Academic literature on the topic 'Obligate intracellular bacteria'
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Journal articles on the topic "Obligate intracellular bacteria"
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Otten, Christian, Matteo Brilli, Waldemar Vollmer, Patrick H. Viollier, and Jeanne Salje. "Peptidoglycan in obligate intracellular bacteria." Molecular Microbiology 107, no. 2 (December 12, 2017): 142–63. http://dx.doi.org/10.1111/mmi.13880.
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McOrist, Steven. "Obligate intracellular bacteria and antibiotic resistance." Trends in Microbiology 8, no. 11 (November 2000): 483–86. http://dx.doi.org/10.1016/s0966-842x(00)01854-0.
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Raoult, Didier. "Antimicrobial activity against obligate intracellular bacteria." Trends in Microbiology 9, no. 1 (January 2001): 14. http://dx.doi.org/10.1016/s0966-842x(00)01861-8.
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Bordenstein, Seth R., and William S. Reznikoff. "Mobile DNA in obligate intracellular bacteria." Nature Reviews Microbiology 3, no. 9 (August 10, 2005): 688–99. http://dx.doi.org/10.1038/nrmicro1233.
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McClure, Erin E., Adela S. Oliva Chávez, Dana K. Shaw, Jason A. Carlyon, Roman R. Ganta, Susan M. Noh, David O. Wood, et al. "Engineering of obligate intracellular bacteria: progress, challenges and paradigms." Nature Reviews Microbiology 15, no. 9 (June 19, 2017): 544–58. http://dx.doi.org/10.1038/nrmicro.2017.59.
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Boichenko, M. N., E. O. Kravtsova, and V. V. Zverev. "Mechanism of intracellular bacterial parasitism." Journal of microbiology, epidemiology and immunobiology, no. 5 (November 21, 2019): 61–72. http://dx.doi.org/10.36233/0372-9311-2019-5-61-72.
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Algorithm of intracellular bacterial parasitism does not depend on if bacterium is obligate or facultative intracellular parasite. Depending on replicative niche’s localization intracellular bacterial parasites are divided onto cellular and vacuolated. Rickettsia spp., Shigella spp., Chlamydia spp. and Listeria monocytogenes use cell’s machinery of actin polymerization during process of their intracellular parasitism. These bacteria possess some of effector’s proteins which contain domains identical to effector proteins from the host cell. Shigella spp. T3SS and autotransporter protein IscA provide this process together with spreading bacteria intra colonic epithelium. In contrast other intracellular bacterial parasites, Listeria monocytogenes switches from dissemination in cytosol to persist in vacuole. In case of Brucella spp. the leading role in the creation of a replicative niche and in the modulation of the innate immune response is played by effector proteins of fourth type secretory system (T4SS).
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Hooppaw, Anna J., and Derek J. Fisher. "A Coming of Age Story: Chlamydia in the Post-Genetic Era." Infection and Immunity 84, no. 3 (December 14, 2015): 612–21. http://dx.doi.org/10.1128/iai.01186-15.
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Chlamydiaspp. are ubiquitous, obligate, intracellular Gram-negative bacterial pathogens that undergo a unique biphasic developmental cycle transitioning between the infectious, extracellular elementary body and the replicative, intracellular reticulate body. The primaryChlamydiaspecies associated with human disease areC. trachomatis, which is the leading cause of both reportable bacterial sexually transmitted infections and preventable blindness, andC. pneumoniae, which infects the respiratory tract and is associated with cardiovascular disease. Collectively, these pathogens are a significant source of morbidity and pose a substantial financial burden on the global economy. Past efforts to elucidate virulence mechanisms of these unique and important pathogens were largely hindered by an absence of genetic methods. Watershed studies in 2011 and 2012 demonstrated that forward and reverse genetic approaches were feasible withChlamydiaand that shuttle vectors could be selected and maintained within the bacterium. While these breakthroughs have led to a steady expansion of the chlamydial genetic tool kit, there are still roads left to be traveled. This minireview provides a synopsis of the currently available genetic methods forChlamydiaalong with a comparison to the methods used in other obligate intracellular bacteria. Limitations and advantages of these techniques will be discussed with an eye toward the methods still needed, and how the current state of the art for genetics in obligate intracellular bacteria could direct future technological advances forChlamydia.
