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Results for “Plant Pathology”

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8 recordsLinked to original sources
USGS2003

Fungal biology and agriculture: revisiting the field

Plant pathology has made significant progress over the years, a process that involved overcoming a variety of conceptual and technological hurdles. Descriptive mycology and the advent of chemical plant-disease management have been followed by biochemical and physiological studies of fungi and their hosts. The later establishment of biochemical genetics along with the introduction of DNA-mediated transformation have set the stage for dissection of gene function and advances in our understanding of fungal cell biology and plant-fungus interactions. Currently, with the advent of high-throughput technologies, we have the capacity to acquire vast data sets that have direct relevance to the numerous subdisciplines within fungal biology and pathology. These data provide unique opportunities for basic research and for engineering solutions to important agricultural problems. However, we also are faced with the challenge of data organization and mining to analyze the relationships between fungal and plant genomes and to elucidate the physiological function of pertinent DNA sequences. We present our perspective of fungal biology and agriculture, including administrative and political challenges to plant protection research.

Molecular Plant-Microbe Interactions↗
USGS2022

Ceratocystis lukuohia-infested ambrosia beetle frass as inoculum for Ceratocystis wilt of ʻōhiʻa (Metrosideros polymorpha)

Metrosideros polymorpha (‘ōhi‘a) trees in Hawaiʻi are dying from two distinct diseases, collectively referred to as rapid ‘ōhi‘a death (ROD), caused by Ceratocystis lukuohia and Ceratocystis huliohia . Boring dust (frass) released when ambrosia beetles attack and colonize infected trees has been suspected as a transmission source. We sampled ambrosia beetle frass from six locations on Hawaiʻi Island and screened samples for Ceratocystis DNA and fungal viability. Ceratocystis DNA was detected in 79% of frass samples and 61% were viable. To assess the infectivity of C . lukuohia -colonized frass, M . polymorpha seedlings were wound-inoculated with frass in growth chamber trials. Wilt incidence was 40% in the first trial and 15% in the second. Frass particles naturally infested with C . lukuohia were treated with a cytoplasmic stain and microscopically examined; thick-walled chlamydospores were found in all samples. The chlamydospores appeared to be derived from aleurioconidia. Ceratocystis survival in frass was assessed in a baiting experiment conducted under varying environmental regimes; viability decreased with increasing temperature, frass age and decreasing humidity. After 6 months, 90% of the samples exhibited viable C . lukuohia at the lowest temperatures. Results confirmed that C . lukuohia chlamydospores are the fungal inoculum within ambrosia beetle frass and can induce wilt when introduced to M . polymorpha wounds. Although ambrosia beetles or other insects may serve as vectors, the present work supports the hypothesis that Ceratocystis species may be dispersed in frass, which can inform ongoing efforts to manage ROD across Hawaiʻi's native forests.

Hawaii↗
USGS2021

Viral-like particles are associated with endosymbiont pathology in Florida corals affected by stony coral tissue loss disease

Stony coral tissue loss disease (SCTLD) was first documented in 2014 near the Port of Miami, Florida, and has since spread north and south along Florida’s Coral Reef, killing large numbers of more than 20 species of coral and leading to the functional extinction of at least one species, Dendrogyra cylindrus . SCTLD is assumed to be caused by bacteria based on presence of different molecular assemblages of bacteria in lesioned compared to apparently healthy tissues, its apparent spread among colonies, and cessation of spread of lesions in individual colonies treated with antibiotics. However, light microscopic examination of tissues of corals affected with SCTLD has not shown bacteria associated with tissue death. Rather, microscopy shows dead and dying coral cells and symbiotic dinoflagellates (endosymbionts) indicating a breakdown of host cell and endosymbiont symbiosis. It is unclear whether host cells die first leading to death of endosymbionts or vice versa. Based on microscopy, hypotheses as to possible causes of SCTLD include infectious agents not visible at the light microscopy level or toxicosis, perhaps originating from endosymbionts. To clarify this, we examined corals affected with SCTLD and apparently healthy corals using transmission electron microscopy. Endosymbionts in SCTLD-affected and apparently healthy corals consistently had varying degrees of pathology associated with elongated particles compatible in morphology with filamentous positive single-stranded RNA viruses of plants termed anisometric viral-like particles (AVLP). There was apparent progression from early to late replication of AVLP in the cytoplasm of endosymbionts adjacent to or at times within chloroplasts, with morphologic changes in chloroplasts consistent with those seen in plant cells infected by viruses. Coral host cell pathology appeared limited to massive proliferation and lysis of mucus cells. Based on these findings, we hypothesize that SCTLD is a viral disease of endosymbionts leading to coral host death. Efforts to confirm the presence of a virus associated with SCTLD through other means would be appropriate. These include showing the presence of a virus through molecular assays such as deep sequencing, attempts to grow this virus in the laboratory through culture of endosymbionts, localization of virus in tissue sections using immunohistochemistry or in situ hybridization, and experimental infection of known-virus-negative corals to replicate disease at the gross and microscopic level.

