Page 48 - Review of Medical Microbiology and Immunology ( PDFDrive )

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CHAPTER 7 Pathogenesis
are often nonpathogenic. For example, the pili of Neisseria
are especially important in cellulitis caused by Streptococcus
gonorrhoeae and E. coli mediate the attachment of the
organisms to the urinary tract epithelium, and the glycoca-
pyogenes.
(2) Coagulase, which is produced by Staphylococcus
lyx of Staphylococcus epidermidis and certain viridans
aureus and accelerates the formation of a fibrin clot from its
streptococci allows the organisms to adhere strongly to the
endothelium of heart valves. The various molecules that
from phagocytosis by walling off the infected area and by
mediate adherence to cell surfaces are called adhesins.
After the bacteria attach, they often form a protective
coating the organisms with a layer of fibrin). Coagulase is
matrix called a biofilm consisting of various polysaccha- precursor, fibrinogen (this clot may protect the bacteria
also produced by Yersinia pestis, the cause of bubonic
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plague. See Chapter 20 for the role of coagulase in the
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rides and proteins. Biofilms form especially on foreign bod-
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ies such as prosthetic joints, prosthetic heart valves, and
pathogenesis of plague.
intravenous catheters, but they also form on native structures
(3) Immunoglobulin A (IgA) protease, which degrades
such as heart valves. Biofilms protect bacteria from both
antibiotics and host immune defenses such as antibodies
and is produced chiefly by N. gonorrhoeae, Haemophilus
and neutrophils. They also retard wound healing resulting
influenzae, and Streptococcus pneumoniae.
in chronic wound infections, especially in diabetics. Biofilms
(4) Leukocidins, which can destroy both neutrophilic
leukocytes and macrophages.
play an important role in the persistence of Pseudomonas in
the lungs of cystic fibrosis patients and in the formation of
In addition to these enzymes, several virulence factors
dental plaque, the precursor of dental caries.
The production of biofilms by bacteria such as
defense mechanisms, especially phagocytosis, to operate
Pseudomonas is controlled by the process of quorum sensing.
effectively.
In quorum sensing, the bacteria grow in a nonaggressive contribute to invasiveness by limiting the ability of the host
manner until a quorum is sensed (i.e., a certain density of
(1) The most important of these antiphagocytic factors
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bacteria has been reached), at which point the synthesis of
is the capsule external to the cell wall of several important
new bacterial virulence factors (e.g., biofilms) that con-
pathogens such as S. pneumoniae and Neisseria meningiti-
tribute to pathogenesis occurs.
Foreign bodies, such as artificial heart valves and artifi-
from adhering to the bacteria; anticapsular antibodies
cial joints, predispose to infections. Bacteria can adhere to
allow more effective phagocytosis to occur (a process called
these surfaces, but phagocytes adhere poorly owing to the
opsonization) (see page 55). The vaccines against S. pneu-
absence of selectins and other binding proteins on the arti-
moniae, H. influenzae, and N. meningitidis contain capsular
ficial surface (see Chapter 8).
polysaccharides that induce protective anticapsular
Some strains of E. coli and Salmonella have surface pro-
antibodies.
teins called curli, which mediate binding of the bacteria to
(2) A second group of antiphagocytic factors are the cell
endothelium and to extracellular proteins such as fibronec-
tin. Curli also interact with serum proteins such as factor
tein of the group A streptococci (S. pyogenes) and protein
XII—a component of the coagulation cascade. Curli, there- wall proteins of the gram-positive cocci, such as the M pro-
A of S. aureus. The M protein is antiphagocytic, and pro-
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fore, are thought to play a role in the production of the
tein A binds to immunoglobulin G (IgG) and prevents the
thrombi seen in the disseminated intravascular coagulation
activation of complement. These virulence factors are
(DIC) associated with sepsis caused by these bacteria (see
the discussion of endotoxin on page 44).
Bacteria can cause two types of inflammation: pyogenic
and granulomatous. In pyogenic (pus-producing) inflam-
3. Invasion, Inflammation, &
mation, neutrophils are the predominant cells. Some of the
most important pyogenic bacteria are the gram-positive
Intracellular Survival
and gram-negative cocci listed in Table 7–8. In granuloma-
One of the two main mechanisms by which bacteria cause
tous inflammation, macrophages and helper T cells pre-
disease is invasion of tissue followed by inflammation.
(The inflammatory response is described in Chapter 8.)
Mycobacterium tuberculosis. No bacterial enzymes or tox-
The other main mechanism, toxin production, and a third
ins that induce granulomas have been identified. Rather, it
mechanism, immunopathogenesis, are described later in dominate. The most important organism in this category is
appears that bacterial antigens stimulate the cell-mediated
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this chapter.
immune system, resulting in sensitized T-lymphocyte and
Several enzymes secreted by invasive bacteria play a role
macrophage activity. Phagocytosis by macrophages kills
in pathogenesis. Among the most prominent are the
following:
macrophages in the granuloma.
Intracellular survival is an important attribute of cer-
(1) Collagenase and hyaluronidase, which degrade
tain bacteria that enhances their ability to cause disease.
collagen and hyaluronic acid, respectively, thereby allowing
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