Biological Sciences

Intracellular Bacteria

Intracellular bacteria are bacteria that live inside host cells. They have evolved mechanisms to invade and survive within host cells, often causing chronic infections. Examples of intracellular bacteria include Chlamydia, Rickettsia, and Mycobacterium tuberculosis.

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4 Key excerpts on "Intracellular Bacteria"

  • Book cover image for: Metabolism and Bacterial Pathogenesis
    • Tyrrell Conway, Paul S. Cohen, Tyrrell Conway, Paul S. Cohen(Authors)
    • 2015(Publication Date)
    • ASM Press
      (Publisher)
    3 ), it is usually detrimental in infections of mammalian cells by Intracellular Bacterial pathogens. In this encounter, a host cell-defense program is initiated, including antimicrobial metabolic reactions aimed to damage the invading pathogen and/or to withdraw essential nutrients, while the intracellular pathogen tries to deprive nutrients from the host cell and to counteract the antimicrobial reactions, resulting in damaging of the host cell. Our knowledge of the metabolic adaptation processes occurring during this liaison and the link between these metabolic changes and the pathogenicity is still rather fragmentary. For these complex metabolic interactions, we coin the term “pathometabolism”. Studies of pathometabolism are not only central for a deeper understanding of bacterial infections caused by Intracellular Bacterial pathogens, but may also provide promising bacterial and host cell targets for the development of novel antimicrobial therapeutic measures.

