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Category: Clinical Microbiology; Bacterial Pathogenesis
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(Chapter 3) Schematic representation of inductive and effector sites of the GALT. Ag, antigen; B, B lymphocyte; CTL, cytotoxic T lymphocyte; DC, dendritic cell; FAE, follicle associated epithelium; FcRn, neonatal Fc receptor; FDC, follicular dendritic cells; GC, germinal center; IE, intraepithelial; IEC, intestinal epithelial cell; IEL, intraepithelial lymphocyte; IFN-γ, interferon-γ; IgA, immunoglobulin A; IgG, immunoglobulin G; IgM, immunoglobulin M; IL, interleukin; LF, lymphoid follicle; LPL, lamina propria lymphocyte; M, microfold-M cell; Mϕ, macrophage; MHC, major histocompatibility complex; MLN, mesenteric lymph node; pIgR, polymeric immunoglobulin receptor; sIgA, secretory IgA; T, T lymphocyte; TGF-β, transforming growth factor-β; Th1, Thelper type 1 lymphocyte; Th2, Thelper type 2 lymphocyte; Treg, regulatory T cell. For other abbreviations, see chapter 3.

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(Chapter 3) Schematic representation of inductive and effector sites of the GALT. Ag, antigen; B, B lymphocyte; CTL, cytotoxic T lymphocyte; DC, dendritic cell; FAE, follicle associated epithelium; FcRn, neonatal Fc receptor; FDC, follicular dendritic cells; GC, germinal center; IE, intraepithelial; IEC, intestinal epithelial cell; IEL, intraepithelial lymphocyte; IFN-γ, interferon-γ; IgA, immunoglobulin A; IgG, immunoglobulin G; IgM, immunoglobulin M; IL, interleukin; LF, lymphoid follicle; LPL, lamina propria lymphocyte; M, microfold-M cell; Mϕ, macrophage; MHC, major histocompatibility complex; MLN, mesenteric lymph node; pIgR, polymeric immunoglobulin receptor; sIgA, secretory IgA; T, T lymphocyte; TGF-β, transforming growth factor-β; Th1, Thelper type 1 lymphocyte; Th2, Thelper type 2 lymphocyte; Treg, regulatory T cell. For other abbreviations, see chapter 3.
(Chapter 4) Confocal laser-scanning micrographs showing P. aeruginosa quorum sensing visualized in the lungs of mice. The cells were tagged with Rfp, and they expressed green fluorescence (Gfp ASV) in response to quorum-sensing signals received from their nearest neighbors (see references 31 and 32 in chapter 4 for details).

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(Chapter 4) Confocal laser-scanning micrographs showing P. aeruginosa quorum sensing visualized in the lungs of mice. The cells were tagged with Rfp, and they expressed green fluorescence (Gfp ASV) in response to quorum-sensing signals received from their nearest neighbors (see references 31 and 32 in chapter 4 for details).
(Chapter 8) (A) CEACAM interactions, cytoskeletal reorganization and transmigration of N. meningitidis and H. influenzae. On interactions of H. influenzae with target CHO cells transfected with CEACAM1, cellular actin is reorganized and filamentous actin (stained with rhodamine-conjugated phalloidin) is colocalized beneath bacterially induced receptor caps. H. influenzae organisms are stained with fluorescein isothiocyanate-conjugated anti-H. influenzae antibodies (150). (B and C) H. influenzae and N. meningitidis transmigration across polarized human epithelial cells was studied using Caco-2 cells as a model system since they express high levels of CEACAMs. x-z sections obtained by confocal imaging show N. meningitidis located within (arrow in panel C) the epithelial cell whereas H. influenzae is often found in junctions between cells (arrows in panel B). Bacteria were labeled using antibodies raised against bacteria and fluorescein isothiocyanate-conjugated secondary antibodies. Filamentous actin was stained with rhodamine-conjugated phalloidin. Different modes of transmigration of N. meningitidis and H. influenzae are similar to those observed in organ culture studies (see Fig. 1 in chapter 8) (M. Soriani and M. Virji, unpublished data). Confocal images were obtained with the help of Mark Jepson in the MRC cell imaging facility at the School of Medical Sciences, University of Bristol.

