Faculty Publications and Presentations

Using Serratia marcescens as a Model to Elucidate Aspects of Germ Genesis in Bacteria

Publication Date


Document Type

Conference Proceeding




For creationists, biblical studies and current microbiological research suggests that factors leading to pathogenicity in bacteria may be attributed to the Fall of man and the Curse on the original “good” creation that is now undergoing decay. The origin of bacterial diseases is complex and multifaceted and may be explained by a combination of factors including mutations, mobile genes, and man’s protective defense mechanisms. The hypothesis is that a common pattern in the origin of bacterial diseases found in many is the modification and displacement of originally “good” bacteria.

A common focus among creationists has been the degeneracy in genomic pathways that lead to pathogenesis. Most bacterial diseases are too complex to be the result of the simple deterioration of a bacterial genome. A more likely genome “recipe” for germ genesis is to reduce, add, and “stir” the DNA. The loss of genomic and metabolic pathways has been typically understated in the evolutionary biology literature.

The bacterium Serratia marcescens may serve as a model for genomic decay leading to pathogenicity. S. marcescens is noted for the production of a bright red pigment called prodigiosin. The metabolic pathways involved in prodigiosin production are numerous and complex, so mutations affecting any of these pathways could result in loss of pigment production. Most (70–93%) Serratia infections are caused by naturally occurring white mutants, which also often bear antigenic flagella and appear to be more host dependent.

In the initial stages, we seek to develop and elucidate a research model using S. marcescens. UV irradiation can transform prodigiosin-producing organisms into nonproducing white mutants. In our experiments to maximize random mutations correlated with loss of prodigiosin, radiation time influenced mortality and the number of white mutants that grew. The degeneracy of prodigiosin production in our experiments have some similarity (i.e., some UV white mutants have greater motility and have lost some metabolic capabilities) to that in clinical strains (933 and WF), suggesting a possible link to pathogenicity. The initiation rate and degree of pathogenicity in the UV white mutants is unknown, but those that develop numerous flagella are more likely to become pathogenic via transduction or another undetermined mechanism. Future investigations will explore this inverse relationship of prodigiosin production with motility (i.e., flagella), pathogenicity, and host dependency. Germ genesis in S. marcescens (from saprophyte to pathogen) appears to be a good model of bacteria that first lost metabolic pathways, then acquired foreign genes (phages), and finally had its DNA “stirred.” A once harmless saprophyte has now become an opportunistic pathogen.