However, the phenomenon was first discovered in 2005 in the isolate EC93 of Escherichia coli found in rat intestine, and, in this case, was mediated by a Type V secretion system.
This isolate dominated the rat's gut flora and appeared to be particularly good at outcompeting lab strains of E. coli when grown in co-culture.
[1][2] Before CDI was discovered in this isolate, the only systems known to mediate direct interbacterial competition by intoxication were toxins secreted into the extracellular space.
[3] The Type IV Secretion System T4SS is found in many species of Gram-negative and Gram-positive bacteria as well as in archea and are typically associated with conjugation or delivery of virulence proteins to eukaryotic cells.
CdiA is predicted to form a filament several nanometers long that extends outward from the CDI+ cell in order to interact with neighbouring bacteria via outer membrane protein receptors to which it will bind.
[6] The Type VI Secretion System T6SS is widely spread amongst Gram-negative bacteria and consists of a protein complex with 13 core components (TssA to TssM), forming a needle-like structure capable of injecting effector molecules into neighbouring target cells similar to the contractile tail of the T4 bacteriophage.
In a similar fashion, the CdiA homolog BcpA in Burkholderia thailandensis causes up-regulation of genes encoding pili and polysaccharides when delivered to sibling cells which are in possession of the immunity protein BcpI.