This Month in Blastocystis Research - AUG 2016

Last month, I asked about your thoughts on Blastocystis and age... is age a limiting factor with regard to the susceptibility to infection/colonisation? One of the reasons why I asked is that we and others have noted that Blastocystis becomes more and more common with age... at least until a certain stage in life (adulthood) and at least in certain countries.

Among the answers I got, I'd like to highlight one from Dr Graham Clark, London School of Hygiene and Tropical Medicine, with whom I've had the tremendous privilege of working for more than 10 years. Dr Clark writes:

In my opinion, prevalence is a mixture of three things: exposure, immunity and ‘loss’.

To illustrate the latter, infection with Entamoeba histolytica (and probably other Entamoeba species) can be lost spontaneously with a half-life of 13 months (in one study at least, Blessmann et al. 2003 J Clin Micro). There is no evidence that immunity is involved, just chance. Extrapolating to Blastocystis, I suspect the same is true – loss can occur spontaneously but what the half-life of colonisation is we have no idea and it would be difficult to evaluate without high resolution genotyping (which is what we used in E. histolytica). If you had a population of infected individuals that were followed over time and a high res[olution] typing method you could calculate rates of loss and of new infections, as we did for E. histolytica.

I do not think there is any evidence for immunity to Blastocystis infection, which leaves exposure. If the rate of exposure is greater than the rate of spontaneous loss then you would get an increase in prevalence with age. I suspect (hope!) exposure is higher in children for behavioural reasons than in adults so you will get a levelling out of prevalence with age to a point where the rate of new infection balances the rate of spontaneous loss. If exposure stays high then this plateau may not be reached.

So why are other parasites different? Probably there is immunity leading to clearance of the infection in children.

Certainly, we have quite good data from Ireland indicating that once established, Blastocystis will keep colonising the GI tract for ages (i.e., many years). Regarding loss, I hope that I'll soon be able to refer to some data that we have obtained in a study on experimental animals.

Exposure is obvisouly something to think about - Blastocystis is transmitted by ingesting food/drink contaminated with Blastocystis and/or improper hygiene. The fact remains that studies using molecular methods for detection have identified most children in Sub-Saharan African study populations as being colonised, while in more developed countries, parasites such as Dientamoeba fragilis are more common in toddlers and smaller children; Blastocystis emerges and gains in prevalence only in teenagers and older individuals... roughly speaking.

One aspect of colonisation that I've been very interested in myself, is whether it's each individual's gut microbiota that "decides" whether Blastocystis colonisation/infection establishes upon exposure. We are seeing some data emerging from a couple of labs on this, and maybe next month I'll be able to bring you up to speed in this matter. To my knowledge, there is not a lot of precedence–if any–for such a situation, but the fact that we have seen quite clear differences in gut microbiota patterns between those who have Blastocystis and those who have not, has left me thinking...

If you want to contribute to the discussion, please drop a line. 

References:

Blessmann, J., Ali, I., Ton Nu, P., Dinh, B., Ngo Viet, T., Le Van, A., Clark, C., & Tannich, E. (2003). Longitudinal Study of Intestinal Entamoeba histolytica Infections in Asymptomatic Adult Carriers Journal of Clinical Microbiology, 41 (10), 4745-4750 DOI: 10.1128/JCM.41.10.4745-4750.2003

Scanlan PD, Stensvold CR, Rajilić-Stojanović M, Heilig HG, De Vos WM, O'Toole PW, & Cotter PD (2014). The microbial eukaryote Blastocystis is a prevalent and diverse member of the healthy human gut microbiota. FEMS microbiology ecology, 90 (1), 326-30 PMID: 25077936

This Month in Blastocystis Research - Interactive Edition

What are your thoughts on Blastocystis carriage and age?

More and more data suggest that the prevalence of Blastocystis carriage increases by age - at least to a certain point.

Some intestinal parasites, such as Cryptosporidium, may not be that uncommon in infants/very young toddlers, while they are much less common in older children and adolescents. Other parasites appear to peak in prevalence around the age of 7, e.g., Dientamoeba fragilis.

