Pallvi Slathia
Aspergillosis is a respiratory disease also known as mycotic pneumonia, brooder pneumonia or pneumomycosis. Chicken, turkey, humans, other animals and less frequently ducks, pigeons, geese and other wild and domestic birds, are all susceptible to this respiratory disease. On some farms, the illness may be endemic in chickens and turkeys. In wild birds, it seems too random and frequently only affects one bird at a time. The typical age of birds with it is 7 to 40 days. From infected animals Aspergillus fumigatus is usually isolated. Infection is brought on by spore inhalation. Acute and chronic manifestations of the disease exist. The acute form affects birds who consume high quantities of spores, but the chronic form affects birds whose immune systems are suppressed. For the diagnosis of aspergillosis in poultry, which requires a range of diagnostic methods, culturing is crucial because the clinical indications are non-specific. Aspergillosis cannot be effectively treated; instead, prevention is the key to keeping the condition under control. To prevent and control the disease, good management techniques like as sanitation, avoiding moist litter or dirt and mouldy or dusty feeds, providing proper ventilation and sanitizing feed and water lines should be used.
Etiology: Aspergillus fungus species is the cause of aspergillosis in chicken. Aspergillus fumigates, A. flavus, A. niger, A. glaucus and A. terreus are the organisms that are most frequently grown from diseased organs in decreasing order. A. fumigatus is one of these species that frequently causes the illness. Common soil saprophytes, which grow on organic matter in warm (>25°C) and humid environments, as well as damaged eggs in hatcheries, are these organisms.
Pathogenesis:Aspergillus has the ability to penetrate eggshells under specific circumstances, contaminating eggs. If the eggs crack during incubation, the Aspergillus spreads to the hatchery. There could be a higher risk of contamination with in-ovo immunisation. It’s also possible that the virus came from heavily polluted litter. Aspergillus conidia enter the pulmonary system through inhalation and become lodged there. On the impacted cells as well as inside of them, hyphae form. Necrosis of the infected tissue is related to the severe inflammatory response to the infection. Many tissues in the body are thought to become infected with Aspergillus through the blood (eyes, brain, air sacs, visceral organs, and bones).
Clinical Signs: A wide range of nonspecific clinical symptoms, such as anorexia, lethargy, ruffled feathers, respiratory symptoms, polydipsia, polyuria, stunting, or abrupt mortality, can indicate acute aspergillosis. The disease, generally known as brooder pneumonia, is very lethal in the first ten days of life and causes severe respiratory distress in chicks that are infected in-ovo or during hatching. In chicken farms, the mortality rate may climb gradually or abruptly, reaching a peak for a few days before reverting to the previous level. Dyspnea, gasping, hyperpnea with panting, non-productive coughing, wheezing, cyanosis, and occasionally nasal discharge are respiratory symptoms.
Dyspnea, depression, dehydration, and emaciation are listed as symptoms of the chronic type. The involvement of the nervous system results in ataxia, tremor, opisthotonos, lateral recumbency, and paresis. One week after an acute incident of aspergillosis, a flock of turkeys was reported to have nervous and ocular issues. Torticollis, seizures, convulsions, lameness, and hind limb paralysis in broiler breeders were linked to cloudiness of the eye with severe conjunctivitis and turbid discharge.
Gross lesions:Although other organs may be affected, the lungs and air sacs are the predominant sites of lesions. Before the onset of clinical indications, the respiratory tract may become severely involved. The size of lesions ranges from milliary (pinhead- or miller-seed-sized), white to yellowish granulomas up to the size of a pea. Approximately spherical granulomatous nodules may also be seen in the parenchyma and serosa of the other affected organs. The syrinx, air sacs, liver, and intestines also contain granulomas. On the dissected surfaces of the lungs, there are single or multiple necrotic regions and consolidated lung parenchyma. There have been reports of pulmonary aspergillosis and mycotic pododermatitis in turkeys. Encrustations, acute inflammation, and rupture of the keratinized epidermis were seen in the footpads.
Histopathology findings: The microscopical examination revealed perivascular edoema and pulmonary and parietal venular congestion. Disseminated granulomatous foci took the place of the lung’s and air sacs’ typical structural organisation. Caseous necrosis and necrotic cellular debris were present in the granulomatous foci’s centre, which was encircled by rims of heterophils, lymphocytes, macrophages, and multinucleated giant cells. The nodules have coagulative necrotic centres inside of them. On the pleura and beneath the pulmonary lobules, there were a few, more severe densification and inflammatory lesions.
Diagnosis: Aspergillosis symptoms are non-specific, making a diagnosis challenging. Furthermore, no single test can guarantee accuracy. The majority of the time, a diagnosis is made based on a combination of data from the patient’s history, clinical presentation, post-mortem findings, haematology, biochemistry, serology, radiographic abnormalities, endoscopy and fungus culture. Since clinical diagnosis is challenging, cases of aspergillosis in birds are frequently determined based on post-mortem discoveries of white caseous nodules in the lungs or air sacs of infected birds. The bird’s past can disclose a traumatic experience, certain underlying environmental elements and an immune-suppressing disease or medication. Additionally, it could indicate vocal changes, persistent debilitating conditions, or an aversion to physical activity. On the serosa and parenchyma of the respiratory tracts and other organs, granulomatous nodules and/or cheesy plaques are seen.
However, the basis for a conclusive diagnosis is the culture-based isolation of an Aspergillus species or the discovery of the organism during a histological investigation.A nodule can be removed for this purpose, crushed on a slide, and then dipped in a solution of 20% potassium hydroxide and lactophenol cotton blue. The hyphae of the fungus are stained with lactophenol cotton blue. Additionally, sputum or nasal swabs can be used to produce wet mounts using 10% KOH, Calcofluor, Parker ink, and/or Gram stain.
The tissue samples, which include the lungs, trachea, pharynx, and thoracic air sacs in addition to other organs, are processed, embedded in paraffin blocks, and stained using the haematoxylin and eosin (HE) procedure. In H & E-stained sections, Aspergillus hyphae stained ineffectively. The hyphae and mycelia can be distinguished and quickly identified using differentiating stains like Periodic acid-Schiff (PAS), Bauer’s, and Gridley’s. To identify the presence of fungus hyphae, special stains like Grocott’s and Gomori Methanamine Silver stain should be used. The pathogenic organism must be isolated by cultivating it on Sabouraud’s glucose agar in order to determine its species with accuracy. The typical conidial head and colony of an Aspergillus species can be seen.
Treatment: Because the fungus is walled off by the inflammatory reaction of the bird and consequently isolated from the blood stream, treatment for aspergillosis is ineffective. If only systemic medications are administered and the tissue infection is severe, this condition has a poor prognosis. Use of one or more systemic antifungal medications is required for the treatment of aspergillosis. Itraconazole, ketoconazole, clotrimazole, miconazole, fluconazole, and Amphotercin B are among the drugs that are frequently utilised. Itraconazole is one of these medications that is used to treat the illness.
Prevention and control: There is no cure for aspergillosis, and immunisation is not an economically viable method of prophylaxis. Decreased exposure to the fungus and related risk factors is therefore necessary for control.By keeping hatcheries clean, Aspergillus fumigatus in young chicken has been somewhat managed. Avoid using mouldy feed or litter to stop the spread of aspergillosis. Antifungal chemicals should be used to treat poultry houses and litter. Any mouldy feed should be removed, the bulk feed container cleaned, and the old litter in the house should be replaced with the fresh. Air ducts and hatching equipment need to be thoroughly cleaned, sterilised, and inspected. Formaldehyde or thiabendazole should be used to fumigate contaminated hatcheries.