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Color Plates

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Color Plate 1.

Artist’s conception of the infection process and the host’s immune response and overresponse: (Blue) site where the presence of bacteria does not result in symptoms–asymptomatic. (Red) site or state where the presence of bacteria can result in symptoms. See the text for more details.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 2.

SNPs, haplotypes, and linkage disequilibrium (LD). (A) Different SNPs on the same chromosome may or may not be inherited together, depending on the local recombination rate. (B) When a recombination event occurs, new recombinant haplotypes are created, thereby increasing haplotype diversity. (C) The extent of LD, or the length of haplotype blocks, before and after the occurrence of the recombination event is shown. Each block of LD is presented in a different color.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 3.

Dynamic outcomes of the modified SIR model with two strains, for different levels of cross-immunity (c in Fig. 2). The proportion of the host population infected with strain A is shown in pink, and the proportion infected with strain B is shown in yellow. Here, strain A has a higher force of infection than strain B. Panela shows no cross-immunity (c = 0); strains circulate independently at a prevalence determined by γ. Panel b shows intermediate cross-immunity (c > 0); strains compete for hosts and suppress each others’ prevalence. Panel c shows high cross-immunity (c close to 1); the strain with the highest force of infection excludes the less competitive strain.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 4.

Effects of cross-immunity on an antigenically variable pathogen population. A hypothetical pathogen population is made up of strains defined by two antigenic loci, represented by the circle and the square, each with two alleles, given by the different colors. This allows for four possible strains. Immune selection will then act to coselect the strains that do not share antigenic determinants and suppress the others, leading to populations dominated by one of two possible subsets of strains, as shown.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 5.

Dynamics resulting from the theoretical framework of Gupta et al. (S. Gupta, M. C. Maiden, I. M. Feavers, S. Nee, R. M. May, and R. M. Anderson, Nat. Med. 2: 437–442, 1996) are shown for (a) low, (b) intermediate, and (c) high levels of cross-immunity, given by the parameter γ. (a) When cross-immunity (γ) is low, all strains will coexist at a prevalence reflecting their intrinsic transmissibility. The different strains will not be competing for hosts, since infection with one strain provides no protection against others. (b) For intermediate values of γ, oscillatory dynamics occur, with subsets of strains that do not share alleles dominating sequentially. Chaotic oscillations can also occur for some parameter values. (c) For high levels of cross-immunity (γ), the competition for susceptible hosts causes two strains that do not share alleles to dominate, since immunity to one will not affect the transmission of the other.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 6.

Prevalence of different combinations of PorA VR1 and VR2 epitopes from the Feavers et al. (I. M. Feavers, A. J. Fox, S. Gray, D. M. Jones, and M. C. Maiden, Clin. Diag. Lab. Immunol. 3: 444–450, 1996) study of disease isolates from the United Kingdom.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 7.

Comparison of stochastic and deterministic formulations of the Gupta et al. (S. Gupta, M. C. Maiden, I. M. Feavers, S. Nee, R. M. May, and R. M. Anderson, Nat. Med. 2: 437–442, 1996) model of cross-immunity. On the left are the outcomes of the deterministic model for low (A), medium (B), and high (C) levels of cross-immunity. “z” on the y-axis represents the proportion of the population immune to a particular strain. The black and grey lines represent different subsets of nonoverlapping combinations of antigenic determinants. For example, for the two-locus, two-allele case, where a and b are alleles at one locus and x and y are alleles at the other, black = ax and by and grey = ay and bx. On the right are the equivalent dynamics for the stochastic system for low (D), medium (E), and high (F) levels of cross-immunity. Taken from Buckee et al. (C. O. Buckee, K. Koelle, M. J. Mustard, and S. Gupta, Proc. Natl. Acad. Sci. USA 101: 10839–10844, 2004).

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 8.

