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Erwinia
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Erwinia
Orchid bacterial leaf blight caused by Erwinia sp.
Scientific classification Edit this classification
Domain: Bacteria
Kingdom: Pseudomonadati
Phylum: Pseudomonadota
Class: Gammaproteobacteria
Order: Enterobacterales
Family: Erwiniaceae
Genus: Erwinia
Winslow et al., 1920
Species

See text

Erwinia is a genus of Enterobacterales bacteria containing mostly plant pathogenic species which was named for the famous plant pathologist, Erwin Frink Smith. It contains Gram-negative bacteria related to Escherichia coli, Shigella, Salmonella, and Yersinia. They are primarily rod-shaped bacteria.

Many infect woody plants. A well-known member of this genus is the species E. amylovora, which causes fire blight on apples, pears, and other Rosaceae crops; E. tracheiphila, though, causes bacterial wilt of cucurbits. Other familiar species, such as E. carotovora (another major cause of plant diseases), are more distantly related to the fire blight bacterium, and have been moved to genera Brenneria, Dickeya, and Pectobacterium.[1]

Erwinia aphidocola and E. persicina species were both observed to be present within the floral nectar microbial community of seven different orchid (Epipactis) flower species.[2] E. aphidicola appears to display characteristics of a pathogen as it had decimated fifty percent of a bean crop in Spain in late 2003.[3]

Erwinia rhapontici has been identified as a plant pathogen that produces a distinct diffusible pink pigment on sucrose-peptone agar and creates pink seeds in the hosts.[4] It is also found to be a wound pathogen[citation needed]. Wound pathogens are replicating microorganisms in a wound that can cause the host injury. It is possible that the bacterium can penetrate though young pea pods through wounds or injuries and infect seeds produced in the pod, causing deformed leaves.[5]

Erwinia uredovora is a bacterium from which Phytoene desaturase was isolated, which is the gene that is inserted into golden rice.

Species

[edit]

Species in Erwinia are:[6]

Dickeya dadantii was formerly classified as Erwinia chrysanthemi.

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Erwinia

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Erwinia is a of Gram-negative, motile, rod-shaped belonging to the family Erwiniaceae within the order , primarily recognized as phytopathogens that cause significant diseases in , including soft rots, wilts, and . These are cosmopolitan, often associated with , , and , and while most species are necrogenic pathogens leading to tissue decay, some are non-pathogenic epiphytes or even beneficial plant growth-promoting . Taxonomically, the genus Erwinia was named after bacteriologist Erwin F. Smith and encompasses that have undergone reclassifications, with some former members like Pectobacterium and Dickeya now in separate genera due to phylogenetic distinctions. Cells are typically straight rods measuring 0.5–1.0 × 1.0–3.0 μm, occurring singly, in pairs, or occasionally in chains, and are equipped with peritrichous flagella for motility. Physiologically, Erwinia species are facultative anaerobes, catalase-positive, - and urease-negative, and capable of fermenting various sugars while producing pectolytic enzymes that degrade cell walls. Their DNA G+C content ranges from 51.1–56.4 mol%, and major cellular fatty acids include C12:0, C14:0, and C16:0. The pathogenic significance of Erwinia lies in its ability to infect a wide range of hosts, particularly , fruits, and ornamentals, often resulting in post-harvest spoilage and economic losses in . Key species include Erwinia amylovora, the responsible for in rosaceous plants like apples and pears, which is transmitted by and can devastate orchards. Transmission frequently occurs via , wounds, or contaminated water, exacerbating disease spread in humid environments. Beyond phytopathology, Erwinia species exhibit diverse ecological roles, including associations with insects as endosymbionts—such as Erwinia dacicola in olive fruit flies, aiding nitrogen metabolism—and rare isolations from human clinical samples, though human infections are infrequent, typically opportunistic, with recent reports of novel species like Erwinia wuhanensis from blood as of 2025. Recent genomic studies have revealed novel species, like Candidatus Erwinia impunctatus from midges, highlighting the genus's adaptability and potential beyond plant hosts. Non-pathogenic strains, such as Erwinia tasmaniensis and Erwinia billingiae, colonize plant surfaces epiphytically and may suppress pathogens or promote growth through antagonistic or symbiotic interactions.

