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New Threats to Rice Production: Emerging Pathogens and their Impact

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Rodrigo Pedrozo, Samuel de Paula, Madison Flasco, Felipe Dalla Lana, Yulin Jia and Camila Nicolli

Submitted: 30 May 2025 Reviewed: 03 June 2025 Published: 09 July 2025

DOI: 10.5772/intechopen.1011393

Rice Cultivation and Consumption - Advancements in Research and Technology IntechOpen
Rice Cultivation and Consumption - Advancements in Research and T... Edited by Min Huang

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Rice Cultivation and Consumption - Advancements in Research and Technology [Working Title]

Dr. Min Huang

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Abstract

Rice (Oryza sativa L.) is a staple food for over 50% of the global population. Biotic and abiotic stresses contribute to about 10–30% annual yield losses in rice cultivation. Among these, rice diseases are major constraints, typically managed through genetic resistance, pesticide application, and cultural practices. However, pathogen evolution, vector dynamics, rising disease incidence, and shifts in geographic distribution have led to the emergence of diseases once considered no or minor threats. In the southern USA, rice hoja blanca virus is of particular concern due to the complexity of the rice-virus-vector interaction. After a 65-year absence, this virus reemerged in the southern United States, affecting a large area, though its distribution is likely underestimated. Another emerging pathogen is Pantoea ananatis, a globally distributed bacteria noted for its ecological plasticity and variable rice symptom expression influenced by environmental conditions. Despite its first report over two decades ago, the mechanisms underlying infection, colonization, and symptom development in rice remain poorly understood. Similarly, the narrow brown leaf spot and rice false smut, both fungal pathogens, have shown increasing incidence in recent years. Substantial knowledge gaps persist in their life cycles, hindering effective management. More specifically, rice false smut exhibits a unique floral infection strategy and remains largely unaddressed in breeding programs, with fungicides providing only limited suppression. This chapter focuses on the pathogen distribution and characterization, symptomatology, epidemiology, detection methods, and management strategies for these emerging rice pathogens, highlighting critical areas for future research.

Keywords

  • Hoja Blanca disease
  • Pantoea ananatis
  • narrow Brown leaf spot
  • Cercospora net blotch
  • Cercospora panicle blight
  • Villosiclava virens
  • outbreaks

1. Introduction

Rice (O. sativa) is cultivated in over 110 countries and serves as the primary staple food for more than half of the global population [1, 2]. The top producing countries are India and China, accounting for 27% each of the global production in the 2024–2025 season [3]. Rice is impacted during the entire growing season by biotic and abiotic stresses [4]. As a result, yield losses are estimated to be around 10–30% annually [5]. Phytopathogens represent significant biotic stresses in rice crops, adversely affecting photosynthesis, nutrient uptake, grain development and milling quality, and ultimately, yield potential [6]. The plant-pathogen interaction can be described as an evolutionary arms race, wherein plants respond to pathogen infection through an innate immune system that facilitates the deployment of defense molecules and the formation of physical barriers [7, 8]. Conversely, pathogens exploit a sophisticated arsenal of effectors to evade host recognition and successfully colonize plant tissues [9, 10]. Genetic resistance remains the most effective and preferred strategy for managing plant pathogens [11]. However, the dynamic interaction between host and pathogen often selects for pathogen variants capable of overcoming host resistance [12]. As a result of evolution, pathogens previously under control can re-emerge or newly emerge as significant threats to cultivated crops by increasing in incidence, expanding their geographic distribution, or broadening their host range [13].

Among the emerging threats to rice production, rice hoja blanca virus (RHBV), Pantoea ananatis, Cercospora disease complex (Cercospora janseana), and rice false smut (RFS) (Ustilaginoidea virens) are of particular concern. This chapter explores the distribution and characterization of each pathogen, addressing key aspects such as morphology and host infection mechanisms. Special attention is given to disease symptoms, key aspects of the pathogen life cycles, and critical epidemiological factors, including conducive environmental conditions and survival strategies. We also review current methods for pathogen detection and management and end with an outlook on future research directions and associated challenges.

2. Rice Hoja Blanca virus

2.1 Virus

Rice hoja blanca virus (RHBV) is a member of the species Tenuivirus oryzalbae, in the genus Tenuivirus, family Phenuiviridae, closely related tenuiviruses include Echinocloa hoja blanca virus and Urochloa hoja blanca virus, assigned to the species Tenuivirus echinochloae and Tenuivirus urochloae, respectively [14, 15]. Like other tenuiviruses, RHBV has a tetrapartite, single stranded, RNA genome. RHBV virions are nonenveloped, spiral, filamentous particles measuring approximately 3 nm in diameter and have varied lengths [16, 17].

RNA1 is approximately 9 kilobases (kb) in size and encodes the RNA-dependent RNA polymerase, with negative polarity. Conversely, RNAs 2–4 utilize ambisense strategy, wherein each RNA component encodes two open reading frames (ORF), one with positive polarity (viral sense) on the 5’ proximal region, and one with negative polarity (complementary sense) at the 3’ proximal region with a noncoding region spanning the two ORFs. RNA2 is approximately 3.6 kb. The viral sense ORF encodes a membrane glycoprotein, and the complementary sense ORF encodes a nonstructural protein (NS2) [18]. RNA3, approximately 2.3 kb, encodes a nonstructural protein (NS3) at the proximal 5’ end and a nucleocapsid protein (NCP) at the 3’ proximal end. NS3 serves as a viral suppressor of RNA silencing (VSR) by binding to double-stranded RNA (dsRNA) and small-interfering RNA (siRNA) and blocking its incorporation into the RNA induced silencing complex (RISC), ultimately halting host immunity responses and allowing for infection [19, 20]. The NCP provides stability to the genome and offers some resistance to degradation by host RNase activity [21]. Finally, RNA4, 2 kb in size, encodes a major nonstructural protein in the viral sense which accumulates in infected plants, and a nonstructural protein (NS4) in the complementary sense [22, 23, 24].

There is little evidence of significant diversity and virulence among RHBV isolates. A study comparing isolates from Colombia and Costa Rica found 98.9 and 98.6% sequence identity of the coding and noncoding regions of RNA3, respectively. Similarly, further comparison of the isolates revealed 96.9 and 91.5% sequence identity in the coding and non-coding regions of RNA4, respectively [25].

2.2 Hoja Blanca disease

RHBV is the causal agent of hoja blanca disease (HBD). As indicated by the name, hoja blanca (white leaf), infected rice plants exhibit chlorotic stripes or complete bleaching (Figure 1a). Beyond foliar symptoms, infected plants are often stunted with reduced root formation, potentially leading to plant death. Panicles exhibit partial or total sterility, while tillers are stunted, discolored, and malformed. Eventually, necrosis of leaf blades begins at the apical portion of leaves and extends to the base of young plants. Mature plants are less likely to exhibit severe symptoms compared to younger plants. In susceptible cultivars, yield losses ranged from 25 to 75% but have been observed to be 100% [26, 27, 28, 29]. These losses included plant death and increased panicle sterility [30, 31].

Figure 1.

Rice plants in Cali, Colombia exhibiting hoja blanca disease symptoms (a) caused by rice hoja blanca virus (RHBV). The rice delphacid, Tagosodes orizicolus, brown plant hopper, is a pest of rice that transmits RHBV in the circulative, propagative manner (b). Females (c) are often larger and lighter in color compared to males (d). Photo credits: Dr. Maribel Cruz Gallego.

HBD was first identified in Cauca Valley, Colombia, in 1935 [28]. High incidence of HBD was not seen again until 1952 in Panama, though little yield loss was observed. In 1956, outbreaks in Cuba and Venezuela recorded crop losses of 25 and 50%, respectively. In Venezuela, all 75,000 acres of rice production exhibited disease symptoms only 90 days after initial disease onset [30]. Ongoing outbreaks were observed throughout Central and Southern America and the Caribbean from 1957 to 1967. Epidemic levels were reported in Latin American countries from 1980 to 1985 [32], with an additional outbreak in Colombia occurring in 1996–1999 [29].

HBD was first observed in the United States in 1957 in Florida, though this outbreak was several hundred miles away from large production areas. Similarly, in 1958, RHB was observed in Mississippi and close to small-scale commercial rice production. Growers and researchers became concerned in 1959 when HBD was found in commercial rice production in the Louisiana “rice belt”. The virus was only found in mature plants and losses were minimal as these plants were destroyed before further spread could occur [26, 30]. After a 65-year hiatus, RHBV reemerged in the United States. Surveys conducted in Texas in 2024 revealed over 800 hectares of infected rice plantings, though this is likely an underestimate of the area impacted [33].

To date, HBD, and subsequently RHBV, is distributed across the western hemisphere in tropical and subtropical America, including Brazil, Belize, Colombia, Costa Rica, Cuba, Dominican Republic, El Salvador, Ecuador, Guatemala, Guyana, Honduras, Mexico, Nicaragua, Panama, Peru, Puerto Rio, Surinam, United States, and Venezuela [29].

2.3 HBD epidemiology

RHBV is not mechanically, or seed transmitted [30, 34]. Rather, the spread of RHBV is largely attributed to the planthopper, Tagosodes orizicolus (Muir) (Hemiptera; Delphacidae), formerly Sogata orizicola (Figure 1b). Within this species, females (Figure 1c) are typically larger than the males (Figure 1d) and lighter in color. Both alate (winged) and brachypterous (wingless) individuals exist in populations, with females more commonly wingless compared to males. Females deposit egg clusters in the midrib of the rice leaf blade. Eggs are typically white, 0.7 mm in length, and sensitive to desiccation. The incubation period prior to nymphal emergence is 1–2 weeks, dependent on temperature. First instars emerge and begin feeding within 24 hours. Each of the five nymphal stages takes 3–7 days. Adults can mate 2 days upon maturation, after which females will lay approximately 160 eggs throughout their lifetime. The time required to complete their lifecycle is temperature dependent, requiring relatively high temperatures (27°C) and high humidity (>80%) [35]. This sap sucking insect typically feeds lower on the plant. In high numbers, this feeding causes yellowing or reddening on young leaves, and results in significant yield losses, referred to as hopper burn.

Tagosodes orizicolus adults and nymphs transmit RHBV in a circulative, propagative manner [36, 37]. When feeding on an infected plant, virions entering the stylet travel to the midgut and perforate the mid-gut barrier to the hemolymph. This acquisition process can take up to 12 hours. Following an incubation period of 20-25 days, the virus reaches the salivary glands of the insect and transmission can occur after 3–7 hours of feeding with a transmission efficiency of 90% following 5 hours of feeding. Viruliferous insect feeding for 24 hours or more on healthy tissue resulted in transmission rates of 100% [36, 37].

While circulating through the insect body, RHBV replicates and infects insect tissues, particularly those of the digestive and respiratory systems [17]. RHBV replication in insects is not ubiquitous but rather driven by recessive gene inheritance [38]. This results in reduced fecundity, nymphal viability, and longevity. Indeed, viruliferous insects deposited one-third as many eggs as healthy individuals. The number of resultant nymphs was similarly decreased. It was noted that overall fertility was reduced for both infected males and females [39, 40]. Transovarial transmission is observed in up to 100% of progeny when the maternal parent is infected with RHBV, and symptoms of infection are exacerbated when the male parent is similarly infected [40]. These nymphs can transmit RHBV shortly after emergence. Following acquisition, whether maternally or by feeding on infected material, insects retain RHBV throughout their lifetime [39]. In natural populations, 5–15% of T. orizicolus are infected and capable of transmitting RHBV. This value is likely influenced by the deleterious impacts of RHBV infection [39].

