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PubMed1999

[The epidemiology of Q fever in the northern area of Huelva, Spain].

OBJECTIVE: The aim of the present study is to know the prevalence, incidence and clinical presentation of the acute Q fever in the north of the Huelva district. METHODOLOGY: a) Prevalence: 1,654 serum were randomly collected from the health district and distributed by their origin, age and sex. The methodology used was the indirect immunofluorescence, Coxiella burnetii phase II as antigen. Were regarded as positives those serum whose titles were equal or higher to 80; b) Incidence: prospective study of every case treated in hospital during 1996-1997 plus every referred patient from the different "Health Centers". An acute case of Q fever was established as a feverish syndrome of more than 2 days plus a title equal or higher to 320 against C. burnetti phase II antigen, and c) Clinical data: all the patients were clerked and similar form was filled up including the following items: pneumonia, hepatitis, headache, persistent fever, etc. RESULTS: a) Prevalence: it was 5.08%, more frequent in men than in women; b) Incidence: 21 new cases over two years, an incidence of 12.70 cases per 100,000 population, and c) CLINICAL PRESENTATION: feverish syndrome plus hepatitis in 100% of the cases, just two pneumonia were recorded and in 4 cases the clinical picture was associated to immunological symptoms with persistent fever. CONCLUSION: A discrepancy between incidence and prevalence has been pointed out which makes us think that the majority of the Q fever cases in this area debut as a self restricted feverish syndrome which does not require specialized treatment.

Adolescent↗
PubMed1993

Chronic Q fever. Ninety-two cases from France, including 27 cases without endocarditis.

OBJECTIVE: Chronic Q fever is seldom recognized; before 1989, only 234 cases had been reported in the literature. The 92 cases of chronic Q fever collected at the French National Reference Center for Rickettsioses from 1982 through 1990 represent the largest series ever reported. PATIENTS: The patients included in the study were diagnosed between July 31, 1982, and August 1, 1990, at the French National Reference Center for Rickettsioses as having chronic Q fever by the following criteria: presence of antibody against Coxiella burnetii phase I antigen at a titer greater than or equal to 800 for IgG and 50 for IgA by the indirect immunofluorescence test. Epidemiologic, clinical, laboratory, and treatment data were collected from 39 different collaborative hospitals throughout France. MAIN OUTCOME MEASURE: For each serologically selected patient, a computerized questionnaire was utilized to record 188 different items of demographic, epidemiologic, clinical, laboratory, and therapeutic data, which were analyzed. RESULTS: Chronic Q fever occurs more frequently in city dwellers than in rural inhabitants, and exposure to domestic ruminants and raw milk is an important feature. Immunocompromising conditions (20.2%) and underlying heart disease (88.4%) or vascular disease are the most important risk factors to consider in potential cases of chronic Q fever. The mortality in these patients with endocarditis was high (23.5%). The clinical spectrum of 84 patients included 57 cases of endocarditis, three cases of vascular prosthesis infection, three cases of aneurysmal infection, three cases of osteoarthritis, four cases with lung localizations, nine asymptomatic cases, three cases of hepatitis, and two cases with cutaneous forms of the disease. CONCLUSIONS: In patients with unexplained fever, negative blood cultures, and a history of underlying vascular or cardiac disease, Q fever should be considered.

Adult↗
PubMed1998

Cytokine dysregulation in the post-Q-fever fatigue syndrome.

The post-Q-fever fatigue syndrome (QFS) (inappropriate fatigue, myalgia and arthralgia, night sweats, changes in mood and sleep patterns) follows about 20% of laboratory-proven, acute primary Q-fever cases. Cytokine dysregulation resulting from chronic immune stimulation and modulation by persistence of Coxiella burnetii cells or their antigens is hypothesized. We studied cytokine release patterns of peripheral blood mononuclear cells (PBMC) stimulated with various ligands in short-term culture, from 18 patients with active QFS, and 27 controls: six with resolving QFS, five who had had acute primary Q-fever without subsequent QFS, eight healthy Q-fever vaccinees and eight healthy subjects without Q-fever antibody. Conditioned media (CM) from PBMC stimulated in short-term culture with Q-fever antigens, PHA or measles antigen (as an unrelated antigen) were assayed for IL-2, IL-4, IL-5, IL-6, IL-10 and IFN gamma by AgEIA, and for IL-1 and TNF alpha/beta by bioassay. Aberrant cytokine release patterns were observed with PBMC from QFS patients when stimulated with Q-fever antigens: an accentuated release of IL-6 which was significantly [p = 0.01, non-parametric one-way analysis of variance (ANOVA)] in excess of medians for all four control groups. With IL-2, the number of responders in the active QFS group was decreased relative to control groups (Fisher's exact test, p = 0.01) whereas the number of IFN gamma responders was increased (Fisher's exact test, p = 0.0008). Significant correlations were observed between concentrations of IL-6 in CM, total symptom scores, and scores for other key symptoms.

