Possible solution to end RTN forever?!?

[Scott Campbell]

Just looking at that one study they suggest RTN or WBD (white band disease) is caused by microorganisms rather than by physiological stress.

The study goes on to say that RTN/STN is a polymicrobial disease associated with multiple specific microorganisms that are consistently associated with diseased samples but absent or undetectable in healthy samples. They say that up to 16 specific microorganisms have been found.

14 bacteria, one archaea, and one ciliate.

Anybody wanna guess which ciliate that was? Yep, it was Philaster Lucinda. So we know this guy is consistently on scene.

Then it says, “One of these, the ciliate Philaster Lucinda has recently been shown to be consistently associated with the coral disease WS in the Pacific and within Aquaria, which all have identical visible and histopathological disease signs, namely the advancing band of cleared skeleton immediately adjacent to visible normal tissues.”

But they still think it’s unlikely to be a primary pathogen of RTN/STN. Which really means nothing to me, because they misidentified a pathogen during the study.

Can anybody help me to understand this? This is why they think that’s it’s not a primary pathogen:

“However, selective elimination of this pathogen using the antibiotic metronidazole failed to arrest disease lesion progression in controlled experiments, indicating that the Philaster ciliate is unlikely to be a primary pathogen of WBD.”

How would this make it unlikely? Not sure I understand.

Let's say a bunch of wildebeest keep showing up dead on the plains of Africa. And researchers consistently find the same 16 animals around the dead wildebeest - vultures, lions, hyenas, etc. So they decide to kill off all the vultures. And it has no impact on the number of dead wildebeest. Wouldn't that be pretty good evidence the vultures are not involved in actually killing the wildebeest?

Just because the Philaster ciliate is "on the scene" doesn't mean it makes sense to kill them all off.

 

[MnFish1]

This... I thought about what I wrote earlier and this is what I should have said instead. Pretty much sums up how I felt.

Unfortunately - this is so vague as to be meaningless - no offense.

 

[Reefahholic]

Can you give the reference? otherwise no one can determine what youre talking abut

I find this extremely interesting too. Yet in the same study they still say it’s “likely” a second cause, but this goes exactly with what I was saying earlier. They are present and waiting for dinner. Even if they’re secondary and not the actual causal agent...could it be that they indeed finish the job rapidly? Errrr...I wanna know the culprit!!!

“To date, the histophagous ciliate, Philaster lucinda, has not been detected in association with healthy corals in the natural environment, yet has been shown to be consistently present in the neighbouring reef environment, particularly associated with numerous marine algal species (Sweet et al. 2013b). It is therefore possible that they remain in these nearby reservoirs until the coral becomes compromised.”

 

[Reefahholic]

Let's say a bunch of wildebeest keep showing up dead on the plains of Africa. And researchers consistently find the same 16 animals around the dead wildebeest - vultures, lions, hyenas, etc. So they decide to kill off all the vultures. And it has no impact on the number of dead wildebeest. Wouldn't that be pretty good evidence the vultures are not involved in actually killing the wildebeest?

Just because the Philaster ciliate is "on the scene" doesn't mean it makes sense to kill them all off.

I understand the first part (makes sense), but didn’t quite understand that last part.

 

[Scott Campbell]

I find this extremely interesting too. Yet in the same study they still say it’s “likely” a second cause, but this goes exactly with what I was saying earlier. They are present and waiting for dinner. Even if they’re secondary and not the actual causal agent...could it be that they indeed finish the job rapidly? Errrr...I wanna know the culprit!!!

“To date, the histophagous ciliate, Philaster lucinda, has not been detected in association with healthy corals in the natural environment, yet has been shown to be consistently present in the neighbouring reef environment, particularly associated with numerous marine algal species (Sweet et al. 2013b). It is therefore possible that they remain in these nearby reservoirs until the coral becomes compromised.”

Indicates they are scavengers - not predators. And probably like most ciliates subsist mainly on microalgae. But won't turn down a dying coral if given the opportunity. If this is the case - why should we eradicate them from our tank?

 

[Scott Campbell]

I understand the first part (makes sense), but didn’t quite understand that last part.

Vultures, like Philaster ciliates, may always be found around dead things. Doesn't mean the vultures or the ciliates killed anything. And taking action to completely remove the vultures (or the ciliates) may actually make the situation worse in unforeseen ways - like giving hyenas more food, allowing hyenas to reproduce more and thereby causing the death of even more wildebeest.

