Studies on an ascitic syndrome in young broilers 2. ultrastructure

Maxwell, M.H.; Robertson, Gavin; Spence, S

doi:10.1080/03079458608436313

Cited by 36 publications

(28 citation statements)

References 12 publications

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“…In addition, it has been reported previously that a white blood cell response to viruses was mainly lymphocytic, and therefore stress, which reduces lymphocyte numbers does increase susceptibility to viruses (Gross, 1962). In an accompanying ultrastructural study (Maxwell et al, 1986) virus particles were identified in tissues from birds with ascites. According to the above criteria therefore, the heterophil-lymphocyte ratio in the present study may reflect a stressful environment which may be exacerbated by, or predispose the birds to abnormal accumulations of virus particles.…”

Section: Discussionmentioning

confidence: 81%

Studies on an ascitic syndrome in young broilers 1. haematology and pathology

1986

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SUMMARYIn the present investigation, the haematology and pathology of young broiler chicks with an ascitic syndrome were examined. Gross changes included cardiomegaly, ascites, congested lungs, shrunken livers, enlarged kidneys, dark breast muscle and congested intestines. Many blood parameters were significantly raised including the packed cell volume (PCV), haemoglobin (Hb), red (Rbc) and white blood cell (Wbc) counts. The heterophils and monocytes were also increased at the expense of the lymphocytes compared with control birds. The histopathology revealed degenerative changes in all organs examined which resembled lesions reported elsewhere in birds maintained at high altitude. In addition, large numbers of infiltrating leukocytes, in particular heterophils, were also present in the tissues. In many cases the syndrome was characterised by congestive heart failure.

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Section: Discussionmentioning

confidence: 81%

Studies on an ascitic syndrome in young broilers 1. haematology and pathology

1986

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“…Cardiomyopathy with viral inclusions has been associated with the development of ascites in other ALV infections, and initial ALV-J isolates came from flocks with a high prevalence of ascites and retroviral particles in the myocardium. 16,17,20,24 One clinical manifestation of ALV-J infection may therefore be dilated cardiomyopathy and congestive heart failure. Inclusions were evident in HE-stained sections from older chickens but not in those from newly hatched chicks.…”

Section: Discussionmentioning

confidence: 99%

“…Initial isolates of ALV-J came from meat-type chicken flocks with a high prevalence of ascites and retroviral particles present in the myocardium. 20,24 Severe body weight suppression, evident as early as 1 week of age, has been seen in meat-type chickens following natural congenital infection with ALV-J. 32 The pathogeneses of these effects have not been elucidated.…”

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confidence: 99%

Localization of Avian Leukosis Virus Subgroup J in Naturally Infected Chickens by RNA In Situ Hybridization

Stedman

Brown

2001

Vet Pathol

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Abstract. The novel subgroup J of avian leukosis virus (ALV-J) has emerged as a significant cause of myeloid neoplasia and weight suppression in broiler chickens. We investigated viral tropism using RNA in situ hybridization (ISH) in naturally infected chickens. Formalin-fixed tissues were collected from 12-day-old embryos (seven infected, two control) and from 0-week-old (four infected, one control), 3-week-old (five infected, one control), 6-week-old (five infected, one control), and 9-week-old (10 infected, two control) chickens naturally infected with ALV-J in ovo. A 636-base antisense riboprobe complementary to the 3Ј and 5Ј ends of the pol and env viral genes, respectively, was constructed. Strong positive staining was present in cardiac myocytes, Purkinje fibers, vascular and pulmonary smooth muscle, renal glomeruli, distal tubules, and pituitary glands. Light staining was present in gastrointestinal smooth muscle, thyroid and adrenal glands, and follicular medullae in the cloacal bursa. Staining was not present in any hematopoietic precursors. Tissues from newly hatched chicks exhibited the strongest and most consistent staining, whereas staining in embryos was minimal. RNA ISH confirmed the presence of ALV-J-specific nucleic acid within cytoplasmic inclusions in cardiac myocytes, Purkinje fibers, pituitary glands, and renal glomeruli. Viral tropism for cardiac myocytes and Purkinje fibers may relate pathogenetically to the cardiomyopathy and congestive heart failure described in index chicken flocks infected with ALV-J. Viral tropism for endocrine organs may relate pathogenetically to the weight suppression associated with infection.

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“…The morphological symptom of PHS is right ventricular failure, often accompanied with thinning of the right ventricular wall (RVW) (2,13,14,18,27,47). Potential explanations of hypoxia and PHS are mismatches of ventilation and perfusion in the lungs (7,35,48), reductions of vascular capacity in the lungs (7,20,21,29,30), hypertrophy of the RVW, an increased blood pressure via the pulmonary artery (3,28,36), persistent heart congestion, hydropericardium, and ascites (22).…”

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confidence: 99%

Pulmonary Hypertension Syndrome in Broilers Caused byEnterococcus faecalis

2001

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A field strain of Enterococcus faecalis was administered to broiler chicks at doses of 0, 3 ؋ 10 6 , 1.5 ؋ 10 7 , and 2 ؋ 10 7 bacteria/bird either intra-abdominally or intravenously. In trials 1 to 3, birds were reared communally in a broiler house on pine shaving litter. In trial 4, challenged and control birds were maintained in separate isolation rooms in metal cages with raised wire floors. Challenged birds exhibited a characteristic cavity or depression in the external wall of the right ventricle. A subjective scoring system was devised to quantify challenge effects by assigning each heart a score of 1 to 4. The average number of birds, over all trials and over all dose levels, exhibiting the ventricular cavity was 93%. This value in controls was 5%. The average heart score for challenged birds was 3.1, and that for controls was 0.20. Heart scores of challenged and control chicks were not different in birds reared communally or in separate isolation rooms. Additionally, both routes of administration were equally effective. Results suggest that challenge with E. faecalis caused pulmonary hypertension.

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Studies on an ascitic syndrome in young broilers 2. ultrastructure

Cited by 36 publications

References 12 publications

Studies on an ascitic syndrome in young broilers 1. haematology and pathology

Studies on an ascitic syndrome in young broilers 1. haematology and pathology

Localization of Avian Leukosis Virus Subgroup J in Naturally Infected Chickens by RNA In Situ Hybridization

Pulmonary Hypertension Syndrome in Broilers Caused byEnterococcus faecalis

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