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Review
. 2015 Jun 11;11(6):e1004823.
doi: 10.1371/journal.ppat.1004823. eCollection 2015 Jun.

Analysis of Bottlenecks in Experimental Models of Infection

Sören Abel  1 , Pia Abel zur Wiesch  2 , Brigid M Davis  3 , Matthew K Waldor  4
Affiliations
Review

Analysis of Bottlenecks in Experimental Models of Infection

Sören Abel et al. PLoS Pathog. .
No abstract available

PubMed Disclaimer

Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. Schematic representation of the effect of bottlenecks on genetic diversity.
Individual pathogens are shown as colored spheres; the colors represent distinguishable markers. The barriers to infection that constitute the bottleneck are shown by the solid bars and the size of the bottleneck is represented by the size of the gap between these bars. Bottlenecks are events that dramatically reduce the original population size, for example, the inoculum in infectious diseases. In the context of infection, the founding population consists of the pathogens that survive passage through the bottleneck and give rise to a population in a new environment, e.g., a new host or anatomical site. Often it is not feasible to sample directly after the bottleneck event (t b); instead, populations are sampled (at time t s) after the passage of time (t), represented by the black arrow. During this time, the founding population often replicates. Wide bottlenecks lead to limited loss of markers (e.g., the magenta and black spheres) and limited changes in the marker frequencies (e.g., over-representation of the blue and under-representation of the olive marker). In contrast, tight bottlenecks lead to stochastic loss of many markers and substantial changes in marker frequencies. These changes can be used to determine the magnitude of bottleneck events and the size of the founding population, even after the population size has increased, provided that the expansion has limited effect on the marker composition (i.e., markers are fitness neutral, and no additional genetic drift occurs).
Fig 2
Fig 2. The mechanisms underlying bottlenecks shape the relationship between inoculum size and founding population size.
Five conceptual examples of how the relationship between the inoculum size and founding population size changes with different types of bottlenecks. (A) An “absolute” bottleneck allows the unobstructed passage of organisms until its capacity is exhausted, thereby defining an upper limit on the number organisms that can pass. (B) During passage through a “fractional” bottleneck, a proportion of the inoculum does not survive. In this scenario, low inoculum sizes can occasionally give rise to infection, even if the expected bottleneck size is below one; however, for simplicity, in the graph, low inocula are set to a founding population size of zero. (C) With a “limited” bottleneck, a fixed amount of the inoculum is killed. (D) With a “cooperative” bottleneck, a population cannot pass through the bottleneck unless a sufficient number of organisms are present in the inoculum. Once the population size crosses this threshold, all organisms become competent for bottleneck passage. (E) In more realistic scenarios, diverse mechanisms of host defense collectively limit the founding population size.
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