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PubMed1964

SOME BIOCHEMICAL CHANGES IN THE GUINEA PIG DURING INFECTION WITH COXIELLA BURNETII.

Paretsky, D. (University of Kansas, Lawrence), C. M. Downs, and C. W. Salmon. Some biochemical changes in the guinea pig during infection with Coxiella burnetii. J. Bacteriol. 88:137-142. 1964.-Guinea pigs infected with Coxiella burnetii, the rickettsial agent of Q fever, were studied for 11 days postinfection. Maximal changes in liver lipids, liver phosphorylase, and uridine diphosphate glucose (UDPG)-glycogen glucosyl-transferase activities occurred 3 to 4 days post-infection. In this period, total liver lipids increased from 1.26 to 5.46 mg/mg of N, with the largest increment in the glyceride fraction. Liver glycogen virtually disappeared by the second day, with no chemically detectable restoration until the eleventh day. A pattern of altered phosphorylase and UDPG-glycogen transglucosylase activities was observed, with maximal phosphorylase and minimal glucosyltransferase activities at the third and fourth days. Histochemical observations confirmed chemical analyses for lipids and glycogen.

Animals↗
PubMed1998

Effect of endocytosis inhibitors on Coxiella burnetii interaction with host cells.

The obligate intracellular rickettsia Coxiella burnetii has previously been reported to reach the intravacuolar compartment of host cells by phagocytosis. With the aim to further examine the mechanisms of C. burnetii internalisation, macrophage monolayers were treated with well characterised inhibitors of endocytosis. The treatment with two general inhibitors, colchicine and methylamine, resulted in a pronounced dose-dependent decrease of radiolabelled phase II rickettsiae retained from the intracellular fraction. A third inhibitor used, amiloride, has been reported to reduce effectively clathrin-independent pinocytic pathways. The internalisation of C. burnetii was shown to be substantially reduced also by amiloride and the effect was dependent on its concentration. The passive role of C. burnetii in the internalisation was verified by using heat-killed C. burnetii. Host cells treated with either of the three inhibitors (amiloride, colchicine and methylamine) showed a similar reduction of intracellular C. burnetii after exposure to killed as well as live organisms. The data presented indicate that different endocytic mechanisms, pinocytosis as well as phagocytosis, may mediate the uptake of C. burnetii by a host cell.

Amiloride↗
PubMed1963

Studies on the physiology of Rickettsiae. IV. Folic acids of Coxiella burnetii.

Mattheis, Martha S. (University of Kansas, Lawrence), M. Silverman, and D. Paretsky. Studies on the physiology of rickettsiae. IV. Folic acids of Coxiella burnetii. J. Bacteriol. 85:37-41. 1963.-Yolk, yolk sac, and embryo tissues of uninfected eggs, and those infected with Coxiella burnetii, were analyzed for folic acid derivatives by employing diethylaminoethyl (DEAE)-cellulose column chromatography. Infected tissues contained quantitatively less folate, but the elution profiles of both infected and uninfected tissues were identical. Purified C. burnetii contained some types of folate apparently unique to these rickettsiae, and not found in infected tissue. The major folate fraction of C. burnetii was partially characterized by (i) elution position from DEAE columns; (ii) treatment with conjugase; (iii) growth response by Lactobacillus casei, Streptococcus faecalis R, and Pediococcus cerevisiae; and (iv) response to oxidation, reduction, and formylation.

Coxiella↗
PubMed1995

Cloning, sequencing and expression of the dnaJ gene of Coxiella burnetii.

A 6-kb EcoRI genomic DNA fragment of Coxiella burnetii, isolated from a recombinant bacteriophage lambda ZapII library, allowed heterologous genetic complementation of Escherichia coli deleted for its dnaJ gene. The C. burnetii dnaJ gene was expressed in E. coli and identified by Western blot analysis using polyclonal antibodies raised against purified E. coli DnaJ protein. Deletion mapping and genetic complementation demonstrated that C. burnetii dnaJ is present on a 2-kb EcoRI-HindIII genomic DNA fragment, from which the nt sequence of the C. burnetii dnaJ gene was determined.

Amino Acid Sequence↗
PubMed1994

Analysis of the rnc locus of Coxiella burnetii.

