Local dispersal of Puccinia striiformis f. sp. tritici from isolated source lesions.

Understanding how disease foci arise from single source lesions has not been well studied. Here, single wheat leaves were inoculated with Puccinia striiformis f. sp. tritici urediniospores, and all wheat leaves within two intersecting 0.3 × 3.0 m transects were sampled in eight replicates over three years. The lesions observed on each of the top three leaves on plants within 1.5 m from the source lesion were three-dimensionally mapped. The total number of lesions within a 1.5 m radius was estimated by dividing the number of lesions observed within each 0.025 m-wide annulus by the fraction of the annulus sampled. The estimated total number of lesions produced within 1.5 m of a single source lesion ranged from 27 to 776, with a mean of 288 lesions. Eighty percent of the lesions were recorded within 0.69 m of the source infection. The proportion of total lesions observed at a given distance from the source was fitted well by the Lomax and Weibull distributions, reflecting the large proportion of lesions arising close to the source, and when fitted to an inverse-power distribution had a slope (b) of 2.5. There were more lesions produced on leaves higher in the canopy than on lower leaves, with more lesions being detected above than below the point of inoculation. Simultaneous measurement of lesion gradients and spore dispersal in the final year of the study suggests that this pattern is due to greater susceptibility of upper leaves, rather than increased dispersal to upper leaves.

Effect of Plant Age and Leaf Position on Susceptibility to Wheat Stripe Rust.

In addition to pathogen propagule dispersal, disease spread requires successful infection of host tissue. In plant disease epidemiology, susceptibility of host tissue is often assumed to be constant. This assumption ignores changes in host phenology due to developmental stage. To examine this assumption, 3-, 4-, and 5-week-old wheat plants were inoculated with equal quantities of urediniospores of Puccinia striiformis f. sp. tritici, the causal agent of wheat stripe rust (WSR). Disease severity on each leaf was assessed and fit by mixed-effect linear model as a function of leaf position and plant age. Younger plants had significantly greater disease severity than older plants, with mean severities of 50.4, 30.1, and 12.9% on plants that were 3, 4, and 5 weeks old, respectively, at time of inoculation. This effect was greater on leaves higher on the plant. Within same-aged plants, younger leaves had significantly greater disease severity than older leaves, with mean severities of 40.2, 34.8, and 17.7% on the uppermost, second, and third leaf, respectively. These results suggest that the vertical distribution of WSR lesions in agricultural fields could be driven by differences in host susceptibility more so than propagule dispersal.

First Report of Resistance to QoI Fungicides in North American Populations of Zymoseptoria tritici, Causal Agent of Septoria Tritici Blotch of Wheat.

