1382 I. 1382 II. 1383 III. 1383 IV. 1384 V. 1386 VI. 1387 VII. 1389 VIII. 1391 1391 References 1391 SUMMARY: In forest ecosystems, ectomycorrhizal and saprotrophic fungi play a central role in the ...breakdown of soil organic matter (SOM). Competition between these two fungal guilds has long been hypothesized to lead to suppression of decomposition rates, a phenomenon known as the ‘Gadgil effect’. In this review, we examine the documentation, generality, and potential mechanisms involved in the ‘Gadgil effect’. We find that the influence of ectomycorrhizal fungi on litter and SOM decomposition is much more variable than previously recognized. To explain the inconsistency in size and direction of the ‘Gadgil effect’, we argue that a better understanding of underlying mechanisms is required. We discuss the strengths and weaknesses of each of the primary mechanisms proposed to date and how using different experimental methods (trenching, girdling, microcosms), as well as considering different temporal and spatial scales, could influence the conclusions drawn about this phenomenon. Finally, we suggest that combining new research tools such as high‐throughput sequencing with experiments utilizing natural environmental gradients will significantly deepen our understanding of the ‘Gadgil effect’ and its consequences on forest soil carbon and nutrient cycling.
Summary Human African trypanosomiasis, or sleeping sickness, is caused by infection with parasites of the genus Trypanosoma , transmitted by the tsetse fly. The disease has two forms, Trypanosoma ...brucei (T b) rhodesiense and T b gambiense ; and is almost always fatal if untreated. Despite a recent reduction in the number of reported cases, patients with African trypanosomiasis continue to present major challenges to clinicians. Because treatment for CNS-stage disease can be very toxic, diagnostic staging to distinguish early-stage from late-stage disease when the CNS in invaded is crucial but remains problematic. Melarsoprol is the only available treatment for late-stage T b rhodesiense infection, but can be lethal to 5% of patients owing to post-treatment reactive encephalopathy. Eflornithine combined with nifurtimox is the first-line treatment for late-stage T b gambiense . New drugs are in the pipeline for treatment of CNS human African trypanosomiasis, giving rise to cautious optimism.
Varicella-zoster virus (VZV) is a pathogenic human herpes virus that causes varicella (chickenpox) as a primary infection, following which it becomes latent in peripheral ganglia. Decades later, the ...virus may reactivate either spontaneously or after a number of triggering factors to cause herpes zoster (shingles). Varicella and its complications are more severe in the immunosuppressed. The most frequent and important complication of VZV reactivation is postherpetic neuralgia, the cause of which is unknown and for which treatment is usually ineffective. Reactivation of VZV may also cause a wide variety of neurological syndromes, the most significant of which is a vasculitis, which is treated with corticosteroids and the antiviral drug acyclovir. Other VZV reactivation complications include an encephalitis, segmental motor weakness and myelopathy, cranial neuropathies, Guillain⁻Barré syndrome, enteric features, and zoster sine herpete, in which the viral reactivation occurs in the absence of the characteristic dermatomally distributed vesicular rash of herpes zoster. There has also been a recent association of VZV with giant cell arteritis and this interesting finding needs further corroboration. Vaccination is now available for the prevention of both varicella in children and herpes zoster in older individuals.
Human African trypanosomiasis (HAT), also known as sleeping sickness, is one of the Africa's 'neglected diseases' and is caused by infection with protozoan parasites of the
Trypanosoma
genus. ...Transmitted by the bite of the tsetse fly, it puts 70 million people at risk throughout sub-Saharan Africa and is usually fatal if untreated or inadequately treated. In this brief overview, some important recent developments in this disease are outlined. These cover various aspects including a reduction in disease incidence, newly recognised parasite reservoir sites in humans, disease outcome, novel diagnostic methods, new and improved treatment, and disease neuropathogenesis.
