Host Pathogen Research Articles

Excess mortality of infected ectotherms induced by warming depends on pathogen kingdom and evolutionary history

Climate change is causing extreme heating events and leading to more infectious disease outbreaks, putting species persistence at risk. The extent to which warming temperatures and infection may together impair host health is unclear. Using a meta-analysis of >190 effect sizes representing 101 ectothermic animal host–pathogen systems, we demonstrate that warming significantly increased the mortality of hosts infected by bacterial pathogens. Pathogens that have been evolutionarily established within the host species showed higher virulence under warmer temperatures, too. Conversely, the effect of warming on novel infections—from pathogens without a shared evolutionary history with the host species—were more pronounced with larger differences between compared temperatures. We found that compared to established infections, novel infections were more deadly at lower/baseline temperatures. Moreover, we revealed that the virulence of fungal pathogens increased only when temperatures were shifted upwards towards the pathogen thermal optimum. The magnitude of all these significant effects was not impacted by host life-stage, immune complexity, pathogen inoculation methods, or exposure time. Overall, our findings reveal distinct patterns in changes of pathogen virulence during warming. We highlight the importance of pathogen taxa, thermal optima, and evolutionary history in determining the impact of global change on infection outcomes.

ChIP-seq and structural analyses delineating the regulatory mechanism of master regulator EsrB in Edwardsiella piscicida.

As a crucial virulence regulator, EsrB possesses a LuxR-like superfamily domain at the C-terminal, which is conserved within the canonical NarL family regulators. Due to its critically important role in virulence and pathogenicity in fish hosts, the DNA binding ability has been believed to allow EsrB to regulate genes associated with the invasion process of host cells and basal metabolism in response to environmental stimuli. The lack of EsrB's crystal structure has been a major obstacle in understanding the molecular mechanisms of EsrB-DNA interaction which choreographs EsrB-mediated pathogenic behavior. Here, we conducted ChIP-seq and solved the crystal structure of the C-terminal of EsrB (EsrBC) at 2.20-Å resolution, which revealed that EsrB preferred to bind to virulence-associated promoters with a distinct 7'-4-7' pseudopalindromic DNA motif and interacted with metabolic-related promoters with a high AT DNA motif in Dulbecco's Modified Eagle's Medium (DMEM) (mimicking in vivo environments). Our results facilitate a detailed understanding of EsrB's regulatory role in Edwardsiella piscicida pathogenesis and expand our knowledge of virulence regulators in the family Hafniaceae.

Pattern Recognition Receptors in Periodontal Disease: Molecular Mechanisms, Signaling Pathways, and Therapeutic Implications

Periodontal disease remains a significant global health concern, characterized by complex host–pathogen interactions leading to tissue destruction. This review explored the role of pattern recognition receptors (PRRs) in the pathogenesis of periodontal disease, synthesizing current knowledge on their molecular mechanisms and potential as therapeutic targets. We examined the diverse family of PRRs, focusing on toll-like receptors (TLRs) and NOD-like receptors (NLRs), elucidating their activation by periodontal pathogens and subsequent downstream signaling cascades. This review highlights the intricate interplay between PRR-mediated pathways, including NF-κB and MAPK signaling, and their impact on inflammatory responses and bone metabolism in periodontal tissues. We discussed the emerging concept of PRR crosstalk and its implications for periodontal homeostasis and disease progression. Furthermore, this review addressed the potential of PRR-targeted therapies, exploring both challenges and opportunities in translating molecular insights into clinical applications. By providing an overview of PRRs in periodontal health and disease, this review aims to stimulate future research directions and inform the development of novel diagnostic and therapeutic strategies in periodontology.