Which is why there has been such vigorous pushback in this thread. It doesn't appear to be as simple as presented.

 

[Reefahholic]

Indicates they are scavengers - not predators. And probably like most ciliates subsist mainly on microalgae. But won't turn down a dying coral if given the opportunity. If this is the case - why should we eradicate them from our tank?

But in the microscopic videos they are clearly observed by themselves munching on the coral in swarms. So let’s say they’re a secondary cause of RTN and the primary is a bacterial infection that really only cause very minimal damage. Then these guys come in like piranha and completely devour the corals. Even though they’re not causal agents it seems to me that they would be the greater threat.

I’m not worried about the fuse burning on a stick of dynamite...I’m worried about the explosion!

 

[Reefahholic]

Vultures, like Philaster ciliates, may always be found around dead things. Doesn't mean the vultures or the ciliates killed anything. And taking action to completely remove the vultures (or the ciliates) may actually make the situation worse in unforeseen ways - like giving hyenas more food, allowing hyenas to reproduce more and thereby causing the death of even more wildebeest.

Which is why there has been such vigorous pushback in this thread. It doesn't appear to be as simple as presented.

I definitely don’t think it’s simple by any means. I do think there’s more than one guilty party, but also think the primary person is the Philaster.

Could it be that we are just not seeing these bacteria because they are ultra small.

One thing that bugs me about that paper is that they make a lot of bold claims in their study, but they won’t come out and say it’s the bacteria for sure. If they’re so sure that the Philaster isn’t primary then why can’t they say who is. Didn’t they perform the same tests for all 16 microorganisms. I sure would have.

 

[Reefahholic]

Discussion
Selective elimination of candidate pathogens using a variety of antibiotics in controlled experiments can aid in the identification of specific roles of these organisms with respect to disease causation. This study shows that the specific form(s) of WS sampled in this study were the result of a polymicrobial disease associated with a number of potential pathogens (15 bacteria and 7 ciliates identified in this study) that were consistently associated with all samples of disease and absent from healthy samples. This result supports previous studies on WS (Sussman et al. 2008; Luna et al. 2010; Sweet & Bythell 2012) as well as others such as white plague (Denner et al. 2003; Pantos et al. 2003; Bythell et al. 2004; Barash et al. 2005; Efrony et al. 2009; Atad et al. 2012) and black band disease (Cooney et al. 2002; Frias‐Lopez et al. 2003) which show multiple specific associates of any given diseased state. The combined elimination of three bacteria and one ciliate ribosomal type from this group of potential pathogens resulted in immediate and complete cessation of disease lesion progression, strongly indicating that one or a consortium of more than one (possibly all 4) of these candidate pathogens can be considered the ‘primary’ pathogen of WS in this instance. Only one of these candidate pathogens has been implicated in WS before, the ciliate Philaster lucinda (Sweet & Bythell 2012), which remains the only specific pathogen associated with the disease in all cases studied to date. However, as we have recently concluded for WBD in Caribbean acroporas, Philaster lucinda is more likely to be a ‘secondary’ pathogen contributing to pathogenesis and not a primary pathogen as the lesion continued to progress even though the ciliate was reduced to undetectable levels in the metronidazole treatment.

To date, the histophagous ciliate, Philaster lucinda, has not been detected in association with healthy corals in the natural environment, yet has been shown to be consistently present in the neighbouring reef environment, particularly associated with numerous marine algal species (Sweet et al. 2013b). It is therefore possible that they remain in these nearby reservoirs until the coral becomes compromised. With this in mind and the fact that two of the antibiotics utilized caused the lesion progression to cessate, the primary pathogen, at least in this instance, appears to be one or a combination of up to three of the bacterial agents. In the absence of the histophagous ciliate, these bacteria cause a degree of tissue necrosis that promotes lesion progression. In the natural disease state, these compromised tissues are apparently consumed by ciliates before necrosis occurs. However, without fine‐scale temporal sampling at the initiation of infection, it cannot be determined whether prior physical disruption by ciliates, or some other primary agent, may allow these specific bacterial agents to infect the tissues, and they may actually still be secondary agents, in a complicated disease process.

In this study, transmission electron microscopy showed the appearance of stress associated with the coral's symbiotic algae in progressive lesions but not in healthy tissues or those treatments which successfully stopped the disease. The symbiotic algae are a vital part of the coral holobiont and dysfunctional or damaged symbionts appear to be part of the aetiology of this disease. Damage to the symbionts may represent an additional stress to the coral and potentially provide a vicious cycle, further reducing host defences. This result, in which the algae are shown to be affected by the disease, is again similar to our recent study on WBD in the Caribbean acroporids.