In the United States, the presence of T. orizicolus corresponded with RHBV presence in the late 1950s [26, 30]. It was not until 2015 that the vector was seen again in the country. Rice fields in Texas exhibited symptoms of hopper burn corresponding to high T. orizicolus populations [41]. Insects from this outbreak and one in 2018 were negative for RHBV following testing via polymerase chain reaction (PCR) [42]. The cyclical nature of T. orizicolus infestations corresponds to RHBV epidemics, indicating vector populations and the environmental conditions supporting them are the driving force of RHBV outbreaks [29].

2.4 RHBV detection

Several lab-based methods have been developed to determine the presence of RHBV in plant and insect tissues. Antibodies targeting the coat protein of the RHBV virion were initially developed when establishing the causal relationship between the filamentous RHBV particles and RHB symptoms in double immunodiffusion tests [16]. Further advancements allow for RHBV detection in both the plant and insect on a microplate for larger scale detection with increased sensitivity via double antibody sandwich-enzyme linked immunosorbent assay (DAS-ELISA) [38, 43].

A PCR assay has been developed to determine the presence of RHBV via amplicons of regions of the NS3 and NS4 ORFs [44]. These primer pairs have been used to detect Peruvian and Colombian isolates of RHBV in plant and insect samples [44], while they were similarly used in Texas, no vector samples tested positive for the virus [42].

2.5 HBD management

Management of HBD targets both RHBV and its vector, T. orizicolus. Insecticidal control is a widely adopted method with limited success. Small-plot studies showed pyrethroids were not effective compared to dinotefuran in Texas [41]. The use of broad-spectrum organo-phosphates and pyrethroids was shown to be deleterious to parasitoids used to control T. orizicolus populations. These biocontrol agents remain a viable option for countries in which the use or importation of chemical pesticides is highly regulated [29].

In addition to rice, the virus and vector have been observed in several weed species. Vector reproductive success has been documented in wild grasses, including Panicum and Echinochloa species, barnyard grass, and jungle rice [36], though deposited eggs are more exposed compared to deposition in Oryza species, leaving them vulnerable to the environment and degradation [45]. Furthermore, E. colona, while prevalent in rice fields and shown to be a host of the virus, does not appear to be an inoculum reservoir for subsequent transmission, but rather a dead end in the transmission cycle [29]. Despite being susceptible to RHBV via natural and experimental settings, wheat, barley, oats, and rye do not appear to be contributors to HBD incidence due to different growing environments compared to rice [29, 30].

The best management practice is to implement varieties resistant to both RHBV and the feeding of T. orizicolus. While this venture has been successful, particularly in cultivar Fedearroz 2000, monocultural practices run the risk of resistance breaking, especially considering complete resistance to RHBV has not been observed in any cultivar [29, 46]. Nevertheless, the South American varieties Fedearroz 2000, Linea 34, and Altamira 1 N show promising resistance to vector feeding and should be a consideration for breeding programs in Central America and the United States [47].

Breeding for resistance to RHBV proves more challenging. Cultivars derived from O. sativa japonica with the QTL, qHBV4.1, showed reduced HBD symptoms upon infection. Within this region, a gene encoding argonaute 4 (AGO4), a key protein in RNA silencing and viral defense in plants, has been implicated in RHBV resistance [46, 48]. Ordinarily, AGO4 binds to dsRNA and siRNA, which is then incorporated into RISC and targeted for degradation. In wildtype Fedearroz 2000, AGO4 expression increased upon insect feeding, and overexpression was maintained in the presence of RHBV; in susceptible varieties or in AGO4 knockout mutants, AGO4 gene expression decreased in the presence of RHBV [48]. The role of the VSR, NS3, in this process warrants further attention. While the presence or absence of this quantitative trait locus (QTL) greatly impacted HBD incidence and severity, complete resistance was not observed, indicating resistance to RHBV is controlled by multiple genes [46]. Additional QTLs of interest different than those of O. sativa japonica have been found in O. sativa indica and provide a promising outlook for future breeding programs.

To assess the potential for resistance, the Alliance of Bioversity International and the International Center for Tropical Agriculture (CIAT) successfully optimized unmanned aerial vehicles (drones) for in-field detection of HBV breeding lines. This tool has allowed for earlier and time-efficient HBV detection when compared to more subjective human observation [49]. Furthermore, the group has developed a reliable, standardized method of insect-mediated transmission assays to determine a breeding line’s susceptibility to RHBV in controlled settings [29].

3. Pantoea ananatis

3.1 Global distribution and pathogen characterization

Pantoea ananatis has emerged as a globally distributed bacterial species. Initially isolated in tropical regions in association with pineapple (Ananas comosus), P. ananatis has since emerged as a notable pathogen across multiple cropping systems, especially rice (O. sativa), a globally important staple food [50, 51, 52]. Its subsequent isolation from economically important crops across multiple continents has expanded our understanding of its ecological breadth and significance [53].

In rice, the pathogen has been linked to both outbreaks and sporadic infections from Asia to the Americas, positioning it as a globally relevant emerging threat [54]. Its occurrence has been documented in several Asian countries (e.g., Japan, China, Philippines, Malaysia, Thailand), African nations (notably Togo), Latin America (Brazil, Argentina), and even in Europe (primarily on other monocots rather than rice), as well as in North America, particularly in the southern United States, including Arkansas and Louisiana [55, 56, 57, 58, 59, 60, 61, 62, 63] field surveys, phytosanitary reports, and active surveillance.

Pantoea ananatis is a bacterial species of growing significance in food production, primarily due to its broad host range, emerging virulence in key crops, and complex ecological behavior. First described in 1989, the genus Pantoea belongs to the Enterobacteriaceae family [64]. The genus name derives from the Greek word Pantoios, meaning “of all sorts or sources,” reflecting its diverse global distribution [65]. Species within this genus are considered highly versatile and ubiquitous, inhabiting a variety of ecological niches and hosts, and some exhibit the ability to interact with both plants and animals [66, 67].

Morphologically, P. ananatis is a Gram-negative, rod-shaped, facultatively anaerobic bacterium, typically measuring 0.5–1.0 μm in diameter and 1.5–2.5 μm in length. It is motile due to the presence of peritrichous flagella and forms distinctive round, yellow-pigmented colonies on nutrient agar, aiding in preliminary identification [68]. The yellow pigmentation results from carotenoid production, which is believed to confer protection against oxidative stress and ultraviolet radiation. Biochemically, P. ananatis exhibits broad metabolic capabilities, utilizing a wide array of carbon sources. Its facultative anaerobic nature allows it to thrive in both oxygen-rich and low-oxygen environments, including plant tissues, soil, and aquatic habitats [69].

For molecular identification, multilocus sequence analysis (MLSA) represents the most robust method for species-level classification [70]. Studies employing sequences of four housekeeping genes have demonstrated that MLSA enables clear differentiation among Pantoea species [67]. Comparative analyses of the gyrB (DNA gyrase subunit B) and rpoB (RNA polymerase beta subunit) gene sequences offer reliable identification of P. ananatis strains, with strong concordance between gyrB sequences and DNA–DNA hybridization values. Advances in genome sequencing have further elucidated the organism’s genetic architecture, uncovering genes linked to plant colonization, virulence, and environmental adaptability [71, 72, 73, 74].

Pantoea ananatis displays pronounced ecological plasticity, largely attributed to its extensive genomic flexibility [75]. While strains share a conserved core genome, they also possess a highly variable accessory genome enriched with genes specific to colonization of diverse hosts, including plants, animals, and insects [76, 77]. This accessory genome, shaped in part by integrated prophages and mobile genetic elements, encodes proteins involved in carbohydrate and amino acid metabolism, host tissue adherence, immune evasion, and potential pathogenicity [69]. Key mobile genetic elements include the large plasmid LPP-1, which harbors genes associated with metabolic diversity, nutrient acquisition (e.g., iron and nitrogen), resistance to antimicrobials and heavy metals, and host interactions [78, 79].

Another major contributor is the Integrative and Conjugative Element (ICE), found in some P. ananatis strains, which encodes proteins involved in antibiosis and stress responses. These elements may confer competitive advantages by producing bacteriocins and putative antibiotics [80]. Such genetic features, particularly mobile elements and accessory proteins are central to the organism’s ability to shift between pathogenic, commensal, and mutualistic lifestyles [80]. The ecological diversity of P. ananatis is further evidenced by its isolation as a pathogen, endophyte, epiphyte, and even from human clinical samples, complicating its detection and management [75].

In addition to its pathogenic potential, P. ananatis has been reported to produce indole-3-acetic acid (IAA), a plant hormone involved in cell elongation and tissue differentiation [81]. IAA acts as a potent growth regulator, exerting physiological effects even at low concentrations and promoting plant cell wall loosening during expansion [82]. Although the complete suite of virulence factors in P. ananatis remains largely undefined, recent genomic studies have begun to shed light on its potential mechanisms of pathogenicity. The genome of a virulent P. ananatis strain isolated from eucalyptus, as well as the type of strain derived from pineapple, have been sequenced using 454 pyrosequencing and Solexa technology, respectively [74]. Preliminary comparative analyses have revealed a lack of the classical Type II, Type III, and Type IV secretion systems, which are typically associated with virulence and often found on pathogenicity islands in both plant- and animal-associated bacteria [69]. Interestingly, P. ananatis possesses a gene cluster showing high homology to components of the Type VI secretion system, a mechanism involved in bacterial competition and host interactions in several Gram-negative pathogens. However, the precise role of this system in P. ananatis pathogenesis has yet to be fully elucidated [83, 84].

Unlike better-characterized host-pathogen systems, there is a scarcity of mechanistic studies detailing how these molecular pathways contribute to infection, colonization, or symptom development in rice. Further research is needed to elucidate the virulence strategies of P. ananatis in this crop, particularly under field conditions where interactions with the plant microbiome and environmental stressors may influence disease expression. As highlighted by Weller-Stuart et al. [69], genomic data provides a foundation for such investigations, but functional validation through mutagenesis and transcriptomic analyses in rice-specific contexts is still lacking.

3.2 Disease symptoms

In rice, the bacterium typically acts as a pathogen, associated with diseases such as sheath rot, grain discoloration, and systemic infections that can reduce yield and grain quality. Symptoms observed in leaves and sheaths of infected rice plants include elongated brown streaks spanning the full length of affected tissues (Figure 2a-d), which often progress from inside out and lead to complete necrosis. In other monocot hosts, symptoms generally present as streaks or blotches parallel to the main leaf veins [85, 86]. Occurrences of P. ananatis-related diseases in rice are generally sporadic in Asia and other production regions, including in the United States, likely reflecting its opportunistic nature.

Figure 2.