Taxonomy

Classification

The genus Erwinia is classified within the domain , phylum , class , order , and family Erwiniaceae. The genus was established by Winslow et al. in 1920, with Erwinia amylovora designated as the . This taxonomic placement reflects its position among primarily associated with plant environments. Phylogenetic studies utilizing 16S rRNA gene have revealed close relationships between Erwinia and other genera in the order , including Escherichia, Shigella, Salmonella, and . These analyses indicate that Erwinia species form distinct clusters within the broader enterobacterial group, supported by similarities ranging from 96% to 99% with related taxa. Complementary whole-genome comparisons have reinforced this positioning, highlighting shared genomic signatures such as conserved housekeeping genes and structures. Delineation of the Erwinia relies on key phenotypic and genotypic criteria, including Gram-negative , facultative anaerobiosis, rod-shaped morphology, negativity, and conferred by peritrichous flagella, alongside a predominantly plant-associated . The was emended in 1998 to restrict membership to species in phylogenetic cluster I based on 16S rRNA data, excluding more divergent groups reclassified elsewhere. A significant taxonomic update occurred in 2016 with the proposal of the family Erwiniaceae, derived from the former through genome-based phylogeny identifying distinct monophyletic clades.

Etymology and History

The genus Erwinia derives its name from Erwin Frink Smith (1854–1927), a pioneering American plant pathologist renowned for his foundational contributions to bacterial phytopathology, including early studies on and soft rot diseases. This follows bacterial conventions, using the scientist's first name rather than surname to form the feminine Latin noun Erwinia. The genus was formally established in 1920 by Winslow et al. in their comprehensive classification of , initially comprising Gram-negative, peritrichously flagellated rods responsible for soft-rot diseases in , with Erwinia amylovora designated as the . This description built on earlier observations of plant-pathogenic enterobacteria, grouping them separately from animal or human pathogens. The genus Erwinia belongs to the order . Key historical milestones include extensive isolations from plant diseases in the 1940s and 1950s, such as William H. Burkholder's 1948 description of Erwinia atroseptica (now Pectobacterium atrosepticum) from potato blackleg and his 1953 report on Erwinia chrysanthemi causing bacterial blight in chrysanthemums. Molecular advancements from the 1980s to 2000s prompted significant reclassifications of non-pathogenic species; for instance, the Erwinia herbicola group, including epiphytic strains, was transferred to the novel genus Pantoea in 1989 based on DNA hybridization and phenotypic data. Similarly, pectinolytic species like Erwinia chrysanthemi were reclassified into the genus Dickeya in 2005 following 16S rRNA and multilocus sequence analyses that highlighted phylogenetic heterogeneity. Influential figures in refining the genus include Erwin F. Smith for early pathological insights, Burkholder for mid-20th-century species delineations, Robert Samson for the 2005 Dickeya proposal, and contemporary taxonomists like Carrie L. Brady, whose phylogenomic studies have addressed ongoing boundary debates. As of 2025, these debates continue, with recent analyses supporting reclassifications such as the transfer of Erwinia gerundensis to the new genus Duffyella based on whole-genome sequencing and average nucleotide identity metrics. Recent additions to the genus include Erwinia pyri, a causing dieback, and Erwinia plantamica, a non-pathogenic species isolated from .

