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Clinical Microbiology Reviews Jan 2017Coxiella burnetii is the agent of Q fever, or "query fever," a zoonosis first described in Australia in 1937. Since this first description, knowledge about this pathogen... (Review)
Review
Coxiella burnetii is the agent of Q fever, or "query fever," a zoonosis first described in Australia in 1937. Since this first description, knowledge about this pathogen and its associated infections has increased dramatically. We review here all the progress made over the last 20 years on this topic. C. burnetii is classically a strict intracellular, Gram-negative bacterium. However, a major step in the characterization of this pathogen was achieved by the establishment of its axenic culture. C. burnetii infects a wide range of animals, from arthropods to humans. The genetic determinants of virulence are now better known, thanks to the achievement of determining the genome sequences of several strains of this species and comparative genomic analyses. Q fever can be found worldwide, but the epidemiological features of this disease vary according to the geographic area considered, including situations where it is endemic or hyperendemic, and the occurrence of large epidemic outbreaks. In recent years, a major breakthrough in the understanding of the natural history of human infection with C. burnetii was the breaking of the old dichotomy between "acute" and "chronic" Q fever. The clinical presentation of C. burnetii infection depends on both the virulence of the infecting C. burnetii strain and specific risks factors in the infected patient. Moreover, no persistent infection can exist without a focus of infection. This paradigm change should allow better diagnosis and management of primary infection and long-term complications in patients with C. burnetii infection.
Topics: Animals; Coxiella burnetii; Genome, Bacterial; Humans; Q Fever; Virulence; Zoonoses
PubMed: 27856520
DOI: 10.1128/CMR.00045-16 -
The American Journal of Tropical... Aug 2022
Topics: Coxiella burnetii; Humans; Q Fever
PubMed: 35977719
DOI: 10.4269/ajtmh.22-0372 -
Frontiers in Cellular and Infection... 2022is an obligate hematophagous parasitic arthropod that is responsible for the transmission of a wide range of zoonotic pathogens including spirochetes of the genus... (Review)
Review
is an obligate hematophagous parasitic arthropod that is responsible for the transmission of a wide range of zoonotic pathogens including spirochetes of the genus spp., , and , which are part the tick´s microbiome. Most of the studies focus on "pathogens" and only very few elucidate the role of "non-pathogenic" symbiotic microorganisms in . While most of the members of the microbiome are leading an intracellular lifestyle, they are able to complement tick´s nutrition and stress response having a great impact on tick´s survival and transmission of pathogens. The composition of the tick´s microbiome is not consistent and can be tied to the environment, tick species, developmental stage, or specific organ or tissue. Ovarian tissue harbors a stable microbiome consisting mainly but not exclusively of endosymbiotic bacteria, while the microbiome of the digestive system is rather unstable, and together with salivary glands, is mostly comprised of pathogens. The most prevalent endosymbionts found in ticks are spp., spp., -like and -like endosymbionts, spp. and Midichloria spp. Since microorganisms can modify ticks' behavior, such as mobility, feeding or saliva production, which results in increased survival rates, we aimed to elucidate the potential, tight relationship, and interaction between bacteria of the microbiome. Here we show that endosymbionts including -like spp., can provide with different types of vitamin B (B2, B6, B7, B9) essential for eukaryotic organisms. Furthermore, we hypothesize that survival of spp., or the bacterial pathogen can be supported by the tick itself since coinfection with symbiotic provides with complete metabolic pathway of folate biosynthesis necessary for DNA synthesis and cell division. Manipulation of tick´s endosymbiotic microbiome could present a perspective way of control and regulation of spread of emerging bacterial pathogens.
Topics: Animals; Ixodes; Microbiota; Coxiella; Symbiosis; Rickettsia; Francisella tularensis
PubMed: 36467722
DOI: 10.3389/fcimb.2022.990889 -
Frontiers in Cellular and Infection... 2023Obligate intracellular pathogens occupy one of two niches - free in the host cell cytoplasm or confined in a membrane-bound vacuole. Pathogens occupying membrane-bound... (Review)
Review
Obligate intracellular pathogens occupy one of two niches - free in the host cell cytoplasm or confined in a membrane-bound vacuole. Pathogens occupying membrane-bound vacuoles are sequestered from the innate immune system and have an extra layer of protection from antimicrobial drugs. However, this lifestyle presents several challenges. First, the bacteria must obtain membrane or membrane components to support vacuole expansion and provide space for the increasing bacteria numbers during the log phase of replication. Second, the vacuole microenvironment must be suitable for the unique metabolic needs of the pathogen. Third, as most obligate intracellular bacterial pathogens have undergone genomic reduction and are not capable of full metabolic independence, the bacteria must have mechanisms to obtain essential nutrients and resources from the host cell. Finally, because they are separated from the host cell by the vacuole membrane, the bacteria must possess mechanisms to manipulate the host cell, typically through a specialized secretion system which crosses the vacuole membrane. While there are common themes, each bacterial pathogen utilizes unique approach to establishing and maintaining their intracellular niches. In this review, we focus on the vacuole-bound intracellular niches of , and .