Symptomatology of Pantoea ananatis infection in rice (O. sativa) observed under experimental field conditions in Arkansas, United States. Panel (a) shows an early-stage infection characterized by a narrow, reddish-brown longitudinal streak along the mid-vein of the leaf blade, commonly referred to as “leaf streak.” This is considered a hallmark symptom of P. ananatis infection in Arkansas experimental rice fields. In panel (b), symptoms progress from initial streaking into more pronounced necrotic lesions, with tissue browning and collapse extending outward from the vascular bundles. This “inside-out” necrosis pattern suggests systemic movement and a strong vascular association of the pathogen. Panel (c) displays linear brown streaks present on the leaf sheath, running parallel to the vascular tissue. The continuity of symptoms between the leaf blade and sheath further supports the hypothesis of vascular systemic infection. Panel (d) shows an infected emerging panicle, where browning and streaking are visible at the base of the panicle and adjacent sheath tissue. This indicates the pathogen’s capacity to invade reproductive structures, potentially impacting grain development.

A particularly noteworthy feature of P. ananatis is the variation in symptom expression on the same host across different geographic regions. In maize, for instance, Brazilian strains cause necrotic or white leaf spots and streaks [85, 87], while in South Africa, the disease manifests primarily as stalk rot [88]. A similar trend is observed in rice: in Japan and several other regions, P. ananatis infects developing seeds, resulting in palea browning, whereas in Australia, it causes stem necrosis [89]. In the United States, divergent symptomatology has also been noted; rice fields in Arkansas exhibit different symptoms compared to those in Louisiana, reinforcing the notion that both environmental conditions and strain-specific factors contribute to this variability [63, 90].

3.3 Epidemiology

The epidemiology of plant diseases caused by P. ananatis remains poorly understood, especially across its diverse range of hosts. Current knowledge suggests that the pathogen can enter host tissues through flowers [91], insect feeding wounds [92], mechanical injuries [93], or direct plant-to-plant contact facilitated by strong winds [89].

Pantoea ananatis is both seed-borne and seed-transmitted in several crops, including onions [94], sudangrass [86], and rice [95]. The recent emergence of bacterial blight and die-back symptoms in eucalyptus in countries that imported seeds from South Africa further supports the likelihood of seed transmission [75]. Similarly, outbreaks of center rot in onions have been associated with the introduction of infested seed into new environments [94]. Although this pathway has not yet been officially documented in rice, it represents a potential phytosanitary risk, particularly as international seed trade intensifies.

Environmental conditions have a substantial impact on disease incidence and severity caused by P. ananatis. In crops such as maize and eucalyptus, the pathogen thrives under moderate temperatures (20–25°C) and high humidity [75]. On sudangrass, however, the most severe infections occur at higher temperatures (32°C) and elevated humidity levels [86]. This trend is mirrored in onion, where P. ananatis becomes active during bulb formation under high moisture conditions and temperatures between 28 and 35°C [96]. In rice, ongoing studies are attempting to define the precise environmental parameters that favor disease development, but preliminary evidence suggests that high humidity and elevated temperatures similarly increase pathogen aggressiveness [97].

3.4 P. ananatis detection

Detection protocols for P. ananatis are still under development. Although primers for detection and diagnosis have been developed, they require further optimization to ensure reliability and specificity for isolates from rice [98]. A semi-selective medium for isolating bacteria of the genus Pantoea has been developed, facilitating preliminary identification and purification of new isolates [99].

3.5 Disease management

Disease management strategies for P. ananatis typically rely on resistant or tolerant cultivars when available. In South Africa, blight and die-back in eucalyptus are effectively managed through the deployment of resistant clones, selected in high-disease nurseries [75]. In maize, Paccola-Meirelles et al. [100] demonstrated that artificial inoculation trials were effective in identifying resistant genotypes. Chemical control of white spot disease in maize with the fungicide Mancozeb has also proven effective when applied early in the disease cycle [101]. In onions, cultural practices such as mulching and modified irrigation systems have been tested. While irrigation method had little impact on disease incidence, using straw mulch or bare soil delayed symptom development by 7–14 days compared to black plastic [102]. For rice, the most practical approach currently available is the early identification, avoidance, and eradication of initial inoculum sources. These preventative actions are considered the most appropriate strategies to manage P. ananatis-associated diseases in rice under field conditions.

4. Cercospora diseases

4.1 Global distribution and pathogen characterization

The rice Cercospora diseases are caused by the ascomycete fungus Cercospora janseana (syn. Cercospora oryzae and Passalora janseana; telemorph: Sphaerulina oryzina) [103, 104, 105]. Cercospora disease in rice was first reported as narrow brown leaf spot in Japan in 1906 [104]. The disease has a global distribution, including most rice-growing regions in Asia, Africa, Australia, North America, Central America, and South America [106]. Cercospora janseana was first reported in the United States in 1935 in Texas [107]. Once considered a minor disease, the incidence and severity has been increasing over the past few decades, mainly in the southern United States rice belt, including major producers like Louisiana, Mississippi, Texas, and Arkansas [108, 109, 110].

Cercospora janseana is classified within the Kingdom Fungi. It belongs to the phylum Ascomycota, which includes fungi that produce spores in sac-like structures called asci [111]. Within this phylum, it falls under the class Dothideomycetes, known for many phytopathogenic species [112, 113, 114]. The pathogen is further categorized in the order Capnodiales and the family Mycosphaerellaceae, which comprises numerous foliar pathogens [115, 116]. Within the genus Cercospora, the species C. janseana is recognized as the causal agent of diseases in rice. Morphologically, C. janseana produces hyaline to light brown conidia, multicellular, and borne on pigmented conidiophores, typical of Cercospora species [117]. This pathogen exhibits a slow growth rate and low sporulation on commonly used culture media, such as potato dextrose agar (PDA) [108, 118]. As a result, efforts have been made to develop a reliable protocol for culturing and inducing sporulation, aiming to facilitate both laboratory and field studies of C. janseana [108].

The infection process of C. janseana begins with the germination of conidia under conditions of high humidity and temperatures ranging from 20 to 28°C [119]. Germ tube grows towards the stomata, where it forms appressoria and penetrates the rice tissues [106, 110, 120]. Cercospora janseana then colonizes the intercellular spaces, spreading longitudinally, with conidiophores emerging through the stomata [110]. This pathogen has a potentially long latent period, leading to delays in the observation of disease symptoms [106]. It has been reported to require from 7 to 66 days after inoculation for the expression of disease symptoms on rice leaves [106, 121].

The molecular mechanisms deployed by C. janseana to decoy the host immune system and successfully invade rice plants are yet to be elucidated. Recently, the reference genome for C. janseana was assembled, and 10,850 genes were identified, including 955 predicted secreted proteins and 361 predicted effector proteins [122]. Future studies will contribute to a better understanding of rice-C. janseana interactions.

4.2 Cercospora diseases

Narrow brown leaf spot (NBLS), caused by the fungus Cercospora janseana, is a recurrent foliar disease of rice that was initially observed affecting only the leaves, where it produced narrow, elongated lesions ranging in color from brown to reddish-brown [109, 123]. However, as the disease has expanded to other parts of the plant, including the sheath and panicle, a revision of both its terminology and management recommendations has become necessary. Following the naming convention used for blast disease, the nomenclature for C. janseana-induced symptoms now reflects the specific plant tissue affected. Thus, the term narrow brown leaf spot (NBLS) is now restricted to lesions on the leaves (Figure 3a). Symptoms appearing on the leaf sheath are referred to as Cercospora net blotch (CNB) (Figure 3b), while those on the panicle rachis and branches are identified as Cercospora panicle blight (CPB) (Figure 3c). When referring to the disease complex as a whole—encompassing symptoms across all tissues—the term Cercospora is being used. This updated terminology improves clarity and facilitates disease management, as recent studies have demonstrated that host resistance and control strategies may differ depending on the infected tissue [124, 125, 126, 127].

Figure 3.

Cercospora diseases symptoms based on a new proposed terminology. (a) Narrow brown leaf spot (NBLS): symptoms on the leaf. (b) Cercospora net blotch (CNB): symptoms on the sheath. (c) Cercospora panicle blight (CPB): symptoms on the panicle.

4.3 Epidemiology

Cercospora janseana conidia are dispersed by wind and rain splashes, infecting leaves through stomata or wounds [106, 110, 124]. This pathogen survives between seasons on crop residues and is favored by warm, humid environments—conditions common in rice-growing regions [126, 127]. Several gaps persist in the epidemiology of the Cercospora diseases. On the host side, factors such as planting date, nutritional imbalances, cultivar susceptibility, and growth stage susceptibility remain under investigation. Regarding the pathogen, the roles of potential alternative hosts and tillage practices in the life cycle of C. janseana, particularly related to survival mechanisms, have yet to be fully elucidated.

4.4 Disease identification and pathogen detection

The identification of diseases caused by C. janseana in rice is based on the symptomology wherein long, narrow, brown lesions on leaves, sometimes with a yellow halo indicate NBLS. Dark brown blotches in net-like patterns on leaf sheaths suggest CNB, and discoloration and decay in panicles, often confused with other panicle diseases, indicates CPB. There is a single report of C. janseana molecular detection and quantification by real-time PCR, aiming to quantify the inoculum build-up over time in treated and non-treated varietal plots at three different planting times [128]. However, there is no description of the specific primers and probe used.

4.5 Disease management

Integrated disease management for C. janseana involves a combination of cultural, chemical, and genetic strategies. Although host resistance is currently limited, ongoing research is investigating resistant rice varieties as a potential long-term solution. Rice varieties carrying the CRSP2.1 resistance gene [129] have been deployed in the southern United States, such as PVL03 [130], CLL16 [131], CLL17 [132], and Avant [133]. These varieties confer different levels of resistance to NBLS, although CNB and CPB can still occur [134].

Crop rotation and residue management are important practices that help reduce inoculum levels in the field by disrupting the pathogen’s life cycle. Lately planted rice develops more NBLS than earlier planted rice [126]. NBLS severity in hybrid genotypes is significantly lower than in inbred genotypes [125]. Chemical control using fungicides such as triazoles and strobilurins can provide partial disease suppression; however, proper resistance management is essential to maintain their effectiveness. The fungicides propiconazole and fluxapyroxad are more effective for NBLS control [124].

Finally, accurate diagnosis is essential for effective disease management, as it allows for proper differentiation of C. janseana from other foliar pathogens, ensuring that control measures are appropriately applied. Similarly, precise identification of panicle diseases is important, as they are often easily mistaken for neck blast in rice [109].

5. Rice false smut

5.1 Global distribution and pathogen characterization

Rice false smut (RFS) is caused by the fungal pathogen Ustilaginoidea virens (Cooke) Takahashi (syn. Villosiclava virens), a nonobligate biotrophic ascomycete that infects rice floral organs. U. virens was first reported in India in 1878 as the causal agent of a minor disease with sporadic occurrence in rice fields [135, 136]. Currently, the RFS pathogen has spread throughout most important rice-growing regions, with reports on six continents and in 57 countries [137]. The RFS worldwide distribution includes 18 countries in Africa, 20 countries in Asia, 2 countries in Australia and Oceania, 1 country in Europe, 8 countries in North America, and 8 countries in South America (Figure 4) [137, 138].

Figure 4.

The RFS global distribution includes 57 countries on six continents.

