Validity and reliability of the Thai version Consumer Assessment of Healthcare Providers and Systems In-Centre Hemodialysis (Thai CAHPS-ICH) survey for maintenance hemodialysis patients.

is an obligate intracellular parasitic protozoan that infects a wide array of warm-blooded animals, including approximately one-third of humans worldwide [–]. Transmission occurs primarily via ingestion of contaminated water or food harbouring oocysts, consumption of undercooked meat containing tissue cysts, or exposure to cat faeces. Once acquired, typically establishes a lifelong latent infection by persisting within host tissues – particularly in the brain – in the form of dormant cysts [–]. Although acute infections can be managed with antiparasitic therapies, these interventions do not eradicate the infection which eventually transitions into a chronic latent phase. There is some evidence from general population studies suggests that latent infection may influence brain structure and neuropsychiatric function. Epidemiological studies have linked seropositivity to increased risk of schizophrenia, anxiety, suicidal behavior, and alterations in personality and impulsivity [–]. Although neuroimaging studies in humans remain limited, a UK Biobank analysis found that higher antibody titers were associated with reduced total grey matter volume, though no associations were observed with specific regional volumes or white matter []. While most chronically infected individuals remain clinically asymptomatic, emerging evidence suggests that latent infection may modify neurological vulnerability to other brain insults, including traumatic brain injury (TBI) [, ]. TBI is a significant health concern worldwide, with millions of individuals affected each year, leading to a broad spectrum of short- and long-term neurological deficits []. These injuries often result in lasting cognitive impairment, increased susceptibility to neurodegenerative diseases, and heightened risk of psychiatric disorders [–]. TBI initiates a cascade of inflammatory responses, cellular damage, and subsequent neural repair mechanisms, which can alter brain function and structure [–]. Recent preclinical studies have found that chronic infection – defined as the latent phase marked by the persistence of tissue cysts in the brain following an acute infection – can interact with TBI-induced alterations and influence outcomes [, ]. This interaction may stem from the parasite’s capacity to modulate the immune system, particularly through cytokine production, and its influence on neurochemical pathways [, , ]. Experimental models have demonstrated that chronic infection leads to increased production of pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α within the brain []. These cytokines are also elevated in response to TBI, where they play a crucial role in the immune response to injury but may additionally contribute to secondary neurotoxicity and exacerbate neuronal damage []. The overlapping immune activation raises the possibility that a concomitant chronic infection could amplify neuroinflammation and neuropathology, thereby worsening neurobehavioral outcomes or delaying recovery, as supported by murine studies showing that infected mice exhibit more pronounced inflammatory responses and neuropathological changes after TBI compared to non-infected controls [, ].