Showing posts with label polyparasitism. Show all posts
Showing posts with label polyparasitism. Show all posts

Sunday, March 16, 2014

What's In A Name?

When people have had their stools examined and are told that they have Blastocystis, most of them will not have a clue about what that is. And eventually they'll be told that it's a parasite. A parasite? As in tapeworm? Ok it's not. But then what? As in malaria? Oh... ok, I see... So it's....? Huh? As in ... what???

Now, which are those parasites in and on your body, and what in fact makes a parasite? Depends on who you ask. For parasitologists and public health/clinical microbiologists, a parasite means something along the lines of a eukaryotic organism (i.e. not a bacterium and not a virus) that is not a fungus and that is capable of living and maybe even multiplying on or inside another organism. Some organisms are considered somewhere in between parasites and fungi, such as microsporidia and Pneumocystis. But whether an organism is a fungus or a parasite is not important in most cases. You will also sometimes see that 'parasite' is used as a term meant to cover living organisms causing disease, and in this sense the term may include for instance bacteria and viruses; for instance. A lot of research deals with 'host-parasite' relationships, evolution of virulence and tolerance in parasites and hosts, respectively; also here, bacteria may be referred to as parasites.

 Mosquitos are practically parasites that may transmit other parasites. Source (eyeweed on Flickr).

The word 'parasite' stems from Greek, and means something like 'eating beside' or 'eating at someone else's table'. Parasitism is a non-mutual symbiotic relationship where one organism (the parasite) benefits at the expense of another (the host).

People like me usually divide parasites (sensu stricto) into protozoa (single-celled) and helminths (multi-cellular; worms). Effectively, this should be protists and helminths, since not all single-celled parasitic eukaryotes are protozoa. Please note that most protists and helminths (the nematode fraction) are free-living, - but some have adapted a parasitic life style and very effectively so.

So, when we're told by doctors that we are in fact hosting parasites, - how do we react? I guess  some of us will be quite alarmed: Creatures eating defenseless hosts from within, castrating them and turning them into zombies come to our minds, for instance Sacculina, Dicrocoelium, and Leucochloridium, just to mention a few ones (if you're not familiar with these ones, I suggest you look them up - you will hardly believe what they are capable of doing, and despite the horrifying subtlety and cold-bloodedness with which these creatures operate, one can hardly help marveling on how cunningly evolution makes way for some organisms' ability to exploit others). Other parasites are known to cause less spectacular phenotypic changes while having huge consequences for human health and disease: Malaria continues to be a significant cause of morbidity and mortality in many larger regions, and recently, diarrhoea caused by species of Cryptospordium was recognised as one of the most significant health issues in infants and toddlers in select sentinel areas sub-Saharan Africa and South Asia.

Some parasites, however, are commensals (ie. they just sit there with a more or less neutral outcome) or even beneficial to the host; for instance, there's evidence of ciliates assisting herbivores in metabolising cellulose. So while, these organisms from one point of view are parasites, the hole symbiotic relationship between these protozoa and herbivores may be seen as mutualistic. Maybe this particular relationship started out as 'parasitsm' but developed into 'mutualism'? There may be a lot more examples of this. Animals usually host various types of parasites, and humans probably used to host a much larger zoo of parasites than many of us do today; what is the public health significance of the recent and rapid 'defaunation' of humans in certain parts of the world?

At least technically, Blastocystis is also a parasite: Sitting in the colon, it lives on food delivered by its host, and thereby it certainly eats at someone else's table. Moreover, the parasite is probably not capable of completing its life cycle without a host. But what does it do apart from eating? Does it do us any good just like the ciliates in the herbivores? Blastocystis has co-evolved with humans (and other host species) and maybe humans have learned to exploit Blastocystis so that it's not only Blastocystis exploiting us? Does Blastocystis compete with other organisms in the gut? Does it secrete substances that impact other organisms including the host, and if so, in what way? What's its impact on the immune system? Etc.

I guess the take-home message here is that 'parasite' is just a word, - a name for something, and there are examples of parasitism turning into mutualism. Not all parasites induce disease, and parasites are not always organisms that should be sought eradicated.