The infection strategy of U. virens is unique. Unlike many foliar pathogens, U. virens invades the spikelets and forms characteristic smut balls that replace developing grains [135]. During the sexual cycle, the fungus forms sclerotia externally on false smut balls [139]. These sclerotia play a pivotal role in the pathogen’s survival and dissemination [4]. Under favorable environmental conditions (increased moisture, light, temperature), sclerotia germinate to produce asci and ascospores, which initiate primary infections and can generate secondary conidia, further promoting disease spread [137, 140]. At the late booting stages, the pathogen spores germinate on the lemma and palea of the developing spikelets, without forming appressoria, and invade the inner space of the spikelet to infect the staminal filaments [141, 142, 143]. In the asexual cycle, U. virens produces thick-walled chlamydospores on the surface of false smut balls, which generate secondary conidia that contribute to disease development as well as serve as a major inoculum source between rice seasons [137].

Ustilaginoidea virens conidia are round to elliptical with diameters ranging from 3 to 5 μm [144]. Conidia are ornamented with spines, usually pointed at the apex or irregularly curved, and approximately 200–500 nm long [144]. In contrast, sclerotia are flat and irregularly oblong or horseshoe-shaped, commonly developing when large temperature differences occur between day and night [135, 145]. This structure can remain dormant and be viable in the field for long periods [140].

Ustilaginoidea virens holds sophisticated mechanisms of infection and survival. Several effectors acting as virulence mechanisms have been identified to be crucial for U. virens. Effectors known to induce necrosis or suppress rice immunity, like SCRE1 and SCRE2, have already been reported [135, 146, 147, 148]. SCRE6, for example, is secreted and translocated into rice cells during infection, where it interacts with OsMPK6 to enhance its stability, suppress rice immunity, and facilitate U. virens infection [149]. OsWRKY31-OsAOC module, a key regulator of broad-spectrum disease resistance, was found to be hijacked by the U. virens secreted effector UvSec117, resulting in the suppression of jasmonic acid-mediated immunity [150]. Also, rice chitin-triggered immunity is suppressed by the U. virens-secreted cytoplasmic effector UvGH18.1 [151, 152]. This virulence factor acts as a chitinase by degrading chitin oligomers and reducing the plant’s reactive oxygen species (ROS) burst, which usually occurs upon pathogen sensing. Despite the findings to date, U. virens molecular mechanisms undermining rice immunity are still an undergoing investigation.

The RFS fungus is an exception among the biotrophs. Unlike other biotrophic fungi, U. virens can be cultured in the laboratory under nutrient-rich conditions such as Richard’s medium or Potato Dextrose Agar [4, 135]. By adopting a temperature range of 25–28°C and a pH of 5.5–7.0, U. virens mycelium and chlamydospores can be obtained on synthetic media [135, 153]. This characteristic can facilitate the study of pathogenicity mechanisms, enhancing the management strategies.

5.2 False smut disease

Recent reports have drawn attention to the increase in RFS incidence levels, thereby turning this pathogen into a re-emerging threat with the potential to cause yield losses commonly ranging from 0.01 to 8.6% [4, 135]. During epidemic seasons, yield losses can reach up to 70%, depending on weather conditions and rice cultivars [137, 154].

False smut affects the rice panicle during the booting to heading stage and is considered an emerging threat due to its increasing incidence in high-yielding and hybrid varieties, especially under favorable environmental conditions. The disease typically starts as small, pale-gray spots on the surface of developing grains (Figure 5a). As the infection progresses, one or more kernels on a panicle are transformed into large, yellowish-green spore balls that replace the normal grain [155]. These smut balls gradually enlarge and turn orange (Figure 5b), olive green, and eventually dark green to black (Figure 5c) as masses of chlamydospores accumulate on the surface [137]. Each smut ball may reach 1–2 cm in diameter and is composed of fungal mycelium, host tissue, and spores. Unlike true smut diseases, where the entire inflorescence is usually affected, false smut affects only a few kernels per panicle, often in a scattered pattern [142, 143]. This patchy infection pattern makes the disease difficult to manage and detect early. The smut balls are covered with a velvety mass of spores and sometimes exhibit a powdery texture. In severe cases, infection leads to grain yield and quality loss, and the presence of mycotoxins such as ustiloxins A and B can pose a food safety concern [135, 156].

Figure 5.

Rice false smut balls on rice kernels. During the cycle, smut balls are initially white-gray (a), enlarging to orange–olive green (b), and becoming green to black balls at maturation (c). Photo credits: Yeshi Wamishe (a).

5.3 Epidemiology

Ustilaginoidea virens survives in rice fields through the production of sclerotia, which have been found in high numbers even in subtropical regions. Although few sclerotia successfully overwinter, each can produce large quantities of ascospores that serve as the primary inoculum during the rice booting stage [140].

Dormant for 2–5 months, but viable up to 5 years under dry and low-temperature conditions, sclerotia germinate under favorable light, temperature, and humidity conditions [145]. Yellow fruiting bodies are produced under a light intensity higher than 250 Lux, combined with day and night temperatures around 31°C and 19°C, respectively [4, 135]. The conducive conditions also include recurrent rainfall periods along with cloudy weather until the next day and a relative humidity above 90% [4, 143]. Also, chlamydospores can germinate under high humidity conditions and produce a high amount of secondary conidia, which may spread by air and rain to infect rice flowers at the late booting stage [4].

Conidia serve as the primary inoculum, and wind and rain aid their dispersal [4, 137]. High nitrogen fertilization, dense planting, and prolonged booting-to-flowering periods increase disease severity [155]. Disease development is closely linked to environmental conditions during the panicle emergence and grain-filling stages, making false smut an unpredictable but recurrent problem. Sclerotia and chlamydospores are responsible for U. virens overwinter survival and serve as a primary inoculum source for the next season [135, 139].

The RFS pathogen can infect seedling roots, but the role of this mechanism in false smut ball epidemiology remains to be elucidated [140, 157]. Additionally, several weed species can act as alternative hosts and pathogen reservoirs during the rice off-season, potentially contributing to the long-term pathogen persistence [135, 137, 139]. Also, the specific contributions of germinating ascospores and chlamydospores in initiating the RFS infection at the booting stage remain unresolved [137].

5.4 Disease identification and pathogen detection

RFS early detection is challenging due to the cryptic nature of infection, which often remains asymptomatic until late stages [157, 158]. Traditional detection relies on visual observation of smut balls during the heading or maturity stage. Molecular methods such as PCR-based assays targeting U. virens-specific genes have improved early detection [159, 160]. Chlamydospores detection in field soil has been successfully achieved through real-time PCR [157]. Also, U. virens infection of rice roots and shoots was detected using a nested PCR with species-specific primers [157]. This advancement may support further investigations to elucidate the missing aspects of the disease cycle, such as the timing and impact of root and leaf sheath colonization and its role in RFS epidemiology. Furthermore, Loop-Mediated Isothermal Amplification (LAMP) detection provides sensitive and rapid diagnostics, supporting laboratory and field-level applications such as quarantine and breeding programs [161].

5.5 Disease management

Integrated disease management is essential to reduce the incidence and severity of rice false smut, relying on a combination of cultural, chemical, biological, and genetic strategies [4, 162]. Cultural practices such as the use of resistant or moderately resistant varieties, maintaining optimal planting density, and applying balanced fertilization, particularly managing nitrogen levels, can help limit disease development [162]. Chemical control remains a key strategy, although fungicide applications at the booting stage have only shown limited effectiveness in suppressing the disease; triazoles (e.g., tebuconazole, propiconazole) and strobilurins (e.g., azoxystrobin) are commonly used [137, 162, 163]. Biological control using antagonistic microorganisms like Bacillus spp. and Trichoderma spp. offers a promising but still underdeveloped alternative, requiring more field-level validation [164]. Efforts in host resistance breeding continue, but progress is hindered by the complex, polygenic nature of resistance and the limited availability of fully resistant rice cultivars [4, 162].

6. Conclusion and future outlook

Rice hoja blanca virus (RHBV) and hoja blanca disease (HBD) remain a constant threat to rice production in the western hemisphere. Climate and production system change is a likely driver in moving vector populations further north into Texas [41, 42], resulting in the reemergence of vector populations and RHBV after a more than 50-year absence [33]. Continued attention to breeding remains paramount to combat both the virus and vector, considering unstable environmental conditions. While the threat of both is well established in Central and South America, understanding the overwintering capabilities of the vector in Texas and Louisiana warrants further research. Indeed, the vector appears to be an established threat in Texas, and cultural practices in Louisiana promoting second ratoon crops and encouraging crawfish production provide year-round feeding and reproductive hosts for the vector. Future research should assess any resistance currently present in rice cultivars grown in the United States and in global rice varieties and incorporate resistance genes for both the vector and RHBV. The knowledge gleaned over nearly a century of RHBV research since its initial detection in 1935 should help handle this recognized but emerging threat.

Pantoea ananatis is an intriguing plant pathogen, especially for rice [50]. Despite advancements in genome sequencing, many aspects of its biology and epidemiology remain unresolved. The pathogen’s life cycle is poorly understood, and the molecular pathways involved in infection, colonization, and symptoms are largely unknown. Future research should focus on elucidating the virulence strategies of P. ananatis, as well as its interactions with the plant microbiome and environmental factors. Moreover, distinct symptomatology reported across different geographic regions [63, 90] suggests environmental influence, highlighting the need for region-specific research. Artificial inoculation and early detection protocols are still under development and are expected to support the screening of rice varieties for resistance.

Cercospora diseases have gained relevance due to their rising severity, particularly in the southern United States [108, 109]. Genetic resistance remains limited, with only a few varieties exhibiting resistance or moderate resistance to narrow brown leaf spot (NBLS), while remaining susceptible to Cercospora net blotch (CNB) and Cercospora panicle blight (CPB) [134]. The resistance gene CRSP2.1 appears vulnerable to newly emerging races of C. janseana [165]. With the recent C. janseana genome assembly [122], future research should prioritize a deeper understanding of the pathogen’s biology and virulence factors undermining host resistance. Furthermore, potential adjustments of fungicide application timing based on the distinct infected tissues (NBLS, CNB, and CPB) and developing an artificial inoculation protocol for resistance screening are relevant areas for future studies. Despite these challenges, advancements in disease identification and a name system based on the infected tissue hold promise for improving technical information exchange and field disease management.

Nearly 150 years after its first report [136], rice false smut (RFS) has reemerged as a significant rice disease. Nonetheless, substantial progress has been made in understanding the life cycle of U. virens, along with the mechanisms underlying its virulence factors, infection process, host colonization, smut ball formation, and survival [141, 146, 147, 149]. Ongoing research focusing on the genome, proteome, and effector biology of U. virens continues to yield valuable insights, including the identification of potential pathogen targets for plant breeding [137, 166]. Future research should prioritize the development of a reliable artificial inoculation protocol, the integration of RFS into breeding program screening protocols, and the advancement of early detection methods to support more effective management strategies. Additionally, future research should aim to dissect key aspects of the U. virens life cycle, particularly the roles of sclerotia and chlamydospores in initiating infection.

While the above-mentioned pathogens certainly serve as a worrisome threat to global rice production, great strides are underway to better our understanding of pathogen life cycles and integrated management strategies to further strengthen the resiliency of this globally essential crop.

Acknowledgments

Camila Nicolli and Samuel de Paula gratefully acknowledge the Arkansas Rice Research and Promotion Board for their generous support through research funding. They also extend their thanks to the Non-Assistance Cooperative Agreement between the Agricultural Research Service (ARS) of the U.S. Department of Agriculture (USDA) and the University of Arkansas, made possible through the collaboration with Dr. Yulin Jia and Dr. Rodrigo Pedrozo of USDA ARS.