The general absence of a significant population of bacteria and a lack of bacterial‐induced necrosis at the disease lesion interface of WS and similar ‘white diseases’ (Ainsworth et al. 2007; Work & Aeby 2011; Sweet & Bythell 2012) have been paradoxical to the finding of multiple bacterial causal agents for the disease by challenge experiments and culture‐independent studies (Ben‐Haim & Rosenberg 2002; Denner et al. 2003; Barash et al. 2005; Gil‐Agudelo et al. 2006; Pantos & Bythell 2006; Luna et al. 2010; Kline & Vollmer 2011; Sweet & Bythell 2012). This finding was also reflected in the present study. The altered histopathology that occurred in the metronidazole treatment may be explained by the lack of ciliates associated with this treatment, which would otherwise have consumed the tissues before necrosis could be detected. In the metronidazole‐treated corals, we were also able to locate numerous rod‐shaped bacteria associated with these fragmented tissues. This may explain why previous studies have failed to find bacteria associated with WS lesions, as infected tissues are rapidly consumed by the ciliates.

One further finding of note is the presence of Bacteriovorax in healthy tissues but absent in diseased samples. Bacteriovorax are predatory bacteria whose presence in host organisms is thought to shape the natural microbial community through trophic interactions (Thurber et al. 2009; Chen et al. 2012). Particularly, Bacteriovorax are known to prey on Gram‐negative bacteria such as members of the genus Vibrio. Its dynamics may therefore be of importance in maintaining a healthy population of microbes, and its subsequent absence in diseased tissues may then allow for pathogenic bacteria to infect (Chen et al. 2012).

Although detection of viruses was not a focus of this study, two main types were observed to be associated with the samples. One, circular, electron dense cored capsid VLP was consistently found in all sample types and appeared to be associated with the coral's symbiotic algae. Similar VLPs have previously been reported in Acropora hyacinthus (Pollock et al. 2014) and found in both healthy and diseased tissues. In contrast, the occurrence of a unique, larger VLP only present in metronidazole‐treated samples warrants further investigation. While this result is not sufficient to imply a role in disease causation, an increasing number of studies are showing the presence of viruses associated with disease lesions (Lohr et al. 2007; Lawrence et al. 2014a,b; Pollock et al. 2014; Yvan et al. 2014) and their role as a potential pathogen requires further study. However, interestingly, the study by Lawrence et al. (2014b) also highlighted the presence of ciliates within the diseased tissues of corals showing signs of Porites tissue loss (PorTL), a disease that fits within the generic description of WS disease.

Significant questions remain over the similarity between WS in the Indo‐Pacific and WBD in the Caribbean and between geographically and temporally separated WS cases. All these diseases are associated with the specific ciliate Philaster lucinda, and it remains the only agent with direct evidence for involvement in pathogenesis as it has been observed to consume intact coral tissues at the lesion interface (Sweet & Bythell 2012). However, we can conclude that the ciliate is a secondary pathogen due to its responses to antibiotic treatment. The diseases are also associated with a specific bacterial consortium that is absent in healthy coral and present in every case of the disease observed at any particular site. Thus, there is no distinction between WBD in the Caribbean and the equally variable geographical presentation of WS in the Pacific, either in associated microbial communities, histopathology or visible disease signs. The question then remains as to whether the different white syndromes and WBD consist of separate types of disease or are a single disease. It is possible that they are clearly separate diseases, caused by specific bacteria, but that the secondary, specific ciliate pathogen and other nonspecific pathogens cause disease signs that are indistinguishable. The fact that none of the specific agents associated with WS in Fiji in this study were previously detected in corals showing signs of WS in the GBR or Solomon Islands (Sweet & Bythell 2012) might suggest that they are separate diseases associated with specific pathogens. However, it is also possible that the bacterial infections are nonspecific and opportunistic (Lesser et al. 2007) and that any of a wide range of potential pathogens can act to cause initial infection and weaken host defences to allow the ciliate pathogens to invade. However, the fact that the bacterial consortium associated with the disease is so consistent between cases (sometimes separated by several km) and that none of these agents can be detected in healthy coral, even with deep sequencing, suggests that WS is not a completely nonspecific infection. Whatever the case, these diseases are certainly polymicrobial diseases, not only with bacteria and ciliates playing different roles in pathogenesis, but with multiple, specific bacterial associates consistently associated with the disease at a particular location and time. Further work is needed to determine whether this is simply a result of the ‘beta diversity’ associated with coral reef environments (whatever specific bacterial pathogens are available in the environment at any one time cause the disease) or whether specific disease consortia are associated with a number of specific diseases. It is also possible that the disease consortia are continually changing, possibly in response to changes in the host defences. This latter hypothesis differs from the hologenome theory of coral disease evolution (Rosenberg et al. 2007) in that changes in microbial consortia rather than individual pathogen selection and evolution would be required to enable coral diseases to persist in the environment.

