided as padding material for birds during transport, or given as bedding or nesting material, or in contaminated food.. (P24.327.w4, P24.327.w26)
  • Outbreaks may be related to the presence of massive numbers of spores. 
  • Infection is by inhalation of spores, with subsequent haematogenous (blood-borne) spread.
  • Infection is more likely in conditions of sub-optimal ventilation and hygiene. (B197.15.w15)
  • Transmission can occur in/on eggs. (J4.122.w1)
  • Damp nest boxes, spoiled food, improperly maintained substrates and accumulation of droppings may all act s source of fungi. (B365.45.w45)

(B15, B36.13.w13, D48, P24.327.w4, P24.327.w26)

  • Aspergillosis has been reported in a wide variety of waterfowl and other birds. It appears likely that all bird species may be susceptible to this infection.
  • Eider ducks (Somateria spp. and Polystica stelleri - Steller's eider), other sea ducks and swans, particularly Cygnus buccinator - Trumpeter swan appear to be particularly susceptible to aspergillosis.
  • In all species stress-related immunosuppression increases susceptibility. This stress may be due to injury, disease, exposure to contaminants (particularly oil - see: Oiling), social stress (including nest defence and parenting demands), management changes (e.g. transport, change of pen, new feeding regime) or poor nutrition.
  • Immature birds appear to be more susceptible than adults.
  • Inappropriate use of antibiotics and steroids may also increase susceptibility. (B197.11.w11)
  • Also associated with Vitamin A Deficiency and with Thiamine Deficiency.

(J7.30.w2, J7.33.w3, J7.43.w1, J7.S1.w4, J8.17.w1,J23.13.w5, B10.26.w10, B11.35.w3, B11.37.w5, B13.46.w1, B15, B16.19.w1, B18, B36.13.w13, B197.11.w11)

  • Aspergillus fumigatus is common in damp soils, decaying vegetation etc.; outbreaks may be related to the presence of massive numbers of spores. Infection is by inhalation of spores, with subsequent haematogenous (blood-borne) spread (J37.13.w1, B13.46.w1, B15, B36.13.w13).
  • Cranes are among the species of birds considered particularly susceptible to aspergillosis [at least in zoos]. (B214.3.28.w17)
  • This is a common cause of respiratory signs in chicks two weeks old or older; also seen in adults. (B12.56.w14)
  • Chicks are particularly susceptible. (B197.9.w9, B336.20.w20, B703.10.w10)
    •  In chicks over 20 days this is relatively common, while bacterial respiratory infection is commoner in younger chicks. (B115.5.w6)
    • Respiratory diseases are more common in chicks being reared by inexperienced/ineffective parents, after cool, rainy weather. (B115.5.w6)
  • Debilitated cranes are particularly susceptible. (B115.8.w8, B703.10.w10)
    • Cranes may be debilitated by other disease, injury, poor nutrition or environmental factors (e.g. adverse weather). (P62.12.w1, B197.9.w9,, B703.10.w10)
    • In captivity, this is a disease associated with stress due to e.g. crowding, inappropriate housing or poor nutrition, leading to decreased resistance to infection. (P62.12.w1)
    • Two cranes developed aspergillosis following pinioning. (B10.24.w46, B485.22.w22)
  • Following treatment for bacterial pneumonia. (B115.8.w8)
  • Grus americana - Whooping cranes may be particularly susceptible due to their elongated and coiled trachea. (J54.32.w1)
    • In the Grus americana - Whooping cranes chicks being raised for direct autumn release (DAR) in Wisconsin, possible factors increasing susceptibility were prolonged cold temperaters and driving rain as stressors in some years, possible air flow problems in some parts of the crane pens, and drainage problems leading to increased energy demands and possible associated stress. Acute infections in chicks up to eight days old were thought probably related to overwhelming exposure. (J54.32.w1)
  • In wild cranes, from mouldy grain left in fields. (P62.12.w1)
  • The source of infection is often considered to be contaminated bedding or flooring:
    • Infection of a litter of four week old rabbits was presumed to be associated with the mouldy grass hay bedding on which they were raised. No further cases occurred after the nesting material was changed. (B608.21.w21)
    • Contaminated commercial bedding was reportedly the cause of an aspergillosis outbreak in mice of an animal care research facility. Therefore it is advisable to consider bedding as a potential source of infection when investigating fungal outbreaks in rabbits. (J213.6.w1)
    • In the reported case of abortion due to aspergillosis, the source of infection was thought to be contaminated flooring. (J213.6.w1)

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Disease has been reported in either the wild or in captivity in:

  • Various seabirds brought into captivity (D48).
  • Scaup, European jay, American coots, passerines; loons (divers) and marine birds in rehabilitation, raptors and penguins in captivity (B36.13.w13).
  • Currawongs, magpies, small passerines, aquatic birds, raptors. (P24.327.w4)
  • Pheasants, herring gulls, jackdaws and woodpigeons with Aspergillus fumigatus, also one woodpigeon with Aspergillus nidulans. (J35.121.w1)
  • Wild woodpigeons, herring gulls and a jackdaw in the UK, with Aspergillus fumigatus, also one woodpigeon with Aspergillus nidulans. (J42.65.w1)
  • Birds (mainly Uria aalge - Common murre) oiled with Kuwait crude following the Torrey Canyon spill.(J7.19.w1)
  • One Podiceps cristatus - Great crested grebe oiled in the Arabian Gulf in 1991. (P1.1991.w1)
  • Two Podiceps nigricollis - Black-necked grebe (15.1%) necropsied after being oiled in the Arabian Gulf spill in 1991. (P14.3.w20)
  • Two guillemots (Uria aalge - Common murre) out of 67 necropsied after being found washed up on beaches in Belgium during the winter of 1993-1994. (J3.143.w8)
  • Both oiled and nonoiled loons during a winter die-off in Florida, USA. (J4.169.w2)
  • Oiled birds (mainly Uria aalge - Common murre, Alca torda - Razorbill, and Fratercula arctica - Atlantic puffin) dying during rehabilitation following the Prestige oil spill, in 2000 (found in 28%). (J1.41.w1)


