This document summarizes various fungal infections that can affect poultry, including aspergillosis, thrush, favus infection, dactyliorosis, histoplasmosis, and cryptococcosis. It provides details on the causative agents, transmission, clinical signs, pathogenesis, lesions, diagnosis, and differential diagnosis for several of the major fungal infections affecting respiratory and digestive tracts of poultry. Aspergillosis, caused by Aspergillus species, is one of the most common fungal infections and typically presents as granulomatous lesions in the lungs and air sacs. Thrush is a yeast infection of the crop typically caused by Candida albicans

1. FUNGAL INFECTIONS IN POULTRY
Avian Pathology 610 (2+1)
Submitted by,
Dr. Rajwardhan
MVSc
Dept. Of Poultry Science
Veterianary College, Bengaluru.

2. 1. Avian aspergillosis.
2. Thrush.
3. Favus infection.
4. Dactyariosis.
5. Histoplasmosis.
6. Cryptococcosis.

3. INTRODUCTION
 Fungi and yeast produce disease in two ways
 First, they invade and destroy body tissues
 Secondly, fungi can infect growing grain or finished
feeds, and produce toxic chemicals (mycotoxins).
 These mycotoxins produce disease or a decrease
in growth (mycotoxicosis) when they are consumed

4.  The respiratory tract, nervous system and eyes
of poultry are commonly infected by fungi.
Infections are usually due to Aspergillus species.
Infection with other fungi are less common

5. INTRODUCTION
 Fungal infections such as histoplasmosis and
cryptococcosis are not common pathogens of
poultry, but they are of public health importance.

6. AVIAN ASPERGILLOSIS
 Aspergillosis is a disease caused by infection
with the genus Aspergillus.
 Manifestations of aspergillosis depend upon
which organs or systems are involved and
whether infection is localised or disseminated

7.  Aspergillosis in birds is usually confined to the
lower pulmonary system with florid lesions in air
sacs and lungs.
 In young poultry it is referred to as brooder
pneumonia
AVIAN ASPERGILLOSIS

8. INTRODUCTION
 Other synonyms are fungal or mycotic
pneumonia, pneumonomycosis, and
bronchomycosis
 Less manifestations relate to infections of the
eye, brain, skin, joints, and viscera.
 It usually means,” pulmonary or respiratory
aspergillosis.

9. ETIOLOGY
 The two major species of fungus Aspergillus which
cause aspergillosis in poultry are,
 Aspergillus fumigatus
 Aspergillus flavus
 Other species include A.terreus, A.glaucus, A.niger.

10.  These organisms are common soil saprophytes,
occurring in decaying vegetative matter and feed
grains.
 They grow on organic matter in warm humid
environments
 Fungal hyphae are 4 -12 μm in diameter and
bear conidiopores producing conidia (spores) 2 -
6 μm in diameter that are easily spread in air.

11. ASPERGILLOSIS: TRANSMISSION
 Infections are acquired from environmental
exposure.
 Infection is by inhalation of spores that usually
originate from infected eggs.
 Contamination of the equipments may result in
hatchery infection.

12. ASPERGILLOSIS: TRANSMISSION

13. ASPERGILLOSIS - TRANSMISSION
 Contaminated feed or poultry house litter also
produce infection

14. ASPERGILLOSIS - PATHOGENESIS

15. ASPERGILLOSIS - CLINICAL SIGNS IN
CHICKS
 Signs are subtle even in cases in which severe
airsacculitis is present

16.  Survived birds – become lethergic and stunted,
develop conjunctival swelling, blindness and
exhibit torticollis and other central nervous
system abnormalities.
 Infected poultry flock – Biphasic mortality pattern.

17.  Acute respiratory disease may cause 5-50%
mortality in the first 1-3 weeks of age.
 Survivors usually develop chronic disease with
up to 5% mortality due to chronic pulmonary
insufficiency, ascites, blindness or neurological
fungal metastasis.

18. ASPERGILLOSIS: LESIONS
 Macroscopical lesions
 Lungs and air sacs
 Granulomas appear as separate 1 -15 mm
diameter white plaques or caseous nodules.
 Composition: Necrotic centres containing
branching, septate, 4-7 μm diameter hyphae.

