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Chapter 21 Images for Students Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 1 Fig21.01a Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Endoflagellum (a) Periplasmic space Outer membrane Endoflagellum Cell body 2 Table21.01 3 Fig21.08 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. (1) Primary infection induces high fever. (2) Initial antibody response at first reduces fever. (3) Reinfection by mutant Borrelia causes a relapse of fever. (1) (4) The immune reaction to second antigen slows symptoms for a time. (5) New antigenic form causes another relapse. (3) (6) Antibody response again reduces symptoms of infection, followed by relapse. (5) 106 98 Third antibody response (2) Third antigenic challenge Second antibody response 100 Second antigenic challenge 102 First antibody response 104 First antigenic challenge Body Temperature F Variable (4) (6) Normal temperature 1 2 4 6 8 10 12 Days 14 16 18 20 22 24 Fig21.11 Intestinal lumen Intestinal lumen Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Cl2 HCO32 Na1 K1 H2 O Cl2 H2O HCO32 H2O Na1 K1 H2O Intestinal cell (a) (b) 1 The Vibrio cholerae cell comes to rest in the protective mucous coating near the cell surface and secretes its toxin, which is a complex protein. Vibrio cholerae 2 The toxin has an affinity for specialized receptors on the glycocalyx and binds there. Cell membrane 3 The active portion of the toxin is released, is transported through the membrane, and enters the cytoplasm. 4 It becomes a signal in a system that converts inactive adenyl cyclase into an active state. 5 This enzyme converts ATP into a molecule called cyclic AMP (cAMP). The cAMP is needed by the cell to control a major membrane pump for negative ions. ions. 6 The result is that the membrane begins to actively pump Cl2, and HCO32 into the intestinal lumen. One additional effect of the toxin is that it overrides the usual controls for the adenyl cyclase/cAMP system so that the cell continues to pump out these ions for an extended time. Glycocalyx 1 Adenyl cyclase, inactive 4 2 3 Cholera toxin molecules Adenyl cyclase, active 1 5 Membrane pump HCO32 HCO32 Cl2 6 Cl2 Cyclic AMP Na1, K1 7 Positive ions (Na1 and K1) follow Na1, K1 the anions and are also lost into the intestinal fluid, along with large H2 O amounts of water, causing secretory diarrhea and dehydration. 7 H2 O (c) 5 Table21.0A 6 Table21.02 7 Fig21.15 8 Fig21.16 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. tick with eggs CNS damage, coma Rash (b) Egg (a) Vascular damage Tick/Dog Infection Human Infection (c) (d) 9 Fig21.25 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Cusp with occlusal surface Crown Enamel Dentin Pulp cavity Gingival crevice Gingiva (gum) Blood vessels and nerves in pulp Root Bone/socket Cementum Periodontal ligament Periodontal membrane Root canal 10 Fig21.26 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Tooth Surface (enamel, root) Pellicle Formation Plaque Formation Acidification and Cavitation Calculus (Tartar) Formation Dental Caries Damage to enamel Gingivitis/Periodontal Disease Tooth Destruction (exposure of dentin, pulp, root) Bone Resorption Tooth Loss 11 Fig21.27 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 6 1 A freshly cleaned tooth surface immediately develops a thin layer of salivary glycoproteins (the acquired pellicle). 2 Fibers of proteins, antibodies, salivary enzymes, bacterial debris, and other salivary molecules adhere to the pellicle (M). 3 The earliest tooth colonizers are the Streptococcus mutans group(s) (S. oralis and S. gordonii). These bacteria have specific receptors that adhere to the outer pellicle molecules. The streptococci likewise bind to each other, forming the initial base of plaque. 4 The next phase involves cell-cell signaling and coaggregation with additional colonists. The most common bacteria to add to the biofilm during this phase are filamentous rods in the genus Actinomyces (A). Other species of Streptococcus (the mutans group) use dietary carbohydrates to secrete glucans that add bulk to the matrix and serve as a source of sugars. 5 Once this initial framework has been laid down, it enters a second phase of aggregation which creates the final dense mat of plaque. Bacteria that colonize at this point are frequently anaerobes such as Fusobacterium (F), Porphyromonas (PO), Prevotella (PR), Veillonella (V), and Treponema (T). 6 See upper left. Initial damage to the enamel occurs when streptococci near the enamel surface ferment the sugars in plaque to lactic, acetic, and other acids. When these acids are trapped against the tooth surface and etch through it, a dental caries has developed. V A S M F PR V S Tooth enamel PO Acquired pellicle T A 1 2 3 4 5 12 Fig21.29 13 TA21.01 14