№ 275/2014 from Jul 21, 2014
A research project headed by the molecular microbiologist Elke Genersch that investigates the "Molecular Pathogenesis of American Foulbrood in the Honeybee" is being supported by the German Research Foundation (DFG) with funds from the Stifterverband für Deutsche Wissenschaft. A spokesperson for the DFG in Bonn said the project is particularly deserving of support because Genersch's research findings represent a breakthrough in bee pathology and will pave the way for an effective therapy. Elke Genersch is on the faculty of the Institute of Microbiology and Epizootics at Freie Universität Berlin and the deputy director of the Institute for Bee Research at Humboldt-Universität zu Berlin. Genersch received a grant of 25,500 euros to explore additional factors involved in the disease. "We can only fight the disease, if we understand it," says Dr. Elke Genersch.
American foulbrood is an animal disease that can destroy entire colonies of bees. The pathogenic agent of this notifiable animal disease is the bacterium Paenibacillus larvae (P. larvae). Larvae that are supposed to grow into bees are decomposed into a slimy, stringy mass. The brood, and often the whole colony, must be destroyed to eliminate the epidemic.
Several years ago Dr. Elke Genersch was able to demonstrate that there are genetically distinct types of P. larvae. Two of them are responsible for the destruction of beehives worldwide: ERIC I and ERIC II. One obvious difference between the two genotypes is the course taken by the disease: ERIC II kills the larvae faster than ERIC I. Genersch and her team hope to find out why this is so as they continue their DFG project on the molecular pathogenesis of American foulbrood.
In 2008 Dr. Elke Genersch and her research team discovered the infection mechanism of the deadly bee disease: the pathogen populates the midgut of the larva and lives from the food ingested by the larva. Once the larval gut is filled to the point of bursting, the bacteria break through the intestinal wall and enter the surrounding tissue. The ERIC I bacterium penetrates through the intestinal wall with the help of toxins. ERIC II has developed a different mechanism: it forms a so-called surface-layer protein on its cell surface, which it uses to attach itself to the intestinal cells of the larva, where it destroys the connections between the epithelial cells.
In order to understand the pathogenesis of this deadly disease, Genersch aims to identify other factors that make the bacterium so dangerous and cause the difference in virulence in the bacteria. She also plans to explore where the bacterium comes from and how it is spread.