Transcript 1 - McGraw-Hill Education

Chapter 21
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1
Fig21.01a
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Endoflagellum
(a)
Periplasmic space
Outer membrane
Endoflagellum
Cell body
2
Table21.01
3
Fig21.08
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(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
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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
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tick
with eggs
CNS
damage,
coma
Rash
(b)
Egg
(a)
Vascular
damage
Tick/Dog Infection
Human Infection
(c)
(d)
9
Fig21.25
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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
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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
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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