Discussion:
Recent studies have identified a possible link between Blastocystis hominis, a common gut eukaryote, and cognitive function. Specifically, various subtypes of Blastocystis have been associated with deficits in executive function and changes in gut bacterial composition, suggesting that Blastocystis colonization may contribute to cognitive impairment through mechanisms involving gut microbiota dysbiosis [4].
Blastocystis is a genetically diverse unicellular parasite found in humans and a wide range of animals. It is classified as a stramenopile. The parasite’s potential to cause gastrointestinal disease in humans is debated, as it has been detected in both symptomatic and asymptomatic individuals [2]. Despite controversies surrounding its pathogenicity, accumulating evidence suggests Blastocystis may cause gastrointestinal symptoms such as diarrhea and abdominal pain, as well as extraintestinal manifestations like urticaria [5]. Diagnosis involves identifying Blastocystis species, usually in its vacuolar form, in stool samples. Molecular methods are primarily used for research purposes. The parasite’s life cycle, including its infectious stage and the significance of its various morphological forms, remains poorly understood despite ongoing studies on its global distribution and host range [2].
The gut microbiota, consisting of bacteria, viruses, fungi, protozoans, and archaea, plays a critical role in maintaining physiological homeostasis, immune system development, and digestion [6]. Dysbiosis, or an imbalance in the gut microbiota, has been linked to numerous diseases, including Parkinson’s disease (PD) [7].
Parkinson’s disease is the second most prevalent neurodegenerative disorder in the United States, marked by the degeneration of dopaminergic neurons in the substantia nigra and the formation of Lewy Bodies. Motor symptoms include resting tremors, bradykinesia, rigidity, shuffling gait, and postural instability. Non-motor symptoms include cognitive impairment, depression, anxiety, autonomic dysfunction, and sensory/sleep disturbances. The causes are a mix of environmental and genetic factors, with an increased risk from head injuries and exposure to toxins [8].
The gut-brain axis enables bidirectional communication between the gut microbiota and the central nervous system (CNS), influencing each other through neural, immune, and endocrine signals [9]. Dysbiosis in PD patients is characterized by specific changes in gut microbial populations, which contribute to the disease’s motor and non-motor symptoms through increased intestinal permeability, systemic inflammation, and disrupted neurotransmitter metabolism [9].
In this case, an elderly male patient with PD developed daily diarrhea that was resistant to loperamide, ciprofloxacin, and metronidazole, along with worsening PD symptoms. Diagnostic tests revealed an infection with Blastocystis hominis, which likely further disrupted his gut microbiota. Blastocystis hominis is a common gut eukaryote found in humans, capable of asymptomatic long-term colonization [10, 11].
It exhibits a dual nature as both a commensal organism, often residing in the gut without causing symptoms, and a potential pathogen under certain conditions [4]. Research has highlighted its association with increased gut bacterial diversity while also disrupting microbial composition, particularly affecting beneficial bacteria such as Bifidobacterium and Lactobacillus [12, 13].
These dual characteristics suggest that Blastocystis hominis may contribute to gut dysbiosis and related health outcomes, depending on its interactions within the gut microbiota.
The intricate relationship between gut microbiome dysbiosis and Parkinson’s disease (PD) is an emerging focus of scientific inquiry [7].
We hypothesize that the pre-existing dysbiosis associated with PD predisposed our patient to infection with Blastocystis hominis, which in turn exacerbated the dysbiosis and aggravated the patient’s PD symptoms. Pre-existing dysbiosis in PD patients typically manifests as an altered gut microbial composition, increased intestinal permeability, and a compromised immune response [9].
In our patient, these factors likely created a conducive environment for B. hominis colonization. Dysbiosis disrupts the normal protective mechanisms of the gut, thereby facilitating the establishment of pathogenic organisms such as B. hominis. Once established, this protozoan parasite may have further disrupted the gut microbiota, exacerbating the dysbiotic state.
Colonization by B. hominis could have intensified the pre-existing dysbiosis through several mechanisms. It may have further altered the gut microbial community, increased intestinal permeability, and induced both local and systemic inflammation. These changes can disrupt the gut-brain axis, which plays a crucial role in the pathophysiology of PD. The exacerbated dysbiosis likely initiated a vicious cycle, where the infection-induced imbalance of the gut microbiota led to increased systemic inflammation and neuroinflammation. These inflammatory processes are known to contribute to the progression of PD.
Furthermore, the disrupted gut microbiome may have impaired the gut’s ability to produce and metabolize neurotransmitters and other bioactive compounds essential for maintaining neurological function. This dysbiosis may have made the patient more susceptible to B. hominis infection, creating a vicious cycle where the infection aggravated gut dysbiosis, exacerbating PD symptoms. Addressing B. hominis infection and restoring gut microbial balance could potentially alleviate some of the PD symptoms by improving gut health and reducing systemic inflammation.