The G143A mutation in cytb (cytochrome b gene) is associated with high levels of resistance to quinone outside inhibitor (QoI or strobilurin) fungicides that disrupt electron transport during cellular respiration (1). The G143A mutation in Zymoseptoria tritici (synonyms: Mycosphaerella graminicola and Septoria tritici), the causal agent of septoria tritici blotch of wheat (Triticum aestivum), was first reported in Europe in 2001 (1). Although Z. tritici has a global distribution (3), G143A mutants of Z. tritici have not been reported outside of Europe. We used PCR-RFLP (4) to estimate the frequencies of G143A mutants in Z. tritici populations at two locations in the Willamette Valley of western Oregon: the Hyslop Crop Science Field Research Laboratory (Hyslop Farm, HF), Benton County (44°37'52.85″ N, 123°11'55.19″ W) and research plots planted in a commercial wheat field in Washington County (45°33'58.53″ N, 123°00'11.78″ W) (North Valley Farm, NVF). Isolates originated from flag leaf collections from two cultivars ('Bobtail' and 'Tubbs 06') made in April and June of 2012 from plants in a replicated fungicide-treatment experiment, with isolates collected from both sprayed and unsprayed plots. Sixteen of the 169 isolates (9.5%) from HF possessed the G143A mutation (7 of 132 isolates from plots not receiving a QoI fungicide and 9 of 37 isolates collected from plots receiving two applications of the QoI azoxystrobin). One hundred forty six of the 175 isolates (83.4%) from NVF were G143A mutants (101 of 129 isolates from plots receiving no QoI fungicide and 45 of 46 isolates from plots receiving two applications of azoxystrobin). Results of phenotypic assays of a subset of 10 isolates from each location (5 mutants, 5 wild types from each location; 20 isolates altogether) supported a high level of resistance to azoxystrobin only in the G143A mutants. All 10 G143A mutants developed colonies after 8 days of growth on YMA plates amended with SHAM (2) and 1 ppm or 10 ppm azoxystrobin, with nine and eight G143A mutant isolates developing colonies on plates amended with 1 ppm and 10 ppm azoxystrobin, respectively. None of the wild-type isolates developed colonies on plates amended with SHAM and 1 ppm azoxystrobin, nor on plates amended with SHAM and 10 ppm azoxystrobin. All 20 isolates developed colonies on YMA plates lacking azoxystrobin, and treatments produced identical results across three replicates. These results are consistent with findings of higher levels of azoxystrobin resistance in G143A mutants compared to wild types in European populations (1). Isolates from HF and NVF differ in their previous exposure to QoI fungicides. The majority of the wheat area at HF is planted to breeding plots that are not sprayed with fungicide. Plots at NVF were planted in a commercial wheat field in a county where most wheat fields were treated with two to three applications of strobilurins each year over the past 4 years. Future monitoring for G143A mutants of Z. tritici throughout its range in North America will be necessary to assess whether strobilurin resistance will spread via wind-dispersal of ascospores or emerge de novo in treated fields. In Europe, stobilurins were first applied to wheat in 1996. G143A mutants of Z. tritici emerged de novo several times (4) and were widespread by 2007. References: (1) B. A. Fraaje et al. Phytopathology 95:933, 2005. (2) J. A. LaMondia. Tob. Sci. 49:1, 2012. (3) E. S. Orton et al. Mol. Plant Pathol. 12:413, 2011. (4) S. F. F. Torriani et al. Pest Manag. Sci. 65:155, 2008.

Intraspecific functional diversity in hosts and its effect on disease risk across a climatic gradient.

The effects of host biodiversity on disease risk may vary greatly depending on host population structure and climatic conditions. Agricultural diseases such as potato late blight, caused by Phytophthora infestans, provide the opportunity to study the effects of intraspecific host diversity that is relatively well-defined in terms of disease resistance phenotypes and may have functional impacts on disease levels. When these systems are present across a climatic gradient, it is also possible to study how season length and conduciveness of the environment to disease may influence the effects of host diversity on disease risk. We developed a simple model of epidemic progress to evaluate the effects on disease risk of season length, environmental disease conduciveness, and host functional divergence for mixtures of a susceptible host and a host with some resistance. Differences in disease levels for the susceptible vs. resistant genotypes shifted over time, with the divergence in disease levels first increasing and then decreasing. Disease reductions from host diversity were greatest for high host divergence and combinations of environmental disease conduciveness and season length that led to moderate disease severity. We also compared the effects of host functional divergence on potato late-blight risk in Ecuador (long seasons), two sites in Peru (intermediate seasons) in El Niño and La Niña years, and the United States (short seasons). There was some evidence for greater disease risk reduction from host diversity where seasons were shorter, probably because of lower regional inoculum loads. There was strong evidence for greater disease reduction when host functional divergence was greater. These results indicate that consideration of season length, environmental conduciveness to disease, and host functional divergence can help to explain the variability in disease response to host diversity.

Specificity of incomplete resistance to Mycosphaerella graminicola in wheat.