Topics: Vacuoles; Coxiella burnetii; Anaplasma phagocytophilum; Chlamydia trachomatis; Ehrlichia chaffeensis
PubMed: 37645379
DOI: 10.3389/fcimb.2023.1206037 -
Canadian Journal of Microbiology Feb 2016Q fever is a zoonosis of worldwide distribution with the exception of New Zealand. It is caused by an intracellular bacterium, Coxiella burnetii. The disease often goes... (Review)
Review
Q fever is a zoonosis of worldwide distribution with the exception of New Zealand. It is caused by an intracellular bacterium, Coxiella burnetii. The disease often goes underdiagnosed because the main manifestation of its acute form is a general self-limiting flu-like syndrome. The Dutch epidemics renewed attention to this disease, which was less considered before. This review summarizes the description of C. burnetii (taxonomy, intracellular cycle, and genome) and Q fever disease (description, diagnosis, epidemiology, and pathogenesis). Finally, vaccination in humans and animals is also considered.
Topics: Animals; Coxiella burnetii; Humans; Q Fever; Vaccination
PubMed: 26730641
DOI: 10.1139/cjm-2015-0551 -
Genome Biology and Evolution Jul 2021Both symbiotic and pathogenic bacteria in the family Coxiellaceae cause morbidity and mortality in humans and animals. For instance, Coxiella-like endosymbionts (CLEs)...
Both symbiotic and pathogenic bacteria in the family Coxiellaceae cause morbidity and mortality in humans and animals. For instance, Coxiella-like endosymbionts (CLEs) improve the reproductive success of ticks-a major disease vector, while Coxiella burnetii causes human Q fever, and uncharacterized coxiellae infect both animals and humans. To better understand the evolution of pathogenesis and symbiosis in this group of intracellular bacteria, we sequenced the genome of a CLE present in the soft tick Ornithodoros amblus (CLEOA) and compared it to the genomes of other bacteria in the order Legionellales. Our analyses confirmed that CLEOA is more closely related to C. burnetii, the human pathogen, than to CLEs in hard ticks, and showed that most clades of CLEs contain both endosymbionts and pathogens, indicating that several CLE lineages have evolved independently from pathogenic Coxiella. We also determined that the last common ancestorof CLEOA and C. burnetii was equipped to infect macrophages and that even though horizontal gene transfer (HGT) contributed significantly to the evolution of C. burnetii, most acquisition events occurred primarily in ancestors predating the CLEOA-C. burnetii divergence. These discoveries clarify the evolution of C. burnetii, which previously was assumed to have emerged when an avirulent tick endosymbiont recently gained virulence factors via HGT. Finally, we identified several metabolic pathways, including heme biosynthesis, that are likely critical to the intracellular growth of the human pathogen but not the tick symbiont, and show that the use of heme analog is a promising approach to controlling C. burnetii infections.
Topics: Animals; Argasidae; Coxiella; Coxiella burnetii; Symbiosis; Ticks
PubMed: 34009306
DOI: 10.1093/gbe/evab108 -
Microbiology Spectrum Feb 2016Intracellular bacterial pathogens have evolved to exploit the protected niche provided within the boundaries of a eukaryotic host cell. Upon entering a host cell, some... (Review)
Review
Intracellular bacterial pathogens have evolved to exploit the protected niche provided within the boundaries of a eukaryotic host cell. Upon entering a host cell, some bacteria can evade the adaptive immune response of its host and replicate in a relatively nutrient-rich environment devoid of competition from other host flora. Growth within a host cell is not without their hazards, however. Many pathogens enter their hosts through receptor-mediated endocytosis or phagocytosis, two intracellular trafficking pathways that terminate in a highly degradative organelle, the phagolysosome. This usually deadly compartment is maintained at a low pH and contains degradative enzymes and reactive oxygen species, resulting in an environment to which few bacterial species are adapted. Some intracellular pathogens, such as Shigella, Listeria, Francisella, and Rickettsia, escape the phagosome to replicate within the cytosol of the host cell. Bacteria that remain within a vacuole either alter the trafficking of their initial phagosomal compartment or adapt to survive within the harsh environment it will soon become. In this chapter, we focus on the mechanisms by which different vacuolar pathogens either evade lysosomal fusion, as in the case of Mycobacterium and Chlamydia, or allow interaction with lysosomes to varying degrees, such as Brucella and Coxiella, and their specific adaptations to inhabit a replicative niche.