Florida↗
USGS2014

Lectins stain cells differentially in the coral, Montipora capitata

A limitation in our understanding of coral disease pathology and cellular pathogenesis is a lack of reagents to characterize coral cells. We evaluated the utility of plant lectins to stain tissues of a dominant coral, Montipora capitata , from Hawaii. Of 22 lectins evaluated, nine of these stained structures in the upper or basal body wall of corals. Specific structures revealed by lectins that were not considered distinct or evident on routine hematoxylin and eosin sections of coral tissues included apical and basal granules in gastrodermis and epidermis, cnidoglandular tract and actinopharynx cell surface membranes, capsules of mature holotrichous isorhizas, and perivitelline and periseminal cells. Plant lectins could prove useful to further our understanding of coral physiology, anatomy, cell biology, and disease pathogenesis.

Hawai'i↗
USGS2018

Exploring the pathology of an epidermal disease affecting a circum-Antarctic sea star

Over the past decade, unusual mortality outbreaks have decimated echinoderm populations over broad geographic regions, raising awareness globally of the importance of investigating such events. Echinoderms are key components of marine benthos for top-down and bottom-up regulations of plants and animals; population declines of these individuals can have significant ecosystem-wide effects. Here we describe the first case study of an outbreak affecting Antarctic echinoderms and consisting of an ulcerative epidermal disease affecting ~10% of the population of the keystone asteroid predator Odontaster validus at Deception Island, Antarctica. This event was first detected in the Austral summer 2012–2013, coinciding with unprecedented high seawater temperatures and increased seismicity. Histological analyses revealed epidermal ulceration, inflammation, and necrosis in diseased animals. Bacterial and fungal alpha diversity was consistently lower and of different composition in lesioned versus unaffected tissues (32.87% and 16.94% shared bacterial and fungal operational taxonomic units OTUs respectively). The microbiome of healthy stars was more consistent across individuals than in diseased specimens suggesting microbial dysbiosis, especially in the lesion fronts. Because these microbes were not associated with tissue damage at the microscopic level, their contribution to the development of epidermal lesions remains unclear. Our study reveals that disease events are reaching echinoderms as far as the polar regions thereby highlighting the need to develop a greater understanding of the microbiology and physiology of marine diseases and ecosystems health, especially in the era of global warming.

Scientific Reports↗
USGS1986

Acute oral toxicity of sodium cyanide in birds

Sensitivities of six avian species, black vulture ( Coragyps atratus ), American kestrel ( Falco sparverius ), Japanese quail ( Coturnix japonica ), domestic chicken ( Gallus domesticus ), eastern screech-owl ( Otus asio ), and European starling ( Sturnus vulgaris ), to acute poisoning by sodium cyanide (NaCN) were compared by single dose LD50's. Three species, domestic chickens, black vultures, and turkey vultures ( Cathartes aura ), were dosed with NaCN to determine cyanide residues in those that died and also in survivors, in addition to postmortem fate. Three flesh-eating species (black vulture, American kestrel, and eastern screech-owl; LD50's 4.0–8.6 mg/kg) were more sensitive to NaCN than three species (Japanese quail, domestic chicken, and European starling; LD50's 9.4–21 mg/kg) that fed predominantly on plant material. Elevated concentrations of cyanide were found in the blood of birds that died of cyanide poisoning; however, concentrations in birds that died overlapped those in survivors. Blood was superior to liver as the tissue of choice for detecting cyanide exposure. No gross pathological changes related to dosing were observed at necropsy.