  • Mallard Anas platyrhynchos (J1.14.w2, J1.5.w1).
  • Domestic Ducks and geese in UK (J3.67.w2).
  • (Argentine) Red shoveler Anas platalea (J3.136.w1).
  • Pintail Anas acuta, shoveler, green-winged teal Anas crecca, mallard Anas platyrhynchos, cinnamon teal Anas cyanoptera, (American) widgeon Anas americana, whistling swan Cygnus columbianus columbianus (J4.99.w1).
  • Eider Somateria mollissima borealis (J5.2.w1).
  • Lesser scaup Aythya affinis, canvasback ducks Aythya valisineria, whistling swans Cygnus (Olor) columbianus in California, USA (J5.8.w2)
  • Upland goose Chloephaga picta , Andean crested duck Lophonetta (Anas) specularioides alticola, red-crested pochard Netta rufina, Maned goose Chenonetta jubata, eider (J7.4.w1).
  • Blue-winged goose Cyanochen cyanopterus, long-tailed duck Clangula hyemalis, mute swan Cygnus olor, kelp goose Chloephaga hybrida, Chiloe wigeon Anas sibilatrix, Brazilian teal Amazonetta brasiliensis, Andean crested duck Lophonetta (Anas) specularioides alticola, Hartlaub's duck Pteronetta hartlaubi Flightless steamer duck Tachyeres spp., Bewick's swan Cygnus columbianus Buick, whistling swan Cygnus columbianus columbianus (J7.5.w1).
  • Greater snow goose Anser caerulescens, ruddy-headed goose Chloephaga rubidiceps, Falkland (upland) goose Chloephaga picta , Andean goose Chloephaga melanoptera, Abyssinian blue-winged goose Cyanochen cyanopterus, New Zealand (Paradise) shelduck Tadorna variegata, Maned goose Chenonetta jubata, Scaup (J7.6.w1).
  • White-fronted goose Anser albifrons (J7.7.w1).
  • Dark-bellied brent goose Branta bernicla on the Wash, UK (J7.25.w1).
  • Eiders, other seaducks (J7.30.w2).
  • Musk duck Biziura lobata adult (in quarantine after transport from Australia), North American ruddy duck Oxyura jamaicensis and white-headed duck Oxyura leucocephala juveniles in the UK (J7.33.w3)
  • Among northern geese in captivity, noted to be particularly problematic in: Emperor geese Anser canagica, red-breasted geese Branta ruficollis, white-fronted geese Anser albifrons (adults); emperor geese Anser canagica, bean geese Anser fabalis, brent geese Branta bernicla and Ross's geese Anser rossii (juveniles), white-fronted geese Anser albifrons , brent geese Branta bernicla, red-breasted geese Branta ruficollis, Ross's geese Anser rossii and Canada geese Branta canadensis (downies). Important in "all goslings except Lesser Whitefronts and Beans" (J7.34.w1).
  • Bewick's Cygnus columbianus bewickii, Black Cygnus atratus, Black-necked Cygnus melanocoryphus, Trumpeter Cygnus buccinator, Whistling Cygnus columbianus columbianus and Whooper Cygnus cygnus swans (J7.43.w1).
  • Canada goose Branta canadensis and blue goose (lesser snow goose) Anser (Chen) caerulescens) (J37.13.w1).
  • All species of swans (B9.6.w1).
  • Wild wood ducks Aix sponsa and mallards Anas platyrhynchos (B15).
  • Canvasback Aythya valisineria on the lower Detroit River, USA (P10.28.w1).


