Cercospora leaf spot, caused by the fungal pathogen Cercospora beticola, is the most destructive foliar disease of sugar beet worldwide. This review discusses C. beticola genetics, genomics, and biology and summarizes our current understanding of the molecular interactions that occur between C. beticola and its sugar beet host. We highlight the known virulence arsenal of C. beticola as well as its ability to overcome currently used disease management strategies. Finally, we discuss future prospects for the study and management of C. beticola infections in the context of newly employed molecular tools to uncover additional information regarding the biology of this pathogen.Taxonomy: Cercospora beticola Sacc.; Kingdom Fungi, Phylum Ascomycota, Class Dothideomycetes, Order Capnodiales, Family Mycosphaerellaceae, Genus Cercospora.Host range: Well‐known pathogen of sugar beet (Beta vulgaris subsp. vulgaris) and most species of the Beta genus. Reported as pathogenic on other members of the Chenopodiaceae (e.g., lamb's quarters, spinach) as well as members of the Acanthaceae (e.g., bear's breeches), Apiaceae (e.g., Apium), Asteraceae (e.g., chrysanthemum, lettuce, safflower), Brassicaceae (e.g., wild mustard), Malvaceae (e.g., Malva), Plumbaginaceae (e.g., Limonium), and Polygonaceae (e.g., broad‐leaved dock) families.Disease symptoms: Leaves infected with C. beticola exhibit circular lesions that are coloured tan to grey in the centre and are often delimited by tan‐brown to reddish‐purple rings. As disease progresses, spots can coalesce to form larger necrotic areas, causing severely infected leaves to wither and die. At the centre of these spots are black spore‐bearing structures (pseudostromata). Older leaves often show symptoms first and younger leaves become infected as the disease progresses.Management: Application of a mixture of fungicides with different modes of action is currently performed although elevated resistance has been documented in most employed fungicide classes. Breeding for high‐yielding cultivars with improved host resistance is an ongoing effort and prudent cultural practices, such as crop rotation, weed host management, and cultivation to reduce infested residue levels, are widely used to manage disease.Useful website: https://www.ncbi.nlm.nih.gov/genome/11237?genome_assembly_id=352037

Bacterial diseases are one of the most important biotic constraints of potato production, especially in tropical and subtropical regions, and in some warm temperate regions of the world. About seven bacterial diseases affect potato worldwide and cause severe damages especially on tubers, the economically most important part of the plant. Bacterial wilt and back leg are considered the most important diseases, whereas potato ring rot, pink eye, and common scab are the minor. Knowledge about zebra chip is extremely rare, as it occurs in a very isolated area and is an emerging disease in New Zealand, Europe, the USA and Mexico. Potato crop losses due to bacterial diseases could be direct and indirect; and they have several dimensions, some with short-term consequences such as yield loss and unmarketability of the produce and others with long-term consequences such as economic, environmental, and social. Some of them are of national and international importance and are the major constraints to clean seed potato production, with considerable indirect effects on trade. This review focuses on Clavibacter spp., Ralstonia spp., Pectobacterium spp., Dickeya spp., Streptomyces spp., and Liberibacter spp. pathogenic to potato, and looks at the respective pathogen in terms of their taxonomy and nomenclature, host range, geographical distribution, symptoms, epidemiology, pathogenicity and resistance, significance and economic losses, and management strategies. Nevertheless, the information collected here deal more with diseases known in developed and developing countries which cause severe economic losses on potato value chain.

