Phytotoxicity of Fusarium, other fungal isolates, and of the phytotoxins fumonisin, fusaric acid, and moniliformin to jimsonweed

Dix isolats fongiques isolés de la stramoine commune (Datura stramonium) et 7 isolats provenant d'espèces cultivées ont été examinés pour la production de phytotoxines et pour leur pouvoir pathogène sur des plantules de stramoine commune cultivées en serre. Quatre isolats de Fusarium moniliforme, trois isolatsde F. semitectum, un isolatde F. oxysporum, un isolatde Cephalosporium spp. et un isolât d'Alternaria crassa prélevés sur des plantules de stramoine commune infectées, et sept isolats supplémentaires de F. moniliforme obtenus de grains et de plantules d'espèces cultivées ont été mis en culture sur du riz (Oryza sativa) autoclave. Les mélanges champignon-riz ont été moulus et leur phytotoxicite sur des plantules de stramoine commune âgées de 1 et 2 semaines a été testée par des applications foliaires. Tous les extraits de riz infestés par un champignon (5 g de mélange riz-champignon 50 ml-1 d'eau) ont causé des dommages ou la mort des plantules, sauf les extraits d'isolats de F. semitectum, Cephalosporium spp. et A. crassa. Les mélanges champignon-riz ont été analysés de façon quantitative pour la présence de phytotoxines du fusarium[fumosinine B1 (FB1), acide fusarique et moniliformine]. Aucun isolât n'a produit plus d'une de ces phytotoxines dans les extraits de champignon-riz. La FB1 était produite par tous les isolats de F. moniliforme isolés selon une échelle de concentration de ≤ 5 à 850 μg mL-1 de mélange champignon-riz. L'isolât de F. oxysporum a produit 3,5 g m L-1 de moniliformine et aucune phytotoxine n'a été détectée dans les extraits de F. semitectum, Cephalosporium spp. ou A. crassa. La fumonisine, l'acide fusarique et la moniliformine appliqués à l'état pur à du feuillage de stramoine commune à 6-50,25-800 et 50-800 μg mL-1 ont causé des symptômes similaires à ceux des isolats fongiques qui avaient produit ces composés. Des tests sur le pouvoir pathogène des spores de tous les isolats sur la stramoine ont indiqué que les isolats étaient avirulents, sauf A. crassa qui a causé des infections seulement après une durée d'humectation ≥ 12 h.Ten fungal isolates from jimsonweed (Datura stramonium L.) and 7 from crop species were examined for phytotoxin production and pathogenicity on jimsonweed seedlings in the greenhouse. Four isolates of Fusarium moniliforme, three F. semitectum isolates, a F. oxysporum isolate, a Cephalosporium spp. isolate, and an Alternaria crassa isolate from diseased jimsonweed seedlings, plus seven additional F. moniliforme isolates from seeds and seedlings of crop species were grown on autoclaved rice (Oryza sativa). The fungus-rice mixtures were ground and tested for phytotoxicity on 1- and 2-wk-old jimsonweed seedlings via foliar application. All fungus-infested rice extracts (5 g fungus-rice mixture 50 mL-1 water) caused injury or mortality to the seedlings except the extracts from isolates of F. semitectum, Cephalosporium spp., and A. crassa. Fungus-rice mixtures were quantitatively analyzed for the presence of Fusarium phytotoxins [fumonisin B1 (FB1 fusaric acid, and moniliformin]. No isolate produced more thanoneof these phytotoxins in the fungus-rice extract. FB1 was produced by ail F. moniliforme isoletes in a concentration range of ≤ 5 to 850 μg mL-1 of fungus-rice extract. The F. oxysporum isolate produced moniliformin at 3.5 g mL-1, and no phytotoxins were detected in extracts of F. semitectum, Cephalosporium spp., or A. crassa. Pure fumonisin, fusaric acid, and moniliformin applied to jimsonweed foliage at 6-50, 25-800, and 50-800 (μg mL-1, respectively, caused symptoms similar to that of the fungal isolates that produced these compounds. Pathogenicity tests of spores of all isolates on jimsonweed indicated that the isolates were avirulent, except for A crassa which infected only after a dew period ≥ 12 h

A Network Approach to Psychosis: Pathways Between Childhood Trauma and Psychotic Symptoms

Childhood trauma (CT) has been identified as a potential risk factor for the onset of psychotic disorders. However, to date, there is limited consensus with respect to which symptoms may ensue after exposure to trauma in early life, and whether specific pathways may account for these associations. The aim of the present study was to use the novel network approach to investigate how different types of traumatic childhood experiences relate to specific symptoms of psychotic disorders and to identify pathways that may be involved in the relationship between CT and psychosis. We used data of patients diagnosed with a psychotic disorder (n = 552) from the longitudinal observational study Genetic Risk and Outcome of Psychosis Project and included the 5 scales of the Childhood Trauma Questionnaire-Short Form and all original symptom dimensions of the Positive and Negative Syndrome Scale. Our results show that all 5 types of CT and positive and negative symptoms of psychosis are connected through symptoms of general psychopathology. These findings are in line with the theory of an affective pathway to psychosis after exposure to CT, with anxiety as a main connective component, but they also point to several additional connective paths between trauma and psychosis: eg, through poor impulse control (connecting abuse to grandiosity, excitement, and hostility) and motor retardation (connecting neglect to most negative symptoms). The results of the current study suggest that multiple paths may exist between trauma and psychosis and may also be useful in mapping potential transdiagnostic processes