  • In captive, and occasionally in free-living, Gruidae - Cranes. (B12.56.w14, B22.24.w16, B115.8.w4, B115.5.w6, B197.9.w9)
  • In a four-month-old Grus japonensis - Red-crowned crane crane chick. (J4.183.w5)
  • In a 42-day-old Grus japonensis - Red-crowned crane crane chick. (J436.25.w1)
  • Systemic aspergillosis was diagnosed in a free-living Florida sandhill crane Grus canadensis praetensis (Grus canadensis - Sandhill crane). (P1.1988.w6)
  • Secondary pneumonic Aspergillus fumigatus infection was present in a Grus canadensis - Sandhill crane with Avian Tuberculosis found at the Platt River, Nebraska, USA in 1978. [1988](J40.52.w2)
  • An aspergilloma due to Aspergillus flavus occurred in a captive crane. (B10.24.w46)
  • Two cranes [species not specified] developed aspergillosis following pinioning. (B10.24.w46, B485.22.w22)
  • Seen in crane(s) at the New York Zoological Park [no details given]. (P1.1986.w4)
  • Fatal infection in one Grus grus - Common crane and three Grus japonensis - Red-crowned crane at ICF, 972-1982. (P92.1.w5)
  • In a three-year old, captive-reared Mississippi sandhill crane (Grus canadensis - Sandhill crane) found caught in a leg-hold trap two years after release. The bird died from capture myopathy [Capture Myopathy]; aspergillosis was noted, considered to have occurred due to chronic debility and stress and to have contributed to the crane's death. (P1.1989.w2)
  • In wild Grus canadensis - Sandhill cranes in Florida while undergoing 3-4 weeks of treatment for a "neck paresis" syndrome thought to be associated with mycotoxins (see: Fusariotoxicosis (Mycotoxicosis) in Waterfowl and Cranes). (P504.2001.w5)
  • Aspergillosis was diagnosed as the cause of death in 7/167 wild Grus grus - Common crane in Germany, 1998-2008, including five males and two females, two adults, one subadult and three juveniles. [2011] (J1.47.w5)
  • Aspergillosis was recorded as the cause of death in seven Grus americana - Whooping cranes at Patuxent Wildlife Research Center, 1982-1995 (three chicks, two juveniles and one adult); aspergillosis tended to develop subsequent to bacterial respiratory infections. (P87.7.w8)
  •  Aspergillosis cased pneumonia in one individual and cardiac inflammation in another, together with aflatoxicosis  associated with mouldy corn (maize),in yearling Florida sandhill cranes translocated to Georgia and held  for soft-release. (P87.8.w9)
  • Very severe, fatal, aspergillosis was seen in two Grus americana - Whooping cranes in Florida, one pre-release and one which had been free-living for about a year. (B702.19.w19)
  • Respiratory aspergillosis was an important cause of death or euthanasia in Grus americana - Whooping cranes chicks being reared from the direct autumn release (DAR) programme in Wisconsin, with seven deaths or euthanasia due to severe respiratory aspergillosis in chicks from 6-72 days old, 2005-2010. (J54.32.w1)


  • In Oryctolagus cuniculus domesticus - Domestic European rabbit
    • Aspergillosis of the skin and lungs has been reported in a whole litter of rabbits that were four weeks old. (B608.21.w21)
    • One commercial rabbitry discovered a subclinical pulmonary aspergillosis in their apparently healthy rabbits; only kits under the age of five weeks were affected. (B614.15.w15; J213.6.w1)
    • Pulmonary granulomas caused by aspergillosis have been reported in laboratory rabbits. (B600.16.w16)
    • There has been one case of Aspergillus fumigatus causing spontaneous abortion in late pregnancy. (J213.6.w1)
  • Reported in hares [probably Lepus europaeus - Brown hare] in Sweden and the UK. (B220)

Further information on Host species has only been incorporated for species groups for which a full Wildpro "Health and Management" module has been completed (i.e. for which a comprehensive literature review has been undertaken). Host species with further information available are listed below:

Host Species List




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Disease has been specifically reported in Free-ranging populations of:

  • Wild woodpigeons, herring gulls and a jackdaw in the UK, with Aspergillus fumigatus, also one woodpigeon with Aspergillus nidulans. (J42.65.w1)
  • Two guillemots (Uria aalge - Common murre) out of 67 necropsied after being found washed up on beaches in Belgium during the winter of 1993-1994. (J3.143.w8)
  • Scaup, European jay, American coots, passerines, sometimes raptors (B36.13.w13).
  • Currawongs, magpies, small passerines, aquastic birds, raptors. (P24.327.w4)
  • Both oiled and nonoiled loons during a winter die-off in Florida, USA. (J4.169.w2)


  • Mallard Anas platyrhynchos (J1.14.w2, J1.5.w1).
  • (Northern) Pintail Anas acuta, (Northern) shoveler Anas clypeata, green-winged teal Anas crecca, mallard Anas platyrhynchos, cinnamon teal Anas cyanoptera, (American) widgeon Anas americana, whistling swan Cygnus columbianus columbianus (J4.99.w1).
  • Lesser scaup Aythya affinis, canvasback ducks Aythya valisineria, whistling swans Cygnus (Olor) columbianus in California, USA (J5.8.w2).
  • White-fronted goose Anser albifrons (J7.7.w1).
  • Dark-bellied brent goose Branta bernicla on the Wash, UK (J7.25.w1).
  • Wild wood ducks Aix sponsa and mallards Anas platyrhynchos (B15).
  • Canvasback Aythya valisineria on the lower Detroit River, USA (P10.28.w1).



Further information on Host species has only been incorporated for species groups for which a full Wildpro "Health and Management" module has been completed (i.e. for which a comprehensive literature review has been undertaken). Host species with further information available are listed below:

Host Species List




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General Information on Environmental Factors/Events and Seasonality

  • Spores can be found in most land-based environments, however rotting or decaying vegetation can provide a particularly spore-rich environment. (B11.18.w29)
  • Most outbreaks in wild birds occur in winter, associated with mouldy silage, corn etc., particularly when other food sources are unavailable, e.g. due to deep snow (B15, B36.13.w13).
  • Greater numbers of air-borne spores may be present in dry, dusty conditions and one outbreak in wild birds was associated with dry, dusty conditions after a three-year drought (J5.8.w2, B15, B36.13.w13).
  • Climatic changes may precipitate release of fungal spores (J8.17.w1).
  • Aspergillus grows readily in moist environments including for example wood shavings, seed hulls and corn cob bedding. (B365.45.w45)
  • 'Brooder pneumonia' is usually seen in spring and is due to Aspergillus-contaminated hatchers or brooders. This form is particularly associated with poorly-ventilated, humid, overcrowded brooders. Broken eggs can provide an excellent growth medium for Aspergillus and therefore a source of spores for newly-hatched birds. Eggs can also be infected in the nest (B11.37.w5, B11.40.w8, B36.13.w13).

