Fig 1.
In vitro versus in vivo bacterial evolution.
Comparison of parameters that differ between bacterial evolution in vitro (flasks) and in vivo (people). HGT, horizontal gene transfer; PK/PD, pharmacokinetics/pharmacodynamics.
Fig 2.
Bacterial evolution during chronic infection.
Pulmonary infection is shown as an example. Infection starts with a population of bacteria entering a new environment, such as the lung. Antibiotics, immune responses, and other pressures exert selection on the bacterial population, causing the emergence of bacterial variants possessing antibiotic resistance and other adaptive traits in a process referred to as pathoadaptation. Bacteria from the adapted population can be transmitted to other individuals or can continue to adapt and cause chronic infection, lasting months to decades.
Fig 3.
Bacterial evolution during acute infection.
(A) Evolution of VRSA during coinfection with MRSA and VRE. While MRSA can be easily transmitted to other patients, VRSA have poor fitness and cannot be transmitted. (B) Different VRE populations in the GI tract and bloodstream of an infected patient. While VRE from the GI tract can be transmitted to other patients, VRE infecting the bloodstream are not transmitted. Conditionally beneficial mutations (shown in green) that are selected during growth in the bloodstream will similarly not be transmitted to other patients. Because anatomical barriers prevent conditionally beneficial adaptations from being transmitted, body sites such as the bloodstream can be considered evolutionary “dead-ends.” GI, gastrointestinal; MRSA, methicillin-resistant S. aureus; VRE, vancomycin-resistant Enterococcus; VRSA, vancomycin-resistant S. aureus.