by Dr. Tara Nath Gaire
Department of Veterinary Medicine and Public Health
Institute of Agriculture and Animal Science (IAAS), Rampur, Chitwan, Nepal.
Complete Article: Avian Aspergillosis by Dr. Tara Nath Gaire
Contents
Abstract … Introduction … Etiology … Growth … Toxins … Epidemiology … Transmission … Pathogenesis … Clinical Signs, Gross Lesions, Histopathology & Diagnosis … Treatments & Acquired Immunity (below) … Prevention and Control … References Cited
Treatments
Treating avian aspergillosis is a challenge due to a number of factors. These include the limited knowledge on the pharmacokinetics of antifungal agents in different bird species, the granulomatous inflammation that makes it difficult for the drug to reach the target fungus, the presence of concurrent disease and/or immunosuppression, and the late stage at which birds are usually presented (McMillan & Petrak, 1989; Flammer, 1993; Orosz & Frazier, 1995). The best way to overcome the disease is topical therapy after removing the granulomatous tracheal lesions by suction (Westerhof, 1995), and this can be used in combination with an early, aggressive systemic antifungal therapy. In most birds, however, granulomatous lesions are difficult to remove because of their location within the respiratory system and because of the risk of surgical trauma and anaesthesia (Hernandez-Divers, 2002). Hence, in most cases, only antifungal therapy is applied. Topical therapy can be administered by nebulization, nasal or air sac flushing, or surgical irrigation of the abdominal cavities (Bauck et al., 1992; Oglesbee, 1997; Abrams et al., 2001), while systemic therapy can be administered intravenously and orally.
The role and prevalence of acquired resistance to antifungal drugs as a potential contributing factor is not well known. Since drug resistance has been increasingly reported in human medicine (Snelders et al., 2008), standardized susceptibility testing is also becoming necessary in avian medicine. Literature regarding in vitro susceptibilities of antifungal agents for avian A. fumigatus strains in birds is scarce. The minimal inhibitory concentration of thiabendazole, 5-fluorocytosine, fluconazole, ketoconazole, caspofungin, amphotericin B, itraconazole and voriconazole for a limited number of A. fumigatus strains isolated from raptors has been determined using non-standardized methods (Redig & Duke, 1985; Silvanose et al., 2006, 2009). Currently, a reference method is available to test the antifungal susceptibility of filamentous fungi (Clinical and Laboratory Standards Institute document M38-A2), thus solving the lack of standardization. Using this method, the in vitro susceptibility of 59 avian A. fumigatusstrains against amphotericin B, itraconazole and voriconazole has been determined. Four isolates showed acquired resistance to both itraconazole and voriconazole, a fact that may harbour implications for the treatment (Beernaert et al., 2009c).
Acquired Immunity
The role of acquired immunity in aspergillosis resolution still remains unclear. A previous nonfatal challenge with A. fumigatus did not protect turkeys against a second inoculation and even worsened airsacculitis severity. Transfer of activated splenocytes from convalescent 12-to-14-week-old Beltsville small white turkeys to naive birds did not confer any protection against experimental infection to the latter. A culture filtrate vaccine, a conidial vaccine, a mycelial vaccine, and 2 germling vaccines were compared in different trials for their protective efficiency against A. fumigatus infection in poults, with limited results. This underlines the actual importance of animal models in therapeutic protocols evaluation.
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