that clog arteries, and cause tissue necrosis. Biofilms consist of
microbial communities of cells attached to a surface (cell
matrix) and generally embedded in a viscous substance rich
in polysaccharides. Biofilms protect bacteria against phagocytosis by immune cells and prevent the penetration of biocides
used to treat patients, at the same time promoting systemic
infections and chronic diseases. Some microbes, such as atypical mycobacteria involved in opportunistic lung infections,
spread and survive in macrophages, which are immune cells of
the host paradoxically specialized in the fight against infectious agents (Sundaramurthy and Pieters 2007).
Another amazing case of weakening of the innate immunity
system with a disease outcome in insects lies in the criminal
alliance between the entomophagous nematodes Steinernema
and Heterorhabditis and the entomopathogenic bacteria
Xenorhabdus and Photorhabdus, respectively (GoodrichBlair and Clarke 2007). Xenorhabdus and Photorhabdus bacteria live symbiotically in intestinal vesicles of the nematodes.
When the larvae of nematodes, living freely in the soil,
encounter and infect an insect host, they metamorphose into
the adult stage, which weakens the immune system of the
insect. Bacteria are then released into the blood of the immunocompromised insect and act as opportunistic agents. They
multiply and release through their secretion systems toxins
that cause septicemia and toxemia, causing the death of the
insect. Necrotic tissues in turn are eaten by the entomophagous
nematode. Inoculation of the asymbiotic nematode or the
bacterium alone does not lead to death of the insect whose
immune system can then effectively eliminate the intruders.
In contrary to opportunistic pathogens that exploit
immune vulnerability of hosts to cause damage, certain
groups of bacteria such as enteropathogens (Campylobacter,
E. coli, Legionella, Listeria, Salmonella, Yersinia) responsible for diarrheal crises that affect hundreds of millions of
people around the world (of which millions will die) are
natural pathogens with invasive capacity and production of
toxins, which give them a virulent character (Cossart and
Sansonetti 2004).
11.4.3.2 Virulence Factors of Pathogens
One of the first virulence factors shared by pathogens of animals
such as enteropathogenic bacteria is the ability to overcome the
physical barrier (skin and mucosa) through an intimate attachment via structures such as adhesins (Ofek et al. 2003).
Adhesins are the first virulence factors of pathogenic bacteria involved in the infection process (Mainil 2013). They
interact with the components, called receptors, present on the
surface of eukaryotic cells or on the surface of the extracellular
matrix leading to the attachment of interacting cells.
Dozens of bacterial adhesins are known and three types of
adhesin–receptor interactions with a certain degree of
specificity have been described. Bacterial lectins are
fimbriae-like structures or have fibrillar proteic nature, which
are classified according to their hemagglutination properties,
and carbohydrate receptors are components of glycoproteins
or glycolipids of cell membranes of the host animal. The
second type includes proteins of the cell wall or membrane
associated or not to bacterial lipopolysaccharides and
peptidoglycans and protein receptors of cytoplasmic
membranes of the host cells. Finally, hydrophobins, present
on the surface of both bacteria (adhesins) and eukaryotic cells
(receptors), are mostly composed of lipid or hydrophobic
domains of proteins.
The adhesion of bacteria to the surface of host cells is
followed by injection of invasive effector molecules via
secretion systems. These secretion systems constitute the
second group of virulence factors, which play a role as
important as adhesins in the establishment of interactions
between microorganisms and hosts. Seven secretion
systems, designated type I to type VII (Fig. 11.15) (Abdallah
et al. 2007; Filloux et al. 2008), have been described and
characterized mainly in pathogenic bacteria and to a lesser
extent in the mutualists (Thanassi and Hultgren 2000). The
type I secretion system (or ABC transporters) is involved in
the transport of a wide variety of substrates (proteins, sugars,
lipids) and many processes of bacterial life per se. This is by
far the most represented secretion system found in many
bacteria. Type II (or typical sec-dependent secretion) and
type V (or autotransporters) systems are mainly used for the
secretion of enzymes and/or other proteins (Sandkvist 2001).
The type III (T3SS) and type IV (T4SS) secretion systems
have evolved for interaction with other organisms (Cascales
and Christie 2003). The T3SS develops a path allowing the
bacterium to inject cytotoxic or cyto-destabilizing factors
directly into the cytoplasm of the target cell. The T4SS,
meanwhile, allows the translocation of nucleoprotein
complexes to hosts, either directly inside the target cell or
via the extracellular medium (Llosa and O’Callaghan 2004).
Mammal cells such as human cells but also plant cells are
potential targets, providing an agronomic and medical interest to the study of these systems. Pili formed by the T3SS
and T4SS are also involved in the attachment process of
bacteria to target cells. The relationships between bacteria
and host cells (animal or plant) via the T3SS and T4SS often
have a pathogenic outcome and sometimes a mutualistic
character (Dale et al. 2002).
