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PubMed1994

[Follow-up studies of the detection of IgG1 antibodies to Coxiella burnetii in blood and milk from cattle in relation to the reproductive cycle and milk production].

During a 14 month period, 36 dairy cattle were selected from a herd (n = 103), after IgG1 antibodies to Coxiella burnetii had repeatedly been detected in blood and milk, as measured by ELISA. ELISA results were analyzed with reference to reproductive cycle, daily milk yield, as well as daily concentration, and output of milk protein. The rate of positive blood samples slightly grew from 47.6% in the non-pregnant period, and 46.8% in the first half of pregnancy to 52.0% in the second half of pregnancy. In contrast, results of milk ELISA changed significantly from non-pregnant period to first, and second half of pregnancy, with increases from 23.8 to 38.5, and 64.6% of positive milk samples. Moreover, milk samples showed negative correlations between ELISA OD405 values and daily milk yield, as well as daily output of milk protein.

Animals↗
PubMed1994

Prevalence of antibodies to Coxiella burnetii in blood donors in the Czech Republic.

In 1988-1993, a total of 3,732 sera of blood donors from two districts (Strakonice and Nový Jicń) of the Czech Republic were tested for antibodies to Coxiella burnetii. Using the complement-fixation test at titers of 8 (10) and higher, the antibodies were detected in 41 (1.1%). No statistically significant difference in seroprevalence between the Strakonice and Nový Jicín districts was found (chi 2 = 2.536, P = 0.112, d.f. = 1). Antibodies were ascertained in 36 donors, 24 of which worked in agriculture. In one donor, antibodies persisted for at least 21 months. The highest ascertained titer was 160.

Agriculture↗
PubMed1997

Comparative efficacy of a Coxiella burnetii chloroform:methanol residue (CMR) vaccine and a licensed cellular vaccine (Q-Vax) in rodents challenged by aerosol.

Q fever is an acute and self-limited febrile illness caused by the obligate intracellular bacterium Coxiella burnetii. While phase I cellular Q fever vaccines are efficacious in humans, vaccination of immune individuals may result in sterile abscesses and granulomas. The chloroform:methanol residue vaccine (CMR) was developed as a safer alternative. The efficacy of a licensed phase I cellular vaccine (Q-Vax) was compared with that of CMR vaccine in A/J mice and Hartley guinea pigs challenged with virulent phase I C. burnetii by aerosol. Both vaccines were efficacious. The CMR vaccine dose required to protect 50% of mice (PD50) against lethal aerosol challenge (11 LD50) was one-third of the Q-Vax dose. However, the PD50 for CMR was four times the Q-Vax dose in guinea pigs challenged by aerosol (60 LD50). It was concluded that CMR is an efficacious alternative to cellular Q fever vaccines for the prevention of Q fever.

Aerosols↗
PubMed1989

Cell-mediated immune response to Coxiella burnetii antigens in Q fever convalescents and vaccinees.

Cellular immunity against phase I and II Coxiella burnetii antigens was evaluated by the lymphocyte blast transformation test in a) Q fever convalescents; b) persons immunized with a chemovaccine against Q fever; and c) control persons. The first two groups consisted of workers in a ricketsiology department. Of the 9 convalescents, all (100%) were positive against phase I antigen and 4 (44.4%) against phase II antigen. Of the 22 vaccinees, 77.3% were positive against phase I antigen and all were negative against phase II antigen. All 10 controls were negative against both antigens.

Antigens, Bacterial↗
PubMed1995

Antibodies to spotted fever group rickettsiae and Coxiella burnetii among domestic animals in southern Croatia.

The sera of dogs, goats, sheep and cattle (total 153) from the Kastelas' bay area (middle part of the eastern coast of the Adriatic Sea) were tested for antibodies against Rickettsia conorii and Coxiella burnetii by a complement fixation test. The overall percentages of positive sera among the tested animals were 23.9% for R. conorii and 16.4% for C. burnetii. The results show that animals in this area are clearly being exposed to spotted fever group rickettsiae as well as to C. burnetii. For comparison, six sheep sera from the flock, living in known Q fever focus in hinterland area and linked with outbreak of Q fever among owners were tested. Antibodies to C. burnetii but not for R. conorii were present in all six sera.

Animals↗
PubMed2004

Improvement of chronic nonspecific symptoms by long-term minocycline treatment in Japanese patients with Coxiella burnetii infection considered to have post-Q fever fatigue syndrome.

