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PubMed1994

Minimizing the risk of Q fever in the hospital setting.

Q fever is caused by a rickettsial microorganism (Coxiella burnetii) harboured in sheep. The highest concentration of organisms are found in birth products. It is a very contagious organism which humans can contract by inhaling aerosolized organisms. Most commonly it leads to an acute 'flu-like illness. Rarely, chronic disease with endocarditis is fatal. Infected patients should be treated with tetracyclines or chloramphenicol. A number of outbreaks have been reported in hospital and research settings. Because of the fear of patients and staff contracting Q fever, Hospital Research Review Boards have increasingly resisted the presence of sheep in medical facilities. The authors have reviewed the circumstances leading to these outbreaks and believe researchers can minimize the risk of Q fever. The most important precautions are to use sheep only from Q fever controlled flocks and, depending on the nature of the research, only male sheep.

Academies and Institutes↗
PubMed2006

National surveillance and the epidemiology of human Q fever in the United States, 1978-2004.

Although Q fever is considered enzootic in the United States, surveillance for human Q fever has been historically limited. From 1978 through 1999, 436 cases (average = 20 per year) of human Q fever were reported. After Q fever became nationally reportable in 1999, 255 human Q fever cases (average = 51 per year) were reported with illness onset during 2000 through 2004. The median age of cases was 51 years, and most cases were male (77%). The average annual incidence of Q fever was 0.28 cases per million persons, and was highest in persons 50-59 years of age (0.39 cases per million). State-specific incidence ranged from a high of 2.40 cases per million persons in Wyoming, to 0 cases in some states. Since Q fever became reportable, case reports have increased by more than 250%. Surveillance for Q fever is essential to establish the distribution and magnitude of disease and to complement U.S. bioterrorism preparedness activities.

Adolescent↗
PubMed1987

The pathology of Q fever hepatitis. A case diagnosed by liver biopsy.

A 52-year-old woman with fever and low grade hepatitis had Q fever, a diagnosis made by the characteristic granulomas, containing fibrin and vacuoles, on liver biopsy and confirmed by serology. Fibrin was demonstrated in the granulomas but Coxiella burnetii antigens were not. The literature on the histopathology of the liver in both acute Q fever and Q fever endocarditis shows that none of the 220 cases of Q fever endocarditis, with one possible exception, had the characteristic granulomas of acute Q fever. Rather they displayed a range from normality through nonspecific reactive hepatitis to occasional nonspecific granulomas. Thus, the characteristic granulomas of acute Q fever appear to be transient even if active infection persists. The definition of chronic Q fever should have a temporal characteristic rather than a serologic one.

Female↗
PubMed2003

[Time course of the levels of antibodies to Coxiella burnetii and detection of C. burnetii-DNA in three imported cases of acute Q fever].

Three patients developed acute Q fever after returning from an inspection tour of farms and abattoirs to Australia. Serum levels of antibodies to Coxiella burnetii and the presence of C. burnetii-DNA in blood samples were examined for more than 100 days. Four-fold raises of IgM and IgG antibodies against C. burnetii phase 2 were observed within the first three weeks in all the three cases. Maximum titers of IgM and IgG antibodies were 1,024-2,048 and 512-4,096, respectively. According to the temporal diagnostic criteria of acute Q fever in the convalescent serum: the IgM titer of > or = 64 and IgG titer of > or = 512 against phase 2, patient A, B and C were determined to be antibody positive for 45, 199 and 122 days, respectively. The result suggests that this standard is practical and reasonable for diagnosis of acute Q fever. C. burnetti-DNA was detected in the sera and buffy coat samples of patient A who developed high fever, severe thrombocytopenia and liver disfunction, but not in those of patient B and C. This study provides useful information for optimization and standardization of Q fever diagnosis in Japan.

Acute Disease↗
PubMed2001

Risks factors and prevention of Q fever endocarditis.

