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PubMed1989

[The effect of serial passage of Coxiella burnetii in chick embryos on pathogen phase variability].

Coxiella burnetii has been investigated in different egg passages (EP-17, 163). Coxiella in EP 163 was completely eliminated from the suspension during the purification but not that in EP 17. It means that the coxiella of the two EP with a seroreaction of phase II are different, and phase II positivity of EP 17 can't be the result of presence of two populations in the suspension or of one mutation during the multiplication in yolk sacs but of a change on the surface of C. burnetii.

Animals↗
PubMed1998

Antigenic characteristic of the lipopolysaccharides of Coxiella burnetii isolates.

Lipopolysaccharides (LPSs) of 8 isolates of Coxiella burnetii from a variety of clinical and geographical sources could be divided into four groups based on molecular heterogeneity in silver-stained sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) profiles in the region of the 10 to 17 kDa. The lipopolysaccharide of group 1 was identified on isolates from acute Q fever patient, milk and tick. The three remaining groups were primarily found on isolates from human cases of chronic Q fever. These LPSs shared many antigenic epitopes, as determined by immunoblotting with mouse anti-C. burnetii antisera.

Animals↗
PubMed1985

Electron microscopic studies of lipopolysaccharides from phase I and phase II Coxiella burnetii.

Lipopolysaccharides from phase I (LPSI) Coxiella burnetii Ohio and Nine Mile strains and from phase II (LPSII) Nine Mile stain were negatively and positively and examined with the electron microscope. The ultrastructure of LPSI and LPSII positively stained with uranyl formate or uranyl acetate was ribbon-like. When negatively stained with uranyl acetate, LPSI was ribbon-like but LPSII exhibited hexagonal lattice structures. However, LPSII stained negatively with sodium phosphotungstate and ammonium molybdate exhibited hexagonal lattice ultrastructures which were not identical to those observed when negatively stained with uranyl acetate. The hexagonal lattice structures formed in vitro were due to the interactions of LPSII and the staining reagents rather than to protein-LPS interactions. The differences in the ultrastructures of LPSI and LPSII are undoubtedly based on variations in their chemical composition.

Coxiella↗
PubMed1993

Spread and distribution of Coxiella burnetii in C57BL/6J (H-2b) and Balb/cJ (H-2d) mice after intraperitoneal infection.

Spread and distribution of Coxiella burnetii were investigated immunocytochemically and antigen dissemination was correlated with light microscopic alterations in Balb/cJ (H-2d) and C57BL/6J (H-2b) mice. Intraperitoneal inoculation of C. burnetii resulted in a self-limiting systemic infection. Gross findings consisted of hepatosplenomegaly and histological lesions were characterized by microabscesses and granulomas in numerous organs including spleen, liver, mesentery, bone marrow, lymph nodes, pancreas, heart and uterus. In addition, splenic lymphoid depletion, venous microthrombi and reduction of bone marrow cells were observed. Coxiella burnetii antigen was demonstrated immunocytochemically in the aforementioned organs, especially in spleen, liver and most of all in the bone marrow. Coxiella antigen was detected in macrophages, macrophage precursor cells, and occasionally endothelial cells. Numerous C. burnetii antigen-positive cells were observed between 5 and 12 days post-infection; thereafter, the amount of C. burnetii antigen decreased rapidly. Immunopositivity was detectable until 30 and 44 days post-infection in the bone marrow of Balb/cJ and C57BL/6J mice, respectively. Severity of histological lesions was associated with presence and clearance of C. burnetii antigen. Specific IgM antibodies were detected 4 days after infection and IgG seroconversion was noticed 7 to 10 days post-infection. Coxiella burnetii-specific IgM and IgG antibodies were still present 150 days after infection. Significant strain-specific differences in the antibody response were not found. The findings demonstrate systemic spread of C. burnetii, especially to bone marrow, spleen and liver, and antigen distribution was closely correlated with the appearance and degree of histological lesions.

Animals↗
PubMed1993

Prevalence of antibodies to Coxiella burnetii in Japan.

We evaluated the prevalence of Coxiella burnetii antibodies in 626 human serum samples (275 from veterinarians, 107 from meat-processing workers, 184 from respiratory-disorder patients, and 60 from healthy humans) by the indirect immunofluorescence test. Of the serum samples examined, 54 (8.6%) and 103 (16.5%) reacted positively to phase I and II antigens, respectively, of C. burnetii. The rates differed for healthy humans and respiratory-disorder patients. Antibody prevalence was high for healthy humans living in close contact with animals (e.g., veterinarians and meat-processing workers).

Antibodies, Bacterial↗
PubMed1963

STUDIES ON THE PHYSIOLOGY OF RICKETTSIAE. V. METABOLISM OF CARBAMYL PHOSPHATE BY COXIELLA BURNETII.

