Schizophrenia is a severe mental illness affecting approximately 1% of the population worldwide. While its exact causes remain unknown, emerging evidence suggests that infections and inflammation may contribute to disease development in a subset of individuals. This review comprehensively summarizes the evidence linking infections, immune system dysfunction, and schizophrenia risk.
Several population-based studies have linked serious prenatal or childhood infections requiring hospitalization to increased risk of later schizophrenia diagnosis, especially in individuals with genetic predisposition. Both central nervous system infections and systemic infections appear to confer risk. Specific pathogens including Toxoplasma gondii, herpesviruses, Chlamydophila, and more have been implicated. Autoimmune diseases are also associated with increased schizophrenia susceptibility, possibly due to blood-brain barrier disruption allowing brain-reactive antibodies access. The recent Coronavirus disease 2019 (COVID-19) pandemic raises questions about SARS-CoV-2 as a risk factor for new-onset psychosis. The mechanisms underlying the infection-schizophrenia link likely involve inflammation, cytokines, microglial activation, and tryptophan/kynurenine pathway modulation. Treatments targeting inflammation showed some efficacy in schizophrenia, further supporting an inflammation hypothesis. While the epidemiological and mechanistic evidence is substantial, further research is needed to conclusively determine the exact mechanisms linking immune dysfunction to schizophrenia requires further study.
The evidence suggests immune system abnormalities likely play a role, perhaps by interacting with genetic and environmental factors, in instigating schizophrenia pathophysiology in a subset of patients. More research is needed to understand these connections more clearly which may aid future prevention and personalized treatment approaches tailored to specific illness subtypes.
Gut microbiota plays a pivotal role in the gut-brain axis and can influence neurodevelopment and mental health outcomes. This review summarizes the current evidence on the associations between gut microbiota alterations and various psychiatric illnesses.
The composition of the gut microbiome evolves from birth through old age, and disruptions during critical periods may increase disease risk. Factors like diet, medications, stress, and infections can disturb the gut microenvironment and lead to dysbiosis. Dysbiosis has been linked to conditions like depression, anxiety, autism, ADHD, and schizophrenia. Proposed mechanisms involve microbial regulation of neurotransmitters, inflammation, oxidative stress, blood-brain barrier permeability, and the immune system. Therapeutic strategies like probiotics, prebiotics, and faecal transplantation may modulate the gut-brain axis and microbial ecosystem. However, more research is needed to elucidate the causal microbiota-psychiatry relationship. Understanding gut-brain interactions may uncover new possibilities for preventing and managing psychiatric disorders.
A growing body of research points to a close relationship between gut microbiota and mental health. While the field is still emerging, dysbiosis of gut microbial ecosystem has been associated with various neuropsychiatric conditions. The underlying mechanisms likely involve the microbiota-gut-brain axis signalling pathways. Additional research with larger samples is required to establish causal links between specific microbial changes and psychiatric outcomes.
Multiple sclerosis (MS) is an inflammatory demyelinating central nervous system disease with diverse clinical manifestations. The present study aimed to compare the psychiatric outcomes of MS patients with full ambulatory versus impaired ambulatory function and identify the potential risk factors for disability in MS. Seventy MS patients were classified into two groups based on their Expanded Disability Status Scale (EDSS) scores, Group A: full ambulatory (EDSS ≤ 4.5) (N = 48), Group B: impaired ambulatory (EDSS ≥ 5) (N = 22). All participants were evaluated by the Socioeconomic Scale, Hamilton Anxiety Scale, Hamilton Depression Scale, Brief Psychiatric Rating Scale, and The Pittsburgh Sleep Quality Index.
In the total cohort (N = 70), females represented (77.1%). The mean age was 31.16 ± 6.46, the mean age of onset was 26 ± 6.083, and the mean disease duration was 5.33 ± 3.653 years which was less in Group A than in Group B. Relapsing–remitting multiple sclerosis (RRMS) was the most common presentation (80%), representing 93.6% of Group A. Group A reported more severe depression and anxiety, while Group B had more poor sleep quality. Correlation analysis showed increased relapses, progressive-relapsing multiple sclerosis (PRMS), cervical or dorsal plaques, sensory or motor manifestations, and precipitancy increased disability, while RRMS type decreased disability.