Assessment of Babesia ovis pathogenicity in goats: implications for transmission dynamics and host resistant

Babesia ovis, commonly associated with ovine babesiosis, poses a significant threat to sheep health, often resulting in severe clinical manifestations and high mortality rates. However, the impact of B. ovis on goats has remained uncertain, prompting us to investigate its pathogenicity in caprine hosts. Experimental infections using B. ovis-infected blood inoculation and infected tick infestation, were conducted on spleen-intact (n=5) and splenectomized (n=5) goats. The experimental infection was performed using fresh blood obtained from a B. ovis-infected splenectomized sheep. One spleen-intact sheep served as a control for the experimental infection with B. ovis-infected Rhipicephalus bursa ticks. While all experimentally infected sheep (#501, #575) displayed severe clinical symptoms and high parasitemia, goats exhibited resistance, showing no significant clinical manifestations or sustained parasitemia. Notably, B. ovis was detected in two spleen-intact goats via nested PCR, prompting further investigation into their role as reservoirs for tick-borne transmission. These goats were then infested with Babesia spp.-free R. bursa larvae (0.1 gr) and adults (50 females and 50 males) for transstadial and transovarial transmission experiments respectively. Results indicated that chronically B. ovis-infected spleen-intact goats are not significant sources for maintaining the tick-borne transmission cycle of the parasite. These findings highlight the differential susceptibility of goats to B. ovis infection compared to sheep and their limited role as reservoirs for parasite transmission. Understanding the role of goats in B. ovis transmission and their resistance mechanisms can inform effective control measures and reduce economic losses in affected regions. Further research into caprine babesiosis and host immunological responses is essential to fully elucidate their possible role as reservoirs of the parasite, and underlying mechanisms of host susceptibility and parasite pathogenesis.

Bacterial-host adhesion dominated by collagen subtypes remodelled by osmotic pressure.

Environmental osmolarity plays a crucial role in regulating the functions and behaviors of both host cells and pathogens. However, it remains unclear whether and how environmental osmotic stimuli modulate bacterial‒host interfacial adhesion. Using single-cell force spectroscopy, we revealed that the interfacial adhesion force depended nonlinearly on the osmotic prestimulation of host cells but not bacteria. Quantitatively, the adhesion force increased dramatically from 25.98 nN under isotonic conditions to 112.45 or 93.10 nN after the host cells were treated with the hypotonic or hypertonic solution. There was a strong correlation between the adhesion force and the number of host cells harboring adherent/internalized bacteria. We further revealed that enhanced overexpression levels of collagen XV and II were responsible for the increases in interfacial adhesion under hypotonic and hypertonic conditions, respectively. This work provides new opportunities for developing host-directed antibacterial strategies related to interfacial adhesion from a mechanobiological perspective.

RXLR effector genes mediate regional adaptation of Phytophthora infestans

AbstractLocal adaptation has been a central theme of eco-evolutionary research for decades. It is generally assumed that plant pathogens are locally adapted due to their standing interactions with biotic and abiotic factors in the ecosystem. Effectors, secreted small proteins encoded by pathogens, play critical roles in host–pathogen interactions, by activating host genotype-specific resistance, suppressing plant immunity, and playing other functions. In this study, we investigated the potential involvement of RXLR effector genes in ecological adaptation by examining the simple sequence repeat (SSR), virulence, and effector profiles in Phytophthora infestans isolates collected from two geographic regions differing in ecological environments. Genotypic analyses with SSR markers and virulence assays showed that the pathogen from the two regions shared genetic background but differed in virulence spectrums. High-throughput sequencing and expression analysis of 24 selected P. infestans isolates further showed variations in the RXLR effector repertoire, ranging from 536 to 548 for each isolate and the expression of effector genes was highly associated with the accumulation of homologous sRNA. Regional specific alleles were detected at 94 RXLR effector genes, and a specific accumulation of homologous 25–26 nt sRNAs was found at 67 RXLR effector genes. Two of the regional specific RXLR effector genes were confirmed to be virulence factors. Taken together, these results suggest that genomic and epigenetic variations in RXLR effector genes contribute significantly to the ecological adaptation of P. infestans populations and that regional specific effector genes will help to understand the adaptive landscape of pathogens and efficient use of host resistance genes.