Kotloff KL, Nataro JP, Blackwelder WC, Nasrin D, Farag TH, Panchalingam S, Wu Y, Sow SO, Sur D, Breiman RF, Faruque AS, Zaidi AK, Saha D, Alonso PL, Tamboura B, Sanogo D, Onwuchekwa U, Manna B, Ramamurthy T, Kanungo S, Ochieng JB, Omore R, Oundo JO, Hossain A, Das SK, Ahmed S, Qureshi S, Quadri F, Adegbola RA, Antonio M, Hossain MJ, Akinsola A, Mandomando I, Nhampossa T, Acácio S, Biswas K, O'Reilly CE, Mintz ED, Berkeley LY, Muhsen K, Sommerfelt H, Robins-Browne RM, & Levine MM (2013). Burden and aetiology of diarrhoeal disease in infants and young children in developing countries (the Global Enteric Multicenter Study, GEMS): a prospective, case-control study. Lancet, 382 (9888), 209-22 PMID: 23680352

Veira DM (1986). The role of ciliate protozoa in nutrition of the ruminant. Journal of Animal Science, 63 (5), 1547-60 PMID: 3098727

Monday, February 3, 2014

This Month In Blastocystis Research (JAN 2014)

Investigations into the 'biodiversity' existing in a given host is interesting for a number of reasons. One of these reasons has to do with how microorganisms present in our bodies may impact each other or the host. Numerous fields of research are developing at the moment at all levels from studies of gut microbes influencing host microRNA response to bacterial infections to epidemiological/public health studies examining the increased morbidity or risk associated with contracting infection/developing disease given that some infection/disease is present already. Sometimes the reverse is seen, namely that co-infection by multiple parasites is associated with a morbidity lower than the morbidity seen when only one of the parasites is present. For instance, a 2012 study saw that children infected by both Plasmodium falciparum (causing malaria) and hookworm had lower odds of anemia and iron deficiency than their counterparts infected with P. falciparum alone. Other authors have recently reviewed what they see as compelling evidence of chronic viral and helminth coinfections capable of modulating deleterious malaria-specific immune responses. Obviously such types of information are critical to the development of control measures against malaria and helminth infections. A Nigerian colleague of mine is currently exploring co-infections in quite a large Nigerian population, and investigating associations between malaria and soil-transmitted helminths; I'm thankful to be involved.

Along these lines, a new paper sees an inverse association between Blastocystis carriage and tuberculosis/Mycobacterium tuberculosis infections (TB). Dr Franke and colleagues carried out a case–control study to examine associations between parasite infection and tuberculosis (TB) in children in Lima, Peru. Logistic regression analyses revealed that Blastocystis infection was strongly associated with a lower risk of TB (P = 0.002). Hence, the study seems to suggest that Blastocystis carriage may protect against TB. The authors hypothesise that a pro-inflammatory/Th1 response potentially elicited by Blastocystis may protect against other infections, such as TB. While we know very little about Blastocystis induced immunity, little seems to suggest that Blastocystis is related to a chronic pro-inflammatory immunological alert. At least the colonic mucosa of patients with Blastocytis appears to be normal by endoscopy. Given the prevalence of Blastocystis that we have found in the aforementioned Nigerian study, I'd suspect very little TB to be present in this cohort...

The authors highlight a major limitation of their finding, namely the one related to the directionality of the association: It might as well be TB 'protecting' against Blastocystis. Maybe the behaviour (and thereby the exposure to Blastocystis) of patients with TB is different from the behaviour of those who do not have TB; I don't think so though.
I could have wished that a similar analysis had been performed using another common micro-eukaryote in children that the authors did not test for, namely Dientamoeba fragilis. It would be useful to know whether the same association could be identified, or whether the association was specific to Blastocystis. In fact, a general analysis of the microbiota (16S/18S) would have been in place here to learn about other factors potentially responsible for the observations.

Btw, there are some ASM conferences coming up this year relevant to the topic:

1. 5th ASM Conference on Beneficial Microbes, September 27-30, 2014, Washington DC.
2. 1st ASM Conference on Polymicrobial Infections, November 13-16, 2014, Washington DC.

