ABSTRACT
The occurrence of Aviadenovirus (FAdV) was investigated in chickens from the poultry industry of Minas Gerais state, Brazil. The investigation was conducted due to the scarcity of recent data in the country and its description in neighboring countries. For this purpose, livers were collected from layer chicks (n=25), older layers (n=25), broilers (n=300), and livers (n=25) and stool (n=25) samples from broiler breeders, representing the major poultry regions of the state. FAdV DNA was demonstrated using a previously described PCR protocol for amplifying part of the hexon gene encoding sequence. FAdV was found in layer chicks (36 percent), widespread (100 percent) in older layers, and with regional differences in broilers (24-86 percent). Although all broiler breeder stools were negative, FAdV DNA was detected in livers (16 percent, 4/25) of stool-negative birds. In order to obtain additional information on the circulation of the infection, livers of subsistence chickens collected from one poultry intensive region, were evaluated (n = 12), with FAdV being detected in all samples. FAdV was found in young and old layers, broilers, broiler breeders and free-range chickens, and results suggest the circulation of FAdV among different types of chickens. The detection in older layer chickens may indicate an extended risk of horizontal transmission in regions of Minas Gerais with mixed activity of egg and meat type chickens and poor biosecurity strategies. The infection in breeders may indicate vertical transmission and the continuous production of infected progenies. The hexon-gene-targeted PCR amplicon sequences aligned with FAdV of species D of Aviadenovirus. Results indicate the necessity for biosecurity, especially for breeders, separating flocks according to origin, age and health status, which will be an advantage regarding any pathogen...
Descreve-se a ocorrência de Aviadenovirus (FAdV) na avicultura mineira. Foram amostrados fígados de poedeiras jovens (n=25) e velhas (n=25) e de frangos de corte (n=300). Em matrizes pesadas foram amostrados fígados (n=25) e fezes (n=25). O estudo envolveu as principais regiões avícolas do Estado de Minas Gerais. O DNA de FAdV foi pesquisado por PCR universal, descrito para a amplificação do gene que codifica o hexon de Aviadenovirus, usando FAdV Phelps como referência. Foi demonstrada a presença do DNA de FAdV em 100 por cento (25/25) das poedeiras velhas (78 semanas de idade) e em 36 por cento (9/25) das jovens (18 dias). Em frangos de corte, a detecção variou entre 24 e 86 por cento. Embora as fezes das matrizes tenham sido negativas, foi obtido o amplicon específico em 4/25 dos fígados dessas mesmas aves, indicando menor sensibilidade para detecção nas fezes. Em amostras da avicultura familiar (fígado), colhidas de uma das regiões de avicultura intensificada, foi detectado o genoma de FAdV em 100 por cento das galinhas (n=12). A constatação de alta disseminação de FAdV em aves da avicultura industrial e familiar de Minas Gerais contribui para o entendimento da epidemiologia de Aviadenovirus. As sequências nucleotídicas dos produtos de PCR alinharam com FAdV da espécie D de Aviadenovirus. A demonstração de FAdV em reprodutores indica risco de transmissão vertical e reforça a necessidade de biosseguridade estrita nesses plantéis. A presença de FAdV em diversos setores avícolas, incluindo poedeiras comerciais, frangos de corte, reprodutores e galinhas da avicultura familiar, recomenda a biosseguridade estrita entre as criações de mesmo tipo e de tipos diferentes de aves. A detecção em matrizes pode indicar a continuada geração de progênies infectadas...
Subject(s)
Animals , Aviadenovirus/isolation & purification , Poultry Diseases/diagnosis , Liver/parasitology , Epidemiology , PoultryABSTRACT
OBJECTIVE@#To detect etiological agents and pathological changes associated with polyserositis in commercial layer chicken.@*METHODS@#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.@*RESULTS@#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).@*CONCLUSIONS@#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.
ABSTRACT
Objective: To detect etiological agents and pathological changes associated with polyserositis in commercial layer chicken. Methods: 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. Results: 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 O
ABSTRACT
Objective:To detect the various bacteriological agents and pathological changes in commercial layer chicken affected with egg yolk peritonitis in Namakkal region of India. Methods: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. Result: 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. Conclusion: 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.