Acute Disease↗
PubMed1992

Susceptibility of some species of rodents to rickettsiae.

The present study was designed to test the susceptibility of free-living rodents, viz Apodemus flavicollis, Microtus arvalis, Clethrionomys glareolus, Mus musculus, and outbred white mice from Dobrá Voda farm, CSFR, to Coxiella burnetii, rickettsiae of the spotted fever group (Rickettsia sibirica, R. conorii, R. slovaca and R. akari) and rickettsiae of typhus group (R. typhi and R. prowazekii) by various routes of administration. The highest levels of antibodies to C. burnetii were found in A. flavicollis and M. arvalis inoculated intraperitoneally and intracerebrally. Antibodies to C. burnetii exerted peak levels between days 13 and 16 in contrast to white mice which showed maximum levels on day 28. When 10(0.5) and 10(0.05) EID50/0.25 ml of C. burnetii was administered intraperitoneally to A. flavicollis, M. arvalis and white mice, the agent was detected only in organs of wild animals. In addition to spleen, the bone marrow appeared as a predilective tissue for the detection of this agent. R. akari at a dose of 10(4.5) EID50/0.25 ml caused overt illness and death in rodents. Antibody levels to R. sibirica and R. conorii were dependent on dosage, route of inoculation and duration of infection, but were not dependent on animal species. Antibodies to R. slovaca and R. akari were dependent on dosage, infection duration and animal species but were not dependent on the route of infection. For R. conorii, R. sibirica and R. slovaca a sharp increase of antibody levels with high titres on days 4-6 and peak levels about day 11 post intraperitoneal infection was characteristic. Antibody level to R. akari increased up to day 21. Spotted fever group rickettsiae in rodents inoculated intraperitoneally were observed in various organs, particularly in tunica vaginalis and spleen at days 2-8 post infection. R. typhi at a dose of 10(4.3) EID50/0.25 ml inoculated intracerebrally or intraperitoneally killed white mice and inoculated intraperitoneally killed C. glareolus and M. musculus. The antibody response of white mice to intraperitoneal, subcutaneous or intranasal inoculation of this rickettsia was low and no antibody was detected following peroral administration. M. musculus did not develop antibodies after intracerebral, intranasal, subcutaneous or peroral inoculation of R. typhi. The target organs for this rickettsia were the spleen and tunica vaginalis. R. prowazekii inoculated intraperitoneally into white mice at a dose of 10(6.5) EID50/0.25 ml and at a dose of 10(4.5) EID50 into C. glareolus was fatal for these rodents.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2002

Q fever--still a query and underestimated infectious disease.

Coxiella burnetii (C.b.) is a strictly intracellular, Gram-negative bacterium. It causes Q fever in humans and animals worldwide. The animal Q fever is sometimes designated "coxiellosis". This infection has many different reservoirs including arthropods, birds and mammals. Domestic animals and pets, are the most frequent source of human infections. Q fever may appear basically in two forms, acute and chronic (persistent). The latter form of Q fever in animals is characteristic by shedding C.b. into the environment during parturition or abortion. Human Q fever results usually from inhalation of contaminated aerosols originating mostly from tissue and body fluids of infected animals. Q fever may appear in humans either in an acute form accompanied mainly by fever (pneumonia, flu-like disease, hepatitis) or in a chronic form (mainly endocarditis). Diagnosis of Q fever is based on isolation of the agent in cell culture, its direct detection, namely by PCR, and serology. Detection of high phase II antibodies titers 1-3 weeks after the onset of symptoms and identification of IgM antibodies are indicative to acute infection. High phase I IgG antibody titers >800 as revealed by microimmunofluorescence offer evidence of chronic C.b. infection. For acute Q fever, a two-weeks-treatment with doxycycline is recommended as the first-line therapy. In the case of Q fever endocarditis a long-term combined antibiotic therapy is necessary to prevent relapses. Application of Q fever vaccines containing or prepared from phase I C.b. corpuscles should be considered at least for professionally exposed groups of the population. Infections caused by C.b. are spread worldwide and may pose serious and often underestimated health problems in human but also in veterinary medicine. Though during the last decades substantial progress in investigation of C.b. has been achieved and many data concerning this pathogen has been accumulated, some questions, namely those related to the pathogenesis of the disease, remain open.

Acute Disease↗
PubMed2004

Q fever pneumonia.