A 3.2 kb EcoRI genomic DNA fragment of Coxiella burnetii was isolated by virtue of its ability to suppress mucoidy in Escherichia coli. Nucleotide sequence analysis revealed the presence of the genes homologous to rnc, era and recO of E. coli. Suppression of capsule synthesis, measured by beta-galactosidase expression in lon- cps-lac fusion strains of E. coli, is caused by gene-dosage effects of the plasmid-borne rnc genes of either C. burnetii or E. coli. The rnc gene of C. burnetii complemented rnc- E. coli hosts for lambda plaque morphology and stimulation of lambda N gene expression. We also demonstrated heterologous complementation of an E. coli strain defective for the expression of Era, an essential protein in E. coli, using the plasmid-borne C. burnetii era. Under the control of the bacteriophage lambda PL promoter, this 3.2 kb EcoRI DNA fragment directed the synthesis in E. coli of three proteins with approximate molecular masses of 35, 27 and 25 kDa. Antibodies against purified E. coli Era protein cross-reacted with the 35 kDa protein of C. burnetii on Western blots.

Amino Acid Sequence↗
PubMed1992

Dynamics of non-specific antibacterial activity of the peritoneal cells of mice induced with Coxiella burnetii antigen.

It was found that primary immunization with Coxiella burnetii antigen increased mouse resistance to Salmonella typhimurium infection as evidenced by acceleration of bacterial elimination from the peritoneal cavity and a decrease in lethality of experimental animals. The existence of two rises of bactericidal activity of mouse peritoneal cells was ascertained: the "early" on days 1 and 2, and the "late" on day 14 after C. burnetii administration. The first rise was accompanied by some increase in the number of peritoneal cells as well as by some change of their qualitative representation. The second increase of antibacterial activity was detected during the pronounced cellular and humoral immune responses to C. burnetii.

Animals↗
PubMed2001

Activation of protein tyrosine kinases by Coxiella burnetii: role in actin cytoskeleton reorganization and bacterial phagocytosis.

Coxiella burnetii, the agent of Q fever, is an obligate intracellular microorganism that grows in monocytes/macrophages. The internalization of virulent organisms by monocytes is lower than that of avirulent variants and is associated with actin cytoskeleton reorganization. We studied the activation of protein tyrosine kinases (PTKs) by C. burnetii in THP-1 monocytes. Virulent organisms induced early PTK activation and the tyrosine phosphorylation of several endogenous substrates, including Hck and Lyn, two Src-related kinases. PTK activation reflects C. burnetii virulence since avirulent variants were unable to stimulate PTK. We also investigated the role of PTK activation in C. burnetii-stimulated F-actin reorganization. Tyrosine-phosphorylated proteins were colocalized with F-actin inside cell protrusions induced by C. burnetii, and PTK activity was increased in Triton X-100-insoluble fractions. In addition, lavendustin A, a PTK inhibitor, and PP1, a Src kinase inhibitor, prevented C. burnetii-induced cell protrusions and F-actin reorganization. We finally assessed the role of PTK activation in bacterial phagocytosis. Pretreatment of THP-1 cells with lavendustin A and PP1 upregulated the uptake of virulent C. burnetii but had no effect on the phagocytosis of avirulent organisms. Thus, it is likely that PTK activation by C. burnetii negatively regulates bacterial uptake by interfering with cytoskeleton organization.

Actins↗
PubMed1996

High incidence of Coxiella burnetii markers in a rural population in France.

Since Coxiella burnetii, the causative agent of Q fever, is often transmitted from goats and sheep to humans through aerosols, we examined the sera from 168 persons involved in goat breeding in the Centre region of France and 40 members of veterinary and medical staff from the same region for the presence of antibodies against C. burnetii. An immunofluorescence assay was used to detect the presence of antibodies of the IgG isotope against epitopes from phase II of C. burnetii, which are the first antibodies to appear in infected people, and from phase I, which reflect more chronic stages of the infection. Our serological survey showed that most of the tested sera were positive for C. burnetii markers, indicating at least an encounter with the bacterium. In the overall population of 208 subjects, 71% of the sera had antibodies against phase II epitopes (titres > or = 1:40). Among the goat farmers and their immediate families, 78% had antibodies against phase II and 33% against phase I (titres > or = 1:40). Considering only high titres (> or = 1:320), though, only 37% of the farmers had antibodies against phase II and 15% against phase I. Only 3 out of 12 veterinarians working in the field had high titres of antibodies against phase II and phase I, while none of 28 members of veterinary and medical laboratories had significant levels of antibodies. These results emphasize the need for closer surveillance of populations at risk for Q fever, to prevent the infection by C. burnetii from reaching chronic stages of the disease.

