Knowledge of the incubation period of infectious diseases (time between host infection and expression of disease symptoms) is crucial to our epidemiological understanding and the design of appropriate prevention and control policies. Plant diseases cause substantial damage to agricultural and arboricultural systems, but there is still very little information about how the incubation period varies within host populations. In this paper, we focus on the incubation period of soilborne plant pathogens, which are difficult to detect as they spread and infect the hosts underground and above-ground symptoms occur considerably later. We conducted experiments on Rhizoctonia solani in sugar beet, as an example patho-system, and used modelling approaches to estimate the incubation period distribution and demonstrate the impact of differing estimations on our epidemiological understanding of plant diseases. We present measurements of the incubation period obtained in field conditions, fit alternative probability models to the data, and show that the incubation period distribution changes with host age. By simulating spatially-explicit epidemiological models with different incubation-period distributions, we study the conditions for a significant time lag between epidemics of cryptic infection and the associated epidemics of symptomatic disease. We examine the sensitivity of this lag to differing distributional assumptions about the incubation period (i.e. exponential versus Gamma). We demonstrate that accurate information about the incubation period distribution of a pathosystem can be critical in assessing the true scale of pathogen invasion behind early disease symptoms in the field; likewise, it can be central to model-based prediction of epidemic risk and evaluation of disease management strategies. Our results highlight that reliance on observation of disease symptoms can cause significant delay in detection of soil-borne pathogen epidemics and mislead practitioners and epidemiologists about the timing, extent, and viability of disease control measures for limiting economic loss.

Plant disease complexes are a playground to investigate coinfections in natural or cultivated systems. Pathogens of such complexes may affect each other through direct and/or indirect interactions and lead to changes in virulence or aggressiveness, offspring production, and transmission. As coinfections by sympatric host‐pathogens can strongly influence pathogen dynamics and their evolutionary trajectories, new insights into the mechanisms of their coexistence is thus of critical importance. In order to characterize differences in ecological niches liable to explain species coexistence on the same host, the inter‐ and intraspecific diversity of the life history traits in natural collections of the two main pathogens (Peyronellaea (formerly Didymella) pinodes [Dp] and Phoma medicaginis var. pinodella [Pmp]) of the ascochyta blight disease complex of pea was evaluated under controlled conditions. Dp strains developed 1.3 times faster and produced longer, mainly bicellular spores and in lower amounts (3.7 times less) than Pmp strains. Pmp strains were separated into two groups, one producing more pycnidiospores, mainly bicellular, with less resources, and the other with mainly unicellular ones. These three groups can be interpreted as three distinct life history strategies: pioneer colonizer (Dp), scavenger (large‐spored Pmp), and intermediate (small‐spored Pmp), allowing differentiation in access to and use of resources. While this experimental work provides new insight into coexistence of two species of the ascochyta blight disease complex of pea, it also raises the question of the benefit of having two distinct life history strategies for one species (Pmp).

The dietary composition and partitioning of food resources between five sympatric species of Platycephalidae inhabiting the coastal waters of New South Wales, Australia was investigated. Samples were collected monthly between March and November 2007 onboard commercial ocean prawn trawlers based in the ports of Yamba and Newcastle. Monthly percentage weight contribution of 12 prey categories was analysed to determine if diet was influenced by the variables: species, location, depth, size and maturity. Of the 959 stomachs from the five species examined, 28-54% contained prey. All Platycephalid species primarily consumed teleosts, however the diversity of prey and the proportion each prey type contributed to the overall diet varied substantially between species. Platycephalus caeruleopunctatus, P. longispinis, P. richardsoni and Ambiserrula jugosa were generalist carnivores and consumed prey from a wide variety of phyla including teleosts, crustaceans, polychaetes, molluscs and echinoderms. In contrast, Ratabulus diversidens were primarily piscivorous.Partitioning of prey resources between species was more evident in waters at Yamba than at Newcastle. Differences in diet between locations were considered a result of differential prey exploitation rather than shifts in the suite of prey consumed. Dietary composition was observed to be influenced by size, maturity status and depth however these differences were not observed for all species.