We examined interactions between wheat (Triticum aestivum) and Mycosphaerella graminicola, causal agent of Septoria tritici blotch, to determine whether specific interactions occur between host and pathogen genotypes that could be involved in eroding resistance. The moderate resistance of the wheat cultivar Madsen has eroded significantly in the Willamette Valley of Oregon since its release in 1990. Foote is a replacement cultivar expressing moderate resistance and was released in 2000. Isolates of M. graminicola were collected from Foote and Madsen in 2004 and 2005 and tested on each cultivar in growth chamber and greenhouse experiments. There was a significant (P

Frequency of sexual recombination by Mycosphaerella graminicola in mild and severe epidemics.

The importance of sexual recombination in determining fungal population structure cannot be inferred solely from the relative abundance of sexual and asexual spores and reproductive structures. To complement a previously reported study of proportions of Mycosphaerella graminicola ascocarps and pycnidia, we investigated the share of sexual recombinants among isolates randomly derived from the same field at the same time. Early in three successive growing seasons (those ending in 1998, 1999, and 2000), field plots of the susceptible winter wheat cultivar Stephens were inoculated with suspensions of two M. graminicola isolates that each had rare alleles at restriction fragment length polymorphism (RFLP) loci. Near harvest time, leaves were randomly sampled from the same plots, and a population of over 100 monopycnidial isolates was created for each year of the experiment. Natural populations were also sampled from noninoculated plots in the 1999 and 2000 seasons, in order to compare allele frequencies. Based on RFLP haplotypes and DNA fingerprints, isolates from the inoculated plots were categorized by both inspection and Bayesian methods as inoculant clones, recombinants, or immigrants. Inoculation in the 2000 season was delayed, and the recovery rate of inoculant types was just 1 to 2%. In 1998, a high-disease year, and 1999, a low-disease year, inoculants comprised 36 and 22 to 23% of end-of-season samples, respectively. In those 2 years, recombinants as a percentage of inoculant descendants (both sexual and asexual) were 35 and 32%, respectively. By comparison, the study of fruiting bodies had found 93 and 32% of M. graminicola fruiting bodies were ascocarps in 1998 and 1999, respectively. These findings support the hypothesis that sexual recombination makes a relatively consistent contribution to M. graminicola population structure, despite differences in epidemic severity and ascocarp proportions.

Sexual reproduction facilitates the adaptation of parasites to antagonistic host environments: Evidence from empirical study in the wheat-Mycosphaerella graminicola system.

Most eukaryotes use sexual reproduction to transmit genetic information from generation to generation despite the advantages offered by asexual reproduction. One theory to explain the origin and maintenance of sexual reproduction hypothesises that sexual recombination generates genetic variation that allows faster adaptation to fluctuating and/or stressful environments. We used a combination of ecological, molecular genetic, statistical and experimental evolution approaches to test this hypothesis in an agricultural plant-pathogen system. We inoculated wheat hosts with 10 strains of the fungal pathogen Mycosphaerella graminicola in a field experiment and estimated the contributions of sexual reproduction, asexual reproduction and immigration to the genetic composition of fungal populations sampled from moderately resistant and susceptible hosts through the course of an epidemic cycle. We found that a significant proportion of the M. graminicola population in the late phase of the epidemic originated from sexual reproduction among isolates that had been introduced into the field plots at the beginning of the epidemic. Recombinants were recovered at a higher frequency on the moderately resistant plant host Madsen than on the susceptible host Stephens. By the end of the growing season, we estimated that approximately 13% of the strains sampled from the resistant host were recombinants, compared with 9% in the samples collected from the susceptible host. We also found that pathogen strains originating from the resistant cultivar displayed higher levels of fitness, virulence and fungicide tolerance than those originating from the susceptible cultivar. Our results provide empirical support for the hypothesis that sexual reproduction facilitates the evolution of parasites to overcome host resistance.

Pyramiding and dissecting disease resistance QTL to barley stripe rust.

