Newcastle disease or Ranikhet disease is implicated to be an important viral infection caused by an enveloped, negative sense RNA virus named Avulavirus and often contributes to the progressive economic losses to the poultry farmers or industries in terms of decline egg production and mortality¹. Velogenic viscerotropic and velogenic neurotropic pathotypes of this virus are demonstrated to be associated with more worrisome mortality pattern in poultry birds followed by mesogenic and lentogenic forms^{2, 3, 4}. The clinically affected birds show several manifestations including dyspnoea, discharge from nostrils and conjunctiva, torticollis, ruffed feathers, prostration, greenish diarrhoea and severe decline in the egg production^{5, 6}. Gross evaluation of the birds after necropsy usually uncover severe haemorrhages on the tip of proventricular glands, haemorrhages throughout the intestinal tract, button ulcers in intestine and bronchopneumonia⁷. Histopathological examination often reflects the necrosis and haemorrhages in various organs including digestive tract, spleen, lungs and various lymphoid tissue (gut associated lymphoid tissues, caecal tonsils). Brain tissue often shows perivascular cuffing and necrosis of Purkinje fibres⁸. In human beings this virus is predicted to produce clinical symptoms including conjunctivitis, headache and fever. So, use of PPEs (personnel protective equipments) and biological safety cabinet during handling of necropsies and samples containing this deadly agent is recommended^{9, 10}. The present manuscript describes a pathomorphological investigation of an outbreak of Newcastle disease in backyard poultry.

Various owners throughout the village reported death of about 100 backyard poultry birds of age 15 days to 8 months after the history of anorexia, decreased egg production, respiratory distress, gasping, air hunger and watery greenish diarrhoea in Balh valley of District Mandi, Himachal Pradesh. Some owners reported 100% mortality of theirs birds flock between the periods of 3-5 days. Clinically sick birds died within 5-6 hours of appearance of clinical signs. Some of the poultry farmers recorded almost 100% mortality in their farms. The birds presented for necropsy were thoroughly examined for pathological alterations and gross lesions were recorded. Representative tissue sections approximately 5 mm thickness from proventriculus, lungs, liver, caeca tonsils, spleen, intestine and brain were collected in 10% neutral buffered formalin (NBF) for the histological investigation. The preserved tissue sections were dehydrated with ascending grades of alcohol, cleared with benzene, impregnated in paraffin wax and sectioned to 4-6 micron thickness with the help of microtome. The processed sections were stained with routine Haematoxylin and Eosin (H&E) stain as per the standard protocol¹¹. The microscopic lesions were recorded and microphotographed.

Gross examination of the necropsied birds reflected the diffuse areas of severe congestion along with multifocal, petechial to ecchymotic haemorrhages and necrotic patches over the lung tissue. Trachea was found to show mild hyperaemia along with mucinous exudates. The brain tissue shows mild congestion on gross examination. Proventriculus revealed typical pin point haemorrhages on their tips in association with slimy mucoid contents distributed throughout the mucosal surface (Fig. 1). Button like ulcerative areas with greenish mucus mixed exudate were quite prominent over the Peyer’s patches in the small intestine (Fig. 2). The small intestine also exhibited the presence of haemorrhages progressive up to caeca tonsils. The liver of the dead birds showed mottled appearance and was friable in consistency.

Histopathological examination of lung sections depicted the presence of eosinophilic oedematous fluid accumulation inside the alveolar spaces along with the infiltration of MNCs (Fig. 3). Microscopic examination of proventriculus reflected desquamated epithelial cells and glandular tissue along with multifocal areas of haemorrhages in association with the infiltration of MNCs mainly lymphocytes in the submucosal layer (Fig. 4). Gut associated lymphoid tissue (GALT) and caecal tonsils revealed the evidence of multiple areas of necrotic changes in the lymphoid follicles (lymphocytic depletion) (Fig. 5) along with haemorrhages at some of the places. Intestinal section exhibited the presence of necrotic changes along with pronounced MNCs infiltration especially lymphocytes. Focal areas of coagulative necrosis and degenerative changes accompanied with increased activity of Kupffer cells and erythrophagocytosis/haemosiderosis were evident in the liver section. Brain tissue showed mild endothelial and glial cells proliferation but no perivascular cuffing was recorded (Fig. 6).

The clinical symptoms including respiratory distress, nervous signs, and greenish diarrhoea with profound mortality in poultry birds in the present report are in accordance with studies carried previously by several researchers^{7, 12, 13}. The haemorrhagic lesions in the proventriculus, caecal tonsils and intestine reported in the present investigation has a parallel correlation with studies concluded previously^{6, 7, 14}. Gross and microscopic examination of lung, trachea and brain tissues have shown almost similar finding compared with the earlier studies^{15, 16, 17}. The present investigation has warranted the adverse trends of mortality associated with Newcastle disease in backyard poultry. The cumulative pathological interventions in various organs and correlation of clinical manifestations with gross and microscopic findings has further supported this outbreak in backyard poultry because of Newcastle disease. The worrisome effects among poultry birds and threat of zoonotic transmission perpetuated by the Newcastle disease signify the urgent need of timely vaccination in poultry birds in the endemic areas.

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