In waterfowl:

  • Aspergillosis has been seen in eider ducklings kept in a hot, humid greenhouse (J5.2.w1).
  • One case in a wild Bewick's swan Cygnus columbianus bewickii was hypothesized to have been associated with the feeding of mouldy bread (J7.14.w4).
  • Spring and autumn peaks were recorded in eiders at Slimbridge (WWT) (J7.30.w2).
  • Outbreaks also occur in seaducks during rehabilitation after oil spills (B11.35.w3, B36.13.w13).
  • Cases in individual birds may occur at any time (B36.13.w13).

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Regions / Countries where the Infectious Agent or Disease has been recorded

Almost worldwide; causative fungi are ubiquitous (B15, B36.13.w13).

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Regions / Countries where the Infectious Agent or Disease has been recorded in Free-ranging populations

Britain, USA (J7.14.w4, B15, B36.13.w13).

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General Investigation / Diagnosis

General Information on Investigation / Diagnosis

  • Diagnosis requires not just culture of the fungus but repeated culture in association with histopathological findings, or culture from a site, such as the blood or brain, which should be sterile. (B365.45.w45)
  • Laparoscopy, cytology, histopathology and culture findings may be involved in diagnosis. (B365.45.w45)

Clinical signs:

  • Not sufficient for diagnosis.
  • May be suggestive. (P24.327.w4)

Clinical pathology:

  • Haematology: typically leucocytosis (heterophilia) and in later stages of infection monocytosis and toxic heterophils. (P24.327.w4)
  • Examination of deep tracheal swabs or air sac swabs for fungal hyphae, in a wet mount with saline or potassium hydroxide (KOH) or stained with lactophenol cotton blue or Gram stain. (P24.327.w4)
    • Hyphae are branching and septate. (P14.4.w28)
  • Culture of tracheal swabs: insert a small, long-handled swab into the trachea when the glottis is widest open, twirl around, withdraw without touching other parts of the oral cavity, and culture on Sabouraud at 37 C. Small white colonies may be visible by 18 hours and are recognisable as Aspergillus sp. by microscopic examination of a wet mount; green-blue colonies by 48 hours. One to four colonies from such a swab is diagnostic; the presence of many colonies indicates a poor prognosis. (B22.23.w1)
  • Endoscopic examination of the trachea and/or air sacs for the presence of fungal lesions. (P24.327.w4)
    • Cloudy air sacs and granulomas may be visible on laparoscopy. (P14.4.w28)
  • Haematology combined with protein electrophoresis, antigen capture tests and ELISA may be used. However positive ELISA results may be difficult to interpret and may only indicate exposure to the organism, not necessarily that it is causing disease. (P24.327.w26)
    • Significant increase in leucocyte count; heterophilia is evident early in the disease course, later monocytosis and in late stages presence of toxic heterophils. (B22.23.w1)
  • Radiography: 
    • Rarely allows a definitive diagnosis, but may be useful in conjunction with other investigations.(P24.327.w4)
    • If lesions are visible radiographically the prognosis is poor. (B22.23.w1, , P24.327.w4)
    • Diffuse cloudiness in the abdominal air sacs generally is visible only late in the course of the disease. Nodular air sacculitis, pulmonary nodules, increased density of the syrinx, ring shadows in the hilum, localised granulomas and, on ventrodorsal radiographs, asymmetric air sac density and extension may be visible. (B365.45.w45)
    • The lungs may show granulomas and hyperinflation. (P14.4.w28)
    • Lack of visible lesions on radiography does not preclude the presence of aspergillosis. (P24.327.w4)
  • Special tests: 
    • Double diffusion precipitation test. (P24.327.w4)
    • ELISA. (P24.327.w4)
      • ELISA is available for raptors, ratites, waterfowl, turkeys and psittacines. (B365.45.w45)
      • ELISAs may be negative in infected birds in acute disease or in immunosuppressed individuals. (B365.45.w45)

Post mortem examination:

  • Carcasses are generally emaciated with chronic infections, but this may not be seen with acute disease or tracheal blockage.
  • Presence of fungal plaques in respiratory tract. (B36.13.w13, P14.4.w28)
    • Typical white to yellow nodules or plaques. (P24.327.w4)
    • Green mould appearance if fruiting bodies are present. (P24.327.w4)
  • Lesions seen at necropsy can be examined in a wet mount with saline or KOH or stained with lactophenol cotton blue or Gram stain. (P24.327.w4)
    • This allows identification of Aspergillus sp., but not which species of Aspergillus is present. (B36.13.w13)
  • Fungus may be cultured from lesions. 
  • Histopathology using special stains may be used visualise Aspergillus structures and to confirm the identity of fungus seen grossly. (B36.13.w13, P24.327.w4)
    • Hyphae are dichotomously branching, 3-6 m thick and regularly septate. (B336.75.w75)

(B36.13.w13, D48, P24.327.w4, P24.327.w26)

WATERFOWL Associated environmental features/events:
  • Stressful events in susceptible species. 
  • Known exposure to mould spores, such as mouldy food in winter when other food sources are unavailable, mouldy litter/bedding. 
  • Dry, dusty conditions. 
  • For 'brooder pneumonia', humid, poorly-ventilated, overcrowded brooders and/or known fungus-infected egg.