Varicella–Zoster virus (VZV) is a pathogenic human alpha herpes virus that causes varicella (chicken pox) as a primary infection and, following a variable period of latency in different ganglionic ...neurons, it reactivates to produce herpes zoster (shingles). The focus of this review is on the wide spectrum of the possible neurological manifestations of VZV reactivation. While the most frequent reactivation syndrome is herpes zoster, this may be followed by the serious and painful post-herpetic neuralgia (PHN) and by many other neurological conditions. Prominent among these conditions is a VZV vasculopathy, but the role of VZV in causing giant cell arteritis (GCA) is currently controversial. VZV reactivation can also cause segmental motor weakness, myelitis, cranial nerve syndromes, Guillain–Barre syndrome, meningoencephalitis, and zoster sine herpete, where a neurological syndrome occurs in the absence of the zoster rash. The field is complicated by the relatively few cases of neurological complications described and by the issue of causation when a neurological condition is not manifest at the same time as the zoster rash.
Fungi represent a large proportion of the genetic diversity on Earth and fungal activity influences the structure of plant and animal communities, as well as rates of ecosystem processes. Large-scale ...DNA-sequencing datasets are beginning to reveal the dimensions of fungal biodiversity, which seem to be fundamentally different to bacteria, plants and animals. In this Review, we describe the patterns of fungal biodiversity that have been revealed by molecular-based studies. Furthermore, we consider the evidence that supports the roles of different candidate drivers of fungal diversity at a range of spatial scales, as well as the role of dispersal limitation in maintaining regional endemism and influencing local community assembly. Finally, we discuss the ecological mechanisms that are likely to be responsible for the high heterogeneity that is observed in fungal communities at local scales.
Trypanosomiasis has been recognized as a scourge in sub-Saharan Africa for centuries. The disease, caused by protozoan parasites of the
genus, is a major cause of mortality and morbidity in animals ...and man. Human African trypanosomiasis (HAT), or sleeping sickness, results from infections with
or
with
accounting for over 95% of infections. Historically there have been major epidemics of the infection, followed by periods of relative disease control. As a result of concerted disease surveillance and treatment programmes, implemented over the last two decades, there has been a significant reduction in the number of cases of human disease reported. However, the recent identification of asymptomatic disease carriers gives cause for some concern. The parasites evade the host immune system by switching their surface coat, comprised of variable surface glycoprotein (VSG). In addition, they have evolved a variety of strategies, including the production of serum resistance associated protein (SRA) and
-specific glycoprotein (TgsGP) to counter host defense molecules. Infection with either disease variant results in an early haemolymphatic-stage followed by a late encephalitic-stage when the parasites migrate into the CNS. The clinical features of HAT are diverse and non-specific with early-stage symptoms common to several infections endemic within sub-Saharan Africa which may result in a delayed or mistaken diagnosis. Migration of the parasites into the CNS marks the onset of late-stage disease. Diverse neurological manifestations can develop accompanied by a neuroinflammatory response, comprised of astrocyte activation, and inflammatory cell infiltration. However, the transition between the early and late-stage is insidious and accurate disease staging, although crucial to optimize chemotherapy, remains problematic with neurological symptoms and neuroinflammatory changes recorded in early-stage infections. Further research is required to develop better diagnostic and staging techniques as well as safer more efficacious drug regimens. Clearer information is also required concerning disease pathogenesis, specifically regarding asymptomatic carriers and the mechanisms employed by the trypanosomes to facilitate progression to the CNS and precipitate late-stage disease. Without progress in these areas it may prove difficult to maintain current control over this historically episodic disease.
Several viruses have the capacity to cause serious infections of the nervous system in patients who are immunosuppressed. Individuals may be immunosuppressed because of primary inherited ...immunodeficiency, secondary immunodeficiency due to particular diseases such as malignancy, administration of immunosuppressant drugs or organ or bone marrow transplantation. The viruses capable of such opportunistic infection of the nervous system include herpes simplex virus (HSV), Varicella-Zoster virus (VZV), Cytomegalovirus (CMV), Epstein –Barr virus (EBV), Human Herpes virus type 6 (HHV-6), JC virus (JCV), enterovirus, measles virus and Covid-19. In most cases it seems likely that immunological defence mechanisms in the immunosuppressed are deficient which creates a suitable environment for certain viruses to become opportunistic in the nervous and other systems. Further research is required both to understand these opportunistic mechanisms in more detail and also to determine how many virus infections are modified by specific inborn errors of immunological responses.
