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Protein A from Staphylococcus aureus was used for differentiating antibodies against Coxiella burnetii according to immunoglobulin classes. Interaction of immune serum with protein A resulted in complete (within the sensitivity limits of the methods used) removal of IgG antibody and had practically no effect on the level of IgM antibody.
Domestic animals are the hosts of several tick species and the reservoirs of some tick-borne pathogens; hence, they play an important role in the circulation of these arthropods and their pathogens in nature. They may act as vectors, but, also, as reservoirs of spotted fever group (SFG) rickettsiae, which are the causative agents of SFG rickettsioses. Q fever is a worldwide zoonosis caused by Coxiella burnetii (C. burnetii), which can be isolated from ticks. A total of 1,848 ticks (954 female, 853 male, and 41 nymph) were collected from dogs, goats, sheep, cattle, and horses in 32 different localities of the Greek island of Cephalonia. Rhipicephalus (Rh.) bursa, Rh. turanicus, Rh. sanguineus, Dermacentor marginatus (D. marginatus), Ixodes gibbosus (I. gibbosus), Haemaphysalis (Ha.) punctata, Ha. sulcata, Hyalomma (Hy.) anatolicum excavatum and Hy. marginatum marginatum were the species identified. C. burnetii and four different SFG rickettsiae, including Rickettsia (R.) conorii, R. massiliae, R. rhipicephali, and R. aeschlimannii were detected using molecular methods. Double infection with R. massiliae and C. burnetii was found in one of the positive ticks.
OBJECTIVE: To comprehensively determine global estimates of Q fever seroprevalence in children and adolescents by conducting a systematic review and meta-analysis. DATA SOURCES: Searches of published articles in MEDLINE, Embase and Scopus databases were conducted from inception until February 2025. STUDY SELECTION: Cross-sectional studies reporting seroprevalence of Q fever/ Coxiella burnetii antibodies, using any established laboratory test, in any population of healthy children and adolescents <20 years old were included. The quality of eligible articles was assessed using a modified Newcastle-Ottawa Scale. DATA EXTRACTION: Data from eligible articles were extracted using a standardized form, which included year of publication, year(s) the study was conducted, numbers of antibody-positive cases/specific population, age, country, geographic region, serology test used and antibody titer cutoff value. DATA SYNTHESIS: DerSimonian and Laird random effects models were used to calculate pooled seroprevalence estimates and 95% confidence intervals in data from 41 eligible articles reporting 42 studies comprising 9841 children and adolescents. Q fever seroprevalence was observed in multiple countries across 7 geographic regions, and varied markedly between countries and regions, with the highest estimate observed by an individual country in Ethiopia (45%) and by region in the Middle East (14%). Seroprevalence estimates were higher in older children and adolescents ≥10 years (15%) compared with younger children <10 years of age (8%). CONCLUSION: Despite varying geographical prevalence, our findings demonstrate that widespread exposure to Q fever antigens occurs across multiple global regions in children and adolescents to potentially serious C. burnetii infection, indicating that diagnostic surveillance and preventive measures should be considered in both endemic and previously unreported areas.
Plaque formation and dye uptake assays were used to measure the MICs of PD 127,391 and PD 131,628 against Rickettsia species. The MICs of PD 127,391 were 0.25 microgram/ml for Rickettsia rickettsii and 0.125 to 0.25 microgram/ml for Rickettsia conorii. The MICs of PD 131,628 were 0.25 to 0.5 microgram/ml for R. rickettsii and 0.5 microgram/ml for R. conorii. As determined by the shell vial technique, 15 strains of Coxiella burnetii were susceptible to PD 127,391 and PD 131,628 (MIC, < or = 1 microgram/ml), while one strain of C. burnetii (MP10) was of intermediate susceptibility.
