288
14.3.2 Pathogenicity
Bacteria have a suite of chemical defences and mechanisms for defence and antagonism against other bacteria. However, the chemical signals between algal and bacterial pathogenic interactions are less well known (Wietz et al. 2013). One advantage
to bacteria in killing their algal host is that it leads to access of metabolites and
nutrients within their host. As such, proximity to the dying host should allow for
more direct benefit. This is the case for some bacteria, in which close association is
a necessity for pathogenicity, with some bacterial pathogens even residing directly
in the algal cell wall (Wang et al. 2010). However, it has been suggested that only a
minority of bacterial pathogens require direct cell-to-cell contact to negatively
affect their host (Mayali and Azam 2004; Demuez et al. 2015). Chemotaxis has
been shown to be an important feature in bacteria obtaining the dissolved organic
matter (DOM) released from lytic algal cells (Stocker et al. 2008; Smriga et al.
2016). Some bacteria may capitalize on this and induce lysis of their algal hosts
(Wang et al. 2010).
A few bacteria have been proposed to have the ability to switch from a mutualistic to pathogenic phase, induced by either molecule made due to aging of the algal
host, the presence of a high nutrient media, accumulation of bacterial QS molecules
or other unknown signals (Seyedsayamdost et al. 2011b; Wang et al. 2014b).
Chemotaxis towards algal products such as DMSP is important for mutualists, as it
can lead to the area around the algae containing higher concentrations. However,
chemotaxis towards DMSP is also important in achieving the quorum of bacteria
needed to achieve the QS signal concentration required to switch to a pathogenic
lifestyle (Lovejoy et al. 1998; Nakashima et al. 2006; Wang and Yuan 2014).
Environmental conditions and nutrient levels are an important factor in generating
an algicidal response in bacteria, as a threshold concentration of bacteria and nutrients is required to stimulate lytic responses (Mayali and Doucette 2002; Amaro
et al. 2005). One example is the bacteria Kordia algicida which has targeted algicidal effects against selected diatom species, as it only releases the algicidal proteases once a quorum has been reached (Paul and Pohnert 2011).
Effects of algicidal bacteria can include decreased chlorophyll and photosynthesis, induction of caspase-like activity and loss of cell wall integrity (Fu et al. 2012;
Mayers et al. 2016). Pathogenicity seems to be a targeted affair, as algicidal bacteria
are often found to kill one strain or species but not another (Mayali and Azam 2004;
Demuez et al. 2015). However, unlike viral killing of algae (Bidle and Vardi 2011),
the main mechanisms and compounds used by the bacteria remain mostly uncharacterized (Mayali and Azam 2004; Seyedsayamdost et al. 2011b). The algicidal bacteria Alteromonas sp. and Thalassobius aestuarii sp. release enzymes that
specifically target the cell wall of the Alexandrium tamarense, including chitinase or
β-glucosidase (Wang et al. 2010). Proteases induced in the stationary phase of
Pseudoalteromonas sp. were implicated in the death of Skeletonema costatum (Lee
et al. 2000; Mitsutani et al. 2001).
Specific algicidal molecules have been harder to identify, although recently the
QS messenger 2-heptyl-4-quinolone (HHQ) (Diggle et al. 2007) produced by
L. Labeeuw et al.
14.3.2 Pathogenicity
Bacteria have a suite of chemical defences and mechanisms for defence and antagonism against other bacteria. However, the chemical signals between algal and bacterial pathogenic interactions are less well known (Wietz et al. 2013). One advantage
to bacteria in killing their algal host is that it leads to access of metabolites and
nutrients within their host. As such, proximity to the dying host should allow for
more direct benefit. This is the case for some bacteria, in which close association is
a necessity for pathogenicity, with some bacterial pathogens even residing directly
in the algal cell wall (Wang et al. 2010). However, it has been suggested that only a
minority of bacterial pathogens require direct cell-to-cell contact to negatively
affect their host (Mayali and Azam 2004; Demuez et al. 2015). Chemotaxis has
been shown to be an important feature in bacteria obtaining the dissolved organic
matter (DOM) released from lytic algal cells (Stocker et al. 2008; Smriga et al.
2016). Some bacteria may capitalize on this and induce lysis of their algal hosts
(Wang et al. 2010).
A few bacteria have been proposed to have the ability to switch from a mutualistic to pathogenic phase, induced by either molecule made due to aging of the algal
host, the presence of a high nutrient media, accumulation of bacterial QS molecules
or other unknown signals (Seyedsayamdost et al. 2011b; Wang et al. 2014b).
Chemotaxis towards algal products such as DMSP is important for mutualists, as it
can lead to the area around the algae containing higher concentrations. However,
chemotaxis towards DMSP is also important in achieving the quorum of bacteria
needed to achieve the QS signal concentration required to switch to a pathogenic
lifestyle (Lovejoy et al. 1998; Nakashima et al. 2006; Wang and Yuan 2014).
Environmental conditions and nutrient levels are an important factor in generating
an algicidal response in bacteria, as a threshold concentration of bacteria and nutrients is required to stimulate lytic responses (Mayali and Doucette 2002; Amaro
et al. 2005). One example is the bacteria Kordia algicida which has targeted algicidal effects against selected diatom species, as it only releases the algicidal proteases once a quorum has been reached (Paul and Pohnert 2011).
Effects of algicidal bacteria can include decreased chlorophyll and photosynthesis, induction of caspase-like activity and loss of cell wall integrity (Fu et al. 2012;
Mayers et al. 2016). Pathogenicity seems to be a targeted affair, as algicidal bacteria
are often found to kill one strain or species but not another (Mayali and Azam 2004;
Demuez et al. 2015). However, unlike viral killing of algae (Bidle and Vardi 2011),
the main mechanisms and compounds used by the bacteria remain mostly uncharacterized (Mayali and Azam 2004; Seyedsayamdost et al. 2011b). The algicidal bacteria Alteromonas sp. and Thalassobius aestuarii sp. release enzymes that
specifically target the cell wall of the Alexandrium tamarense, including chitinase or
β-glucosidase (Wang et al. 2010). Proteases induced in the stationary phase of
Pseudoalteromonas sp. were implicated in the death of Skeletonema costatum (Lee
et al. 2000; Mitsutani et al. 2001).
Specific algicidal molecules have been harder to identify, although recently the
QS messenger 2-heptyl-4-quinolone (HHQ) (Diggle et al. 2007) produced by
L. Labeeuw et al.