Characteristics

Morphology and Physiology

Erwinia species are Gram-stain-negative rods measuring 0.5–1.0 μm in width and 1.0–3.0 μm in length, occurring singly, in pairs, or occasionally in short chains. These bacteria are motile, possessing peritrichous flagella that enable swimming motility. On solid media such as nutrient agar, they form round, convex, and often mucoid colonies, which can appear creamy white to beige depending on the species and conditions. Major cellular fatty acids include C12:0, C14:0, and C16:0. Physiologically, Erwinia bacteria are facultatively anaerobic, capable of growth under aerobic or microaerophilic conditions, though anaerobic growth may be weak in some species. They are catalase-positive and oxidase-negative, and they ferment glucose to produce acid but no gas, either aerobically or anaerobically. Optimal growth occurs at 27–30°C, with a maximum of around 40°C, and they thrive on nutrient-rich media such as or yeast extract-peptone agar. Pathogenic strains produce extracellular enzymes including and , which contribute to tissue degradation. Pigmentation varies among species; for instance, Erwinia rhapontici produces a characteristic diffusible pink pigment on media like sucrose-peptone , responsible for symptoms such as pink seed discoloration. In contrast, species like Erwinia amylovora are typically non-pigmented, forming white or cream-colored colonies.

Genomics and Molecular Features

The genomes of Erwinia species typically consist of a single circular ranging from 3.5 to 5.5 Mb in size, with some strains harboring additional plasmids that contribute to . For instance, Erwinia amylovora has a chromosome of approximately 3.8–4.0 Mb, while Dickeya dadantii (formerly Erwinia chrysanthemi) has one of approximately 4.9 Mb. The is generally 51.1–56.4 mol%, reflecting adaptation to plant-associated lifestyles within the order. These compact genomes encode core functions for metabolism, motility, and , with plasmids often carrying accessory genes for or resistance. Key gene clusters underpin Erwinia's molecular capabilities, particularly in pathogenesis and environmental adaptation. The hrp and hrc gene clusters encode the type III secretion system (T3SS), a syringe-like apparatus essential for injecting effector proteins into host cells. Pectinolytic genes such as pel (pectate lyases) and peh (polygalacturonases) form clusters that enable tissue degradation by breaking down plant cell walls. In pigment biosynthesis, species like Pantoea ananatis (formerly Erwinia uredovora) feature the crtI gene encoding phytoene desaturase, which produces carotenoids for photoprotection and signaling. Molecular tools have advanced Erwinia strain differentiation and genomic analysis. (MLST) targets housekeeping genes to resolve phylogenetic relationships and track outbreaks. Average nucleotide identity (ANI) values exceeding 95–96% confirm species boundaries, as demonstrated in delineating novel Erwinia taxa. CRISPR-Cas systems, identified in several genomes, provide adaptive immunity against phages and enable precise applications. Comparative genomics reveals extensive horizontal gene transfer (HGT) from related , shaping Erwinia's accessory genome. Studies highlight HGT events involving islands and metabolic pathways, enhancing adaptability to diverse hosts. Recent 2020s analyses have uncovered mechanisms mediated by acyl-homoserine lactones (AHLs), which regulate collective behaviors like formation and gene across strains.

Ecology and Distribution

Natural Habitats

Erwinia species primarily inhabit , bodies, and surfaces, including the (above-ground parts like leaves and flowers) and (root zones). In , these bacteria can survive for extended periods, with some species persisting up to 6 months under favorable conditions, particularly in association with . They are often epiphytic on healthy surfaces, colonizing flowers and leaves without causing immediate harm, as seen with Erwinia amylovora growing on stigmas of plants at concentrations exceeding 10^6 cells per flower. In the , (formerly classified as Erwinia carotovora) is commonly present on roots of various species, thriving in nutrient-rich environments near tissues. Geographically, Erwinia bacteria are distributed worldwide, with a prevalence in temperate regions due to their adaptation to moderate climates. Erwinia amylovora is native to and has spread extensively to , parts of (including recent confirmations in southern and as of 2025), the , forming continuous infected zones across western and beyond. In contrast, Erwinia tracheiphila is more restricted to warmer temperate areas, particularly the Midwestern and , aligning with the range of its primary insect vectors. These distributions reflect historical introductions and favorable climatic conditions for persistence and spread. Erwinia species thrive in moist environments, such as those provided by , , or high (>55% relative humidity), which facilitate epiphytic growth and dispersal on surfaces. Survival is enhanced in wet soils and water-saturated conditions, with overwintering occurring in plant debris where remain viable through . They are also associated with insect vectors for dissemination, including pollinators like honeybees for E. amylovora (surviving up to 10 days on insects) and cucumber beetles for E. tracheiphila, which carry the bacteria in their guts. Motility via peritrichous flagella aids in short-distance movement across wet surfaces. Non-plant reservoirs are uncommon but documented, with rare isolations of Erwinia-like organisms from mammals, including vital organs of deer (over 40% of examined populations) and occasional sources. In aquatic environments, (formerly classified as Erwinia carotovora) has been detected in lakes, streams, and irrigation water, serving as potential sources for contamination of agricultural systems. These extra-plant niches underscore the bacteria's broad environmental adaptability, though plant-associated habitats remain dominant.

