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Zymoseptoria tritici is the causal agent of septoria tritici blotch ( STB), a foliar wheat disease important worldwide. Succinate dehydrogenase inhibitors ( SDHIs) have been used in cereals for effective control of STB for several years, but resistance towards SDHIs has been reported in several phytopathogenic fungi. Resistance mechanisms are target-site mutations in the genes coding for subunits B, C and D of the succinate dehydrogenase ( SDH) enzyme. Previous monitoring data in Europe indicated the presence of single isolates of Z. tritici with reduced SDHI sensitivity. These isolates carried mutations leading to amino acid exchanges: C-T79N, C-W80S in 2012; C-N86S in 2013; B-N225T and C-T79N in 2014; and C-V166M, B-T268I, C-N86S, C-T79N and C-H152R in 2015. The current study provides results from microtitre and greenhouse experiments to give an insight into the impact of different mutations in field isolates on various SDHIs. In microtitre tests, the highest EC50 values for all tested SDHIs were obtained with mutants carrying C-H152R. Curative greenhouse tests with various SDHIs confirmed the findings of microtitre tests that isolates with C-H152R are, in general, controlled with lower efficacy than isolates carrying B-T268I, C-T79N and C-N86S. SDHI-resistant isolates of Z. tritici found in the field were shown to have cross-resistance towards all SDHIs tested. So far, SDHI-resistant isolates of Z. tritici have been found in low frequencies in Europe. Therefore, FRAC recommendations for resistance management in cereals, including a limited number of applications, alternation and combination with other MOAs, should be followed to prolong SDHI field efficacy. [ABSTRACT FROM AUTHOR]

In order to study the variety of infectious pancreatic necrosis virus ( IPNV) strains involved in outbreaks of infectious pancreatic necrosis ( IPN) in Atlantic salmon fish farms, samples were collected from 19 different outbreaks of IPN in the northern part of Norway. The main objective of this study was to examine whether IPNV isolates of different virulence were involved in the outbreaks and could explain the variable IPN protection observed in vaccinated post-smolts in the field. Both the molecular basis of virulence of all field isolates and virulence expressed by mortality after bath challenge of unvaccinated post-smolts with eight of the isolates were studied. Very little variation among the field isolates was detected when the 578-bp variable region encoding the VP2 protein known to be involved in virulence was sequenced. The cumulative mortality after experimental challenge with field isolates genetically characterized as highly virulent was always high (40-56%), while the cumulative mortality of the same strains in vaccinated post-smolts during the field outbreaks varied from 1 to 50%. Although the tested samples came from fish vaccinated with the same vaccine product, the protection against IPN varied. These results demonstrate that differences in virulence of the isolates were not the main reason for the variation in mortality in the field outbreaks. Most of the field isolates were of high virulence, which is shown in experimental challenges to be important for mortality, but clearly other factors that might affect the susceptibility of IPN also play an important role in the outcome of an IPNV infection. [ABSTRACT FROM AUTHOR]

Plasmodium falciparum infection can lead to a life threatening disease and the pathogenetic mechanisms of severe manifestations are not fully understood. Here, we investigated the capacity of P. falciparum -parasitized red blood cells (PRBC) from 45 children with clinical malaria to induce endothelial cell (EC) apoptosis. In all subjects, PRBC that cytoadhered to ECs could be found albeit to a variable degree. By contrast, PRBC that induce EC apoptosis were found only in nine (20%) subjects. Interestingly, children with neurological manifestations were significantly more likely to harbour apoptogenic strains. There was no quantitative relationship between the capacity of these isolates to cytoadhere and apoptosis induction. We hypothesize that P. falciparum -encoded molecules could be responsible for apoptosis induction and therefore suggest new insights in the pathogenesis of P. falciparum malaria. Further investigations are currently in progress to determine whether these results can be confirmed and to identify putative parasite apoptogenic factors. [ABSTRACT FROM AUTHOR]