Mallavia, L. (University of Kansas, Lawrence) and D. Paretsky. Studies on the physiology of rickettsiae. V. Metabolism of carbamyl phosphate by Coxiella burnetii. J. Bacteriol. 86:232-238. 1963.-Preparations of disrupted Coxiella burnetii catalyze synthesis of citrulline from ornithine and carbamyl phosphate at an optimal pH of 7.0 to 7.5. Rickettsial synthesis of the pyrimidine precursor, ureidosuccinate, is demonstrated and confirmed by isolating C(14)-labeled ureidosuccinate from reaction mixtures of carbamyl phosphate and labeled aspartate. The data suggest a further rickettsial synthesis of orotate and imply rickettsial competence for host-independent pyrimidine synthesis.

Amino Acids↗
PubMed2001

Characterization of a stress-induced alternate sigma factor, RpoS, of Coxiella burnetii and its expression during the development cycle.

Coxiella burnetii is an obligate intracellular bacterium that resides in an acidified phagolysosome and has a remarkable ability to persist in the extracellular environment. C. burnetii has evolved a developmental cycle that includes at least two morphologic forms, designated large cell variants (LCV) and small cell variants (SCV). Based on differential protein expression, distinct ultrastructures, and different metabolic activities, we speculated that LCV and SCV are similar to typical logarithmic- and stationary-phase growth stages. We hypothesized that the alternate sigma factor, RpoS, a global regulator of genes expressed under stationary-phase, starvation, and stress conditions in many bacteria, regulates differential expression in life cycle variants of C. burnetii. To test this hypothesis, we cloned and characterized the major sigma factor, encoded by an rpoD homologue, and the stress response sigma factor, encoded by an rpoS homologue. The rpoS gene was cloned by complementation of an Escherichia coli rpoS null mutant containing an RpoS-dependent lacZ fusion (osmY::lacZ). Expression of C. burnetii rpoS was regulated by growth phase in E. coli (induced upon entry into stationary phase). A glutathione S-transferase-RpoS fusion protein was used to develop polyclonal antiserum against C. burnetii RpoS. Western blot analysis detected abundant RpoS in LCV but not in SCV. These results suggest that LCV and SCV are not comparable to logarithmic and stationary phases of growth and may represent a novel adaptation for survival in both the phagolysosome and the extracellular environment.

Alternative Splicing↗
PubMed1994

Survival of the Q fever agent Coxiella burnetii in the phagolysosome.

The Q fever agent, Coxiella burnetii, thrives in the acidic environment of the phagolysosome of the host cell. How this obligate intracellular agent manages to survive within this hostile milieu is unknown; however, several of its enzymes may eliminate or prevent the formation of toxic oxygen metabolites by the host cell. Also implicated as virulence factors are its surface lipopolysaccharide and plasmids.

Acid Phosphatase↗
PubMed2003

Complete genome sequence of the Q-fever pathogen Coxiella burnetii.

The 1,995,275-bp genome of Coxiella burnetii, Nine Mile phase I RSA493, a highly virulent zoonotic pathogen and category B bioterrorism agent, was sequenced by the random shotgun method. This bacterium is an obligate intracellular acidophile that is highly adapted for life within the eukaryotic phagolysosome. Genome analysis revealed many genes with potential roles in adhesion, invasion, intracellular trafficking, host-cell modulation, and detoxification. A previously uncharacterized 13-member family of ankyrin repeat-containing proteins is implicated in the pathogenesis of this organism. Although the lifestyle and parasitic strategies of C. burnetii resemble that of Rickettsiae and Chlamydiae, their genome architectures differ considerably in terms of presence of mobile elements, extent of genome reduction, metabolic capabilities, and transporter profiles. The presence of 83 pseudogenes displays an ongoing process of gene degradation. Unlike other obligate intracellular bacteria, 32 insertion sequences are found dispersed in the chromosome, indicating some plasticity in the C. burnetii genome. These analyses suggest that the obligate intracellular lifestyle of C. burnetii may be a relatively recent innovation.

Bacterial Adhesion↗
PubMed1995

Sequencing and linkage analysis of a Coxiella burnetii 2.1 kb NotI fragment.

Most of the Coxiella burnetii isolates (72 of 80) available in our institute share a 2.1 kb NotI fragment. Sequence analysis revealed two incomplete open reading frames (ORF) for putative genes hemA and bcR coding for glutamyl-tRNA-reductase and bicyclomycin resistance protein, respectively. Upon completing the ORF for the hemA gene by sequencing the adjacent NotI/EcoRI fragment a third ORF for the putative prfA gene was determined coding for release factor 1, an enzyme catalysing the last step in protein biosynthesis.