The authors thank Dr. Maribel Cruz Gallego from the Centro Internacional de Agricultura Tropical (CIAT) for providing the HBD symptomatic field and planthopper photos.

USDA is an equal opportunity provider and employer. The findings and conclusions are those of the author(s) and do not represent official USDA or U.S. Government policy or determination.

Conflict of interest

The authors declare no conflict of interest.

References

  1. 1. Fukagawa NK, Ziska LH. Rice: Importance for global nutrition. Journal of Nutritional Science and Vitaminology (Tokyo). 2019;65:S2-S3. DOI: 10.3177/jnsv.65.S2
  2. 2. Sen S, Chakraborty R, Kalita P. Rice - not just a staple food: A comprehensive review on its phytochemicals and therapeutic potential. Trends in Food Science and Technology. 2020;97:265-285. DOI: 10.1016/j.tifs.2020.01.022
  3. 3. United States Department of Agriculture Foreign Agricultural Service. World Agricultural Production. 2025. Available from: https://www.fas.usda.gov/data/world-agricultural-production-05122025
  4. 4. Debnath P, Mahawar S, Singh G. A review on accessible techniques for the management of rice false smut: Recent research and future outlook. Planta. 2025;261:137. DOI: 10.1007/s00425-025-04706-0
  5. 5. Savary S, Willocquet L, Pethybridge SJ, Esker P, McRoberts N, Nelson A. The global burden of pathogens and pests on major food crops. Nature Ecology & Evolution. 2019;3:430-439. DOI: 10.1038/s41559-018-0793-y
  6. 6. Liu Z, Zhu Y, Shi H, Qiu J, Ding X, Kou Y. Recent progress in rice broad-spectrum disease resistance. International Journal of Molecular Sciences. 2021;22:11658. DOI: 10.3390/ijms222111658
  7. 7. Nishad R, Ahmed T, Rahman VJ, Kareem A. Modulation of plant defense system in response to microbial interactions. Frontiers in Microbiology. 2020;11:1298. DOI: 10.3389/fmicb.2020.01298
  8. 8. Jones JDG, Dangl JL. The plant immune system. Nature. 2006;444:323-329. DOI: 10.1038/nature05286
  9. 9. McCombe CL, Wegner A, Wirtz L, Zamora CS, Casanova F, Aditya S, et al. Plant pathogenic fungi hijack phosphate signaling with conserved enzymatic effectors. Science. 2025;387:955-962. DOI: 10.1126/science.adl5764
  10. 10. Oliveira-Garcia E, Yan X, Oses-Ruiz M, de Paula S, Talbot NJ. Effector-triggered susceptibility by the rice blast fungus Magnaporthe oryzae. The New Phytologist. 2024;241:1007-1020. DOI: 10.1111/nph.19446
  11. 11. Leclerc M, Clément JAJ, Andrivon D, Hamelin FM. Assessing the effects of quantitative host resistance on the life-history traits of sporulating parasites with growing lesions. Proceedings of the Royal Society B: Biological Sciences. 2019;286:20191244. DOI: 10.1098/rspb.2019.1244
  12. 12. Trivedi P, Wang N. Host immune responses accelerate pathogen evolution. The ISME Journal. 2014;8:727-731. DOI: 10.1038/ismej.2013.215
  13. 13. Ristaino JB, Anderson PK, Bebber DP, Brauman KA, Cunniffe NJ, Fedoroff NV, et al. The persistent threat of emerging plant disease pandemics to global food security. Proceedings of the National Academy of Sciences. 2021;118:e2022239118. DOI: 10.1073/pnas.2022239118
  14. 14. de Miranda JR, Muñoz M, Wu R, Espinoza AM. Phylogenetic placement of a novel Tenuivirus from the grass Urochloa plantaginea. Virus Genes. 2001;22:329-333. DOI: 10.1023/A:1011122508545
  15. 15. de Miranda JR, Muñoz M, Madriz J, Wu R, Espinoza AM. Sequence of Echinochloa hoja blanca tenuivirus RNA-3. Virus Genes. 1996;13:65-68. DOI: 10.1007/BF00576980
  16. 16. Morales FJ, Niessen AI. Association of spiral filamentous viruslike particles with rice hoja blanca. Phytopathology. 1983;73:971. DOI: 10.1094/Phyto-73-971
  17. 17. Shikata E, Galvez GE. Fine flexuous threadlike particles in cells of plants and insect hosts infected with rice hoja blanca virus. Virology. 1969;39:635-641. DOI: 10.1016/0042-6822(69)90002-6
  18. 18. de Miranda JR, Hull R, Espinoza AM. Sequence of the PV2 gene of rice hoja blanca tenuivirus RNA-2. Virus Genes. 1995;10:205-209. DOI: 10.1007/BF01701809
  19. 19. Yang X, Tan SH, Teh YJ, Yuan YA. Structural implications into dsRNA binding and RNA silencing suppression by NS3 protein of Rice Hoja Blanca Tenuivirus. RNA. 2011;17:903-911. DOI: 10.1261/rna.2552811
  20. 20. Shen M, Xu Y, Jia R, Zhou X, Ye K. Size-independent and noncooperative recognition of dsRNA by the rice stripe virus RNA silencing suppressor NS3. Journal of Molecular Biology. 2010;404:665-679. DOI: 10.1016/j.jmb.2010.10.007
  21. 21. Lu G, Li J, Zhou Y, Zhou X, Tao X. Model-based structural and functional characterization of the rice stripe tenuivirus nucleocapsid protein interacting with viral genomic RNA. Virology. 2017;506:73-83. DOI: 10.1016/j.virol.2017.03.010
  22. 22. Jimenez J, Carvajal-Yepes M, Leiva AM, Cruz M, Romero LE, Bolaños CA, et al. Complete genome sequence of Rice hoja blanca tenuivirus isolated from a susceptible rice cultivar in Colombia. Genome Announcements. 2018;6:e01490-17. DOI: 10.1128/genomeA.01490-17
  23. 23. Ramirez B-C, Macaya G, Calvert LA, Haenni A-L. Rice hoja blanca virus genome characterization and expression in vitro. The Journal of General Virology. 1992;73:1457-1464. DOI: 10.1099/0022-1317-73-6-1457
  24. 24. Ramirez B-C, Lozano I, Constantino L-M, Haenni A-L, Calvert LA. Complete nucleotide sequence and coding strategy of rice hoja blanca virus RNA4. The Journal of General Virology. 1993;74:2463-2468. DOI: 10.1099/0022-1317-74-11-2463
  25. 25. de Miranda JR, Ramirez B-C, Munõz M, Lozano I, Wu R, Haenni A-L, et al. Comparison of Colombian and costa Rican strains of Rice Hoja Blanca Tenuivirus. Virus Genes. 1997;15:191-193. DOI: 10.1023/A:1007974728671
  26. 26. Atkins JG, Adair CR. Recent discovery of hoja blanca, a new rice disease in Florida, and varietal resistance tests in Cuba and Venezuela. Plant Disease Report. 1957;41:911-915. DOI: 10.1079/cabicompendium.4761
  27. 27. Jennings PR. Estimating yield loss in rice caused by hoja blanca. Phytopathology. 1963;53:492. DOI: 10.5555/19631102923
  28. 28. Garcés-Orejuela C, Jennings PR, Skiles RL. Hoja blanca of rice and the history of the disease in Colombia. Plant Disease Report. 1958;42:750-751
  29. 29. Morales FJ, Jennings PR. Rice hoja blanca: A complex plant-virus-vector pathosystem. CABI Reviews. 2010;5:1-16. DOI: 10.1079/PAVSNNR20105043
  30. 30. United States Department of Agriculture. Hoja Blanca: Serious Threat to Rice Crops. Agricultural Research Service - Crop Research Division Entomology Research Division and Plant Pest Control Division ARS. Washington D.C; 1960. Available from: https://archive.org/details/hojablancaseriou57unit/mode/2up mode/2up?view=theater
  31. 31. Hill L. Louisiana faces hoja blanca: A serious new rice disease. Louisiana Agricultural Extension Service. 1960;1267:3-8
  32. 32. Vargas JP. La hoja blanca: descalabro de CICA-8. Arroz. 1985;34:18-19
  33. 33. Zhou Z-G, Bernaola L, Sarkar N, Bradshaw G, Rustom S, Khanal S. Texas ratoon rice: New hoja blanca disease and rice delphacid alert. Rice Farming. 2025. Available from: https://www.ricefarming.com/departments/feature/texas-ratoon-rice-new-hoja-blanca-disease-and-rice-delphacid-alert/
  34. 34. Murphy FA, Fauquet CM, Bishop DHL, Ghabrial SA, Jarvis AW, Martelli GP, et al. The viruses. In: Murphy FA, Fauquet CM, Bishop DHL, Ghabrial SA, Jarvis AW, Martelli GP, Mayo MA, Summers MD, editors. Virus Taxonomy: Classification and Nomenclature of Viruses Sixth Report of the International Committee on Taxonomy of Viruses. Vienna: Springer; 1995. pp. 15-507
  35. 35. Everett T. Vectors of hoja blanca virus: The virus diseases of the rice plant. CABI Compendium. 1969:111-121
  36. 36. Mcguire J, Mcmillan WW, Lamey HA. Hoja blanca disease of rice and its insect vector. Rice Journal. 1960;63:15-28
  37. 37. Mcmillian WW, Mcguire JU, Lamey HA. Hoja blanca transmission studies on rice. Journal of Economic Entomology. 1962;55:796-797. DOI: 10.1093/jee/55.5.796
  38. 38. Zeigler RS, Morales FJ. Genetic determination of replication of rice hoja blanca virus within its planthopper vector, Sogatodes oryzicola. Phytopathology. 1990;80:559-566. DOI: 10.1094/Phyto-80-559
  39. 39. Galvez GE. Transmission studies of the hoja blanca virus with highly active, virus-free colonies of Sogatodes oryzicola. Phytopathology. 1968;58:818-821
  40. 40. Jennings PR. The effect of the hoja blanca virus on its insect vector. Phytopathology. 1971;61:142-143. DOI: 10.1094/Phyto-61-142
  41. 41. Way MO, Vyavhare SS, Mock C, Mock W, Metz K, McKamey SH, et al. Outbreak of Tagosodes orizicolus (Muir) in Texas rice. Southwestern Entomologist. 2016;41:871-874. DOI: 10.3958/059.041.0329
  42. 42. Martin JE, Bernal Jimenez EK, Cruz MG, Zhu-Salzman K, Way MO, Badillo-Vargas IE. Assessing the potential infection of Tagosodes orizicolus (Hemiptera: Delphacidae) by rice hoja blanca virus in Texas. Journal of Economic Entomology. 2020;113:1018-1022. DOI: 10.1093/jee/toz321
  43. 43. Marys E, Carballo O. Development of a diagnostic tool for the rice “hoja blanca” virus in Venezuela. Interciencia. 2007;32:262-265
  44. 44. Bolaños C, Leiva AM, Saavedra J, Bruzzone C, Cruz M, Cuellar WJ. Occurrence and molecular detection of Rice hoja blanca virus (genus Tenuivirus) in Peru. Plant Disease. 2017;101:1070-1070. DOI: 10.1094/PDIS-12-16-1797-PDN