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(Chapter 8) (A) CEACAM interactions, cytoskeletal reorganization and transmigration of N. meningitidis and H. influenzae. On interactions of H. influenzae with target CHO cells transfected with CEACAM1, cellular actin is reorganized and filamentous actin (stained with rhodamine-conjugated phalloidin) is colocalized beneath bacterially induced receptor caps. H. influenzae organisms are stained with fluorescein isothiocyanate-conjugated anti-H. influenzae antibodies (150). (B and C) H. influenzae and N. meningitidis transmigration across polarized human epithelial cells was studied using Caco-2 cells as a model system since they express high levels of CEACAMs. x-z sections obtained by confocal imaging show N. meningitidis located within (arrow in panel C) the epithelial cell whereas H. influenzae is often found in junctions between cells (arrows in panel B). Bacteria were labeled using antibodies raised against bacteria and fluorescein isothiocyanate-conjugated secondary antibodies. Filamentous actin was stained with rhodamine-conjugated phalloidin. Different modes of transmigration of N. meningitidis and H. influenzae are similar to those observed in organ culture studies (see Fig. 1 in chapter 8) (M. Soriani and M. Virji, unpublished data). Confocal images were obtained with the help of Mark Jepson in the MRC cell imaging facility at the School of Medical Sciences, University of Bristol.
(Chapter 16) Micrographs of bacterial flagella. (A) V. cholerae O395 producing a sheathed polar flagellum. (B) S. enterica producing multiple peritrichous flagella. (C) EHEC EDL933 producing various flagella. (D) Flagellar structures isolated from an ETEC strain, demonstrating the flexible nature of the filaments. (E) Flagellar hook attached to the flagellum (arrows). (F) High magnification of a flagellum, showing the helical nature of the filament. (G and H) Flagella (green-fluorescent structures) produced by adhering EPEC to HeLa cells tethering bacteria to the inert substratum and to the cultured cells. (I) Scanning electron micrograph of EPEC adhering to HeLa cells and producing multiple interconnecting flagellar structures.

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(Chapter 16) Micrographs of bacterial flagella. (A) V. cholerae O395 producing a sheathed polar flagellum. (B) S. enterica producing multiple peritrichous flagella. (C) EHEC EDL933 producing various flagella. (D) Flagellar structures isolated from an ETEC strain, demonstrating the flexible nature of the filaments. (E) Flagellar hook attached to the flagellum (arrows). (F) High magnification of a flagellum, showing the helical nature of the filament. (G and H) Flagella (green-fluorescent structures) produced by adhering EPEC to HeLa cells tethering bacteria to the inert substratum and to the cultured cells. (I) Scanning electron micrograph of EPEC adhering to HeLa cells and producing multiple interconnecting flagellar structures.
(Chapter 21) Colonization by S. enterica serotype Typhimurium of the bovine (A and B) and murine (C) mucosa. (A and B) Detection of serotype Typhimurium in sections of the bovine ileal mucosa collected at 15 min (A) and 2 h (B) after inoculation of bovine ligated loops by immunohistochemistry using rabbit anti-O4,5 antiserum (brown precipitate). The center of each microscopic field shows a domed villus of a Peyer's patch lymphoid follicle. The sections were counterstained with hematoxylin (blue signal). Reprinted from B. P. Reis, S. Zhang, R. M. Tsolis, A. J. Bäumler, L. G. Adams, and R. L. Santos, Vet. Microbiol. 97:269–277, 2003, with permission from the publisher. (C) Section of the murine cecum collected 5 days after oral infection with a lethal dose of serotype Typhimurium (109 CFU/animal), showing bacterial microcolonies lining the epithelial surface. Serotype Typhimurium was detected by fluorescence microscopy using sheep anti-somatic (O4) antiserum and donkey anti-sheep immunoglobulin Alexa-Fluor 488 (green signal). Sections were counterstained with Hoechst nuclear stain (blue signal).

