Experimental Production of Ascites in Broiler Chickens Using Infectious Bronchitis Virus and Escherichia coli

Tottori, Junichi; Yamaguchi, R.; Murakawa, Yasushi; Satô, Mizuho; Uchida, Kôji; Tateyama, Susumu

doi:10.2307/1592462

Cited by 28 publications

(10 citation statements)

References 21 publications

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“…Ascites outbreaks have been attributed in several reports to poor air quality (e.g., dusty conditions), poor ventilation (e.g., elevated ammonia, carbon monoxide, or carbon dioxide levels), and respiratory damage or airway obstruction due to pathogens or pulmonary inflammation (Wideman, 1984(Wideman, , 1988Julian and Goryo, 1990;Shlosberg et al, 1992Shlosberg et al, , 1996aBottje and Wideman, 1995;Tottori et al, 1997;Wideman et al, 1997;Bottje et al, 1998). Exposure to bacterial lipopolysaccharide (LPS, endotoxin) has been used to experimentally simulate the responses of broiler lungs to inflammatory responses.…”

Section: Mediators Of Pulmonary Vasoconstrictionmentioning

confidence: 99%

“…The respiratory tract is constantly challenged with aerosolized bacteria (e.g., poultry house "dust") or bacteria translocated into the blood from the gastrointestinal tract or integument. Administering LPS intravenously or via an inhaled aerosol triggers pulmonary hypertension attributable to vasoconstriction (Wideman et al, , 2009Chapman et al, 2005Chapman et al, , 2008Lorenzoni and Wideman, 2008b), and respiratory exposure to E. coli amplifies the incidence of PAH (Tottori et al, 1997;Yamaguchi et al, 2000). The pulmonary hypertension elicited by LPS in mammals has been associated with the release or synthesis of several vasoconstrictors, including ET-1, platelet activating factor, TxA 2 , and 5-HT .…”

Section: Mediators Of Pulmonary Vasoconstrictionmentioning

confidence: 99%

See 1 more Smart Citation

Pulmonary arterial hypertension (ascites syndrome) in broilers: A review

Wideman¹,

Rhoads

Erf³

et al. 2013

Poultry Science

174

180

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Section: Mediators Of Pulmonary Vasoconstrictionmentioning

confidence: 99%

Section: Mediators Of Pulmonary Vasoconstrictionmentioning

confidence: 99%

Pulmonary arterial hypertension (ascites syndrome) in broilers: A review

Wideman¹,

Rhoads

Erf³

et al. 2013

Poultry Science

174

180

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“…Respiratory disease could cause hypoxic hypoxaemia and induce polycythaemia (Tottori et al, 1997). Fibrosis following lung damage from infection and inhaled or ingested toxins can reduce capillary size, restricting blood flow and causing PH (Julian, 1993;Witschi, 1996).…”

Section: The Lungs and Air Sacs As Physiological Triggers Of The Asmentioning

confidence: 99%

Physiological, management and environmental triggers of the ascites syndrome: A review

2000

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In meat-type chickens, an inadequacy of vascular capacity for blood flow through the lung to provide the tissues with the oxygen needed for rapid growth is the primary cause of pulmonary hypertensioninduced ascites. There are a variety of other factors that can trigger the ascites syndrome. These factors may cause increased blood flow because of a higher metabolic rate (cold, heat, certain nutrients, chemicals, etc.) or they may cause pulmonary hypertension-induced ascites in rapidly growing chickens because of greater resistance to blood flow in the lung by: (i) increased blood viscosity or red blood cell rigidity; or (ii) reduced vascular capacity in the lung. Some secondary factors, such as high sodium from salt in feed or water, may cause both increased flow and increased resistance to flow. Measures to reduce the ascites syndrome must address the primary genetic cause of insufficient vascular flow capacity in the lung and oxygen delivery to tissues, and the secondary factors that increase oxygen requirement, blood flow and the resistance to blood flow in the lung.

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“…The heritability of RV:TV is approximately half that of the clinical condition of ascites (Lubritz et al, 1995). It has been demonstrated that elevated RV:TV ratios can be induced by the experimental intratracheal inoculation of infectious bronchitis virus or Escherichia coli (Tottori et al, 1997). These agents could not be recovered from the birds by the time the clinical signs of ascites developed.…”

Section: The Role Of Infectious Agentsmentioning

confidence: 99%

Ascites in poultry: Recent investigations

Currie¹

1999

Avian Pathology

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In recent years, ascites research has centred on gaining an increased understanding of pulmonary hypertension syndrome together with the potential role of primary cardiac pathologies. The impact at a cellular level of factors which trigger ascites and substances that protect against it has also been documented. Primary pulmonary hypertension has been induced when birds are exposed to hypoxia during incubation. The conditions experienced during this phase of development may impact on the ability of the bird to regulate its basal metabolic rate through endocrine signals controlled by thyroid activity. The extent of ventilation in the lung in¯uences the ability of the bird to oxygenate haemoglobin. Ventilation/ perfusion mismatches may occur prior to or post-hatching. This factor has been studied extensively using the pulmonary artery/bronchus clamp model. At high altitude, a decreased ventilation/perfusion ratio may occur following the effective increase in physiological dead space due to the lowered oxygen tension at the level of the parabronchi. This explains the mechanism by which ascites is triggered by hypoxia in this particular situation. The effects of ascites are ameliorated by the use of b 2 agonists and dietary arginine, which act by increasing ventilation and blood¯ow in the lungs and thus correcting a ventilation/perfusion mismatch. Transient bacterial and viral infections may also in¯uence the induction of pulmonary hypertension. The increases in blood viscosity associated with ascites are most probably a consequence of the condition rather than a cause. A bird may alleviate the effects of pulmonary hypertension by decreasing blood viscosity through inhibition of platelet function, increased erythrocyte deformability and the production of coronary relaxants. Evidence is accumulating that primary cardiac pathology may be associated with a number of ascites cases. Broilers that subsequently develop ascites, exhibit lower heart rates than their normal¯ock mates. Furthermore, during ascites, hypoxic broilers exhibit bradycardia as opposed to the expected tachycardia. In these cases, a tachycardia induced by feed restriction may protect the bird by raising its cardiac output. Right atrio-ventricular regurgitant¯ow velocities in chickens are relatively slow compared with similar regurgitant¯ows induced by pulmonary hypertension in other species. The conduction system in the avian heart is specialized and contains a recurrent bundle branch that innervates the right atrio-ventricular valve, thus initiating active valve closure before right ventricular systole. This predisposes the heart to right ventricular volume overload through a valvular incompetance following a failure of valvular innervation. The resultant elevated diastolic wall stress can trigger the production of angiotensin II and its converting enzyme, which mediate ventricular hypertrophy. Subclinical myocardial damage, irrespective of its cause, can be detected by the presence of troponin T in the blood. Reactive oxygen species may damage cell me...

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Experimental Production of Ascites in Broiler Chickens Using Infectious Bronchitis Virus and Escherichia coli

Cited by 28 publications

References 21 publications

Pulmonary arterial hypertension (ascites syndrome) in broilers: A review

Pulmonary arterial hypertension (ascites syndrome) in broilers: A review

Physiological, management and environmental triggers of the ascites syndrome: A review

Ascites in poultry: Recent investigations

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