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Zientz, Evelyn, Thomas Dandekar, and Roy Gross. "Metabolic Interdependence of Obligate Intracellular Bacteria and Their Insect Hosts." Microbiology and Molecular Biology Reviews 68, no. 4 (December 2004): 745–70. http://dx.doi.org/10.1128/mmbr.68.4.745-770.2004.
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SUMMARY Mutualistic associations of obligate intracellular bacteria and insects have attracted much interest in the past few years due to the evolutionary consequences for their genome structure. However, much less attention has been paid to the metabolic ramifications for these endosymbiotic microorganisms, which have to compete with but also to adapt to another metabolism—that of the host cell. This review attempts to provide insights into the complex physiological interactions and the evolution of metabolic pathways of several mutualistic bacteria of aphids, ants, and tsetse flies and their insect hosts.
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Martinson, Vincent G., Ryan M. R. Gawryluk, Brent E. Gowen, Caitlin I. Curtis, John Jaenike, and Steve J. Perlman. "Multiple origins of obligate nematode and insect symbionts by a clade of bacteria closely related to plant pathogens." Proceedings of the National Academy of Sciences 117, no. 50 (November 30, 2020): 31979–86. http://dx.doi.org/10.1073/pnas.2000860117.
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Obligate symbioses involving intracellular bacteria have transformed eukaryotic life, from providing aerobic respiration and photosynthesis to enabling colonization of previously inaccessible niches, such as feeding on xylem and phloem, and surviving in deep-sea hydrothermal vents. A major challenge in the study of obligate symbioses is to understand how they arise. Because the best studied obligate symbioses are ancient, it is especially challenging to identify early or intermediate stages. Here we report the discovery of a nascent obligate symbiosis in Howardula aoronymphium, a well-studied nematode parasite of Drosophila flies. We have found that H. aoronymphium and its sister species harbor a maternally inherited intracellular bacterial symbiont. We never find the symbiont in nematode-free flies, and virtually all nematodes in the field and the laboratory are infected. Treating nematodes with antibiotics causes a severe reduction in fly infection success. The association is recent, as more distantly related insect-parasitic tylenchid nematodes do not host these endosymbionts. We also report that the Howardula nematode symbiont is a member of a widespread monophyletic group of invertebrate host-associated microbes that has independently given rise to at least four obligate symbioses, one in nematodes and three in insects, and that is sister to Pectobacterium, a lineage of plant pathogenic bacteria. Comparative genomic analysis of this group, which we name Candidatus Symbiopectobacterium, shows signatures of genome erosion characteristic of early stages of symbiosis, with the Howardula symbiont’s genome containing over a thousand predicted pseudogenes, comprising a third of its genome.
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Libbing, Cassandra L., Adam R. McDevitt, Rea-Mae P. Azcueta, Ahila Ahila, and Minal Mulye. "Lipid Droplets: A Significant but Understudied Contributor of Host–Bacterial Interactions." Cells 8, no. 4 (April 15, 2019): 354. http://dx.doi.org/10.3390/cells8040354.
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Lipid droplets (LDs) are cytosolic lipid storage organelles that are important for cellular lipid metabolism, energy homeostasis, cell signaling, and inflammation. Several bacterial, viral and protozoal pathogens exploit host LDs to promote infection, thus emphasizing the importance of LDs at the host–pathogen interface. In this review, we discuss the thus far reported relation between host LDs and bacterial pathogens including obligate and facultative intracellular bacteria, and extracellular bacteria. Although there is less evidence for a LD–extracellular bacterial interaction compared to interactions with intracellular bacteria, in this review, we attempt to compare the bacterial mechanisms that target LDs, the host signaling pathways involved and the utilization of LDs by these bacteria. Many intracellular bacteria employ unique mechanisms to target host LDs and potentially obtain nutrients and lipids for vacuolar biogenesis and/or immune evasion. However, extracellular bacteria utilize LDs to either promote host tissue damage or induce host death. We also identify several areas that require further investigation. Along with identifying LD interactions with bacteria besides the ones reported, the precise mechanisms of LD targeting and how LDs benefit pathogens should be explored for the bacteria discussed in the review. Elucidating LD–bacterial interactions promises critical insight into a novel host–pathogen interaction.