 

[crusso1993]

Discussion
Selective elimination of candidate pathogens using a variety of antibiotics in controlled experiments can aid in the identification of specific roles of these organisms with respect to disease causation. This study shows that the specific form(s) of WS sampled in this study were the result of a polymicrobial disease associated with a number of potential pathogens (15 bacteria and 7 ciliates identified in this study) that were consistently associated with all samples of disease and absent from healthy samples. This result supports previous studies on WS (Sussman et al. 2008; Luna et al. 2010; Sweet & Bythell 2012) as well as others such as white plague (Denner et al. 2003; Pantos et al. 2003; Bythell et al. 2004; Barash et al. 2005; Efrony et al. 2009; Atad et al. 2012) and black band disease (Cooney et al. 2002; Frias‐Lopez et al. 2003) which show multiple specific associates of any given diseased state. The combined elimination of three bacteria and one ciliate ribosomal type from this group of potential pathogens resulted in immediate and complete cessation of disease lesion progression, strongly indicating that one or a consortium of more than one (possibly all 4) of these candidate pathogens can be considered the ‘primary’ pathogen of WS in this instance. Only one of these candidate pathogens has been implicated in WS before, the ciliate Philaster lucinda (Sweet & Bythell 2012), which remains the only specific pathogen associated with the disease in all cases studied to date. However, as we have recently concluded for WBD in Caribbean acroporas, Philaster lucinda is more likely to be a ‘secondary’ pathogen contributing to pathogenesis and not a primary pathogen as the lesion continued to progress even though the ciliate was reduced to undetectable levels in the metronidazole treatment.

To date, the histophagous ciliate, Philaster lucinda, has not been detected in association with healthy corals in the natural environment, yet has been shown to be consistently present in the neighbouring reef environment, particularly associated with numerous marine algal species (Sweet et al. 2013b). It is therefore possible that they remain in these nearby reservoirs until the coral becomes compromised. With this in mind and the fact that two of the antibiotics utilized caused the lesion progression to cessate, the primary pathogen, at least in this instance, appears to be one or a combination of up to three of the bacterial agents. In the absence of the histophagous ciliate, these bacteria cause a degree of tissue necrosis that promotes lesion progression. In the natural disease state, these compromised tissues are apparently consumed by ciliates before necrosis occurs. However, without fine‐scale temporal sampling at the initiation of infection, it cannot be determined whether prior physical disruption by ciliates, or some other primary agent, may allow these specific bacterial agents to infect the tissues, and they may actually still be secondary agents, in a complicated disease process.

In this study, transmission electron microscopy showed the appearance of stress associated with the coral's symbiotic algae in progressive lesions but not in healthy tissues or those treatments which successfully stopped the disease. The symbiotic algae are a vital part of the coral holobiont and dysfunctional or damaged symbionts appear to be part of the aetiology of this disease. Damage to the symbionts may represent an additional stress to the coral and potentially provide a vicious cycle, further reducing host defences. This result, in which the algae are shown to be affected by the disease, is again similar to our recent study on WBD in the Caribbean acroporids.

The general absence of a significant population of bacteria and a lack of bacterial‐induced necrosis at the disease lesion interface of WS and similar ‘white diseases’ (Ainsworth et al. 2007; Work & Aeby 2011; Sweet & Bythell 2012) have been paradoxical to the finding of multiple bacterial causal agents for the disease by challenge experiments and culture‐independent studies (Ben‐Haim & Rosenberg 2002; Denner et al. 2003; Barash et al. 2005; Gil‐Agudelo et al. 2006; Pantos & Bythell 2006; Luna et al. 2010; Kline & Vollmer 2011; Sweet & Bythell 2012). This finding was also reflected in the present study. The altered histopathology that occurred in the metronidazole treatment may be explained by the lack of ciliates associated with this treatment, which would otherwise have consumed the tissues before necrosis could be detected. In the metronidazole‐treated corals, we were also able to locate numerous rod‐shaped bacteria associated with these fragmented tissues. This may explain why previous studies have failed to find bacteria associated with WS lesions, as infected tissues are rapidly consumed by the ciliates.