Quantitative resistance (QR) to disease is usually more durable than qualitative resistance, but its genetic basis is not well understood. We used the barley/barley stripe rust pathosystem as a model for the characterization of the QR phenotype and associated genomic regions. As an intermediate step in the preparation of near-isogenic lines representing individual QTL alleles and combinations of QTL alleles in a homogeneous genetic background, we developed a set of QTL introgression lines in a susceptible background. These intermediate barley near-isogenic (i-BISON) lines represent disease resistance QTL combined in one-, two-, and three-way combinations in a susceptible background. We measured four components of disease resistance on the i-BISON lines: latent period, infection efficiency, lesion size, and pustule density. The greatest differences between the target QTL introgressions and the susceptible controls were for the latter three traits. On average, however, the QTL introgressions also had longer latent periods than the susceptible parent (Baronesse). There were significant differences in the magnitudes of effects of different QTL alleles. The 4H QTL allele had the largest effect, followed by the alleles on 1H and 5H. Pyramiding multiple QTL alleles led to higher levels of resistance in terms of all components of QR except latent period.

Effect of population size on the estimation of QTL: a test using resistance to barley stripe rust.

The limited population sizes used in many quantitative trait locus (QTL) detection experiments can lead to underestimation of QTL number, overestimation of QTL effects, and failure to quantify QTL interactions. We used the barley/barley stripe rust pathosystem to evaluate the effect of population size on the estimation of QTL parameters. We generated a large (n = 409) population of doubled haploid lines derived from the cross of two inbred lines, BCD47 and Baronesse. This population was evaluated for barley stripe rust severity in the Toluca Valley, Mexico, and in Washington State, USA, under field conditions. BCD47 was the principal donor of resistance QTL alleles, but the susceptible parent also contributed some resistance alleles. The major QTL, located on the long arm of chromosome 4H, close to the Mlo gene, accounted for up to 34% of the phenotypic variance. Subpopulations of different sizes were generated using three methods-resampling, selective genotyping, and selective phenotyping-to evaluate the effect of population size on the estimation of QTL parameters. In all cases, the number of QTL detected increased with population size. QTL with large effects were detected even in small populations, but QTL with small effects were detected only by increasing population size. Selective genotyping and/or selective phenotyping approaches could be effective strategies for reducing the costs associated with conducting QTL analysis in large populations. The method of choice will depend on the relative costs of genotyping versus phenotyping.

Use of multiline cultivars and cultivar mixtures for disease management.

The usefulness of mixtures (multiline cultivars and cultivar mixtures) for disease management has been well demonstrated for rusts and powdery mildews of small grain crops. Such mixtures are more useful under some epidemiological conditions than under others, and experimental methodology, especially problems of scale, may be crucial in evaluating the potential efficacy of mixtures on disease. There are now examples of mixtures providing both low and high degrees of disease control for a wide range of pathosystems, including crops with large plants, and pathogens that demonstrate low host specificity, or are splash dispersed, soilborne, or insect vectored. Though most analyses of pathogen evolution in mixtures consider static costs of virulence to be the main mechanism countering selection for pathogen complexity, many other potential mechanisms need to be investigated. Agronomic and marketing considerations must be carefully evaluated when implementing mixture approaches to crop management. Practical difficulties associated with mixtures have often been overestimated, however, and mixtures will likely play an increasingly important role as we develop more sustainable agricultural systems.

Sensitivity of Wheat Genotypes to a Toxic Fraction Produced by Cephalosporium gramineum and Correlation with Disease Susceptibility.

