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PubMed2001

Relationships between the shedding of Coxiella burnetii, clinical signs and serological responses of 34 sheep.

Two abortions associated with Coxiella burnetii occurred in a group of 34 pregnant ewes. The seroprevalence of C. burnetii infection was studied by using an ELISA and the immunofluorescence (IF) assay was applied to the contents of vaginal swabs. In addition, a PCR assay, with primers based on a transposon-like repetitive region of the C. burnetii genome (trans-PcR), was used for the highly sensitive and specific detection of C. burnetii in vaginal swabs, milk and faeces. Of the 34 animals tested at parturition, eight (24 per cent) were positive by ELISA, 11 (32 per cent) were positive by IF, and 15 (44 per cent) were positive when the vaginal swab extract was subjected to the trans-PCR assay. C. burnetii was therefore detected by PCR in the vaginal swabs of seven seronegative ewes. However, five weeks after lambing, 16 (47 per cent) of the animals tested were ELISA positive but only two animals (6 per cent) were positive by PCR. Among the ELISA- and PCR-positive animals, eight (25 per cent) shed coxiella in their milk and six (18 per cent) did so in their faeces.

Abortion, Veterinary↗

PubMed2000

Seroprevalence of Coxiella burnetii infection in southern Taiwan.

BACKGROUND AND PURPOSE: The emergence of infection with Coxiella burnetii, the causative organism of Q fever, has been only recently recognized in Taiwan. Several cases of acute Q fever infection have been described, but the prevalence of antibodies to C. burnetii in the general population in Taiwan has not been reported. Thus, we studied the seroprevalence of C. burnetii infection in southern Taiwan. METHODS: We conducted a retrospective serosurvey to examine the prevalence of C. burnetii infection among subjects admitted to a rural hospital in Taiwan for various reasons, and among presumably healthy attendees of a routine physical examination clinic of an urban public hospital. The diagnosis of C. burnetii infection required the presence of antibodies to both phase I and II antigens (titer > or = 1:16) or only to phase II antigens (titer > or = 1:256), as detected by indirect immunofluorescence assay. RESULTS: The prevalence of C. burnetii infection was 4.2% in both the in-patient (15/357) and physical examination participant (11/259) populations. None of these subjects had signs compatible with acute Q fever (febrile illness within the past 3 months). The antibody prevalence rate was higher in males than in females, and peaked in persons aged 61 to 70 years. CONCLUSIONS: These data suggest that C. burnetii infection is not rare in southern Taiwan and does not cause clinical symptoms in all infected patients.

Adolescent↗

PubMed2000

Coxiella burnetii exhibits morphological change and delays phagolysosomal fusion after internalization by J774A.1 cells.

Coxiella burnetii, the etiological agent of Q fever, is an obligate intracellular bacterium proliferating within the harsh environment of the phagolysosome. Mechanisms controlling trafficking to, and survival of pathogens within, the phagolysosome are unknown. Two distinct morphological variants have been implicated as playing a role in C. burnetii survival. The dormant small-cell variant (SCV) is resistant to extracellular stresses and the more metabolically active large-cell variant (LCV) is sensitive to environmental stresses. To document changes in the ratio of SCVs to LCVs in response to environment, a protein specific to SCV, ScvA, was quantitated. During the first 2 h after internalization of C. burnetii by J774A.1 cells, the level of ScvA decreased, indicating a change from a population containing primarily SCVs to one containing primarily LCVs. In vitro experiments showed that 2 h of incubation at pH 5.5 caused a significant decrease in ScvA in contrast to incubation at pH 4.5. Measuring in vitro internalization of [(35)S]methionine-[(35)S]cysteine in response to pH, we found the uptake to be optimal at pH 5.5. To explore the possibility that after uptake C. burnetii was able to delay phagolysosomal fusion, we used thorium dioxide and acid phosphatase to label phagolysosomes during infection of J774A.1 cells. We determined that viable C. burnetii was able to delay phagolysosomal fusion. This is the first time that a delay in phagolysosomal fusion has been shown to be a part of the infection process of this pathogenic microorganism.

