Studies on the aetiology of hydropericardium syndrome (Angara disease) in broilers

Afzal, M.; Muneer, R.; Stein, George

doi:10.1136/vr.128.25.591

Cited by 51 publications

(31 citation statements)

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“…These findings also suggest that immunosuppressive agents increase the virulence and/or pathogenic potential of NDV and/or ADV as reported earlier (Markowski-Grimsrud and Schat, 2003;Shivachandra et al, 2003). The post-challenge clinical signs, mortality rates and gross lesions observed in birds following NDV and ADV challenges are consistent with earlier reports (Muneer et al, 1989;Afzal et al, 1991;Chaudhry, 1991;Naeem et al, 1995;Nakamura et al, 1999;Ganesh and Raghavan, 2000;Balamurugan and Kataria, 2004;Kapczynski and King, 2005). The observation that peak mortality occurred between the 3rd and 5th days post-ADV challenge is in agreement with the findings of Kumar and colleagues (1997).…”

Section: Discussionsupporting

confidence: 92%

Effects of Polyether Ionophores on the Protective Immune Responses of Broiler Chickens against Angara Disease and Newcastle Disease Viruses

et al. 2007

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Immunization against Angara disease virus (ADV), a serotype 4 avian adenovirus, and Newcastle disease virus (NDV), an avian paramyxovirus serotype 1, is the mainstay of a broiler vaccination programme, while polyether ionophores usually form an essential component of a broiler medication programme in most parts of India and Pakistan. The role of polyether ionophores in the protective immune responses of broiler chickens vaccinated and challenged with ADV and NDV was investigated. A total of 1600 birds were divided into eight groups of 200 birds each. First four groups were vaccinated against NDV and ADV, while the remaining four served as unvaccinated controls. The first 3 groups of birds were administered salinomycin, monensin and cyclophosphamide (CYP), respectively. The last group served as an untreated control. The same treatment schedule was also followed for the next four unvaccinated groups. The post-vaccination and post-challenge serological responses to NDV and ADV, body and lymphoid organ weight gains, post-challenge survival rate and detection of NDV and ADV in the tissues of infected birds were evaluated. Birds administered salinomycin showed a significant stimulation of protective immune responses against both NDV and ADV as compared to the untreated and CYP-treated birds. Monensin also enhanced the protective immune responses against both viruses but the effect was not statistically significant. Thus, it is concluded that monensin and salinomycin augment the anti-NDV and anti-ADV immune responses in broiler chickens, which supports their use in poultry flocks.

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Section: Discussionsupporting

confidence: 92%

Effects of Polyether Ionophores on the Protective Immune Responses of Broiler Chickens against Angara Disease and Newcastle Disease Viruses

et al. 2007

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“…In 1987, Angara disease (hydropericardium syndrome) occurred in Pakistan (Qureshi, 1988(Qureshi, , 1989Anjum et al, 1989a;Jaffery, 1989;Niazi et al, 1989). Adenovirus has been isolated from affected broilers and is thought to cause the myocardial damage that results in ascites (Afzal & Ahmad, 1990;Anjum, 1990;Afzal et al, 1991). A similar disease has been reported from Iraq (Abdul-Aziz & Al-Attar, 1991).…”

Section: Valvular Insufficiency and Right Ventricular Failure Causingmentioning

confidence: 89%

Ascites in poultry

1993

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SUMMARYResearch on ascites occurring in meat-type chickens reared at moderate and low altitude has shown that the pathogenesis is similar to that of the high altitude disease. Pulmonary hypertension (PH) caused by increased blood flow or increased resistance to flow in the lung results in right ventricular hypertrophy (RVH), valvular insufficiency, increased venous pressure and ascites. The structure of the avian heart, with its thin-walled right ventricle and muscular right atrioventricular valve, allows PH to induce heart failure quickly. The sudden increase in pulmonary hypertension syndrome (PHS) in meat-type chickens in the 1980s was associated with a rapid increase in growth rate and feed conversion. This was a result of a combination of genetic selection for fast-growing, heavy broilers with low feed conversion and a more dense, high caloric, pelleted food that supplied all the nutrients required for rapid growth and encouraged a high nutrient intake. PHS in meat-type chickens is usually primary pulmonary hypertension, that is, PH that occurs without evidence of prior heart or lung disease that could account for the increase in blood flow or resistance to flow that results in the increased pressure in the pulmonary arteries. The lungs of birds are firm and fixed in the thoracic cavity and they do not expand to draw air into the lung. The blood and air capillaries form a rigid network that allows only minimal expansion of the blood capillaries when more blood flow is required. Air is moved through the lung by abdominal movement which draws air in and out of the air sacs. The anatomy and physiology of the avian respiratory system are important in the susceptibility of meat-type chickens to PHS. The small stature of the modern meat-type chicken, the large, heavy breast mass, the pressure from abdominal contents on air sacs, and the small lung volume compared to body weight, may all be involved in the increased incidence of PHS. There is limited space for blood flow in the avian lung. Factors that increase blood flow or increase resistance to flow are additive. Increased blood viscosity caused by the polycythaemia of hypoxia, or increased erythrocyte rigidity of high Na + , are more likely to produce PH in fast-growing than in slow-growing birds. Increased flow due to cold exposure is also additive. Ascites caused by PH is a production-related disease at low altitude. It can be prevented easily by restricting growth rate. It is possible that some meat-type chickens of the phenotype we have created have reached the limit of blood flow through their lungs and that future improvements in growth rate will only be possible if the lung and abdominal cavity capacities are enlarged.

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“…Since then, HPS has been reported in Iraq, Kuwait, India, Mexico, Ecuador, Peru, Chile, Korea, and Japan. [1][2][3][4]8,11,14 From these cases, an adenovirus, which was either isolated from, or visualized electron microscopically, in the liver of affected chickens, has been implicated in the syndrome. 6 The syndrome has been reproduced by inoculation of isolated Fowl adenovirus (FAdV) strains 8,11,15,18 ; hence, the syndrome is also called infectious hydropericardium.…”

Section: Introductionmentioning

confidence: 99%

Characterization of Fowl Adenovirus Serotype 4 Isolated from Chickens with Hydropericardium Syndrome Based on Analysis of the Short Fiber Protein Gene

2010

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The sequences of short fiber genes of the Fowl adenovirus serotype 4 (FAdV-4), including isolates from chickens with hydropericardium syndrome (HPS), in Japan, India, and Pakistan were compared. By phylogenetic analysis based on complete nucleotide sequences of this gene, FAdV-4 strains from HPS (HPS-FAdV-4) in Japan, India, and Pakistan fell into a different cluster from FAdV-4 strains not derived from HPS. Hydropericardium syndrome-FAdV-4 isolates were differentiated from other FAdV-4 strains by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis using the enzyme the Alu I. The use of PCR-RFLP analysis of short fiber genes may be useful to distinguish among FAdV-4 strains.

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Studies on the aetiology of hydropericardium syndrome (Angara disease) in broilers

Cited by 51 publications

References 0 publications

Effects of Polyether Ionophores on the Protective Immune Responses of Broiler Chickens against Angara Disease and Newcastle Disease Viruses

Effects of Polyether Ionophores on the Protective Immune Responses of Broiler Chickens against Angara Disease and Newcastle Disease Viruses

Ascites in poultry

Characterization of Fowl Adenovirus Serotype 4 Isolated from Chickens with Hydropericardium Syndrome Based on Analysis of the Short Fiber Protein Gene

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