  45. 45. Cordero AD, Newsom LD. Suitability of Oryza and other grasses as hosts of Sogata orizicola Muir. Journal of Economic Entomology. 1962;55:868-871. DOI: 10.1093/jee/55.6.868
  46. 46. Silva A, Montoya ME, Quintero C, Cuasquer J, Tohme J, Graterol E, et al. Genetic bases of resistance to the rice hoja blanca disease deciphered by a quantitative trait locus approach. G3: Genes, Genomes, Genetics. 2023;13:jkad223. DOI: 10.1093/g3journal/jkad223
  47. 47. Kraus EC, Guerra R, Stout MJ. Evaluation of south American rice varieties for resistance to rice delphacid: Potential sources for breeding programs. Southwestern Entomologist. 2020;45:79-88. DOI: 10.3958/059.045.0109
  48. 48. Ñañez J, Valdes S, Cruz Gallego M, Rebolledo MC, Lorieux M, Alvarez MF, et al. Revealing the role of the AGO4 gene against rice hoja blanca virus: From transformation to protein structure. Frontiers in Plant Science. 2025;16:1-11. DOI: 10.3389/fpls.2025.1517321
  49. 49. Delgado C, Benitez H, Cruz M, Selvaraj M. Digital disease phenotyping. In: IGARSS 2019-2019 IEEE International Geoscience and Remote Sensing Symposium. Yokohama: IEEE; 2019. pp. 5702-5705
  50. 50. Xie GL. First report of Palea browning in China and characterization of the causal organism by phenotypic tests and biolog. International Rice Research Notes. 2001;26:25-26
  51. 51. Kim YC, Kim KC, Choi BH. Palea browning disease of rice caused by Erwinia herbicola and ice nucleation activity of the pathogenic bacterium. Korean Journal Plant Pathology. 1989;5:72-79
  52. 52. Tabei H, Azegami K, Fukuda T. Infection site of rice grain with Erwinia herbicola, the causal agent of bacterial Palea browning of rice. Japanese Journal of Phytopathology. 1988;54:637-639. DOI: 10.3186/jjphytopath.54.637
  53. 53. Lv L, Luo J, Ahmed T, Zaki HEM, Tian Y, Shahid MS, et al. Beneficial effect and potential risk of Pantoea on rice production. Plants. 2022;11:2608. DOI: 10.3390/plants11192608
  54. 54. Azizi MMF, Ismail SI, Ina-Salwany MY, Hata EM, Zulperi D. The emergence of Pantoea species as a future threat to global rice production. Journal of Plant Protection Research. 2020;60:327-335. DOI: 10.24425/jppr.2020.133958
  55. 55. Xue Y, Hu M, Chen S, Hu A, Li S, Han H, et al. Enterobacter asburiae and Pantoea ananatis causing rice bacterial blight in China. Plant Disease. 2021;105:2078-2088. DOI: 10.1094/PDIS-10-20-2292-RE
  56. 56. Mondal KK, Mani C, Singh J, Kim J-G, Mudgett MB. A new leaf blight of rice caused by Pantoea ananatis in India. Plant Disease. 2011;95:1582-1582. DOI: 10.1094/PDIS-06-11-0533
  57. 57. Yu L, Yang C, Ji Z, Zeng Y, Liang Y, Hou Y. First report of new bacterial leaf blight of rice caused by Pantoea ananatis in Southeast China. Plant Disease. 2022;106:310. DOI: 10.1094/PDIS-05-21-0988-PDN
  58. 58. Toh WK, Loh PC, Wong HL. First report of leaf blight of rice caused by Pantoea ananatis and Pantoea dispersa in Malaysia. Plant Disease. 2019;103:1764-1764. DOI: 10.1094/PDIS-12-18-2299-PDN
  59. 59. Kini K, Agnimonhan R, Afolabi O, Soglonou B, Silué D, Koebnik R. First report of a new bacterial leaf blight of rice caused by Pantoea ananatis and Pantoea stewartii in Togo. Plant Disease. 2017;101:241. DOI: 10.1094/PDIS-06-16-0939-PDN
  60. 60. Arayaskul N, Poompouang S, Lithanatudom P, Lithanatudom SK. First report of a leaf blight in rice (O. sativa) caused by Pantoea ananatis and Pantoea stewartii in Thailand. Plant Disease. 2020;104:562. DOI: 10.1094/PDIS-05-19-1038-PDN
  61. 61. Choi O-H, Kim H-Y, Lee Y-S, Kim J-W, Moon J-S, Hwang I-G. First report of sheath rot of rice caused by Pantoea ananatis in Korea. Plant Pathology Journal. 2012;28:331-331. DOI: 10.5423/PPJ.DR.08.2011.0150
  62. 62. Egorova M, Mazurin E, Ignatov AN. First report of Pantoea ananatis causing grain discolouration and leaf blight of rice in Russia. New Disease Reports. 2015;32:21-21. DOI: 10.5197/j.2044-0588.2015.032.021
  63. 63. Luna E, Lang J, McClung A, Wamishe Y, Jia Y, Leach JE. First report of rice bacterial leaf blight disease caused by Pantoea ananatis in the United States. Plant Disease. 2023;107:2214. DOI: 10.1094/PDIS-08-22-2014-PDN
  64. 64. Gavini F, Mergaert J, Beji A, Mielcarek C, Izard D, Kersters K, et al. Transfer of Enterobacter agglomerans (Beijerinck 1888) Ewing and fife 1972 to Pantoea gen. Nov. as Pantoea agglomerans comb. nov. and description of Pantoea dispersa sp. nov. International Journal of Systematic Bacteriology. 1989;39:337-345. DOI: 10.1099/00207713-39-3-337
  65. 65. Greyling I, Pantoea spp. Associated with Leaf and Stem Diseases of Eucalyptus [Thesis]. Pretoria: University of Pretoria; 2007. Available from: https://repository.up.ac.za/items/981372a5-c014-4528-95d7-43519faa703d
  66. 66. Mergaert J, Verdonck L, Kersters K. Transfer of Erwinia ananas (synonym, Erwinia uredovora) and Erwinia stewartii to the genus Pantoea emend. as Pantoea ananas (Serrano 1928) comb. nov. and Pantoea stewartii (Smith 1898) comb. nov., respectively, and description of Pantoea stewartii subsp. indologenes subsp. nov. International Journal of Systematic Bacteriology. 1993;43:162-173. DOI: 10.1099/00207713-43-1-162
  67. 67. Brady C, Cleenwerck I, Venter S, Vancanneyt M, Swings J, Coutinho T. Phylogeny and identification of Pantoea species associated with plants, humans and the natural environment based on multilocus sequence analysis (MLSA). Systematic and Applied Microbiology. 2008;31:447-460. DOI: 10.1016/j.syapm.2008.09.004
  68. 68. Dye DW. A taxonomic study of the genus Erwinia. IV. ‘Atypical’ Erwinias. New Zealand Journal of Science. 1969;12:833-839
  69. 69. Weller-Stuart T, De Maayer P, Coutinho T. Pantoea ananatis: Genomic insights into a versatile pathogen. Molecular Plant Pathology. 2017;18:1191-1198. DOI: 10.1111/mpp.12517
  70. 70. Gevers D, Cohan FM, Lawrence JG, Spratt BG, Coenye T, Feil EJ, et al. Re-evaluating prokaryotic species. Nature Reviews. Microbiology. 2005;3:733-739. DOI: 10.1038/nrmicro1236
  71. 71. De Maayer P, Venter SN, Kamber T, Duffy B, Coutinho TA, Smits TH. Comparative genomics of the type VI secretion systems of Pantoea and Erwinia species reveals the presence of putative effector islands that may be translocated by the VgrG and hcp proteins. BMC Genomics. 2011;12:576. DOI: 10.1186/1471-2164-12-576
  72. 72. Choi O, Lim JY, Seo Y-S, Hwang I, Kim J. Complete genome sequence of the rice pathogen Pantoea ananatis strain PA13. Journal of Bacteriology. 2012;194:531-531. DOI: 10.1128/JB.06450-11
  73. 73. Adam Z, Tambong JT, Lewis CT, Lévesque CA, Chen W, Bromfield ESP, et al. Draft genome sequence of Pantoea ananatis strain LMG 2665T, a bacterial pathogen of pineapple fruitlets. Genome Announcements. 2014;2:e00489-14. DOI: 10.1128/genomeA.00489-14
  74. 74. De Maayer P, Chan WY, Venter SN, Toth IK, Birch PRJ, Joubert F, et al. Genome sequence of Pantoea ananatis LMG20103, the causative agent of eucalyptus blight and dieback. Journal of Bacteriology. 2010;192:2936-2937. DOI: 10.1128/JB.00060-10
  75. 75. Coutinho TA, Venter SN. Pantoea ananatis: An unconventional plant pathogen. Molecular Plant Pathology. 2009;10:325-335. DOI: 10.1111/j.1364-3703.2009.00542.x
  76. 76. Sheibani-Tezerji R, Naveed M, Jehl M-A, Sessitsch A, Rattei T, Mitter B. The genomes of closely related Pantoea ananatis maize seed endophytes having different effects on the host plant differ in secretion system genes and mobile genetic elements. Frontiers in Microbiology. 2015;6:440. DOI: 10.3389/fmicb.2015.00440
  77. 77. De Maayer P, Chan W, Rubagotti E, Venter SN, Toth IK, Birch PRJ, et al. Analysis of the Pantoea ananatis pan-genome reveals factors underlying its ability to colonize and interact with plant, insect and vertebrate hosts. BMC Genomics. 2014;15:404. DOI: 10.1186/1471-2164-15-404
  78. 78. De Maayer P, Chan W-Y, Blom J, Venter SN, Duffy B, Smits THM, et al. The large universal Pantoea plasmid LPP-1 plays a major role in biological and ecological diversification. BMC Genomics. 2012;13:625. DOI: 10.1186/1471-2164-13-625
  79. 79. De Maayer P, Chan WY, Rezzonico F, Bühlmann A, Venter SN, Blom J, et al. Complete genome sequence of clinical isolate Pantoea ananatis LMG 5342. Journal of Bacteriology. 2012;194:1615-1616. DOI: 10.1128/JB.06715-11
  80. 80. De Maayer P, Chan W-Y, Martin DAJ, Blom J, Venter SN, Duffy B, et al. Integrative conjugative elements of the ICEPan family play a potential role in Pantoea ananatis ecological diversification and antibiosis. Frontiers in Microbiology. 2015;6:576. DOI: 10.3389/fmicb.2015.00576
  81. 81. Mano H, Morisaki H. Endophytic bacteria in the rice plant. Microbes and Environments. 2008;23:109-117. DOI: 10.1264/jsme2.23.109
  82. 82. Brandl MT, Lindow SE. Contribution of Indole-3-acetic acid production to the epiphytic fitness of Erwinia herbicola. Applied and Environmental Microbiology. 1998;64:3256-3263. DOI: 10.1128/AEM.64.9.3256-3263.1998
  83. 83. Pukatzki S, Ma AT, Sturtevant D, Krastins B, Sarracino D, Nelson WC, et al. Identification of a conserved bacterial protein secretion system in vibrio cholerae using the Dictyostelium host model system. National Academy of Sciences of the United States of America. 2006;103:1528-1533. DOI: 10.1073/pnas.0510322103
