Biomedical subjects

V S Davis

Publications and source records attributed to V S Davis.

5 recordsLinked to original sources

PubMed1992

Self-audits. First step in TQM.

In the fall of 1987, West Paces Medical Center (WPMC), a 294-bed hospital in Atlanta, made a commitment to a new way of management, one that would make it a learning organization. The commitment would not be just to a higher quality of service, but would be a change in the way of doing business. The three components included in the hospital's quality improvement process were customer mindedness, process mindedness and statistical mindedness. West Paces employees concentrated on understanding customers and their needs, learning how they should perform each day to satisfy those needs, and routinely measuring the improvements made in daily processes. Led by Vicki S. Davis, director of quality resources, WPMC implemented, in November 1987, a program based on W. Edwards Deming's quality management method. One year later, 54 department managers had been trained in quality improvement. Davis shares her account of the quality improvement process on the following pages.

Georgia↗

PubMed1990

Adapting the polymerase chain reaction to a double-stranded RNA genome.

We have adapted the polymerase chain reaction (PCR) to a double-stranded RNA (dsRNA) target without possessing unambiguous sequence information. Infectious bursal disease virus of chickens, a member of the binavirus group, has a dsRNA genome which is resistant to denaturation and subsequent enzyme modification. The only published sequence information was for a strain of virus unavailable to us. We have used a quick primer binding assay to select appropriate primers and have combined a simple denaturation method with reverse transcription and subsequent polymerization using the cDNA template to yield amplified product easily detectable by ethidium bromide staining. By varying the times of denaturation, annealing, and polymerization and by reducing the total number of amplification cycles, artifacts have been eliminated when using purified genome as the template. This allowed us to obtain partial sequence information for one viral strain. We have enhanced the utility of our method by optimizing a rapid cell lysis and capsid digestion protocol such that no purification steps are required from initial tissue handling through final PCR product. Total time for all procedures involved no more than 6 h. This technique should be applicable to all other members of the Birnaviradae family and to any other species of dsRNA.

Animals↗

PubMedDate not supplied

Molecular detection of infectious bursal disease virus by polymerase chain reaction.

The polymerase chain reaction (PCR) technique was applied to the detection of infectious bursal disease virus (IBDV). Reverse transcription followed by the PCR was used to amplify a portion of IBDV genome. A set of primers that specify a 150-base-pair segment of IBDV genome was chosen from an Australian strain of IBDV. Standard challenge strain and variant strains A, D, E, G, and GLS-5 of IBDV serotype 1 and OH strain of serotype 2 from infected bursae were subjected to reverse transcription, followed by 30 cycles of PCR. A single band of the PCR product (DNA) of the expected size from each strain of IBDV was visible on polyacrylamide gels stained with ethidium bromide. Using the same primers, no PCR product was detected from genomic nucleic acids of turkey hemorrhagic enteritis virus, infectious bronchitis virus, reovirus, Salmonella enteritidis, Escherichia coli, and uninfected bursae. The PCR could be efficiently performed on serially diluted IBDV RNA and could detect 2 femtograms of IBDV RNA. The identity of the PCR products was confirmed by direct sequencing. The PCR is a specific and sensitive method for the detection of IBDV.

Animals↗

PubMedDate not supplied

Random cDNA probes to infectious bursal disease virus.

Viruses from three commercially available modified-live infectious bursal disease virus vaccines were propagated in tissue culture. Following this, a series of 32P-labeled probes was generated using the entire RNA genome as template for formation of randomly primed cDNAs. These probes were tested against dot blots of the three vaccine strains, as well as the USDA standard challenge strain and one field-origin strain. Dot blots were made of both crude tissue extract and LiCl-precipitated RNA genome. All three probes detected the standard challenge and field strains. Although differences in probe binding could be quantified among the strains, cross-hybridization indicated considerable homology within genomic regions preferentially transcribed under the experimental conditions.

Animals↗

PubMedDate not supplied

History of infectious bursal disease in the U.S.A.--the first two decades.

Infectious bursal disease (IBD) emerged in 1957 as a clinical entity responsible for acute morbidity and mortality in broilers on the Delmarva peninsula. The condition spread rapidly and was recognized throughout the U.S. broiler and commercial egg production areas by 1965. Early attempts to isolate the etiologic agent were impeded by a lack of specific-pathogen-free (SPF) eggs and by deficiencies in viral and serologic techniques. By 1967, the highly infectious nature of the agent was recognized. Reliable methods were developed to isolate the virus in embryonated eggs and to adapt it to tissue culture. The agent was characterized as a virus belonging to a new taxonomic group in 1976. The immunosuppressive property of IBD virus was first recognized in 1970 and was confirmed in structured trials in 1976. An early method of control involved planned infection of chickens. This technique lowered IBD mortality but often resulted in immunosuppression and further dissemination of field virus. A live attenuated vaccine was then developed, based on mild field isolates passaged in SPF eggs. This vaccine was federally licensed as the first of its kind for interstate use in 1968. It remains widely used today in breeders as a primer and in the control of very virulent IBD in many countries. The first two decades following emergence of IBD were characterized by close cooperation among scientists in academia, the biologics industry, and the USDA. By 1976, mortality caused by IBD was effectively controlled by vaccination. However, the more subtle effects of immunosuppression and the tremendous economic impact of the disease were just starting to be appreciated. Recognition of Delaware variants in the mid-1980s and emergence of very virulent forms of the condition in Europe and Asia beginning in 1989 attest to the continuing importance of IBD.

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