Topics: Adaptation, Psychological; Animals; Bacteria; Bacterial Infections; Bacterial Physiological Phenomena; Brucella; Chlamydia; Coxiella; Eukaryotic Cells; Humans; Lysosomes; Mycobacterium
PubMed: 26999394
DOI: 10.1128/microbiolspec.VMBF-0014-2015 -
Frontiers in Cellular and Infection... 2022is a zoonotic pathogen responsible for the human disease Q fever. While an inactivated whole cell vaccine exists for this disease, its widespread use is precluded by a... (Review)
Review
is a zoonotic pathogen responsible for the human disease Q fever. While an inactivated whole cell vaccine exists for this disease, its widespread use is precluded by a post vaccination hypersensitivity response. Efforts for the development of an improved Q fever vaccine are intricately connected to the availability of appropriate animal models of human disease. Accordingly, small mammals and non-human primates have been utilized for vaccine-challenge and post vaccination hypersensitivity modeling. Here, we review the animal models historically utilized in Q fever vaccine development, describe recent advances in this area, discuss the limitations and strengths of these models, and summarize the needs and criteria for future modeling efforts. In summary, while many useful models for Q fever vaccine development exist, there remains room for growth and expansion of these models which will in turn increase our understanding of host interactions.
Topics: Animals; Bacterial Vaccines; Coxiella burnetii; Mammals; Models, Animal; Q Fever; Vaccine Development
PubMed: 35223553
DOI: 10.3389/fcimb.2022.828784 -
Annals of Agricultural and... 2013Q fever is an infectious disease of humans and animals caused by Gram-negative coccobacillus Coxiella burnetii, belonging to the Legionellales order, Coxiellaceae... (Review)
Review
Q fever is an infectious disease of humans and animals caused by Gram-negative coccobacillus Coxiella burnetii, belonging to the Legionellales order, Coxiellaceae family. The presented study compares selected features of the bacteria genome, including chromosome and plasmids QpH1, QpRS, QpDG and QpDV. The pathomechanism of infection--starting from internalization of the bacteria to its release from infected cell are thoroughly described. The drugs of choice for the treatment of acute Q fever are tetracyclines, macrolides and quinolones. Some other antimicrobials are also active against C. burnetii, namely, telitromycines and tigecyclines (glicylcycline). Q-VAX vaccine induces strong and long-term immunity in humans. Coxevac vaccine for goat and sheep can reduce the number of infections and abortions, as well as decrease the environmental transmission of the pathogen. Using the microarrays technique, about 50 proteins has been identified which could be used in the future for the production of vaccine against Q fever. The routine method of C. burnetii culture is proliferation within cell lines; however, an artificial culture medium has recently been developed. The growth of bacteria in a reduced oxygen (2.5%) atmosphere was obtained after just 6 days. In serology, using the IF method as positive titers, the IgM antibody level >1:64 and IgG antibody level >1:256 (against II phase antigens) has been considered. In molecular diagnostics of C. burnetii infection, the most frequently used method is PCR and its modifications; namely, nested PCR and real time PCR which detect target sequences, such as htpAB and IS1111, chromosome genes (com1), genes specific for different types of plasmids and transposase genes. Although Q fever was diagnosed in Poland in 1956, the data about the occurrence of the disease are incomplete. Comprehensive studies on the current status of Q fever in Poland, with special focus on pathogen reservoirs and vectors, the sources of infection and molecular characteristics of bacteria should be conducted.
Topics: Animals; Anti-Bacterial Agents; Antibodies, Bacterial; Bacterial Vaccines; Coxiella burnetii; Genome, Bacterial; Humans; Livestock; Plasmids; Poland; Polymerase Chain Reaction; Q Fever
PubMed: 23772566
DOI: No ID Found -
Frontiers in Cellular and Infection... 2017Cholesterol is a multifunctional lipid that plays important metabolic and structural roles in the eukaryotic cell. Despite having diverse lifestyles, the obligate... (Review)
Review
Cholesterol is a multifunctional lipid that plays important metabolic and structural roles in the eukaryotic cell. Despite having diverse lifestyles, the obligate intracellular bacterial pathogens all target cholesterol during host cell colonization as a potential source of membrane, as well as a means to manipulate host cell signaling and trafficking. To promote host cell entry, these pathogens utilize cholesterol-rich microdomains known as lipid rafts, which serve as organizational and functional platforms for host signaling pathways involved in phagocytosis. Once a pathogen gains entrance to the intracellular space, it can manipulate host cholesterol trafficking pathways to access nutrient-rich vesicles or acquire membrane components for the bacteria or bacteria-containing vacuole. To acquire cholesterol, these pathogens specifically target host cholesterol metabolism, uptake, efflux, and storage. In this review, we examine the strategies obligate intracellular bacterial pathogens employ to manipulate cholesterol during host cell colonization. Understanding how obligate intracellular pathogens target and use host cholesterol provides critical insight into the host-pathogen relationship.
Topics: Anaplasma; Bacteria; Biological Transport; Chlamydia; Cholesterol; Coxiella; Cytoplasm; Ehrlichia; Eukaryotic Cells; Host-Pathogen Interactions; Humans; Lipid Droplets; Membrane Microdomains; Phagocytosis; Rickettsia; Vacuoles
PubMed: 28529926
DOI: 10.3389/fcimb.2017.00165