Schematic illustration of MLST. Seven loci spread around the genome, shown in red on the S. pneumoniae genome (left) as an example, are amplified by PCR, and internal fragments are sequenced. For each locus, each different sequence is defined as an allele and is assigned a unique integer. The combination of the seven integers is the allelic profile and in turn determines the sequence type (ST) of the isolate.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 9.

(A) Schematic organization of the fungal cell wall. The major structural components are shown in the figure. This figure has also been presented previously (M. Molina, C. Gil, J. Pla, J. Arrovo, and C. Nombela, Microsc. Res. Tech. 51: 601–612, 2000). (B) Biogenesis of cell wall proteins. After cytoplasmic synthesis of the protein moiety, N- and O-linked glycosylation occurs at the endoplasmic reticulum. Proteins are exported through the cytoplasmic membrane, and some of them acquire a GPI anchor signal that enables its anchoring to the cellular surface, while other get cross-linked through other means. β-mannosylated proteins are also found on the cellular surface. Nonconventional secreted proteins and capsule are also represented in this figure.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 10.

Examples of interaction of cell wall components with mammalian cells are shown. The upper layer represents a mucosal surface, while the part schematically depicts the role of signalling through PAMPs-PRR in an immune cell.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 11.

Mobile genes location. Frequency of horizontally transferred genes (HGT[AQ6]), phage-related sequences (Phage), insertion sequences (IS), and antibiotic-resistance genes (Resistance) along the chromosomes of S. aureus Mu50 (a) and E. coli K-12 (b). The genome is divided into quadrants, according to the distance from the replication origin, with quadrant 4 being the closest to the terminus. Some genes appear to increase in number closer to the replication terminus.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 12.

IS expansions in human-related species. DNA sequence similarities between pairs of paralogous genes (in blue) and between pairs of IS elements (in red) across different bacteria are shown. The chromosomal location of the first gene for each pair is shown on the x axis. Bacteria specialized in humans, in agricultural plants, and in farm animals are shown on the left, whereas related species which are not human specialists are on the right. Human-associated species show a recent explosion of IS elements across their genomes. Other human specialists such as Shigella flexneri or Salmonella enterica serovar Typhi show similar patterns. Reprinted from Trends in Microbiology (A. Mira, R. Pushker, and F. Rodriguez-Valera, Trends Microbiol., 14: 200–206, 2006) with permission from Elsevier.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 13.

Diagram of a genomic island (left). int, integrase gene; a, b, structural genes; IS, insertion sequence; DR, direct repeat. The main features of genomic islands are given on the right.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 14.

Diagram of the uropathogenic strain E. coli 536. The major virulence factors are indicated. Gene clusters located on pathogenicity islands (PAIs) I to V as well as on genomic islands (GEIs) VI to IX, which encode virulence as well as fitness factors, are indicated in the chromosome.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 15.

Comparison of genomic island II (GEI II) of the commensal E. coli Nissle 1917 and a pathogenicity island (PAI) of the uropathogenic strain CFT073. Gene clusters encoding major virulence factors, which are part of the genome of uropathogenic strain CFT073, are not present in the genome of strain Nissle 1917.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 16.

Model of the integron recombination molecular mechanism using a single-strand (ss) attC substrate folded through pairing of the imperfect palindromic sequences. Steps are identical to classical site-specific recombination steps catalyzed by other Y- recombinases, up to the HJ intermediate. Classical resolution through the A axis reverses the recombination to the original substrates, while resolution through the B axis, giving rise to covalently closed linear molecules, is abortive. The nonabortive productive resolution necessitates a replication step. Putative integrase binding domains are indicated by boxes. Red lines in the last panel show the neosynthesized strands.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 17.

