Detailed Clinical and Pathological Characteristics
|
IN BIRDS
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 |
IN BIRDS
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:
|
| 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) |
| LAGOMORPHS |
Clinical
Findings
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:
|
Incubation |
- 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). |
| LAGOMORPHS |
-- |
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)
|
| 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). |
| LAGOMORPHS |
Aspergillosis is not a
commonly reported disease of rabbits.
|
Pathology |
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)
Acute:
- 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)
Subacute:
Chronic:
- 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)
Ocular:
- Keratitis and uveitis (mixed Aspergillus and Candida
infection) has been described. (B365.45.w45)
Histopathology:
- 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)
|
| WATERFOWL |
Acute:
- 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).
Chronic:
- 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 Sabourauds dextrose agar (J5.5.w1).
|
| 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)
|
Disease has been reported in either the wild or in captivity
in:
|
BIRDS
- 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)
WATERFOWL
- 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)
LAGOMORPHS
- 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" volume 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 |
WATERFOWL
LAGOMORPHS
|
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 µm 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.
Clinical:
- 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 (3µm), 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 |
| LAGOMORPHS |
- 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 |
|
 |
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)
|
| WATERFOWL |
- 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)
(B11.18.w9, B13.35.w2, B22.23.w1,
B197.11.w11). |
| LAGOMORPHS |
-- |
| Related Techniques |
|
 |
|
|
| Vaccination |
- 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). |
| LAGOMORPHS |
-- |
| Prophylactic Treatment |
BIRDS |
-
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)
|
| WATERFOWL |
|
| LAGOMORPHS |
--
|
| Related Techniques |
|
 |
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:
(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)
|
| Related Techniques |
|
 |