A proposed new selective growth medium for the isolation of enteroaggregative shiga-toxigenic strains of the emerging pathogen Escherichia coli O104:H4
3rd International Congress on Bacteriology and Infectious Diseases
August 04-06, 2015 Valencia, Spain

Kei Amemiya

Keynote: J Bacteriol Parasitol


The year 2011 was an eventful year for infectious emerging pathogens especially for the European continent. The shiga-toxin
producing Escherichia coli O104:H4 was responsible for one of the largest outbreaks of gastroenteritis centered primarily
in Germany leading in many cases to the life-threatening hemolytic uremic syndrome. In the same year in the United States
there were at least two smaller outbreaks of food poisoning caused by E. coli O157:H7. The outbreak in Germany was found
to be associated with contaminated bean sprouts while those in the US were associated with hazelnuts and romaine lettuce.
Strains of E. coli O104:H4 were received from the Centers for Disease Control and Prevention. Comparative biochemical
studies were performed with E. coli O157:H7 and E. coli O104:H4 using Biolog GEN III microplates and selective differential
plates for identification of metabolic differences. It was also noticed the ability of the E. coli O104:H4 strains to form biofilms
and their ability to bind Congo Red. The ability to activate the host innate immune response was also evaluated using human
embryonic kidney (HEK) cells transfected with individual Toll-like receptors (TLR). It was during the course of these studies
that it was found that E. coli O104:H4 could grow in the special medium used to measure TLR activation but neither E. coli
ATCC25922 nor E. coli O157:H7 could not. With the result of these studies, a solid medium was devised that could support
growth of E. coli O104:H4 but not E. coli O157:H7 or E. coli ATCC25922. The results of the studies will be presented with the
proposed new selective medium that could potentially be used to differentiate enteroaggregative STEC stains of E. coli O14:H4
from E. coli O157:H7.

Biography :

Kei Amemiya received his Doctoral degree from Rutgers University in Microbiology in 1973. He did his Postgraduate studies in Gene Regulation in the laboratory
of Lucy Shapiro at Albert Einstein College of Medicine, Bronx, NY. Later, he went to the National Institute of Neurological Diseases and Stroke in 1986, where
he examined gene regulation in JC virus that caused the demyelinating disease progressive multifocal leuko-encephalopathy in immune suppressed patients. In
1999, he went to the US Army Medical Research Institute of Infectious Diseases, Bacteriology Division, where he has been involved in vaccine development for
Burkholderiamallei and Yersinia pestis. His primary interest has been in the immune response and innate immunity in animal models.