A review of Sutherland, K.P., Shaban, S., Joyner, J.L., Porter, J. & Lipp, E.K., (2011), Human Pathogen Shown to Cause Disease in the Threatened Eklhorn Coral Acropora palmata, PloS one.
Acropora palmata, one of the most common coral in the Caribbean has become critically endangered. This is largely due to the disease acroporid serratiosis (APS), known as white pox, which is unique to this coral species. It is caused by the bacterium Serratia marcescens, an opportunistic human pathogen that has been associated with waterborne infections in tropical freshwaters. During an outbreak in 2003, one strain of S.marcescens, strain PDR60, was observed on diseased A.palmata and in untreated human sewage, as well as on several non-host corals, suggesting a link between the coral disease and wastewater.
APS has satisfied Koch’s postulates, however only with the strain PDL100. The authors attempt to determine that PDR60 is a coral pathogen by using challenge experiments. They inoculated 8 isolates of Serratia marcescens of 3 different strains, from offshore reefs and wastewater in Florida Keys, onto healthy A.palmata fragements, to determine infectivity. They also wanted to establish whether humans are the source and if other marine invertebrates acted as reservoirs of the pathogen.
Their results confirmed strain PDR60 as a coral pathogen as it satisfied Koch’s postulates. When the disease occurred, the coral began by releasing mucus which reduced water clarity and had a distinct smell. This was followed by a tissue bleb adjacent to the inoculation region and lastly, the tissue lifting off the skeleton in stringy fragments. This whole process was completed in 24hours.
They found the same effects on A.palmata inoculated with strains from wastewater and from non-host corals and snails. The only variation was the degree of pathogenic effect. For example, strain PDR60 from wastewater caused disease signs in 4-10 days, whereas strains from non-host corals showed a more delayed pathogenic effect, taking around 20 days to show signs. These results confirm that non-host coral and snails, who are not affected by the pathogen, act as interepizootic reservoirs or vectors for the disease, which is later transferred to other coral through release of pathogen-containing layers of the coral. Moreover, it confirms that strains found to cause the disease in as little as 4 days, are found in human wastewater and that we infact are a source of the disease.
Interestingly, A.palmata inoculated with an isolate from APS-affected corals remained healthy for the entire of the experiment, showing that this isolate of strain PDR60 is non-virulent or that the corals used were resistant to APS. Previous studies looking at strain PDL100 and also V.shiloi have suggested evidence for the evolution of hosts resistant to these pathogens.
Overall, a really good study with clear, convincing results that expand our understanding of APS transmission and factors that drive its emergence in the marine environment. It also establishes humans as the source and provides vital results to support ongoing improvements to wastewater treatments and urge large parts of the Caribbean to begin taking action against untreated waste, to help protect the reef ecosystems. It would be interesting for further studies to look at host resistance or susceptibility to the pathogen. Also previous work has found that strain PDL100 is not well adapted to the marine environment and can only persist for 15hours. However, survival and proliferation was observed when it is in the A.palmata surface mucopolysaccharide layer, where it survived for 11 days. It would be interesting to expand on this mechanism too.
4 comments:
Normally we talk about zoonotic diseases being passed along from wildlife to humans, I thought it was really interesting how this study changed the dynamics of the system, showing humans passing on diseases to wildlife instead. They refer to it as 'reverse zoonosis' and point out that its all the more interesting as it involves the jump of a pathogen from vertebrate to invertebrate and terrestrial to marine.
Hi Jelena
I was just wondering if the authors said what caused the different time periods for infection to show from different sources? Is it a result of different number of cells being present? For example, non-host carol strains had far less cell numbers than wastewater. Or was it always different strains?
Lee
Hi Lee,
Sorry about the late reply, lack of internet at the moment!
The paper doesn't go into too many details about the different time periods. It just says this showed the difference in infectivity and virulence of the strains, as for example they found that coral was resistant to some of the strains. The examples they gave on the varying time periods focused on the different strains on the different hosts, so I'm going to assume that it is to do with them rather then cell count.
From their results they did also suggest that stressors other than S.marcescens infection can contribute to tissue loss, so perhaps this could have been a factor seeing as they kept the corals in different control environments.
Hope you had a good Christmas!
Jelena
I think the most important feature of this paper is that thauthors went to considerable lengths to follow the genetic makeup of the strains - they used PFGE as a genetic fingerprinting technique. What they haven't yet explained is why this particular strain is able to establish itself in a marine host (and in the coral grazing snails as a reservoir) - which is the core of their 'reverse zoonosis' concept.
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