Coxiella burnetii causes acute and chronic Q fever. To evaluate the risk factors of development of chronic endocarditis following Q fever and to assess the best preventive therapy, a retrospective study of patients diagnosed as having Q fever during 1985-2000 was conducted. Twelve patients with acute Q fever who developed endocarditis and 102 patients with Q fever endocarditis were included in the study. When compared to 200 control patients with acute Q fever, preexisting valvular disease (P<10(-7)), especially a prosthetic valve (P=.01), were encountered more often among patients with endocarditis. Among patients with valvular defects, we estimate the risk of developing endocarditis to be 39%. A combination of doxycycline plus hydroxychloroquine was better at preventing the development of endocarditis than doxycycline alone (P=.009). Our results should encourage physicians to detect valvular lesions in patients with acute Q fever and to search for acute Q fever in patients with a valvulopathy and unexplained fever. A proper treatment for such patients and a scheduled follow-up should reduce the risk of developing endocarditis.

Aged↗
PubMed1980

Chronic Q fever endocarditis.

Eight patients with chronic Q fever endocarditis were treated with tetracycline for up to 40 months. In addition, five of these patients received co-trimoxazole. Six patients had prosthetic valves. Two patients who had Q fever endocarditis on their native valves required valve replacement because of haemodynamic difficulties: in only one did the Q fever endocarditis contribute to the haemodynamic difficulty. One patient died. It is suggested that medical treatment is continued until clinically and haematologically there is no evidence of endocarditis and the Q fever phase 1 antibody titre is less than 200. No recurrence of Q fever endocarditis has been detected in three of our patients who have now stopped treatment.

Adult↗
PubMed1999

Short report: prevalence of antibodies against spotted fever, murine typhus, and Q fever rickettsiae in humans living in Zambia.

The causative agents of rickettsial diseases (Rickettsia conorii, R. typhi, and Coxiella burnetii) have been reported throughout the African continent. However, there have been no reports on epidemiologic surveys of these infections in Zambia. This study was designed to clarify the prevalence of three rickettsioses in 377 humans in Zambia. The seroprevalence of antibodies against R. conorii, R. typhi, and C. burnetii was 16.7%, 5.0%, and 8.2%, respectively. The rates of antibody positivity against R. conorii and C. burnetii were higher in the eastern (23.1% and 11.8%) and western (16.8% and 7.4%) areas of Zambia than in the northern (3.0% and 3.0%) area of this country. There was little difference among the three areas in the distribution of antibodies against R. typhi. Since cattle breeding is more extensive in the western and eastern areas than in the northern area, it is thought that cattle-breeding areas are foci of R. conorii and C. burnetii infections in Zambia.

Adolescent↗
PubMed2003

The effect of C. burnetii infection on the quality of life of patients following an outbreak of Q fever.

Sixty-six cases of Q fever were diagnosed in people affiliated with a goat-farming co-operative in rural Newfoundland in the spring of 1999. Follow-up studies which included administration of the Short Form 36 Health Survey (SF-36) were conducted 3 and 27 months after the initial outbreak to prospectively follow the effects of acute Q fever on the quality of life of the participants. Twenty-seven months after the outbreak 51% of those who had Q fever reported persistent symptoms including seven participants whose symptoms had initially resolved 3 months after the outbreak. Individuals with Q fever had significantly lower scores on five of the eight scales in the SF-36 and lower scores in the mental and physical summary scales compared to uninfected controls. Although this supports the hypothesis of a 'post Q fever fatigue syndrome' (QFFS), further study is warranted.

Case-Control Studies↗
PubMed2003

Significance of Q fever serologic diagnosis in clinically suspect patients.

Q fever is caused by C. burnetii, an intracellular obligate bacterium. For clinical confirmation of Q fever, diagnosis of interstitial pneumonia is of significance. The acute disease varies in severity from minor to fatal, with the possibility of serious complications. Chronic endocarditis is a well-known outcome. Symptoms of Q fever can vary; fixing diagnosis is done by serology with the phase I and the phase II antibody. We tested 44 sera of 31 clinically suspect patients. From these, 22 patients were taken to the infection clinic, 8 to the pulmonary clinic, and one to the general hospital. From the 31 patients, 21 patients had one serum, 7 patients, 2 sera, and 3 patients, 3 sera. Blood samples were collected by vein puncture, and serum samples were kept at -20 degrees C until testing. All sera were processed by indirect immunofluorescent assay (IFA) Q fever IgM and IgG. Of 44 processed sera, 21 were seropositive. Specific IgM antibody was found in sera of 6 patients (19.4%), and specific IgG antibody in sera of 16 patients (51.2%). In sera of 15 clinically suspect patients (48.3%), no specific anticoxiella antibody was found. From these results we can confirm the importance of serology in laboratory diagnosis and clinical affirmation of suspect Q fever. Indirect immunofluorescent assay (IFA) is reliable and appropriate for daily, routine diagnosis of human Q fever.

