| 期刊全称 | Bacterial Infection: Close Encounters at the Host Pathogen Interface | | 影响因子2023 | Peter K. Vogt,Michael J. Mahan | | 视频video | http://file.papertrans.cn/181/180286/180286.mp4 | | 学科分类 | Current Topics in Microbiology and Immunology | | 图书封面 |  | | 影响因子 | When it comes to bacterial disease, we are living in a state of false security. Antibiotics have indeed brought unprecedented health benefits, protection from and cure of bacterial diseases during the past 50 years. But there are ominous signs that the fortress and the defenses built on antibiotics are crumbling. They are crum bling because we wittingly or unwittingly created selective con ditions for the emergence of superior pathogens that can no longer be controlled by antibiotics. There are numerous warnings. After a long period of eclipse tuberculosis has now emerged as a serious threat unchecked by antibiotic treatment. Recent years have seen reports of cholera epidemics, of anthrax infections, of serious problems with Salmonella and even with E. coli, just to name a few. Mankind is in a race with microbial invaders. The challenge is to anticipate and respond to developments that affect the precarious balance between man and microbe. This will re quire new knowledge and it will take time for an effective appli cation of that knowledge. | | Pindex | Book 1998 |
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Front Matter |
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Abstract
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| 2 |
,In Vivo Gene Expression: Contributions to Infection, Virulence, and Pathogenesis, |
C. P. Conner,D. M. Heithoff,M. J. Mahan |
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Abstract
Pathogenic bacteria are distinguished by their ability to proliferate within host cells or fluids that are forbidden to commensal species. Viewed from this perspective, bacterial products that lead to enhanced growth and persistence at these sites are key attributes that determine a microbe’s pathogenic potential (. 1996; . et al. 1997). Many virulence determinants that contribute to this unique ability share a common phenotype, i.e., induction in host tissues. In this review, we will describe two complementary genetic strategies developed in . that allow the isolation of bacterial genes induced or required during infection. The identification of such genes and the products they encode provides a means to understand their contributions to infection, virulence, and pathogenesis.
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| 3 |
,Anthrax Pathogenesis and Host Response, |
P. Hanna |
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Abstract
Anthrax has been both a scourge and a fundamental model for infectious disease studies for over a century. Death associated with systemic anthrax is mimicked in animals challenged with anthrax lethal toxin, a virulence factor believed to affect only macrophages. Animals depleted of macrophages become resistant to the toxin, while reintroduction of cultured macrophages into depleted animals restores sensitivity. These studies and others implicate an active role for the innate immune system in the demise of the anthrax victim. Many of the molecular factors and events in the cascade of lethal events during anthrax infections have now been identified. Other recent overviews of anthrax pathogenesis and toxins include those by . (1986), . (1990), . (1995), and . and . (1997).
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| 4 |
,New Insights into the Genetics and Regulation of Expression of , Enterotoxin, |
B. A. McClane |
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Abstract
The bacterial genus . includes many gram-positive, anaerobic, sporeforming species, a number of which are responsible for significant human and veterinary diseases (. et al. 1997). As their outstanding virulence attribute, these pathogenic Clostridia share the ability to elaborate extremely potent protein toxins (. et al. 1997). With the recent development of tools and techniques for analyzing clostridial genetics (. et al. 1997), it is now becoming feasible to investigate the genetics and regulation of expression of these clostridial toxins.