PURPOSE OF REVIEW: In this era of emerging infectious diseases and bioterrorism it is important to be up to date with the diagnosis and management of Q fever pneumonia. RECENT FINDINGS: A considerable amount of new information has emerged regarding the pathogenesis of Coxiella burnetii infection. The complete genome of this microorganism has now been sequenced and there are several unique features. The spectrum of manifestations of infection due to C. burnetii continues to expand. Some of the more recently described findings are acalculous cholecystitis, rhabdomyolysis, long-term persistence of Coxiella, post Q fever fatigue syndrome, and hemolytic uremic syndrome. Pneumonia as a manifestation of acute Q fever shows tremendous geographic variation, being common in one area of a country such as Spain but not in another area. SUMMARY: Pneumonia continues to be an important manifestation of infection with C. burnetii. It responds to treatment with doxycycline, quinolones or macrolides.

Anti-Bacterial Agents↗
PubMed1988

A heat shock operon in Coxiella burnetti produces a major antigen homologous to a protein in both mycobacteria and Escherichia coli.

A gene library from the DNA of Coxiella burnetii has been constructed in the cosmid vector pHC79. A particular clone, pJB196, reacted strongly with Coxiella-specific antibodies elicited in a number of different species of animals. This clone produced two abundant C. burnetii-specific polypeptides, a 14-kilodalton nonimmunoreactive protein and a 62-kilodalton immunoreactive protein. Sequencing identified two open reading frames, encoding polypeptides of 10.5 and 58.3 kilodaltons. The only transcriptional control element observed on the 5' side of the initiation codon resembled a heat shock promoter. This heat shock promoter was functionally regulated in Escherichia coli, since both proteins were produced by growth conditions at 37 degrees C and neither protein was detected at 23 degrees C. There were four sequences from the literature that were highly homologous (greater than 50%) to the 62-kilodalton protein from C. burnetii. Three were from Mycobacterium species and represent the immunodominant antigen of this genus. The other was from E. coli, detected as a gene that complements or suppresses a temperature-sensitive RNase activity. Since the recombinant protein was immunogenic, it may serve as an efficacious vaccine against C. burnetii and other pathogenic microorganisms that express the conserved antigen.

Amino Acid Sequence↗
PubMed1987

Q fever in France.

In France Q fever is a notifiable disease, but information could only be obtained from fragmental inquiries. Routine serologic examination of 75 901 sera during the years 1982-85 showed 430 Q fever positive sera (mean rate 0.57%). Our laboratory could confirm 135 cases of clinical Q fever. In the region of Dijon, 4.4% of the country population was seropositive, but among breeders 25% were positive. 36 persons (8%) among 245 employees of the departmental veterinary services were seropositive, some with very high titers, but without obvious clinical symptoms. It seems that infection by Coxiella burnetii is still largely underestimated.

Animal Husbandry↗
PubMedDate not supplied

[Q fever in a 5-year-old girl].

The first case of Q fever in Poland in a 5-year girl is presented. A girl is inhabitant of the Lublin region where this disease is of endemic character. Q fever was diagnosed on the base of the clinical examinations and serological tests. The course of the disease was acute. Doxycycline and lincomycin were given. A short time lapse between the treatment and eradication of Coxiella burnetii antigen indicates rather spontaneous recovery.

Antigens, Bacterial↗
PubMed1987

Epidemiology of Q fever in Italy and in other Mediterranean countries.

The history of Q fever in Italy may be divided into three periods: epidemic in character after the Second World War, endemic occurrence from 1960 to 1980, and sporadic occurrence at present. Clinical symptoms are unspecific, and diagnosis must be confirmed by serology and isolation of the causative agent. The reported incidence is consequently underestimated. Results are reported of a seroepidemiologic survey in animals and humans in the Italian region and western Sicily. In the Mediterranean area several epidemic foci are still present. The need of further studies to evaluate the incidence of Q fever and to shed more light upon the epidemiology of Coxiella burnetii infections is stressed.

Africa, Northern↗
PubMed1989

Clinical aspects and prevention of Q fever in animals.

In recent years, in the Federal Republic of Germany an increase in the prevalence of Coxiella burnetii infections in cattle has been well documented and its association with infertility problems in this species has been postulated by a number of authors. Investigations on this problem have been hampered by the fact that another intracellular agent, Chlamydia psittaci, which may also cause infertility, is also highly prevalent in the cattle population. Vaccination trials with a commercial egg-propagated inactivated vaccine against both agents have indicated that fertility in infected flocks may be improved significantly by application of such a vaccine. However, since this combined vaccine occasionally induces severe local reactions in vaccinated animals, it still needs further improvement. Limited experiments with more purified experimental C. burnetii vaccines have shown that Q fever in cattle may be prevented by vaccination of young uninfected animals only. In this way herds free of C. burnetii may be established.