Multi-infections may result in either competitive exclusion or coexistence on the same host of pathogen genotypes belonging to the same or different species. Epidemiological consequences of multiple infections, particularly how the development and transmission of a pathogen can be modified by the presence of another pathogen, are well documented. However, understanding how life history strategies of each pathogen modulate co-infection outcomes remains quite elusive. To analyze how co-infection drives changes in life history traits and affects coexistence in epidemic pathogens, we infected detached pea stipules with two fungal species, Peyronellaea pinodes and Phoma medicaginis var. pinodella (considering two strains per species), part of the ascochyta blight complex but presenting different life history strategies. All pairwise combinations (including self-pairs) between two strains of each species were tested. Strains were inoculated simultaneously, but apart from one another on the stipule. For each strain, four life history traits were measured: incubation period, necrosis area six days after inoculation, latent period and offspring production. Results show that, in co-infection, when resources are highly allocated to lesion development, the time between inoculation and the appearance of reproduction structures (latent period) and offspring production decreased, and vice-versa relative to single infections. The direction and/or magnitude of these responses to co-infection depend on the co-infecting strains. Moreover, these changes were always higher in self-pairs than in mixed co-infections. These results suggest facilitation between co-infecting strains, resulting in the selection of an intermediate level of virulence (here measured as the lesion development) at the expense of pathogen offspring production. This strategy allows the development and reproduction of each co-infecting strain when sharing limited resources. However, the direction and strength of these life history traits variations in co-infection depend on the life history strategy of the co-infecting strains, with a clear difference between 'opportunists', 'scavengers' and 'pioneer colonisers'.

Assessing life-history traits of parasites on resistant hosts is crucial in evolutionary ecology. In the particular case of sporulating pathogens with growing lesions, phenotyping is difficult because one needs to disentangle properly pathogen spread from sporulation. By considering Phytophthora infestans on potato, we use mathematical modelling to tackle this issue and refine the assessment of pathogen response to quantitative host resistance. We elaborate a parsimonious leaf-scale model by convolving a lesion growth model and a sporulation function, after a latency period. This model is fitted to data obtained on two isolates inoculated on three cultivars with contrasted resistance level. Our results confirm a significant host–pathogen interaction on the various estimated traits, and a reduction of both pathogen spread and spore production, induced by host resistance. Most interestingly, we highlight that quantitative resistance also changes the sporulation function, the mode of which is significantly time-lagged. This alteration of the infectious period distribution on resistant hosts may have strong impacts on the dynamics of parasite populations, and should be considered when assessing the durability of disease control tactics based on plant resistance management. This inter-disciplinary work also supports the relevance of mechanistic models for analysing phenotypic data of plant–pathogen interactions.

Understanding the transmission of plant pathogen inoculum during the periods when the host plants are not present is crucial for predicting the initiation of epidemics and optimizing mitigation strategies. However, inoculum production at the end of the cropping season, survival during the intercrop period, and the emergence or release of inoculum can be highly variable, difficult to assess, and generally inferred indirectly from symptom data. As a result, a lack of large datasets hampers the study of these epidemiological processes. Here, inoculum production was studied in Leptosphaeria maculans, the cause of phoma stem canker of oilseed rape. The fungus survives on stubble left in the field, from which ascospores are released at the beginning of the next cropping season. An image processing framework was developed to estimate the density of fruiting bodies produced on stem pieces following incubation in field conditions, and a quality assessment of the processing chain was performed. A total of 2540 standardized RGB digital images of stems were then analysed, collected from 27 oilseed rape fields in Brittany over four cropping seasons. Manual post‐processing removed 16% of the pictures, e.g. when moisture‐induced darkening of the oilseed rape stems caused overestimation of the area covered with fruiting bodies. The potential level of inoculum increased with increasing phoma stem canker severity at harvest, and depended on the source field and the cropping season. This work shows how image‐based phenotyping generates high‐throughput disease data, opening up the prospect of substantially increased precision in epidemiological studies.

Until recently, genotypes of Phytophthora infestans were regionally distributed in Europe, with populations in western Europe being dominated by clonal lineages and those in northern Europe being genetically diverse due to frequent sexual reproduction. However, since 2013, a new clonal lineage (EU_41_A2) has successfully established itself and expanded in the sexually recombining P. infestans populations of northern Europe. The objective of this study was to study phenotypic traits of the new clonal lineage of P. infestans, which may explain its successful establishment and expansion within sexually recombining populations. Fungicide sensitivity, aggressiveness and virulence profiles of isolates of EU_41_A2 were analyzed and compared to those of the local sexual populations from Denmark, Norway, and Estonia. None of the phenotypic data obtained from the isolates collected from Denmark, Estonia and Norway independently explained the invasive success of EU_41_A2 within sexual Nordic populations. Therefore, we hypothesize that the expansion of this new genotype could result from a combination of fitness traits and more favorable environmental conditions that have emerged due to climate change.

No abstract