Journal of Wildlife Diseases↗
USGS1998

Epizootic vacuolar myelinopathy of the central nervous system of bald eagles ( Haliaeetus leucocephalus ) and American coots ( Fulica americana )

Unprecedented mortality occurred in bald eagles ( Haliaeetus leucocephalus ) at DeGray Lake, Arkansas, during the winters of 1994-1995 and 1996-1997. The first eagles were found dead during November, soon after arrival from fall migration, and deaths continued into January during both episodes. In total, 29 eagles died at or near DeGray Lake in the winter of 1994-1995 and 26 died in the winter of 1996-1997; no eagle mortality was noted during the same months of the intervening winter or in the earlier history of the lake. During the mortality events, sick eagles were observed overflying perches or colliding with rock walls. Signs of incoordination and limb paresis were also observed in American coots ( Fulica americana ) during the episodes of eagle mortality, but mortality in coots was minimal. No consistent abnormalities were seen on gross necropsy of either species. No microscopic findings in organs other than the central nervous system (CNS) could explain the cause of death. By light microscopy, all 26 eagles examined and 62/77 (81%) coots had striking, diffuse, spongy degeneration of the white matter of the CNS. Vacuolation occurred in all myelinated CNS tissue, including the cerebellar folia and medulla oblongata, but was most prominent in the optic tectum. In the spinal cord, vacuoles were concentrated near the gray matter, and occasional swollen axons were seen. Vacuoles were uniformly present in optic nerves but were not evident in the retina or peripheral or autonomic nerves. Cellular inflammatory response to the lesion was distinctly lacking. Vacuoles were 8-50 microns in diameter and occurred individually, in clusters, or in rows. In sections stained by luxol fast blue/periodic acid-Schiff stain, the vacuoles were delimited and transected by myelin strands. Transmission electron microscopy revealed intramyelinic vacuoles formed in the myelin sheaths by splitting of one or more myelin lamellae at the intraperiodic line. This lesion is characteristic of toxicity from hexachlorophene, triethyltin, bromethalin, isonicotinic acid hydrazide, and certain exotic plant toxins; however, despite exhaustive testing, no etiology was determined for the DeGray Lake mortality events. This is the first report of vacuolar myelinopathy associated with spontaneous mortality in wild birds.

Arkansas↗
USGS2026

Diverse novel and avian-associated viruses in the ileal viromes of northern mockingbird (Mimus polyglottos)

Viruses are the most abundant and diverse organisms on Earth, though only a small portion cause disease. Understanding viral diversity is key to understanding and predicting pathogen emergence and zoonotic spillover. Here, we use meta-transcriptomic sequencing to examine the viral communities in the ileum of 25 Northern Mockingbirds ( Mimus polyglottos ) from various locations across Texas. We assembled high-quality genomes of 43 viral species (40 species identified to 13 families, one to kingdom, and two to realm), 38 of which were novel. They tentatively represent avian- (n = 3), arthropod- (n = 21), plant- (n = 5) and fungi- (n = 4) associated, or other (n = 10) viruses. The arthropod-associated Dicistroviridae family was the most dominant, comprising known and potentially new species. Of potential epidemiological importance were three novel and avian-associated viruses: members of the families Hepeviridae and Picornaviridae , and a new Matryoshka RNA virus. The Matryoshka RNA virus 8 (MaRNAV-8) is sister to other Matryoshka RNA viruses, and its co-occurrence with haemosporida further supports the nested virus-parasite-vector-vertebrate host relationship of this group of viruses, with potential implications for parasite evolution, fitness and load and vector competence. The Picornaviridae virus is a member of an avian hepatovirus clade, found nested within a clade containing both the mammalian pathogens Hepatovirus A – I and the avian Tremovirus pathogens, suggestive of a newly discovered pathogen of Northern Mockingbird. Although the recovered Hepeviridae virus is of unknown pathology, its family members include the Hepatitis E viruses. With the great diversity and novelty described from ileal viromes, discriminating potential pathogens and commensal microbiota from viruses associated with food items remains challenging. A deeper understanding of virus transmission and the risk of potential zoonosis can be enhanced by tracking viruses through the food web and via inter-specific and predator-prey interactions, particular in areas subject to land-use change, where human-wildlife interactions are increased and the risks from emerging pathogens of veterinary and medical importance are more pronounced.

Texas↗