Aspergillosis

Aspergillosis

Article originally written by Poonam Neupane , B.V.Sc&A.H ….IAAS,Paklihawa

Introduction

Aspergillosis is defined as a disease caused by infection with the genus Aspergillus, which is composed of approximately 600 Species. Manifestations of aspergillosis depend upon which organs or systems are involved and whether infection is localized or disseminated. Aspergillosis in birds is usually confined to the lower pulmonary system with florid lesions in air sacs and lungs.

In young poultry, the disease is referred to as brooder pneumonia. Other synonyms for avian aspergillosis include fungal or mycotic pneumonia, pneumonomycosis, bronchomycosis, and colloquialisms such as “asper” and “air sac.” Less common manifestations relate to infections of the eye, brain, skin, joints, and viscera.

Etiology

The principal agent causing aspergillosis in poultry is Aspergillus fumigatus. Isolation of A. flavusis less common. Other speciesrarely isolated include A. terreus, A. glaucus, A. nidulans, A. niger, A. amstelodami, and A. nigrescens.

Transmission

Aspergillosis is not a transmissible disease. Infections are acquired from environmental exposure. Disturbances of soil ormovement of hay, compost, or litter can produce aerosols that furnish occasion for respiratory exposure to conidia. Fresh litter contaminated with A. fumigatus can precipitate outbreaks of aspergillosis.

Feed with high moisture content above 14% favors the growth of Aspergillosis.

Immunosuppression and excessive use of antibiotics makes the bird more susceptible to disease.

Transmission may also take place via contaminated egg shell.

Pathogenesis

The widespread distribution of the organism ensures inhalation of conidia by susceptible hosts. The conidia are small enough, 2–3 μm in diameter, to bypass the physical barriers of the upper respiratory tract and are deposited deep in the pulmonary system. A. fumigatus produces a number of proteolytic enzymes that can degrade host tissues, especially components of the extracellular matrix.

Signs and symptoms

Dyspnea, gasping, and accelerated breathing may be present.

When these signs are associated with other respiratory diseases, such as infectious bronchitis and infectious laryngotracheitis, they often are accompanied by gurgling and rattling noises, whereas in aspergillosis there usually is no sound. Other symptoms include thirst, loss of appetite, emaciation.

Gasping

Gross lesions

At 24 hours, white miliary foci were present on air sac membranes, and lung lesions consisted of straw-colored gelatinous sub pleural edema. Air sacs became progressively thicker and opaque and supported granulomata that increased in size andchanged shape from raised domes (1 mm) to flat or umbilicated plaques (2–5 mm), which tended to coalesce.In advanced cases of aspergillosis, the organism can sporulate on the surface of the caseous lesions and on the walls of the thickened air sacs  as evidenced by visible greenish gray mold growth.Caseous, gelatinous, or less commonly mucopurulent exudate may be present in the syrinx in infected birds.

Lesions in brain tissue were white to yellow circumscribed areas usually visible on the brain surface. They were present either in the cerebellum or cerebrum or less frequently in both.

Microscopic lesions

Air sac membranes were thickened up to 100-fold by massive infiltrates of heterophils, multinucleate giant cells, and other leukocytes. Germinating conidia were seen in the membrane interstitium, and lymphohistiocyticperivasculitis was discernable in less severely affected areas.

Granulomas had centers composed of necrotic cellular debris and heterophils with a peripheral palisade of epithelioid macrophages and aggregates of lymphocytes.

Examination of pyogranulomas stained with Gomori’smethenamine silver stain revealed large numbers of germinating conidia centrally and hyphae extending peripherally through the layer of macrophages.

Lung lesions consisted of heterophilic and lymphohistiocytic or granulomatous pleuritic and pneumonia with edema and hemorrhage in the initial 48 hours, but had progressed to extensive effacement of parenchymal architecture by necrosis, hemorrhage, and massive infiltrates of leukocytes by 72 hours.

Septate hyphae were mostly localized to areas of necrosis and aggregates of multinucleate giant cells.

Brain lesions consisted of solitary abscesses with necrotic centers infiltrated with heterophils and surrounded by giant cells. Hyphae were seen in the central area of some lesions.

Diagnosis

Aspergillosis usually is diagnosed at postmortem examination, often based upon the observation of white caseous nodules in the lungs or air sacs of affected birds.

Biopsy specimens of infected material were obtained for histologic evaluation and bacterial and fungal examination and culture. Although it is sometimes possible to observe fungal growth and sporulation on the caseous nodules or plaques, especially in the air sacs, confirmation should be made by cultural isolation and identification of the causative fungus. With use of Radiology/ endoscopy. Demonstration of fungal hyphae protruding from the giant cells on staining with PAS or fungal stain.

Differential diagnosis

           The clinical signs of avian aspergillosis are nonspecific and dependent upon the organ systems involved. Pulmonary aspergillosis usually is differentiated from other avian respiratory diseases by the granulomatous lesions observed at necropsy.

Exudative fibrinous or purulent airsacculitis and pneumonia are also frequently seen in cases of    mycoplasmosis, colibacillosis, fowl cholera, and chlamydophilosis. Mycobacteriosis and other mycoses should also be considered when granulomas predominate.

References;

Diseases of Poultry, 12th Edition5

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