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.

Ultrastructural Alterations in Hela Cells Induced by Spider Venom

1967 ◽  
Vol 25 ◽  
pp. 20-21
Author(s):  
Dale E. McClendon ◽  
Paul N. Morgan ◽  
Bernard L. Soloff
Keyword(s):  
Growth Medium ◽  
Mammalian Cells ◽  
Carcinoma Cells ◽  
Venom Protein ◽  
Sterile Saline ◽  
Carbon Coated ◽  
Available Information ◽  
Loxosceles Reclusa ◽  
Essential Growth ◽  
Solution Cultures

It has been observed that minute amounts of venom from the brown recluse spider, Loxosceles reclusa, are capable of producing cytotoxic changes in cultures of certain mammalian cells (Morgan and Felton, 1965). Since there is little available information concerning the effect of venoms on susceptible cells, we have attempted to characterize, at the electron microscope level, the cytotoxic changes produced by the venom of this spider.Cultures of human epithelial carcinoma cells, strain HeLa, were initiated on sterile, carbon coated coverslips contained in Leighton tubes. Each culture was seeded with approximately 1x105 cells contained in 1.5 ml of a modified Eagle's minimum essential growth medium prepared in Hank's balanced salt solution. Cultures were incubated at 36° C. for three days prior to the addition of venom. The venom was collected from female brown recluse spiders and diluted in sterile saline. Protein determinations on the venom-were made according to the spectrophotometric method of Waddell (1956). Approximately 10 μg venom protein per ml of fresh medium was added to each culture after discarding the old growth medium. Control cultures were treated similarly, except that no venom was added. All cultures were reincubated at 36° C.

scholarly journals Comparative biofilm assays using Enterococcus faecalis OG1RF identify new determinants of biofilm formation

2021 ◽  
Author(s):  
Julia L. E. Willett ◽  
Jennifer L. Dale ◽  
Lucy M. Kwiatkowski ◽  
Jennifer L. Powers ◽  
Michelle L. Korir ◽  
...  
Keyword(s):  
Enterococcus Faecalis ◽  
Growth Medium ◽  
Biofilm Formation ◽  
Time Course ◽  
Opportunistic Pathogen ◽  
Genetic Determinants ◽  
Experimental Conditions ◽  
Biofilm Reactors ◽  
Biofilm Architecture ◽  
Biofilm Development

AbstractEnterococcus faecalis is a common commensal organism and a prolific nosocomial pathogen that causes biofilm-associated infections. Numerous E. faecalis OG1RF genes required for biofilm formation have been identified, but few studies have compared genetic determinants of biofilm formation and biofilm morphology across multiple conditions. Here, we cultured transposon (Tn) libraries in CDC biofilm reactors in two different media and used Tn sequencing (TnSeq) to identify core and accessory biofilm determinants, including many genes that are poorly characterized or annotated as hypothetical. Multiple secondary assays (96-well plates, submerged Aclar, and MultiRep biofilm reactors) were used to validate phenotypes of new biofilm determinants. We quantified biofilm cells and used fluorescence microscopy to visualize biofilms formed by 6 Tn mutants identified using TnSeq and found that disrupting these genes (OG1RF_10350, prsA, tig, OG1RF_10576, OG1RF_11288, and OG1RF_11456) leads to significant time- and medium-dependent changes in biofilm architecture. Structural predictions revealed potential roles in cell wall homeostasis for OG1RF_10350 and OG1RF_11288 and signaling for OG1RF_11456. Additionally, we identified growth medium-specific hallmarks of OG1RF biofilm morphology. This study demonstrates how E. faecalis biofilm architecture is modulated by growth medium and experimental conditions, and identifies multiple new genetic determinants of biofilm formation.ImportanceE. faecalis is an opportunistic pathogen and a leading cause of hospital-acquired infections, in part due to its ability to form biofilms. A complete understanding of the genes required for E. faecalis biofilm formation as well as specific features of biofilm morphology related to nutrient availability and growth conditions is crucial for understanding how E. faecalis biofilm-associated infections develop and resist treatment in patients. We employed a comprehensive approach to analysis of biofilm determinants by combining TnSeq primary screens with secondary phenotypic validation using diverse biofilm assays. This enabled identification of numerous core (important under many conditions) and accessory (important under specific conditions) biofilm determinants in E. faecalis OG1RF. We found multiple genes whose disruption results in drastic changes to OG1RF biofilm morphology. These results expand our understanding of the genetic requirements for biofilm formation in E. faecalis that affect the time course of biofilm development as well as the response to specific nutritional conditions.

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