Topic
Pathogen
About: Pathogen is a research topic. Over the lifetime, 3108 publications have been published within this topic receiving 122742 citations. The topic is also known as: infectious agent & germ.
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TL;DR: This review summarizes the virtual explosion of information regarding the epidemiology, biochemistry, mechanisms of action, and genetic basis of these urovirulence factors that has occurred in the past decade and identifies areas in need of further study.
Abstract: Uropathogenic strains of Escherichia coli are characterized by the expression of distinctive bacterial properties, products, or structures referred to as virulence factors because they help the organism overcome host defenses and colonize or invade the urinary tract. Virulence factors of recognized importance in the pathogenesis of urinary tract infection (UTI) include adhesins (P fimbriae, certain other mannose-resistant adhesins, and type 1 fimbriae), the aerobactin system, hemolysin, K capsule, and resistance to serum killing. This review summarizes the virtual explosion of information regarding the epidemiology, biochemistry, mechanisms of action, and genetic basis of these urovirulence factors that has occurred in the past decade and identifies areas in need of further study. Virulence factor expression is more common among certain genetically related groups of E. coli which constitute virulent clones within the larger E. coli population. In general, the more virulence factors a strain expresses, the more severe an infection it is able to cause. Certain virulence factors specifically favor the development of pyelonephritis, others favor cystitis, and others favor asymptomatic bacteriuria. The currently defined virulence factors clearly contribute to the virulence of wild-type strains but are usually insufficient in themselves to transform an avirulent organism into a pathogen, demonstrating that other as-yet-undefined virulence properties await discovery. Virulence factor testing is a useful epidemiological and research tool but as yet has no defined clinical role. Immunological and biochemical anti-virulence factor interventions are effective in animal models of UTI and hold promise for the prevention of UTI in humans. Images
1,290 citations
TL;DR: It is reported that persistence of M. tuberculosis in mice is facilitated by isocitrate lyase (ICL), an enzyme essential for the metabolism of fatty acids, an observation with important implications for the treatment of chronic tuberculosis.
Abstract: Mycobacterium tuberculosis claims more human lives each year than any other bacterial pathogen. Infection is maintained in spite of acquired immunity and resists eradication by antimicrobials. Despite an urgent need for new therapies targeting persistent bacteria, our knowledge of bacterial metabolism throughout the course of infection remains rudimentary. Here we report that persistence of M. tuberculosis in mice is facilitated by isocitrate lyase (ICL), an enzyme essential for the metabolism of fatty acids. Disruption of the icl gene attenuated bacterial persistence and virulence in immune-competent mice without affecting bacterial growth during the acute phase of infection. A link between the requirement for ICL and the immune status of the host was established by the restored virulence of delta icl bacteria in interferon-gamma knockout mice. This link was apparent at the level of the infected macrophage: Activation of infected macrophages increased expression of ICL, and the delta icl mutant was markedly attenuated for survival in activated but not resting macrophages. These data suggest that the metabolism of M. tuberculosis in vivo is profoundly influenced by the host response to infection, an observation with important implications for the treatment of chronic tuberculosis.
1,281 citations
TL;DR: This Review describes how S. pneumoniae uses its armamentarium of virulence factors to colonize the upper and lower respiratory tracts of the host and cause disease.
Abstract: Streptococcus pneumoniae is a Gram-positive bacterial pathogen that colonizes the mucosal surfaces of the host nasopharynx and upper airway. Through a combination of virulence-factor activity and an ability to evade the early components of the host immune response, this organism can spread from the upper respiratory tract to the sterile regions of the lower respiratory tract, which leads to pneumonia. In this Review, we describe how S. pneumoniae uses its armamentarium of virulence factors to colonize the upper and lower respiratory tracts of the host and cause disease.
1,090 citations
TL;DR: Arabidopsis, a tractable genetic system, is shown to develop resistance to a bacterial and a fungal pathogen following 2,6-dichloroisonicotinic acid (INA) treatment and three proteins that accumulated to high levels in the apoplast in response to INA treatment were purified and characterized.
Abstract: Acquired resistance is an important component of the complex disease resistance mechanism in plants, which can result from either pathogen infection or treatment with synthetic, resistance-inducing compounds In this study, Arabidopsis, a tractable genetic system, is shown to develop resistance to a bacterial and a fungal pathogen following 2,6-dichloroisonicotinic acid (INA) treatment Three proteins that accumulated to high levels in the apoplast in response to INA treatment were purified and characterized Expression of the genes corresponding to these proteins was induced by INA, pathogen infection, and salicylic acid, the latter being a putative endogenous signal for acquired resistance Arabidopsis should serve as a genetic model for studies of this type of immune response in plants
1,052 citations
TL;DR: Observations indicate that there is an ongqing evolution of the host plant's ability to recognize pathogen races that were previously unrecognized while the pathogen evolves to avoid recognition by a previously resistant host.
Abstract: Plant disease resistance to pathogens such as fungi, bacteria, and viruses often depends on whether the plant is able to recognize the pathogen early in the infection process. The recognition event leads to a rapid tissue necrosis at the site of infection, which is called the HR. The HR deprives the pathogen of nutrients and/or releases toxic molecules, thereby confining pathogen growth to a small region of the plant. This response provides resistance to the great majority of potential pathogens (nonhost or species resistance). For a given plant species, a much more limited number of true pathogens exhibit the ability to evade the host recognition system and grow extensively within the plant without evoking host necrosis at a11 or only after considerable delay. In this case, the plant exhibits susceptibility and the extensive growth of the successful pathogen can cause varying degrees of damage. However, certain races within pathogenic bacteria1 or funga1 species are recognized by certain cultivars or genotypes of the host plant species and the HR is triggered. These observations indicate that there is an ongqing evolution of the host plant's ability to recognize pathogen races that were previously unrecognized while the pathogen evolves to avoid recognition by a previously resistant host. Recognition of pathogens triggers a large range of inducible defense mechanisms that are believed to contribute to overall resistance in the plant. The mechanisms induced at the site of infection and associated with the HR include synthesis of antimicrobial compounds called phytoalexins, synthesis of hydrolytic enzymes that attack fungi and bacteria, and alterations in the synthesis of cell-wall structural proteins (for
863 citations