22. Aspergillosis pathological lesions on
internal organs

23. Aspergillosis pathological lesions on air sacs

24. Aspergillosis lesions on air sacs

25. Aspergillosis lesions on air sacs

27.  Older lesions
 Contain pleomorphic hyphae up to 12 μm in dia.
 Air-filled cavities may appear green to black due
to development of pigmented conidiophores
 Fungi tend to proliferate within the granuloma and
rarely invade adjacent tissue in immunocompetent
birds.

28.  Trachea: Yellow caseous plaques adherent to the
mucosal surface.
 Syrinx: Caseous, gelatinous, or less commonly
mucopurulent exudate.
 Brain: white to yellow circumscribed areas either
in cerebellum or cerebrum.
 Ocular form: Extensive keratoconjunctivitis

30. Microscopical lesions
 Air sacs
 Thickening due to massive infiltration of
heterophils, multinucleated giant cells and other
types of leukocytes
 Germinating conidia were seen in the membrane
interstitium, and lymphohistiocytic perivasculitisin
less severely affected area

31.  Granulomas composing central necrotic cellular
debris and heterophils with peripheral palisade of
epitheliod macrophages and aggregates of
lymphocytes

32. DIAGNOSIS
 Aspergillosis can be made on PM
lesions: Especially white caseous nodules in
lungs, or airsacs. Exudate plugs in tracheal and
bronchial lumen
 Demonstration of branched, septate Aspergillus
hyphae in the lesions
 Under microscopic, using impression smears of
lesions

34.  Using tissue sections
 Routine haematoxylin & eosin
 Periodic Acid-Schiff (PAS)
 Grocott’s Methenamine-Silver (GMS)
 Confirmation should also be made by cultural
isolation and identification of the causative fungus

35.  Although A.fumigatus is the most likely agent of
avian aspergillosis, other species of fungi can
cause the disease. Therefore, isolates should be
identified
 Granulomas or plaques may be cultured on
Sabouraud dextrose agar with antibiotics
 Serological tests are of limited value due to non-
specific nature of the antigen.

36. DIFFERENTIAL DIAGNOSIS
 The clinical signs of avian aspergillosis are dependent
upon the organ systems involved
 Pulmonary aspergillosis is differentiated from other
respiratory diseases by granulamatous lesions at
necropsy
 Exudative fibrinous or purulent air sacculitis and
pneumonia are also frequently seen in the following cases
 Mycoplasmosis
 Colibacillosis
 Fowl cholera
 Chlamydiosis
 If granulamatous lesions predominate , the following ones
should also be considered
 Mycobacteriosis
 Other mycoses

37. THRUSH (CROP MYCOSIS, CANDIDIASIS)
 Moniliasis, Oidiomycosis, sour crop and Mycosis
of the digestive tract.
 Oral, oesophageal or crop candidiasis occurs
quite commonly, but rarly causes clinical signs.

38. AETIOLOGY
 Crop mycosis is usually caused by Candida
albicans, a dimorphic yeast. It appears as
round to oval 3-4 μm budding yeasts
(blastospores) on epithelial surfaces, or as
branching septate hyphae or pseudohyphae in
deeper tissues.

39.  C. albicans is ubiquitous in the environment,
and is usually present in the upper
gastrointestinal tract of normal birds.
 Candidial overgrowth occurs in prolonged
administration of antibiotics.
 Antibiotics suppress normal bacterial flora, thus
allowing Candida to proliferate.

40.  Other risk factors include highly contaminated
drinkers or feeders, eating litter, immuno
suppression, environmental stress, or nutritional
disease.
 Infections are more common in birds under 3
weeks of age. This suggests acquired or age
resistance. Mortality directly due to candidiasis is
almost non-existent. Most signs are due to other
concurrent diseases, or reduced feed intake.