Interactions with Hosts and Environment

Erwinia species exhibit a broad host range, primarily targeting woody and herbaceous , with Erwinia amylovora specializing in members of the family, including over 200 species predominantly in the subfamily Maloideae such as apples ( spp.) and pears (Pyrus spp.). Before initiating , these often adopt endophytic or epiphytic lifestyles, colonizing internal tissues or surfaces asymptomatically, which facilitates persistence and eventual opportunistic pathogenesis in susceptible hosts. Transmission of Erwinia occurs through diverse vectors, including insects like bees, ants, flies, and wasps that carry bacterial ooze from infected tissues to flowers or wounds, as seen in the bee-mediated spread of fire blight caused by E. amylovora. Additional dissemination happens via rain splash, wind-driven dispersal of contaminated droplets, and mechanical means such as pruning tools, enabling short- and long-distance movement within and between plant populations. Some Erwinia species also form non-pathogenic associations with , acting as endosymbionts. For example, Erwinia dacicola resides in the gut of the (Bactrocera oleae), aiding in and potentially benefiting the host . Ecologically, Erwinia alters microbiomes by outcompeting beneficial for nutrients such as on flower surfaces, thereby disrupting community structure and reducing microbial diversity in infected tissues. This competition can suppress protective endophytes, enhancing pathogen dominance during outbreaks. Furthermore, through enzymatic degradation of polymers like via secreted polysaccharidases, Erwinia contributes to nutrient cycling by breaking down cell walls, releasing carbon and other elements into the ecosystem. Environmental factors significantly influence Erwinia dynamics, with —particularly warmer temperatures—projected to expand the pathogen's geographic distribution by favoring survival and vector activity in previously unsuitable regions. formation on plant surfaces, mediated by exopolysaccharides, enhances persistence under fluctuating conditions like humidity and temperature, allowing overwintering and reinfection cycles.