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| 5 |
,Identification of Virulence Determinants in Pathogenic Mycobacteria, |
J. E. Clark-Curtiss |
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Abstract
Few infectious organisms have wreaked so much suffering upon the human race as members of the genus .. From ancient times, the major pathogenic mycobacterial species, . and .; have afflicted humans, causing not only overt disease, but also immeasurable fear and distress. Lesions suggestive of spinal tuberculosis have been found in the skeleton of a neolithic man (c. 4000 B.C.) and in Egyptian mummies dating from 3700–1000 B.C.(Morse et al. 1964; Grange 1989). Ancient medical writings from China (c. 250 B.C.) and India (between 600 and 400 B.C.) describe skin diseases characterized by nodulation, hair loss, disturbed pigmentation, anesthesia, and ulceration that are suggestive of leprosy (. 1989; . and . 1932; K.N.N.S. . 1909), although skeletal lesions characteristic of leprosy have not been identified in skeletons earlier than one dating from 350 A.D. (. 1989). . (1989) pointed out that the term “lepra” or “lepros” used in the Talmud and Old and New Testaments was different from the words used to describe leprosy in biblical times; “lepra” or “lepros” referred to specific scaling skin diseases such as psoriasis. However, the context in which the words “lepra” or “lepros” were used
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| 6 |
,Mechanisms of Pathogenesis of Staphylococcal and Streptococcal Superantigens, |
J. V. Rago,P. M. Schlievert |
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Abstract
In order to infect a host successfully, to access nutrients, and to promote the progression of disease, many pathogenic bacteria, such as the staphylococci and streptococci, produce exoproteins which enhance microbial virulence. Among these proteins is the family of toxins known today as the superantigens (SAg). This family includes the pyrogenic toxin SAg (PTSAg), such as the staphylococcal enterotoxins (SE, serotypes A-E, G, H), group A streptococcal pyrogenic exotoxins (SPE, serotypes A-C and possibly F), streptococcal SAg (SSA), and staphylococcal toxic shock syndrome toxin (TSST)-1. The following is a review of the biochemistry, structure, and mechanisms of pathogenicity of the PTSAg and the shared and unique properties of each. The properties of other relevant superantigenic proteins such as the staphylococcal exfoliative toxins (ETA, ETB) will also be discussed.
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| 7 |
,Intracellular Multiplication of ,: Human Pathogen or Accidental Tourist?, |
H. A. Shuman,M. Purcell,G. Segal,L. Hales,L. A. Wiater |
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Abstract
Pathogens which secrete toxins and otherwise damage host cells and tissues from the outside have been studied from a variety of approaches. In many cases it has been possible to purify toxins as well as their receptors and targets. In some cases (e.g., diphtheria toxin, pertussis toxin), the basis of toxin activity is understood at the molecular level. For these organisms, it is possible to describe at least one important aspect of the pathogenesis of the disease carefully enough to devise specific hypotheses that lead to a relatively deep understanding of the basis of pathogenesis.
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| 8 |
,Fe(III) Periplasm-to-Cytosol Transporters of Gram-Negative Pathogens, |
T. A. Mietzner,S. B. Tencza,P. Adhikari,K. G. Vaughan,A. J. Nowalk |
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Abstract
Iron acquisition by bacteria is a concept that is embedded in both classical microbiology and contemporary biochemistry. Early work by . (1949) defined the bacterial requirement for iron and allowed . and . (. 1985) to deduce that the bacteriostatic property of serum could be reversed by the inclusion of iron. This in turn led to the contributions of . and colleagues (1987) toward defining the biology of bacterial, fungal, and plant siderophores; this is a concept that is now accepted as a necessary, but by itself insufficient contributor to the virulence of many bacterial pathogens (. 1978, 1984). Focused studies on bacterial iron acquisition have set up a dichotomy of iron transport systems for gram-negative pathogens: those that employ a siderophore-mediated mechanism (. 1980, 1981, 1991, 1995; . 1987) and those that utilize a mechanism involving transferrin-bound iron (. and . 1989; . and . 1992). The culmination of these studies is a broad literature describing the molecular and biochemical basis for high-affinity iron transport.
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,Molecular Pathogenesis of Urinary Tract Infections, |
S. E. F. D’Orazio,C. M. Collins |
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Abstract
Urinary tract infection (UTI) is the most common bacterial infection of the human body. It has been estimated that there are as many as 8 million visits a year to physicians’ offices for treatment of the symptoms of UTI and more than 100 000 hospital admissions for serious infections (US . 1990). In addition, the urinary tract is usually the most common source of bacteremia in hospitals and nursing homes. The presence of bacteria in urine (bacteriuria) alone is not necessarily indicative of a UTI; significant bacterial counts (> 10. cfu/ml) and pyuria are the classic signs of UTI. Infections can range from mild, asymptomatic episodes of bladder infection (cystitis) to more severe, life-threatening complications of the kidney, such as acute pyelonephritis.
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Back Matter |
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Abstract
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