This chapter discusses the major potato diseases worldwide: late blight, early blight, wart, and powdery scab. Late blight, caused by the oomycete Phytophthora infestans, continues to be the main biotic constraint of potato production. Annual losses have been estimated to be about €6.1 billion, with major consequences to food security, especially in developing countries. Symptoms of the disease can be seen in leaves (water-soaked light to dark brown spots), stems (brown spots), and tubers (slightly depressed areas with reddish-brown color). High humidity and mild temperatures are essential for disease development and, under optimal conditions, the disease can destroy a field in a few days. Phytophthora infestans evolves continuously, mainly through recombination and migration from other areas. Thus, monitoring of P. infestans populations is critical for the design of effective management strategies. Fungicides remain as the most common tactic for late blight management, but environmental considerations are increasing the pressure to use host resistance, sanitation, and other measures. New solutions being developed to manage late blight include, among others, smart phone-based decision support systems linked to portable molecular diagnostics kits that can disseminate disease information rapidly to a large number of farmers. Emerging research topics on P. infestans include the role of the pathogen–microbiota interaction in promotion or suppression of the disease, as well as the metabolism of P. infestans. The fungus Alternaria solani is the main pathogen causing early blight on potatoes. Early blight can be found in most potato-growing countries. Typical symptoms on the leaves are dark brown to black spots with concentric rings (target spot). In susceptible potato cultivars in particular, as well as in locations (especially in warmer areas) with increased occurrence of A. solani, the disease can cause considerable yield losses. Integrated pest management to control early blight requires the implementation of several approaches. The disease is primarily controlled by the use of cultural practices (to reduce the soil born inoculum), less susceptible cultivars and the use of pesticides. But there is a loss in sensitivity toward two groups of fungicides described. The loss in sensitivity towards succinate dehydrogenase inhibitor (SDHI) and Quinone outside inhibitor (QoI) fungicides are caused by different point mutations. In many countries the occurrence of SDHI and QoI mutants is reported. Therefore, the control of early blight will be a considerable challenge in the future. The increasing importance of early blight in potatoes is due to a number of factors. Synchytrium endobioticum is a soil-borne biotrophic fungus causing potato wart disease of cultivated potato. The fungus originates from the Andean zones of South America, from where it spread first to Europe in the late of the nineteenth century. Presently, the geographical distribution of this pathogen includes almost all European and Mediterranean Plant Protection Organization (EPPO) countries, Asia, North and South America as well as Oceania (New Zealand). The typical symptoms of cauliflower-like galls could develop on all meristematic tissues of potato except roots. S. endobioticum produces summer sporangia with mobile zoospores that can move in the soil. Winter (resting) sporangia are the dormant structures by which the fungus disperses to establish new infections. They can survive more than 40 years without plant hosts. The pathogen does not produce hyphae. Its long persistence in soil and the severe losses it inflicts to potato crops have prompted its inclusion into the A2 quarantine list of EPPO. Since the discovery of pathotype 2(G1) in Germany, more than 40 pathotypes were reported in Europe. In Europe, pathotypes 1(D1), 2(G1), 6(O1), and 18(T1) are the most relevant. Other pathotypes occur mainly in the rainy mountainous areas of central and eastern Europe. S. endobioticum is a still serious problem for crop production in countries with moderate climates. The strategies to confine the disease are strict quarantine and phytosanitary measures, and the cultivation of resistance cultivars of potato. Spongospora subterranea causes root galling and tuber powdery scab leading to quality and yield losses in seed and ware crops worldwide and is also important as the natural vector of potato mop-top virus (PMTV), an economically important tuber blemish disease of potato. S. subterranea spreads by movement of infected seed tubers and soil and can survive long periods in soils and some asymptomatic hosts. Powdery scab is particularly favored by cool, damp conditions and is an intractable disease. Avoidance is the best control for powdery scab, but once soil is infested with S. subterranea, cultural practices and chemical treatments are ineffective control methods, and host resistance appears to be the most promising mechanism for long-term management. Although sources of host resistance have been identified, they are not widely deployed in practice. S. subterranea is an unculturable biotroph, making research difficult. Recent progress in understanding the biology of S. subterranea as a result of the application of basic molecular techniques, and future opportunities to further advance knowledge of this understudied pathogen, and the virus that it vectors, are included.

Cercospora leaf spot (CLS), caused by the fungal pathogen Cercospora beticola, is the most destructive disease of sugar beet worldwide. Although growing CLS-tolerant varieties is helpful, disease management currently requires timely application of fungicides. However, overreliance on fungicides has led to the emergence of fungicide resistance in many C. beticola populations, resulting in multiple epidemics in recent years. Therefore, this study focused on developing a fungicide resistance detection “toolbox” for early detection of C. beticola in sugar beet leaves and mutations associated with different fungicides in the pathogen population. A loop-mediated isothermal amplification (LAMP) method was developed for rapid detection of C. beticola in infected sugar beet leaves. The LAMP primers specific to C. beticola (Cb-LAMP) assay was able to detect C. beticola in inoculated sugar beet leaves as early as 1 day postinoculation. A quinone outside inhibitor (QoI)-LAMP assay was also developed to detect the G143A mutation in cytochrome b associated with QoI resistance in C. beticola. The assay detected the mutation in C. beticola both in vitro and in planta with 100% accuracy. We also developed a probe-based quantitative PCR (qPCR) assay for detecting an E198A mutation in β-tubulin associated with benzimidazole resistance and a probe-based qPCR assay for detection of mutations in cytochrome P450-dependent sterol 14α-demethylase (Cyp51) associated with resistance to sterol demethylation inhibitor fungicides. The primers and probes used in the assay were highly efficient and precise in differentiating the corresponding fungicide-resistant mutants from sensitive wild-type isolates.