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(Chapter 21) Colonization by S. enterica serotype Typhimurium of the bovine (A and B) and murine (C) mucosa. (A and B) Detection of serotype Typhimurium in sections of the bovine ileal mucosa collected at 15 min (A) and 2 h (B) after inoculation of bovine ligated loops by immunohistochemistry using rabbit anti-O4,5 antiserum (brown precipitate). The center of each microscopic field shows a domed villus of a Peyer's patch lymphoid follicle. The sections were counterstained with hematoxylin (blue signal). Reprinted from B. P. Reis, S. Zhang, R. M. Tsolis, A. J. Bäumler, L. G. Adams, and R. L. Santos, Vet. Microbiol. 97:269–277, 2003, with permission from the publisher. (C) Section of the murine cecum collected 5 days after oral infection with a lethal dose of serotype Typhimurium (109 CFU/animal), showing bacterial microcolonies lining the epithelial surface. Serotype Typhimurium was detected by fluorescence microscopy using sheep anti-somatic (O4) antiserum and donkey anti-sheep immunoglobulin Alexa-Fluor 488 (green signal). Sections were counterstained with Hoechst nuclear stain (blue signal).
(Chapter 22) Life cycle of E. histolytica. Infection is initiated by ingestion of the cyst from fecally contaminated food or water. Excystation in the intestine to the trophozoite form leads to colonization in 90% or more of individuals and invasion in 10% or fewer. Colonization leads to the production of new cysts that are formed via a quorum-sensing-like interaction of amebae that requires the Gal/GalNAc lectin. Invasion is mediated by amebic contact-dependent cytotoxicity as well as via neutrophil-mediated damage.

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(Chapter 22) Life cycle of E. histolytica. Infection is initiated by ingestion of the cyst from fecally contaminated food or water. Excystation in the intestine to the trophozoite form leads to colonization in 90% or more of individuals and invasion in 10% or fewer. Colonization leads to the production of new cysts that are formed via a quorum-sensing-like interaction of amebae that requires the Gal/GalNAc lectin. Invasion is mediated by amebic contact-dependent cytotoxicity as well as via neutrophil-mediated damage.
(Chapter 22) Amebic colitis in a human viewed by endoscopy. Note the raised white ulcerations in the intestinal epithelium. Reprinted from R. Haque, C. Huston, M. Hughes, E. Houpt, and W. A. Petri, N. Engl. J. Med 348:1565–1573, 2003, with permission from the publisher. © 2003 Massachusetts Medical Society. All rights reserved.

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(Chapter 22) Amebic colitis in a human viewed by endoscopy. Note the raised white ulcerations in the intestinal epithelium. Reprinted from R. Haque, C. Huston, M. Hughes, E. Houpt, and W. A. Petri, N. Engl. J. Med 348:1565–1573, 2003, with permission from the publisher. © 2003 Massachusetts Medical Society. All rights reserved.
(Chapter 24) Structural changes occurring in the interdomain region of the FimH lectin domain during SMD simulations. Lateral (A) and end-on (B) views of residues A150 to T158 of the linker chain (light yellow) lying between the 3-4 loop (blue) and the 9-10 loop (red). These loops are identified by the β-strands that they connect, and the residue and strand numbers reflect the terminology published with the crystal structure (20). Six hydrogen bonds that anchor the linker chain to the 3–4 and 9–10 loops in the crystal structure are shown as dashed lines. (C and D) Lateral view similar to that shown in panel A, illustrating linker chain extension (C) and loop region deformation (D). Reprinted from W. E. Thomas, E. Trintchina, M. Forero, V. Vogel, and E. V. Sokurenko, Cell 109:913–923, 2002, with permission from Elsevier.

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(Chapter 24) Structural changes occurring in the interdomain region of the FimH lectin domain during SMD simulations. Lateral (A) and end-on (B) views of residues A150 to T158 of the linker chain (light yellow) lying between the 3-4 loop (blue) and the 9-10 loop (red). These loops are identified by the β-strands that they connect, and the residue and strand numbers reflect the terminology published with the crystal structure (20). Six hydrogen bonds that anchor the linker chain to the 3–4 and 9–10 loops in the crystal structure are shown as dashed lines. (C and D) Lateral view similar to that shown in panel A, illustrating linker chain extension (C) and loop region deformation (D). Reprinted from W. E. Thomas, E. Trintchina, M. Forero, V. Vogel, and E. V. Sokurenko, Cell 109:913–923, 2002, with permission from Elsevier.
(Chapter 26) Hematoxylin-and-eosin- and alizarin red S-stained sections of P. mirabilis-infected mouse bladders. (A and B) Hematoxylin-and-eosin-stained (A) and alizarin red S-stained (B) consecutive sections of a mouse bladder that developed a macroscopically visible stone after infection by P. mirabilis. (C and D) Hematoxylin-and-eosin-stained (C) and alizarin red S-stained (D) consecutive sections of a mouse bladder that developed mild urolithiasis due to P. mirabilis infection. (E and F) Magnified views of areas in panel B to show alizarin red S-stained mineral deposits on the bladder epithelium. Scale bars, 400 μm (A to D) and 100 μm (E and F). Reprinted with permission from X. Li, H. Zhao, C. V. Lockatell, C. B. Drachenberg, D. E. Johnson, and H. L. Mobley, Infect. Immun. 70:389–394, 2002.