Full ambulatory MS patients had high anxiety and depression, while impaired ambulatory MS patients had poor sleep quality. Associated factors for disability were frequent relapses, plaque location, MS subtype, sphincter, and sensory symptoms.
Myasthenia gravis is an autoimmune neuromuscular junction disorder characterized by fatigable muscle weakness and autoantibodies. Frequent associations exist between myasthenia gravis and thymic abnormalities, including hyperplasia and thymoma. Several autoimmune illnesses have been identified to be associated with thymoma; however, a few case reports have linked thymoma and achalasia, and the underlying mechanism is unknown.
A 43-year-old man with thymoma-associated myasthenia gravis presented with dysphagia that was refractory to conventional treatment of myasthenia gravis. This dysphagia was challenging to diagnose even after multiple gastroenterology consults and upper endoscopy. The diagnosis of achalasia type II was established after a comprehensive evaluation, including upper endoscopy, barium swallow, and high-resolution esophageal manometry. The patient underwent elective pneumatic balloon dilatation, which successfully alleviated his dysphagia.
This case confirmed the association between myasthenia gravis secondary to thymoma and achalasia and showed how the diagnosis of achalasia was challenging. Awareness of this association is crucial for early diagnosis and treatment, improving affected patients’ quality of life.
Background: Epilepsy is a prevalent neurological illness, impacting about 70 million individuals around the world. Although a large number of patients are controlled with anti-seizure drugs (ASDs), 30%–40% of patients fail to be controlled and develop drugresistant epilepsy (DRE). Objectives: This study aimed to identify miRNa-223 expression and serum level of high mobility group box 1 (HMGB1) as biomarkers for detecting DRE. Methodology: This case-control study comprised 96 subjects categorized to three groups: group I: 46 patients with genetically presumed epilepsy who having DRE; group II: 25 patients with medically controlled genetically presumed epilepsy and group III: 25 healthy individuals. MiRNA-223 expression level was measured by real-time PCR and serum HMGB1 was estimated by ELISA technique. Results: MiRNA-223 expression serum HMGB1 and hs-CRP levels in epilepsy patients were considerably greater than in patients with controlled epilepsy and in healthy controls (p<0.001 for all). The predictive ability of miRNA, HMGB1 and hs-CRP for the detection of epilepsy and DRE using the ROC curve analysis revealed good sensitivities and specificities. Conclusion: MiRNA-223 expression and serum HMGB1 and hs-CRP levels are important biomarkers for diagnosis of epilepsy in suspicious cases. They are also significant for predicting DRE which may pave the way to the development of new antiepileptogenic drugs.
Infective endocarditis infects the heart's inner surface, mostly the valves. It is a lethal disease with a high rate of morbidity and fatality. It mostly caused by bacteria, but fungi can also cause it. Microbiological diagnosis relies on blood culture. Molecular and biochemical indicators add to diagnosis, particularly in culture-negative patients. This study aimed to decide the role of 16s rRNA, procalcitonin, and high sensitivity C reactive protein (hsCRP) in the diagnosis of culture negative infective endocarditis (CNIE) in Assiut university hospitals. This cross-sectional study included 60 patients who were admitted to cardiac hospitals with suspected infective endocarditis according to modified DUKE criteria. A group of 20 apparently healthy subjects served as a control group for investigation of inflammatory biomarkers. We performed blood culture, biochemical markers and molecular investigations. Of the 60 patients, there were 46 (76.7%) culture positives and 14 (23.3%) culture negatives. Staphylococcus aureus was the most prevalent pathogen in culture positive patients, followed by enterococcus and klebsiella. Linezolid and imipenem were the most sensitive antibiotics for Gram-positive and Gram-negative bacteria, respectively. Amplification of bacterial 16S rRNA gene, after DNA extraction from whole blood samples, was positive in 11/14 cases (78.5%) of culture negative patients and in 42/46 cases (91.3%) of culture positive patients. The range of procalcitonin in culture positive patients was (0.32- 89) ng/ml, significantly higher than in culture negative patients (0.02- 8.8) ng/ml, and in the control group (0.01-0.08) ng/ml. hsCRP showed the same pattern. In conclusion, our data suggest that PCR was the most accurate diagnostic tool for diagnosing CNIE, followed by procalcitonin, and hsCRP, respectively.