Dissertations / Theses on the topic "Obligate intracellular bacteria"
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Bekebrede, Hannah S. "Random Mutagenesis for the Discovery of Obligate Intracellular Bacterial In vivo Virulence Genes." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1574767897548976.
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Hebert, Kathryn S. "Investigation of Anaplasma phagocytophilum and Anaplasma marginale adhesin-host cell interactions." VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4130.
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Anaplasma phagocytophilum and A. marginale are the etiologic agents of bovine anaplasmosis and human granulocytic anaplasmosis, respectively. As obligate intracellular pathogens, binding and entry of host cells is a prerequisite for survival. The molecular events associated with these processes are poorly understood. Identifying the adhesins mediating binding, delineating their key functional domains, and determining the molecular determinants to which they bind not only benefits better understanding of Anaplasma spp. pathobiology, but could also benefit the development of novel approaches for protecting against infection. We previously demonstrated that A. phagocytophilum outer membrane protein A (ApOmpA) is critical for bacterial binding and entry host through recognition of α2,3-sialic acid and α1,3-fucose of its receptors, including 6-sulfo-sLex. In this study, we determined that two amino acids, G61 and K64, within its binding domain (ApOmpA59-74), are essential for ApOmpA function. We also confirmed the ability of ApOmpA to act as an adhesin and invasin as it conferred adhesiveness and invasiveness to inert beads. We next extended our studies to A. marginale as it also expresses OmpA (AmOmpA) and its role in infection has not been studied. Molecular models of ApOmpA and AmOmpA were nearly identical, especially in the ApOmpA binding domain and its counterpart in AmOmpA. Antisera raised against AmOmpA or its putative binding domain inhibit A. marginale infection. AmOmpA G55 and K58 are contributory and K59 is essential for AmOmpA to bind to host cells. AmOmpA binding is dependent on α2,3-sialic acid and α1,3-fucose. Coating inert beads with AmOmpA conferred the ability to bind to and be taken up by host cells, confirming that it acts as an adhesin and invasin. 6-sulfo-sLex is dispensable for AmOmpA binding and A. marginale infection. ApOmpA works cooperatively with Asp14 (14-kDa A. phagocytophilum surface protein) to promote optimal infection of host cells. We found that Asp14 is conserved across A. phagocytophilum strains and in A. marginale and confirmed the ability of Asp14 to act as an adhesin and invasin as it conferred adhesiveness and invasiveness to inert beads. Collectively, this work advances our understanding of A. phagocytophilum and A. marginale adhesion and invasion of host cells.
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Evans, Sean M. "Orientia tsutsugamushi secretes two ankyrin repeat-containing effectors via a type 1 secretion system to inhibit host NF-κB function." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4813.
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Scrub typhus is a potentially fatal infection that threatens one billion persons in the Asia-Pacific region and is caused by the obligate intracellular bacterium, Orientia tsutsugamushi. How this organism facilitates its intracellular survival and pathogenesis is poorly understood. Intracellular bacterial pathogens utilize the Type 1 (T1SS) or Type 4 secretion system (T4SS) to translocate ankyrin repeat-containing proteins (Anks) into the host cell to modulate host cell processes. The O. tsutsugamushi genome encodes one of the largest known bacterial Ank libraries as well as Type 1 and Type 4 secretion systems (T1SS and T4SS), which are expressed during infection. In silico analyses of the Anks’ C-termini revealed that they possess characteristics of T1SS secretion signals. Escherichia coli expressing a functional T1SS was able to secrete chimeric hemolysin proteins bearing the C-termini of 19 of 20 O. tsutsugamushi Anks. In addition to infecting endothelial cells, O. tsutsugamushi infects professional phagocytes. To better understand why these innate immune cells are unable to eliminate O. tsutsugamushi, we addressed the activity of host NF-κB proinflammatory transcription factor. Screening of O. tsutsugamushi infected cells at an MOI of 1 revealed inhibition of NF-κB nuclear accumulation as early as 8 hours in HeLa and bone-marrow derived macrophage cells. When stimulating infected cells with TNF-α, IκBα degradation still occurs, however NF-κB dependent gene transcription remains downregulated. Immunofluorescence microscopic analysis of TNF-α treated cells ectopically expressing all O. tsutsugamushi Anks revealed that two nuclear trafficking Anks, Ank1 and Ank6, result in a significant decrease in NF-κB nuclear accumulation. Additionally, these Anks also significantly inhibited NF-κB dependent gene transcription. Co-immunoprecipitation experiments revealed that both Anks interact with importin-β1, exportin-1, and the p65 NF-κB subunit. Treating cells with importazole significantly reduces the nuclear accumulation of Ank1 and Ank6. Finally, treating infected cells or cells ectopically expressing Ank1 or Ank6 with leptomycin B resulted in restoration of NF-κB nuclear accumulation. With these data, we propose that O. tsutsugamushi secretes Ank1 and Ank6 to initially interact with importin-β1, which permits their nuclear entry where they then interact with NF-κB and subsequently exportin-1 to prevent NF-κB nuclear accumulation.