Applications of Nanotechnology in Combating Fungal Diseases in Humans: An Updated Review

In recent years, fungal infections caused by filamentous fungi have posed a serious threat to public health worldwide. Fungi such as Aspergillus, Coccidioides, and Mucorales (the most common filamentous fungi), as well as Candida auris (a non-filamentous fungus), can cause infections in humans. It can cause serious life-threatening diseases in individuals with weakened immune systems, patients infected with HIV/AIDS, uncontrolled diabetes, blood disorders, organ transplants, and chemotherapy. In this review, we describe the available nan formulations (metallic and polymeric nanoparticles) that have been developed to enhance efficacy and reduce the number of adverse effects following the administration of conventional antifungals. The burden posed by fungal infections on human health is increasing worldwide. Fungi such as Aspergillus, Candida, and Cryptococcus are among the most common pathogens responsible for human diseases, accounting for over 90% of infection-related deaths. Moreover, effective antifungal treatments are not available, primarily due to host toxicity, pathogen resistance, and immunodeficiency. In recent years, nanomaterials have proven to be not only more efficient antifungal therapeutic agents but also capable of overcoming fungal drug resistance".

Recent progress in the understanding of Citrus Huanglongbing: from the perspective of pathogen and citrus host.

Citrus Huanglongbing (HLB) is a devastating disease spread by citrus psyllid, causing severe losses to the global citrus industry. The transmission of HLB is mainly influenced by both the pathogen and the citrus psyllid. The unculturable nature of the HLB bacteria (Candidatus Liberibacter asiaticus, CLas) and the susceptibility of all commercial citrus varieties made it extremely difficult to study the mechanisms of resistance and susceptibility. In recent years, new progress has been made in understanding the virulence factors of CLas as well as the defense strategies of citrus host against the attack of CLas. This paper reviews the recent advances in the pathogenic mechanisms of CLas, the screening of agents targeting the CLas, including antimicrobial peptides, metabolites and chemicals, the citrus host defense response to CLas, and strategies to enhance citrus defense. Future challenges that need to be addressed are also discussed.

Characterization of a Highly Virulent Klebsiella michiganensis Strain Isolated from a Preterm Infant with Sepsis.

Klebsiella michiganensis is an opportunistic pathogen that causes an increasing number of serious infections. This study aimed to investigate the etiology of the severe clinical symptoms of sepsis in preterm infants and the characterization of K. michiganensis isolates. Whole-genome sequencing (WGS) was performed on three strains isolated from an infected preterm infant. Additionally, the genomic sequences of 534 K. michiganensis strains were obtained from the NCBI database. To gain deeper insights into these strains, we utilized the Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), Clusters of Orthologous Groups (COG), and Pathogen Host Interactions (PHI) database annotation tools for comprehensive gene function analyses. Moreover, the multilocus sequence typing (MLST), EasyCGtree, and virulence factor database (VFDB) were employed to determine the sequence types (STs), construct phylogenetic trees, and identify potential virulence factors. Sequence analysis found that the three isolated strains had identical sequence characteristics and did not correspond to any of the known ST types. Virulence factor analysis revealed that the three strains harbored mrkABCDFHIJ, fimABCDEFGHIK, entABCDEFS, fepABCD, and capsule genes. These virulence factors are likely to play crucial roles in enhancing adhesion and metabolic capabilities, resisting phagocytosis (inducing immune cell damage), and ultimately contributing to prolonged bacteremia. The phylogenetic tree and comparative genomics of virulence factors showed the genetic and virulence factor diversity of the currently reported K. michiganensis strains. We identified a novel strain of K. michiganensis that exhibits high virulence and leads to severe septicemia phenotypes in preterm infants. Furthermore, comparative genomic analysis of previously reported K. michiganensis strains revealed the existence of three clades. This comprehensive analysis provides novel insights into the genetic relationships and virulence factor profiles of diverse strains of K. michiganensis. In future, it will be necessary to investigate the concept of the high virulence of K. michiganensis to determine the treatment method.

Candida albicans infection model in Drosophila melanogaster suggests a strain-specific virulent factor boosting a stormy innate immune response.