The rate and extent of coliphage Q beta RNA translation by cell-free extracts prepared from Coxiella burnetii were studied. When translations were conducted at temperatures elevated above 37 degrees C, both polypeptide elongation and frequency of initiation were by comparison increased. The ratios of products synthesized from the polycistronic phage mRNA also changed upon increases in translation temperature, especially at 45 degrees C. Although the organism is a moderate acidophile, initiation of protein synthesis in extracts did not occur below pH 6.2, and was superior when the pH was 6.8-7.2. The results are discussed in context with the known physiological characteristics of this obligate intracellular bacterium.
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The dynamics of antibody response in guinea pigs infected with Coxiella burnetii was investigated by microagglutination (MA) and complement-fixation (CF) tests with different preparations of C. burnetii antigens. At the onset of antibody response the highest antibody titres were detected by the MA test with natural antigen 2, later on by the MA test with artificial antigen 2. Throughtout the 1-year period of observation, the CF antibody levels were usually lower and, with the exception of the highest infectious doses, the CF antibodies appeared later than agglutinating antibodies. There was no difference in the appearance of agglutinating and CF antibodies directed to antigen 1. Inactivation of the sera caused a marked decrease in antibody titres when tested with artificial antigen 2, whereas the antibody levels remained unchanged when tested with natural antigen 2.
Two-component regulatory systems play important roles in the adaptive responses of many bacteria to environmental changes. The sensor proteins of these systems are highly conserved near their C-termini. We exploited this feature to isolate a gene encoding a putative sensor component from the obligate intracellular rickettsial parasite Coxiella burnetii (Cb). Using degenerate primers and the polymerase chain reaction (PCR), we isolated a DNA fragment from a genomic library of Cb containing an open reading frame (ORF), sufficient to encode a 48-kDa protein. Sequence comparison revealed that the deduced protein shared high homology to members of the bacterial sensor protein family, particularly at three conserved regions of the C terminus. When the Cb sensor-like gene was cloned into a high-copy-number vector and introduced into an E. coli strain (phoM, phoR), the mutant expressed low levels of alkaline phosphatase activity, suggesting that the gene functioned as a sensor protein in E. coli. Consequently, we designated this gene qrsA (for Q fever agent regulatory sensor-like gene). Because two-component regulatory systems have been implicated in a variety of cellular processes, including virulence determinants in some pathogenic bacteria, the identification of qrsA in Cb may shed light on how the pathogen adapts to extracellular changes during infection, as it proliferates in the phagolysosome.
Killed Coxiella burnetii (C.b.) cells in phase II but not in phase I had a mild stimulatory effect on hexose monophosphate shunt (HMPS) and superoxide anion production by human polymorphonuclear (PMN) leukocytes. Preincubation of C.b. cells of either phase with serum of a leukocyte donor lacking detectable antibodies to C.b. did not affect the studied activities of PMN leukocytes. In contrast, both HMPS stimulation and superoxide production were enhanced by specific opsonization of C.b. cells with rabbit immune sera containing corresponding phase I and/or phase II antibodies. Stimulatory effect was observed also with lipopolysaccharide-protein-phospholipid (LPS-Pr-Pl) complex but not with lipopolysaccharide-protein (LPS-Pr) complex and with purified lipopolysaccharide (LPS) isolated from phase I C.b. cells. Possible consequences of these findings for explanation of C.b. resistance to intracellular killing by professional phagocytes are discussed.
We describe the case of a 35-year-old man who presented with pneumonia and encephalitis due to Coxiella burnetii. The neurological manifestations of Q fever are discussed and we suggest that C. burnetii be included in the differential diagnosis of patients with pneumonia and encephalitis.