Pathogenicity

Diseases Caused

Erwinia species are phytopathogenic primarily responsible for destructive diseases in various crops, leading to significant agricultural losses through symptoms such as wilting, rot, and tissue . While classic soft rots were historically attributed to Erwinia, many such species have been reclassified to genera like Pectobacterium and Dickeya; current Erwinia species cause diseases such as , , and pink seed. Among the most notorious is , caused by E. amylovora, which primarily affects fruits like apples and pears. This disease manifests as blossom blight, where infected flowers wilt and turn black, progressing to blackened shoots with a scorched appearance and oozing cankers that exude a creamy bacterial slime, especially during humid conditions. First reported in the 1790s in , fire blight has caused substantial economic impacts, with annual losses and control costs exceeding $100 million in the United States alone. Recent epidemics have been exacerbated by warmer, wetter springs, resulting in annual losses of up to $22 million in affected regions as of 2023. Another major disease is bacterial wilt of cucurbits, induced by E. tracheiphila, which targets crops such as cucumbers, squash, and melons. Symptoms begin with vascular , where leaves droop during the day and may recover at night, eventually leading to permanent yellowing, browning, and stem collapse as the bacterium clogs the plant's water-conducting tissues. This disease has caused severe epidemics in U.S. production, particularly in the Midwest and Northeast, with yield losses reaching up to 80% in susceptible cucurbit fields. Transmission often occurs via cucumber beetle vectors, amplifying outbreaks in warm, humid environments. E. rhapontici is associated with pink seed and crown rot, affecting like peas and such as and . Infected seeds develop a characteristic to pigmentation and become shriveled, leading to poor and seedling damping-off, while crown rot causes and lower stem decay with pinkish lesions. These symptoms reduce seedling vigor and establishment, impacting and crop yields across regions like and other grain-producing areas. Notably, E. aphidicola has been linked to aphid-transmitted wilts in beans (), causing over 50% crop loss in protected cultivation in southeastern in 2003. Epidemiologically, Erwinia outbreaks are frequently tied to favorable weather conditions, such as wet springs that promote bacterial dissemination and infection. Global spread has been facilitated by in infected plant material, enabling the pathogen to establish in new regions like and from its North American origins.

Virulence Mechanisms

Erwinia species employ sophisticated secretion systems to deliver factors into hosts. The (T3SS), encoded by hrp/hrc gene clusters, forms a needle-like apparatus that injects effector proteins directly into host cells to suppress immune responses. For instance, in Erwinia amylovora, the effector HrpN, a harpin protein, facilitates the translocation of other effectors like DspA/E while contributing to callose deposition in host tissues, thereby modulating defense signaling. In contrast, the type II secretion system secretes exoenzymes into the , enabling tissue maceration in soft-rot species such as Dickeya dadantii (formerly Erwinia chrysanthemi). Enzymatic degradation is central to Erwinia's necrotrophic strategy, with and dismantling cell walls to facilitate invasion. Pectate lyases, such as PelC in D. dadantii (formerly E. chrysanthemi), cleave polymers, promoting tissue softening and nutrient release; mutants lacking these enzymes exhibit reduced on host . complement this by hydrolyzing , further compromising structural integrity. Additionally, (HR) elicitors like HrpN trigger localized in non-host , potentially aiding in symptom development or immune evasion in compatible hosts. Toxins and secondary metabolites enhance Erwinia's pathogenicity by directly damaging host tissues and securing resources. In E. amylovora, the amylovorin induces and in susceptible species, correlating with symptom progression during infection. , such as desferrioxamine E, chelate iron in the iron-limited plant , supporting bacterial proliferation and virulence; disruption of siderophore biosynthesis impairs systemic infection. Gene regulation coordinates these factors in response to host cues. Quorum sensing via N-acyl homoserine lactones in species like Pectobacterium carotovorum (formerly Erwinia carotovora) activates virulence gene expression at high population densities, including exoenzyme production. The hrpL sigma factor specifically regulates T3SS expression in E. amylovora, integrating environmental signals like low pH and plant-derived compounds to induce pathogenicity under in planta conditions. Erwinia manipulates host physiology to evade immunity and promote . Effectors such as DspA/E in E. amylovora interact with kinases to suppress pattern-triggered immunity, allowing unchecked . Furthermore, production of (IAA), an mimic, disrupts hormonal balance, enhancing tissue susceptibility and bacterial multiplication in host vasculature.