Pathogens drive the evolution of host defence strategies, with both innate and adaptive immune systems playing key roles. Priming enhances the innate immune system's readiness by functionally reprogramming immune cells after initial exposure to stimuli, like β-glucans. In this sense, Drosophila melanogaster is a valuable model to evaluate the role of innate immunity to control infections. In this study we aimed to set light on the immune priming effect of oral treatment with heat-killed M. manresensis and two different heat-killed C. albicans isolates upon systemic infection by C. albicans in the D. melanogaster model. A clinical and a control ATCC 90028 Candida albicans strain were used. Flies were primed through oral administration of heat-killed C. albicans (hkCa), both clinical and control, and hk-Mycolicibacterium manresensis. After priming, flies were systemically infected with both C. albicans isolates. Host survival, pathogen load, and immune response in response to treatment and infection were evaluated. Both treatments showed a significant capacity to enhance the expression of antimicrobial peptides, in particular Diptericin, and Drosomycin in males. This response had a marked sexual dimorphism due to the difference in Upd3, Nox, and Duox expression. Surprisingly, even when priming was able to avoid the growth of both C. albicans strains, survival was not improved in the case of the clinical isolate, causing an unexpected mortality rate in hours, regardless of the host's sex. Gene expression analysis 24 hours post-infection showed an exacerbated increase in Diptericin, Drosomycin and Upd3 expression upon infection with the clinical strain. Data herein suggests the presence of a strain-specific component in C. albicans as the booster of a "stormy" innate immune response, which must be further investigated, and position D. melanogaster as a useful model for evaluating virulent factors related to the modulation of the innate immunity.

Zinc metalloprotease FgM35, which targets the wheat zinc-binding protein TaZnBP, contributes to the virulence of Fusarium graminearum

Metalloproteinases are ubiquitous in organisms. Most metalloproteinases secreted by pathogenic microorganisms are also called virulence factors, because they degrade proteins in the external tissues of the host, thereby reducing the host’s immunity and increasing its susceptibility to disease. Zinc metalloproteinase is one of the most common metalloproteinases. In our report, we studied the biological function of zinc metalloprotease FgM35 in Fusarium graminearum and the pathogen–host interaction during infection. We found that the asexual and sexual reproduction of the deletion mutant ΔFgM35 were affected, as well as the tolerance of F. graminearum to metal stress. In addition, deletion of FgM35 reduced the virulence of F. graminearum. The wheat target TaZnBP was screened using a wheat yeast cDNA library, and the interaction between FgM35 and TaZnBP was verified by HADDOCK molecular docking, yeast two-hybrid, Bi-FC, Luc, and Co-IP assays. The contribution of TaZnBP to plant immunity was also demonstrated. In summary, our work revealed the indispensable role of FgM35 in the reproductive process and the pathogenicity of F. graminearum, and it identified the interaction between FgM35 and TaZnBP as well as the function of TaZnBP. This provides a theoretical basis for further study of the function of metalloproteinases in pathogen–host interactions.

Plant cell wall structure and dynamics in plant-pathogen interactions and pathogen defence.

Plant cell walls delimit plant cells from their environment and provide mechanical stability to withstand internal turgor pressure as well as external influences. Environmental factors can be beneficial or harmful for the plants and vary substantially depending on prevailing combinations of climate conditions and stress exposure. Consequently, the physicochemical properties of plant cell walls need to be adaptive, and their functional integrity needs to be monitored by the plant. One major threat to plants is posed by phytopathogens, which employ a diversity of infection strategies and lifestyles to colonise host tissues. During these interactions, the plant cell wall represents a barrier that impedes the colonisation of host tissues and pathogen spread. In a tussle over maintenance and breakdown, plant cell walls can be rapidly and efficiently remodelled by enzymatic activities of plant and pathogen origin, heavily influencing the outcome of plant-pathogen interactions. We review the role of locally and systemically induced cell wall remodelling and the importance of tissue-dependent cell wall properties for the interaction with pathogens. Furthermore, we discuss the importance of cell wall-dependent signalling for defence response induction and the influence of abiotic factors on cell wall integrity and cell wall-associated pathogen resistance mechanisms.

Cold snaps lead to a 5-fold increase or a 3-fold decrease in disease proliferation depending on the baseline temperature

BackgroundClimate change is driving increased extreme weather events that can impact ecology by moderating host–pathogen interactions. To date, few studies have explored how cold snaps affect disease prevalence and proliferation. Using the Daphnia magna–Ordospora colligata host-parasite system, a popular model system for environmentally transmitted diseases, the amplitude and duration of cold snaps were manipulated at four baseline temperatures, 10 days post-exposure, with O. colligata fitness recorded at the individual level.ResultsCold snaps induced a fivefold increase or a threefold decrease in parasite burden relative to baseline temperature, with complex nuances and varied outcomes resulting from different treatment combinations. Both amplitude and duration can interact with the baseline temperature highlighting the complexity and baseline dependence of cold snaps. Furthermore, parasite fitness, i.e., infection prevalence and burden, were simultaneously altered in opposite directions in the same cold snap treatment.ConclusionsWe found that cold snaps can yield complicated outcomes that are unique from other types of temperature variation (for example, heatwaves). These results underpin the challenges and complexity in understanding and predicting how climate and extreme weather may alter disease under global change.