41. CLINICAL SIGNS
 Infections are common, but clinical signs are
seen in only severely affected birds.
 Birds with superficial oral, oesophageal or crop
infections fail to gain weight.
 In rare cases there is systemic invasion, and
signs of neurological, renal, or intestinal
disease may be present

49. PATHOGENESIS AND LESIONS
 Candida are acquired by ingestion.
 They then become part of the normal flora of the
mouth, oesophagus, and crop.
 With inhibition of competing microflora (by
antibiotics) or immunosuppression, fungi
proliferate on the surface, and hyphae or
pseudohyphae penetrate superficial epithelial
layers.

50.  This penetration stimulates epithelial
hyperplasia, and pseudomembrane or
diphtheritic membrane formation.
 The membrane appears grossly as multifocal to
confluent layers of white cheesy material in the
crop and sometimes in the oesophagus and
pharynx.

51.  Candidial thick tangled mass and membranes
are usualIy adherent. They cannot be washed
away like normal accumulations of mucus.
Inflammatory response to mucosal candidiasis
is mild, unless ulceration is produced.

52. DIAGNOSIS
 Pseudomembranes and diphtheritic membranes
in the crop, oesophagus and mouth are highly
suggestive of candidiasis.
 Wet mount by scraping.
 Corn meal agar or Biggy agar

53. FAVUS INFECTION
 This disease is no longer important in commercial
poultry.
 Dermatophytosis, dermatomycosis, ringworm, and
favus are terms applied to the condition of fungal
infections of skin
 The term favus usually is used to denote the disease
in poultry
 Favus has a world wide distribution but its occurrence
is sporadic

54.  The disease is contagious and is transmissible in
humans
 The primary etiologic agent of favus is
Microsporum gallinae (previously, Trichophyton
gallinae)
 The incidence have been reported in the
chicken, turkey, duck, quail, and canary
 M.gallinae favus may be more common in

55. FAVUS – PATHOGENESIS

63. FAVUS – DIAGNOSIS

64. DACTYLARIOSIS
 This is a new fungal disease of chickens
caused by the thermophilic fungus Dactylaria
gallopava.
 Young chickens and turkey poults rapidly
develop neurological disease. Sometimes,
pulmonary lesions similar to those of
aspergillosis are seen

65.  Usually, there is also involvement of the
nervous system. I nfected chicks and poults
develop torticollis, paresis, and incoordination.
In rare cases, pulmonary granulomas develop
and cause dyspnoea as in aspergillosis.
DACTYLARIOSIS

66. PATHOGENESIS AND LESIONS
 Spores reach the brain haematogenously and
produce the main lesions of meningeal and
encephalitic necrosis. This lesion is most
common in the cerebellum, but can appear
anywhere in the brain.

67.  It differs from the mycotic encephalitis of
aspergillosis by having more malacia and
haemorrhage and having far greater number of
giant cells. Grossly, ocular and pulmonary
lesions appear similar to aspergillosis, but
microscopically are less well organized and
have greater number of giant cells.
PATHOGENESIS AND LESIONS

68. DIAGNOSIS
 Clinical signs and gross lesions are not
specific enough to allow diagnosis. Brain
lesions should be examined microscopically.
Those containing pigmented 2μm diameter
hyphae and large number of giant cells are
diagnostic for dactylariosis. The fungus can
be cultured from brain lesions on Sabouraud
dextrose agar with added antibiotics.

69. HISTOPLASMOSIS
 This disease is not of economic importance to
the poultry industry, but it is considered because
of its public health significance.
 It is caused by the fungus Histoplasma
capsulatum, and has been reported usually in
zoo birds, and sometimes, in chicken and
turkey.
 It is an infectious and not contagious disease of
human and lower animals. The disease

70. Histoplasma capsulatum thrives best in soils that have
accumulated droppings from chickens, pigeons, starlings,
other birds, and bats.

71.  1. Histoplasmosis is common in bird dropings.
 2. Protective equipment is necessary for cleaning the
dropings.
 3. Birds dropings carries the Histoplasmosis.
 4. Microscopic view of Histoplasmosis.
1 2 3 4

73. CRYPTOCOCCOSIS
 Cryptococcosis is a disease of humans and
animals, and It is caused by the fungus
Cryptococcus neoformans.
 In humans, it is characterized by a meningitis.
 Although the disease is not of economic
importance in poultry, there are many
sporadic cases from zoo birds.