Agricultural Workers' Diseases↗
PubMed2003

Interleukin-4 induces Coxiella burnetii replication in human monocytes but not in macrophages.

Coxiella burnetii, an obligate intracellular bacterium, is the agent of Q fever. The chronic disease is characterized by impaired cell-mediated immune response and microbicidal activity of monocytes. We hypothesized that interleukin(IL)-4, a Th2 cytokine, interferes with the fate of C. burnetii inside monocytes. C. burnetii survived without multiplication in resting monocytes, but replicated in IL-4-treated monocytes. The effect of IL-4 is specific for monocytes since IL-4 did not stimulate C. burnetii replication in monocyte-derived macrophages. The effects of IL-4 on bacterial replication and on tumor necrosis factor (TNF) production in monocytes were apparently not related. Although IL-4 inhibited C. burnetii-stimulated release of TNF, the addition of recombinant TNF to IL-4-treated monocytes did not prevent the IL-4 effect. These results suggest that IL-4 enables monocytes to support C. burnetii replication and a Th2 polarization of immune response that may interfere with immune control of Q fever.

Cell Division↗
PubMed1999

Intraspecies diversity of Coxiella burnetii as revealed by com1 and mucZ sequence comparison.

Coxiella burnetii is classified within the gamma subgroup of the Proteobacteria. All strains tested to date have an identical 16S rRNA sequence but 20 different genotypes have been determined by pulsed field gel electrophoresis (PFGE). In this study, intraspecies genetic diversity was investigated by sequence comparison of 715 bp of the Com1 encoding gene (com1) and 774 bp of the MucZ encoding gene (mucZ) in 37 strains isolated from animals and humans with acute or chronic Q fever in Europe, North America and Africa. Five and four groups were established from sequence analysis of com1 and mucZ, respectively. Neither relation of the defined groups to geographical distribution of the isolates was noted nor relation to disease form (acute/chronic). The same isolates were grouped together regardless of the gene being investigated. Comparison of the five proposed groups to previous groups, yielded after digestion by NotI PFGE, allowed for an intermediate classification of C. burnetii isolates between those obtained by using 16S rDNA (one group) and PFGE (20 groups).

Animals↗
PubMed2000

Reduced transendothelial migration of monocytes infected by Coxiella burnetii.

The migratory properties of THP1 monocytes infected by Coxiella burnetii were determined in a transmigration assay across a human microvascular endothelial cell monolayer. Transendothelial migration of monocytes infected by virulent, but not avirulent, C. burnetii was inhibited. This inhibition was observed in spite of conserved adherence properties of infected monocytes.

Animals↗
PubMed1994

In vivo endogenous spore formation by Coxiella burnetii in Q fever endocarditis.

AIMS: To determine whether Coxiella burnetii, the aetiological agent of Q fever, undergoes endogenous spore-like formation, the crucial stage of the developmental cycle, in the infected cardiac valves of patients with chronic Q fever endocarditis. METHODS: Surgically removed valves from three cases of Q fever endocarditis were processed for electron microscopy. Sections were stained with potassium permanganate and uranyl acetate before being extensively examined by transmission electron microscopy. RESULTS: In all three cases endogenous spore-like formation was seen in the infected cardiac valves. CONCLUSIONS: As the factors that govern sporogenesis in C burnetii are still largely unknown, it is uncertain how important are the implications of the discovery of endogenous spore-like formation in Q fever endocarditis. However, this finding may add new dimensions to current thinking about the treatment of chronic Q fever.

Adult↗
PubMed2000

In vitro activities of telithromycin (HMR 3647) against Rickettsia rickettsii, Rickettsia conorii, Rickettsia africae, Rickettsia typhi, Rickettsia prowazekii, Coxiella burnetii, Bartonella henselae, Bartonella quintana, Bartonella bacilliformis, and Ehrlichia chaffeensis.

In vitro activities of telithromycin compared to those of erythromycin against Rickettsia spp., Bartonella spp., Coxiella burnetii, and Ehrlichia chaffeensis were determined. Telithromycin was more active than erythromycin against Rickettsia, Bartonella, and Coxiella burnetii, with MICs of 0.5 microg/ml, 0.003 to 0.015 microg/ml, and 1 microg/ml, respectively, but was inactive against Ehrlichia chaffeensis.

