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PubMed1978

Comparison of ribosomes from Coxiella burnetii and Escherichia coli by gel electrophoresis, protein synthesis, and immunological techniques.

Ribosomes and postribiosomal supernatant fluid (S-100) were isolated from Coxiella burnetii. The ribosomes functioned in polyuridylic acid-directed polyphenylalanine synthesis in the presence of S-100 from either C. burnetii or Escherichia coli. C. burnetii S-100 promoted translation with E. coli ribosomes. Antisera against E. coli elongation factor G and ribosomal proteins L7/L12 cross-reacted with rickettsial S-100 and ribosomes, respectively. Ribosomal proteins were analyzed by two-dimensional gel electrophoresis.

Bacterial Proteins↗
PubMed2000

Repeated pregnancies in BALB/c mice infected with Coxiella burnetii cause disseminated infection, resulting in stillbirth and endocarditis.

Q fever is a widespread zoonosis caused by the obligate intracellular bacterium Coxiella burnetii. Although this highly virulent organism is most concentrated in mammals during parturition, there are few reports on the manifestations of perinatal Q fever in the human and animal host. The affinity of C. burnetii to pregnancy and its abortifacient potential were investigated in a murine animal model. Intraperitoneal infection of female BALB/c mice with C. burnetii, followed by repeated pregnancies over a 2-year period, resulted in persistent infection associated with abortion and perinatal death, with a statistically significant decrease in viable offspring. In addition, endocarditis occurred in 2 of the adult animals, and C. burnetii antigen and DNA were detected in their heart valves. Taken together, these results demonstrate the abortifacient potential of C. burnetii and the increased risk of persistent infection and endocarditis in pregnant mice, probably related to a decline in cellular immunity during pregnancy.

Animals↗
PubMed1986

Characterization of a phase I Coxiella burnetii chloroform-methanol residue vaccine that induces active immunity against Q fever in C57BL/10 ScN mice.

The effect of phase I Coxiella burnetii chloroform-methanol residue vaccine (CMRV) on the response of murine splenic lymphocytes to mitogenic and antigenic stimuli was evaluated in C57BL/10 ScN endotoxinnonresponder mice with an in vitro lymphocyte proliferation assay. Intraperitoneal injection of phase I CMRV resulted in antibody production against phases I and II antigens. Lymphocytes were responsive in vitro to concanavalin A, phytohemagglutinin, pokeweed mitogen, and specific recall antigens. Antibodies against phases I and II antigens were not detected after intraperitoneal injection of chloroform-methanol extract (CME). Lymphocytes also were only slightly hyporesponsive to mitogens. Reconstitution of the CMRV with the CME of phase I whole cells restored the immunopathological reactions that were associated with the phase I whole cell vaccine (WCV). The CMRV was more mitogenic than the WCV for lymphocytes from mice injected with saline. Lymphocytes from phase I WCV-injected mice were negatively modulated with nontoxic concentrations of homologous WCV or CMRV. Lymphocytes from phase I CMRV-injected mice were only slightly hyporesponsive to mitogens and were significantly stimulated by antigens of either WCV or CMRV as recall antigens. Vaccination of mice with 100 micrograms of CMRV, CME, or WCV provided 80, 0, or 50% protection, respectively, against a lethal intraperitoneal challenge with viable phase I C. burnetii. The epitopes which induce immunological hyporesponsiveness, negative modulation, and the death of lymphocytes were fractionated into the CMRV and CME. The CMRV provides at least one of the determinants which induce immunosuppression, whereas CME contains specific or nonspecific components or both. Collectively, these results show that the CMRV may be a potential candidate to replace the WCV currently used for human vaccination.

Animals↗
PubMed1985

Histological changes in mouse liver and spleen caused by different Coxiella burnetii antigenic preparations.

The effect was examined on mouse liver and spleen (inbred line A) of intraperitoneal (i.p.) inoculation of phase I Coxiella burnetii (C.b.) cells either untreated or treated with chloroform-methanol (CM) mixture in comparison to the trichloracetic acid extract (TCAE) from phase I C.b.) cells. The phase I C.b. cells were highly toxic as manifested by marked hepatosplenomegaly accompanied with hyperplastic, degenerative and necrotic changes in the liver. By contrast, phase I CM--treated C.b. cells and TCAE were nontoxic as evidenced by the absence of any distinct pathological changes in mouse viscera.

Animals↗
PubMed1989

Endotoxicosis induced by Coxiella burnetii lipopolysaccharide stimulates a ribosomal protein S6 kinase: some properties of the partially purified enzyme.

