scholarly journals Morphological changes in heart and lungs of broilers experiencing pulmonary hypertension syndrome caused by Enterococcus faecalis

2002 ◽  
Vol 81 (3) ◽  
pp. 365-370 ◽  
Author(s):  
J.D. Tankson ◽  
J.P. Thaxton ◽  
Y. Vizzier-Thaxton
Keyword(s):  
Pulmonary Hypertension ◽  
Enterococcus Faecalis ◽  
Morphological Changes ◽  
Pulmonary Hypertension Syndrome

Pulmonary Hypertension Syndrome in Young Chickens Challenged with Frozen and Autoclaved Cultures of Enterococcus faecalis

2002 ◽  
Vol 227 (9) ◽  
pp. 812-816 ◽  
Author(s):  
J. D. Tankson ◽  
J. P. Thaxton ◽  
Y. Vizzier-Thaxton
Keyword(s):  
Pulmonary Hypertension ◽  
Enterococcus Faecalis ◽  
Growth Medium ◽  
Ascites Fluid ◽  
Pulmonary Hypertension Syndrome ◽  
Sterile Saline ◽  
Unknown Substance ◽  
Live Culture ◽  
Similar Incidence

Enterococcus faecalis, when administered in a growth medium or sterile saline, will cause pulmonary hypertension syndrome (PHS) in chickens. The objective of this study was to determine if frozen and/or autoclaved cultures of E. faecalis retain ability to evoke PHS. In Trial 1, chicks were inoculated with 3.6 × 107 E. faecalis (IA) in tryptic soy broth (TSB) from either a live culture or one that had been autoclaved (120°C for 20 min). Controls received TSB. Autoclaved and live cultures produced the same degree of PHS in a majority of the birds. Trial 2 used the same protocol, except a frozen (–70°C for 60 min) culture of E. faecalis was compared with the control. The results agreed with those of Trial 1, i.e., the frozen culture also produced PHS. Trial 3 was conducted to determine if E. faecalis caused PHS by producing and releasing some unknown substance into the supernatant. Incidence of PHS was based on percentage of birds exhibiting ascites fluid at 24 hr after challenge. Controls received sterile, frozen, or autoclaved TSB. As compared with controls, those birds that received challenge with E. faecalis alone, supernatant alone, and E. faecalis plus supernatant from live cultures exhibited similar incidence of ascites, whereas birds that received E. faecalis plus supernatant and supernatant alone from cultures that had been either frozen or autoclaved exhibited elevated incidence of ascites as compared with controls. Also, with frozen and autoclaved cultures, those birds that received only pelleted E. faecalis exhibited incidence of ascites that did not differ from controls. Apparently, E. faecalis produces PHS in chicks by producing and releasing an unknown toxin.

scholarly journals Pulmonary Hypertension Syndrome in Broilers Caused by Enterococcus faecalis

2001 ◽  
Vol 69 (10) ◽  
pp. 6318-6322 ◽  
Author(s):  
J. D. Tankson ◽  
J. P. Thaxton ◽  
Y. Vizzier-Thaxton
Keyword(s):  
Pulmonary Hypertension ◽  
Enterococcus Faecalis ◽  
Broiler Chicks ◽  
Pulmonary Hypertension Syndrome ◽  
Routes Of Administration ◽  
Heart Score ◽  
The Right ◽  
And Control ◽  
Dose Levels ◽  
Broiler House

ABSTRACT A field strain of Enterococcus faecalis was administered to broiler chicks at doses of 0, 3 × 106, 1.5 × 107, and 2 × 107 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.

scholarly journals Endothelin in the perinatal circulation

2003 ◽  
Vol 81 (6) ◽  
pp. 644-653 ◽  
Author(s):  
Thérèse Perreault ◽  
Flavio Coceani
Keyword(s):  
Pulmonary Hypertension ◽  
Transition Period ◽  
Morphological Changes ◽  
Ductus Arteriosus ◽  
Negative Inotropic Effect ◽  
Pulmonary Vasculature ◽  
Practical Applications ◽  
Neonatal Cardiomyocytes ◽  
Nitric Oxide Formation ◽  
Pulmonary Vasoconstriction

During the fetal period, blood is oxygenated through the placenta, and most of the cardiac output bypasses the lung through the ductus arteriosus. At birth, pulmonary vascular resistance falls with the initiation of ventilation. Coincidentally, the ductus arteriosus constricts. Endothelin-1 (ET-1) appears to play an important role during that transition period and postnatally. ET-1 can dramatically increase resistance in the placental microcirculation and may be involved in blood flow redistribution with hypoxia. At birth, the increase in oxygen tension is important in triggering ductus vasoconstriction. It is proposed that oxygen triggers closure of the ductus arteriosus by activating a specific, cytochrome P450-linked reaction, which in turn stimulates the synthesis of ET-1. On the neonatal heart, ET-1 has a positive chronotropic but negative inotropic effect. In the newborn piglet and the fetal lamb, both term and preterm, ET-1 causes a potent, long-lasting pulmonary vasoconstriction. Furthermore, a transient dilator response has been identified, and it is ascribed to nitric oxide formation. ET receptors are abundant in the piglet pulmonary vasculature. They are predominantly of the ETA constrictor subtype, though ETB2 constrictor receptors may also be present in certain species. The dilator response is linked to the ETB1 receptor, and the number of ETB1 receptors is reduced in hypoxia-induced pulmonary hypertension. ET-1 appears to be a causative agent in the pathogenesis of hypoxia- and hyperoxia-induced pulmonary hypertension as demonstrated by reversal of hemodynamic and morphological changes with treatment with an ETA receptor antagonist. Findings are amenable to practical applications in the management of infants with pulmonary hypertension or requiring persistent patency of the ductus arteriosus.Key words: ductus arteriosus, neonatal pulmonary circulation, neonatal pulmonary hypertension, neonatal cardiomyocytes, fetus.

Sign in / Sign up

Export Citation Format

Share Document