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.