Species

Validly Published Species

The genus Erwinia encompasses 21 validly published as of 2025, primarily plant-associated within the family Erwiniaceae. These are defined by their valid publication in the International Journal of Systematic and Evolutionary Microbiology or equivalent validation lists, with Erwinia amylovora designated as the . Erwinia amylovora (Burrill 1882) Winslow et al. 1920 is the and a well-known phytopathogen responsible for , primarily affecting members of the family such as apples and pears. First validly described in 1920, it exhibits a global distribution, with significant economic impacts in fruit production regions worldwide. Erwinia tracheiphila (Smith 1895) Bergey et al. 1923 causes in cucurbits, including cucumbers, melons, and squash, leading to vascular blockage and plant collapse. Isolated as early as 1901 but validly named in 1923, this species is predominantly reported in the United States, with limited occurrences elsewhere. Erwinia aphidicola Janda et al. 2003 is associated with and causes and in beans and other . Described in 2003 based on strains from insect vectors, it highlights the role of entomopathogenic transmission in Erwinia . Erwinia persicina Hao et al. (corrig. ex persicinus) produces a characteristic pigment and is implicated in soft rot diseases of various , including and ornamentals. Validly published in , it is distinguished by its pigmentation and enzymatic profile. Erwinia rhapontici (Millard 1924) Burkholder 1948 causes crown rot in and , often resulting in discoloration of seeds and vascular tissues. Validly named in 1948 from earlier isolations, it is a necrotrophic adapted to temperate crops. Among other valid species, Erwinia billingiae Samson et al. 2005 is notable for its association with plant surfaces and potential biocontrol properties against pathogens. Erwinia aeris Guo et al. 2025, a novel species isolated from the surface of an ore in , demonstrates associations outside plant hosts. In contrast, Erwinia herbicola (Löhnis 1911) Bergey et al. 1923 has been reclassified to the genus as Pantoea agglomerans, reflecting phylogenetic rearrangements. Several species originally classified within the genus Erwinia have undergone significant taxonomic reclassifications into distinct genera, primarily driven by advances in molecular phylogeny. Notably, Erwinia carotovora, a causative agent of soft rot in various plants, was reassigned to the genus Pectobacterium in 1999, reflecting its pectinolytic activity and genetic divergence from core Erwinia taxa. Similarly, Erwinia chrysanthemi was transferred to the genus Dickeya in 2005, establishing Dickeya as a separate entity for aggressive necrotrophic pathogens affecting a wide array of monocot and dicot hosts. Additionally, Erwinia herbicola, an epiphytic bacterium associated with plant surfaces, was reclassified as Pantoea agglomerans in 1989, highlighting its closer affiliation with non-pathogenic or opportunistic enterobacteria. These reclassifications were substantiated by molecular evidence, including DNA-DNA hybridization (DDH) values typically below 70% and average nucleotide identity (ANI) thresholds under 95-96%, which fall short of genus-level similarity criteria. Furthermore, differences in pathogenicity profiles contributed to the separations; for instance, Dickeya species demonstrate a broader host range and more aggressive tissue maceration than retained Erwinia pathogens, supported by distinct genomic signatures in clusters. The genus Erwinia maintains phylogenetic proximity to several related genera within the family Erwiniaceae, including Brenneria and Samsonia, forming a alongside Pectobacterium and Dickeya based on multi-locus analyses of genes. Brenneria encompasses species like Brenneria quercina (formerly Erwinia quercina), which causes diseases in trees, while Samsonia includes rare pathogens isolated from necrotic lesions. These genera share a conserved enterobacterial core , encompassing essential metabolic and replication functions, but diverge in effector proteins secreted via type III systems, enabling host-specific interactions and ecological adaptations.