Animals↗
PubMed1999

Survival of Mycobacterium avium and Mycobacterium tuberculosis in acidified vacuoles of murine macrophages.

Despite the antimicrobial mechanisms of vertebrate phagocytes, mycobacteria can survive within the phagosomes of these cells. These organisms use various strategies to evade destruction, including inhibition of acidification of the phagosome and inhibition of phagosome-lysosome fusion. In contrast to mycobacteria, Coxiella burnetii, the etiologic agent of Q fever, inhabits a spacious acidified intracellular vacuole which is prone to fusion with other vacuoles of the host cell, including phagosomes containing mycobacteria. The Coxiella-infected cell thus provides a unique model for investigating the survival of mycobacteria in an acidified phagosome-like compartment. In the present study, murine bone marrow-derived macrophages were infected with either Mycobacterium avium or Mycobacterium tuberculosis and then coinfected with C. burnetii. We observed that the majority of phagocytosed mycobacteria colocalized to the C. burnetii-containing vacuole, which maintained its acidic properties. In coinfected macrophages, the growth of M. avium was not impaired following fusion with the acidified vacuole. In contrast, the growth rate of M. tuberculosis was reduced in acidified vacuoles. These results suggest that although both species of mycobacteria inhibit phagosome-lysosome fusion, they may be differentially susceptible to the toxic effects of the acidic environment in the mature phagolysosome.

Animals↗
PubMed1981

Fatty acid composition of rickettsiae.

The fatty acid compositions of selected strains of rickettsiae were studied by gas-liquid chromatography. The profiles of all the rickettsiae except Coxiella burnetii were qualitatively similar. The fatty acid composition of C. burnetii was similar to that of certain Legionella species.

Coxiella↗
PubMed1985

Cellular immunity in Q fever: specific lymphocyte unresponsiveness in Q fever endocarditis.

Human infection with the rickettsia Coxiella burnetii presents as acute influenza-like primary Q fever, subacute granulomatous hepatitis, or chronic endocarditis with hepatitis. To investigate whether persistent infection is associated with a possible immunologic defect, we tested lymphocyte proliferation specific for Coxiella in vitro in peripheral blood mononuclear cells from patients and controls. All four patients with endocarditis had profound lymphocyte unresponsiveness to Coxiella antigens with normal proliferation to control antigens. Hepatitis and primary Q fever were associated with vigorous responses in vitro to Coxiella antigens. Suppression of lymphocyte unresponsiveness was in part mediated by an antigen-nonspecific, glass-adherent cell. We hypothesize that specific T cell unresponsiveness is an important factor in persistent infection with C. burnetii and offer in vitro lymphocyte stimulation as a more specific diagnostic test to distinguish cases of endocarditis among those with chronic hepatitis due to Q fever.

Adult↗
PubMed1985

Cellular immunity in Q fever: modulation of responsiveness by a suppressor T cell-monocyte circuit.

Human infection with the rickettsia Coxiella burnetii presents as an acute flulike primary Q fever, as a subacute granulomatous hepatitis, or, rarely, as chronic endocarditis. We have previously described lymphocyte unresponsiveness to Coxiella antigen in patients with Q fever endocarditis. This unresponsiveness was antigen specific and was mediated in part by adherent suppressor cells. In this report we show that the adherent suppressor cells work via prostaglandin E2 (PGE2)4 production. Addition of the cyclooxygenase inhibitor indomethacin to cultures of PBMC from patients with endocarditis or chronic laboratory exposure resulted in consistent increases in Coxiella-specific lymphocyte proliferation. The degree of increase in proliferation induced by indomethacin correlated strongly with the amount of PGE2 produced in a 4-hr culture stimulated by Coxiella antigen, but it also correlated with the sensitivity to inhibition of mitogenesis by PGE2. The suppressor mechanism was antigen nonspecific, because induction of suppression in vitro by Coxiella antigen also suppressed Candida-induced proliferation when both antigens were present in the same culture. Addition of indomethacin to these antigen cocultures totally reversed the Coxiella-induced suppression, confirming the evidence above that the nonspecific effector mechanism of suppression was prostaglandin (PG)-mediated. Elicitation of suppression, however, was antigen specific and involved a T cell-monocyte suppressor circuit. Supernatants from Coxiella-stimulated immune T cells and from the suppressor subset (OKT8+-enriched) of those T cells, but not unstimulated immune cells, induced augmented PGE2 production by unrelated nonimmune PBMC. We conclude that the lymphocyte unresponsiveness characterizing patients with Q fever endocarditis is modulated in part by an antigen-specific T suppressor cell which secretes a lymphokine to stimulate PGE2 production by adherent cells.

Adult↗