Aspergillus species are widely distributed throughout the world and can develop parasitic and saprophytic ways of life, allowing Aspergillus to infect living hosts, including plants, insects, birds and mammals. The most common form of aspergillosis in poultry and other birds is respiratory infection. Clinical manifestations depend on the infective dose, pre-existing diseases, and the immune response of the host. The aim of the present research was to study aspergillosis in domestic and wild birds from Argentina. We carried out morphological and molecular identification, and determination of antifungal susceptibility against seven antifungal drugs. Six birds from different cities of Buenos Aires Province of Argentina were studied. Three of the samples belonged to broiler chicks, while the other three belonged to an eagle, a pheasant, and a kelp gull. Two isolates were identified as Aspergillus fumigatus by morphological characteristics and growth at 50 °C. Morphology and BenA sequencing enabled us to identify three isolates as Aspergillus flavus, and one as Aspergillus sydowii. All antifungal drugs tested showed low MIC values, ranging from 0.008 to 1 mg/L. Aspergillosis in birds causes high economic losses and could be controlled by sanitation, avoidance of moldy food, nest and litter and reducing stress factors.

Objective: This case report aims to discuss the veterinary approach taken to control a case of aspergillosis outbreak on a duck farm. Materials and Methods: A broiler duck farm with a population of 900 Muscovy ducks was having a complaint of a 5% mortality rate in their 3-week-old ducklings. Upon presentation, 10% of the ducks appeared to be listless, dyspneic, ruffled feathers, and cyanotic. Postmortem examination of the dead birds was conducted. The collected samples were subjected to isolation and iden¬tification of the associated Aspergillus fumigatus under the microscope using the scotch tape method. Results: Postmortem examination revealed whitish to creamy caseous nodules in the lungs, tho¬racic air sacs, gizzard, proventriculus, and intestines. Granuloma lesions and infiltration of inflam¬matory cells were observed in the lung and liver tissues. As for therapeutic management, all ducks were treated with copper sulfate, erythromycin, and multivitamins as the fungicide, antibiotic, and supplement, respectively, via drinking water. Conclusion: There is no effective treatment for Aspergillosis as the spores are difficult to destroy completely. Nonetheless, the disease can be controlled and prevented effectively with proper farm sanitation and providing a suitable feed storage environment to inhibit the growth of this opportunistic fungus. [J Adv Vet Anim Res 2020; 7(4.000): 692-697]

Purified lipopolysaccharides (LPS) from 16 serotypes of Pasteurella multocida were complexed with Aspergillus fumigatus ribosomes. The complexes were used as inocula to prepare antisera, in chickens, for somatic antigen typing by the gel diffusion precipitin test (GDPT). Antisera made against 15 of 16 LPS reacted with their respective specific heat-stable antigens in the GDPT and homologous LPS in the passive hemagglutination test. Antisera could not be made against serotype 15 LPS. Correlation was not observed between intensity of the precipitin reaction in the GDPT and titer to homologous LPS in the passive hemagglutination test. Most antisera cross-related with other heat-stable antigens of other serotypes in the GDPT. Many of these cross-reactions were eliminated by dilution. Cross-reactions that occurred in the GDPT with antisera made against LPS of serotypes 2, 5, 7 and 8 could not be eliminated by dilution.