ABSTRACT Cephalosporium stripe is an important disease of winter wheat (Triticum aestivum) in several areas of the world, especially where stubble mulch and early seeding are practiced to maintain soil moisture and prevent erosion. We developed a procedure to mass-produce a toxic fraction produced by Cephalosporium gramineum through a modification of the method of Kobayashi and Ui. Exposure of excised wheat leaves to a concentration of 60 mul/ml of the toxic fraction for 72 h produced distinct wilting symptoms that allowed us to distinguish toxin-sensitive wheat genotypes in a repeatable manner. Twenty wheat genotypes belonging to four distinct germ plasm groups (common, club, durum, and synthetic) were evaluated. Variation in toxin sensitivity of wheat genotypes was mostly at the level of the germ plasm group, and all differences among the four germ plasm groups were highly significant (P < 0.001) based on linear contrasts. Seventeen winter wheat genotypes representing the common, club, and durum germ plasm groups were planted in C. gramineum-infested fields at two locations. The logarithm of the percentage of tillers showing whitehead symptoms at each of the two locations was significantly (P < 0.0001) correlated with wilting symptoms measured by the toxin assay (r = 0.80 and 0.84). The common wheat genotypes were all sensitive to the toxic fraction, but showed a substantial range of disease reactions in the field. However, we found no case of a toxin-insensitive genotype being susceptible in the field. These results suggest that toxin insensitivity may be an important mechanism of resistance to Cephalosporium stripe, but that other mechanisms are operative as well. The toxin assay may be useful as an initial screening procedure to reduce the number of genotypes to be tested in the field.

The effects of host diversity and other management components on epidemics of potato late blight in the humid highland tropics.

ABSTRACT A field study at three highland sites near Quito, Ecuador, was conducted to determine whether host-diversity effects on potato late blight would be as important as recently found in studies conducted in temperate areas. We compared three potato mixtures and use of mixtures in combination with different planting densities and two fungicide regimes. Treatment comparisons were made by absolute and relative measures of host-diversity effects and incorporating a truncated area under the disease progress curve as a means of standardizing comparisons across sites. Potato-faba intercrops consisting of only 10% potato provided an estimate of the effects of dilution of susceptible host tissue. Host-diversity effects were very different across study sites, with a large host-diversity effect for reduced disease only at the site most distant from commercial potato production. Planting density had little influence on host-diversity effects or on late blight in single-genotype stands. Fungicide use in combination with potato mixtures enhanced a host-diversity effect for reduced late blight. Potato-faba intercrops produced only a small decrease in potato late blight. Effects of host diversity on yield were variable, with the greatest increase in yield for mixtures treated with fungicides at the site most distant from commercial potato production. The effects of host diversity on late blight severity may be less consistent in the tropical highlands than in the temperate zone, but can contribute to integrated disease management.

Using Restriction Fragment Length Polymorphisms to Assess Temporal Variation and Estimate the Number of Ascospores that Initiate Epidemics in Field Populations of Mycosphaerella graminicola.

ABSTRACT Restriction fragment length polymorphisms (RFLPs) and DNA fingerprints were used to assess temporal variation and estimate the effective population size of the wheat pathogen Mycosphaerella graminicola over a 6-year period. In each year, the fungal population was founded by ascospores originating from outside the sampled fields. A total of 605 fungal isolates were included in this study. Our results indicate that the genetic structure of these M. graminicola populations were stable over the 6-year period. The common alleles at each RFLP locus were present at similar frequencies each year. More than 99% of gene diversity was distributed within populations sampled from the same year and less than 1% was attributed to differences among years. The lack of population differentiation among collections taken in different years indicated that the effective size of the source population was sufficiently large that genetic drift was insignificant in this location. It also suggests that the initial colonists from ascospore founder populations were a fair reflection of the source population. We estimate that the effective sizes of these field populations ranged from 3,400 to 700,000 individuals, depending on the size of the field sampled and assumptions about mutation rates. Estimates of the number of ascospores initiating epidemics of leaf blotch disease in each field plot and factors that contribute to the large effective population size of M. graminicola are discussed.

Effects of competition on resistance gene polymorphism in a plant/pathogen system.

