Causal beliefs about mental illness: A scoping review.

Research on causal beliefs about mental illness-the beliefs people hold about what causes a particular mental illness, or mental illnesses in general-is split across a number of theories and disciplines. Although research on this subject has provided a number of insights and practical applications, the diversity of theories, terminology, and keywords makes it challenging for a new reader to gain a comprehensive understanding. We sought to address this by conducting a systematic scoping review of research on causal beliefs. This review included English-language articles from any year that mentioned causal beliefs for mental illness in their title or abstract. We identified articles in two stages. In the first stage, we used a narrow set of search terms referring specifically to causal beliefs (1227 records identified, 417 included). In the second stage, we used a comprehensive set of terms relevant to research on causal beliefs (10,418 records identified, 3838 included). We analyzed articles qualitatively, organizing them into one of five theories or categories: the common-sense model of self-regulation, explanatory models, mental health literacy, biogenetic causal beliefs, and other research on causal beliefs. We provide a comprehensive summary of these literatures in terms of their history, typical research questions and study design, findings, and practical applications. These theories differ in their theoretical orientation towards causal beliefs, research methods, findings, and applications. However, they broadly share a view of causal beliefs as multifaceted, culturally determined, and relevant for additional psychosocial variables such as mental illness stigma and help-seeking. We conclude by making recommendations for researchers, clinicians, public health messaging, and for individuals with mental illness.

Failed Eradication Therapy of New-Onset Pseudomonas aeruginosa Infections in Children With Cystic Fibrosis Is Associated With Bacterial Resistance to Neutrophil Functions.

BACKGROUND: Antibiotics, such as inhaled tobramycin, are used to eradicate new-onset Pseudomonas aeruginosa (PA) infections in patients with cystic fibrosis (CF) but frequently fail due to reasons poorly understood. We hypothesized that PA isolates' resistance to neutrophil antibacterial functions was associated with failed eradication in patients harboring those strains. METHODS: We analyzed all PA isolates from a cohort of 39 CF children with new-onset PA infections undergoing tobramycin eradication therapy, where 30 patients had eradicated and 9 patients had persistent infection. We characterized several bacterial phenotypes and measured the isolates' susceptibility to neutrophil antibacterial functions using in vitro assays of phagocytosis and intracellular bacterial killing. RESULTS: PA isolates from persistent infections were more resistant to neutrophil functions, with lower phagocytosis and intracellular bacterial killing compared to those from eradicated infections. In multivariable analyses, in vitro neutrophil responses were positively associated with twitching motility, and negatively with mucoidy. In vitro neutrophil phagocytosis was a predictor of persistent infection following tobramycin even after adjustment for clinical risk factors. CONCLUSIONS: PA isolates from new-onset CF infection show strain-specific susceptibility to neutrophil antibacterial functions, and infection with PA isolates resistant to neutrophil phagocytosis is an independent risk factor for failed tobramycin eradication.

Pseudomonas aeruginosa in Chronic Lung Infections: How to Adapt Within the Host?

Bacteria that readily adapt to different natural environments, can also exploit this versatility upon infection of the host to persist. Pseudomonas aeruginosa, a ubiquitous Gram-negative bacterium, is harmless to healthy individuals, and yet a formidable opportunistic pathogen in compromised hosts. When pathogenic, P. aeruginosa causes invasive and highly lethal disease in certain compromised hosts. In others, such as individuals with the genetic disease cystic fibrosis, this pathogen causes chronic lung infections which persist for decades. During chronic lung infections, P. aeruginosa adapts to the host environment by evolving toward a state of reduced bacterial invasiveness that favors bacterial persistence without causing overwhelming host injury. Host responses to chronic P. aeruginosa infections are complex and dynamic, ranging from vigorous activation of innate immune responses that are ineffective at eradicating the infecting bacteria, to relative host tolerance and dampened activation of host immunity. This review will examine how P. aeruginosa subverts host defenses and modulates immune and inflammatory responses during chronic infection. This dynamic interplay between host and pathogen is a major determinant in the pathogenesis of chronic P. aeruginosa lung infections.