One further finding of note is the presence of Bacteriovorax in healthy tissues but absent in diseased samples. Bacteriovorax are predatory bacteria whose presence in host organisms is thought to shape the natural microbial community through trophic interactions (Thurber et al. 2009; Chen et al. 2012). Particularly, Bacteriovorax are known to prey on Gram‐negative bacteria such as members of the genus Vibrio. Its dynamics may therefore be of importance in maintaining a healthy population of microbes, and its subsequent absence in diseased tissues may then allow for pathogenic bacteria to infect (Chen et al. 2012).

Although detection of viruses was not a focus of this study, two main types were observed to be associated with the samples. One, circular, electron dense cored capsid VLP was consistently found in all sample types and appeared to be associated with the coral's symbiotic algae. Similar VLPs have previously been reported in Acropora hyacinthus (Pollock et al. 2014) and found in both healthy and diseased tissues. In contrast, the occurrence of a unique, larger VLP only present in metronidazole‐treated samples warrants further investigation. While this result is not sufficient to imply a role in disease causation, an increasing number of studies are showing the presence of viruses associated with disease lesions (Lohr et al. 2007; Lawrence et al. 2014a,b; Pollock et al. 2014; Yvan et al. 2014) and their role as a potential pathogen requires further study. However, interestingly, the study by Lawrence et al. (2014b) also highlighted the presence of ciliates within the diseased tissues of corals showing signs of Porites tissue loss (PorTL), a disease that fits within the generic description of WS disease.

Significant questions remain over the similarity between WS in the Indo‐Pacific and WBD in the Caribbean and between geographically and temporally separated WS cases. All these diseases are associated with the specific ciliate Philaster lucinda, and it remains the only agent with direct evidence for involvement in pathogenesis as it has been observed to consume intact coral tissues at the lesion interface (Sweet & Bythell 2012). However, we can conclude that the ciliate is a secondary pathogen due to its responses to antibiotic treatment. The diseases are also associated with a specific bacterial consortium that is absent in healthy coral and present in every case of the disease observed at any particular site. Thus, there is no distinction between WBD in the Caribbean and the equally variable geographical presentation of WS in the Pacific, either in associated microbial communities, histopathology or visible disease signs. The question then remains as to whether the different white syndromes and WBD consist of separate types of disease or are a single disease. It is possible that they are clearly separate diseases, caused by specific bacteria, but that the secondary, specific ciliate pathogen and other nonspecific pathogens cause disease signs that are indistinguishable. The fact that none of the specific agents associated with WS in Fiji in this study were previously detected in corals showing signs of WS in the GBR or Solomon Islands (Sweet & Bythell 2012) might suggest that they are separate diseases associated with specific pathogens. However, it is also possible that the bacterial infections are nonspecific and opportunistic (Lesser et al. 2007) and that any of a wide range of potential pathogens can act to cause initial infection and weaken host defences to allow the ciliate pathogens to invade. However, the fact that the bacterial consortium associated with the disease is so consistent between cases (sometimes separated by several km) and that none of these agents can be detected in healthy coral, even with deep sequencing, suggests that WS is not a completely nonspecific infection. Whatever the case, these diseases are certainly polymicrobial diseases, not only with bacteria and ciliates playing different roles in pathogenesis, but with multiple, specific bacterial associates consistently associated with the disease at a particular location and time. Further work is needed to determine whether this is simply a result of the ‘beta diversity’ associated with coral reef environments (whatever specific bacterial pathogens are available in the environment at any one time cause the disease) or whether specific disease consortia are associated with a number of specific diseases. It is also possible that the disease consortia are continually changing, possibly in response to changes in the host defences. This latter hypothesis differs from the hologenome theory of coral disease evolution (Rosenberg et al. 2007) in that changes in microbial consortia rather than individual pathogen selection and evolution would be required to enable coral diseases to persist in the environment.

Just to bring a little light heartedness to this thread which, by the way, I've been following since the onset;
this is easily the longest single comment I've seen in any thread! So, you've got that going for you!

 

[MnFish1]

Forgetting anol

Well, I was just making a point. You really didn’t understand what you were taking about even though you google it. It’s ok though. Let’s move on.