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(Chapter 26) Hematoxylin-and-eosin- and alizarin red S-stained sections of P. mirabilis-infected mouse bladders. (A and B) Hematoxylin-and-eosin-stained (A) and alizarin red S-stained (B) consecutive sections of a mouse bladder that developed a macroscopically visible stone after infection by P. mirabilis. (C and D) Hematoxylin-and-eosin-stained (C) and alizarin red S-stained (D) consecutive sections of a mouse bladder that developed mild urolithiasis due to P. mirabilis infection. (E and F) Magnified views of areas in panel B to show alizarin red S-stained mineral deposits on the bladder epithelium. Scale bars, 400 μm (A to D) and 100 μm (E and F). Reprinted with permission from X. Li, H. Zhao, C. V. Lockatell, C. B. Drachenberg, D. E. Johnson, and H. L. Mobley, Infect. Immun. 70:389–394, 2002.
(Chapter 28) Within a short time after birth, a relatively diverse group of bacteria colonize the mucosal surfaces of the gut and perirurethra. Illustrated here are bifidobacteria (yellow), lactobacilli (blue rods), streptococci (light blue cocci), and coliforms (red, rod shaped).

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(Chapter 28) Within a short time after birth, a relatively diverse group of bacteria colonize the mucosal surfaces of the gut and perirurethra. Illustrated here are bifidobacteria (yellow), lactobacilli (blue rods), streptococci (light blue cocci), and coliforms (red, rod shaped).
(Chapter 28) Three types of biofilms found on the vaginal epithelial mucosa. The so-called normal (N) state is when lactobacilli and often bifidobacteria dominate the microbiota. The intermediate (I) state is a transition between normal and BV, with more gram-negative anaerobes such as Gardnerella and Prevotella and enterococci; the BV state includes dense microcolonies of gram-negative anaerobes or other pathogens, with no or very few lactobacilli (105). The ability of the gram-negative pathogens to invade the epithelium has been shown for E. coli in the bladder (4) but has not been shown to date for vaginal pathogens.

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(Chapter 28) Three types of biofilms found on the vaginal epithelial mucosa. The so-called normal (N) state is when lactobacilli and often bifidobacteria dominate the microbiota. The intermediate (I) state is a transition between normal and BV, with more gram-negative anaerobes such as Gardnerella and Prevotella and enterococci; the BV state includes dense microcolonies of gram-negative anaerobes or other pathogens, with no or very few lactobacilli (105). The ability of the gram-negative pathogens to invade the epithelium has been shown for E. coli in the bladder (4) but has not been shown to date for vaginal pathogens.
(Chapter 28) Deconvolution micrograph showing a 5-day E. coli biofilm protruding from a glass surface (DAPI live blue stain about five layers thick) into which L. rhamnosus GR-1 (Texas Red X stain) has penetrated after addition on day 2. The white line shows the outline of the biofilm.

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(Chapter 28) Deconvolution micrograph showing a 5-day E. coli biofilm protruding from a glass surface (DAPI live blue stain about five layers thick) into which L. rhamnosus GR-1 (Texas Red X stain) has penetrated after addition on day 2. The white line shows the outline of the biofilm.
(Chapter 28) E. coli Hu734 after 96 h, grown in a four-chamber Lab-Tek coverglass system, stained with live/dead stain. Live cells are stained with SYTO 9 green-fluorescent nucleic acid stain, and dead cells are stained with propidium iodide red-fluorescent nucleic acid stain.

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(Chapter 28) E. coli Hu734 after 96 h, grown in a four-chamber Lab-Tek coverglass system, stained with live/dead stain. Live cells are stained with SYTO 9 green-fluorescent nucleic acid stain, and dead cells are stained with propidium iodide red-fluorescent nucleic acid stain.