Puccinia striiformis, a fungal pathogen, has been shown to cause direct, negative frequency-dependent selection on its host, wheat (Triticum aestivum). This disease-induced frequency-dependent selection was not sufficient to maintain polymorphism for resistance genes in the host populations. The present study examines whether interactions between disease and competition could impact upon the maintenance of genetic polymorphism in a highly self-pollinated species such as wheat, where strong associations between traits are likely. Four different two-way mixtures of wheat genotypes, susceptible to different races of P. striiformis, were planted at different frequencies in both the presence and absence of disease. In order to examine the influence of competition and disease on the maintenance of genetic polymorphism, relationships between host absolute fitness and host frequency were studied for each genotype in the mixtures of plants both in the presence and in the absence of disease. In the absence of disease, the absolute fitness of the stronger competitor was often negatively frequency-dependent, or else it did not vary with host frequency; the absolute fitness of the weaker competitor was often positively frequency-dependent. Disease typically rendered the slopes between absolute fitness and genotype frequency more negative for the stronger competitor. However, the influence of disease was not strong enough to reverse the sign of the slope between absolute fitness and genotype frequency for the genotype that was the weaker competitor in the absence of disease. Thus, disease was unable to reverse the relative ranking of the two genotypes caused by competition and create the negative frequency dependence on both genotypes in a mixture that is required for the maintenance of genetic polymorphism.

Disease, frequency-dependent selection, and genetic polymorphisms: experiments with stripe rust and wheat.

Pathogens have the potential to maintain genetic polymorphisms by creating frequency-dependent selection on their host. This can occur when a rare host genotype is less likely to be attacked by a pathogen (frequency-dependent disease attack) and has higher fitness at low frequency (negative frequency-dependent selection). In this study, we used wheat genotypes that were susceptible to different races of the pathogen Puccinia striiformis to test whether disease created frequency-selection on its host and whether such selection could maintain polymorphisms for resistance genes in the wheat populations. Four different two-way mixtures of wheat genotypes were planted at different frequencies in both the presence and absence of disease. Disease created frequency-dependent selection on its host in some populations. Unknown factors other than disease also created frequency-dependent selection in this system because, in some instances, rare genotype advantage was observed in the absence of disease. Although the pathogen created frequency-dependent selection on its host, this selection was not sufficient to maintain genetic polymorphism in the host populations. In all cases where frequency-dependent selection occurred only in the diseased plots, one of the two genotypes was predicted to dominate in the population and the same genotype was predicted to dominate in both the presence and absence of disease. Only in cases where frequency-dependent selection was not caused by disease was there evidence that genetic polymorphisms would be maintained in the population. The frequency-dependent selection described in this study is a consequence of epidemiological effects of disease and differs from the time-lagged frequency-dependent selection resulting from coevolution between hosts and parasites. The impact of this direct frequency-dependent selection on the maintenance of genetic polymorphisms in the host population is discussed.

Genetic diversity and disease control in rice.

Crop heterogeneity is a possible solution to the vulnerability of monocultured crops to disease. Both theory and observation indicate that genetic heterogeneity provides greater disease suppression when used over large areas, though experimental data are lacking. Here we report a unique cooperation among farmers, researchers and extension personnel in Yunnan Province, China--genetically diversified rice crops were planted in all the rice fields in five townships in 1998 and ten townships in 1999. Control plots of monocultured crops allowed us to calculate the effect of diversity on the severity of rice blast, the major disease of rice. Disease-susceptible rice varieties planted in mixtures with resistant varieties had 89% greater yield and blast was 94% less severe than when they were grown in monoculture. The experiment was so successful that fungicidal sprays were no longer applied by the end of the two-year programme. Our results support the view that intraspecific crop diversification provides an ecological approach to disease control that can be highly effective over a large area and contribute to the sustainability of crop production.

Host diversity can reduce potato late blight severity for focal and general patterns of primary inoculum.

