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PubMed1999

Long term vascular complications of Coxiella burnetii infection in Switzerland: cohort study.

OBJECTIVE: To evaluate the range of long term vascular manifestations of Coxiella burnetii infection. DESIGN: Cohort study in Switzerland of people affected in 1983 by the largest reported outbreak of Q fever and who were followed up 12 years later. Follow up information about possible vascular disease and endocarditis was obtained through a mailed questionnaire and death certificates. SETTING: Val de Bagnes, a rural Alpine valley in Switzerland. PARTICIPANTS: 2044 (87%) of 2355 people who had serum testing for Coxiella burnetii infection in 1983: 1247 were classed as not having been infected, 411 were classed as having been acutely infected, and 386 were classed as having been infected before 1983. MAIN OUTCOME MEASURES: Relative risk controlled for age and sex and 12 year risk of vascular diseases and endocarditis among infected participants as compared with those who had never been infected. RESULTS: The 12 year risk of endocarditis or venous thromboembolic disease was not increased among those who had been acutely infected. The 12 year risk of arterial disease was significantly higher among those who had been acutely infected (7%) as compared with those who had never been infected (4%) (relative risk 2.2, 95% confidence interval 1.4 to 3.6). Specifically, there was an increased risk of developing a cerebrovascular accident (relative risk 3.7, 1.6 to 8.4) and cardiac ischaemia (relative risk 1.9, 1.04 to 3.4). 12 year mortality was significantly higher among the 411 people who had been acutely infected in 1983 (9.7%; age adjusted relative risk 1.8, 1.2 to 2.6) when compared with the 1247 participants who had remained serologically negative in 1983 (7.0%). CONCLUSIONS: Coxiella burnetii infection may cause long term complications including vascular disease.

Adult↗

PubMed2001

[Prosthetic valve endocarditis due to Coxiella burnetii: six cases].

PURPOSE: Prosthetic valve endocarditis is a dangerous complication of valvular surgery (3-6%). Among involved pathogens, Coxiella burnetii is an occasional agent, though isolated with increasing frequency. We report our experience with this peculiar endocarditis and lay stress on specific diagnostic and therapeutic difficulties. METHODS: Between 1990 and 1995, six patients retrospectively met the diagnosis criteria for definite endocarditis due to Coxiella burnetii. RESULTS: Five Algerian men and one French woman presented with prosthetic valve endocarditis with negative blood cultures (on bioprosthesis: four cases, on mechanical valve: two cases). The main clinical and biological feature was febrile congestive heart failure with hepatomegaly, splenomegaly, hepatic and renal abnormalities, inflammatory syndrome, hypergammaglobulinemia, anemia and lymphopenia. Serological testing for Coxiella burnetii provided diagnosis in all cases. Echocardiography displayed vegetations in all cases. Valvular replacement was performed in four patients. With antibiotic therapy including doxycycline or/and hydroxychloroquine, quinolones or rifampicine, all patients experienced complete clinical, biological and echographic remission. CONCLUSION: Q fever prosthetic valve endocarditis presents as a systemic disorder occurring in patients with valvular heart disease. From now on, early diagnosis and efficient medical treatment may provide permanent prosthetic sterilization.

Adult↗

PubMed2002

Permeability of Coxiella burnetii to ribonucleosides.

Knowledge about transport in Coxiella burnetii, an obligate phagolysosomal parasite, is incomplete. The authors investigated the capability of isolated, intact, host-free Coxiella to transport ribonucleosides while incubated at a pH value typical of lysosomes. Because of the low activities and limitations of obtaining experimental quantities of isolated, purified Coxiella, incorporation of substrate into nucleic acid was used as a trap for determination of uptake abilities. Virulent wild-type (phase I) organisms possessed uptake capability for all ribonucleosides. Both phase I and phase II (avirulent) organisms incorporated the purine nucleosides guanosine, adenosine and inosine, and showed a more limited uptake of thymidine and uridine. Both phases were poorly active in cytidine uptake. Neither phase of the organism was capable of transport and incorporation of NTPs, CMP, cytosine or uracil. Water space experiments confirmed that the uptake process concentrated the purine nucleosides within the cytoplasm of both wild-type and phase II Coxiella via a low-pH-dependent mechanism. Comparison of uptake rates in Escherichia coli versus Coxiella verified that the incorporation of ribonucleosides by Coxiella is a slow process. It is concluded that Coxiella possesses some transport pathways consistent with utilization of pools of nucleosides found within its host cell lysosomal pathway.