Meanwhile, Blastocystis appear to increase in prevalence by age until mature adulthood... why is that? And what does it tell us? Please comment! I'm not having all the answers to these questions myself, and if some interesting suggestions pop up, I'll post them! You only need a Google account to be able to comment. If you don't have one, please send your comment using

crs[at]blastocystis.net 

For those interested in Blastocystis carriage in association with age, I have listed a couple of relevant recent studies below.

References:

Forsell J, Granlund M, Samuelsson L, Koskiniemi S, Edebro H, & Evengård B (2016). High occurrence of Blastocystis sp. subtypes 1-3 and Giardia intestinalis assemblage B among patients in Zanzibar, Tanzania. Parasites & Vectors, 9 (1) PMID: 27356981  

Poulsen CS, Efunshile AM, Nelson JA, & Stensvold CR (2016). Epidemiological Aspects of Blastocystis Colonization in Children in Ilero, Nigeria. The American Journal of Tropical Medicine and Hygiene, 95 (1), 175-9 PMID: 27139454

This Month in Blastocystis Research (JUN 2016) - FMT Edition

From time to time, I've been touching upon the concept of faecal microbiota transplantion (FMT) in my blog posts. Now, there is a chance to familiarize yourself a lot more with this therapeutic approach to treating recurrent Clostridium difficile infection and other types of gastrointestinal diseases.

In my opinion, one of the more interesting aspects of FMT is to obtain knowledge about what microbes are actually being transferred (what microbes are allowed in stool selected for FMT?), and what are in fact the components in faecal transplants resulting in the high treatment success rates generally observed?

I dedicate this month's post to the launching of an online course in Faecal Microbiota Transplantation (FMT) supported and developed by United European Gastroenterology (UEG) in collaboration with leading Italian gastroenterologists, including Dr Gianluca Ianiro, who was recently appointed as a new member of the UEG Young Talent Group. I was lucky to involved in the editing of the course.

Targeted learners include not only gastroenterologists, but also endoscopists, internists, paediatricians, endocrinologists, surgeons, infectious disease specialists and clinical microbiologists who are interested in gut microbiota and who deal with diseases associated with gut microbiota perturbation (recurrent CDI, IBD, IBS, obesity, diabetes and other metabolic disorders).

If you wish to take the course, it can be accessed through your myUEG account.

For general information about UEG, please go here. And for more information on UEG Education, please go here.

This Month in Blastocystis Research (MAY 2016)

Very much belated, I'm back to give you the MAY entry of the 2016 "This Month in Blastocystis Research" blog series.

I'm basically just going to highlight a few papers and some other interesting things.

Ever since our metagenomics paper came out, it's as if the interest in Blastocystis in a gut microbiota context is exploding. If you put "Blastocystis microbiota" into the search box in PubMed, today you will get 20 hits, most of which papers are extremely interesting and of course very central to this type of research. Given the number of times I've addressed the relevance of studying Blastocystis in relation to gut microbiota diversity on this blog, I'll try not to flog it to death this time!

Over at Gut Microbiota For Health, a blog was posted a week ago summarising the recent findings of Audebert and colleagues and comparing them to data coming out from our lab. You can read the blog here. Using the Ion Torrent PGM sequencing platform, 16S rDNA gene sequencing was performed on genomic DNAs extracted from Blastocystis-positive and - negative stool samples. What Audebert hypothesised was that if Blastocystis is associated to intestinal disease such as for instance diarrhoea, one would expect to find a higher degree of microbiota perturbation (dysbiosis) in Blastocystis carriers than in non-carriers. Meanwhile, and similar to what we have have published, they reported that gut microbiota diversity is higher in Blastocystis carriers than in non-carriers, indicating that Blastocystis is generally a marker of a healthy gut microbiota rather than a perturbed one. Again similar to what we found in the metagenomics paper, Audebert et al. saw that the bacterial families Ruminococcaceae and Prevotellaceae were also more abundant in carriers than in Blastocystis-negative patients, while Enterobacteriaceae were enriched in Blastocystis-negative patients. What is also really interesting is the fact that the genera Faecalibacterium and Roseburia had a significantly higher abundance in Blastocystis-positive patients. These genera contain bacteria that produce butyrate which has a lot of important and beneficial functions. Loss of butyrate producers is seen for instance in patients with inflammatory bowel disease. The group used some of the same methods as we used in our study presented recently at ECCMID, including rarefaction analysis and calculation of Chao1 indices.