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Olsen, Michelle Toomey. "Cellular, molecular, and evolutionary mechanisms of Wolbachia stem cell niche tropism in Drosophila." Thesis, 2015. https://hdl.handle.net/2144/15441.
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The intracellular bacteria Wolbachia infect up to 40% of all insect species, including the vectors of prevalent infectious diseases such as Dengue and malaria. Even though Wolbachia infections are the largest pandemic on this planet, the cellular and molecular mechanisms for bacterial spreading in nature are still unknown. Wolbachia are mainly vertically transmitted through the egg cytoplasm, however there is also evidence of extensive horizontal transmission. We have found that Wolbachia target the stem cell niches in the Drosophila ovary to enhance germline colonization and subsequent vertical transmission. This tropism is pervasive across the Drosophila genus, with the pattern of targeting being evolutionarily conserved. Phylogenetic analyses, confirmed by hybrid introgression and transinfection experiments, demonstrate that bacterial factors are the major determinants of differential patterns of niche tropism. Furthermore, bacterial load is increased in germline cells passing through infected niches, supporting previous findings suggesting a contribution of Wolbachia from stem cell niches towards vertical transmission.
If niche tropism is important for Wolbachia transmission through the germline, evolutionary theory predicts that there should be no selective pressure to maintain niche tropism in males. Indeed, we have found that tropism to the stem cell niche in the testis, known as the hub, is not evolutionarily conserved. Towards identifying the cellular and molecular mechanisms of stem cell niche tropism, we investigated hub targeting of closely related Wolbachia strains (wMel-like strains: wMel, wMel2, and wMel3; wMelCS-like strains: wMelCS, wMelCS2, and wMelPop). wMel-like and wMelCS-like Wolbachia strains differ in their frequencies and densities of hub infection. The targeting differences of these strains of Wolbachia indicate that this phenotype is rapidly evolving, as they shared a common ancestor only 8,000 years ago. With the plethora of tools available in D. melanogaster, a candidate gene approach was used to target host proteins enriched in the stem cell niche in the testis for RNAi mediated gene knockdown in the hub. We have identified Drosophila stem cell related signaling pathways that promote Wolbachia accumulation. Unraveling the cellular and molecular bases of tissue tropism is fundamental to understanding Wolbachia-host interactions.2017-01-01T00:00:00Z
Books on the topic "Obligate intracellular bacteria"
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Harper, Angela. Nutritional studies on the obligate intracellular bacterium Chlamydia trachomatis. Birmingham: University of Birmingham, 1995.
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Matthews, Philippa C. Infections caused by obligate intracellular bacteria. Edited by Philippa C. Matthews. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198737773.003.0006.
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This chapter consists of short notes, diagrams, and tables to summarize infections caused by obligate intracellular bacteria. The chapter begins with a classification system to divide these organisms into Rickettsia, Anaplasma, Chlamydia, Coxiella, and Bartonella species. Separate sections then follow on the infections of most clinical significance for the tropics and subtropics, including the typhus group (caused by rickettsial infection) and Q fever. For ease of reference, each topic is broken down into sections, including classification, epidemiology, microbiology, pathophysiology, clinical syndromes, diagnosis, treatment, and prevention.
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Angelakis, Emmanouil, and Didier Raoult. Scrub typhus. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0013.