Animals↗

PubMed1996

Retrospective survey of chronic Q fever in Japan by using PCR to detect Coxiella burnetii DNA in paraffin-embedded clinical samples.

We used PCR to detect Coxiella burnetii DNA in paraffin-embedded tissues obtained from patients with chronic endocarditis in which the etiological agent had been unknown. On the basis of the published nucleotide sequence of the C. burnetii htpB gene, primers were chosen to produce an amplified fragment of 285 bp. A total of 60 samples from 56 patients were tested for the presence of C. burnetii DNA. Five samples from four patients were found to be positive. All of the amplified DNA fragments possessed a TthHB8I restriction site, as predicted from the published sequence of C. burnetii. In one of the four positive patients, rickettsia-like particles were found in sections of tissue stained by Gimenez's method. This is the first report of chronic Q fever in Japan.

Base Sequence↗

PubMed2005

Virulent Coxiella burnetii does not activate human dendritic cells: role of lipopolysaccharide as a shielding molecule.

Coxiella burnetii is an obligate intracellular bacterium and the etiological agent of the zoonotic disease Q fever. Acute human Q fever is characterized by flu-like symptoms that, in some cases, can result in a persistent infection that may reactivate months or years after initial exposure. Mechanisms by which this obligate parasite evades clearance by the host immune response during persistent infection are unknown. Here, we characterized the interaction of C. burnetii with dendritic cells (DC), critical components of both innate and adaptive immunity. Human DC were infected with two isogenic C. burnetii strains that differ in LPS length. Infection by the Nine Mile phase I (NMI) strain, which is fully virulent and produces full-length LPS, did not result in DC maturation. In contrast, infection by the avirulent Nine Mile phase II strain, producing a severely truncated LPS, resulted in toll-like receptor 4-independent DC maturation and approximately 10-fold more IL-12 and TNF production. NMI did not actively inhibit DC maturation as NMI-infected DC subsequently matured if treated with Escherichia coli LPS or Nine Mile phase II. Furthermore, removal of LPS from NMI dramatically increased its ability to stimulate DC. We propose a model whereby LPS of virulent C. burnetii masks toll-like receptor ligands from innate immune recognition by DC, thereby allowing replication without significant maturation or inflammatory cytokine production. This immune evasion strategy may allow C. burnetii to persist in an immunocompetent host.

Coxiella burnetii↗

PubMed2006

Infective endocarditis due to Bartonella spp. and Coxiella burnetii: experience at a cardiology hospital in Sao Paulo, Brazil.

Bartonella spp. and Coxiella burnetii are recognized as causative agents of blood culture-negative endocarditis (BCNE) in humans and there are no studies of their occurrences in Brazil. The purpose of this study is to investigate Bartonella spp. and C. burnetii as a causative agent of culture-negative endocarditis patients at a cardiology hospital in São Paulo, Brazil. From January 2004 to December 2004 patients with a diagnosis of endocarditis at our Institute were identified and recorded prospectively. They were considered to have possible or definite endocarditis according to the modified Duke criteria. Those with blood culture-negative were tested serologically using the indirect immunofluorescent assay (IFA) for Bartonella henselae, B. quintana, and C. burnetii. IFA-IgG titers >800 for Bartonella spp. and C. burnetii were considered positive. A total of 61 patients with endocarditis diagnosis were evaluated, 17 (27%) were culture-negative. Two have had IgG titer greater than 800 (>/=3,200) against Bartonella spp. and one against C. burnetii (phase I and II>/=6,400). Those with Bartonella-induced endocarditis had a fatal disease. Necropsy showed calcifications and extensive destruction of the valve tissue, which is diffusely infiltrated with mononuclear inflammatory cells predominantly by foamy macrophages. The patient with C. burnetii endocarditis received specific antibiotic therapy. Reports of infective endocartitis due to Bartonella spp. and C. burnetii in Brazil reveal the importance of investigating the infectious agents in culture-negative endocarditis.

Adult↗

PubMed2005

Specificity of Legionella pneumophila and Coxiella burnetii vacuoles and versatility of Legionella pneumophila revealed by coinfection.