Strategic genetic insights and integrated approaches for successful management of blackleg in canola/rapeseed farming

AbstractThis review describes a triumphant narrative in the battle against the devastating plant pathogen complex, Leptosphaeria maculans and L. biglobosa, and the success of the world's second‐largest oilseed crop, canola/oilseed rape. Emphasizing global collaborations, the article explores successfully mitigating this destructive disease in canola/rapeseed production across Australia, Canada and Europe. It highlights how strategies may vary between continents to adapt to specific contexts. While initial resistance (R) genes proved effective, the evolution of the pathogen under crop‐induced disease pressure led to the breakdown of these genes. Now, growers in these regions have been equipped with new tools, allowing them to make informed decisions that help to keep the disease at generally low levels. A pivotal factor in this success has been a deepened understanding of the intricate science underlying the host–pathogen interaction. Concerted efforts of individual laboratories and collaborative initiatives have played an essential role in this success, including novel methods for disease control based on extensive research that has translated into developing highly resistant varieties, enhanced pathogen monitoring, improved cultivar recommendation and integrated management strategies. The review showcases many milestone advancements, including the cloning of numerous avirulence genes within the pathogen, characterization of specific R genes, the development of various molecular tools for monitoring both pathogen and host, the introduction of groundbreaking disease management strategies such as R gene labelling, rotation and stacking, and establishment of a universal pathogen isolate collection that facilitates the exchange of information among multiple laboratories and adds a new dimension to this triumph.

Characterization of NFDQ1 in Cryptosporidium parvum

BackgroundCryptosporidium spp. are important zoonotic parasites that can cause moderate to severe diarrhea in humans and animals. Among the three Cryptosporidium species infecting the intestines of calves, Cryptosporidium parvum has a broad host range and causes severe diarrhea in calves, while Cryptosporidium bovis and Cryptosporidium ryanae mainly infect calves without obvious clinical symptoms. Comparative genomic analysis revealed differences in the copy number of genes encoding the nonfinancial disclosure quality (NFDQ) secretory protein family among the three species, suggesting that this protein family may be associated with the host range or pathogenicity of Cryptosporidium spp. To understand the function of cgd8_10 encoded NFDQ1, tagged and knockout strains were constructed and characterized in this study.MethodsTo determine the localization of NFDQ1, we used clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9) technology to tag the C-terminus of NFDQ1 with three hemagglutinin epitopes (3 × HA). The tagged strain was constructed, and the genomic insertion was confirmed by polymerase chain reaction (PCR). Immunofluorescence assays were performed to observe the localization of NFDQ1 both in extracellular sporozoites and at various intracellular developmental stages. Immunoelectron microscopy was used to study the ultrastructural localization of NFDQ1. Then, the ΔNFDQ1 strain was generated by CRISPR/Cas9 and the in vitro growth assay on HCT-8 cells was used to analyze of phenotypic changes after knockout NFDQ1 in parasites.ResultsThe NFDQ1 tagging and knockout stains were successfully constructed by CRISPR/Cas9 technology and the insertions of transgenic strains were validated by PCR. The expression of NFDQ1 was validated in parasite by western blot. Immunofluorescence and immune-electron microscopy assay showed that NFDQ1 expressed in both asexual and sexual stages of C. parvum, where it was localized to the cytoplasm of the parasite. Upon ablation of NFDQ1, the ΔNFDQ1 strain showed an apparent growth retardation during sexual replication in vitro.ConclusionsNFDQ1 is a cytoplasmic protein without specific localization to secretory organelles, and it may participate in C. parvum growth during sexual reproduction. Future study should determine the role of NFDQ1 following C. parvum infection in vivo.Graphical

Novel Fosfomycin Resistance Mechanism in Pseudomonas entomophila Due to Atypical Pho Regulon Control of GlpT

