Infection with the intestinal protozoan parasite Giardia lamblia is common in developing countries and is often seen in travelers returning from endemic areas . It is also a frequent cause of waterborne outbreaks in industrialized countries, but it is generally regarded as an uncomplicated infection for which there is effective antibiotic treatment. Although long term abdominal symptoms following acute giardiasis have been observed by clinicians in individual patients for decades, studies on post-giardiasis functional gastrointestinal disorders (FGID)  and chronic fatigue  have only recently been reported after a waterborne outbreak in Bergen in 2004 .
FGID are a group of disorders characterized by recurring or chronic gastrointestinal symptoms without an identifiable disease process . Irritable bowel syndrome (IBS) and functional dyspepsia (FD) are the best described FGID. Fatigue is a frequent symptom in FGID patients [3, 6]. One study has found that 14% of IBS patients also have chronic fatigue syndrome (CFS), while six studies report that 35-92% of CFS patients also have IBS . Researchers of FGID as well as CFS [8, 9] rarely control for this co-morbidity, even though they are focusing on the same pathophysiologic mechanisms, such as low grade inflammation, immunological dysfunction, neuroendocrine dysfunction, sensory hypersensitivity, sustained stress responses and adverse life events underlying the symptomatology. FGID and CFS share the characteristics of female preponderance, both are diagnoses relying on symptom criteria alone, and in many cases the onset is preceded by an acute infection .
Many studies have been reported regarding differences in activation and function in peripheral blood lymphocyte subsets in CFS. These have given inconsistent results, and are reviewed by Natelson et al., with some studies finding altered natural killer (NK)-cell levels and some finding lowered CD4:CD8 ratios, but most studies find normal T, B and NK cell levels in CFS . More recent studies have reported a decrease in the CD56brightCD16- NK-cell subset and increased CD4CD25FoxP3 regulatory T-cells , and CD26 expressed on T-cells and NK-cells (marked with CD2) has been put forward as a promising biomarker in CFS .
Studies looking at peripheral blood lymphocyte subsets in FGID have not identified differences in regulatory T-cells  or lymphocyte subsets, but have found increased levels of B-cells expressing IgG or co-stimulatory molecules CD80 or CD86 and T-cells expressing β7+HLADR+ and CD69+ in IBS-patients compared to controls [15–17].
When the onset of FGID or CFS is associated with an acute infection, it is often termed post-infectious CFS (PI-CFS) [18, 19] or FGID (PI-FGID)  or in the case of IBS, post-infectious IBS (PI-IBS) . A meta-analysis of PI-IBS estimates that the risk of having IBS one year after an acute gastroenteritis is approximately sixfold . Until recently few studies of FGID and CFS separated between infection-related onset and a less defined onset in these disorders.
The immune responses to Giardia infection are known to include both innate and adaptive components . Important roles have been shown for mast cells and IL-6 , as well as for B-cell antibody production [24, 25]. In mice αβ-TCR-expressing T-cells are required to control infection  and CD4 T-cell depletion results in chronic infection . CD8 T-cells seems not to be important for the control of infection in mice, but contribute to the giardiasis related intestinal mucosal injury . Beige mice, which are deficient in NK-cells, have been shown to clear Giardia infection equally fast as immunocompetent mice .
The present study, performed in a well-defined group of patients with clinically observed post-infectious FGID and CFS after a common eliciting Giardia infection, was done to evaluate a wide array of lymphocyte subsets, including many of the previously reported markers of immune dysfunction in CFS and FGID.