This study demonstrated over a 2-fold risk of IBS among those with an antecedent Giardia infection and an unexposed reference population after adjusting for covariates. While several studies have described the incidence of FGD following bacterial and viral IGE few have examined their incidence subsequent to parasitic infection [8, 14].

The incidence of Giardia reported here is lower than recorded in another recently published study in this population. Specifically, the Medical Surveillance Monthly Report (MSMR) published in October of 2013 cites an 11-year surveillance period of the US Armed Forces for gastrointestinal infections [15]. The authors reported an incidence rate of giardiasis of 6.2 per 100,000. The study reported here utilized data from 1998 to 2009, while the MSMR focused on 2002–2012 [15]. The highest rates of Giardia from the MSMR study were in 2002–2006 and from 2008 to 2012 [15]. Case diagnosis year was not available, precluding annual comparisons across the two studies. One potential reason for the difference in incidence estimates could be variable inclusion criteria. For inclusion in this study, a subject could not have a prior documented medical encounter with any of the outcomes of interest (IBS, GERD, constipation, dyspepsia) to help cut down on the likelihood that the outcome of interest could be attributed to something other than the parasitic exposure. If a participant had a prior medical encounter with one of the outcomes of interest it would underestimate the incidence.

The results of this study are consistent with other studies reporting an increase in IBS after enteric infection [16–18]. While not specific to parasitic infections, two recent meta-analyses have shown that the risk increases 6- to 7-fold after IGE and remains elevated for at least 2 to 3 years after the initial infection [9, 10]. In only one prior study has antecedent Giardia infection been linked to IBS. Following a Giardia outbreak in Bergen, Norway, investigators found a 46.1 % IBS prevalence in exposed subjects (46.1 %) compared to 14.0 % in the control subjects (aRR: 3.4, 95 % CI: 2.9, 3.8) [17]. Similarly, we found a 2.1 increase risk in IBS following sporadic Giardia infections compared to an uninfected reference population. The estimate reported here (aRR: 2.1) is lower than that reported in prior systematic reviews or in the prior G. lamblia outbreak possibly due to case definitions, study design and/or differences in study populations. The Bergen study used a questionnaire mailed to participants with standardized questions where IBS was defined according to the Rome III criteria, whereas we relied on passive surveillance through DoD medical encounters [17].

Evidence of the association between acute IGE and development of functional dyspepsia has been accumulating in the literature over the past decade. The findings of this study support the growing body of evidence demonstrating an association between acute GI infection and functional dyspepsia [16, 18]. FGD was the third most prevalent FGD found within the study population (overall estimate of 3.5 %); however, this is probably an underestimate. Most studies show the prevalence of post-infectious FD around 10 % [11]. Quigley and Lacy reported a prevalence of 12–15 % among the general US population [19]. A meta-analysis in 2013 estimated a pooled OR of 2.18 (95 % CI: 1.70, 2.81) for the risk of developing FD following IGE [12]. Dizdar recently reported that patients with abdominal symptoms after acute Giardia infection had evidence of enhanced visceral sensitivity, and 15 of the 22 patients had evidence of FD indicating that dyspepsia may be attributed to increased visceral sensitivity that persists after initial infection [16]. A recent study [16].

This study found a similar trend with more cases having a GERD diagnosis (32.5 %) compared to controls (17.3 %); however, this was not significant in multivariate analyses. A 2012 study looking at three recent norovirus outbreaks found the risk of GERD is higher among those who had an IGE diagnosis during a confirmed outbreak (aRR: 1.39, 95 % CI: 1.07, 1.81) [20]. The potential association between Giardia and functional dyspepsia needs further study.

The mechanisms by which Giardia infection may induce chronic, long-term FGD are unclear. Recently, researchers at the University of Calgary have shown that infection with Giardia can induce functional changes in commensal flora composition in a nematode model [21]. In a healthy host, it may be that these infections trigger the intestinal dysbiosis and altered sensory perception common noted in many FGDs [22]. Additionally, Giardia has been shown to disrupt tight junctions, which perhaps alters gut permeability in a way that alters normal homeostasis and host-microbiota interactions [23]. The link between giardiasis and post-infectious sequelae is likely the result of a multi-factorial process in a susceptible host and understanding these processes and host characteristics is an ongoing area of research across multiple institutions.

Psychological comorbidities, such as stress and anxiety, are associated with an increased IBS risk, and often the two conditions occur together [14, 24, 25]. In fact, we observed a stronger association between axis I disorders and FGDs then was observed with our exposure of interest (ie, Giardia infection). Several studies have demonstrated a similar association between axis I disorders and IBS [8, 9, 24, 25]. Additionally, traumatic life events can often precede the onset of functional bowel disorders [26]. A meta-analysis conducted in 2002 found that psychiatric comorbidities were present in up to 94 % of patients with chronic gastrointestinal disorders, including IBS [27]. We observed an increase in the risk of IBS, GERD, dyspepsia, and constipation in subjects with preceding axis I diagnoses after controlling for relevant covariates and exposures. These results are consistent with observed associations between psychological co-morbidities and IBS [9, 10]. It is important to note, that the associations between giardia and chronic GI disorders were noted to be significant when controlling for these important known covariates. Interactions between IGE and psychological co morbidities were difficult to investigate due to low numbers of each individual comorbidity.

Limitations inherent in our study may impact the generalizability of these results. Giardia infections were identified exclusively among males in this study population, perhaps not unsurprising given the study population and the inclusion criteria. Interactions between covariates were not investigated due to a small sample size of the outcome of interest and relatively low numbers of participants within each subcategory of covariates. FGD diagnoses are complicated by their functional nature and the lack of diagnostic tests [7]. It is also possible that the observed findings could be the result of an unmeasured confounder; however, no confounders have been proposed to date that would differentially affect the exposed cohort. The etiology of enteric infection is also complicated by poor diagnostic test utilization and a low rate of care-seeking behavior in persons with IGE. The utilization of ICD9-CM codes to identify exposures and outcomes can be problematic and has been described elsewhere [28].