OBJECTIVE: To address the presence of post-Q fever fatigue syndrome (post-QFS) in Japan, and to evaluate the efficacy of minocycline for this condition. PATIENTS AND METHODS: In 20 Coxiella burnetii (C. burnetii) seropositive patients with persistent nonspecific symptoms including general fatigue, low-grade fever, myalgia and arthralgia, changes in subjective symptoms, C. burnetii antibody titers and C. burnetii DNA were evaluated after antibiotic treatment. RESULTS: After treatment mainly with minocycline (100 mg/day for 3 months), the clinical picture improved in all 20 patients as evidenced by decreases in body temperature (13/17), general fatigue (20/20) and headache (9/12). The mean performance status (PS) score improved from 5.0 to 1.8 (p<0.01). All 7 who had been positive for C. burnetii DNA, became negative together with an improvement in subjective symptoms. Indirect immunofluorescence tests demonstrated 6 of the 20 patients to be positive for C. burnetii IgM antibody to phase II antigen (1:32), and 18 to be positive for IgG antibody (1:128, 1:256). Antibody titers of both IgM (6/6, 1:16) and IgG (18/18, 1:16) decreased markedly after treatment. CONCLUSION: These results of an open label study in Japan suggest that minocycline administration is useful for improving chronic nonspecific symptoms considered to be post-Q fever fatigue syndrome caused by C. burnetii infection.

Adult↗
PubMed1990

Isolated Coxiella burnetii synthesizes DNA during acid activation in the absence of host cells.

Two populations of Coxiella burnetii were isolated from fibroblast tissue cultures and examined for their ability to synthesize DNA when incubated in a defined medium. Both the populations released by mechanical lysis of heavily infected host cells, as well as those recovered from the tissue culture medium, incorporated H3 32PO4 into DNA. Incorporation occurred at pH 4.5 but not at pH 7.0, and proceeded for 12-15 h. When incorporation of [3H]thymidine was studied, only the organisms obtained by mechanical lysis of host cells were active. Those which had been released by natural means into the tissue culture medium, and then recovered for study, did not incorporate precursor thymidine but were extremely active in protein biosynthesis. In mechanically released organisms, thymidine incorporation was inhibited immediately by rifamycin (40 microM) and hydroxyurea (10 mM), but it was not affected by chloramphenicol (310 microM) until 4 h after addition of the drug. Incorporation of H3 32PO4 by both populations of organisms was also inhibited by rifamycin, chloramphenicol and hydroxyurea, but the time sequence of inhibition differed. Southern hybridization utilizing 32P-labelled DNA suggested that both populations synthesized authentic chromosomal DNA sequences, as well as QpH1 plasmid DNA, during acid activation of metabolism.

Blotting, Southern↗
PubMed2000

The detection of Coxiella burnetii from ovine genital swabs, milk and fecal samples by the use of a single touchdown polymerase chain reaction.

The polymerase chain reaction (PCR), targeting the repetitive transposon-like region of Coxiella burnetii (Trans-PCR), was evaluated for its ability to detect directly C. burnetii in genital swabs, milk and fecal specimens of ewes. By using a combination of centrifugation step, DNA purification using Qiamp Tissue kit followed by Trans-PCR assay, the efficiency for detection of coxiella in ewes milk samples was further improved and one C. burnetii-cell could be detected in 1ml of milk. In addition, an effective, simple and rapid method to remove PCR-inhibitory substances from fecal specimens by simply diluting the DNA template to 1:100 is described, which made the detection of one microorganism per mg of sample then possible. The results obtained from seropositive ewes proved that C. burnetii could also be detected in milk and fecal samples of naturally infected animals.

Animals↗
PubMed2002

Coxiella burnetii survival in THP-1 monocytes involves the impairment of phagosome maturation: IFN-gamma mediates its restoration and bacterial killing.

The subversion of microbicidal functions of macrophages by intracellular pathogens is critical for their survival and pathogenicity. The replication of Coxiella burnetii, the agent of Q fever, in acidic phagolysosomes of nonphagocytic cells has been considered as a paradigm of intracellular life of bacteria. We show in this study that C. burnetii survival in THP-1 monocytes was not related to phagosomal pH because bacterial vacuoles were acidic independently of C. burnetii virulence. In contrast, virulent C. burnetii escapes killing in resting THP-1 cells by preventing phagosome maturation. Indeed, C. burnetii vacuoles did not fuse with lysosomes because they were devoid of cathepsin D, and did not accumulate lysosomal trackers; the acquisition of markers of late endosomes and late endosomes-early lysosomes was conserved. In contrast, avirulent variants of C. burnetii were eliminated by monocytes and their vacuoles accumulated late endosomal and lysosomal markers. The fate of virulent C. burnetii in THP-1 monocytes depends on cell activation. Monocyte activation by IFN-gamma restored C. burnetii killing and phagosome maturation as assessed by colocalization of C. burnetii with active cathepsin D. In addition, when IFN-gamma was added before cell infection, it was able to stimulate C. burnetii killing but it also induced vacuolar alkalinization. These findings suggest that IFN-gamma mediates C. burnetii killing via two distinct mechanisms, phagosome maturation, and phagosome alkalinization. Thus, the tuning of vacuole biogenesis is likely a key part of C. burnetii survival and the pathophysiology of Q fever.