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Bacteria of the genus Rickettsia are obligate intracellular rods that retained basic fuchsin when stained by the method of Gimenez. This genus has long been used as a generic term of small intracellular bacteria. However, taxonomic progress made over the last years has deeply modified the definition of “rickettsia”. As a result, in 1995 the position of R. tsutsugamushi has reclassified from the genus Rickettsia into a separate new genus, Orientia (Tamura et al. 1995).Scrub typhus, also known as ‘tsutsugamushi fever’, occurs only in Asia and is a chigger-borne zoonosis. The disease is acute, febrile, potentially fatal and has been known for centuries in China where it was probably described as early as in the fourth century BC (Parola and Raoult 2006). These last years this infection has been re-emerging because of descriptions of strains of O. tsutsugamushi with reduced susceptibility to antibiotics and of the surprising interactions between scrub typhus and the human immunodeficiency virus (HIV). It is estimated that more than a million cases of scrub typhus are transmitted annually in Asia and more than a billion people are at risk (Rosenberg 1997).
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Fletcher, Tom, and Nick Beeching. Rickettsial infection. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0314.
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Rickettsial infections are caused by a variety of obligate intracellular, Gram-negative bacteria from the genera Rickettsia, Orientia, Ehrlichia, and Anaplasma. Rickettsia is further subdivided into the spotted fever group and the typhus group. Bartonella and Coxiella burnetii bacteria are similar to rickettsiae and cause similar diseases. The range of recognized spotted fever group infections is rapidly expanding, complementing long-recognized examples such as Rocky Mountain spotted fever (Rickettsia rickettsii) in the US, and Australian tick typhus (Rickettsia australis), as well as those in southern Europe and Africa. Animals are the predominant reservoir of infection, and transmission to people is usually through ticks, mites, fleas, or lice, during blood-feeding or from scarification of faeces deposited on the skin. This chapter focuses on the two of the most relevant infections encountered in UK practice: African tick typhus, and Q fever.
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Sun, Lisa, and Michael V. Johnston. Rickettsial Diseases. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0157.
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Tick-borne rickettsioses are emerging as more important health problems throughout the world. The spotted fever group including Rickettsia rickettsia can cause encephalopathy, meningitis and brain damage by selectively targeting capillary endothelial cells in the brain, and stimulating inflammation, capillary leakage, hemorrhage, and intravascular coagulation. Rickettsia are are arthropod-borne gram-negative coccobacilli bacteria and are obligate intracellular organisms that do not survive in artificial medium. In North and South America, the most common rickettsial disorder is rocky mountain spotted fever (RMSF) transmitted by the dog tick Dermacentor variabilis or the wood tick Dermacentor andersoni. A characteristic “starry sky” pattern can be seen on MRI imaging of the brain in some patients with RMSF encephalopathy and is thought to reflect the organisms targeting of brain endothelial cells in capillaries the white matter. Early treatment with doxycycline is curative and reverses signs of encephalopathy if given within a few day of onset, but delayed treatment can be associated with permanent neurological disability. The typhus group of rickettsia bacteria include R. prowazekii, which causes epidemic typhus and R. typhi, which causes murine typhus (endemic) typhus in tropical and subtropical parts of the world. Flying squirrels and humans carry R prowazekii and rats are carry R. typhi. Q fever caused by the rickettsia organism Coxiella burnetti is transmitted from farm animals including sheep and is seen throughout the world including the United States.
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Birtles, Richard. Other bacterial diseasesAnaplasmosis, ehrlichiosis and neorickettsiosis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0020.
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In 2001, taxonomic reorganization of the bacterial genera Anaplasma, Ehrlichia, Cowdria and Neorickettsia resulted in the transfer of numerous species between these taxa, and the renaming of the transferred species to reflect their new taxonomic position (Dumler et al. 2001). Among the members of these genera, there are four species of established zoonotic importance, which are therefore the subject of this chapter. Two of these species were affected by the changes outlined above.Although these four species possess markedly different ecologies, they share the fundamental biological character of being obligate intracellular bacteria that reside within vacuoles of eukaryotic cells. This lifestyle underlies their fastidious nature in the laboratory and hence our limited knowledge of their biology and pathogenicity. Nonetheless, despite this shortfall, all four are associated with diseases of established or emerging importance: E. chaffeensis provokes human monocytic ehrlichiosis (HME), E. ewingii causes human ewingii ehrlichiosis (HEE), A. phagocytophilum causes human granulocytic anaplasmosis (HGA), N. sennetsu is the agent of sennetsu neorickettsiosis.The first three pathogens are transmitted by hard (ixodid) ticks and are encountered across the temperate zones of the northern hemisphere (and maybe beyond), although the vast majority of human infections caused by them are currently reported in the USA. There, HME and HGA are second only to Lyme disease (caused by Borrelia burgdorferi) in terms of public health significance. Furthermore, given that there is evidence of increasing population sizes and changing distributions for ixodid species (Scharlemann et al. 2008), it is not unreasonable to predict that the infections they transmit will present an increased medical burden in the future. N. sennetsu remains an enigmatic pathogen; case reports remain scarce, but serological surveys suggest high levels of exposure. The widespread consumption of raw fish across east Asia presents specific infection risks to this region, and an increased awareness that sennetsu neorickettsiosis is among the infections that can be acquired from this source is required before its public health importance can be accurately assessed.