  • Dyspnoea. Non-specific signs in highly-susceptible species.
  • Deep tracheal culture: This is possible without anaesthesia in waterfowl. Bend the aluminium handle of the swab to give a slight curvature, insert through the glottis when widest open, during inspiration. Insert as far as possible, twirl around, withdraw (without contacting the mouth). Inoculate onto a Sabouraud dextrose agar culture plate and incubate at 37C. Small white colonies may be visible at 18 hours, definitive blue-green colonies by 48 hours. Even one colony should be considered significant in association with a suggestive history and clinical signs, although Aspergillus can be cultured from the trachea of normal birds; 1-4 is usual in clinical cases, large numbers suggest a poor prognosis (B22.23.w1).
  • Endoscopic examination: This should be carried out under gaseous anaesthesia. The trachea should be viewed directly and rapidly (as the bird must be removed from the anaesthetic apparatus). The abdominal and posterior thoracic airsacs may be examined by standard methods as for endoscopic sex determination. Air sacs may be thickened. Fungal plaques are yellowish or green-blue, resembling bread mould, and may be discoid or coalescing. Examination of an endoscopic sample using lactophenol cotton blue for the narrow, septate hyphae and typical conidia. Culture can be used to give a definite identification of the fungus if no conidia are present.
  • Clinical pathology: An ELISA is available which can detect antibodies within a week of exposure to an infective dose of spores. Titres rise before clinical signs are evident and fall following successful treatment. An optical density reading above 0.121, or above 0.220 in swans, may indicate a positive immune reaction (P4.1994.w1, B22.23.w1, B197.11.w11)
  • Haematology: Increased total white cell count. Heterophilia is evident early in the development of the disease, later monocytosis and toxic heterophils can be seen. (J3.130.w1, B22.23.w1, J3.114.w3)
  • Radiography may reveal advanced lesions. Absence of radiological signs (air sac cloudiness or discrete granulomas) does not indicate a negative diagnosis.

Post mortem examination:

  • Whole carcasses should be examined. Detection of typical fungal plaques. Lesions can be extensive. In one whistling swan Cygnus columbianus it was described that "Its body cavity was a mass of greenish hyphae" (J5.8.w2)
  • Gross lesions (white to green fungal plaques) are characteristic; diagnosis can be confirmed by demonstration or growth of the fungus from the plaques. (D48)
  • Fungal hyphae can be demonstrated in plaques or granulomas. These can be visualised by digesting a portion of the lesion in 20% potassium hydroxide or sodium hydroxide, staining with a drop of lactophenol cotton blue or blue-black permanent ink, and looking for the narrow (3m), septate, highly branched fungal hyphae.
  • Specific identification of Aspergillus is possible from the conidia (spores), if present.
  • Histopathology: fungal hyphae and conidia (spores) may be detected in the air sacs with haematoxylin and eosin stain; stains such as methenamine silver will show hyphae clearly.
  • Culture from lesions are required for identification if no conidia are present. Culture requires media containing antibiotics to avoid bacterial overgrowth.

B10.26.w10, B15, B22.23.w1, B36.13.w13, B197.11.w11

  • On necropsy, typical lesions are highly suggestive. (P62.12.w1)
    • Impression smears of lesions to show fungal hyphae and distinguish granulomatous lesions from those of Avian Tuberculosis. (P62.12.w1)
    • Histopathology with PAS or silver stains to demonstrate fungal elements. (P62.12.w1)
  • Culture. Culture and identification for fungi as well as for bacteria should be carried out in cranes with respiratory signs. (B115.8.w8, P62.12.w1)
  • Radiography. (B115.8.w8)
  • May be diagnosed due to failure of antibacterial treatment for respiratory disease. (B115.8.w8)
  • In a four-month-old Grus japonensis - Red-crowned crane crane chick, histology and microbiology revealed Aspergillus fumigatus "vigorously propagating" in the lesions seen as nodules/necrotic lesions. (J436.25.w1)
  • In a 42-day-old Grus japonensis - Red-crowned crane chick. (J4.183.w5)
    • Presence of fungal hyphae in the granulomata, revealed by silver stains.
    • Lack of acid-fast bacilli (therefore not tuberculosis).
    • Fungal culture: Aspergillus flavus isolated on Sabouraud dextrose agar, from the thoracic and intestinal lesions.