Blood Bactericidal Activity↗
PubMed1990

Mixed infection of Rickettsiella phytoseiuli and Coxiella burnetii in Dermacentor reticulatus female ticks: electron microscope study.

Mixed infection of Rickettsiella phytoseiuli and Coxiella burnetii was investigated in hemolymph and organs of experimentally infected females of Dermacentor reticulatus ticks. Following intracoelomic infection, both agents, with the exception of Gene's organ, multiplied well in the cells of the tick host's organs. Two out of six developmental stages of R. phytoseiuli, i.e., crystal-forming and small dark particles, in dual infection with C. burnetii revealed marked morphological alterations. C. burnetii in the presence of R. phytoseiuli penetrated into the cortical layer of the synganglion and into the alveoli of the second and third type of salivary glands, but did not occur in the single infection.

Animals↗
PubMed2004

Effect of sex on Coxiella burnetii infection: protective role of 17beta-estradiol.

Q fever is a zoonosis caused by Coxiella burnetii and recently has been recognized as a potential agent of bioterrorism. In Q fever, men are symptomatic more often than women, despite equal seroprevalence. We hypothesized that sex hormones play a role in the pathogenesis of C. burnetii infection. When C57/BL6 mice were injected with C. burnetii, bacteria load and granuloma numbers were lower in females than in males. Ovarectomized mice showed increased bacteria load in the spleen and the liver, similar to that found in males. The granuloma number was also increased in ovarectomized mice and reached the levels found in males. Tissue infection and granulomatous response are largely under the control of estrogens: treatment of ovarectomized mice with 17beta-estradiol reduced both bacteria loads and granuloma numbers. These results show that sex hormones control host response to C. burnetii infection and may account for host-dependent clinical presentation of Q fever.

Animals↗
PubMed1997

The number and proportion of Vgamma9 Vdelta2 T cells rise significantly in the peripheral blood of patients after the onset of acute Coxiella burnetii infection.

We conducted serial studies on peripheral blood lymphocytes from four patients with acute Coxiella burnetii infection. These studies revealed that the proportion of gammadelta T cells in these patients significantly increased after the onset of disease (mean, 16%; range, 13%-30%) as compared with that in five healthy controls (mean, 4%; range, 0.5%-7%; P < .0055) and that in five controls with pneumonia (mean, 2%; range, 1%-3%; P < .0014). Most of the gammadelta T cells from these patients expressed the Vgamma9 Vdelta2 gene product. During the acute phase of disease, most gammadelta T cells expressed the activation marker human leukocyte antigen DR but not CD25. During this phase, gammadelta T cell activation was higher than alphabeta T cell activation. Our findings indicate that gammadelta T cells are predominantly involved in the acute immune response to C. burnetii.

Acute Disease↗
PubMed1977

Lesions in guinea pigs infected with Coxiella burnetii strain M-44.

Guinea pigs inoculated with the live M-44 vaccine strain of Coxiella burnetii were examined grossly and microscopically for the presence of Q fever-related lesions. Mild myocarditis was observed in 38% of the infected animals but in none of the control animals. Livers showed significant incidence of hepatitis, necrosis, and granuloma formation, especially during the first eight days of the infection. A much lower incidence of splenitis was also found but was considered to be of borderline significance. Generally, lesions were mild in nature, and none seemed to endanger the life of the animal or to cause observable distress.

Adrenal Glands↗
PubMed2001

Lack of association between Kawasaki syndrome and infection with Rickettsia conorii, Rickettsia typhi, Coxiella burnetii or Ehrlichia phagocytophila group.

BACKGROUND: The etiology of Kawasaki syndrome (KS) is unknown. Rickettsiae, intracellular microorganisms that invade the vascular endothelium, might cause KS. OBJECTIVES: To investigate whether there is an association between KS and infection with Rickettsia conorii, Rickettsia typhi, Coxiella burnetii or Ehrlichia phagocytophila group. METHODS: All children who were diagnosed with KS at the University of Athens Second Department of Pediatrics from December, 1999, through November, 2000, were prospectively studied. Paired serum specimens were obtained from all patients and antibody titers against R. conorii, R. typhi, C. burnetii and E. phagocytophila group were assessed by microimmunofluorescence assay. RESULTS: Eleven children with a median age of 2.5 years were included in the study. A 15-month-old child had a 4-fold rise of antibody titers against C. burnetii, which is indicative of acute Q fever. The patient had a history of recent exposure to possible sources of C. burnetii. The remaining patients tested negative for the presence of antibodies against R. conorii, R. typhi, C. burnetii and E. phagocytophila group. CONCLUSIONS: Our study does not provide serologic evidence that KS is the result of infection with R. conorii, R. typhi, C. burnetii or E. phagocytophila group. It is suggested that C. burnetii may cause a KS-like illness in young children.

