Table 1.
Published Works Using Skyline Plots to Estimate Demographic Changes in Bacteria.
| Species | Conclusion | TMRCA | Authors’ Comments |
|---|---|---|---|
| Bordetella pertussis | Expansion | 200 Y | Surprisingly, vaccination was followed by increase not decrease in Ne.u, suggesting diversification of lineages escaping the vaccine (Bart et al. 2014) |
| Clostridium difficile | Expansion | 35 Y | Population expansion coincides with the first reports of hospital outbreaks (He et al. 2010). Recombination tracts removed |
| Escherichia coli | Expansion | 140 MY | A population bottleneck had a founding effect by purging diversity and leading to the formation of the extant major groups of E. coli (Wirth et al. 2006). 50-fold population expansion in the last 5 MY. Mentions the caveat of recombination |
| Legionella pneumophila | Expansion | 20 Y | Correlation between population and reported number of clinical cases (Sanchez-Buso et al. 2014). Recombination tracts removed |
| Moraxella catarrhalis | Expansion | 50 MY | The populations of antibiotic resistant isolates expand faster than those of sensitive bacteria (Wirth et al. 2007). Recombination tracts removed |
| Mycobacterium tuberculosis | All expansion | 70 KY, 6.6 KY, 40Y | (1) Concludes about a parallel evolution between human (mitochondria) and this clade’s Ne caused by a tight host-parasite association (Comas et al. 2013). (2) One expansion is associated with the industrial revolution, another with the first world war, and a recent contraction is associated with the introduction of antibiotherapy (Merker et al. 2015). (3) Expansion is associated with acquisition of multi-drug resistance (Eldholm et al. 2015) |
| Mycoplasma gallisepticum | Expansion | 17 Y | Population expansion (Delaney et al. 2012) |
| Neisseria gonorrhoeae | Expansion, contraction | 40 Ya, 120 Y | (1) Population expansion measured in housekeeping functions parallels the number of clinical cases, but not when measured in an antibiotic resistance gene, suggesting it has been subject to positive selection. Results could be used in managing resistance (Tazi et al. 2010). Found no recombination events in the set. (2) Suggests that demographic changes are associated with selective sweeps caused by antibiotic resistance, crack epidemics and urban-planning. Ne decrease associated with 5× decrease in the prevalence of this obligatory human pathogen (Perez-Losada et al. 2007). Recombination tracts were removed |
| Pseudomonas aeruginosa | Expansion | 0.005/ntb | Assigns the presence of a recent selective sweep (Guttman et al. 2008) |
| Pseudomonas fluorescens | Stable | 0.07/ntb | Suggests ancient rapid growth followed by stabilization, but very close strains are absent (Guttman et al. 2008) |
| Pseudomonas syringae | Stable | 0.1/ntb | Suggests it is an endemic pathogen (Sarkar and Guttman 2004) |
| Salmonella enterica serovar Paratyphi A | Expansion | 450 Y | Population contraction associated with the introduction of antibiotics, followed by expansion that would be associated with environmental changes (Zhou et al. 2014). Recombination tracts removed |
| Salmonella enterica serovar Typhi | All expansion | 10–71 KY, 25 Y | (1) Steady increase in population size in the last 3,000 years. Recombinant SNPs removed and strong selection checked (Roumagnac et al. 2006). (2) Expansion is consistent with epidemiological data reporting drug-resistant isolates. Recombinant regions removed (Wong et al. 2015) |
| Shigella sonnei | Stable | 500 Y | The population size was found to be constant through time (Holt et al. 2012) |
| Staphylococcus aureus | Expansion | 20 Y, 50 Y, 30 Y | (1) Rampant expansion might have followed trans-Atlantic spread (Nubel et al. 2010). (2) Phylodynamics analysis used to estimate epidemiological parameters such as the potential reproductive number. No signs of recombination identified (Prosperi et al. 2013). (3) Fit between demographic expansion and the epidemiology of the CC80 clone (Stegger et al. 2014) |
| Streptococcus pneumoniae | Contraction | 15 Y | Population expansion and then contraction fits the observed number of clinical cases (Croucher et al. 2014). Recombination tracts removed |
| Streptococcus pyogenes | Expansion | 80 Y | Associates population expansion with the acquisition of super-antigens (Davies et al. 2015). Recombination tracts removed |
| Streptococcus suis | Expansion | 90 Y | Correlates population expansion with the introduction of new methods used for improved pig genetics (Weinert et al. 2015). Recombination tracts removed |
| Thiomonas spp | Expansion | 7 MY | The demographic history matches the glacial cycles (Liao and Huang 2012) |
| Vibrio cholerae | Expansion | 3 Y | Association with the history of the progression of an epidemic (Azarian et al. 2014). Found no evidence for recombination |
Note—We show the TMRCA, the conclusion of the work, and the authors' justifications of the results. Multiple studies published for a given species are indicated as multiple lines in the column TMRCA and by the respective numbers in the last column.
aTMRCA not indicated. The value indicates the span of the X-axis on the skyline plot.
bStudies did not perform time calibration and present only the number of mutations per site.