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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 -
Frontiers in Cellular and Infection... 2022HIF1α is an important transcription factor regulating not only cellular responses to hypoxia, but also anti-infective defense responses. We recently showed that HIF1α...
HIF1α is an important transcription factor regulating not only cellular responses to hypoxia, but also anti-infective defense responses. We recently showed that HIF1α hampers replication of the obligate intracellular pathogen which causes the zoonotic disease Q fever. Prior to development of chronic Q fever, it is assumed that the bacteria enter a persistent state. As HIF1α and/or hypoxia might be involved in the induction of persistence, we analyzed the role of HIF1α and hypoxia in the interaction of macrophages with to understand how the bacteria manipulate HIF1α stability and activity. We demonstrate that a -infection initially induces HIF1α stabilization, which decreases then over the course of an infection. This reduction depends on bacterial viability and a functional type IV secretion system (T4SS). While neither the responsible T4SS effector protein(s) nor the molecular mechanism leading to this partial HIF1α destabilization have been identified, our results demonstrate that influences the expression of HIF1α target genes in multiple ways. Therefore, a infection promotes HIF1α-mediated upregulation of several metabolic target genes; affects apoptosis-regulators towards a more pro-apoptotic signature; and under hypoxic conditions, shifts the ratio of the inflammatory genes analyzed towards a pro-inflammatory profile. Taken together, modulates HIF1α in a still elusive manner and alters the expression of multiple HIF1α target genes.
Topics: Coxiella burnetii; Gene Expression; Host-Pathogen Interactions; Humans; Hypoxia; Q Fever; Type IV Secretion Systems
PubMed: 35755850
DOI: 10.3389/fcimb.2022.867689 -
The American Journal of Tropical... Aug 2022
Topics: Coxiella burnetii; Humans; Q Fever
PubMed: 35977719
DOI: 10.4269/ajtmh.22-0372 -
Microbes and Infection Apr 2020Coxiella burnetii is an intracellular bacterium that causes acute and chronic Q fever. This unique pathogen has been historically challenging to study due to obstacles... (Review)
Review
Coxiella burnetii is an intracellular bacterium that causes acute and chronic Q fever. This unique pathogen has been historically challenging to study due to obstacles in genetically manipulating the organism and the inability of small animal models to fully mimic human Q fever. Here, we review the current state of C. burnetii research, highlighting new approaches that allow the mechanistic study of infection in disease relevant settings.
Topics: Animals; Coxiella burnetii; Cytoplasm; Disease Models, Animal; Global Health; Humans; Macrophages; Q Fever
PubMed: 31574310
DOI: 10.1016/j.micinf.2019.09.001 -
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 -
BMC Veterinary Research Jul 2022Q fever is one of the most important zoonotic diseases caused by Coxiella burnetii. Although Q fever is an endemic disease in Iran, epidemiological data on C. burnetii...
BACKGROUND
Q fever is one of the most important zoonotic diseases caused by Coxiella burnetii. Although Q fever is an endemic disease in Iran, epidemiological data on C. burnetii infection are not yet complete in reservoirs and vectors in some parts of Iran. This survey investigated C. burnetii infection in small ruminants (sheep and goat blood samples) and their ticks in western Iran (Kurdistan province) in 2020. The presence of C. burnetii DNA was identified in these samples by targeting the IS1111 gene using the quantitative PCR (qPCR) method.
RESULTS
Out of 250 blood samples (232 sheep and 18 goats), C. burnetii was detected in two samples (0.8%) belonging to the sheep (0.9%). In addition, 34 of 244 collected ticks (13.9%) from infested animals (244) were positive for C. burnetii infection. The highest prevalence of infection was found in Dermacentor marginatus (18.3%) and Haemaphysalis concinna (12.5%).
CONCLUSIONS
The present study showed that ticks could have a possible role in the epidemiology of Q fever in Iran.