Human African trypanosomiasis (HAT), also known as sleeping sickness, is a major cause of mortality and morbidity in sub-Saharan Africa. We hypothesised that recent findings of neurological features ...and parasite brain infiltration occurring at much earlier stages in HAT than previously thought could be explained by early activation of host genetic programmes controlling CNS disease. Accordingly, a transcriptomal analysis was performed on brain tissue at 0, 7, 14, 21 and 28dpi from the HAT CD1/GVR35 mouse model. Up to 21dpi, most parasites are restricted to the blood and lymphatic system. Thereafter the trypanosomes enter the brain initiating the encephalitic stage. Analysis of ten different time point Comparison pairings, revealed a dynamic transcriptome comprising four message populations. All 7dpi Comparisons had by far more differentially expressed genes compared to all others. Prior to invasion of the parenchyma, by 7dpi, ~2,000 genes were up-regulated, denoted 7dpi↑ in contrast to a down regulated population 7dpi↓ also numbering ~2,000. However, by 14dpi both patterns had returned to around the pre-infected levels. The third, 28dpi↑ featured over three hundred transcripts which had increased modestly up to14dpi, thereafter were significantly up-regulated and peaked at 28dpi. The fourth, a minor population, 7dpi↑-28dpi↑, had similar elevated levels at 7dpi and 28dpi. KEGG and GO enrichment analysis predicted a diverse phenotype by 7dpi with changes to innate and adaptive immunity, a Type I interferon response, neurotransmission, synaptic plasticity, pleiotropic signalling, circadian activity and vascular permeability without disruption of the blood brain barrier. This key observation is consistent with recent rodent model neuroinvasion studies and clinical reports of Stage 1 HAT patients exhibiting CNS symptoms. Together, these findings challenge the strict Stage1/Stage2 phenotypic demarcation in HAT and show that that significant neurological, and immune changes can be detected prior to the onset of CNS disease.
Knowns and unknowns of the soil fungal necrobiome Kennedy, Peter G.; Maillard, François
Trends in microbiology (Regular ed.),
February 2023, 2023-02-00, 20230201, Letnik:
31, Številka:
2
Journal Article
Recenzirano
Dead microbial cells, commonly referred to as necromass, are increasingly recognized as an important source of both persistent carbon as well as nutrient availability in soils. Studies of the ...microbial communities associated with decomposing fungal necromass have accumulated rapidly in recent years across a range of different terrestrial ecosystems. Here we identify the primary ecological patterns regarding the structure and dynamics of the fungal necrobiome as well as highlight new research frontiers that will likely be key to gaining a full understanding of fungal necrobiome composition and its associated role in soil biogeochemical cycling. Because many members of the fungal necrobiome are culturable, combining laboratory functional assays with field-based surveys and experiments will allow ongoing studies of the fungal necrobiome to move from largely descriptive to increasingly predictive.
Fungal necromass is a dominant component of the dead microbial cells associated with persistent carbon in soils as well as a significant source of nutrient availability for plant and microbial uptake.Recent molecular-based analyses of decomposing fungal necromass in a range of ecosystems have found a selective but dynamic microbial community that is codominated by bacteria and fungi.Despite considerable taxonomic and functional variation in the fungal necrobiome over time, there appears to be a consistent set of bacteria and fungi encountered on decomposing fungal necromass across geographically and vegetatively diverse ecosystems.The most abundant microbial taxa found in molecular surveys of decomposing fungal necromass are culturable, so both laboratory assays and manipulative ecological experiments should be conducted to better understand the processes underlying fungal necrobiome assembly.
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