Microbial Translocation in Patients with Parkinson’s Disease in Zambia: a Case Control Study

Abstract BACKGROUND Over the past few years evidence has emerged that Parkinson’s disease (PD) could originate from the gastrointestinal tract. Gut leakiness in patients who are genetically susceptible to PD might be an important early component to initiation and progression of the disease, via microbial translocation mechanisms, but this has not been explored in Zambia. OBJECTIVES To study the association of microbial translocation in patients with Parkinson’s disease (PD) in Zambia. METHODS We conducted a case control study at the University Teaching Hospital in Lusaka Zambia between October 2019 and March 2020. We enrolled, consecutively 22 PD patients (20 previously diagnosed and 2 newly diagnosed) presenting to the neurology clinic and compared them to 44 unmatched controls from the PD patient household and non-household individuals. We measured plasma lipopolysaccharide binding protein (LBP) levels to assess systemic exposure to gut bacterial endotoxin lipopolysaccharide (LPS) and 16S ribosomal RNA (16S rRNA) gene copy number was quantified by quantitative real-time polymerase chain reaction. RESULTS Using Fischer’s exact test there was no significant difference in the 16S rRNA gene copy number between the cases and controls (P-value: 0.122). In both groups the levels were very low to undetectable. Lipopolysaccharide binding protein levels were similar in both groups. CONCLUSION This data suggests that the markers of microbial translocation, 16S rRNA gene copy number and lipopolysaccharide binding protein levels, in Zambian patients with Parkinson’s disease are similar to those without Parkinson’s disease.