Legionella pneumophila and Coxiella burnetii are phylogenetically related intracellular bacteria that cause aerosol-transmitted lung infections. In host cells both pathogens proliferate in vacuoles whose biogenesis displays some common features. To test the functional similarity of their respective intracellular niches, African green monkey kidney epithelial (Vero) cells, A/J mouse bone marrow-derived macrophages, human macrophages, and human dendritic cells (DC) containing mature C. burnetii replication vacuoles were superinfected with L. pneumophila, and then the acidity, lysosome-associated membrane protein (LAMP) content, and cohabitation of mature replication vacuoles was assessed. In all cell types, wild-type L. pneumophila occupied distinct vacuoles in close association with acidic, LAMP-positive C. burnetii replication vacuoles. In murine macrophages, but not primate macrophages, DC, or epithelial cells, L. pneumophila replication vacuoles were acidic and LAMP positive. Unlike wild-type L. pneumophila, type IV secretion-deficient dotA mutants trafficked to lysosome-like C. burnetii vacuoles in Vero cells where they survived but failed to replicate. In primate macrophages, DC, or epithelial cells, growth of L. pneumophila was as robust in superinfected cell cultures as in those singly infected. Thus, despite their noted similarities, L. pneumophila and C. burnetii are exquisitely adapted for replication in unique replication vacuoles, and factors that maintain the C. burnetii replication vacuole do not alter biogenesis of an adjacent L. pneumophila replication vacuole. Moreover, L. pneumophila can replicate efficiently in either lysosomal vacuoles of A/J mouse cells or in nonlysosomal vacuoles of primate cells.

Animals↗

PubMed1985

Nature and linkage type of fatty acids present in lipopolysaccharides of phase I and II Coxiella burnetii.

The constituent fatty acids of lipopolysaccharides (LPS) of Coxiella burnetii (phase I and II) were qualitatively and quantitatively analysed by combined gas-liquid chromatography/mass spectrometry. The total fatty acid content (per mg LPS) was determined as 90.0 nmol (2.3 wt%) for LPS of phase I cells (LPS I) and 179.1 nmol (4.8 wt%) for LPS of phase II cells (LPS II). Of the 24 different acyl residues characterized (12 to 18 carbon atoms), nine were 3-hydroxy fatty acids (normal, iso- and anteiso-branched) which quantitatively predominated. All 3-hydroxylated fatty acids were found to possess the (R)-configuration, to be exclusively amide-linked and to be acylated at their 3-hydroxyl group. Ester-linked nonhydroxylated fatty acids (normal, iso- and anteiso-branched) were present but ester-bound 3-hydroxy- or 3-acyloxyacyl residues were lacking from C. burnetii LPS I and LPS II. As the major acyl group (R)-3-(12-methyl-tetradecanoyloxy)-12-methyl-tetradecanoic acid was identified. Our results show that the complex fatty acid spectrum of C. burnetii differs considerably from that of LPS of other Gram-negative bacteria. They further suggest an enormous heterogeneity of the lipid A component of C. burnetii LPS I and LPS II.

Chromatography, Gas↗

PubMed1993

Hairy cell transformation of human peripheral blood lymphocytes by Coxiella burnetii.

Hairy cell (HC) transformation of human peripheral blood lymphocytes (PBL) by Coxiella burnetii was studied to clarify the significance of persistency of C. burnetii in a hairy cell line (designated "TOL"). TOL cells which exhibited HC characteristics in hairy cell leukemia (HCL) were persistently infected with C. burnetii. Two strains of C. burnetii, our isolate from TOL cells and the original isolate in 1935, the Nine Mile strain from American Type Culture Collection (ATCC, U.S.A), were inoculated to PBL cultures. HC transformation not only by our isolates (87%) but also by Nine Mile strain (100%) was demonstrated in an average of 20 days. The original observation that Coxiella induced HC transformation in vitro was also confirmed in experiments with PBL exposed to C. burnetii in vivo. Spontaneous development of HC were observed in cultures of PBL only from coxiellemic cases (12/24) but not from C. burnetii negative cases (0/57). All HC cell lines (34) as determined by their morphology and cytochemical markers of HC in HCL remained infected with C. burnetii invariably.

