Trends in Microbiology最新文献

Small colony variants (SCVs) of Staphylococcus aureus are a relatively rare but clinically significant growth morphotype. Infections with SCVs are frequently difficult to treat, inherently antibiotic-resistant, and can lead to persistent infections. Despite a long history of research, the molecular underpinnings of this morphotype and their impact on the clinical trajectory of infections remain unclear. However, a growing body of literature indicates that SCVs are caused by a diverse range of molecular factors. These recent findings suggest that SCVs should be thought of as an ensemble collection of loosely related phenotypes, and not as a single phenomenon. This review describes the diverse mechanisms currently known to contribute to SCVs and proposes an ensemble model for conceptualizing this morphotype.

Decomposer microbial communities are gatekeepers in the redistribution of carbon and nutrients from dead animals (carrion) to terrestrial ecosystems. The flush of decomposition products from a carcass creates a hot spot of microbial activity in the soil below, and the animal's microbiome is released into the environment, mixing with soil communities. Changes in soil physicochemistry, especially reduced oxygen, temporarily constrain microbial nutrient cycling, and influence the timing of these processes and the fate of carrion resources. Carcass-related factors, such as mass, tissue composition, or even microbiome composition may also influence the functional assembly and succession of decomposer communities. Understanding these local scale microbially mediated processes is important for predicting consequences of carrion decomposition beyond the hot spot and hot moment.

Cryptococcosis imposes a considerable burden on public health, and emerging drug responses to anticryptococcal drugs remain to be addressed. In this forum article we discuss the emerging drug responses of Cryptococcus, focusing on the critical nature of understanding such responses in order to improve the effectiveness of anticryptococcal therapeutics.

The small intestinal microbiota (SIM) is essential for gastrointestinal health, influencing digestion, immune modulation, and nutrient metabolism. Unlike the colonic microbiota, the SIM has been poorly characterized due to sampling challenges and ethical considerations. Current evidence suggests that the SIM consists of five core genera and additional segment-specific taxa. These bacteria closely interact with the human host, regulating nutrient absorption and metabolism. Recent work suggests the presence of two forms of small intestinal bacterial overgrowth, one dominated by oral bacteria (SIOBO) and a second dominated by coliform bacteria. Less invasive sampling techniques, omics approaches, and mechanistic studies will allow a more comprehensive understanding of the SIM, paving the way for interventions engineering the SIM towards better health.

Plants have developed very diverse strategies to defend themselves against viral pathogens, among which plant hormones play pivotal roles. In response, some viruses have also deployed multifunctional viral effectors that effectively hijack key component hubs to counter or evade plant immune surveillance. Although significant progress has been made toward understanding counter-defense strategies that manipulate plant hormone regulatory molecules, these efforts have often been limited to an individual virus or specific host target/pathway. This review provides new insights into broad-spectrum antiviral responses in rice triggered by key components of phytohormone signaling, and highlights the common features of counter-defense strategies employed by distinct rice-infecting RNA viruses. These strategies involve the secretion of multifunctional virulence effectors that target the sophisticated phytohormone system, dampening immune responses by engaging with the same host targets. Additionally, the review provides an in-depth exploration of various viral effectors, emphasizing tertiary structure-based research and shared host targets. Understanding these conserved characteristics in detail may pave the way for molecular drug design, opening new opportunities to enhance broad-spectrum antiviral trials through precise engineering.

Many pathogens are hard to eradicate, even in the absence of genetically detectable antimicrobial resistance mechanisms and despite proven antibiotic susceptibility. The fraction of clonal bacteria that temporarily elude effective antibiotic treatments is commonly known as 'antibiotic persisters.' Over the past decade, there has been a growing body of research highlighting the pivotal role played by the cellular host in the development of persisters. In parallel, this research has also sought to elucidate the molecular mechanisms underlying the formation of intracellular antibiotic persisters and has demonstrated a prominent role for the bacterial stress response. However, questions remain regarding the conditions leading to the formation of stress-induced persisters among a clonal population of intracellular bacteria and despite an ostensibly uniform environment. In this opinion, following a brief review of the current state of knowledge regarding intracellular antibiotic persisters, we explore the ways in which macrophage functional heterogeneity and bacterial phenotypic heterogeneity may contribute to the emergence of these persisters. We propose that the degree of mismatch between the macrophage permissiveness and the bacterial preparedness to invade and thrive intracellularly may explain the formation of stress-induced nonreplicating intracellular persisters.

Nematodes do not merely siphon off plant resources but also sabotage the plant's mutualistic relationships with beneficial microbes. Yang and colleagues elegantly elucidated this generalizable molecular antagonism, revealing how Heterodera glycines, the notorious soybean cyst nematode (SCN), suppresses beneficial microbial symbiosis through a specific chitinase, HgCht2.

While the opportunistic human pathogens Cryptococcus neoformans and Cryptococcus gattii are often isolated from plants and plant-related material, evidence suggests that these Cryptococcus species do not directly infect plants. Studies find that plants are important for Cryptococcus mating and dispersal. However, these studies have not provided enough detail about how plants and these fungi interact, especially in ways that could show the fungi are capable of causing disease. This review synthesizes recent findings from studies utilizing different plant models associated with the ecology of C. neoformans and C. gattii. Unanswered questions about their environmental role are highlighted. Overall, current research indicates that Cryptococcus utilizes plants as a substrate rather than harming them, arguing against Cryptococcus as a genuine plant pathogen. We hypothesize that plants represent reservoirs that aid dispersal, not hosts vulnerable to infection.