Animals↗

PubMed1996

Isolation of Coxiella burnetii from children with influenza-like symptoms in Japan.

The prevalence of Coxiella burnetii antibodies was investigated by indirect immunofluorescence (IF) test in 55 paired sera (acute and convalescent phases) of school children who had influenza-like symptoms. Of the convalescent serum samples examined, 18 (32.7%) sera reacted positively to phase II antigen of C. burnetii. Coxiella-like organism was isolated from the sera of 13 children after injection of the 18 acute phase sera into mice. The organism was identified as C. burnetii by Giemsa staining and the IF antigen test of mouse spleen smears, the polymerase chain reaction (PCR) method, electron microscopic observations of the mouse spleen cells, and the IF antibody test of mouse sera. This is the first report of isolation of C. burnetii from serum specimens of children having influenza-like symptoms. The evidence that C. burnetii was isolated from people indigenous to Japan at a considerably high incidence suggested that C. burnetii may be widespread as a cause of influenza-like symptoms in Japan.

Acute Disease↗

PubMed1999

Induced production of nitric oxide and sensitivity of alveolar macrophages derived from mice with different sensitivity to Coxiella burnetii.

We compared in vitro sensitivities to Coxiella burnetii of alveolar macrophages, derived from mice sensitive and resistant to C. burnetii, respectively, and examined the role of nitric oxide (NO) in the C. burnetii infection. Alveolar macrophages of sensitive A/J mice showed a larger population of C. burnetii antigen-positive cells than those of resistant C57BL/6 mice. C. burnetii induced NO production in alveolar macrophages, but N-methyl-L-arginine and sodium nitroprusside (SNP), NO inhibitor and donor, respectively, did not inhibit the infection. Thus the NO induction seems to be independent of the cell defense mechanism against the C. burnetii infection.

Animals↗

PubMed1993

A sporulation gene in Coxiella burnetii?

During a search for conserved target sequences on the genome of Coxiella burnetii for a diagnostic PCR a NotI/EcoRV DNA fragment was cloned and sequenced from the isolate "Nine Mile", Phase I (sequence data are registered under accession number X70045 in data bases EMBL, GENEBANK and DDBJ). On this fragment we have found a sequence of 1741 base pairs which showed an exceptionally high homology (60% on the nucleic acid level and 49.6% on the amino acid level) to the sporulation gene "spoIIIE" of the gram-positive bacterium Bacillus subtilis. This is first evidence of the molecular basis for formation of spores in Coxiella burnetii which has been postulated in the literature by electron microscopic investigations.

Amino Acid Sequence↗

PubMed1999

Early cytokine induction in mouse P388D1 macrophages infected by Coxiella burnetii.

