Aspergillosis is a non-contagious respiratory disease caused by fungal species known as aspergillus affecting chickens, ducks, turkey and many other bird species. Mainly seen in 7-40 days old birds. Aspergillus fumigatus is the main cause of this disease. Infection occurs through inhalation of spores, typically from contaminated litter or other contaminations in hatchery. After inhalation spores mainly penetrate the respiratory system causing granulomas. Itraconazole is one of these drugs that can be used to treat the disease.Prevention is best method of controlling this disease as treatment is not effective. Adequate managemental practices such as sanitation, disinfection and ventilation must be adopted. Handling infected birds and animals, inhaling spores from infected feed and litter, poor sanitation and hygiene, and eating undercooked contaminated poultry are all ways for it to spread to humans.

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Chickens affected with Newcastle disease virus (NDV) genotype XIII and pigeons affected with genotype II were characterized for virulence and found to be velogenic and lentogenic respectively, based on protein translation of Fusion protein (F) gene and by Mean death time (MDT) and Intracerebral Pathogenicity Index (ICPI). Clinically, respiratory and/or enteric manifestations were exhibited by the chickens, whereas pigeons showed predominantly neurological signs. It was therefore pertinent to describe the salient pathological features or differences during spontaneous infections in the respective hosts. Disease was suspected in two flocks of backyard fowl (Gallus gallus domesticus) showing 100% morbidity and 86% mortality; and in six flocks of domesticated pigeons (Columba livia domestica) exhibiting 21.68% morbidity and 14.16% mortality in a study from August 2017 to July 2018. Gross lesions and microscopic lesions were typical for those described for ND, but viscerotropic lesions were prominent in fowls, while neurotropic lesions were more vivid in pigeons. Gross lesions were suggestive of vascular injury with haemorrhagic tracheitis, enteritis and sometimes petechiae observed in other organs. No prominent gross lesions were observed in the nervous tissue except in some birds showing congestion of meninges. Histologically, haemorrhages, mononuclear infiltration and lymphoid depletion were common. Lesions in nervous tissue were more pronounced in pigeons and represented focal gliosis, loss of Nissl substances and neuronal degeneration, satellitosis and neuronophagia. There was focal gliosis of the nerve tracts in the cerebellum indicating demyelination of nerve tracts. Consistent presence perivascular oedema, endothelial hypertrophy, necrosis and medial hyalinization were noteworthy. In some cases, vacuolation was observed in Purkinjee cells together with presence of intracytoplasmic inclusions. It is speculated that the relatively less pathogenic pigeon strain has sufficient time to generate an overt neurological lesion than the virulent fowl strain. The present findings highlight the salient differences in host pathology in chicken and pigeons and are believed to assist in diagnosis of the disease, particularly while attributing a particular pathotype to a prevalent strain.