1. Table 5.1

2. Figure 5.1 Trade-offs in virulence evolution

3. Table 5.2

4. Figure 5.2 Serial passage increases virulence in the new, experimental host (A), whereas it decreases virulence in the original, natural host (B)

5. Figure 5.3 (A) In the healthy gut, the immune systems maintains microorganisms as commensals. (B) Breached defenses produce pathological inflammation, and infection may follow. (C) Genes and environment factore combine to produce mixtures of immune states

6. Figure 5.3 (A) In the healthy gut, the immune systems maintains microorganisms as commensals

7. Figure 5.3 (B) Breached defenses produce pathological inflammation, and infection may follow. (C) Genes and environmental factors combine to produce mixtures of immune states

8. Figure 5.4 The skin microbiota converse with the immune system, eliciting the production of complement and interleukins

9. Figure 5.5 Five potential mechanisms with which the skin microbiota could initiate or amplify skin disorders; they may often act in combination

10. Table 5.3

11. Figure 5.6 The mispairing of simple sequence repeats causes frame shifts, resulting in amino acid substitutions in bacterial surface proteins

12. Figure 5.7 Variation in the cell surface of H. influenzae

13. Figure 5.8 Plasmodium merozoites evade attack with variable surface properties generated by both allelic polymorphism and variable expression from multigene families

14. Table 4.4

15. Figure 5.9 Mortality from infectious disease declined dramatically in the United States after 1900

16. Figure Bacteria can acquire resistance genes through any of three mechanisms: transformation, transduction, and conjugation. Abr, antibiotic resistance determinants

17. Figure 5. 11 Transposable elements that confer antibiotic resistance
Figure Transposable elements that confer antibiotic resistance. int1, gene for integrase; att1, primary recombination site; attC, integrase substrates; Pc, promoter driving expression

18. Figure 5.12 Phage therapy has a long history and some success