On gut parasites and chronic fatigue

An interesting exchange on Twitter prompted this short post regarding a paper by Naess and colleagues* (full-text) on Giardia lamblia gastroenteritis and chronic fatigue syndrome (CFS). The tweets concerned another parasitic nasty called Toxomplasma gondii which has featured quite a bit on a sister blog with regards to its link to various behaviourally-defined conditions. I thought that T.gondii was a spine-tingling protozoa until someone posted about these other chaps and their brain-eating, behaviour-changing and belly exploding antics (pass the sauce, please).

Giardia lamblia is quite a special  protozoa in terms of its survival, persistence and ability to link into quite a few other health complaints particularly of the gastrointestinal variety and specifically links to lactose intolerance. The current observations by Naess et al are interesting in that based on an examination of over 1200 patients with laboratory-confirmed giardiasis following a large community outbreak in Bergen, Norway, approximately 5% of cases (58/1262) were diagnosed with CFS as classified by the CDC criteria (see here for a related post on the trials and tribulations of diagnosing CFS/ME).

Even assuming a CFS prevalence of 1% previously noted in children (not adults) in the UK, the 5% figure seems high bearing in mind correlation is not necessarily causation. What can perhaps be ascertained from this latest study is that it might be a good idea to screen for giardiasis where active functional bowel issues are present alongside fatigue-related conditions and further research on any mechanism of parasitic infection linked to long-term fatigue might be advisable.

* Naess H. et al. Chronic fatigue syndrome after Giardia enteritis: clinical characteristics, disability and long-term sickness absence. BMC Gastroenterology. February 2012.
DOI: 10.1186/1471-230X-12-13

Parasitic infection, coeliac disease and inflammation

My day-to-day job does not normally include giving lectures and presentations but today was an exception. I was asked to give a short talk on autism, and specifically some of the more 'somatic' research aspects to the condition. One of the issues that cropped up during that talk was some discussion on how we might think that we are in charge of our behaviour, but more often than not external environmental forces might also influence us. By environment, I mean the physical environment we can see and interact with but also the more hidden aspects. Words like Toxoplasma gondii and schizophrenia were used as examples, but also some speculative suggestions about how other 'parasitic' infections might affect our health and wellbeing.

Such discussion brings me neatly to a recent paper by Henry McSorley and colleagues from Australia published in PLoS ONE. The crux of the paper (which is open-access) is that purposeful infection with hookworm might have some interesting positive effects on various aspects of inflammation in relation to coeliac (celiac) disease (CD).

I must admit that I have covered parasitic infection in a previous post on autism (here); the conclusion being that our modern-day obsession with hygiene leads to the eradication of certain parasitic species which have evolved alongside us, and with it, a suggested increase in things like inflammation and conditions manifesting inflammation.

It does appear that similar findings were reported by McSorley and colleagues, where:

• A 2-stage clinical trial was undertaken. Trial 1: 20 participants in total with CD and on a gluten-free diet; 10 were randomly infected with the larvae of the hookworm (Necator americanus) administered via the skin, the controls were given topically administered chilli pepper. At 20 weeks post-infection (with a top-up at 5 weeks), a gluten-challenge was given. Trial 2: a follow-up control participants, infecting 7 of them with hookworm, top-up infection and gluten challenge.
• Levels of duodenal interferon-gamma (IF-y) (sorry about the lack of Greek gamma symbols) and the cytokine IL-17A were significantly decreased in the hookworm infected group from Trial 1 post gluten challenge. This and other results led the authors to assume that helminth therapy might skew the immune response in CD towards a Th2 phenotype; in effect, a more anti-inflammatory response (see this article for a better description of Th1 and Th2).

I must point out that I am in no way advocating such parasite therapy for anyone. I am also under no illusion that these results suggest a simple relationship between parasite and inflammation because they do not. I am however drawn (again!) to the notion that such parasites might carry some important evolutionary function for human health and as such, our recent leanings towards cleanliness (next to Godliness apparently) and sterility might just be to the detriment of our health.

* McSorley HJ. et al. Suppression of inflammatory immune responses in celiac disease by experimental hookworm infection. PLoS ONE. September 2011.