Rabbits were given T-2 mycotoxin orally at 0, 0.25, 0.5, and 0.75 mg/kg of body weight/day for 21 days. Only rabbits in the 0.75 mg/kg/day group (4 of 5 rabbits) died. Alveolar macrophages were harvested on day 22 and used for in vitro phagocytosis of killed Aspergillus fumigatus conidia. Cultures included sera from untreated rabbits or rabbits treated with T-2. Phagocytosis was significantly (P < 0.01) reduced in cultures that used serum from rabbits treated with 0.5 mg of T-2kg/day and alveolar macrophages from untreated rabbits or rabbits treated with T-2. There was little reduction in phagocytosis when alveolar macrophages from rabbits treated with T-2 and normal serum were used. Ingestion of 0.5 mg of T-2 toxin/kg/day significantly (P < 0.05) reduced weight gain, serum alkaline phosphatase activity, serum sorbitol dehydrogenase activity, and serum bacteriostasis. Similar changes were found in the 0.75 mg/kg/day group, as well as a significant (P < 0.05) reduction in PCV, total WBC, and differential leukocyte counts. Neutrophil counts decreased, but not significantly (0.05 < P < 0.10). Significant changes were not detected in alanine transaminase activity, aspartate transaminase activity, blood urea nitrogen concentration, or complement hemolytic activity. Histopathologic changes consisting of centrilobular hepatocellular swelling, mild portal and periportal fibrosis and lymphocyte necrosis within secondary lymphoid tissues developed in most rabbits treated with T-2. Thymic atrophy, bile duct reduplication, and lymphocyte depletion of secondary lymphoid tissues developed in the group given 0.75 mg/kg/day. Severity of lymphoid depletion in secondary lymphoid tissues was greatest in the appendix and decreased in the following order: appendix > sacculus rotundus > ileal Peyer patches > lymph nodes and spleen. In this study, we provide additional data showing that, at these oral doses of T-2 toxin, rabbits could be immunosuppressed, as evidenced by reduced alveolar macrophage phagocytosis and histopathologic changes in lymphoid tissues. Also, these doses caused reductions in weight gain, certain hematologic factors, and serum alkaline phosphatase and sorbitol dehydrogenase activities.

The influence of immunosuppression by T-2 mycotoxin on the fungal disease aspergillosis was investigated in rabbits. Four groups of rabbits (groups 1A, 1B, 3A, and 3B) were given 0.5 mg of T-2 toxin/kg of body weight/day, PO; in addition, rabbits of groups 3A and 3B were exposed to aerosols of Aspergillus fumigatus conidia from days 7 through 16. Rabbits of groups 2A and 2B were exposed to A fumigatus aerosols, but were not given T-2 toxin, and rabbits of group 0 served as controls. Two rabbits of group 1A, 1 rabbit of group 1B, and 1 rabbit of group 3A died before scheduled necropsy. Rabbits of groups 1A, 2A and 3A were killed and necropsied on day 17, and the remaining rabbits (groups 0, 1B, 2B, and 3B) were killed and necropsied on day 28. Changes caused by T-2 toxin included leukopenia, marginal anemia, and increased number of and morphologic changes in nucleated erythrocytes by day 21, followed by a regenerative hematologic response. Serum alkaline phosphatase and sorbitol dehydrogenase activities and antibody response to A fumigatus (as measuredby an indirect hemagglutination test) were decreased by T-2 toxin ingestion. Rabbits with aspergillosis had leukocytosis, increased PCV, and increased antibody response to A fumigatus. Histologic lesions consisting of centrilobular hepatocellular swelling, portal and periportal fibrosis, and lymphocyte necrosis and/or depletion within secondary lymphoid tissue were observed in most rabbits treated with T-2 toxin. Normal defense mechanisms against A fumigatus infection were compromised by T-2 treatment, as evidenced by the severity and extent of lung lesions, greater number of hyphal elements observed, and greater number of colonies of A fumigatus isolated from rabbits of groups 3A and 3B. There were no significant changes in group-0 rabbits.

Sarcocystis cruzi, pregnant cows, plasma alpha-fetoprotein concentrations, cannot be used as diagnostic tool for fetal death

A three years old male Jackass penguin(Spheniscus demersus) showed anorexia, depression, respiratory problem for a few days, followed by clinical treatment for 20 days resulted in death. Grossly, multiple white nodules measuring 2~3 mm in diameter were observed in the surface of and inside lung, liver, kidney, thoracic wall. Microscopically, granuloma formations were observed in the lung and liver. The margin of granuloma surrounded by connective tissue barrier and infiltrated lymphocytes, and also observed giant cell near the granuloma.