  • Demonstration of the organism on histopathology. (B614.15.w15)
    • Typical septate fungal hyphae in association with granulomas. More visible on staining with PAS or methenamine silver. (B613.6.w6)
  • Aspergillus spp. can be isolated by culture. (B608.21.w21)
Related Techniques
WaterfowlINDEXDisInvTrCntr.gif (2325 bytes)

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Similar Diseases (Differential Diagnosis)

WATERFOWL Other causes of sudden death (B197.11.w11). Avian tuberculosis (disseminated granulomas) (see: Avian Tuberculosis) (J42.65.w1); Anatipestifer infection (air sacculitis) (see: Anatipestifer Infection); Lead poisoning (generalised weakness and emaciation) (see: Lead Poisoning). (B15, B36.13.w13); gapeworm (see: Gapeworm Infection (with special reference to Waterfowl)), trichomoniasis (see:Trichomoniasis (Flagellate Infection) in Birds (with special reference to Waterfowl)) paratuberculosis, colibacillosis, salmonellosis. (B197.11.w11)

From radiographic findings of localised masses: Neoplasia, bacterial granulomas. (B365.45.w45)

  • In a 42-day-old Grus japonensis - Red-crowned crane chick with a large, cavitated mass: neoplasia, avian tuberculosis. Note: the masses would have been highly visible on radiography. (J4.183.w5)

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Treatment and Control

Specific Medical Treatment

  • Note: weeks to months of treatment are required. (P14.4.w28)
  • Treatment of individual infected birds may not be possible in a "heard health" situation, such as during rehabilitation of large numbers of oiled birds. (see: Oiling) (P14.4.w28)
  • Treatment is rarely successful; since disease is generally diagnosed when well advanced. Prevention is preferred. (B284.18.w18; B363.9.w9, B365.45.w45, P14.4.w28)
  • Treatment is unlikely to be successful unless the disease is diagnosed and treatment started at an early stage of infection. (D48, P24.327.w4).
    • Treatment after the onset of clinical signs is generally ineffective due to the extent of lesions by this stage of infection. (P24.327.w4)
  • Itraconazole (Sporanox, Janssen) is the drug of choice for treatment. (P24.327.w4)
    • Other drugs which may be used include amphotericin-B, 5-fluorocysteine, ketaconazole, fluconazole, enilconazole. (P24.327.w4)
  • Itraconazole, 15 mg/k twice daily for one week, then once daily until a month after remission of clinical signs, plus Amphotericin B, 1.5 mg/kg intravenously three times daily through an indwelling catheter (sutured into the basilic or jugular vein), plus clotrimazole, 1-2 ml of a 10 mg/ml solution in polyethylene glycol, given for one hour per day by nebulisation for two months. (B11.3.w28)
  • Itraconazole: 5 - 10 mg/kg twice daily orally. Increased absorption at low pH; this can be given in orange juice or a cola drink. It is metabolised by the liver. (P14.4.w28)
  • Amphotericin B (fungicidal):
    • Intravenously: 1.5 mg/kg two to three times daily for five days, then five days without the drug, repeated as required. (P14.4.w28)
    • Intratracheally, 1 mg/kg two to three times daily, or by nebulisation. (P14.4.w28)
    • Can be given in combination with flucytosine or itraconazole. (P14.4.w28)
  • Ketoconazole:
    • 20-30 mg/kg orally twice daily for at least 21 days. Note: Aspergillus spp. are often resistant to this drug. (P14.4.w28)
  • 5-fluorocytosine / flucytosine: 
    • 75-100 mg/kg twice daily for clinical treatment. Note: bone marrow toxicity; blood cell counts should be carried out frequently. (P14.4.w28)
  • Fluconazole: 2-5 mg/kg per day. Good bioavailability, therefore this drug is preferred for cases involving brain or eye. (P14.4.w28)
  • Antifungal drugs. Several drugs have been used, alone or in combination, including amphotericin B, 5-flurocytosine, ketoconazole, miconazole, enilconazole, itraconazole, rifampicin and dimethyldithiocarbonate. These have been variously administered orally, intravenously, into the trachea or by nebulization. An initial short course of Amphotericin B (preferably by nebulization or directly into the airsacs, since it has poor penetration), is suggested as a part of most treatment regimens, since it has a faster onset of action than the izole antifungal agents do. 
  • Oral 5-flurocytosine (5-FC), 40-50 mg/kg three times daily (total daily dose 120-150mg/kg) has been found effective used alone or (in more severe cases) in combination with amphotericin B (1.5mg/kg intravenously, three times daily and 1.0mg/kg intratracheally twice daily). (B22.23.w1)
  • Fluconazole (10-25 mg/kg twice daily), alone or with 5-flurocytosine may also be effective.
  • Ketoconazole and miconazole appear to be less effective.
  • Itraconazole (Sporanox, Janssen, 10 mg/ml peppermint-flavoured liquid), has also been used at a dose rate of 10mg/kg orally twice daily, together with nebulisation with amphotericin B for 20 minutes, three times daily. Itraconazole appears to be less hepatotoxic than other drugs in this group (J3.130.w1).
  • Itraconazole 10-15 mg/kg orally combined with intratracheal enilconazole (in a 1:10 dilution, to give 0.5 mL/kg, twice daily), and amphotericin B for the first 3-5 days (1.5 mg/kg intravenously three times daily). Give 15 mL/kg fluids intravenously with this to reduce risk of renal toxicity if the bird is dehydrated). Continue intertracheal treatment until two weeks after lesions have disappeared and parenteral (itraconazole) treatment for two months. (B11.18.w9)
  • Treatment with antifungal agents should continue until the levels of antibodies have fallen to background levels; this normally takes four to six weeks. (B197.11.w11)
  • Voriconazole has been shown useful for treatment of raptors, at 12.5 mg/kg orally every 12 hours for three days then every 24 hours. (B703.10.w10)

(B11.18.w9, B13.35.w2, B22.23.w1, B197.11.w11).