Blood Cells↗

PubMed2004

Link between impaired maturation of phagosomes and defective Coxiella burnetii killing in patients with chronic Q fever.

Q fever is caused by Coxiella burnetii, a bacterium that survives in monocytes/macrophages by resisting their natural microbicidal activity. Because the link between bacterial killing and phagosome maturation has yet to be demonstrated, we evaluated responses in monocytes from both immunologically naive control subjects and patients with various manifestations of Q fever. Monocytes from patients with chronic Q fever in evolution, who do not control the infection, exhibited defective phagosome maturation and impaired C. burnetii killing. Both responses were stimulated in patients recovering from Q fever. Phagosome maturation and C. burnetii killing were significantly correlated. Defective phagosome maturation and impaired C. burnetii killing were induced by adding interleukin (IL)-10 to monocytes from convalescent patients and were restored by IL-10 neutralization in chronic Q fever in evolution. We show that phagosome maturation and microbial killing are linked in Q fever and that IL-10 regulates both features of microbicidal activity.

Adult↗

PubMed2000

Detection of serum antibodies to Bartonella henselae and Coxiella burnetii from Japanese children and pregnant women.

The participation of Bartonella henselae and Coxiella burnetii in the pathogenesis of fever of unknown origin (FUO) and lymphadenopathy has not been completely clarified. Prevalence of these two agents in Japanese children is also unknown. Serum IgG and IgM antibodies to B. henselae and to C. burnetii were examined by the indirect fluorescence antibody assay. Enzyme immunoassay kits were used to detect serum IgG and IgA antibodies against Chlamydia trachomatis. Out of 200 healthy normal pregnant women, two (1.0%) had serum IgG antibodies to B. henselae, four (2.0%) to C. burnetii and 49 (24.5%) to C. trachomatis. Out of 29 patients with FUO, one (3.4%) had serum IgG antibodies to B. henselae, four (13.8%) to C. burnetii and none to C. trachomatis. Out of 31 patients with cervical lymphadenopathy, three (9.6%) had serum IgG antibodies to B. henselae, two (6.5%) to C. burnetii and none to C. trachomatis. Out of 22 patients with generalized lymphadenopathy, one (4.5%) had serum IgG antibodies to B. henselae, three (13.6%) to C. burnetii and none to C. trachomatis. Prevalences of serum antibodies to C. burnetii in the patients with FUO and generalized lymphadenopathy and to B. henselae in the patients with cervical lymphadenopathy were significantly higher than those of normal pregnant women (Welch's t-test; P<0.01). These two agents may have some roles in the pathogenesis of FUO and lymphadenopathy in Japanese children.

Adolescent↗

PubMed1993

Acid phosphatase activity in Coxiella burnetii: a possible virulence factor.

High-speed supernatant fluids derived from sonicated Coxiella burnetii contained considerable acid phosphatase activity when assayed by using 4-methylumbelliferylphosphate; they also contained a factor that blocked superoxide anion production by human neutrophils stimulated with formyl-Met-Leu-Phe. The pH optimum of the enzyme was approximately 5.0. The level of phosphatase activity detected in several isolates of C. burnetii implicated in acute (Nine Mile) and chronic (S Q217, PRS Q177, K Q154) Q fever was 25 to 60 times greater than that reported in other microorganisms, including Leishmania and Legionella spp. The enzyme was found in rickettsiae grown in different hosts (L929 cells and embryonated eggs) and, in the case of L929 cells, for both short periods (less than a month) and the long term (years). Cytochemical techniques coupled with electron microscopy localized the phosphatase activity to the periplasmic gap in the parasite. Ion-exchange chromatography revealed a major species of the enzyme and showed that the enzyme of the parasite was distinct from that of the host cell (L929 fibroblasts); its apparent molecular weight was 74,000. Phosphatase inhibitors (i.e., molybdate heteropolyanions) had differential effects on the phosphatases of the parasite and host cell. C. burnetii supernatant fluid inhibited superoxide anion production by formyl-Met-Leu-Phe-stimulated human neutrophils; molybdate inhibitors reversed the inhibition. Treatment of C. burnetii-infected L929 cells with one of the molybdate compounds (complex B') significantly reduced the level of infection and did not affect the viability or growth of the host cell. These data suggest that the acid phosphatase of the parasite may be a major virulence determinant, allowing the agent to avoid being killed during uptake by phagocytes and subsequently in the phagolysosome.