ABSTRACT The use of host diversity as a tool for management of potato late blight has not been viewed as promising in the past. But the increasing importance of late blight internationally has brought new consideration to all potential management tools. We studied the effect of host diversity on epidemics of potato late blight in Oregon, where there was little outside inoculum. The experimental system consisted of susceptible potato cv. Red LaSoda and a highly resistant breeding selection, inoculated with local isolates of US-8 Phytophthora infestans. Potatoes were grown in single-genotype plots and also in a mixture of 10 susceptible and 26 resistant potato plants. Half of the plots received inoculation evenly throughout the plot (general inoculation) and half received an equal quantity of inoculum in only one corner of the plot (focal inoculation). The area under the disease progress curve (AUDPC) was greater in single genotype stands of susceptible cv. Red LaSoda inoculated throughout the plot than with stands inoculated in one focus. The host-diversity effect on foliar late blight was significant in both years of the investigation; the AUDPC was reduced by an average of 37% in 1997 and 36% in 1998, compared with the mean disease level for the potato genotypes grown separately. Though the evidence for influence of inoculum pattern on host-diversity effects was weak (P = 0.15), in both years there was a trend toward greater host-diversity effects for general inoculation. Statistical significance of host-diversity effects on tuber yield and blight were found only in one of the two years. In that year, tuber yield from both the resistant and susceptible cultivar was increased in mixtures compared with single genotype stands and tuber blight was decreased in mixtures for susceptible cv. Red LaSoda.

Effects of planting density and the composition of wheat cultivar mixtures on stripe rust: an analysis taking into account limits to the replication of controls.

ABSTRACT The effect of plant density on disease is not well understood in populations of a single host plant genotype and has been studied even less in mixtures of host genotypes. We performed an experiment to evaluate the effect of wheat planting density on infection by Puccinia striiformis in experimental plots with a single wheat genotype and in plots with two genotypes making up a range of frequencies. Stripe rust severity in single-genotype plots increased with planting density in 1997 but decreased with planting density in 1998. Disease in host mixtures was compared to the weighted mean of disease levels in the corresponding single-genotype plots. The design of the field experiment included limited replication of these reference treatments (that is, there was not a unique pair of single-genotype plots for each mixture plot); therefore, we devised an analysis based on collapsing the data into independent mean observations. Disease reduction due to host diversity was less when one genotype predominated than when both host genotypes were present at nearly equal frequencies. The greatest mean host-diversity effect for reduced disease was at the intermediate planting density of 250 seeds per m(2).

Estimation of rates of recombination and migration in populations of plant pathogens-a reply.

ABSTRACT We find that the maximum likelihood method proposed by J. K. M. Brown has deficiencies that limit its usefulness for actual data sets. We propose two alternative statistical methods based on maximum likelihood that could be used to quantify rates of recombination and immigration in fungal populations. We also show that minor modification of our original method, which was based upon posterior probabilities, leads to a result that is identical to one of the maximum likelihood methods. Our previous estimates of the relative contributions of sexual reproduction, asexual reproduction, and immigration to the genetic structure of a Mycosphaerella graminicola population did not change significantly following reanalysis of our data with these new methods.

Epidemiology in mixed host populations.

ABSTRACT Although plant disease epidemiology has focused on populations in which all host plants have the same genotype, mixtures of host genotypes are more typical of natural populations and offer promising options for deployment of resistance genes in agriculture. In this review, we discuss Leonard's classic model of the effects of host genotype diversity on disease and its predictions of disease level based on the proportion of susceptible host tissue. As a refinement to Leonard's model, the spatial structure of host and pathogen population can be taken into account by considering factors such as autoinfection, interaction between host size and pathogen dispersal gradients, lesion expansion, and host carrying capacity for disease. The genetic composition of the host population also can be taken into account by considering differences in race-specific resistance among host genotypes, compensation, plant competition, and competitive interactions among pathogen genotypes. The magnitude of host-diversity effects for particular host-pathogen systems can be predicted by considering how the inherent characteristics of a system causes it to differ from the assumptions of the classic model. Because of the limited number of studies comparing host-diversity effects in different systems, it is difficult at this point to make more than qualitative predictions. Environmental conditions and management decisions also influence host-diversity effects on disease through their effect on factors such as host density and epidemic length and intensity.