Brooder Pneumonia) a Common Economic, Mismanagement Problem in Commercial and Backyard Poultry
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/ 2018 – 2019 / Aspergillosis (Brooder Pneumonia) A common economic, mismanagement problem in commercial and backyard poultry. It is caused by infection with the genus Aspergillus, lesions of aspergillosis depend upon which systems are involved and whether the infection is localized or disseminated. Aspergillosis in birds is usually confined to the lower pulmonary system with severe lesions in air sacs and lung with less common lesions can be seen in the eye, brain, skin, joints, and viscera. The disease synonyms as brooder pneumonia, mycotic pneumonia, pneumonomycosis. Etiology: Aspergillus fumigatus, Aspergillus flavus, and Aspergillus niger are the most common pathogens were isolated from affected lesions. Fungal hyphae are 4-12 μm in diameter and bear conidiophores producing conidia (spores) 2-6 μm in diameter that are easily spread in the air. The organism grows rapidly on Sabouraud dextrose, Czapek’s solution, or potato dextrose agar (25–37°C) with colonies having a diameter of approximately 3 - 4 cm in 7 days. The flat colonies are white at first and then bluish green as conidia begin to mature, especially near the center of the colony. As the colony matures, the conidial masses become gray-green, and the colony edge remains white. Aspergillus spp. produce toxins that can cause interfere with resistance to various infections (immunosuppression) Hyphae measure 3 - 7 μm in diameter, have parallel sides, are septate, and branch dichotomously. The conidiophore gradually enlarges distally to form a flask-shaped vesicle. The vesicle is 20 - 30 μm in diameter with a single series of phialides (conidiogenous cells) over the distal half. The phialides (6 - 8 μm in length) are arranged upward paralleling the axis of the conidiophore. Aspergillus fumigatus grows well with chicken feather keratin. The optimum temperature for rapid culture of A. fumigatus is 40°C. Conidiophore with flask-shaped vesicle, phialides, and columnar mass of chains of conidia 1 / 2018 – 2019 / Public Health Significance Aspergillosis is not a zoonotic or contagious disease. Allergic pneumonitis can develop in those with frequent exposure to moldy ha. Severely immunocompromised individuals are at risk for developing opportunistic infections, including aspergillosis. Influencing factors Cold stress, high ammonia concentrations, dusty environments, concurrent debilitating factors and immunosuppression increase the risk of sever infection. Concentrated exposure to spores, immunosuppression, or stressors increase the risk and severity of disease. Spread: Exposure is by inhalation of spores. These often originate from infected eggs that are opened during incubation or hatching, releasing large numbers of spores and contaminating hatch mates. Aspergillosis can also be produced by inhalation of spores from contaminated feed or poultry house litter. Fungal growth in wet litter produces large numbers of spores that become aerosolized as this litter is dried. Incubation Period: In an outbreak the mortality totaling 75% began at 5 days, reached a peak at 15 days, and subsided after three weeks. Pathogenesis: Airborne conidia (‘spores’) come to rest on conjunctival, nasal, tracheal, parabronchial and air sac epithelium, where they may germinate and initiate granulomas at these sites. In acute form, the infection rapidly disseminated haematogenously to other tissues and producing lesions in the brain, pericardium, bone marrow, kidney, and other soft tissues. Fungal proliferation tends to be confined within the expanding granulomas and is rarely able to invade adjacent tissues in immunocompetent birds. In chronic form, especially in adult, cause impedance of pulmonary blood flow caused by enlarging pulmonary granulomas and this causes right-ventricular dilatation and ascites. Another cause of mortality is aspergillosis induced exudate that becomes lodged in the trachea or syrinx, producing acute respiratory embarrassment and sometimes asphyxiation in chronically infected individuals. 2 / 2018 – 2019 / Clinical Signs: Infected poultry flocks often exhibit a biphasic mortality pattern. Acute respiratory disease may cause 5–50% mortality in the first 1–3 weeks of age. Survivors often develop chronic disease with up to 5% mortality due to chronic pulmonary insufficiency, ascites, blindness or neurological fungal metastasis. Within the first 3–5 days neonates infected in the hatchery become dyspneic, with open-mouthed breathing (gaspers) due to progressive airway obstruction. Survivors may become lethargic and stunted, develop conjunctival swelling and blindness and exhibit torticollis and other central nervous system abnormalities. Older individuals may remain sub clinically affected for some time, only to develop slowly progressive respiratory embarrassment as their increasing body weight places demands on a reduced functional pulmonary mass. They may also become asphyxiated as a result of blockage of the airways. A common feature of dyspnea associated with aspergillosis is the lack of rales or other respiratory noises. Post Mortem Lesions: Lesions are found in the respiratory tract, including particularly the trachea, bronchi, lungs and air sacs. Occasionally lesions are seen in the viscera, the eye and the brain. The lesions appear as white or pale yellow granulomatous, discrete nodules of 1-9 mm in the lungs, often surrounded by pneumonic tissue, as plaques in the air sacs, as caseous exudate in the trachea, as focal plaques on the surface of the brain and meninges and as fungal keratoconjunctivitis or panophthalmitis in the eye. The lesions that develop in the air sacs are often dark green-brown because of the development of fungal conidiophores, which are pigmented. Histopathology: Granulomatous airsacculitis and pleuritis were seen, were thickened up to 100-fold by massive infiltrates of heterophils, multinucleate giant cells, and other leukocytes. Granulomas had centers composed of necrotic cellular debris and heterophils with a peripheral palisade of epithelioid macrophages and aggregates of lymphocytes. 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. Eye lesions were characterized by edema, which was infiltrated heavily with heterophils and mononuclear cells. Trachea lesions consist of fungi mycelia and pyogranulomatous exudate and the mucosa is necrotic with infiltration of macrophages and fibroplasia is evident in the adjacent tracheal wall. 3 / 2018 – 2019 / Hyphae of Aspergillus fumigatus in lesion material prepared as a wet mount in 20% KOH and ink dye. Differential Diagnosis: The clinical signs of avian aspergillosis are nonspecific and dependent upon the organ systems involved. Mycoplasmosis, colibacillosis, fowl cholera, and chlamydophilosis. Control 1- Removing infected litter or covering it with fresh material. 2- Use of an appropriate disinfectant spray. 3- Clinically affected birds should be culled. 4- The premises should be cleaned and disinfected. 5- Hatchery equipment should be disinfected and monitored. 6- Wet litter or soil or feeds should be avoided. 7- Eggs should be disinfected before incubation. Treatment: The most active drugs against this Aspergillus spp. were nystatin, amphotericin B, crystal violet, brilliant green, hamycin and itraconazole. 4.