Acid Phosphatase↗

PubMedDate not supplied

[An experimental infection of Hyalomma asiaticum and Ornithodoros papillipes ticks with a single and combined infection with Coxiella burnetii and Dermacentroxenus sibericus].

Experimental infection of H. asiaticum and O. papillipes with Coxiella burnetii and R. (D.) sibericus in different succession and individual study of these arthropods by means of the fluorescent antibodies method, ordinary microscopy and titration on laboratory animals have revealed an ambiguous outcome of the development of combined rickettsial infection in these ticks. The first agent obtained by the vector either prevents utterly the reproduction of the heterologous agent or inhibits its activity. At the concurrent infection of the ticks with two species of rickettsiae the reproduction of the both agents takes place but against a background of intersuppression of their reproduction. The development of the combined rickettsial infection in ticks is an example of "irregular competition" of species as one of the types of competitive relationships.

Animals↗

PubMed2005

Replication of Coxiella burnetii is inhibited in CHO K-1 cells treated with inhibitors of cholesterol metabolism.

Coxiella burnetii directs the synthesis of a large parasitophorous vacuole (PV) that is required for its replication. While some lysosomal characteristics of the PV have been described, the origin and composition of the PV membrane remain largely undefined. Cholesterol is an essential component of mammalian membranes where it lends mechanical stability and serves as a platform for signaling proteins. Using infected Chinese hamster ovary cells as a model, we examined whether cholesterol is trafficked to the C. burnetii PV membrane and the effects of inhibitors of cholesterol metabolism on C. burnetii replication. When infected cells were stained with filipin, a fluorescent polyene antifungal agent that binds cholesterol, obvious staining of PV was observed indicating the PV membrane is cholesterol-rich. Furthermore, replication of C. burnetii was significantly inhibited in cells treated with the cholesterol metabolism inhibitors lovastatin, ketoconazole, imipramine, progesterone, and U18666A. These data suggest that cholesterol is an important component of the C. burnetii PV membrane and that normal cellular cholesterol metabolism is required for optimal C. burnetii replication.

Animals↗

PubMed1992

Ultrastructure of viable and inactivated Coxiella burnetii after inoculation of mice.

C3HA mice were inoculated intraperitoneally (i.p.) with viable Coxiella burnetii (C.b.) (strain Apodemus flavicollis-Luga, phase I) or C.b. antigen (formalin-inactivated C.b.); pieces of spleen, liver, omentum, kidney, and suspension of peritoneal macrophages were examined by electron microscopy at 1, 7, 14, 21, 28, and 42 days post-infection (p.i.). Two main types of viable C.b. cells--small dense (DC) and bacteria-like (BC)--were found in omentum, spleen, and peritoneal exudate cells beginning from the 1st day p.i. but maximal amount they reached in spleen at day 14. Some parasitophorous vacuoles contained damaged BC or lysing C.b. cells. C.b. corpuscular antigen was found in phagosomes in ultrathin sections of spleen macrophages until 28 days p.i. By 7 days p.i. in omentum 3 types of parasitophorous phagosomes were described which were supposed to be the sites of the antigen utilization. It is assumed that most BC are destroyed in omentum macrophages during the 1st week after i.p. injection of the antigen, and DC can persist in spleen at least for one month.

Animals↗

PubMed1981

Immunological and biological characterization of Coxiella burnetii, phases I and II, separated from host components.

