Fig 1.
Experimental design for quantifying how prior exposure to Mycoplasma gallisepticum alters host heterogeneity in susceptibility in house finches (n = 150 for final analysis).
Five weeks after one of three prior exposure (PE) treatments (none, low, or high dose; left panel), all birds received a secondary dose challenge (right panel) to assess heterogeneity in susceptibility. Our primary data set was whether birds became infected (0|1) in response to a given secondary dose (right). *However, to improve model fits, we also used bird responses to low-dose PE treatment (left, asterisk), which fell intermediate to our highest secondary challenge doses (300 and 7000 Color Changing Units [CCU]/mL), to quantify the proportion of birds with no prior exposure (at the time of low-dose PE) that become infected at a 750 CCU/mL dose. Figure created with Biorender.com.
Fig 2.
Dose response curves for house finch susceptibility to secondary challenge with Mycoplasma gallisepticum across prior exposure treatments.
Points (+/- 1SE) show the fraction of individual birds (n = 10–12 birds for most points; individual responses are 0|1) infected at each secondary exposure dose, shown as Color Changing Units (CCU)/uL. Lines indicate model fits, with blue indicating gamma (heterogeneous) model fits, and red dashed lines indicating homogeneous model fits. Panel labels show prior exposure treatment (birds in the no prior exposure treatment were pathogen-naive at the time of secondary dose challenge). In hosts with prior pathogen exposure (low and high-dose prior exposure groups), the gamma model (which accounts for inter-individual heterogeneity) was better supported via likelihood ratio tests.
Fig 3.
Host susceptibility distributions for house finches from variable prior exposure treatments: no prior exposure (A,B); low-dose (C); or high-dose (D). Colored lines show estimated susceptibility distributions from either homogeneously (A) or gamma-distributed (B-D) models (note distinct axes for the two models). In (A), host infection probability per 1000 bacterial particles (p) is shown as the single best fit parameter p (dotted vertical lines represent 1 standard error) for the homogeneous model, which was the best fit model for the no prior exposure group (see Results). In (B-D), the best fit parameters (shape and scale) for gamma distributions (teal lines) are listed for each group, and vertical gray lines indicate mean susceptibility (x) for that treatment. Lighter shading represents 95% confidence regions for gamma distributions, obtained by bootstrapping chi-squared residuals to create 1,000 pseudoreplicates of infection data and then refitting the model to pseudoreplicates, as per [20,46]. The gamma model was the best fit for only the low-dose and high-dose groups. Gamma estimates are also shown for the no prior exposure group (B) because this allowed more equivalent comparisons for certain SIR simulations (see Methods).
Fig 4.
Cumulative epidemic size (proportion of individuals who ever entered the infectious class) (A,B); dynamics of cumulative infections and deaths (top: C, D; deaths: dashed lines) over time, and numbers of infectious hosts over time (bottom: C, D) in our SIR model, as a function of prior exposure (abbreviated as “exp.”) treatment (x-axis for A,B; columns for C,D). Total starting population was 100; darker shading within color represents individuals (within cumulative totals) that did not survive the epidemic. Blue bars and lines use fitted heterogeneous susceptibility (gamma distribution) for all prior exposure groups (Fig 3 and S1 Table). Red bars and lines assume homogeneous susceptibility for all groups, with mean susceptibility for each group equal to that of the fitted heterogeneous distribution for that treatment group. Left panels (A,C) use fitted mortality rates, whereby estimated mortality rates declined with prior exposure, while right panels (B,D) assume the fixed mortality rate of all groups is equal to that of the no prior exposure birds.