Anti-Bacterial Agents↗
PubMedDate not supplied

Protein-tyrosine phosphatase activity of Coxiella burnetii that inhibits human neutrophils.

Supernatants prepared from disrupted Coxiella burnetii possess acid phosphatase (ACP) activity that apparently accounts for the inhibition of the metabolic burst of formyl-Met-Leu-Phe(fMLP)-stimulated human neutrophils. Results are presented regarding purification and biochemical-biological characterization of the ACP. The highly purified enzyme, which exhibited an apparent M(r) of 91 K and optimal activity at pH 5.0, also inhibited neutrophils. The enzyme retained full activity at pH 4.5, 5.5, and 7.4, when incubated overnight at 0 degrees C and room temperature; at pH 5.5, it retained full activity after overnight incubation at 37 degrees C. Apparently, the enzyme contains asparagine-linked but not serine- or threonine-linked glycan residues since its treatment with N-glycosidase F (PNGase F) decreased its M(r) to 87 K and no changes were detected with O-glycosidase. The enzyme's capacity to hydrolyze phosphate from a number of phosphate-containing compounds was examined; five phosphocompounds were significantly hydrolyzed: 5'-CMP > fructose 1,6-diphosphate > tyrosine phosphate > 3'-AMP > 5'-AMP. The ACP also dephosphorylated (32)P-Raytide, a phosphotyrosine-containing peptide. Dephosphorylation of Raytide was inhibited by the following phosphatase inhibitors: sodium molybdate, potassium fluoride, sodium ortho-vanadate and D2, a heteropolymolybdate compound. These results indicate that C. burnetii ACP may play a role in disrupting tyrosine phosphorylation/dephosphorylation reactions associated with the signal transduction pathway culminating in the metabolic burst. Interestingly, Western blot analysis of ACP-inhibited neutrophils showed a marked increase in tyrosine phosphorylation of a 44 K protein as compared to uninhibited cells.

Acid Phosphatase↗
PubMed1993

[Experimental studies on the development of an antigen-capture test (Capture-ELIFA) for the detection of Coxiella burnetii in cow's milk as a possible alternative to animal studies].

A sensitive and specific Capture-ELIFA (Enzyme-linked-Immunofluorescent Assay) for the detection of Coxiella burnetii was developed using a monoclonal antibody and a rabbit immune serum, both directed against Coxiella burnetii, strain Nine Mile, phase I. A combination of centrifugation, Pronase-K-digestion and heat treatment proved to be advantageous for concentrating, exposure and inactivating of Coxiella antigens in milk samples. Using this method of sample preparation 4 x 10(3) coxiella particles/ml could be detected in experimentally contaminated milk samples by the optimized Capture-ELIFA. Preliminary results of comparative investigations indicate that the Capture-ELIFA is more sensitive than the inoculation of guinea pigs and subsequent detection of seroconversion.

Animal Testing Alternatives↗
PubMed1978

Influence of mild acid hydrolysis on the antigenic properties of phase I Coxiella burnetii.

Mild acid hydrolysis of phase I Coxiella burnetii cells gradually cleaved off polysaccharide chains, which contain determinants of antigen 1, thus unmasking determinants of the diagnostically important antigen 2. This artificial phase I to phase II conversion was reflected by changed serological activity in the complement-fixation (CF) test and by changed nonspecific phagocytosis. The product of mild acid hydrolysis can serve as a complex diagnostic preparation, because it reacts in the CF test with antibodies directed to both C. burnetii antigens.

Animals↗
PubMed2007

Prevalence of Coxiella burnetii DNA in vaginal and uterine samples from healthy cats of north-central Colorado.

Q fever is a worldwide zoonotic disease caused by Coxiella burnetii. Although traditionally associated with livestock exposure, human infection has also been documented from contact with parturient cats. The goal of this study was to determine the prevalence of C burnetii DNA in uterine and vaginal tissues from healthy client-owned and shelter cats of north-central Colorado using polymerase chain reaction assay. Coxiella burnetii was not amplified from vaginal samples of any cat or uterine biopsies of shelter cats. However, a nucleotide sequence with 99% homology to C burnetii DNA was amplified from four of 47 (8.5%) uterine biopsies of client-owned cats. This study demonstrates that clinically normal cats in north-central Colorado can harbor C burnetii. Care should be taken when attending to parturient cats and contact with parturient secretions should be avoided. Additional studies are indicated to further characterize the role of cats in zoonotic Q fever.

Animals↗