The schematic presentation of electro-karyotypes of the C. albicans parental strains 3153A, CAF4-2, and SGY-243, as well as their survivors in four adverse environments and their phenotypic revertants. The numbers at the bottom of the figure denote independently derived mutants that were analyzed. For Foar mutants, 10 subclones from three independent mutants are summarized instead of the original mutants. Different colors indicate all homologs of specific chromosomes that are implicated in the four different phenotypes. The green color of the band corresponding to the co-migrating Ch6b and Ch7a of 3153A denotes only Ch6b. Altered chromosomes having unusual sizes are marked with chromosome numbers. Δ denotes the SOU1 gene. • denotes multiple CSU genes. * denotes a level of DNA less then either one or two copies. x denotes strains with the same pattern except for the ChR. The array of lines for ChR in some strains represents inseparable bands on a gel that reflects instability of the size of this chromosome. Densitometry was used to determine chromosome copy number in the appropriate bands. (A) Strain 3153A; (B and C) major and minor types of Sou+ mutants, respectively; (D) Sou phenotypic revertants; (E) two major types of Foar mutants; (F) Foas phenotypic revertants; (G) two major types of Aru+ mutants; (H) minor types of Aru+ mutants; (I) strain CAF4-2; (J, K, and L) same as panels B, C, and D, respectively; (M) strain SGY-243; (N and O) Flur mutants derived after short and long exposure to fluconazole, respectively. Adapted from E. Rustchenko, p. 91–102, in S. G. Pandalai, ed., Recent Research Developments in Bacteriology, 2003).

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 18.

Modular structure of the genetic plasmid region hosting an important gene of antibiotic resistance, bla CTX-M-9, encoding resistance to broad-spectrum cephalosporins (in red). Each row corresponds to a particular variant found in clinical strains in a single hospital (1996–2003). The multimodular structure related to the In60 integron backbone offers a number of different variants, most of them linked to another multimodular variable structure derived from the transposon Tn402. At their turn many of these multimodules are inserted in another multimodular variable structure, originated in the Tn21 transposon; see the transposition module and the mercury-resistance module flanking the former insertions. Finally, the entire Tn21-like transposons are modules themselves that are inserted in classic multimodular plasmids of IncHI2, IncP1-α, and IncFI groups. For details, see C. Novais, R. Cantón, A. Valverde, E. Machado, J. C. Galán, L. Peixe, A. Carattoli, F. Baquero, and T. M. Coque, Antimicrob. Agents Chemother. 50: 2741–2750, 2006.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 19.

Quinolones induce the transcription of recA, umuC, and dinB genes, as demonstrated by lacZ fusions. Induction of transcription is observed as a blue-green color produced by the increased activity of beta-galactosidase (LacZ) on the substrate X-Gal (present in the plates) whose hydrolysis gives this color. Intensity of the color reflects the increase in transcription of the genes.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 20.

Mechanism of multidrug resistance in the first European MRSA isolate.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 21.

Global spread of pandemic MRSA clones. Adapted with permission from M. Aires de Sousa, and H. de Lencastre, FEMS Immunol. Med. Microbiol. 40: 101–111, 2004.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 22.

Evolution of MRSA clones from the Archaic MRSA in Denmark. Adapted from A. R. Gomes, H. Westh, and H. de Lencastre, Antimicrob. Agents Chemother., 50: 3237–3244, 2006.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 23.

Schematic diagram of the possible evolutionary lineages for emergence of pandemic strains of V. cholerae. Lineages are based on the existence of intermediate strains carrying combinations of horizontally acquired gene clusters and other considerations. Colored ellipses describe strains that exist, whereas black ellipses designate strains that could hypothetically exist but have not yet been isolated. Blue arrows represent horizontal gene transfer events that are the most likely to have occurred based on the existence of intermediate strains that have similar polymorphic markers (for example, ribotypes and allelic types of variable genes such as tcpA, rstR, and toxT, among others). Black arrows represent other transfer events that are hypothetically possible but for which critical intermediate strains have not been documented. Abbreviations: CTX, cholera toxin phage; EPS, extracellular protein secretion gene cluster; HAP, hemagglutinin protease gene; O1 and O139, various O antigen gene clusters; RTX, repeat in toxin gene cluster; TCP, toxin coregulated pilus gene cluster (also referred to as VPI); VPI, Vibrio pathogenicity island; VPI-2, the island that includes the nanH gene cluster; VSP, Vibrio seventh pandemic island; VSP-1 and VSP-2, the islands found in seventh pandemic El Tor strains and eighth pandemic O139 strains.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 24.