Background/Objectives: Pseudomonas entomophila is a ubiquitous bacterium capable of killing insects of different orders and has become a model for host–pathogen studies and a promising tool for biological pest control. In the human pathogen Pseudomonas aeruginosa, spontaneous resistance to fosfomycin arises almost exclusively from mutations in the glycerol-3-phosphate transporter (GlpT), the drug’s sole entry route in this species. Here, we investigated whether this specificity is conserved in P. entomophila, as it could provide a valuable marker system for studying mutation rates and spectra and for selection in genetic engineering. Methods: We isolated 16 independent spontaneous fosfomycin-resistant mutants in P. entomophila, and studied the genetic basis of the resistance using a combination of sequencing, phenotyping and computational approaches. Results: We only found two mutants without alterations in glpT or any of its known regulatory elements. Whole-genome sequencing revealed unique inactivating mutations in phoU, a key regulator of the phosphate starvation (Pho) regulon. Computational analyses identified a PhoB binding site in the glpT promoter, and experiments showed that phoU inactivation reduced glpT expression nearly 20-fold. While placing a sugar-phosphate transporter under the Pho regulon may seem advantageous, bioinformatic analysis shows this configuration is atypical among pseudomonads. Conclusions: this atypical Pho regulon control of GlpT probably reflects the peculiarities of P. entomophila’s habitat and lifestyle; highlighting how readily regulatory evolution can lead to the rapid divergence of resistance mechanisms, even among closely related species.

Scots Pines With Tolerance to Melampsora pinitorqua and Diplodia sapinea Show Distinct Metabolic Profiles.

Diplodia sapinea causes Diplodia tip blight (DTB) and is recognised as an opportunistic necrotrophic pathogen affecting conifers. While DTB is associated with abiotic stress, the impact of biotic stress in the host on D. sapinea's lifestyle shift is unknown. Observed co-occurrences of D. sapinea and Melampsora pinitorqua, causing pine twisting rust on Scots pine (Pinus sylvestris), instigated an investigation into their interaction with and influence on the defence mechanisms of the host. We hypothesised that M. pinitorqua infections predispose the trees to D. sapinea by stressing the host and altering the shoot metabolites. Pines in a plantation were sampled over time to study pathogen biomass and host metabolites. Symptoms of both pathogens were consistent over years, and the preceding season's symptoms affected the metabolic profiles pre-infection and M. pinitorqua's proliferation. Symptoms of M. pinitorqua altered shoot metabolites more than fungal biomass, with co-symptomatic trees exhibiting elevated M. pinitorqua biomass. Specific phenolic compounds had a strong positive association with the shoot symptom × D. sapinea interaction. D. sapinea's biomass presymptoms was independent of previous disease symptoms and infection by M. pinitorqua. Some trees showed disease tolerance, with delayed rust infections and minimal DTB symptoms. Further investigations on this trait are needed.

Genomic characterization of Pantoea dispersa A003 isolated from a clinical patient

IntroductionPantoea dispersa is a Gram-negative bacterium generally considered as a plant pathogen and rarely causes human infections. To date, there have been 13 studies that have documented clinical infections linked to P. dispersa, with a primary emphasis on the initial identification of this pathogen. The genomic features and the mechanisms underlying the pathogenesis of P. dispersa remain largely uninvestigated. In the present study, we describe a clinical infection caused by P. dispersa and provide the first genomic analysis of this bacterium.MethodsThe bacterial strain designated A003 was isolated from blood samples. Preliminary identification of strain A003 was conducted using matrix-assisted laser desorption ionization time-of-flight (MALDI-TOF) technology (VITEK® MS, bioMérieux, France). Biochemical and antimicrobial susceptibility assessments were carried out utilizing the VITEK-2 compact automated microbial analysis system (bioMérieux, France). Additionally, whole genome sequencing and subsequent analysis were performed to further elucidate the potential pathogenicity.ResultsThe bacterial isolate was cultured overnight at 35°C in a CO2-enriched environment on Columbia blood agar, resulting in the appearance of a white, smooth, Gram-negative rod-shaped bacterium with diameters ranging from 1 to 2 mm. Identification of strain A003 was achieved with a high confidence level of 99.9% as P. dispersa using MALDI-TOF mass spectrometry. The average nucleotide identity (ANI) value between strain A003 and the reference strain P. dispersa DSM 30073T was 98.08%, while the DNA–DNA hybridization (DDH) value was 84.10% (Formula 2) based on genome sequencing data, which further confirmed that A003 belonged to the P. dispersa species. Comprehensive analysis revealed the presence of 372 virulence factors, 15 antibiotic resistance genes, 222 carbohydrate-active enzymes, and 666 genes related to Type III secretion system (T3SS) effector proteins, as identified through the core databases of VFDB (Virulence Factors of Pathogenic Bacteria), CARD (Comprehensive Antibiotic Resistance Database), CAZY (Carbohydrate-Active enZYmes Database), and T3SS. The virulence factors included type IV pili (TFP), type VI secretion system, flagella, iron uptake system, and ompA, which are implicated in bacterial pathogenicity. The antibiotic resistance profile indicated resistance to fluoroquinolones, cephalosporins, penams, macrolides, and aminoglycosides, as annotated by the CARD database.ConclusionThe draft genome sequenced represents the inaugural genomic sequence of P. dispersa derived from clinical sources. This advancement may enhance clinical practitioners’ comprehension of the organism’s clinical attributes and serve as a foundational resource for future research into its virulence, antibiotic resistance, and host–pathogen interactions.