Q-fever is caused by Coxiella burnetii, which is an obligate intracellular bacterium with a broad spectrum of host cells, including macrophages. Cytokines produced from macrophages infected by intracellular bacteria play a critical role in the expression of innate immune responses as well as in the subsequent triggering of protective acquired cell-mediated immunity. We followed the induction and secretion of the pro-inflammatory cytokines interleukin 1 alpha (IL-1alpha), tumor necrosis factor alpha (TNF-alpha), and interleukin 12 (IL-12) in the macrophage-like mouse cell line P388D1 during the initial phase of an in vitro infection by virulent C. burnetii Nine Mile. Secretion of IL-1alpha and TNF-alpha were observed within 3 h post-inoculation. IL-12, however, was not detected in cell supernatants. Two forms of C. burnetii exist, virulent phase I and avirulent phase II organisms. To determine whether the cytokine response was dependent on the form of C. burnetii, the induction of IL-1alpha and TNF-alpha in infected P388D1 cells was compared. Both cytokines were produced by macrophages early after infection with Phase I bacteria. A similar induction of TNF-alpha was observed after infection with the avirulent Phase II bacteria, but no IL-1alpha induction could be detected. As the only difference identified between the two forms of C. burnetii is the composition of their lipopolysaccharides (LPS), the ability of each of the purified LPS from the two variants to induce IL-1alpha was investigated. Purified C. burnetii LPS induced a moderate IL-1alpha response in comparison to that induced by the efficient stimulator E. coli LPS. Furthermore, there was no significant difference in action between Phase I and Phase II LPS preparations. We thus postulate that factors other than LPS differ between the two variants of C. burnetii, and these differences may account for differences in IL-1alpha induction.

Animals↗

PubMed1990

[Endocarditis caused by Coxiella burnetii in aortic prosthesis. Presentation of a case with a fatal course].

A case of endocarditis caused by Coxiella burnetii in a patient with an aortic Starr-Edwards prosthesis is described. The diagnosis was made by detecting high titres of antibody against Coxiella burnetii phase I antigens. After 15 weeks of chemotherapy with tetracycline and cotrimoxazole, aortic prosthetic valve replacement was carried out because of haemodynamic deterioration and he died 4 days later. The histologic picture of the excised valve was consistent with endocarditis. Coxiella burnetii should be considered in the differential diagnosis of culture-negative endocarditis in our country, especially when the patient has not receiving antibiotic treatment in the last 2 weeks.

Adult↗

PubMed2007

Vanin-1 controls granuloma formation and macrophage polarization in Coxiella burnetii infection.

Q fever is caused by Coxiella burnetii, a bacterium that survives in MPhi. Vanin-1 is a membrane-anchored pantetheinase that controls tissue inflammation. Consequently, Vanin-1-deficient mice represent a unique mouse model in which stress-induced inflammation is limited by the reaction of resident tissue cells. To investigate the contribution of host tissues in the control of a bacterial infection, we infected Vanin-1-deficient mice with C. burnetii. Mortality and morbidity of mice were not affected. The lack of Vanin-1 had no effect on C. burnetii clearance but decreased the formation of granulomas in spleen and liver. Granuloma formation depends upon MPhi recruitment and activation in these tissues. Whereas the former was slightly impaired in mutant mice, the lack of Vanin-1 significantly affected the activation pattern of BM-derived MPhi stimulated by C. burnetii. While their microbicidal activity against C. burnetii was moderately impaired, they exhibited decreased inducible nitric oxide synthase (iNOS) and MCP-1 gene expression, and increased IL-10 and arginase expression. In liver from mutant mice, increased arginase expression and decreased expression of MCP-1 and iNOS were reminiscent of MPhi data. These results suggest a role of Vanin-1 in granuloma formation in response to C. burnetii by skewing MPhi activation toward an M2 program.

Amidohydrolases↗

PubMed1994

[Acute respiratory insufficiency secondary to Coxiella burnetii pneumonia: a rare complication].

Acute respiratory failure secondary to Coxiella burnetii infection is an extremely rare but serious complication that usually has a good prognosis after appropriate treatment. We describe a female patient who developed acute respiratory failure secondary to Coxiella burnetii pneumonia requiring mechanical ventilation and antibiotic therapy.

Acute Disease↗

PubMed1964

METABOLIC ACTIVITY IN COXIELLA BURNETII.