Guinea pig endotoxicosis induced by lipopolysaccharide from Coxiella burnetii Nine Mile phase I stimulates phosphorylation of liver ribosomal protein S6, with a 50% increase at 12 h postinoculation. The responsible protein kinase (S6PK) has been partially purified from liver; its activity is independent of cyclic AMP and of Ca2+ plus phosphatidyl serine or diacylglycerol. The preparation has an apparent optimum concentration of 20 mM Mg2+, while Ca2+ and Mn2+ are each inhibitory at 2 mM. The apparent Km for ATP is 30 microM with intact ribosomes. Because of the central role of phosphorylation in metabolic regulation and a purported role of phosphorylated S6 in protein synthesis, the lipopolysaccharide-induced stimulation of S6PK suggests a significant regulatory role of such enzymes in the pathobiochemistry of Q fever infection and endotoxicosis.

Animals↗
PubMed2002

Chronic fatigue following infection by Coxiella burnetii (Q fever): ten-year follow-up of the 1989 UK outbreak cohort.

BACKGROUND: Some patients exposed to Q fever (Coxiella burnetii infection) may develop chronic fatigue. AIM: To determine whether subjects involved in the West Midlands Q fever outbreak of 1989 had increased fatigue, compared to non-exposed controls, 10 years after exposure. DESIGN: Matched cohort study comparing cases to age-, sex- and smoking-history-matched controls not exposed to Q fever. METHODS: A postal questionnaire was sent to subjects at home, followed by further assessment in hospital, including a physical examination and blood tests. RESULTS: Of 108 Q-exposed subjects, 70 (64.8%) had fatigue, 37 idiopathic chronic fatigue (ICF) (34.3%), vs. 29/80 (36.3%) and 12 (15.0%), respectively, in controls. In 77 matched pairs, fatigue was commoner in Q-exposed subjects than in controls: 50 (64.9%) vs. 27 (35.1%), p<0.0001. ICF was found in 25 (32.5%) of Q-exposed patients and 11(14.3%) of controls (p=0.01). There were 36 (46.8%) GHQ cases in Q-exposed subjects, vs. 18 (23.4%) controls (p=0.004). A matched analysis of those more intensively studied showed fatigue in 48 (66.7%) Q-exposed patients and 25 (34.7%) controls, (p<0.0001), ICF in 25 (34.7%) Q-exposed and 10 (13.9%) controls (p=0.004), and chronic fatigue syndrome (CFS) in 14 (19.4%) Q-exposed patients and three (4.2%) controls (p=0.003). Thirty-four (47.2%) Q-exposed patients were GHQ cases compared to 17 (23.6%) controls (p=0.004). DISCUSSION: Subjects who were exposed to Coxiella in 1989 had more fatigue than did controls, and some fulfilled the criteria for CFS. Whether this is due to ongoing antigen persistence or to the psychological effects of prolonged medical follow-up is uncertain.

Case-Control Studies↗
PubMed2001

Coxiella burnetii infection in C.B-17 scid-bg mice xenotransplanted with fetal bovine tissue.

Two from a group of approximately 50 C.B-17 scid-bg mice were examined because of lethargy, dehydration, and rough coat. Three months prior to development of clinical signs of disease, mice of this study had been surgically implanted with fetal bovine liver, thymus, and lymph node. At necropsy, marked splenomegaly and mild hepatomegaly were observed in both animals. Large areas of necrosis and inflammation, with associated intracytoplasmic granular basophilic inclusions, were observed in histologic sections of multiple organs. Aerobic and anaerobic culturing of the liver yielded negative results. Six months after the initial case, four more reconstituted scid-bg mice from a different fetal donor had identical clinical, gross, and histologic signs of disease. To determine whether the basophilic inclusions represented an infective agent, 4-month-old immune-naive C.B-17 scid-bg mice were inoculated intraperitoneally with a liver and spleen homogenate from an affected mouse. Two weeks after inoculation, mice developed clinical signs of disease and lesions identical to those seen in the signal mice. On ultrastructural examination of the liver, pleomorphic bacteria were found in large cytoplasmic vacuoles of hepatocytes. Bacterial DNA was amplified from the liver, using primers that amplify a segment of the 16S rRNA gene from many bacterial species. Sequencing of the polymerase chain reaction (PCR) product revealed gene sequence identical to that of Coxiella burnetii, the agent of Q-fever. These results highlight the need to consider infective agents of the donor species when working with xenografted animals.

Abdomen↗
PubMed1983

Estimation of the cytoplasmic pH of Coxiella burnetii and effect of substrate oxidation on proton motive force.