Boutonneuse Fever↗
PubMedDate not supplied

Serosurvey for Cowdria ruminantium, Coxiella burnetii, and Spotted fever group rickettsiae in ostriches (Struthio camelus) from Zimbabwe.

Sera from 216 ostriches on nine farms around Zimbabwe were examined by indirect fluorescent antibody (IFA) testing for the presence of antibodies reactive with Cowdria ruminantium, Coxiella burnetii, and Rickettsia africae, a spotted fever group rickettsia. Although no reactive antibodies could be detected to C. ruminantium or C. burnetii, 51/216 (35%) sera reacted with R. africae. The seroprevalence in ostriches from the south of Zimbabwe was significantly higher than in birds from the north (P < 0.01). Immunoblots of four sera positive by IFA (> 1/160) showed antibodies reactive with antigens of R. africae that also were recognized by pooled sera from mice inoculated with the organism. No reactive antibodies could be detected in six sera negative by IFA.

Animals↗
PubMed2003

Coxiella burnetii avoids macrophage phagocytosis by interfering with spatial distribution of complement receptor 3.

Phagocytosis is a highly localized event requiring the formation of spatially and temporally restricted signals. Numerous microorganisms have taken advantage of this property to invade host cells. Coxiella burnetii, the agent of Q fever, is an obligate intracellular bacterium that has developed a survival strategy in macrophages based on subversion of receptor-mediated phagocytosis. The uptake of C. burnetii is mediated by alpha(v)beta(3) integrin and is restricted by impaired cross-talk of alpha(v)beta(3) integrin and complement receptor 3 (CR3) (CD11b/CD18). In this study, we showed that CR3 molecules remained outside the pseudopodal extensions induced by C. burnetii in THP-1 monocytes, although alpha(v)beta(3) integrin was present in the pseudopods. Chemoattractants such as RANTES restored CR3 localization to the front of pseudopodal extensions and increased C. burnetii phagocytosis, demonstrating that the localization of CR3 is critical for bacterial uptake. In addition, monocyte activation due to the expression of HIV-1 Nef protein also restored CR3-mediated phagocytosis of C. burnetii by allowing CR3 redistribution toward bacterial-induced pseudopods. The redistribution of CR3 and increased C. burnetii phagocytosis in THP-1 cells stimulated by RANTES or expressing Nef were associated with the inhibition of intracellular replication of C. burnetii. Hence, the localization of CR3 is critical for bacterial phagocytosis and also for the control of bacterial replication. This study describes a nonpreviously reported strategy of phagocytosis subversion by intracellular pathogens based on altered localization of monocyte receptors.

Animals↗
PubMed1999

Subversion of monocyte functions by coxiella burnetii: impairment of the cross-talk between alphavbeta3 integrin and CR3.

Several intracellular pathogens exploit macrophages as a niche for survival and replication. The success of this strategy requires the subversion or the avoidance of microbicidal functions of macrophages. Coxiella burnetii, the agent of Q fever, is a strictly intracellular bacterium that multiplies in myeloid cells. The survival of C. burnetii may depend on the selective use of macrophage receptors. Virulent C. burnetii organisms were poorly internalized but survived successfully in human monocytes, whereas avirulent variants were efficiently phagocytosed but were also rapidly eliminated. The uptake of avirulent organisms was mediated by leukocyte response integrin (alphavbeta3 integrin) and CR3 (alphaMbeta2 integrin), as demonstrated by using specific Abs and RGD sequence-containing peptides. The phagocytic efficiency of CR3 depends on its activation via alphavbeta3 integrin and integrin-associated protein. Indeed, CR3-mediated phagocytosis of avirulent C. burnetii was abrogated in macrophages from integrin-associated protein-/- mice. In contrast, the internalization of virulent C. burnetii organisms involved the engagement of alphavbeta3 integrin but not that of CR3. The pretreatment of monocytes with virulent C. burnetii organisms prevented the CR3-mediated phagocytosis of zymosan particles and CR3 activation assessed by the expression of the 24 neo-epitope. We conclude that the virulence of C. burnetii is associated with the engagement of alphavbeta3 integrin and the impairment of CR3 activity, which probably results from uncoupling alphavbeta3 integrin from integrin-associated protein. This study describes a strategy not previously reported of phagocytosis modulation by intracellular pathogens.

Antigens, CD↗