  84. 84. Mattinen L, Somervuo P, Nykyri J, Nissinen R, Kouvonen P, Corthals G, et al. Microarray profiling of host-extract-induced genes and characterization of the type VI secretion cluster in the potato pathogen Pectobacterium atrosepticum. Microbiology. 2008;154:2387-2396. DOI: 10.1099/mic.0.2008/017582-0
  85. 85. Paccola-Meirelles LD, Ferreira AS, Meirelles WF, Marriel IE, Casela CR. Detection of a bacterium associated with a leaf spot disease of maize in Brazil. Journal of Phytopathology. 2001;149:275-279. DOI: 10.1046/j.1439-0434.2001.00614.x
  86. 86. Azad HR, Holmes GJ, Cooksey DA. A new leaf blotch disease of sudangrass caused by Pantoea ananas and Pantoea stewartii. Plant Disease. 2000;84:973-979. DOI: 10.1094/PDIS.2000.84.9.973
  87. 87. Bomfeti CA, Souza-Paccola EA, Massola Júnior NS, Marriel IE, Meirelles WF, Casela CR, et al. Localization of Pantoea ananatis inside lesions of maize white spot disease using transmission electron microscopy and molecular techniques. Tropical Plant Pathology. 2008;33:63-66. DOI: 10.1590/S1982-56762008000100010
  88. 88. Goszczynska T, Botha WJ, Venter SN, Coutinho TA. Isolation and identification of the causal agent of brown stalk rot, a new disease of maize in South Africa. Plant Disease. 2007;91:711-718. DOI: 10.1094/PDIS-91-6-0711
  89. 89. Cother EJ, Reinke R, McKenzie C, Lanoiselet VM, Noble DH. An unusual stem necrosis of rice caused by Pantoea ananas and the first record of this pathogen on rice in Australia. Australasian Plant Pathology. 2004;33:495. DOI: 10.1071/AP04053
  90. 90. Bruno J, Barphagha I, Ontoy J, Dalla Lana F, Ham JH. First report of Pantoea ananatis causing bacterial leaf and panicle blight of rice in Louisiana, U.S.a. Plant Disease. 2025;109:932. DOI: 10.1094/PDIS-08-24-1731-PDN
  91. 91. Hasegawa M, Azegami K, Yoshida H, Otani H. Behavior of Erwinia ananas transformed with bioluminescence genes on rice plants. Journal of General Plant Pathology. 2003;69:267-270. DOI: 10.1007/s10327-003-0046-y
  92. 92. Gitaitis RD, Walcott RR, Wells ML, Perez JCD, Sanders FH. Transmission of Pantoea ananatis, causal agent of center rot of onion, by tobacco thrips, Frankliniella fusca. Plant Disease. 2003;87:675-678. DOI: 10.1094/PDIS.2003.87.6.675
  93. 93. Serrano FB. Bacterial fruitlet brown-rot of pineapple in the Philippines. The Philippine Journal of Science. 1928;36:271-305
  94. 94. Walcott RR, Gitaitis RD, Castro AC, Sanders FH, Diaz-Perez JC. Natural infestation of onion seed by Pantoea ananatis, causal agent of center rot. Plant Disease. 2002;86:106-111. DOI: 10.1094/PDIS.2002.86.2.106
  95. 95. Azegami K, Ozaki K, Matsuda A. Bacterial Palea browning, a new disease of rice caused by Erwinia herbicola. Bulletin of the National Institute of Agricultural Science. 1983;C39:1-12
  96. 96. Schwartz HF, Otto KL, Gent DH. Relation of temperature and rainfall to development of Xanthomonas and Pantoea leaf blights of onion in Colorado. Plant Disease. 2003;87:11-14. DOI: 10.1094/PDIS.2003.87.1.11
  97. 97. Pedrozo R, Huang Y, Nicolli CP, Jia Y. Elucidating the role of seeds as primary inoculum source of Pantoea ananatis in rice production. In: 40th Rice Technical Working Group (RTWG). New Orleans, Louisiana: The Rice Technical Working Group; 2025
  98. 98. Asselin JAE, Bonasera JM, Beer SV. PCR primers for detection of Pantoea ananatis, Burkholderia spp., and Enterobacter sp. from onion. Plant Disease. 2016;100:836-846. DOI: 10.1094/PDIS-08-15-0941-RE
  99. 99. Kini K, Dossa R, Dossou B, Mariko M, Koebnik R, Silué D. A semi-selective medium to isolate and identify bacteria of the genus Pantoea. Journal of General Plant Pathology. 2019;85:424-427. DOI: 10.1007/s10327-019-00862-w
  100. 100. Paccola-Meirelles LD, Meirelles WF, Parentoni SN, Marriel IE, Ferreira AS, Casela CR. Reaction of maize inbred lines to the bacterium Pantoea ananas isolated from Phaeosphaeria leaf spot lesions. Crop Breeding and Applied Biotechnology. 2002;2:587-590
  101. 101. Bomfeti CA, Meirelles WF, Souza-Paccola EA, Casela CR, da Ferreira AS, Marriel IE, et al. Evaluation of commercial chemical products, in vitro and in vivo in the control of foliar disease, maize white spot, caused by Pantoea ananais. Summa Phytopathologica. 2007;33:63-67. DOI: 10.1590/S0100-54052007000100009
  102. 102. Gitaitis RD, Walcott RR, Sanders HF, Zolobowska L, Diaz-Perez JC. Effects of mulch and irrigation system on sweet onion: II. The epidemiology of center rot. Journal of the American Society for Horticultural Science. 2004;129:225-230. DOI: 10.21273/JASHS.129.2.0225
  103. 103. Hollier C. Narrow brown leaf spot. In: Webster RK, Gunnel PS, editors. Compendium of Rice Diseases. St. Paul, MN: APS Press; 1992. p. 18
  104. 104. Miyake I. Studien uber die pilze der reispflazane in Japan. Journal of the College of Agriculture Imperial University of Tokyo. 1910;2:237-276
  105. 105. Deighton FC. Sphaerulina oryzina, the perfect state of Cercospora oryzae. Transactions of the British Mycological Society. 1967;50:499. DOI: 10.1016/S0007-1536(67)80019-6
  106. 106. Biswas A. Narrow brown leaf spot disease of rice: A review. Journal of Mycopathological Research. 2006;44:113-115
  107. 107. Tullis EC. Cercospora oryzae on rice in the United States. Phytopathology. 1937;27:1005-1008
  108. 108. Uppala SS, Zhou X-G, Liu B, Wu M. Plant-based culture media for improved growth and sporulation of Cercospora janseana. Plant Disease. 2019;103:504-508. DOI: 10.1094/PDIS-05-18-0814-RE
  109. 109. Nicolli C, Pereira JS, Pedrozo R. Cercospora Diseases in Rice. Agriculture and Natural Resources. Stuttgart: University of Arkansas System Division of Agriculture; 2025. p. 4. Available from: https://www.uaex.uada.edu/publications/pdf/FSA2213.pdf
  110. 110. Mew TW, Misra JK. Narrow Brown Leaf Spot: Cercospora Janseana. A Manual of Rice Seed Health Testing. Manila, Philippines: International Rice Research Institute; 1994. pp. 77-78
  111. 111. Volk TJ. Fungi. In: Levin SA, editor. Encyclopedia of Biodiversity. 2nd ed. Cambridge, Massachusetts: Academic Press; 2013. pp. 624-640. DOI: 10.1016/B978-0-12-384719-5.00062-9
  112. 112. Muria-Gonzalez MJ, Chooi Y, Breen S, Solomon PS. The past, present and future of secondary metabolite research in the Dothideomycetes. Molecular Plant Pathology. 2015;16:92-107. DOI: 10.1111/mpp.12162
  113. 113. Ohm RA, Feau N, Henrissat B, Schoch CL, Horwitz BA, Barry KW, et al. Diverse lifestyles and strategies of plant pathogenesis encoded in the genomes of eighteen Dothideomycetes fungi. PLoS Pathogens. 2012;8:e1003037. DOI: 10.1371/journal.ppat.1003037
  114. 114. Center for Invasive Species and Ecosystem Health. Narrow Brown Leaf Spot (Cercospora janseana (Racib.) Constant.). Invasive.org. 2018. Available from: https://www.invasive.org/browse/subinfo.cfm?sub=56020&fam=318
  115. 115. Farr DF, Bills GF, Chamuris GP, Rossman AY. Fungi on Plants and Plant Products in the United States. St. Paul, MN: APS Press; 1995
  116. 116. Videira SIR, Groenewald JZ, Nakashima C, Braun U, Barreto RW, de Wit PJGM, et al. Mycosphaerellaceae: Chaos or clarity? Studies in Mycology. 2017;87:257-421. DOI: 10.1016/j.simyco.2017.09.003
  117. 117. Tondok ET, Sa’adah RNH. Isolation and morphological characterization of Cercospora janseana infecting rice leaves. Jurnal Fitopatologi Indonesia. 2023;18:255-263. DOI: 10.14692/jfi.18.6.255-263
  118. 118. Kaur K, Hollier C. Effect of amended media, temperature, and light on the growth and development of Cercospora janseana. In: American Phytopathological Society Annual Meeting. Austin, TX: APS Press; 2013
  119. 119. Sah DN, Rush MC. Physiological races of Cercospora oryzae in the southern United States. Plant Disease. 1988;72:262-264
  120. 120. Ou SH. Rice Diseases. 2nd ed. Kew, UK: Commonwealth Mycological Institute; 1985
  121. 121. Searight J. Population Genomic Characterization of Cercospora Janseana on Rice in the Southern United States [Thesis]. Baton Rouge: Louisiana State University; 2022 Available from: https://repository.lsu.edu/gradschool_theses/5686
  122. 122. Searight J, Famoso AN, Zhou X-G, Doyle VP, Richards JK. A high-quality genome assembly for Cercospora janseana, causal agent of narrow brown leaf spot of rice. Molecular Plant-Microbe Interactions. 2023;36:666-669. DOI: 10.1094/MPMI-10-22-0222-A
  123. 123. Groth DE, Lee F. Rice diseases. In: Smith CW, Dilday RH, editors. Rice: Origin, History, Technology, and Production. Hoboken, NJ: Wiley; 2003. pp. 413-436
  124. 124. Uppala S, Zhou XG. Field efficacy of fungicides for management of sheath blight and narrow brown leaf spot of rice. Crop Protection. 2018;104:72-77. DOI: 10.1016/j.cropro.2017.10.017
  125. 125. Shi J, Zhou X-G, Yan Z, Tabien RE, Wilson LT, Wang L. Hybrid rice outperforms inbred rice in resistance to sheath blight and narrow brown leaf spot. Plant Disease. 2021;105:2981-2989. DOI: 10.1094/PDIS-11-20-2391-RE
  126. 126. Mani KK, Hollier CA, Groth DE. Effect of cultivar susceptibility and planting date on narrow brown leaf spot progression in rice. Crop Protection. 2017;102:88-93. DOI: 10.1016/j.cropro.2017.08.004
  127. 127. Uppala S, Zhou XG. Optimum timing of propiconazole to manage narrow brown leaf spot in the main and ratoon rice crops in Texas. Crop Protection. 2019;124:104854. DOI: 10.1016/j.cropro.2019.104854