A sublethal-challenge model was established in BALB/c mice by using protection from the development of severe splenomegaly as an indicator of vaccinogenic activity for evaluation of the protective efficacies of vaccine candidates. To determine the immunodominant antigens as defined by reaction to an infection-derived antibody, mouse sera from different stages of experimental infection with various doses of Coxiella burnetii were tested by immunoblotting. Proteins with molecular masses of 14, 16, 21, 28, 32, 45 to 50, 57, and 60 kDa were recognized as immunodominant antigens. Antibody responses in whole-cell antigen (WCA)-vaccinated mice were compared with those in unvaccinated mice by immunoblotting using two-dimensional gel-separated C. burnetii antigens. The results indicated that there were significantly different antibody responses during different stages of vaccination and challenge, suggesting that several specific immunogenic antigens may play critical roles in the protection of mice against challenge. To clone these immunogenic antigens, a genomic DNA library of Nine Mile phase I was screened with convalescent-phase antisera from mice. Eighteen novel immunoreactive proteins with molecular masses ranging from approximately 14 to 67 kDa were cloned and identified. Interestingly, several recombinant proteins reacted with sera from both early-stage infected and WCA-vaccinated prechallenged mice. These results suggest that these proteins may play critical roles in the development of protective immunity and that they are logical candidates for vaccine and serodiagnostic reagents.
Virulence of four Coxiella burnettii phase I strains associated with acute (Nine Mile and Luga strains) and chronic (S and Priscilla strains) forms of Q fever, respectively, for outbred guinea pigs and inbred BALB/c mice was compared. In guinea pigs exposed to infectious aerosol, virulence of the strains Nine Mile, Luga and S was similar, because they all caused lethal infection and high febrile reaction (FR). By contrast, exposure to similar doses of the strain Priscilla resulted in the non-lethal infection manifested only by low, dispersed and protracted FR during a 20 day-period of observation. Lower virulence of the strain Priscilla than of the strains Nine Mile and S was observed also in guinea pigs infected intraperitoneally (ip). In mice, comparable degree of multiplication in the spleen on day 6 post ip infection was observed with the strains Nine Mile, Luga and S, but not with the strain Priscilla, namely when lower infectious doses were used. Whereas the highest doses (10(7) EID50) of the strains Nine Mile and S were lethal for mice during the second week post infection (p.i.), the strains Luga and Priscilla did not kill mice with 10-times lower (10(6) EID50) doses. At the same time agglutination antibody response detected 4 weeks p.i. was very similar in guinea pigs with all strains under study and in mice it did not differ markedly, reflecting the infectious dose used.
BACKGROUND AND PURPOSE: Q fever is a disease of humans. Vaccines to prevent this disease have demonstrated efficacy in rodents and must also be evaluated for efficacy in a nonhuman primate model. Preliminary to vaccine efficacy experiments, cynomolgus and rhesus monkeys were evaluated as suitable experimental models of acute Q fever. METHODS: Both species of monkeys were challenged with aerosolized 10(5) virulent phase-I Coxiella burnetii Henzerling strain, and clinical and serologic responses were determined. RESULTS: Radiographic changes were observed in seven of eight monkeys of both species; however, changes in cynomolgus monkeys tended to be more significant. Between 7 and 10 days after challenge, all rhesus monkeys and 88% of cynomolgus monkeys were bacteremic. Sequential increases in antibody responses to C. burnetii phase-I and phase-II whole cells and phase-I lipopolysaccharide were observed in both species. Although the maximal rectal temperature increase was similar in both species, duration of fever was slightly longer in rhesus monkeys. Clinical features were similar to those described in human acute Q fever patients. CONCLUSIONS: On the basis of the more pronounced radiographic changes in cynomolgus monkeys, we favor use of this species for future studies of vaccine efficacy.
Patients with Q fever and legionellosis may present identical clinical symptom. Differentiation of these diseases is made by serology, mainly the indirect immunofluorescence assay (IFA). Using IFA the authors tested 154 Q fever positive sera from 55 patients with acute Q fever and 28 patients with chronic Q fever for Legionella pneumophila antibodies and 57 sera from 57 patients with legionellosis for Coxiella burnetii antibodies. Of the 211 sera tested, four sera from different patients had antibodies to both C. burnetii and L. pneumophila. Using cross-adsorption studies and protein immunoblotting, no cross-reaction between C. burnetii and L. pneumophila antibodies could be identified. The moderate antibody titers against L. pneumophila in two Q fever patients and vice versa for one legionellosis patient are consistent with the incidence of seroprevalence in healthy blood donors and were not due to cross-reactivity. One patient was identified with concurrent Q fever and legionellosis.
