A.R Khosravi - Department of Mycology, Faculty of Veterinary Medicine, Tehran University, Tehran - Iran
R Naghshineh - Department of Pathology, Tehran University, Tehran - Iran
A.A Ashkar - Department of Immunology and Microbiology, Ferdosi University, M ashhad - Iran

In this study, 60 female New Zealand white rabbits were chosen and divided into 3 groups. The animals in group 1&2 were immunosuppressed with dexamethazone and cyclosporin A (CY A) respectively. TI1e animals in group 3 (control animals) were not immunosuppressed. In each group, half of the rabbits were infected intratracheally and the other half were infected intravenously with 4 x 105 .conidia of Aspergillus fumigatus. None of the 20 control animals showed any clinical symptoms. All the rabbits ingroups 1&2, which were infected intravenously, developed clinical signs of invasive aspergillosis. However, of these 2 groups the rabbits whi ch were given the conidia intratracheally , only 7 o f 10 animals in group 1 demonstrated clinical signs of aspergillosis. At autopsythere was macroscopic and microscopic evidence of invasive aspergillosis. Histopathological examination revealed hyphae invasion in liver, lung, brain and spleen. We conclude, in natural conditions that aspergillosis is initiated by inhalation of airbon1 condidia, cortison-treatedpatients are more susceptible to invasive aspergillosis than individuals who received CY -A.

Aspergillus Fumigatus, Cyclosporine A, Dexamethasone