The magnitude of the proton motive force generated during in vitro substrate oxidation by Coxiella burnetii was examined. The intracellular pH of C. burnetii varied from about 5.1 to 6.95 in resting cells over an extracellular pH range of 2 to 7. Similarly, delta psi varied from about 15 mV to -58 mV over approximately the same range of extracellular pH. Both components of the proton motive force increased during substrate oxidation, resulting in an increase in proton motive force from about -92 mV in resting cells to -153 mV in cells metabolizing glutamate at pH 4.2. The respiration-dependent increase in proton motive force was blocked by respiratory inhibitors, but the delta pH was not abolished even by the addition of proton ionophores such as carbonyl cyanide-m-chlorophenyl hydrazone or 2,4-dinitrophenol. Because of this apparently passive component of delta pH maintenance, the largest proton motive force was obtained at an extracellular pH too low to permit respiration. C. burnetii appears, therefore, to behave in many respects like other acidophilic bacteria. Such responses are proposed to contribute to the extreme resistance of C. burnetii to environmental conditions and subsequent activation upon entry into the phagolysosome of eucaryotic cells in which this organism multiplies.

2,4-Dinitrophenol↗
PubMed1987

Comparative virulence of intra- and interstrain lipopolysaccharide variants of Coxiella burnetii in the guinea pig model.

We compared the relative infectivity and virulence of lipopolysaccharide (LPS) variants of the Nine Mile strain of Coxiella burnetii with those of the Priscilla strain, a representative of endocarditis-type strains. In agreement with results of previous studies, Nine Mile phase I (9mi/I) organisms were highly infectious, eliciting seroconversion and fever with inocula containing as few as four organisms. Viable 9mi/I was recovered from the spleens of infected animals 30 days postinfection. Nine Mile phase II (9mi/II) organisms did not elicit fever or seroconversion except with very large inocula, and viable organisms could not be recovered at 30 days postinfection. The Nine Mile/Crazy variant, bearing the intermediate-type LPS, was also highly infectious, as determined by fever response and seroconversion, although, as with 9mi/II, viable organisms could not be recovered 30 days postinfection. The Priscilla strain in phase I (Pris/I) was as infectious as 9mi/I, as determined by seroconversion and its presence in the spleen 30 days postinfection; but in contrast to 9mi/I, more than 10(5) Pris/I isolates were required to induce fever. The temporal appearances of anti-phase I and II antibodies were similar for the two strains. A variety of serological techniques measuring antibody response against whole-cell and purified LPS antigens in agglutination, immunofluorescence, enzyme-linked immunosorbent, and immunoblot assays did not demonstrate sufficient specificity to distinguish between 9mi/I and Pris/I infections. Results of vaccine cross-challenge experiments showed a significant degree of protection between homologous and heterologous challenge strains. protection between homologous

Animals↗
PubMed1997

Coxiella burnetii: the 'query' fever bacterium. A model of immune subversion by a strictly intracellular microorganism.

Although substantial progress occurred in the knowledge of Coxiella burnetii during the past years, the pathophysiology of Q fever is still obscure. Emerging evidence from clinical investigations suggested that certain disorders of cell-mediated immunity play a pivotal role in Q fever and especially in its chronic form. This review analyses the potential strategies that C. burnetii, a strictly intracellular pathogen, use to divert microbicidal mechanisms of macrophages and to depress protective T-cell mediated immunity. The role of monocytes in the induction of Q fever is specifically discussed.

Humans↗
PubMed1989

Chemical composition of phase I Coxiella burnetii soluble antigen prepared by trichloroacetic acid extraction.

Optimal conditions of extraction (time and temperature) by trichloroacetic acid of soluble antigen from phase I Coxiella burnetii (TCAE), possessing protective properties and used as a chemovaccine against Q fever in men, were studied. Extracts prepared under various conditions were analysed for their polysaccharide, protein and phosphorus contents. Forty-five min of extraction at 0 degrees C were sufficient to obtain a soluble antigen reacting in immunodiffusion with hyperimmune rabbit antiserum. The polysaccharide contents decreased with prolonged extraction at 0 degrees C. At higher extraction temperatures (37 and 100 degrees C), the polysaccharide contents increased while that of proteins decreased. TCAE prepared at 100 degrees C gave no positive immunodiffusion reaction.

Animals↗
PubMed1985

3-C-branched aldoses in lipopolysaccharide of phase I Coxiella burnetii and their role as immunodominant factors.