Aldehyde Oxidoreductases↗
PubMed2000

[Acute and chronic Q fever; epidemiology, symptoms, diagnosis and therapy of infection caused by Coxiella burnetii].

Q fever is a zoonosis caused by Coxiella burnetii, an obligate intracellular bacterium. Domestic ungulates and parturient cats are the primary reservoirs of infection. The animals excrete the bacterium in urine, faeces, milk and amniotic fluid. After desiccation the micro-organism spreads via aerosols. After inhalation or ingestion and an incubation period of 2-6 weeks acute Q fever may develop with atypical pneumonia and hepatitis as major clinical symptoms. The infection also may present as a flu-like illness or remain asymptomatic. Generally, the prognosis is favourable. However, endocarditis or another chronic form of Q fever occasionally develops with possibly fatal outcome. Diagnosis relies upon serologic testing with an indirect immunofluorescence method. Doxycycline is the antibiotic of choice in the treatment of Q fever. Endocarditis needs therapy for years with the addition of rifampin or hydroxychloroquine. Q fever is poorly recognised due to the variety of clinical presentations.

Acute Disease↗
PubMed1992

[Acute meningoencephalitis caused by Coxiella burnetii with periodic EEG complexes].

Q fever is a zoonosis found worldwide and is produced by Coxiella burnetii. It may be acute or chronic with neurological manifestations being infrequent. Several cases of acute encephalitis or meningoencephalitis have been described, generally with an evolution towards cure regardless of the use of selective antibiotic treatment. Recently the authors had the opportunity to study a 33 year old male presenting acute meningoencephalitis in which the clinical manifestations, CSF findings (increase in cellularity with lymphocytic predominance and excess proteins ) and neurophysiological findings (appearance of periodic bilateral complexes in the EEG) suggested the diagnosis of herpetic meningoencephalitis. Treatment with acyclovir was initiated. However, serologic studies demonstrated, a posteriori, that the germ responsible had been Coxiella burnetii. The patient evolved satisfactorily with no specific treatment and the EEG anomalies disappeared within a few days. The authors insist on the need to include Q Fever in the diagnostic differential of acute meningoencephalitis and emphasize the possibility that germs of a non viral nature may produce periodic EEG complexes in all that similar to those found in herpetic encephalitis.

Acute Disease↗
PubMed1962

Studies on the physiology of rickettsiae. III. Glucose phosphorylation and hexokinase activity in Coxiella burnetii.

Paretsky, D. (University of Kansas, Lawrence), R. A. Consigli, and C. M. Downs. Studies on the physiology of rickettsiae. III. Glucose phosphorylation and hexokinase activity in Coxiella burnetii. J. Bacteriol. 83:538-543. 1962.-Disrupted Coxiella burnetii preparations phosphorylate glucose by a hexokinase system. Glucose-6-phosphate-P(32), synthesized by the rickettsiae in the presence of P(32)-labeled carbamyl phosphate and glucose, has been isolated as the barium salt and by ion exchange and paper chromatography. C. burnetii hexokinase activity is inhibited by high concentrations of adenosine mono-, di-, and triphosphates, suggesting similarities to hexokinase from other sources.

Carbohydrate Metabolism↗
PubMed1995

Coxiella burnetii infection in subjects with HIV infection and HIV infection in patients with Q fever.

The objective of the study was to determine whether HIV infection favors the acquisition of Coxiella burnetii infection or increases the frequency of symptomatic Coxiella infections. A total of 754 subjects were tested for Coxiella antibodies: 596 intravenous drug users (IVDUs) (306 HIV-infected IVDUs matched by aged and sex with 291 non-HIV-infected IVDUs), and 157 healthy puerperal women matched to the IVDU women. A total of 520 patients with Q fever were tested for HIV antibodies. The seroprevalence of Coxiella antibodies was similar in the 2 groups of IVDUs (19.3% of HIV + IVDUs vs 22.9% of HIV - IVDUs). Likewise, there was no difference in the prevalence of Coxiella antibodies in the groups of IVDU women and healthy women. Of the 520 subjects with acute Q fever, diagnosed between 1987 and 1992, only 4 (0.77%) had HIV infection. The proportions of HIV-infected subjects in the population of patients, with Q fever, of 20-39 years of age (the age of maximum incidence of both HIV and Coxiella infection in our region), coincided with the estimated proportions of HIV subjects in the respective general populations of the province. In conclusion, infection by Coxiella burnetii was not more frequent among HIV-infected subjects. It is not likely that Coxiella infection produces symptomatic infections more often in HIV-infected subjects.

Adolescent↗
PubMed2003

Seroprevalence of infection by Coxiella burnetii in Canary Islands (Spain).