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Sillis, Margaret, and David Longbottom. Chlamydiosis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0017.
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Chlamydial pathogens cause a wide-range of infections and disease, known as chlamydioses, in humans, other mammals and birds. The causative organisms are Gram-negative obligate intracellular bacteria that undergo a unique biphasic developmental cycle involving the infectious elementary body and the metabolically-active, non-infectious reticulate body. At least two species, Chlamydophila psittaci and Chlamydophila abortus, are recognized as causes of zoonotic infections in humans worldwide, mainly affecting persons exposed to infected psittacine and other birds, especially ducks, turkeys, and pigeons, and less commonly to animals, particularly sheep. Outbreaks occur amongst aviary workers, poultry processing workers, and veterinarians. Infection is transmitted through inhalation of infected aerosols contaminated by avian droppings, nasal discharges, or products of ovine gestation or abortion. Person to person transmission is rare. Control strategies have met with variable success depending on the degree of compliance or enforcement of legislation. In the United Kingdom control is secondary, resulting from protection of national poultry flocks by preventing the importation of Newcastle disease virus using quarantine measures. Improved standards of husbandry, transport conditions, and chemoprophylaxis are useful for controlling reactivation of latent avian chlamydial infection. Vaccination has had limited effect in controlling ovine infection. Improved education of persons in occupational risk groups and the requirement for notification may encourage a more energetic approach to its control.
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Burdmann, Emmanuel A., and Vivekanad Jha. Rickettsiosis. Edited by Vivekanand Jha. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0193.
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Rickettsiae are obligate intracellular bacteria transmitted by arthropods to a vertebrate host. Clinically relevant rickettsioses have a similar clinical pattern, manifesting as an acute febrile disease accompanied by headache, articular and muscle pain, and malaise.Epidemic typhus is a worldwide distributed disease caused by the Rickettsia prowazekii, with a human louse as a vector. Data on epidemic typhus-related renal injury is extremely scarce.Murine typhus is caused by the Rickettsia typhi and has a rodent flea as the vector. It is one of the most frequent rickettsioses, and is usually a self-limited febrile illness. Proteinuria, haematuria, elevations in serum creatinine (SCr) and/or blood urea nitrogen (BUN) and AKI have been reported. The real frequency of renal involvement in murine typhus is unknown. Renal abnormalities recover after the infectious disease resolution.Scrub typhus, caused by the Orientia tsutsugamushi, has the Leptotrombidium mite larva as vector. It is endemic in the Tsutsugamushi triangle delimited by Japan, Australia, India, and Siberia. It can manifest either as a self-limiting disease or as a severe, life-threatening multiorgan illness. Early administration of adequate antibiotics is essential to prevent adverse outcomes. Proteinuria, haematuria, and acute kidney injury (AKI) are frequent.Tick-borne rickettsioses are caused by bacteria from the spotted fever group and have ticks as vectors. Rocky Mountain spotted fever (RMSF) is caused by Rickettsia rickettsii. It is the most severe of the spotted fever rickettsial diseases, causing significant morbidity and lethality. RMSF occurs in North, Central, and South America. Renal impairment is frequent in severe forms of RMSF. Mediterranean spotted fever is caused by Rickettsia conorii, and is endemic in the Mediterranean area. It is usually a benign disease, but may have a severe course, clinically similar to RMSF. Haematuria, proteinuria, increased serum creatinine, and AKI may occur. Japanese spotted fever is caused by Rickettsia japonica. Lethal cases are reported yearly and AKI has occurred in the context of multiple organ failure.