Topics: Animals; Coxiella burnetii; Goat Diseases; Goats; Iran; Q Fever; Ruminants; Sheep; Sheep Diseases; Ticks
PubMed: 35902914
DOI: 10.1186/s12917-022-03396-0 -
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 -
Clinical Microbiology Reviews Oct 1999Q fever is a zoonosis with a worldwide distribution with the exception of New Zealand. The disease is caused by Coxiella burnetii, a strictly intracellular,... (Review)
Review
Q fever is a zoonosis with a worldwide distribution with the exception of New Zealand. The disease is caused by Coxiella burnetii, a strictly intracellular, gram-negative bacterium. Many species of mammals, birds, and ticks are reservoirs of C. burnetii in nature. C. burnetii infection is most often latent in animals, with persistent shedding of bacteria into the environment. However, in females intermittent high-level shedding occurs at the time of parturition, with millions of bacteria being released per gram of placenta. Humans are usually infected by contaminated aerosols from domestic animals, particularly after contact with parturient females and their birth products. Although often asymptomatic, Q fever may manifest in humans as an acute disease (mainly as a self-limited febrile illness, pneumonia, or hepatitis) or as a chronic disease (mainly endocarditis), especially in patients with previous valvulopathy and to a lesser extent in immunocompromised hosts and in pregnant women. Specific diagnosis of Q fever remains based upon serology. Immunoglobulin M (IgM) and IgG antiphase II antibodies are detected 2 to 3 weeks after infection with C. burnetii, whereas the presence of IgG antiphase I C. burnetii antibodies at titers of >/=1:800 by microimmunofluorescence is indicative of chronic Q fever. The tetracyclines are still considered the mainstay of antibiotic therapy of acute Q fever, whereas antibiotic combinations administered over prolonged periods are necessary to prevent relapses in Q fever endocarditis patients. Although the protective role of Q fever vaccination with whole-cell extracts has been established, the population which should be primarily vaccinated remains to be clearly identified. Vaccination should probably be considered in the population at high risk for Q fever endocarditis.
Topics: Animals; Bacterial Vaccines; Coxiella burnetii; Female; Humans; Incidence; Pregnancy; Q Fever
PubMed: 10515901
DOI: 10.1128/CMR.12.4.518 -
International Journal of Molecular... Jan 2023Infection by , the etiological agent of Q fever, poses the risk of causing severe obstetrical complications in pregnant women. is known for its placental tropism based...
Infection by , the etiological agent of Q fever, poses the risk of causing severe obstetrical complications in pregnant women. is known for its placental tropism based on animal models of infection. The Nine Mile strain has been mostly used to study pathogenicity but the contribution of human isolates to pathogenicity is poorly understood. In this study, we compared five isolates from human placentas with strains including Nine Mile (NM) as reference. Comparative genomic analysis revealed that the Cb122 isolate was distinct from other placental isolates and the NM strain with a set of unique genes involved in energy generation and a type 1 secretion system. The infection of Balb/C mice with the Cb122 isolate showed higher virulence than that of NM or other placental isolates. We evaluated the pathogenicity of the Cb122 isolate by in vitro and ex vivo experiments. As is known to infect and survive within macrophages, we isolated monocytes and placental macrophages from healthy donors and infected them with the Cb122 isolate and the reference strain. We showed that bacteria from the Cb122 isolate were less internalized by monocyte-derived macrophages (MDM) than NM bacteria but the reference strain and the Cb122 isolate were similarly internalized by placental macrophages. The Cb122 isolate and the reference strain survived similarly in the two macrophage types. While the Cb122 isolate and the NM strain stimulated a poorly inflammatory program in MDM, they elicited an inflammatory program in placenta macrophages. We also reported that the Cb122 isolate and NM strain were internalized by trophoblastic cell lines and primary trophoblasts without specific replicative profiles. Placental explants were then infected with the Cb122 isolate and the NM strain. The bacteria from the Cb122 isolate were enriched in the chorionic villous foetal side. It is likely that the Cb122 isolate exhibited increased virulence in the multicellular environment provided by explants. Taken together, these results showed that the placental isolate of exhibits a specific infectious profile but its pathogenic role is not as high as the host immune response in pregnant women.
Topics: Animals; Mice; Female; Humans; Pregnancy; Coxiella burnetii; Placenta; Q Fever; Macrophages; Trophoblasts
PubMed: 36674725
DOI: 10.3390/ijms24021209