Im beginning against all odds that you are some kind of plant here. I understood completely what I was talking about. should I call the mods or reefsquad to help as you did previously - what the heck are you talking about here seriously?

 

[MnFish1]

Discussion
Selective elimination of candidate pathogens using a variety of antibiotics in controlled experiments can aid in the identification of specific roles of these organisms with respect to disease causation. This study shows that the specific form(s) of WS sampled in this study were the result of a polymicrobial disease associated with a number of potential pathogens (15 bacteria and 7 ciliates identified in this study) that were consistently associated with all samples of disease and absent from healthy samples. This result supports previous studies on WS (Sussman et al. 2008; Luna et al. 2010; Sweet & Bythell 2012) as well as others such as white plague (Denner et al. 2003; Pantos et al. 2003; Bythell et al. 2004; Barash et al. 2005; Efrony et al. 2009; Atad et al. 2012) and black band disease (Cooney et al. 2002; Frias‐Lopez et al. 2003) which show multiple specific associates of any given diseased state. The combined elimination of three bacteria and one ciliate ribosomal type from this group of potential pathogens resulted in immediate and complete cessation of disease lesion progression, strongly indicating that one or a consortium of more than one (possibly all 4) of these candidate pathogens can be considered the ‘primary’ pathogen of WS in this instance. Only one of these candidate pathogens has been implicated in WS before, the ciliate Philaster lucinda (Sweet & Bythell 2012), which remains the only specific pathogen associated with the disease in all cases studied to date. However, as we have recently concluded for WBD in Caribbean acroporas, Philaster lucinda is more likely to be a ‘secondary’ pathogen contributing to pathogenesis and not a primary pathogen as the lesion continued to progress even though the ciliate was reduced to undetectable levels in the metronidazole treatment.

To date, the histophagous ciliate, Philaster lucinda, has not been detected in association with healthy corals in the natural environment, yet has been shown to be consistently present in the neighbouring reef environment, particularly associated with numerous marine algal species (Sweet et al. 2013b). It is therefore possible that they remain in these nearby reservoirs until the coral becomes compromised. With this in mind and the fact that two of the antibiotics utilized caused the lesion progression to cessate, the primary pathogen, at least in this instance, appears to be one or a combination of up to three of the bacterial agents. In the absence of the histophagous ciliate, these bacteria cause a degree of tissue necrosis that promotes lesion progression. In the natural disease state, these compromised tissues are apparently consumed by ciliates before necrosis occurs. However, without fine‐scale temporal sampling at the initiation of infection, it cannot be determined whether prior physical disruption by ciliates, or some other primary agent, may allow these specific bacterial agents to infect the tissues, and they may actually still be secondary agents, in a complicated disease process.

In this study, transmission electron microscopy showed the appearance of stress associated with the coral's symbiotic algae in progressive lesions but not in healthy tissues or those treatments which successfully stopped the disease. The symbiotic algae are a vital part of the coral holobiont and dysfunctional or damaged symbionts appear to be part of the aetiology of this disease. Damage to the symbionts may represent an additional stress to the coral and potentially provide a vicious cycle, further reducing host defences. This result, in which the algae are shown to be affected by the disease, is again similar to our recent study on WBD in the Caribbean acroporids.

The general absence of a significant population of bacteria and a lack of bacterial‐induced necrosis at the disease lesion interface of WS and similar ‘white diseases’ (Ainsworth et al. 2007; Work & Aeby 2011; Sweet & Bythell 2012) have been paradoxical to the finding of multiple bacterial causal agents for the disease by challenge experiments and culture‐independent studies (Ben‐Haim & Rosenberg 2002; Denner et al. 2003; Barash et al. 2005; Gil‐Agudelo et al. 2006; Pantos & Bythell 2006; Luna et al. 2010; Kline & Vollmer 2011; Sweet & Bythell 2012). This finding was also reflected in the present study. The altered histopathology that occurred in the metronidazole treatment may be explained by the lack of ciliates associated with this treatment, which would otherwise have consumed the tissues before necrosis could be detected. In the metronidazole‐treated corals, we were also able to locate numerous rod‐shaped bacteria associated with these fragmented tissues. This may explain why previous studies have failed to find bacteria associated with WS lesions, as infected tissues are rapidly consumed by the ciliates.