Circular genome map of L. monocytogenes EGDe and strain-specific genes between EGDe and L. innocua CLIP11262. From the outside: circle 1, L. monocytogenes genes on the plus and minus strands, respectively; circle 2, genes specific to L. monocytogenes EGDe with respect to L. innocua CLIP11262; circle 3, L. innocua CLIP11262-specific genes with respect to L. monocytogenes EGDe; circle 4, G/C bias (G+C/G-C) of L. monocytogenes with <32.5% G+C in light yellow, between 32.5 and 43.5% G+C in yellow, and >43.5% G+C in dark yellow. The scale in megabases is indicated on the outside of the genomes with the origin of replication being at position 0.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 25.

The internalin family of proteins. Homologous regions of internalin family members are depicted in the same color. Subfamily 1 includes internalins with an LPXTG amino acid motif, and these are covalently linked to the cell wall. Sub-family 2 includes internalin B, which is loosely associated to the cell wall through its GW modules. Subfamily 3 contains five internalins that are predicted to be secreted. Reproduced with permission from M. Hamon, H. Bierne, and P. Cossart, Nat. Rev. Microbiol. 4: 423–434, 2006.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 26.

Schematic presentation of the virulence gene cluster in Listeria and its comparison to the orthologous region in Bacillus subtilis. Orthologous genes among the different Listeria spp. are depicted in the same color. The gene cluster is flanked by the housekeeping genes (light blue arrows) prs and ldh in all six species of Listeria; these genes are also present in B. subtilis. Known virulence genes are depicted in red. Adapted from P. L. Glaser et al., Science 294: 849–852, 2001; M. W. Schmid et al., Syst. Appl. Microbiol. 28: 1–18, 2005; and Chakraborty, 2006))

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 27.

Schematic representation of the inlAB locus and the flanking regions of L. monocytogenes and L. innocua and its hypothetical ancestral organization. EGD, F6854, CLIP80459, F2365, H7858 are L. monocytogenes strain designations. Clip 11262 is an L. innocua strain designation. Orthologous genes are depicted in the same color. Red, inlAB locus; dotted lines, specific regions with respect to the other genomes; lmo, gene names of L. monocytogenes EGDe; lm4b, gene names of L. monocytogenes CLIP80459; lmof2365, gene names of L. monocytogenes F2365; lmoh 7858, gene names of L. monocytogenes H7858; lin, gene names of L. innocua CLIP11262; star; pseudogenes.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 29.

Population snapshot of 229 E. faecalis isolates based on MLST allelic profiles using the eBURST algorithm. This snapshot shows all clonal complexes, singletons, and patterns of evolutionary descent. The sizes of the circles indicate their prevalences in the MLST database. Numbers correspond to the sequence types (STs), black lines connect single-locus variants, and blue lines connect double-locus variants (STs that differ in two of the seven housekeeping genes). The high-risk enterococcal clonal complexes CC2 and CC9 exclusively contain hospital-related isolates. This figure was published in Curr. Op. Microbiol., volume 9, H. L. Leavis, M. J. Bonten, and R. J. Willems, Identification of high-risk enterococcal clonal complexes: global dispersion and antibiotic resistance, p. 454–460. Copyright Elsevier 2006.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 30.

