Source: NORTH CAROLINA STATE UNIV submitted to NRP
VIRULENCE DETERMINANTS OF HIGH PATHOGENIC ENTEROCOCCUS CECORUM
Sponsoring Institution
National Institute of Food and Agriculture
Project Status
COMPLETE
Funding Source
Reporting Frequency
Annual
Accession No.
1001638
Grant No.
(N/A)
Cumulative Award Amt.
(N/A)
Proposal No.
(N/A)
Multistate No.
(N/A)
Project Start Date
Sep 25, 2013
Project End Date
Sep 30, 2014
Grant Year
(N/A)
Program Code
[(N/A)]- (N/A)
Recipient Organization
NORTH CAROLINA STATE UNIV
(N/A)
RALEIGH,NC 27695
Performing Department
Population Health and Pathobiology
Non Technical Summary
High pathogenic strains of Enterococcus cecorum (EC) continue to cause economic losses to the broiler chicken industry in all of the top 5 broiler producing states including North Carolina. Routine farm hygiene procedures and antimicrobial therapy have proven insufficient to control outbreaks of pathogenic EC; therefore, it is apparent that a safe and efficacious vaccine will be essential to control this important emerging pathogen of broilers. Through previous CVM Research Grants, we have identified 4 virulence gene targets, cbp2, lpxtg3, capC and capD which are 1) homologous to known virulence genes of other Gram positive organisms and 2) significantly enriched in pathogenic EC. We hypothesize that these genes contribute to virulence in pathogenic EC.
Animal Health Component
30%
Research Effort Categories
Basic
20%
Applied
30%
Developmental
50%
Classification

Knowledge Area (KA)Subject of Investigation (SOI)Field of Science (FOS)Percent
3113299109030%
3113260116020%
3113299110050%
Goals / Objectives
Our overall goal is to produce a safe and effective, modified live vaccine to control EC-associated disease. This proposal will produce attenuated strains of pathogenic EC which are the necessary first step in vaccine development.
Project Methods
We have recently developed an embryo lethality assay (ELA). As this bioassay successfully identifies virulent strains; we will employ the ELA to screen our mutant strains for attenuation. Once attenuation is confirmed in the ELA, we will assess the ability of attenuated strains to 1) bind collagen and 2) evade macrophage killing. A collagen binding assay will be utilized which allows for quantification of bacteria attached to collagen in microtiter plate wells by staining with crystal violet (CV) as previously described.15 Chicken type II collagen (Sigma-Aldrich) is commercially available and will be used to coat flat bottom microtiter plates. Wells will be blocked with BSA, washed with PBS, inoculated with 107 cfu/per well of each bacterial strain and incubated at 37°C and 5% CO2 overnight. Adhered bacteria will be stained with crystal violet; washed twice with PBS and adhered bacteria will be quantified by solubilizing the crystal violet in ethanol/acetone (80:20) and measuring the absorbance at 595nm. Absorbance values will be compared using a Student's t-test. A macrophage killing assay will be performed using established methods.16-19 Chicken peritoneal phagocytes will be infected in vivo by inoculating 108 cfu of EC into the coelom of healthy 6-9 week old chickens. Phagocytes will be collected 4 hr later by flushing the coelomic cavity with sterile heparinized (.5U/ml) saline and this coelomic wash will be centrifuged at 100Xg for 25 min. Collected phagocytes will be washed with PBS, re-suspended in RPMI with vancomycin (1 μg/ml), mutanolysin (400 U/ml) and lysozyme (0.94mg/ml) and incubated at 37°C and 5% CO2 for 2 hr to kill extracellular bacteria.19 Following trypan-blue staining to enumerate live leukocytes, equal numbers of phagocytes will be seeded into a 96 well plate at 0.5x106 WBC/well. One set of triplicate wells will be immediately lysed (T0) with TritonX-100, and viable EC enumerated (CFUs) using serial dilutions and plate counts. The remaining wells will be incubated in RPMI without antibiotics for up to 72 hr with sets of wells collected for intracellular bacterial counts at 6, 24, 48 and 72 hr. Percent survival will be calculated and compared between wild-type and deletion mutants using a Student's t-test.

Progress 09/25/13 to 09/30/14

Outputs
Target Audience: Poultry Industry, USDA Changes/Problems: A major roadblock to this work was the genetic manipulation of EC. Despite the frequent genetic exchange typical of EC, targeted mutagenesis is complicated by the fact that our pathogenic EC are resistant to multiple antibiotics and grow poorly on the minimal media required in selection protocols. As such, we have had to take multiple approaches. In our first approach we used strains which utilize erythromycin in the primary selection. Due to innate erythromycin resistance in EC, we had to exchange this marker with a chloramphenicol resistance gene which was amplified and cloned into the pCJK47 plasmid from Dr. Jose Lemos at the University of Rochester Medical Center. While we were able to exchange this selection marker; low frequency of transduction with this plasmid made it clear that more efficient method was needed. To this end we developed a new collaboration with Dr. Lynn Hancock at the University of Kansas and acquired a temperature sensitive plasmid pLT06. In addition we have generated primer pairs needed to generate in-frame deletions of our four target genes cbp2, lpxtg3, capC and capD. We now have all the materials and methodologies needed to generate these mutants and have overcome this roadblock. What opportunities for training and professional development has the project provided? During this project we also trained a current second year veterinary student in general laboratory practices, microbiology and basic molecular biology techniques. How have the results been disseminated to communities of interest? Nothing Reported What do you plan to do during the next reporting period to accomplish the goals? Nothing Reported

Impacts
What was accomplished under these goals? Pathogenic Enterococcus cecorum (EC) causes infection of the spine of broiler chickens, which results in paralysis and up to a 15% loss of a flock as it nears market weight. To protect rural economies, global food security, and improve animal welfare, there is a critical need to control pathogenic EC on a national scale. To date, attempts to control pathogenic EC through standard farm hygiene and antibiotic therapy have failed. Also, the rapid and recent emergence of this disease has made its identification confusing. Our long term goal is to control pathogenic EC through a combined vaccination program. In this program, a killed vaccine for broiler-breeder hens and a modified live vaccine for broilers are combined to disrupt the early steps of EC infection which occur in the first 1-4 weeks of life. This vaccine strategy should decrease the impact of this important disease of poultry. In this work we made significant progress in the development of tools and methods needed to select the strains for the killed vaccine and to make the modified live vaccine.

Publications