Mild acid hydrolysis with 1% acetic acid (100 degrees C, 15-60 min) of lipopolysaccharide (LPS) isolated from Coxiella burnetii phase I cells leads to a drastic decrease in its serological reactivity as shown by the passive hemolysis test. This decrease in reactivity occurs parallel or even prior to the cleavage of LPS into free lipid A and the polysaccharide moiety. During this mild hydrolysis two unusual sugars (X and Y) are released from the LPS, which were obtained in pure state by thin-layer chromatography. Analysis of their alditol acetate derivatives by gas chromatography/mass spectrometry revealed that sugar X is a 6-deoxy-3-C-methyl-hexose and sugar Y a 3-C-(hydroxymethyl)-pentose. Using a range of authentic standards and different thin-layer and gas chromatographic conditions, X could be recognized as 6-deoxy-3-C-methyl-gulose (virenose), very probably as the L form of this sugar (L-virenose). Y has been identified as 3-C-(hydroxymethyl)-lyxose (dihydrohydroxystreptose) by comparing it with newly synthesized 3-C-(hydroxymethyl)-pentoses (Dahlman, O., Garegg, P. J., Mayer, H., Schramek, S., unpublished results). Both branched sugars are (at least partially) in terminal positions since methylation analysis of LPS afforded (mainly) their permethylated derivatives. This analysis further showed virenose to be linked in C. burnetii phase I LPS as pyranose and dihydro-hydroxystreptose as furanose. The terminal linkage and the chemical nature of X and Y are in accordance with the observed acid-lability of the serological determinants.

Carbohydrates↗
PubMed2001

Bronchiolitis obliterans with organizing pneumonia associated with acute Coxiella burnetii infection.

We report the case of a 62-year-old man who developed bronchiolitis obliterans with organizing pneumonia (BOOP) associated with acute Coxiella burnetii infection. The diagnosis of BOOP was made by fiber-optic transbronchial biopsy. Treatment with corticosteroids resulted in rapid clinical improvement and complete resolution of airspace opacities. To the best of our knowledge, this is the first well-documented case of BOOP associated with C. burnetii infection. This case suggests that this infection might trigger the development of BOOP.

Acute Disease↗
PubMed1966

Quantitative assay of Coxiella burnetii in mice.

Experimental data are presented which demonstrate that the complement-fixing antibody response in individual mice can be used for quantitative assay of Coxiella burnetii. The method allows the replacement of a single guinea pig with a single mouse, thus resulting in considerable savings in caging requirements and animal costs.

Animals↗
PubMed1989

[Incidence of Coxiella burnetii and Rickettsiae from the RMSF group in the sub-Alpine region in Austria].

Investigations were carried out on small mammals to determine further distribution of Coxiella burnetii and Rickettsia RMSF-group in the Alpine and sub-Alpine regions. In altitudes of 1,200-2,400 m antibodies against Clethrionomys glareolus, Apodemus flavicollis, Sorex alpinus, Sorex minutus and Microtus agrestis were demonstrated. These findings emphasize that in the entire Alpine and sub-Alpine regions of Austria the occurrence of C. burnetii and RMSF-group rickettsia is to be expected.

Animals↗
PubMed1991

Antigenic differences between Coxiella burnetii cells revealed by postembedding immunoelectron microscopy and immunoblotting.

The aim of this study was to investigate the antigenic structures of the morphologically distinct cells of the Coxiella burnetii developmental cycle. Postembedding immunoelectron microscopy with polyclonal antibodies produced in rabbits to (i) phase I cells, (ii) a chloroform-methanol residue fraction of cells, (iii) the cell walls (CW) of large and small cells and small dense cells (SDC), and (iv) the peptidoglycan-protein complexes of small cells and SDC labelled the continuum of morphologically distinct cells. But these antibodies did not distinguish between the antigenic structures of the various cells. Monoclonal antibodies to the phase I lipopolysaccharide labelled the CW of a majority of the smaller cells, but there was diminished reactivity to the larger cells. Although monoclonal antibodies to a 29.5-kDa outer membrane protein labelled the CW of the large mother cells, the large cells, and the small cells, a minority of the SDC with compact CW were not labelled. The endogenous spore within the mother cell was not labelled by the polyclonal or monoclonal antibodies to cellular components. A selected population of SDC was prepared by osmotic lysis of large cells, differential centrifugation, Renografin step-gradient fractionation, and breakage of the small cells in a French press at 20,000 lb/in2. The pressure-resistant SDC collected as fraction CL did not contain the 29.5-kDa protein, as evidenced by the lack of (i) Coomassie brilliant blue staining of protein in the 29.5-kDa region of sodium dodecyl sulfate-polyacrylamide gels and (ii) reactivity of the 29.5-kDa protein antigenic epitopes in immunoblotting with monoclonal antibodies to the protein. In contrast, CW of the pressure-sensitive small cells contained the 29.5-kDa protein. Therefore, the observed ultrastructural differences between large and small cells and SDC reflect differences in sensitivity to breakage by pressure treatment and in cell-associated antigens. Although the process of differentiation in C. burnetii remains an enigma, we have taken steps toward identifying cellular antigens as markers of differentiation. The pressure-resistant SDC in fraction CL that are devoid of the 29.5-kDa protein may be useful for answering questions about the physiological events required for triggering outgrowth and sequential regulation of the Coxiella developmental cycle.

Animals↗