    GENERAL CONSIDERATIONS

    The Intracellular Bacterial Pathogens
    Intracellular Bacteria that may cause severe infections in humans (which are exclusively discussed here), are characterized by their ability to actively invade human and other mammalian cells (and eventually also cells of lower eukaryotic organisms), efficiently replicate intracellularly, and finally exit the infected cells and reinfect new host cells. “Facultative intracellular” bacteria may grow intracellularly within suitable host cells or extracellularly in various natural and artificial environments. The so-called “obligate intracellular” bacteria are thought to exclusively replicate within appropriate host cells. However, recent investigations show that even these bacterial pathogens may thrive in axenic media (4 5 ). Within the infected host cells Intracellular Bacteria may replicate in specifically modified pathogen-containing vacuoles (PCV) (6 ). Typical representatives of this group belong to the genera Salmonella, Mycobacteria, Brucella, Legionella, Coxiella, and Chlamydia . The other group of Intracellular Bacterial pathogens, including members of the genera Shigella, Listeria, Rickettsia and Francisella , escapes into the host cell’s cytosol where these bacteria actively replicate (6 ).
    All Intracellular Bacteria must import basic nutrients from the host cell, including one or more suitable carbon, nitrogen, and sulphur sources and metal ions. Some Intracellular Bacteria require, in addition, several amino acids, nucleotides, vitamins, fatty acids, and even adenosine triphosphate (ATP) and nicotinamide adenine dinucleotide (NAD). The cytosolically replicating Intracellular Bacteria obviously have direct access to these host nutrients that are either taken up or produced by the host cells. Pathogens residing in PCVs, on the other hand, must transport cytosolic host nutrients across the vacuolar membrane. Depending on the pathogen, this membrane may obtain nutrient transporters by fusion with endocytic vesicles, including lysosomes, (macro)pinosomes, or exocytic vesicles, that contain enzymes, transporters, and/or nutrients (7 13
  • Book cover image for: Concepts in Vaccine Development
    • Stefan H. E. Kaufmann(Author)
    • 2012(Publication Date)
    • De Gruyter
      (Publisher)
    2. General Principles of Immunology 2.1 Basic Principles of Immunity Against Intracellular Bacteria and Protozoa Gudrun Szalay and Stefan H. E. Kaufmann 2.1.1 Introduction Intracellular pathogens comprise bacteria as well as protozoa. The major common feature of these pathogens is their intracellular life-style (Hahn and Kaufmann, 1981 ; Moulder, 1985; Kaufmann, 1993; Kaufmann, 1994). Intracellular living implies in-vasion of and permanent residence inside host cells. An additional requirement for in-tracellular living is the low intrinsic toxicity of intracellular pathogens because toxins would impair their habitat. Intracellular pathogens are found in mononuclear phago-cytes (MP) and various other tissue cells, in particular hepatocytes, epithelial cells, and endothelial cells (Kaufmann, 1993; Kaufmann, 1994). The intracellular bacte-ria can be further distinguished according to their capacity to survive outside of host cells: a) Facultative Intracellular Bacteria predominantly live inside host cells but are also capable of replicating in the extracellular space. Their preferred habitat are MP. Mycobacterium tuberculosis, the causative agent of tuberculosis, is the medically most important representative of this group (Bloom, 1994). Worldwide, this dis-ease causes enormous health problems, which increased in recent years in parallel with the emergence of multidrug resistant strains. Other facultative intracellular pathogens are Salmonella typhi, a gram negative rod causing typhoid fever, Le-gionella pneumophila responsible for Legionnaire's disease, and the gram pos-itive rod, Listeria monocytogenes, the etiologic agent of listeriosis (Finlay and Falkow, 1989; Barbaree et al., 1993; Kaufmann, 1988). Disease is transmitted orally by contaminated food as is the case with S. typhi and L. monocytogenes or is air-borne as for M. tuberculosis and L. pneumophila.
  • Book cover image for: Biology of the Prokaryotes
    • Joseph W. Lengeler, Gerhart Drews, Hans G. Schlegel(Authors)
    • 2009(Publication Date)
    • Wiley-Blackwell
      (Publisher)
    33 Prokaryotes in Medicine 827 Table 33.7 Intracellular Bacteria Fig.33.12 Electron micrograph of Gram-negative bacteria before (a) and after (b. c) Invasion Into epithelial cells. N, nucleus of epithelial cell; C, cytoplasm of epithelial cell. Bars. 0.5 in a-c 33.3.2 Invasins Contribute to the Entry of Pathogens Into Host Cells A number of microbial pathogens do not multiply extracellularly. but rather invade cells of the host organ- isms. Once in the cell, these intracellular pathogens are able to surviveand even multiply within the invaded cells. The term "invasion" describes processes triggered by intracellular pathogens that lead to their uptake and intracellular survival within host cells. Virulence factors involved in entry are designated as invasins. Diarrheal disease Diarrheal disease Dysenteria Rocky Mountain spotted fever Typhus Q fever Trachoma leprosy Shigellosis Typhoid fever Listeriosis Tuberculosis legionnaires' disease Bubonic plague Obligate intracellular Rickettsia rickettsii Rickettsia prowazekii Coxiella bumetii Chlamydia trachomatis Mycobacterium leprae Facultative intracellular Salmonella typhimurium Yersinia enterocolitica Enteropathogenic Escherichia coli Shigella spp. Salmonella enterica Listeria monocytogenes Mycobacterium tuberculosis Legionella pneumophila Yersinia pestis The fimbrial adhesin gene clusters of pathogenic Escherichia coli and the genes coding for type IV fimbriae of various other organisms, including Neisseria gonorrhoeae, Vibrio choleme or Pseudomonas aeruginosa (Tab. 33.6), have been studied in detail. In the case ofthe E. coli adhesins, large operons of about 10 kbp are necessary to encode fimbrial adhesins. The correspond- ing operon consists of structural genes encoding major and minor adhesin subunit proteins and genes encoding proteins involved in the transport of the fimbria I subunits through the periplasmic space and the outer membrane (see also Chapters 19.4 and 23.8).
  • Book cover image for: Microbial Pathogens and Human Diseases
    • N A Khan(Author)
    • 2008(Publication Date)
    • CRC Press
      (Publisher)
    To achieve this, the majority of the meningitis-causing bacteria have evolved mechanisms to invade the host cells. This ability allows bacteria to cross a biological barrier as well as protects them from an overwhelming immune response and to hide from antimicrobials circulating into the bloodstream. Again, different bacteria use diverse proteins/toxins to invade into the host cells. The bacterial invasion of the host cells involve host cell cytoskeletal rearrangements (Fig. 17). Cytoskeleton is a network of filaments just beneath the plasma membrane that provides structural support to the cells. The ability of the bacteria to manipulate cytoskeletal proteins to gain entry into the host cells is crucial to remain viable and cross the barrier for the onset of the disease. 2.5 Evasion of Host Killing Mechanisms and Intracellular Multiplication Once taken up, the bacteria use diverse strategies to avoid host cell killing (Fig. 17). For example, Listeria monocytogenes invade the intestinal epithelial cells escape phagosome, multiply and move from one cell to another adjacent cell eventually reaching the bloodstream. In contrast, Salmonella Fig. 17 Bacteria induces cytoskeletal rearrangements resulting in its uptake. Once inside the host cell, the bacteria use diverse mechanisms (indicated by A, B, C) to evade intracellular killing. 145 spp. invade intestinal epithelial cells and then infect the underlying macrophages. Once inside the macrophages, the bacteria inhibit fusion of lysosomes with phagosome. Similarly, Mycobacterium tuberculosis inhibit fusion of lysosomes with phagosome in macrophages. Other bacteria such as Staphylococcus aureus produce catalase and superoxide dismutase which detoxify toxic oxygen radicals and survive macrophage onslaught (Fig. 17). Other mechanisms of avoiding host cell killing are to destroy the host and/or phagocytic cells.
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