To detect the various bacteriological agents and pathological changes in commercial layer chicken affected with egg yolk peritonitis in Namakkal region of India. A total of 6 572 layer chicken from 85 commercial farms were subjected for the study, out of which 1 715 showed various types of oviduct abnormalities. Among the 1 715, 264 birds from six farms were identified as egg peritonitis on the basis of postmortem examination. Trachea, lung, heart blood, liver, peritoneal exudate, oviduct (infundibulum, magnum, uterus) and cloacal swabs were collected from the 264 birds with egg peritonitis lesion for screening of bacterial agents. Signalment, clinical signs and pathological changes were recorded in the affected flocks. The results of the present investigation indicated that the E. coli associated egg peritonitis was responsible for 15.39% of the reproductive tract abnormalities in commercial layers between 21 and 80 week of age. In the affected flocks egg production drop and mortality varied from 3% to 20% and 0.5% to 7.0% respectively. It was noticed during peak egg production (21 to 60 week) and southwest monsoon season (58%). Statistical analysis of age, season and egg production by Chi square test of independence revealed highly significant difference. E. coli was isolated as a pure culture and concurrent with other bacterial agents in 226 and 38 birds respectively. Among the fifteen E. coli serotypes identified serotype O166, O64 and O111 were predominant. Necropsy examination of affected birds revealed the presence of amorphous or insipissiated yolk material in the abdominal cavity with inflammatory changes in the ovary, oviduct and intestine. Microscopically the oviduct surface epithelium showed degeneration and desquamation, moderate to marked infiltration of inflammatory cells especially heterophils and lymphocytes in various regions and lumen contained serofibrinous exudate, inflammatory and desquamated epithelial cells with bacterial microcolonies. Ovarian follicles revealed hyperemia, degeneration of granulosa cells and infiltration of inflammatory cells. Intestine showed degenerative, necrotic and inflammatory lesion. The findings of this study showed that the egg peritonitis might be caused by either the translocation of intestinal E. coli into the peritoneal cavity or by the movement of cloacal E. coli into the oviduct followed by ascension of these bacteria up the oviduct, through the infundibulum, and into the peritoneal cavity. To control the egg peritonitis faecal contamination with E. coli should be minimized.

To detect etiological agents and pathological changes associated with polyserositis in commercial layer chicken. Ten commercial layer flocks which had a sudden increase in mortality and a drop in egg production with lesions suggestive of colisepticemia were investigated. Flock details and pathological changes were recorded in affected flocks to assess the prevalence and impact of polyserositis on commercial layer chicken. Trachea, heart blood, liver, oviduct, cloacal swab, poultry house environment samples, water and feed samples were screened for bacteriological agents. Pooled tissue (trachea, lung, spleen, caecal tonsil, kidney and oviduct) samples from colisepticemia cases were screened for viral agents. Serum samples collected from affected flocks were screened for Newcastle disease virus, infectious bronchitis virus and egg drop syndrome-76 virus by haemagglutination inhibition test, and for Mycoplasma gallisepticum and Mycoplasma synoviae by enzyme linked immunosorbent assay. On necropsy examination of dead birds, fibrinous polyserositis and congestion of various visceral organs were noticed. Microscopically, deciliation and hypertrophy of mucus glands showed in the tracheal epithelium. Vascular derangements and infiltration of inflammatory cells showed in the lungs and air sac. Fibrinous polyserositis, focal necrosis and infiltration of inflammatory cells showed in parenchyma of heart and liver. Inflammatory changes were observed in the ovary and oviduct. Escherichia coli (E. coli) was isolated as a pure culture from 108 birds and from the poultry house environment of the ten affected flocks. Among the eight E. coli serotypes, identified serotypes O78 and O111 were predominant. In colisepticemia affected flocks egg production drop and mortality varied from 3%-10% and 2%-5%, respectively and occured during the peak egg production (21 to 40 weeks) and southwest monsoon season (June to September). The present study revealed that the colisepticemia inducing E. coli isolates were derived from the layer house environment. Hence, the incidences of colisepticemia can be minimized by effectively reducing the bacterial load in the layer house environment through appropriate biosecurity measures.

Infectious laryngotracheitis (ILT) is a severe upper respiratory disease highly contagious in chickens that causes a huge economic impact on the poultry industry all over the world. The current study aimed to design a multi-epitope-based vaccine candidate using envelope glycoprotein B and glycoprotein D of the ILT virus using an immune informatics approach. The glycoproteins B and D are crucial for attachment as well as entry of ILT virus inside the cell, which makes them a potential option for designing vaccine candidates. The prediction of epitopes, viz. helper T lymphocyte, cytotoxic T lymphocyte and interferon-gamma producing epitopes, was performed and high-scoring predicted epitopes were joined in an organized manner using suitable linkers to design the final vaccine candidate. The avian beta-defensin 1 was included as an adjuvant in the amino-terminal of the vaccine design that possesses antimicrobial activity and histidine residues at the carboxy-terminal for the purpose of purification. The final vaccine candidate was evaluated for its physicochemical characteristics, solubility, antigenicity, stability, and allergenicity and validated for its modeling. Molecular docking, binding affinity, and interacting residues between the vaccine candidate and immune receptors, viz. TLR 3, MHC Class I and Class II were assessed. Further, to assess the immune response profile generated by the final vaccine design, an insilico immune simulation study was also performed. The findings of this study revealed that the final vaccine candidate was antigenic, nonallergenic, stable, interacted with immune receptors, and able to produce antibodies as well as cellular immune responses against ILTV infection.

Background: Respiratory diseases are very common in goats and cause severe economic loss to the rural poor farmers. Proper identification of the actual pathogen(s) responsible for the respiratory infections is critical for timely and proper management of those diseases. The present communication describes the spontaneous occurrence of concurrent Peste des petits ruminants (PPR) and contagious caprine pleuro-pneumonia (CCPP) in a goat flock. Methods: An outbreak of respiratory disease in a goat flock consisting of 45 Tellicherry cross bred animals in varying age groups was investigated during the month of February 2019 in Namakkal district of Tamil Nadu. Information of disease outbreak and flock details were collected. Samples from live (nasal, ocular and rectal swabs) and dead (lung, spleen and mesenteric lymph nodes) were collected for detection of Peste des petits ruminants virus (PPRV) and Mycoplasma capricolum subsp.capripneumoniae (MCCP) antigen by polymerase chain reaction. Tissues from heart, lung, liver, kidney, intestine, spleen and lymph node were collected in 10% neutral buffered formalin for histopathological examination. Result: Out of 45 goats at risk, 23 showed clinical signs and 17 died of disease conditions with morbidity, mortality and case fatality rate of 51.11%, 37.77% and 73.91% respectively. PPR was confirmed by RT-PCR with M gene specific primers (191bp) and CCPP was confirmed by PCR with 16S rRNA gene fragment (316 bp). Affected animals showed clinical signs of pyrexia, anorexia, marked depression, mild erosions in the oral mucosa, nasal and ocular discharge, coughing and diarrhoea. Necropsy examination revealed congested oral mucosa, extensive pleuritis with large fibrin clots on lung surface and greyish pink consolidation of cranial lobes and anterior parts of diaphragmatic lobes. On section, consolidated areas were granular in appearance. Histopathology of lung revealed thickening of pleura, interlobular septa and alveolar wall by fibrin deposition and infiltration of inflammatory cells. Pulmonary congestion, infiltration of neutrophils and mononuclear cells, syncytial cell formation with eosinophilic intracytoplasmic and intranuclear inclusions were also noticed. Visceral organs showed degenerative and necrotic changes.