Together with colleagues at the Technical University of Denmark, we were lucky to have The European Journal of Clinical Microbiology and Infection publish our novel data on associations between common single-celled intestinal parasites--Blastocystis and Dientamoeba--and groups of intestinal bacteria, as evidenced by qPCR assays. We confirmed the findings from our metagenomics study, by finding a relatively lower abundance of Bacteroides in the parasite-positive samples than in the -negative ones.

By the way, on the Gut Microbiota For Health site you will find an e-learning course on Microbiota provided by the Gut Microbiota and Health Section of the European Society of Neurogastroenterology and Motility (ESNM) and developed for gastroenterologists.

Speaking of e-learning and gastroenterology: For a couple of years, I've had the immense pleasure of being part of the United European Gastroenterology e-learning task force. We host a resource - UEG Education - developed mainly for gastroenterologists, boasting e-learning courses, "Decide-on-the-Spot" series, "Mistakes in..." series, blogs, and other features. I have included a UEG widget in the right side bar of my blog - please click it!

Back to Blastocystis! Graham Clark and I published a personal view on the current status of Blastocystis in Parasitology International, in which we summarise the development and recent advances in Blastocystis research. The article is expected to form part of a special section/issue dedicated to Blastocystis to commemorate last year's 1st International Blastocystis Symposium in Ankara.

My colleague Juan-David Ramirez and his colleauges published data from a subtyping study from South America including 346 samples. More than 85% of the subtypes found belonged to either ST1, ST2, and ST3 as expected, while the rest belonged to ST4, ST5, ST6, ST7, ST8, ST12 and what they call a new subtype. I think this is the first time ST12 has been reported in humans. Despite the fact that the authors accounted for the databases that they used for subtype and allele calling, there is no mention on the criteria by which the subtypes were called in the NCBI database (i.e., in those cases where no hits could be found at the online Blastocystis database). For instance, what level of similarity was used to identify three samples as ST12? On the same note, which level of similarity was used to identify nine samples as belonging to a "novel subtype" (also, - was it the same sequence across the nine samples?). When dealing with a potentially novel subtype, usually the entire SSU rRNA gene is seqeunced and subjected to phylogenetic analysis, and sequences have not yet been made public in GenBank, so there is no possibility to work with the data so as to validate the findings (which are highly accurate, I'm sure). I think this information is critical to interpreting the data. Nontheless, the work that went into the sampling and the lab work should be highly accredited.

References:

Andersen LO, Bonde I, Nielsen HB, & Stensvold CR (2015). A retrospective metagenomics approach to studying Blastocystis. FEMS microbiology ecology, 91 (7) PMID: 26130823

Audebert C, Even G, Cian A, Blastocystis Investigation Group, Loywick A, Merlin S, Viscogliosi E, & Chabé M (2016). Colonization with the enteric protozoa Blastocystis is associated with increased diversity of human gut bacterial microbiota. Scientific reports, 6 PMID: 27147260  

O'Brien Andersen L, Karim AB, Roager HM, Vigsnæs LK, Krogfelt KA, Licht TR, & Stensvold CR (2016). Associations between common intestinal parasites and bacteria in humans as revealed by qPCR. European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology PMID: 27230509 

Ramírez JD, Sánchez A, Hernández C, Flórez C, Bernal MC, Giraldo JC, Reyes P, López MC, García L, Cooper PJ, Vicuña Y, Mongi F, & Casero RD (2016). Geographic distribution of human Blastocystis subtypes in South America. Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases, 41, 32-5 PMID: 27034056

Stensvold CR, & Clark CG (2016). Current status of Blastocystis: A personal view. Parasitology international PMID: 27247124