Search

Most Varroa induced colony losses occur during the autumn or winter season as a consequence of an elevated Varroa infestation level and an insufficient health status of the adult bees. Even with an initial low Varroa infestation in early spring, critical mite and virus infection levels can be reached before winter if colonies continuously rear brood throughout the whole season. To overcome this challenge, beekeepers can artificially interrupt brood production by suitable management procedures, depending on their type of beekeeping operation. To assess their efficacy, associated workload, and impact on colony development, different methods for brood interruption (queen caging with the combination of oxalic acid treatment, total brood removal, trapping comb technique) were tested during two seasons in 11 locations on 370 colonies in 10 European countries. A protocol was developed to standardize the methods' application across different environmental conditions. The efficacy of queen caging depended on the mode of oxalic acid application and ranged from 48.16% to 89.57% mite removal. The highest efficacies were achieved with trickling a 4.2% solution (89.57%) and with the sublimation of 2 g of oxalic acid (average of 88.25%) in the broodless period. The efficacy of the purely biotechnical, chemical-free trapping comb and brood removal methods did not differ significantly from the queen caging groups. We conclude that a proper application of one of the described brood interruption methods can significantly contribute to an efficient Varroa control and to the production of honey bee products meeting the highest quality and food-safety standards.

Most Varroa induced colony losses occur during the autumn or winter season as a consequence of an elevated Varroa infestation level and an insufficient health status of the adult bees. Even with an initial low Varroa infestation in early spring, critical mite and virus infection levels can be reached before winter if colonies continuously rear brood throughout the whole season. To overcome this challenge, beekeepers can artificially interrupt brood production by suitable management procedures, depending on their type of beekeeping operation. To assess their efficacy, associated workload, and impact on colony development, different methods for brood interruption (queen caging with the combination of oxalic acid treatment, total brood removal, trapping comb technique) were tested during two seasons in 11 locations on 370 colonies in 10 European countries. A protocol was developed to standardize the methods' application across different environmental conditions. The efficacy of queen caging depended on the mode of oxalic acid application and ranged from 48.16% to 89.57% mite removal. The highest efficacies were achieved with trickling a 4.2% solution (89.57%) and with the sublimation of 2 g of oxalic acid (average of 88.25%) in the broodless period. The efficacy of the purely biotechnical, chemical-free trapping comb and brood removal methods did not differ significantly from the queen caging groups. We conclude that a proper application of one of the described brood interruption methods can significantly contribute to an efficient Varroa control and to the production of honey bee products meeting the highest quality and food-safety standards.

IMPORTANCE: Diverse models have been developed to predict psychosis in patients with clinical high-risk (CHR) states. Whether prediction can be improved by efficiently combining clinical and biological models and by broadening the risk spectrum to young patients with depressive syndromes remains unclear. OBJECTIVES: To evaluate whether psychosis transition can be predicted in patients with CHR or recent-onset depression (ROD) using multimodal machine learning that optimally integrates clinical and neurocognitive data, structural magnetic resonance imaging (sMRI), and polygenic risk scores (PRS) for schizophrenia; to assess models' geographic generalizability; to test and integrate clinicians' predictions; and to maximize clinical utility by building a sequential prognostic system. DESIGN, SETTING, AND PARTICIPANTS: This multisite, longitudinal prognostic study performed in 7 academic early recognition services in 5 European countries followed up patients with CHR syndromes or ROD and healthy volunteers. The referred sample of 167 patients with CHR syndromes and 167 with ROD was recruited from February 1, 2014, to May 31, 2017, of whom 26 (23 with CHR syndromes and 3 with ROD) developed psychosis. Patients with 18-month follow-up (n = 246) were used for model training and leave-one-site-out cross-validation. The remaining 88 patients with nontransition served as the validation of model specificity. Three hundred thirty-four healthy volunteers provided a normative sample for prognostic signature evaluation. Three independent Swiss projects contributed a further 45 cases with psychosis transition and 600 with nontransition for the external validation of clinical-neurocognitive, sMRI-based, and combined models. Data were analyzed from January 1, 2019, to March 31, 2020. MAIN OUTCOMES AND MEASURES: Accuracy and generalizability of prognostic systems. RESULTS: A total of 668 individuals (334 patients and 334 controls) were included in the analysis (mean [SD] age, 25.1 [5.

As early detection of symptoms in the subclinical to clinical psychosis spectrum may improve health outcomes, knowing the probabilistic susceptibility of developing a disorder could guide mitigation measures and clinical intervention. In this context, polygenic risk scores (PRSs) quantifying the additive effects of multiple common genetic variants hold the potential to predict complex diseases and index severity gradients. PRSs for schizophrenia (SZ) and bipolar disorder (BD) were computed using Bayesian regression and continuous shrinkage priors based on the latest SZ and BD genome-wide association studies (Psychiatric Genomics Consortium, third release). Eight well-phenotyped groups (n = 1580; 56% males) were assessed: control (n = 305), lower (n = 117) and higher (n = 113) schizotypy (both groups of healthy individuals), at-risk for psychosis (n = 120), BD type-I (n = 359), BD type-II (n = 96), schizoaffective disorder (n = 86), and SZ groups (n = 384). PRS differences were investigated for binary traits and the quantitative Positive and Negative Syndrome Scale. Both BD-PRS and SZ-PRS significantly differentiated controls from at-risk and clinical groups (Nagelkerke's pseudo-R2: 1.3-7.7%), except for BD type-II for SZ-PRS. Out of 28 pairwise comparisons for SZ-PRS and BD-PRS, 9 and 12, respectively, reached the Bonferroni-corrected significance. BD-PRS differed between control and at-risk groups, but not between at-risk and BD type-I groups. There was no difference between controls and schizotypy. SZ-PRSs, but not BD-PRSs, were positively associated with transdiagnostic symptomology. Overall, PRSs support the continuum model across the psychosis spectrum at the genomic level with possible irregularities for schizotypy. The at-risk state demands heightened clinical attention and research addressing symptom course specifiers. Continued efforts are needed to refine the diagnostic and prognostic accuracy of PRSs in mental healthcare.

There is growing evidence that reward processing is disturbed in schizophrenia. However, it is uncertain whether this dysfunction predates or is secondary to the onset of psychosis. Studying 21 unmedicated persons at risk for psychosis plus 24 healthy controls (HCs) we used a incentive delay paradigm with monetary rewards during functional magnetic resonance imaging. During processing of reward information, at-risk individuals performed similarly well to controls and recruited the same brain areas. However, while anticipating rewards, the high-risk sample exhibited additional activation in the posterior cingulate cortex, and the medio- and superior frontal gyrus, whereas no significant group differences were found after rewards were administered. Importantly, symptom dimensions were differentially associated with anticipation and outcome of the reward. Positive symptoms were correlated with the anticipation signal in the ventral striatum (VS) and the right anterior insula (rAI). Negative symptoms were inversely linked to outcome-related signal within the VS, and depressive symptoms to outcome-related signal within the medial orbitofrontal cortex (mOFC). Our findings provide evidence for a reward-associated dysregulation that can be compensated by recruitment of additional prefrontal areas. We propose that stronger activations within VS and rAI when anticipating a reward reflect abnormal processing of potential future rewards. Moreover, according to the aberrant salience theory of psychosis, this may predispose a person to positive symptoms. Additionally, we report evidence that negative and depressive symptoms are differentially associated with the receipt of a reward, which might demonstrate a broader vulnerability to motivational and affective symptoms in persons at-risk for psychosis.