The generation time of a single cell is the duration T_G of a cell cycle, measured as the time between two consecutive mitoses.

In a bacteria population the single-cell generation time varies during the development of the population. Each phase of this evolution has its own single-cell generation time T_G or its specific generation time distribution T_{G, min} ... T_{G, max}. When giving the single-cell generation time one has to specify the phase of the development in which one has measured it.

One distinguishes the following phases of the development (Stephen T. Abedon, Important words and concepts (3/10/01) from Chapter 6, Black, J. G. (1999). Microbiology. Principles and Explorations. 4th ed., Prentice Hall, Ohio State University, Mansfield, OH 44903, USA):

1. lag phase A, no cell diviaion. This lag in division is associated with a physiological adaptation to the new environment, by the cells, prior to their resumption of division. That is, cells may increase in size during this time, but simply do not undergo binary fission.
2. log phase B during which binary fission occurs. This phase of growth is called logarithmic or exponential because the rate of increase in cell number is a multiplicative function of cell number. The generation time of the population (sensu stricto) is the time it takes for the population in phase B to double in number of bacteria.
3. Continuous culture phase C.
4. Decline (die-off, kill) phase.  Typically this die-off occurs exponentially in time. This death occurs because vegetative cells can survive exposure to harsh conditions (few nutrients, too many toxins, antibiotics) for only so long.

• Agger WA, Callister SM, Jobe DA, In vitro susceptibilities of Borrelia burgdorferi to five oral cephalosporins and ceftriaxone, Antimicrob Agents Chemother 1992;Aug;36(8):1788-90.
• Heinemann M, Trautmann M, Sepsis und Antibiotika-induzierte Freisetzung von Endotoxinen: Konsequenzen für die Therapie? Chemotherapie-Journal, 8. Jahrgang, Heft 5, 1999.
• Preac-Mursic V, Marget W, Busch U, Pleterski D, Rigler S, Hagl S , Kill Kinetics of Borrelia burgdorferi, Infection, 24: 9 - 16, 1996.

 

• the generation time T_G (in absence of the cell wall antibiotic) and
• the kill kinetics half life T_S (in the presence of the cell wall antibiotic)

(Here is an explanation for it:

In principle, the population can be killed with the same rate as it is cell dividing (1.), with a smaller rate (2.) or a larger rate (3.):

1. If the cell wall antibiotic
• (a) is effective only in the growth phase B (Burrascano J, Diagnostic Hints And Treatment Guidelines For Lyme And Other Tick Borne Illnesses, Treatment Resistance) and
• (b) each cell division leads to cell death,
T_S = T_G.
2. If the cell wall antibiotic does not kill each cell that divides, some  cells survive and thus the killing (in the presence of the antibiotc) is slower than the cell division in the absence of the antibiotic. In other words: T_S is the upper limit of the Bb generation time T_G (i.e. T_S > T_G). The Bb generation time is then smaller than the above mentioned 10 ... 12 hours. This is consistent with the culture experiments by e.g. Pollack et al.

Pollack RJ, Telford SR 3rd und Spielman A, Standardization of medium for culturing Lyme disease spirochetes, J Clin Microbiol 1993,May;31(5):1251-5.

3. If the cell wall antibiotic kills the cell that is dividing plus other cells, killing (in the presence of the antibiotic) is faster than cell division (in the absence of the antibiotic):

T_S < T_G.

Interestingly, it has been observed that in the presence of the antibiotic up to twice as many cells die per unit time as would divide in the absence of the antibiotic. In other words: 1/2 T_G < T_S < T_G.

Koop AH, Neef C, van Gils SA. A mathematical model for the efficacy and toxicity of aminoglycoside (April 2003). Workshop "Predictive Value of PK/PD models of antimicrobial drugs". Leiden University Medical Center, Leiden, The Netherlands, 4 - 5. September 2003.
Mouton JW, Vinks AA, Punt NC. Pharmacokinetic-Pharmacodynamic Modeling of activity of ceftazidime during continuous and intermittent infusion. Antimicrobial Agents and Chemotherapy 1997;1(4):733-738.
Vinks AA, Punt NC and Mouton JW. Pharmacokinetic-Pharmacodynamic Modeling of Bacterial Growth and Killing using the Modified Zhi Emax model. Workshop "Predictive Value of PK/PD models of antimicrobial drugs". Leiden University Medical Center, Leiden, The Netherlands, 4 - 5. September 2003.

Some related basics in pharmakodynamics.