Dual infection of cells may divert pathogens to intracellular compartments different from those occupied in mono-infected cells. In the present studies, mouse bone marrow in vitro-derived macrophages were first infected with virulent Mycobacterium avium, which are normally singly lodged within tight phagosomes. These phagosomes do not mature; they undergo homotypic fusion with early endosomes and do not fuse with lysosomes. Seven days later, the cultures were superinfected with phase II (non-virulent) Coxiella burnetii, organisms sheltered in lysosome- (or prelysosome)-like, multi-occupancy phagosomes. The latter can attain large size and engage in efficient homo- and heterotypic fusion with other phagosomes. Cultures were fixed for transmission electron microscopy 6, 12, 24, and 48 h later. Other M. avium-infected cultures were superinfected with amastigotes of the trypanosomatid flagellate Leishmania amazonensis, which are also sheltered in lysosome- (or prelysosome)-like multi-occupancy vacuoles, and fixed at the same time periods. Chimeric phagosomes containing both M. avium and C. burnetii, were found already at 6 h and the proportion of M. avium that colocalized with C. burnetii in the same phagosomes reached over 90% after 48 h. In such phagosomes, both organisms were ultrastructurally well preserved. In contrast, colocalization of M. avium and L. amazonensis was rarely found. Speculative scenarios that could underlie the formation of chimeric phagosomes could involve delayed maturation of C. burnetii-containing phagosomes in presence of M. avium, which would allow for fusion of C. burnetii- and M. avium-containing phagosomes; the production, by C. burnetii, of molecules that upregulate the fusion of M. avium-containing phagosomes with those that contain C. burnetii; and the secretion of factors that could favour the survival of M. avium within chimeric vacuoles.
Haemocytes of laboratory bred half-engorged Hyalomma dromedarii ticks phagocytized intracoelomally inoculated Coxiella burnetii organisms. Significantly higher phagocytosis of phase II than phase I C. burnetii was observed, irrespective of whether live, killed untreated or killed organisms treated with chloroform-methanol (CM) mixture were used. However, HCl- or KIO4-treated phase I cells were phagocytized to a similar extent as phase II cells. More consistent results were obtained with haemocytes of male than of female ticks. Phagocytosis of phase I killed and live organisms was significantly increased by their preincubation with phase I but not with phase II immune rabbit sera.
The paper presents data of the long-term (1975-1994) study of Q fever in Carpathian region [correction of Forecarpathia] (Ivano-Frankivs'k and Chernivtsi provinces) and dynamics of epidemiologic manifestations of this disease during the recent years. It is shown that after Q fever outbreaks in 1975-1977, people sick for it have been recorded sporadically, and a considerable decrease of epidemiological manifestations of Coxiella burnetii circulation is observed in the late years. This is accompanied by the decrease of the immune stratum among the population from 10.1% to 1.6-2.8%. In the authors opinion there is the interepizootic period now when the agent population remains in the phase of reservation that requires devoting much attention to the future appearance of its epidemiologically dangerous variants. The expediency of the purposeful examination of the profile therapeutic patients for Q fever and a necessity of special study of the chronic form of this infection are emphasized.
Splenomegaly induced in mice inoculated intraperitoneally (i.p.) with purified formalin-killed phase I and phase II Coxiella burnetii (C.b.) cells was dose-dependent. The phase I cells induced higher splenomegaly than phase II cells. The splenomegaly-inducing ability of phase I cells was reduced upon incubation with phase I but not with phase II antiserum, whereas the phase II cells preincubated with phase I or phase II immune sera induced higher splenomegaly than the phase II cells alone. Phase I cells caused lower splenomegaly in mice previously immunized with C.b. The splenomegaly-inducing ability of phase I cells was abolished by mild acid hydrolysis, by treatment either with phenol-chloroform-petroleum ether (PCP) or with a chloroform-methanol (CM) mixture. However, either the CM or the PCP-treated phase I cells retained their capacity to protect mice challenged with virulent phase I C.b.