Like the bacterial symbiotic islands, genetic determinants
of virulence factors of pathogenic bacteria can be located in
a region of the genome designated pathogenicity island (or
PAI) (Hacker and Kaper 2000). Discovered for the first time
in pathogenic E. coli, genome analysis showed the presence
of PAIs in many other bacterial pathogens of animals. With a
428
Y. Moe ¨nne-Loccoz et al.
microbial communities of cells attached to a surface (cell
matrix) and generally embedded in a viscous substance rich
in polysaccharides. Biofilms protect bacteria against phagocytosis by immune cells and prevent the penetration of biocides
used to treat patients, at the same time promoting systemic
infections and chronic diseases. Some microbes, such as atypical mycobacteria involved in opportunistic lung infections,
spread and survive in macrophages, which are immune cells of
the host paradoxically specialized in the fight against infectious agents (Sundaramurthy and Pieters 2007).
Another amazing case of weakening of the innate immunity
system with a disease outcome in insects lies in the criminal
alliance between the entomophagous nematodes Steinernema
and Heterorhabditis and the entomopathogenic bacteria
Xenorhabdus and Photorhabdus, respectively (GoodrichBlair and Clarke 2007). Xenorhabdus and Photorhabdus bacteria live symbiotically in intestinal vesicles of the nematodes.
When the larvae of nematodes, living freely in the soil,
encounter and infect an insect host, they metamorphose into
the adult stage, which weakens the immune system of the
insect. Bacteria are then released into the blood of the immunocompromised insect and act as opportunistic agents. They
multiply and release through their secretion systems toxins
that cause septicemia and toxemia, causing the death of the
insect. Necrotic tissues in turn are eaten by the entomophagous
nematode. Inoculation of the asymbiotic nematode or the
bacterium alone does not lead to death of the insect whose
immune system can then effectively eliminate the intruders.
In contrary to opportunistic pathogens that exploit
immune vulnerability of hosts to cause damage, certain
groups of bacteria such as enteropathogens (Campylobacter,
E. coli, Legionella, Listeria, Salmonella, Yersinia) responsible for diarrheal crises that affect hundreds of millions of
people around the world (of which millions will die) are
natural pathogens with invasive capacity and production of
toxins, which give them a virulent character (Cossart and
Sansonetti 2004).
11.4.3.2 Virulence Factors of Pathogens
One of the first virulence factors shared by pathogens of animals
such as enteropathogenic bacteria is the ability to overcome the
physical barrier (skin and mucosa) through an intimate attachment via structures such as adhesins (Ofek et al. 2003).
Adhesins are the first virulence factors of pathogenic bacteria involved in the infection process (Mainil 2013). They
interact with the components, called receptors, present on the
surface of eukaryotic cells or on the surface of the extracellular
matrix leading to the attachment of interacting cells.
Dozens of bacterial adhesins are known and three types of
adhesin–receptor interactions with a certain degree of
specificity have been described. Bacterial lectins are
fimbriae-like structures or have fibrillar proteic nature, which
are classified according to their hemagglutination properties,
and carbohydrate receptors are components of glycoproteins
or glycolipids of cell membranes of the host animal. The
second type includes proteins of the cell wall or membrane
associated or not to bacterial lipopolysaccharides and
peptidoglycans and protein receptors of cytoplasmic
membranes of the host cells. Finally, hydrophobins, present
on the surface of both bacteria (adhesins) and eukaryotic cells
(receptors), are mostly composed of lipid or hydrophobic
domains of proteins.
The adhesion of bacteria to the surface of host cells is
followed by injection of invasive effector molecules via
secretion systems. These secretion systems constitute the
second group of virulence factors, which play a role as
important as adhesins in the establishment of interactions
between microorganisms and hosts. Seven secretion
systems, designated type I to type VII (Fig. 11.15) (Abdallah
et al. 2007; Filloux et al. 2008), have been described and
characterized mainly in pathogenic bacteria and to a lesser
extent in the mutualists (Thanassi and Hultgren 2000). The
type I secretion system (or ABC transporters) is involved in
the transport of a wide variety of substrates (proteins, sugars,
lipids) and many processes of bacterial life per se. This is by
far the most represented secretion system found in many
bacteria. Type II (or typical sec-dependent secretion) and
type V (or autotransporters) systems are mainly used for the
secretion of enzymes and/or other proteins (Sandkvist 2001).
The type III (T3SS) and type IV (T4SS) secretion systems
have evolved for interaction with other organisms (Cascales
and Christie 2003). The T3SS develops a path allowing the
bacterium to inject cytotoxic or cyto-destabilizing factors
directly into the cytoplasm of the target cell. The T4SS,
meanwhile, allows the translocation of nucleoprotein
complexes to hosts, either directly inside the target cell or
via the extracellular medium (Llosa and O’Callaghan 2004).
Mammal cells such as human cells but also plant cells are
potential targets, providing an agronomic and medical interest to the study of these systems. Pili formed by the T3SS
and T4SS are also involved in the attachment process of
bacteria to target cells. The relationships between bacteria
and host cells (animal or plant) via the T3SS and T4SS often
have a pathogenic outcome and sometimes a mutualistic
character (Dale et al. 2002).
Like the bacterial symbiotic islands, genetic determinants
of virulence factors of pathogenic bacteria can be located in
a region of the genome designated pathogenicity island (or
PAI) (Hacker and Kaper 2000). Discovered for the first time
in pathogenic E. coli, genome analysis showed the presence
of PAIs in many other bacterial pathogens of animals. With a
428
Y. Moe ¨nne-Loccoz et al.