Clostridium perfringens is a Gram-positive anaerobe that in both humans and animals is the causative agent of a range of histotoxic and enterotoxic diseases; primarily because it produces many different potent protein toxins. In the early 1970s genetic studies on C. perfringens were limited to isolating mutants by chemical mutagenesis; subsequent studies were focussed on the search for conjugative antibiotic resistance plasmids. These plasmids provided the tools for the development of genetic methods of analysis in C. perfringens; tools which then were used to analyse the role of various toxins in disease. Plasmid biology reserach and bacterial pathogenesis studies came together when it was realised that the division of C. perfringens isolates into five, and now seven, toxinotypes was determined primarily by the presence or absence of conjugative plasmids. There are two major families of conjugative toxin and antibiotic resistance plasmids in C. perfringens. The more common Tcp plasmids carry one or more of the genes for C. perfringens-enterotoxin (CPE), beta-toxin, epsilon-toxin, iota-toxin, NetB-toxin, NetF-toxin or antibiotic resistance. The tetracycline resistance plasmid pCW3 has been used as the paradigm C. perfringens plasmid for genetic and structural studies on the tcp-encoded conjugation process and plasmid maintenance. Both genetic and biophysical studies have shown that the ability of a single C. perfringens cell to carry up to five different Tcp toxin plasmids is dependent upon the specific partitioning system carried by each of these plasmids. Genetic studies have led to the identification of at least nine genes that are required for efficient conjugative transfer and the structure of three of these gene products has been determined. The latter studies have provided novel functional insights into the potential mechanism of DNA transfer in the Tcp-mediated conjugation process.