Book chapters on the topic "Obligate intracellular bacteria"
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Nguyen, Bidong, and Raphael Valdivia. "A Chemical Mutagenesis Approach to Identify Virulence Determinants in the Obligate Intracellular Pathogen Chlamydia trachomatis." In Host-Bacteria Interactions, 347–58. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1261-2_20.
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Dumler, J. Stephen. "General Approaches to Identification of Mycoplasma , Ureaplasma , and Obligate Intracellular Bacteria." In Manual of Clinical Microbiology, 1082–87. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555817381.ch61.
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Parola, Philippe, and Didier Raoult. "Rickettsioses." In Oxford Textbook of Medicine, 903–19. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.070639.
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Rickettsioses are zoonoses caused by obligate Gram-negative intracellular bacteria of the order Rickettsiales, comprising (1) rickettsioses due to bacteria of the genus Rickettsia, including spotted fever groups and typhus groups (Rickettsiaceae), (2) ehrlichioses and anaplasmoses due to bacteria of the Anaplasmataceae, and (3) scrub typhus due to ...
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"Chlamydia." In Oxford Handbook of Genitourinary Medicine, HIV, and Sexual Health, edited by Laura Mitchell, Bridie Howe, D. Ashley Price, Babiker Elawad, and K. Nathan Sankar, 149–60. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198783497.003.0009.
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Chlamydia trachomatis is a sexually transmitted infection caused by an obligate intracellular bacteria. It is the most common bacterial STI in the UK, with highest prevalence among 16–25-year-olds, with incidence rates up to 10%. Public health campaigns like the Chlamydia Screening Programme in the UK, have helped to increase testing rates within this age group. Concordance of infection between couples is 75%, reduced to 40% by consistent condom use. This chapter discusses aetiology, epidemiology, clinical features, diagnostics, and management of adults with anogenital and extragenital chlamydia. Partner notification is a key part of management. Management in pregnancy and neonates is also included.
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"General Approaches to Identification of Mycoplasma, Ureaplasma, and Obligate Intracellular Bacteria." In Manual of Clinical Microbiology, 10th Edition, 964–69. American Society of Microbiology, 2011. http://dx.doi.org/10.1128/9781555816728.ch58.
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Griffiths, Karolina, Carole Eldin, Didier Raoult, and Philippe Parola. "Rickettsioses." In Oxford Textbook of Medicine, edited by Christopher P. Conlon, 1230–51. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0144.
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Rickettsioses are mild to life-threatening zoonoses caused by obligate intracellular bacteria of the order Rickettsiales (family Rickettsiaceae). Arthropods, including ticks, fleas, and mites, are implicated as their vectors, reservoirs, or amplifiers. With an increasing number of new pathogens and recognition of new pathogenicity and affected geographical areas over the past few decades, there is a better understanding of the scope and importance of these pathogens, particularly as a paradigm to understanding emerging and remerging infections. The taxonomy has undergone numerous changes, with now three main groups classified as rickettsioses according to morphological, antigenic and metabolic characteristics: (1) Rickettsioses due to the bacteria of the genus Rickettsia, including the spotted fever group, typhus groups (Rickettsiaceae), (2) Ehrlichioses and Anaplasmoses due to bacteria of the Anaplasmataceae and (3) scrub typhus due to Orientia tsutsugamushi.
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Paris, Daniel H., and Nicholas P. J. Day. "Scrub typhus." In Oxford Textbook of Medicine, edited by Christopher P. Conlon, 1252–57. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0145.
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Orientia spp. are obligate intracellular Gram-negative bacteria that cause scrub typhus, historically known as ‘tsutsugamushi disease’, a febrile illness characterized by early non-specific ‘flu-like’ symptoms, and sometimes a diffuse, macular, or maculopapular rash and/or a necrotic lesion eschar at the inoculation site. Leptotrombidium mites transmit Orientia spp. to humans via the bite of the larval stage, while all mite stages act as bacterial reservoirs through vertical transovarial and transstadial transmission. Scrub typhus is a leading cause of treatable undifferentiated febrile illness in many regions of Asia, and unfortunately remains an underappreciated neglected disease, mainly due to diagnostic difficulties and lack of awareness among medical staff. Complications include meningo-encephalitis, respiratory and renal failure, and severe multiorgan failure. Scrub typhus can be treated effectively with tetracyclines, macrolides, and chloramphenicol. Humans are dead-end hosts and do not participate in the Orientia life cycle, hence treatment does not affect overall disease incidence.