OBJECTIVES THE AIMS OF OUR STUDY WERE: (i) to know the seroprevalence of Coxiella burnetii infection in the Canary Islands, (ii) to evaluate its epidemiologic features and (iii) to compare the rates of seroprevalence using two different cut-offs (1:20 and 1:80) for the diagnosis of past infection. METHODS: We analysed a representative sample of the canarian population. 662 sera were tested. For the detection of IgG and IgM antibodies against C. burnetii phase II antigens an immuofluorescence assay was used. The serologic screening for IgG detection begun with a 1:20 dilution. A titer of IgG > or = 1:80 along with a negative IgM were used as criteria for previous infection. RESULTS: At an IgG antibody titer against C. burnetii of 1:80 as diagnostic for past infection, the observed global seroprevalence was 21.5%. If the cut-off used was 1:20, the observed prevalence increased up to 35.8% (p = 0.001). Significantly different seroprevalence rates were obtained at these different cut-offs when results were analysed for groups of age and socioeconomic status, but not for either the island of origin or for farmers. CONCLUSION: Our results strongly suggest that Coxiella burnetii infection is endemic in all the Canary Islands. Although it is more frequent in males above 30 years old, it do affect people of all ages, and thus it should be borne in mind in the face of any acute febrile syndrome.

Antibodies, Bacterial↗
PubMed2005

Survival of Trypanosoma cruzi metacyclic trypomastigotes within Coxiella burnetii vacuoles: differentiation and replication within an acidic milieu.

Coxiella burnetii, the etiological agent of Q fever, is an obligate intracellular bacterium that resides within acidified vacuoles with secondary lysosomal characteristics. Infective stages of Trypanosoma cruzi, the causative agent of Chagas' disease, actively invade a wide variety of cells, a process followed by lysosomal recruitment. Recently, we have investigated and characterized early events that occur in Vero cells persistently colonized with C. burnetii when doubly infected with T. cruzi trypomastigote forms. Kinetic studies of trypomastigote transfer indicated that parasitophorous vacuoles (PV) of metacyclic trypomastigotes are rapidly and efficiently fused to C. burnetii vacuoles. Based on these observations we have investigated the behavior of metacyclic trypomastigotes within C. burnetii vacuoles beyond 12 h of co-infection inside Vero cells. Using indirect immunofluorescence with MAb against different developmental stages, it was possible to follow the T. cruzi differentiation process within C. burnetii vacuoles after up to 96 h post-invasion. We observed that metacyclic trypomastigotes began to differentiate after 12 h of infection, and 24 h later amastigotes were the prevailing forms within C. burnetii vacuoles. T. cruzi amastigote replication within C. burnetii vacuoles was confirmed using video and time-lapse confocal microscopy and around 36 h of co-infection, cytokinesis took about 70 min to occur. After 72 h, we observed that amastigote forms seemed to escape from C. burnetii vacuoles. Labeling of amastigotes within C. burnetii vacuoles using a polyclonal antibody to C9 complement protein suggested that TcTOX (T. cruzi hemolysin) could play a role in parasite escape from C. burnetii. We concluded that T. cruzi has an outstanding adaptation capability and can survive within a hostile milieu such as C. burnetii vacuoles.

Animals↗
PubMed2003

Evaluation of Coxiella burnetii antibiotic susceptibilities by real-time PCR assay.

Coxiella burnetii is an obligate intracellular bacterium. The inability to cultivate this organism on axenic medium has made calculation of infectious units challenging and prevents the use of conventional antibiotic susceptibility assays. A rapid and reliable real-time PCR assay was developed to quantify C. burnetii cells from J774.16 mouse macrophage cells and was applied to antibiotic susceptibility testing of C. burnetii Nine Mile, phase I. For calculation of bacterial replication, real-time PCR performed equally as well as immunofluorescent-antibody (IFA) assay when J774.16 cells were infected with 10-fold serial dilutions of C. burnetii and was significantly (P < 0.05) more repeatable than IFA when 2-fold dilutions were used. Newly infected murine macrophage-like J774.16 cells were treated with 8 microg of chloramphenicol per ml, 4 microg of tetracycline per ml, 4 microg of rifampin per ml, 4 microg of ampicillin per ml, or 1 microg of ciprofloxacin per ml. After 6 days of treatment, tetracycline, rifampin, and ampicillin significantly (P < 0.01) inhibited the replication of C. burnetii, while chloramphenicol and ciprofloxacin did not. In general, these results are consistent with those from prior reports on the efficacy of these antibiotics against C. burnetii Nine Mile, phase I, and indicate that a real-time PCR-based assay is an appropriate alternative to the present methodology for evaluation of the antibiotic susceptibilities of C. burnetii.

Ampicillin↗