Genome resource announcement for emerging pathogen Bipolaris gigantea, isolated from Microstegium vimineum

Bipolaris gigantea is a pathogen of the invasive grass Microstegium vimineum and an emerging pathogen of other hosts such as hemp and barley, causing characteristic eyespot foliar lesions. The fungus is characterized by long pale hyaline conidia measuring about 300 to 350 μm. Previously, this pathogen was classified in the Drechslera genus, and recently reassigned as Bipolaris based on molecular identification. Here, we generated a high-quality draft genome sequence of B. gigantea isolate BGF using long and short read DNA sequencing. The assembled genome, 30.23 Mb in size with a BUSCO completeness score of 98.4%, exhibited synteny with the common grass pathogen B. sorokiniana isolate 10943. Average nucleotide identity (ANI) and single nucleotide polymorphisms (SNP) analyses revealed high sequence identity with B. gigantea isolates from Cannabis sativa fields in Kentucky. This research provides a genomic resource that will contribute to future studies to understand the host range evolution and pathogenicity of this novel pathogen.

Unravelling the Current Status of Rice Stripe Mosaic Virus: Its Geographical Spread, Biology, Epidemiology, and Management

Rice stripe mosaic virus (RSMV) belongs to the Cytorhabdovirus species in the Rhabdoviridae family. Recently, RSMV was widely spread in East Asia and caused severe yield losses. RSMV is transmitted by the planthopper vectors, Recilia dorsalis, Nephotettix virescens, and Nilaparvata lugens, that mostly affect rice. The adult vectors can hibernate, transmit the virus, lay eggs on rice plants, and, finally, multiply in subsequent generations, resulting in new infection outbreaks. RSMV-infected rice varieties display striped mosaicism, mild dwarfism, stiff and twisted leaves, delayed heading, short panicles with large unfilled grains, and yield reduction. In nature, the infection of multiple pathogens in the same host is widespread, which is defined as co-infection. It can be antagonistic or synergistic. Pathological synergistic effects between RSMV and other viruses can generate strains with new genetic characteristics, leading to unpredictable epidemiological consequences. After the first identification of RSMV in 2015, significant advancements in understanding the disease’s characteristics, symptoms, cycles, geographic distribution, potential vectors, and synergistic interaction, as well as its management strategies, were developed. To reduce the damage due to RSMV infection, many scientists have recommended pest control techniques to target adult vectors. It is also essential to confirm the actual time of monitoring, development of resistant varieties, and changes in cultivation systems. Due to the limitations of the conventional plant disease control technologies, improvements in efficiency and safety are in high demand. Therefore, to find efficient and environmentally safe controls to mitigate these challenges, reviews of research are the foremost step. In this review, we summarize the basic epidemiological information about the origin of RSMV and its infection symptoms in the field, synergistic interaction with viruses during co-transmission, yield losses, formulation of the disease cycle, and control strategies from several case studies. Finally, we recommend the formulation of the disease cycle and management strategies of RSMV infection.