  • Multiple antifungal drug therapy has been highly successful. (B12.56.w14, B197.9.w9) This consists of at least two weeks of treatment, continued for a further two weeks if signs have not fully resolved by the end of the first two weeks: (B197.9.w9) A combination of systemic treatment and nebulisation of antifungal agents is used. (B12.56.w14, B197.9.w9, B336.20.w20)
    • Oral Itraconazole, 10 mg/kg. (B197.9.w9)
      • Each 100 mg capsule contains about 285-290 granules, therefore each granule contains about 0.35 mg. Count out the appropriate number of granules and give mixed with food or inside a treat such as a cleaned smelt. (B197.9.w9)
    • Nebulised Clotrimazole, 10 mg/mL in polyethylene glycol (Island Pharmacy Services, Woodruff, Wisconsin, USA). 
      • Place the crane in a small cage, sufficiently large for the bird to stand up and turn around. Place 3-5 mL of the clotrimazole in an "up-mist" medication nebuliser connected to an oxygen source at 5-8 L/minute (to get proper nebulisation). Give three times daily for 20 minutes each time. (B197.9.w9)
    • Oral (usually) or intramuscular Enrofloxacin at 15 mg/k against secondary bacterial infections. (B197.9.w9)
    • Note: no toxicity problems have resulted from this treatment regime. (B197.9.w9)
  • Itraconazole 10 mg/kg (correct number of granules counted and given mixed in 1-3 mL orange juice), given orally by tube every 12 hours, plus nebulisation for total 60 minutes per day with either 5-10 mg Amphotericin B (in 15 mL water) or 3 mL of a 10 mg/mL Clotrimazole in glycerol glycolate. (B12.56.w14, B336.20.w20)
  • Nebulization with clotrimazine (preferable) or amphotericin B. Oral itraconazole or fluconazole, intravenous or intra-tracheal amphotericin B. (B115.8.w4)
  • Note: treatment is generally "unrewarding" in individuals with severe clinical signs. (B12.56.w14, B336.20.w20)
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General Nursing and Surgical Techniques

  • Supportive care including fluids, nutritional support and treatment of any secondary bacterial infections is very important. (P14.4.w28)

Surgical removal of lesions restricting air flow in major airways:

  • Granulomatous lesions should be debrided if possible. (B365.45.w45)
  • Fungal masses at the tracheal bifurcation or in the syrinx may be removed manually via the trachea. (P24.327.w4) under endoscopic guidance.
    • Effective treatment is possible in highly dyspnoeic birds if mechanical blockage is the main cause of the dyspnoea. 
  • Removal of masses in air sacs is difficult but useful if possible.
  • N.B. physical removal of masses must be carried out in conjunction with medical treatment with antifungal agents.

(B13.35.w2, B22.23.w1, B197.11.w11)

  • Good supportive care is important alongside specific therapy. (B197.9.w9)
  • Supportive care:
    • Keep in a non-stressful, warm (70-85 F/21-29 C) environment. (B115.8.w4)
    • Give systemic antibiotics - gentamicin, trimethoprim/sulphadiazine, amikacin, piperazine sodium or enrofloxacin (B115.8.w4) to prevent secondary bacterial infections. (B197.9.w9)
    • Consider intramuscular A, D and E vitamins. (B115.8.w4)
    • Consider fluids, intravenously or subcutaneously as required. (B115.8.w4)
    • If weight loss is noted, supplemental feeding is required. (B115.8.w4)
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Preventative Measures

  • Autogenous vaccines may reduce mortality during an outbreak and may sometimes be use for prevention of disease in susceptible species. (B365.45.w45)
WATERFOWL Results of trials have been mixed. However, vaccination with a heat-killed culture filtrate preparation, alone or in combination with prophylactic 5-FC (5-flurocytosine) in birds considered at risk may be useful (B15, B22.23.w1).
Prophylactic Treatment


  • Avoid broad or prolonged use of antibiotics. (P4.1990.w1, P14.4.w28)

  • Avoid use of immunosuppressive drugs. (P14.4.w28)

Prophylactic treatment is recommended for susceptible species under conditions of stress, including injury, management changes, rehabilitation, oiling and lead poisoning (see: Lead Poisoning in Waterfowl). (B11.3.w28, B22.23.w1, B188)

  • Itraconazole is recommended for prophylaxis. (B284.18.w18)
  • Itraconazole for 1-2 weeks. (P24.327.w4)
    • 15 mg/kg once daily orally in susceptible birds. (J312.16.w1, P24.327.w26)
  • Itraconazole 10 mg/kg orally twice daily for up to one week, then 10 mg/kg orally once daily for up to three weeks. (B11.3.w28, B197.15.w15)
  • Itraconazole at 15 mg/kg orally once daily in Uria aalge - Common murre (guillemot) was adequate to maintain therapeutic drug levels for 24 hours. It was noted that occurence of aspergillosis was lower in murres treated with the drug than in those not given the prophylactic medication. The only difference in blood values was a significantly higher alkaline phosphatase at 48 hours after dosing in birds given 20 mg/kg (P60.1.w12)
  • Nebulisation with amphotericin-B for one week. (P24.327.w4)
  • 5-fluorocytosine, 50-60 mg/kg twice daily for two weeks. (B22.23.w1, P24.327.w4)
  • Fluconazole 15 mg/kg twice daily orally or via a nebuliser. (P24.327.w26)
  • Itraconazole (Sporanox) at 15 mg/kg bodyweight orally once daily. Beads from time-release capsules can be soaked for several hours in a mildly acidic liquid such as cola (flat), then mixed using a syringe. When this is made up the concentration (mg/ml) of the slurry should be recorded. (D133.5.w5)
  • Serological monitoring of at-risk populations using four times a year may be useful to ensure early detection. (B197.11.w11)
  • Prophylactic treatment may be useful in species known to be susceptible when under stressful conditions, for example eider ducks and trumpeter swans, which have been a) injured; b) stressed by a change in management (such as movement between collections); c) brought in from the wild for treatment and rehabilitation, particularly if oiled. Oral administration of 5-fluorocytosine (5-FC), 50-60 mg/kg twice daily for two weeks has been recommended in these circumstances (B22.23.w1, B197.11.w11).
  • Itraconazole (Sporanox, Janssen, 10mg/ml peppermint-flavoured liquid), has also been used prophylactically at a dose rate of 10mg/kg orally for ten days. Itraconazole appears to be less hepatotoxic than other drugs in this group (J3.130.w1).
  • Ensure the thiamine level of the is sufficient for fish-eaters (J23.13.w5).