One further finding of note is the presence of Bacteriovorax in healthy tissues but absent in diseased samples. Bacteriovorax are predatory bacteria whose presence in host organisms is thought to shape the natural microbial community through trophic interactions (Thurber et al. 2009; Chen et al. 2012). Particularly, Bacteriovorax are known to prey on Gram‐negative bacteria such as members of the genus Vibrio. Its dynamics may therefore be of importance in maintaining a healthy population of microbes, and its subsequent absence in diseased tissues may then allow for pathogenic bacteria to infect (Chen et al. 2012).

Although detection of viruses was not a focus of this study, two main types were observed to be associated with the samples. One, circular, electron dense cored capsid VLP was consistently found in all sample types and appeared to be associated with the coral's symbiotic algae. Similar VLPs have previously been reported in Acropora hyacinthus (Pollock et al. 2014) and found in both healthy and diseased tissues. In contrast, the occurrence of a unique, larger VLP only present in metronidazole‐treated samples warrants further investigation. While this result is not sufficient to imply a role in disease causation, an increasing number of studies are showing the presence of viruses associated with disease lesions (Lohr et al. 2007; Lawrence et al. 2014a,b; Pollock et al. 2014; Yvan et al. 2014) and their role as a potential pathogen requires further study. However, interestingly, the study by Lawrence et al. (2014b) also highlighted the presence of ciliates within the diseased tissues of corals showing signs of Porites tissue loss (PorTL), a disease that fits within the generic description of WS disease.

Significant questions remain over the similarity between WS in the Indo‐Pacific and WBD in the Caribbean and between geographically and temporally separated WS cases. All these diseases are associated with the specific ciliate Philaster lucinda, and it remains the only agent with direct evidence for involvement in pathogenesis as it has been observed to consume intact coral tissues at the lesion interface (Sweet & Bythell 2012). However, we can conclude that the ciliate is a secondary pathogen due to its responses to antibiotic treatment. The diseases are also associated with a specific bacterial consortium that is absent in healthy coral and present in every case of the disease observed at any particular site. Thus, there is no distinction between WBD in the Caribbean and the equally variable geographical presentation of WS in the Pacific, either in associated microbial communities, histopathology or visible disease signs. The question then remains as to whether the different white syndromes and WBD consist of separate types of disease or are a single disease. It is possible that they are clearly separate diseases, caused by specific bacteria, but that the secondary, specific ciliate pathogen and other nonspecific pathogens cause disease signs that are indistinguishable. The fact that none of the specific agents associated with WS in Fiji in this study were previously detected in corals showing signs of WS in the GBR or Solomon Islands (Sweet & Bythell 2012) might suggest that they are separate diseases associated with specific pathogens. However, it is also possible that the bacterial infections are nonspecific and opportunistic (Lesser et al. 2007) and that any of a wide range of potential pathogens can act to cause initial infection and weaken host defences to allow the ciliate pathogens to invade. However, the fact that the bacterial consortium associated with the disease is so consistent between cases (sometimes separated by several km) and that none of these agents can be detected in healthy coral, even with deep sequencing, suggests that WS is not a completely nonspecific infection. Whatever the case, these diseases are certainly polymicrobial diseases, not only with bacteria and ciliates playing different roles in pathogenesis, but with multiple, specific bacterial associates consistently associated with the disease at a particular location and time. Further work is needed to determine whether this is simply a result of the ‘beta diversity’ associated with coral reef environments (whatever specific bacterial pathogens are available in the environment at any one time cause the disease) or whether specific disease consortia are associated with a number of specific diseases. It is also possible that the disease consortia are continually changing, possibly in response to changes in the host defences. This latter hypothesis differs from the hologenome theory of coral disease evolution (Rosenberg et al. 2007) in that changes in microbial consortia rather than individual pathogen selection and evolution would be required to enable coral diseases to persist in the environment.

Frankly this is mumbo jumbo - there is a lot of information - which none of us (including me) wants to read. But it doesnt suggest you're correct in any sense.

 

[Reefahholic]

I think this answers one of my questions:

In the metronidazole‐treated corals, we were also able to locate numerous rod‐shaped bacteria associated with these fragmented tissues. This may explain why previous studies have failed to find bacteria associated with WS lesions, as infected tissues are rapidly consumed by the ciliates.

 

[MnFish1]

But in the microscopic videos they are clearly observed by themselves munching on the coral in swarms. So let’s say they’re a secondary cause of RTN and the primary is a bacterial infection that really only cause very minimal damage. Then these guys come in like piranha and completely devour the corals. Even though they’re not causal agents it seems to me that they would be the greater threat.

