Abstract
The variable severity of Burkholderia cepacia complex infections in cystic fibrosis (CF) has recently been ascribed to differences in the virulence between genomovars. Specifically, genomovar III isolates have been associated with higher transmission rates and adverse outcomes compared to other B cepacia genomovars, and consequently further segregation between genomovar III and non-genomovar III B cepacia infected patients is advocated in some centres. The important role of non-genomovar III isolates is presented in the context of a clinical case whereby a patient with long-standing pulmonary infection with B multiovorans developed bacteremic infection reminiscent of the fatal 'cepacia syndrome'.