147
inhalation of spores. The disease is caused by the systemic effects of the anthrax
toxins and a capsule that prevents phagocytosis of this pathogen. The 2011 anthrax
attacks that followed the 9/11 terrorist attack in the US led to the rise of panic in the
general public, and infusion of funds towards the discovery of novel therapeutics
and vaccines [14].
Francisella tularensis causes tularemia, which is classically considered a zoonotic disease and the incidence of human infection is low. F. tularensis is a highly
infectious pathogen, with as few as 10 organisms being capable of causing disease
in humans [15]. The disease can have a number of clinical presentations, and does
not spread from person-to-person [16–19].
Due to its high infectivity and lethality in humans, F. tularensis has been classified as a high-risk agent for bioterrorism. Furthermore, there is little information on
F. tularensis pathogenesis, and the only vaccine; F. tularensis live vaccine strain,
LVS, is not readily available and poorly characterized [20].
F. tularensis seems to employ a secretion system named type six secretion system (T6SS) to deliver effectors into the host cell, but the role of this system in
pathogenesis is still not very well defined [21].
Yersinia pestis is the causative agent of bubonic plague that has a mortality rate
of 30 to 60%. Unlike anthrax and tularemia, Y. pestis can spread from person-toperson. Pseumonic plague is fatal if left untreated, and is considered the main potential form of a. Y. pestis infects the host through flea bites (bubonic) or air droplets
(pneumonic) biothreat. However, plague has a long history as being used as a biological weapon dating back to ancient China and medieval Europe [22] Y. pestis
encodes a T3SS and a plasminogen activated protease that are necessary for virulence in pneumonic plague [23].
9.4 Bacterial Toxins at the Host/Bacterium Interface
The most recognizable bacterial virulence factors are toxins. These are bacterial
proteins that damage host cells. Toxins have different modes of action, and tend to
be classified according to their origin and mode of action. The lipopolysaccharide
(LPS) that is a structural component of the bacterial outer membrane is known as
endotoxin. The LPS from Gram-negative bacteria is highly toxic and is named
endotoxin, given that it is embedded in the membrane. Most toxins, however, are
exotoxins, which are not structural components of the bacterial cell and are secreted
or exported. They comprise bacterial proteins that are toxic to mammalian cells.
They are found in both Gram-positive and Gram-negative bacteria. Toxin nomenclature is based on their target (e.g.: neurotoxin, leukotoxin, hepatotoxin, etc),
named according to the bacterial species that produces them or the disease they
cause (e..g.: cholera toxin, Shiga toxin, botulinum toxin, tetanus toxin); based on
the type of activity they have (e.g.: adenylate cyclase, lecithinase), or are designated
by letters (e.g. exotoxin A of Pseudomonas aeruginosa). The majority of bacterial
toxins are encoded on mobile genetic elements such as bacteriophages (e.g.
9 Bacterial Threats to Human Health and Food Supply
inhalation of spores. The disease is caused by the systemic effects of the anthrax
toxins and a capsule that prevents phagocytosis of this pathogen. The 2011 anthrax
attacks that followed the 9/11 terrorist attack in the US led to the rise of panic in the
general public, and infusion of funds towards the discovery of novel therapeutics
and vaccines [14].
Francisella tularensis causes tularemia, which is classically considered a zoonotic disease and the incidence of human infection is low. F. tularensis is a highly
infectious pathogen, with as few as 10 organisms being capable of causing disease
in humans [15]. The disease can have a number of clinical presentations, and does
not spread from person-to-person [16–19].
Due to its high infectivity and lethality in humans, F. tularensis has been classified as a high-risk agent for bioterrorism. Furthermore, there is little information on
F. tularensis pathogenesis, and the only vaccine; F. tularensis live vaccine strain,
LVS, is not readily available and poorly characterized [20].
F. tularensis seems to employ a secretion system named type six secretion system (T6SS) to deliver effectors into the host cell, but the role of this system in
pathogenesis is still not very well defined [21].
Yersinia pestis is the causative agent of bubonic plague that has a mortality rate
of 30 to 60%. Unlike anthrax and tularemia, Y. pestis can spread from person-toperson. Pseumonic plague is fatal if left untreated, and is considered the main potential form of a. Y. pestis infects the host through flea bites (bubonic) or air droplets
(pneumonic) biothreat. However, plague has a long history as being used as a biological weapon dating back to ancient China and medieval Europe [22] Y. pestis
encodes a T3SS and a plasminogen activated protease that are necessary for virulence in pneumonic plague [23].
9.4 Bacterial Toxins at the Host/Bacterium Interface
The most recognizable bacterial virulence factors are toxins. These are bacterial
proteins that damage host cells. Toxins have different modes of action, and tend to
be classified according to their origin and mode of action. The lipopolysaccharide
(LPS) that is a structural component of the bacterial outer membrane is known as
endotoxin. The LPS from Gram-negative bacteria is highly toxic and is named
endotoxin, given that it is embedded in the membrane. Most toxins, however, are
exotoxins, which are not structural components of the bacterial cell and are secreted
or exported. They comprise bacterial proteins that are toxic to mammalian cells.
They are found in both Gram-positive and Gram-negative bacteria. Toxin nomenclature is based on their target (e.g.: neurotoxin, leukotoxin, hepatotoxin, etc),
named according to the bacterial species that produces them or the disease they
cause (e..g.: cholera toxin, Shiga toxin, botulinum toxin, tetanus toxin); based on
the type of activity they have (e.g.: adenylate cyclase, lecithinase), or are designated
by letters (e.g. exotoxin A of Pseudomonas aeruginosa). The majority of bacterial
toxins are encoded on mobile genetic elements such as bacteriophages (e.g.
9 Bacterial Threats to Human Health and Food Supply