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Environmental and Population Control Measures

General Environment Changes, Cleaning and Disinfection Maintain an environment which minimises opportunities for proliferation of mould. (B22.23.w1)
  • Ensure adequate ventilation is provided, with 10 to 15 air changes per hour. (P24.327.w26); about 15 air changes per hour (J312.16.w1).
  • Minimise exposure of birds to spores:
    • Avoid the development of damp food dumps on which fungus can grow.
    • Ensure that when feeding wild birds, feeders used are of a design which allows complete cleaning, and clean feeders thoroughly. (B36.13.w13, D48)
    • Avoid the use of organic damp material around birds.
    • Avoid use of straw as bedding material. (P24.327.w4)
      • Particularly ensure that hay and straw are never used as bedding for seabirds. (B284.18.w18)
    • Ensure any bedding materials provided are clean and dry. (P24.327.w4)
    • Ensure traveling boxes are stored properly and are not allowed to become mouldy. (B11.18.w29)
    • Keep birds away from fields containing mouldy agricultural waste material such as maize (corn), peanuts, straw or hay. (B36.13.w13)
    • Keep birds away from mouldy straw or fermenting heaps of weed seeds. (J35.121.w1)

(B36.13.w13, B284.18.w18, D48, P24.327.w4)

In oiled bird rehabilitation:

  • Ensure correct housing and substrates, avoiding straw or other absorbent materials which may become and remain moist. (P4.1990.w1)

  • Ensure good ventilation, using adequate exhaust fans. (P4.1990.w1)

    • Facilities should be designed, preferably in advance of a spill, with a minimum of six to eight, and preferably 15, air changes per hour, in animal holding rooms. (P14.4.w28)

  • Separate any individual birds which are obviously ill. (P4.1990.w1)

  • Minimise stress: ensure birds are provided with an appropriate environment, plenty of cover and minimal noise disturbance. (P24.327.w4)

  • Use an appropriate disinfectant in animal holding areas. (J7.19.w1)

In waterfowl:
  • Minimise stress. Minimise exposure to spores. Ensure adequate ventilation.
  • Maintain a clean environment as free as possible of mould spores:
  • Remove old food, straw, grass cuttings, old sacs etc., particularly from dark, damp areas. If items are very mouldy when moved, dampen first with disinfectant to avoid spreading spores while removing.
  • Clean out the remains of food in bins before re-filling. Always buy good quality food, store in a cool dry place and never use feed which appears mouldy or has a musty odor.
  • Always clean out nesting materials after incubation before a nest is re-used. Ensure bedding and nesting materials are clean and mould-free. Use good-quality, bright-yellow, clean-smelling straw rather than hay or sawdust.
  • Boil sacks in disinfectant and dry thoroughly by hanging in the sun before use.
  • Wash concrete areas regularly, into a drain.
  • Use fungicides, for example around nest boxes. Thiabendazole (Mertect 340-F (MSD AGVET, Merck & Co., Raleigh, North Carolina, 27609 USA), which is safe for use on fruit and vegetables for human consumption, has been used to control fungal growth in both poultry litter and zoo situations. (J5.31.w3, P9.1.w2).
  • Remove eggs from ground-level nests soon after laying (B11.37.w5).
  • Thoroughly clean all incubators, hatchers and brooders at the end and beginning of each breeding season.
  • Fumigate incubators and vacant rooms (See: Formaledehyde fumigation of incubators).
  • For wild waterfowl: Avoid dumping mouldy waste grains etc. where wild birds are known to feed. Where birds are at risk from mouldy food an alternative food source should be provided if possible.

(J7.10.w1, B10.26.w10, B13.35.w2, B13.46.w1, B15, B22.23.w1, B36.13.w13, B197.11.w11)

Population Control Measures
  • Discourage wild birds from using a known mouldy food source: scare away if possible and provide alternative feed (B15, B36.13.w13). 
Isolation, Quarantine and Screening
  • Screen incoming birds with ELISA and treat birds with values above established normals for the species with 5-fluorocytosine until values return to normal background levels. (B22.23.w1)
    • This requires normal ELISA values to be established for different species. (B22.23.w1)
  • Infected birds should be isolated in an area with separate ventilation from other birds. (P14.4.w28)
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