I’m not worried about the fuse burning on a stick of dynamite...I’m worried about the explosion!

I think you have a secondary agenda - its probably my mistake - but your lack of objectivity surprises me

 

[MnFish1]

I think this answers one of my questions:

In the metronidazole‐treated corals, we were also able to locate numerous rod‐shaped bacteria associated with these fragmented tissues. This may explain why previous studies have failed to find bacteria associated with WS lesions, as infected tissues are rapidly consumed by the ciliates.

and this came fromwhere?

 

[CJS80]

The altered histopathology that occurred in the metronidazole treatment may be explained by the lack of ciliates associated with this treatment, which would otherwise have consumed the tissues before necrosis could be detected. In the metronidazole‐treated corals, we were also able to locate numerous rod‐shaped bacteria associated with these fragmented tissues. This may explain why previous studies have failed to find bacteria associated with WS lesions, as infected tissues are rapidly consumed by the ciliates.

I believe he is referencing this statement from this article. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4964940/

 

[Frogger]

I am naturally skeptical when I hear something that is too good to be true. I will reserve judgement on this product until further information from other sources is available.

"Build a better mousetrap and the world will beat a path to your door". If indeed this product works as good as the good doctor says we will hear about all the successes soon enough.

There is nothing wrong with after spending time doing research selling a product to make the research worth while. You can't really expect someone to do it for free. Almost every medical drug breakthrough is the result of this process.

 

[Nami]

Going by this concept, wouldn't this imply that if I start a new tank, with fresh RODI saltwater and grow a single piece of acro inside, it is very unlikely to get rtn/stn since there is very low chance of the parasite being introduced.

 

[Jose Mayo]

"Build a better mousetrap and the world will beat a path to your door". If indeed this product works as good as the good doctor says we will hear about all the successes soon enough.

There is nothing wrong with after spending time doing research selling a product to make the research worth while. You can't really expect someone to do it for free. Almost every medical drug breakthrough is the result of this process.

In fact, there is nothing wrong with making money ... as long as you deliver what you promised in exchange for the money.

There is also nothing wrong with sharing with others, even without receiving money, something that our feeling says can benefit everyone and that, for us, also came from other sources without giving money, such as the knowledge we receive and transmit in the forums of the whole world ... humans are like this; we are often only supportive, others only self-seeking.

Regarding the issue of this topic, considering that a solution is offered for payment, what I think is of interest to us as a probable consumer, is not to pay to see but to pay for what is seen, proven and accepted.

Regards

 

[Reefahholic]

In fact, there is nothing wrong with making money ... as long as you deliver what you promised in exchange for the money.

There is also nothing wrong with sharing with others, even without receiving money, something that our feeling says can benefit everyone and that, for us, also came from other sources without giving money, such as the knowledge we receive and transmit in the forums of the whole world ... humans are like this; we are often only supportive, others only self-seeking.

Regarding the issue of this topic, considering that a solution is offered for payment, what I think is of interest to us as a probable consumer, is not to pay to see but to pay for what is seen, proven and accepted.

Regards

Agreed

I think we need to start looking around at 100X+. It's just hard for me to believe that something of that size would even come close to RTN of a full Acropora colony in 24 hrs. I don't think the numbers are there either.

In a lot of these studies you hear...

In most cases....
It's likely...
Most probably...
It appears to be...

All this means to me is that they still don't know what's going on. That one study that was quoted above and below found 16 suspects. Out of those 16 the Philaster L. ciliate's were the most consistent microorganisms present. Even in the studies they point out that they've been caught eating live tissue, dead tissue, and zooxanthellae. It's one of the only suspects caught eating live coral tissue, but then they rule the Philaster's out.?? But remember....they misidentified one of the pathogens. I just don't trust the study. Not to mention they used a Transmission Electron Microscope. This is roughly a $95,000 microscope that offers the most powerful magnification- potentially over one million times or more than a compound microscope and yet they can't identify if one of the 14 bacteria's found was the causation.? This is hard to believe.

Can anybody remember from reading any of these studies where it actually mentions what's eating intact coral tissue other than the Philaster Lucinda? Please site the source below. Here's the source stating what I've just written:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4964940/

All these diseases are associated with the specific ciliate Philaster lucinda, and it remains the only agent with direct evidence for involvement in pathogenesis as it has been observed to consume intact coral tissues at the lesion interface (Sweet & Bythell 2012).