On a different note, there is a paper out by Dr Poirier and his colleauges who have been publishing extensively on Blastocystis, and who were the first ever to sequence and annotate a nuclear genome of Blastocystis. In this new article the authors present a new set of primers applicable to all subtypes of Blastocystis found in humans and targeting the DNA of the mitochondrion-like organelle (MLO). This is reminiscent of the primers used for barcoding (18S analysis), and indeed the primers were validated using strains for which 18S data were available.

The paper highlights a variety of interesting topics and discusses the overall applicability of the two methods  (18S barcoding vs. subtyping using the single-copy MLO rDNA). In both of these scenarios the authors cloned the resulting PCR products to compare intra-isolate genetic variability - something which in itself is very interesting. However, cloning of PCR products is something that is not regularly done in most labs due to time and money constraints. Direct sequencing of barcode products reveals the predominating strain in a mixture, given that no other causes of preferential template amplification exist (e.g. selective primers) and hence shows the consensus sequence; sequence traces may partially or completely fail to reflect cases of mixed infection. However, the issue of not detecting mixed ST infections or mixtures of the same subtype is generally recognised.

The authors present a phylogenetic analysis of the MLO rDNA sequences included and come up with a tree topology different to the one usually seen. Usually, ST1, ST2 and ST5 cluster together, ST3, ST4, and ST8 go together, and ST6, ST7, and ST9 go together. Here, ST1 goes with ST2 and ST3. When I studied the MLOs of Blastocystis on genome level, one of my aims was to see if I could identify evolutionary patterns that had so far not been appreciated and that could be exploited in new hypotheses on the epidemiology and clinical significance of the parasite. Also, as the authors suggest here, mitochondrial DNA is haploid and therefore extremely useful when unambiguous base calling is important as it is in typing schemes. However, so far, when doing phylogenetic analysis of MLO nt sequences and even concatenated MLO nad proteins, we have obtained tree topologies identical to that seen when the 18S gene is used. Maybe the different topology seen here may be due to the way the alignment was constructed/edited? In any case, bootstraps are very low, but if confirmed the finding is very interesting.

If you have half an hour, treat yourself to "A resurgence in Field Research is Essential to Better Understand the Diversity, Ecology, and Evolution of Microbial Eukaryotes".


Archambaud C, Sismeiro O, Toedling J, Soubigou G, Bécavin C, Lechat P, Lebreton A, Ciaudo C, & Cossart P (2013). The intestinal microbiota interferes with the microRNA response upon oral Listeria infection. mBio, 4 (6) PMID: 24327339

Franke MF, Del Castillo H, Pereda Y, Lecca L, Fuertes J, Cárdenas L, Becerra MC, Bayona J, & Murray M (2013). Parasite Infection and Tuberculosis Disease among Children: A Case-Control Study. The American Journal of Tropical Medicine and Hygiene PMID: 24379242 

Frosch AE, & John CC (2012). Immunomodulation in Plasmodium falciparum malaria: experiments in nature and their conflicting implications for potential therapeutic agents. Expert Review of Anti-Infective Therapy, 10 (11), 1343-56 PMID: 23241191

Heger TJ, Edgcomb VP, Kim E, Lukeš J, Leander BS, & Yubuki N (2013). A Resurgence in Field Research is Essential to Better Understand the Diversity, Ecology, and Evolution of Microbial Eukaryotes. The Journal of Eukaryotic Microbiology PMID: 24325268

Poirier P, Meloni D, Nourrisson C, Wawrzyniak I, Viscogliosi E, Livrelli V, & Delbac F (2014). Molecular subtyping of Blastocystis spp. using a new rDNA marker from the mitochondria-like organelle genome. Parasitology, 1-12 PMID: 24467909 

Righetti AA, Glinz D, Adiossan LG, Koua AY, Niamké S, Hurrell RF, Wegmüller R, N'Goran EK, & Utzinger J (2012). Interactions and potential implications of Plasmodium falciparum-hookworm coinfection in different age groups in south-central Côte d'Ivoire. PLoS Neglected Tropical Diseases, 6 (11) PMID: 23133691