How Bacterial Pathogens Penetrate Host Defenses

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How Bacterial Pathogens Penetrate Host Defenses
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Although some pathogens can cause damage on
the surface of tissues, most must penetrate
tissues to cause disease. Here we will consider
several factors that contribute to the
ability of bacteria to invade a host.
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Capsules
Recall from Chapter 4 that some bacteria make
glycocalyx material that forms capsules around
their cell walls this property increases the
virulence of the species. The capsule resists the
hosts defenses by impairing phagocytosis, the
process by which certain cells of the body engulf
and destroy microbes (see Chapter 16, ). The
chemical nature of the capsule appears to prevent
the phagocytic cell from adhering to the
bacterium. However, the human body can produce
antibodies against the capsule, and when these
antibodies are present on the capsule surface,
the encapsulated bacteria are easily destroyed by
phagocytosis.      One bacterium that owes its
virulence to the presence of a polysaccharide
capsule is Streptococcus pneumoniae, the
causative agent of pneumococcal pneumonia (see
Figure 24.13, ). Some strains of this organism
have capsules, and others do not. Strains with
capsules are virulent, but strains without
capsules are avirulent because they are
susceptible to phagocytosis. Other bacteria that
produce capsules related to virulence are
Klebsiella pneumoniae, a causative agent of
bacterial pneumonia Haemophilus influenzae, a
cause of pneumonia and meningitis in children
Bacillus anthracis, the cause of anthrax and
Yersinia pestis, the causative agent of plague.
Keep in mind that capsules are not the only cause
of virulence. Many nonpathogenic bacteria produce
capsules, and the virulence of some pathogens is
not related to the presence of a capsule.the
presence of a capsule .
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Cell Wall ComponentsThe cell walls of certain
bacteria contain chemical substances that
contribute to virulence. For example,
Streptococcus pyogenes produces a heat-resistant
and acid-resistant protein called M protein (see
Figure 21.5, ). This protein is found on both the
cell surface and fimbriae. The M protein mediates
attachment of the bacterium to epithelial cells
of the host and helps the bacterium resist
phagocytosis by white blood cells. The protein
thereby increases the virulence of the
microorganism. Immunity to S. pyogenes depends on
the bodys production of an antibody specific to
M protein. Neisseria gonorrhoeae grows inside
human epithelial cells and leukocytes. These
bacteria use fimbriae and an outer membrane
protein called Opa to attach to host cells.
Following attachment by both Opa and fimbriae,
the host cells take in the bacteria. (Bacteria
that produce Opa form opaque colonies in culture
media.) The waxy lipid (mycolic acid) that makes
up the cell wall of Mycobacterium tuberculosis
also increases virulence by resisting digestion
by phagocytes. In fact, M. tuberculosis can even
multiply inside phagocytes.
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Enzymes
The virulence of some bacteria is thought to be
aided by the production of extracellular enzymes
(exoenzymes) and related substances. These
chemicals can digest materials between cells and
form or digest blood clots, among other
functions.  Coagulases are bacterial enzymes
that coagulate (clot) the fibrinogen in blood.
Fibrinogen, a plasma protein produced by the
liver, is converted by coagulases into fibrin,
the threads that form a blood clot. The fibrin
clot may protect the bacterium from phagocytosis
and isolate it from other defenses of the host.
Coagulases are produced by some members of the
genus Staphylococcus they may be involved in the
walling-off process in boils produced by
staphylococci. However, some staphylococci that
do not produce coagulases are still virulent.
(Capsules may be more important to their
virulence.)  Bacterial kinases are bacterial
enzymes that break down fibrin and thus digest
clots formed by the body to isolate the
infection. One of the better-known kinases is
fibrinolysin (streptokinase), which is produced
by such streptococci as Streptococcus pyogenes.
Another kinase, staphylokinase, is produced by
Staphylococcus aureus. Injected directly into the
blood, streptokinase has been used successfully
to remove some types of blood clots in cases of
heart attacks due to obstructed coronary
arteries. 
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Hyaluronidase is another enzyme secreted by
certain bacteria, such as streptococci. It
hydrolyzes hyaluronic acid, a type of
polysaccharide that holds together certain cells
of the body, particularly cells in connective
tissue. This digesting action is thought to be
involved in the tissue blackening of infected
wounds and to help the microorganism spread from
its initial site of infection. Hyaluronidase is
also produced by some clostridia that cause gas
gangrene. For therapeutic use, hyaluronidase may
be mixed with a drug to promote the spread of the
drug through a body tissue. Another enzyme,
collagenase, produced by several species of
Clostridium, facilitates the spread of gas
gangrene. Collagenase breaks down the protein
collagen, which forms the connective tissue of
muscles and other body organs and tissues. As a
defense against adherence of pathogens to mucosal
surfaces, the body produces a class of antibodies
called IgA antibodies. There are some pathogens
with the ability to produce enzymes, called IgA
proteases, that can destroy these antibodies. N.
gonorrhoeae has this ability, as does N.
meningitidis (me-nin-ji'ti-dis), the causative
agent of meningococcal meningitis, and other
microbes that infect the central nervous system.
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Antigenic Variation
n Chapter 17 you will learn that adaptive
(acquired) immunity refers to a specific
defensive response of the body to an infection or
to antigens. In the presence of antigens the body
produces proteins called antibodies, which bind
to the antigens and inactivate or destroy them.
However, some pathogens can alter their surface
antigens, by a process called antigenic
variation. Thus, by the time the body mounts an
immune response against a pathogen, the pathogen
has already altered its antigens and is
unaffected by the antibodies. Some microbes can
activate alternative genes, resulting in
antigenic changes. For example, N. gonorrhoeae
has several copies of the Opa-encoding gene,
resulting in cells with different antigens and in
cells that express different antigens over
time.      A wide range of microbes is capable
of antigenic variation. Examples include
Influenzavirus, the causative agent of influenza
(flu) Neisseria gonorrhoeae, the causative agent
of gonorrhea and Trypanosoma brucei gambiense
(tri-pa'no-so-mä brüs'e gam-be-ens'), the
causative agent of African trypanosomiasis
(sleeping sickness).