  128. 128. Mani KK, Chanda A, Hollier C. Detection and Quantification of Cercospora Janseana by Real Time PCR Technique. Southern Division of the American Phytopathological Society. Dallas, TX: Phytopathology; 2014. pp. S2.1-S2.11
  129. 129. Addison CK, Angira B, Cerioli T, Groth DE, Richards JK, Linscombe SD, et al. Identification and mapping of a novel resistance gene to the rice pathogen, Cercospora janseana. Theoretical and Applied Genetics. 2021;134:2221-2234. DOI: 10.1007/s00122-021-03821-2
  130. 130. Angira B, Linscombe SD, Webster EP, Webster C, Harrell DL, Groth DE, et al. Registration of ‘PVL03’ rice. Journal of Plant Registrations. 2024;18:303-309. DOI: 10.1002/plr2.20333
  131. 131. Moldenhauer KAK. Rice cultivar ‘CLL16’. United States: United States Patent; 2021. pp. 1-32
  132. 132. Angira B, Linscombe SD, Webster EP, Webster C, Harrell DL, Groth DE, et al. Registration of ‘CLL17’ rice. Journal of Plant Registrations. 2024;18:296-302. DOI: 10.1002/plr2.20332
  133. 133. Angira B, Linscombe S, Webster C, Kongchum M, Dalla-Lana F, Wilson B, et al. Registration of ‘Avant’ rice. Journal of Plant Registrations. 2025;19:e20411. DOI: 10.1002/plr2.20411
  134. 134. Levy R, Pabuayon ILB, Wenefrida I, Utomo HS, Famoso AN, Fontenot KA, et al. Rice Varieties and Management Tips. Baton Rouge: Louisiana State University Agricultural Center; 2023. Available from: https://www.lsuagcenter.com/profiles/astrahan/articles/page1669217585621
  135. 135. Sun W, Fan J, Fang A, Li Y, Tariqjaveed M, Li D, et al. Ustilaginoidea virens : Insights into an emerging rice pathogen. Annual Review of Phytopathology. 2020;58:363-385. DOI: 10.1146/annurev-phyto-010820-012908
  136. 136. Cooke MC. Some extra-European fungi. Grevillea. 1878;7:1-3
  137. 137. Khanal S, Gaire SP, Zhou X-G. Kernel smut and false smut: The old-emerging diseases of rice—A review. Phytopathology. 2023;113:931-944. DOI: 10.1094/PHYTO-06-22-0226-RVW
  138. 138. Dangi B, Khanal S, Shah S. A review on rice false smut, it’s distribution, identification and management practices. Acta Scientific Agriculture. 2020;4:48-54. DOI: 10.31080/ASAG.2020.04.0924
  139. 139. Fan J, Yang J, Wang Y, Li G, Li Y, Huang F, et al. Current understanding on Villosiclava virens, a unique flower-infecting fungus causing rice false smut disease. Molecular Plant Pathology. 2016;17:1321-1330. DOI: 10.1111/mpp.12362
  140. 140. Yong M, Deng Q, Fan L, Miao J, Lai C, Chen H, et al. The role of Ustilaginoidea virens sclerotia in increasing incidence of rice false smut disease in the subtropical zone in China. European Journal of Plant Pathology. 2018;150:669-677. DOI: 10.1007/s10658-017-1312-8
  141. 141. Tang Y-X, Jin J, Hu D-W, ong M-L, Xu Y, He L-P. Elucidation of the infection process of Ustilaginoidea virens (teleomorph: Villosiclava virens) in rice spikelets. Plant Pathology. 2013;62:1-8. DOI: 10.1111/j.1365-3059.2012.02629.x
  142. 142. Fan J, Liu J, Gong Z, Xu P, Hu X, Wu J, et al. The false smut pathogen Ustilaginoidea virens requires rice stamens for false smut ball formation. Environmental Microbiology. 2020;22:646-659. DOI: 10.1111/1462-2920.14881
  143. 143. Ashizawa T, Takahashi M, Arai M, Arie T. Rice false smut pathogen, Ustilaginoidea virens, invades through small gap at the apex of a rice spikelet before heading. Journal of General Plant Pathology. 2012;78:255-259. DOI: 10.1007/s10327-012-0389-3
  144. 144. Kim KW, Park EW. Ultrastructure of spined conidia and hyphae of the rice false smut fungus Ustilaginoidea virens. Micron. 2007;38:626-631. DOI: 10.1016/j.micron.2006.09.006
  145. 145. Fan L, Yong M, Li D, Liu Y, Lai C, Chen H, et al. Effect of temperature on the development of sclerotia in Villosiclava virens. Journal of Integrative Agriculture. 2016;15:2550-2555. DOI: 10.1016/S2095-3119(16)61400-4
  146. 146. Zhang N, Yang J, Fang A, Wang J, Li D, Li Y, et al. The essential effector SCRE1 in Ustilaginoidea virens suppresses rice immunity via a small peptide region. Molecular Plant Pathology. 2020;21:445-459. DOI: 10.1111/mpp.12894
  147. 147. Fang A, Gao H, Zhang N, Zheng X, Qiu S, Li Y, et al. A novel effector gene SCRE2 contributes to full virulence of Ustilaginoidea virens to rice. Frontiers in Microbiology. 2019;10:845. DOI: 10.3389/fmicb.2019.00845
  148. 148. Fang A, Han Y, Zhang N, Zhang M, Liu L, Li S, et al. Identification and characterization of plant cell death–inducing secreted proteins from Ustilaginoidea virens. Molecular Plant-Microbe Interactions. 2016;29:405-416. DOI: 10.1094/MPMI-09-15-0200-R
  149. 149. Zheng X, Fang A, Qiu S, Zhao G, Wang J, Wang S, et al. Ustilaginoidea virens secretes a family of phosphatases that stabilize the negative immune regulator OsMPK6 and suppress plant immunity. The Plant Cell. 2022;34:3088-3109. DOI: 10.1093/plcell/koac154
  150. 150. Duan Y, Yang G, Tang J, Fang Y, Wang H, Wang Z, et al. Ustilaginoidea virens secreted effector UvSec117 hijacks OsWRKY3-OsAOC module to suppress jasmonic acid-mediated immunity in rice. Plant Biotechnology Journal. 2024;22:3342-3344. DOI: 10.1111/pbi.14452
  151. 151. Li G-B, Liu J, He J-X, Li G-M, Zhao Y-D, Liu X-L, et al. Rice false smut virulence protein subverts host chitin perception and signaling at lemma and Palea for floral infection. The Plant Cell. 2024;36:2000-2020. DOI: 10.1093/plcell/koae027
  152. 152. Li G-B, He J-X, Wu J-L, Wang H, Zhang X, Liu J, et al. Overproduction of OsRACK1A, an effector-targeted scaffold protein promoting OsRBOHB-mediated ROS production, confers rice floral resistance to false smut disease without yield penalty. Molecular Plant. 2022;15:1790-1806. DOI: 10.1016/j.molp.2022.10.009
  153. 153. Hu M, Luo L, Wang S, Liu Y, Li J. Infection processes of Ustilaginoidea virens during artificial inoculation of rice panicles. European Journal of Plant Pathology. 2014;139:67-77. DOI: 10.1007/s10658-013-0364-7
  154. 154. Molla KA. A trick for a treat: False smut pathogen manipulates plant defense to gain access to rice flower. The Plant Cell. 2024;36:1598-1599. DOI: 10.1093/plcell/koae048
  155. 155. Nicolli C, de Paula S. Rice false smut. Agriculture and Natural Resources. University of Arkansas System Division of Agriculture; [Internet]. 2025. p. 4. Available from: https://www.uaex.uada.edu/publications/pdf/FSA7582.pdf
  156. 156. Shan T, Sun W, Wang X, Fu X, Sun W, Zhou L. Purification of ustiloxins a and B from rice false smut balls by macroporous resins. Molecules. 2013;18:8181-8199. DOI: 10.3390/molecules18078181
  157. 157. Tanaka E, Kumagawa T, Ito N, Nakanishi A, Ohta Y, Suzuki E, et al. Colonization of the vegetative stage of rice plants by the false smut fungus Villosiclava virens, as revealed by a combination of species-specific detection methods. Plant Pathology. 2017;66:56-66. DOI: 10.1111/ppa.12540
  158. 158. Fan J, Guo X-Y, Huang F, Li Y, Liu Y-F, Li L, et al. Epiphytic colonization of Ustilaginoidea virens on biotic and abiotic surfaces implies the widespread presence of primary inoculum for rice false smut disease. Plant Pathology. 2014;63:937-945. DOI: 10.1111/ppa.12167
  159. 159. Tang J, Zheng L, Jia Q, Liu H, Hsiang T, Huang J. PCR markers derived from comparative genomics for detection and identification of the rice pathogen Ustilaginoidea virens in plant tissues. Plant Disease. 2017;101:1515-1521. DOI: 10.1094/PDIS-08-16-1088-RE
  160. 160. Li H, Ni DH, Duan YB, Chen Y, Li J, Song FS, et al. Quantitative detection of the rice false smut pathogen Ustilaginoidea virens by real-time PCR. Genetics and Molecular Research. 2013;12:6433-6441. DOI: 10.4238/2013.December.10.4
  161. 161. Ayyanar K, Sekhar YC, Chellappan G, Iruthayasamy J, Subramanian R, Swarna Lakshmi KR, et al. Rapid and early detection of rice false smut pathogen Ustilaginoidea virens (cook) (Takahashi) using loop-mediated isothermal amplification (LAMP). Journal of Plant Pathology. 2025;107:1091-1104. DOI: 10.1007/s42161-025-01881-7
  162. 162. Sunani SK, Koti PS, Sunitha NC, Choudhary M, Jeevan B, Anilkumar C, et al. Ustilaginoidea virens, an emerging pathogen of rice: The dynamic interplay between the pathogen virulence strategies and host defense. Planta. 2024;260:92. DOI: 10.1007/s00425-024-04523-x
  163. 163. Zhou L, Mubeen M, Iftikhar Y, Zheng H, Zhang Z, Wen J, et al. Rice false smut pathogen: Implications for mycotoxin contamination, current status, and future perspectives. Frontiers in Microbiology. 2024;15:1344831. DOI: 10.3389/fmicb.2024.1344831
  164. 164. Baite MS, Prabhukarthikeyan SR, Raghu S. Biological control of a fungus Ustilaginoidea virens causing false smut of rice. BioControl. 2022;67:357-363. DOI: 10.1007/s10526-022-10148-4
  165. 165. Blanchard T, Richards J. One Pathogen, Two Diseases and the Research Trying to Understand all Three. Baton Rouge: Louisiana State University Agricultural Center; 2024. Available from: https://www.lsuagcenter.com/articles/page1732640012604
  166. 166. Kumagai T, Ishii T, Terai G, Umemura M, Machida M, Asai K. Genome sequence of Ustilaginoidea virens IPU010, a rice pathogenic fungus causing false smut. Genome Announcements. 2016;4:e00306-16. DOI: 10.1128/genomeA.00306-16

Written By

Rodrigo Pedrozo, Samuel de Paula, Madison Flasco, Felipe Dalla Lana, Yulin Jia and Camila Nicolli

Submitted: 30 May 2025 Reviewed: 03 June 2025 Published: 09 July 2025