Management and Control

Prevention Strategies

Cultural practices form the foundation of preventing Erwinia infections, particularly in susceptible crops like apples and pears affected by E. amylovora. Sanitation involves promptly removing and destroying infected plant parts, such as blighted shoots and cankers, with pruning cuts made at least 8-12 inches below visible symptoms during dry conditions to minimize bacterial spread through tools or wounds. Selecting resistant cultivars, such as the Geneva series apple rootstocks (e.g., Geneva 16 and Geneva 30), significantly reduces susceptibility to fire blight by limiting bacterial establishment in root and shoot tissues. Additionally, site selection plays a key role; planting in well-drained soils with good air circulation avoids excess moisture that favors bacterial proliferation, as poorly drained sites increase infection risk. Quarantine measures and vigilant monitoring are essential for containing Erwinia species across borders and within regions. In the , E. amylovora is classified as a protected zone pest, with strict import restrictions requiring phytosanitary certificates confirming the absence of the in host plants from third countries. Routine scouting in orchards, combined with sensitive detection tools like nested PCR assays, enables early identification of asymptomatic infections in plant material, allowing for timely isolation and preventing establishment. Biological controls offer environmentally friendly options to suppress Erwinia populations before infections occur. Antagonistic , such as Pseudomonas fluorescens strains, compete with E. amylovora for nutrients and produce inhibitory compounds like siderophores and antibiotics, reducing bacterial density on floral surfaces when applied preventively. As of 2025, new biocontrol options like Serenade Optimum have shown promise in suppressing in apples and pears. Bacteriophages specific to Erwinia species, including isolates effective against E. amylovora, lyse target upon application to blossoms, providing targeted suppression without broad impacts on beneficial . Vector management targets insects that mechanically disseminate Erwinia ooze, particularly during bloom. Insecticides applied against and populations, which can carry bacteria on their bodies, have been shown to lower incidence by interrupting transmission pathways. For honeybees, a primary vector, hive treatments involving dispensers loaded with antagonistic bacteria like coat foraging bees, enabling them to deliver biocontrol agents to flowers while reducing pickup and spread.

Treatment and Eradication Methods

Chemical controls for Erwinia infections primarily target bacterial populations on plant surfaces and within tissues, with copper-based bactericides such as being a longstanding option for managing caused by Erwinia amylovora. , a combination of and lime, provides protective action by releasing ions that disrupt bacterial cell membranes, and it is particularly effective when applied during or pre-bloom to limit initial infections. Antibiotics like have been widely used for control, applied during bloom to suppress bacterial entry into flowers, but resistance emerged in the due to repeated applications, with streptomycin-resistant strains now prevalent in regions like the . Oxytetracycline offers an alternative with lower resistance risk, achieving 60% control in trials when injected into trunks for systemic delivery against shoot blight. For post-infection management, kasugamycin demonstrates efficacy comparable to or better than in reducing E. amylovora populations after , targeting factors like exopolysaccharides without promoting widespread resistance. In soft rot diseases caused by species like (formerly Erwinia carotovora), compounds provide limited protective sprays, but no curative chemicals exist once infection is established. Physical methods focus on direct removal or inactivation of infected material to halt spread. , or the complete removal and destruction of infected or branches, is essential for containing outbreaks; for , pruning should extend 12-18 inches below visible symptoms in older wood, performed during dry summer or winter periods when are inactive. treatments, such as hot dips at 45-52°C for 20-30 minutes, effectively eradicate E. amylovora from materials like scion buds without severely damaging viability, offering a non-chemical option for clean production. Flaming or burning of debris and prunings destroys overwintering , reducing inoculum sources in orchards, though care must be taken to avoid fire hazards and comply with local regulations. For soft rot, immediate disposal of wilted via prevents secondary spread through wounds. Integrated pest management (IPM) for Erwinia combines these approaches with precise timing to minimize chemical use and resistance development. Applications of antibiotics or are timed to coincide with bloom stages when E. amylovora is most vulnerable, often guided by disease forecasting models like Maryblyt to predict risk based on and . Post- sprays with kasugamycin target early shoot , integrated with to remove cankers and limit bacterial ooze, achieving synergistic control in high-risk orchards. This holistic strategy emphasizes monitoring and sanitation to sustain long-term efficacy. Eradication efforts have helped maintain low prevalence in some regions through rigorous programs. For example, manages isolated outbreaks of (E. amylovora) through strict , of imports, and . However, challenges persist with antibiotic resistance; as of 2025, streptomycin-resistant E. amylovora has been confirmed in new U.S. states like , complicating control and necessitating rotation with alternatives like oxytetracycline. Regional campaigns combining and chemical interventions have eradicated isolated outbreaks elsewhere, but complete elimination remains difficult in endemic areas due to the bacterium's persistence in reservoirs.

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