Ormsbee, Richard A. (Rocky Mountain Laboratory, Hamilton, Mont.), and Marius G. Peacock. Metabolic activity in Coxiella burnetii. J. Bacteriol. 88:1205-1210. 1964.-Purified suspensions of Coxiella burnetii were shown to utilize alpha-ketoglutarate, succinate, fumarate, malate, oxaloacetate, pyruvate, glutamate, and serine. The addition of nicotinamide adenine dinucleotide(+) was necessary to elicit the maximal rate of oxygen uptake with l-glutamate as substrate, but was unnecessary when other substrates were employed. It was concluded that the Krebs cycle of intermediary carbohydrate metabolism probably operates within C. burnetii, and that pyruvate is the chief energy source.

Acetates↗

PubMed2002

[Bacillus anthracis, prions, Coxiella burnetii].

The detection kits for Bacillus anthracis, an isoform of host prion and Coxiella burnetii, using genetic technology are still not generalized. For B. anthracis target genes for detection would be genes of toxins. Although it is difficult to detect prions related to prion diseases before death, some mutants of prion gene in leukocytes and 14-3-3 proteins in cerebrospinal fluid are detectable in living patients suffering from Creutzfeldt-Jakob disease. The gene of superoxide dismutase in Coxiella burnetii is a useful target for detecting this Rickettsiae.

Animals↗

PubMed2004

Initial peptide mass fingerprinting analysis of proteins obtained by lysis of Coxiella burnetii cells.

Whereas the complete genome of Coxiella burnetii (C.b.), the etiological agent of Q-fever, has recently been published (Seshadri et al., Proc. Natl. Acad. Sci. USA. 100, 5455-5460, 2003), the C.b. proteome is still under study. Using the bioinformatic approach, we found in total 309 proteins on two dimensional electroctrophoretic images of C.b. whole cell lysates. Eighteen major protein species were subjected to peptide mass fingerprinting and identified as the products of 6 known open reading frames (ORFs): the chaperone DnaK (heat shock 70 K protein), chaperonin 60 K (GroEL protein, heat shock protein B), DnaJ-like protein djlA (mucoidy activation protein mucZ), elongation factor Ts (EF-Ts), ribosomal protein L7/L12, and chaperonin 10 K (GroES protein, heat shock protein A).

Bacteria↗

PubMed2005

Lack of association between serological evidence of past Coxiella burnetii infection and incident ischaemic heart disease: nested case-control study.

BACKGROUND: Coxiella burnetii causes the common worldwide zoonotic infection, Q fever. It has been previously suggested that patients who had recovered from acute Q fever (whether symptomatic or otherwise) may be at increased risk of ischaemic heart disease. We undertook this study to determine if past infection with Coxiella burnetii, the aetiological agent of Q fever, is a risk factor for the subsequent development of ischaemic heart disease. METHODS: A nested case-control study within the Prospective Epidemiological Study of Myocardial Infarction (PRIME). The PRIME study is a cohort study of 10,593 middle-aged men undertaken in France and Northern Ireland in the 1990s. A total of 335 incident cases of ischaemic heart disease (IHD) were identified and each case was matched to 2 IHD free controls. Q fever seropositivity was determined using a commercial IgG ELISA method. RESULTS: Seroprevalence of Q fever in the controls from Northern Ireland and France were 7.8% and 9.0% respectively. No association was seen between seropositivity and age, smoking, lipid levels, or inflammatory markers. The unadjusted odds ratio (95% CI) for Q fever seropositivity in cases compared to controls was 0.95 (0.59, 1.57). The relationship was substantially unaltered following adjustment for cardiovascular risk factors and potential confounders. CONCLUSION: Serological evidence of past infection with C. burnetii was not found to be associated with an increased risk of IHD.

Antibodies, Bacterial↗

PubMed1961

Synthesis of serine by Coxiella burnetii.

Myers, W. F. (University of Kansas, Lawrence) and D. Paretsky. Synthesis of serine by Coxiella burnetii. J. Bacteriol. 82:761-763. 1961.-Enzyme preparations from suspensions of purified Coxiella burnetii are capable of synthesizing serine from formaldehyde and glycine-2-C(14) in the presence of tetrahydrofolic acid. Evidence for the reaction is obtained by isolating and identifying radioactive serine and serine derivatives. The data suggest a role for folic acid in these rickettsiae, and extend the knowledge of host-independent biosynthetic competencies of these highly parasitic microorganisms.