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Jeffery-Smith, Anna, and C. Y. William Tong. "The Biology of Viruses." In Tutorial Topics in Infection for the Combined Infection Training Programme. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198801740.003.0008.
Full textAbstract:
In order to be classified as a virus, certain criteria have to be fulfilled. Viruses must ● Be only capable of growth and multiplication within living cells, i.e. obligate intracellular parasite. Host cells could include humans, animals, insects, plants, protozoa, or even bacteria. ● Have a nucleic acid genome (either RNA or DNA, but not both) surrounded by a protein coat (capsid). ● Have no semipermeable membrane, though some have an envelope formed of phospholipids and proteins. ● Be inert outside of the host cell. Enveloped viruses are susceptible to inactivation by organic solvents such as alcohol. ● Perform replication by independent synthesis of components followed by assembly (c.f. binary fission in bacteria). Viruses are considered as a bundle of genetic programmes encoded in nucleic acids and packaged with a capsid +/ - envelope protein, which can be activated on entry into a host cell (compare this with computer viruses packaged in an enticing way in order to infect and take over control of your PC). Although they share some similarities in their properties, mycoplasma and chlamydia are true bacteria. The virion (assembled infectious particle) consists of viral nucleic acid and capsid. The nucleic acid of a virus can either be ribonucleic acid (RNA) or deoxyribonucleic acid (DNA), and the amount of genetic material varies widely, with some viruses able to encode a few proteins and others having genetic material that encodes hundreds of proteins. In association with the nucleic acid there may be non- structural viral proteins, such as a viral polymerase. The nucleic acid and non- structural proteins are protected by a surrounding layer of capsid proteins. The capsid includes proteins which can attach to host cell receptors. The proteins and the cell receptors to which they bind determine a virus’ tropism, i.e., the ability to bind to and enter different cell types. The term nucleocapsid refers to the nucleic acid core surrounded by capsid protein. Some viruses also have an envelope made up of phospholipids and proteins surrounding the nucleocapsid. This envelope can be formed by the host cell membrane during the process of a virus budding from a cell during replication.
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William Tong, C. Y. "Antivirals." In Tutorial Topics in Infection for the Combined Infection Training Programme. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198801740.003.0059.
Full textAbstract:
Viruses are obligate intracellular pathogens that utilize many of the host metabolic machineries for reproduction. Unlike the binary fission of bacteria, the replication process of viruses is more like a production line with a final assembly process to produce their progenies. Any agents used to prevent viral replication must be specific to the virus and cause as little problem for the host as possible. The rate of virus replication can also cause problems. In rapidly reproducing viruses, the high replication rate generates mutants that could be selected for resistance to antivirals. On the other hand, viruses could remain latent with little metabolic activity. None of the current antivirals are effective against latent viruses. The life cycle of a typical virus goes through the following stages: ● Attachment; ● Entry and uncoating; ● Replication of viral nucleic acid; ● Establishing latency or persistent infection (in some viruses); ● Translation of viral protein and post-translational modifications; ● Secretion and assembly of viral particles; and ● Release from host cells. Each of these steps can be used as antiviral targets. The most common strategy is to use a nucleoside analogue as a false substrate. However, such a false substrate can also be taken up by host polymerase and could result in toxicity, e.g. mitochondrial toxicity in some of the earlier antiretroviral drugs. The most successful example to circumvent this problem is aciclovir, which is the prodrug of the active agent aciclovir tri-phosphate. Aciclovir is a substrate for the viral enzyme thymidine kinase carried by the herpes simplex virus (HSV) and varicella-zoster virus (VZV), which converts it into aciclovir monophosphate. As this only happens inside cells infected by HSV or VZV, it is concentrated only in infected cells. Host enzymes then add further phosphates to form the active agent aciclovir triphosphate, which has a higher affinity to viral polymerase than host polymerase. It acts as a false substrate for the viral polymerase and results in premature termination of nucleic acid replication. A similar mechanism is utilized in ganciclovir against cytomegalovirus (CMV). The viral phosphate kinase involved in the case of CMV is the UL97 protein.