Coxiella burnetii, phase I and II, cells cultivated in the yolk sac of chicken embryos were separated from host cell components by two cycles of isopycnic Renografin gradient centrifugation. Initial steps in the purification of viable C. burnetii involved differential centrifugation and sedimentation through an aqueous solution of 30% sucrose and 7.6% Renografin. After the first, but not the second, cycle of Renografin gradient centrifugation, the cells were passed through microfilter glass filters which facilitated the removal of host components. The integrity of morphologically different cell variants was maintained during purification procedures by suspending highly purified C. burnetii in phosphate-buffered saline-sucrose solutions. C. burnetii, phases I and II, obtained by these methods appeared to be free from host cell components by serological methods while retaining morphological integrity and infectivity for yolk sacs and experimental animals. Average yields of C. burnetii were 2.83, 1.5, and 0.84 mg (dry weight) per yolk sac of the Ohio strain (phase I), 9 Mile strain (phase I), and 9 Mile strain (phase II), respectively. Recovery of phase I cells averaged about 70%, whereas the recovery of phage II cells was approximately 40%. The temporal sequence of phase I and II antibody response was demonstrated in infected and vaccinated animals. Also, no antibody response in mice and guinea pigs to yolk sac antigens was detectable after two injections of vaccine or viable cells. Importantly, this is the first report of the separation of viable phase II cells of C. burnetii free of host components.

Animals↗

PubMed1981

Stability of the adenosine 5'-triphosphate pool in Coxiella burnetii: influence of pH and substrate.

The ability of Coxiella burnetii to couple oxidation of metabolic substrates to adenosine 5'-triphosphate (ATP) synthesis in axenic reaction buffers was examined. Pyruvate, succinate, and glutamate were catabolized and incorporated at the highest rates of 11 substrates tested. Glutamate oxidation, however, resulted in the greatest stability of the ATP pool and highest intracellular ATP levels over a 48-h period. At pH 4.5, the optimum for metabolism by C. burnetii, glutamate oxidation resulted in maintenance of the ATP pool at a concentration of approximately 0.7 nmol of ATP per mg of dry weight over a 96-h period. In the absence of substrate, ATP declined by 96 h to less than 0.01 nmol/mg of dry weight. When cells were maintained at pH 7.0 in the presence or absence of glutamate, ATP pools were considerably more stable, presumably due to the minimal metabolic activity displayed by C. burnetii at pH 7. The stability of the ATP pool reflected viability as there was greater than an 8-log decrease in viable C. burnetii after incubation for 7 days at pH 4.5 in the absence of glutamate. Viability was retained in the presence of glutamate at pH 4.5 or 7.0 in the absence of any added substrate. The stability of the ATP pool was due to endogenous synthesis of ATP coupled to substrate oxidation as shown by depression of ATP levels in the presence of inhibitors of electron transport or oxidative phosphorylation. In addition, the adenylate energy charge increased from an initial value of 0.57 to 0.73 during glutamate oxidation with a concomitant rise in the total adenylate pool size. C. burnetii therefore appears able to regulate endogenous ATP levels in response to substrate availability and pH, thus effecting a conservation of metabolic energy in neutral or alkaline environments. Such a mechanism has been proposed to play a role in the resistance of C. burnetii to environmental conditions and subsequent activation upon entry into the phagolysosome in which this organism replicates.

Adenosine Monophosphate↗

PubMedDate not supplied

Experimental Coxiella burnetii infection in pregnant goats: excretion routes.

Q fever is a widespread zoonosis caused by Coxiella burnetii. Infected animals, shedding bacteria by different routes, constitute contamination sources for humans and the environment. To study Coxiella excretion, pregnant goats were inoculated by the subcutaneous route in a site localized just in front of the shoulder at 90 days of gestation with 3 doses of bacteria (10(8), 10(6) or 10(4) i.d.). All the goats aborted whatever the dose used. Coxiella were found by PCR and immunofluorescence tests in all placentas and in several organs of at least one fetus per goat. At abortion, all the goats excreted bacteria in vaginal discharges up to 14 days and in milk samples up to 52 days. A few goats excreted Coxiella in their feces before abortion, and all goats, excreted bacteria in their feces after abortion. Antibody titers against Coxiella increased from 21 days post inoculation to the end of the experiment. For a Q fever diagnostic, detection by PCR and immunofluorescence tests of Coxiella in parturition products and vaginal secretions at abortion should be preferred to serological tests.

Abortion, Veterinary↗