Coxiella↗

PubMed1998

High seroprevalence of Coxiella burnetii infection in Eastern Cantabria (Spain).

BACKGROUND: Coxiella burnetii is the causative agent of Q fever, a worldwide zoonosis which shows a wide diversity of clinical manifestations. The objective of this seroepidemiological study was to estimate the prevalence of antibodies to C. burnetii in a representative population of the Eastern area of the Cantabrian Community (Northern Spain). METHODS: A cross-sectional study was conducted in 595 subjects from Eastern Cantabria. Four different zones (one urban and three rural zones) were defined according to the geographical characteristics of the area and the economic activities of the population. The population sample for this study was collected between December 1994 and March 1995, and was stratified by age, sex and municipality of residence. IgG and IgM antibodies against C. burnetii were assayed by an indirect immunofluorescence technique. RESULTS: The prevalence of anti-phase II Coxiella IgG (titre > or = 1:16) was 48.6% (95% confidence interval: 44.6-52.6%), with 81.3% havinga titre of > or = 1:64. The prevalence of IgG increased with age, ranging from 12.0% in people < 15 years to 70.3% in those > 65 years (P < 0.001). The antibody detection rate was higher in males (53.6%) than in females (43.3%) (P < 0.01). The prevalence of anti-phase II Coxiella IgG was less among subjects living in the urban zone (32.8%) than in those living in the other three rural zones: the two situated on the coast (54.0% and 54.9% respectively) and the inner mountainous zone (82.3%) (P < 0.001). CONCLUSIONS: The prevalence of C. burnetii infection observed in this study is one of the highest reported in Europe. The eastern area of Cantabria is a hyperendemic area for Q fever.

Adolescent↗

PubMed2003

Coxiella burnetii pneumonia.

This report reviews the pulmonary and extrapulmonary manifestation of infections due to Coxiella burnetii. Q fever, a zoonosis, is due to infection with C. burnetii. This spore-forming microorganism is a small gram-negative coccobacillus that is an obligate intracellular parasite. The most common animal reservoirs are goats, cattle, sheep, cats, and occasionally dogs. The organism reaches high concentrations in the placenta of infected animals. Aerosolisation occurs at the time of parturition and infection follows inhalation of this aerosol. There are three distinct clinical syndromes of the acute form of the illness: nonspecific febrile illness, pneumonia, and hepatitis. The chronic form of Q fever is almost always endocarditis, but occasionally it is manifest as hepatitis, osteomyelitis or endovascular infection. The pneumonic form of the illness can range from very mild-to-severe pneumonia requiring assisted ventilation. Multiple round opacities are a common finding on chest radiography. Treatment with doxycycline or a fluoroquinolone is preferred. Susceptibility to macrolides is variable. In conclusion, Coxiella burnetii pneumonia should be considered when there is a suitable exposure history and when outbreaks of a pneumonic illness are being investigated.

Anti-Bacterial Agents↗

PubMed1981

Role of antibody in Coxiella burnetii infection.

BALB/c mice infected with Coxiella burnetii phase I developed a state of acquired resistance which could be detected during week 2 postinfection. Immune serum, administered to normal mice 24 h before challenge with C. burnetii, appeared to accelerate the development of resistance. An increased clearance rate could be measured in these serum recipients 1 week postinfection. Simultaneous administration of immune serum and C. burnetii did not affect the normal clearance rate of rickettsiae from the spleens of infected mice during week 1, but enhanced clearance of the organism by 14 days postchallenge. Passive transfer of immune serum 24 h after challenge of normal mice with viable C. burnetii had no effect on rickettsial growth within the spleens of animals treated in this fashion. Treatment of athymic mice with immune serum 24 h before challenge with C. burnetii had no effect on rickettsial multiplication within the spleens of these T-cell-deficient animals.

Adjuvants, Immunologic↗