Global distribution of major M. tuberculosis clades. (A) Distribution of M. tuberculosis spoligotype clades on the SNP-based phylogeny. Reproduced from I. Filliol, A. S. Motiwala, M. Cavatore, et al., J. Bacteriol. 188: 759–772, 2006 with permission. (B) Examples of spoligotyping profiles of three M. tuberculosis genotypes, Beijing, X2, and T1. (C) Global incidence distribution of the major M. tuberculosis clades Beijing, X, T, Haarlem, Latin American and Mediterranean (LAM), Central Asian (CAS), East African-Indian (EAI), and Africa (M. africanum). “Other” includes orphan genotypes. Adapted from I. Filliol et al., J. Bacteriol. 188: 759–772, 2006.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 31.

The M. tuberculosis W-Beijing genotype. (A) Global distribution of the W-Beijing genotype worldwide. Adapted from J. R. Glynn, J. Whitely, P. J. Bifani, K. Kremer, and D. van Soolingen, Emerg. Infect. Dis. 8: 843–849, 2002. (B) Distribution of streptomycin resistance among W-Beijing and other strains in Hong Kong (study 1), Ho Chi Minh City (study 2), Jakarta (study 3) and Azerbaijan (study 4). Adapted from [Chan, 2001; Anh, 2000; van Crevel, 2001; Pfyffer, 2001]. (C) Comparative virulence of M. tuberculosis H37Rv (black line) and two strains of the Beijing family (red lines). The results indicate the percent survival of mice infected intratracheally with the various strains. Adapted from B. Lopez, D. Aguilar, H. Orozco, et al., Clin. Exp. Immunol. 133: 30–37, 2003.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 32.

Confocal micrograph of a group of mouse neuroblastoma (N2-A) cells infected with fluorochrome (FITC)-labelled M. pneumoniae at 72 h postinfection. Yellow-green fluorescent signal of (FITC)-labeled M. pneumoniae organisms is detected throughout the cell cytoplasma in colocalization with the red color of the cytoplasmic tubulin fluorescent signal. Blue indicates the fluorescent signal from the cell nucleus. A cluster of extracellular M. pneumoniae cells is observed as a yellow-green cup located at the upper left part of the figure. Bar = 100 μm.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 33.

Contribution of individual serogroups to invasive pneumococcal disease in children.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 34.

eBURST analysis of MLST database isolates. 2,338 STs are shown. Each circle represents one ST. The area of each is proportional to the ST’s frequency among database isolates. Lines between STs represent single-locus variants. –, no other relationships are inferred.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 35.

C. neoformans micrographs. (A) India ink staining. (B) Fluorescently labeled C. neoformans. Rhodamine (red), mAb to the C. neoformans capsule; blue, calcofluor, which stains the cell wall. (C) Scanning electron microscopy of a budding C. neoformans cell. Scale bar, 5 μ in all cases. (D) Melanin ghost from C. neoformans cells grown in the presence of -DOPA. Pictures by S. Frasés and O. Zaragoza.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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Color Plate 36.

Interaction of C. neoformans with different hosts. (A) Micrograph of C. elegans with C. neoformans within the gastrointestinal tract (thin white arrows, representative C. neoformans cells). White thick arrows, pharyngeal grinder organ, which functions to disrupt ingested organisms. Black and gray arrows point to the intestinal lumen. (Courtesy of Dr. Mylonakis. Reprinted from F. M. Mylonakis, F. M. Ausubel, J. R. Perfect, J. Heitman, and S. B. Calderwood, Proc. Natl. Acad. Sci. USA 99: 15675–15680, 2002). (B) Acanthamoeba castellanii with ingested C. neoformans (grey arrows) stained with a mAb to the capsule and horseradish peroxidase. (C) Giemsa staining of peritoneal macrophages after phagocytosis of C. neoformans (black arrows). Note how some of the C. neoformans cells are budding (white arrows). Courtesy of T. Zhang. (D and E) Hematoxylineosin staining of lung tissues sections. (D) Lung from naïve mice; (E) lung from mice intratracheally infected with C. neoformans. Notice how in lungs from infected mice the alveolar spaces are filled up with C. neoformans and inflammatory cells.

Citation: Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J. 2008. Color Plates, In Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC.
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