Bosnia and Herzegovina↗
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↗
PubMed1994

Serotyping Coxiella burnetii isolates from acute and chronic Q fever patients by using monoclonal antibodies.

Four mouse monoclonal antibodies reacting with Coxiella burnetti lipopolysaccharide antigens were produced and used in serotyping 17 C. burnetii isolates from acute Q fever and Q fever endocarditis patients in France. Two monoclonal antibodies (1B2 and 3B6) were considered specific for the Priscilla strain, a representative of Q fever endocarditis isolates, and did not react with the Nine Mile strain, which is representative of acute Q fever isolates. Monoclonal antibodies Nos. 1B2 and 3B6 reacted with 75% (3/4) acute Q fever isolates and 85% (11/13) of endocarditis isolates from France. It is reasonable to conclude that Priscilla-like strains cause both acute Q fever and Q fever endocarditis. The hypothesis that Priscilla-like strains only are associated with Q fever endocarditis should be reconsidered.

Acute Disease↗
PubMedDate not supplied

Q fever urban cases in Romania.

Q fever urban sporadic cases in Romania in the 1981-87 period are reviewed as concerns their incidence, seasonality and epidemiological data. Urban cases represented 76.8% as against 23.2% rural cases from the 134 Q fever sporadic cases detected in this period. Cases were distributed throughout all months with peaks during April (18.4% of cases) and June (19.4%). Infections were not related to contact with livestock or domestic birds or with raw milk drinking. Cases could not be identified as Q fever occupational ones. 36.7% of patients were working in nonalimentary industry and only 12.6% were involved in meat industry, veterinary or human medical practices. New studies concerning unusual sources of urban infection such as dogs, cats or urban street pigeons are emphasized.

Humans↗
PubMed2004

Q fever (coxiellosis): epidemiology and pathogenesis.

Q fever is a widespread zoonosis caused by the Gram-negative bacterium Coxiella burnetii. Aborting domestic ruminants are the main sources of human infection but the reservoir of infection is extremely wide. In humans, Q fever may occur as acute pneumonia, hepatitis or flu-like illness or may take a severe chronic form, characterized by endocarditis, chronic hepatitis and chronic fatigue syndrome. In animals, the main clinical manifestation is late abortion. Infection with C. burnetii can be diagnosed using cultural, serological and genetic methods but because the organism is potentially dangerous and requires specialized skills only specialist laboratories are capable of undertaking diagnostic tests. This paper provides a brief overview of the epidemiology and pathogenesis of Q fever (coxiellosis).

Abortion, Induced↗
PubMed2006

[Clinical manifestation of Q fever and tuberculosis, similarly caused by intracellular parasites].

Q fever is a generic term for pneumonia, bronchitis, etc. caused by infection with Coxiella burnetii, a rickettsia-related species of bacteria, in humans. Q-fever is a transient and acute febrile illness that takes a course similar to influenza, and its clinical picture greatly differs from that of tuberculosis that takes a chronic course. The reason for this is thought to be because the generation time of C. burnetii is extremely short (several tens of minutes) compared with Mycobacterium tuberculosis, though those are similar intracellular parasites. Q fever is fourth- or fifth-ranked among the community-acquired pneumonias in the United States and Europe but has a good prognosis with 1-2% of mortality even in the cases that follow a natural course without treatment. Meanwhile, there is a chronic type that follows a protracted course or has a poor prognosis. Therefore, cases definitely diagnosed with Q fever or strongly suspected of Q fever should seek aggressive treatment. Q fever is definitely diagnosed by confirming significant increase in serum antibody titer, but the patients should be followed because in many cases it takes a long time before serum antibody titer increases. Beta-lactams are ineffective against C. burnetii, an obligate intracellular parasite. Although tetracyclines, macrolides, quinolones, rifampicin, etc. are used effectively in the treatment of Q fever, many cases appear to improve by beta-lactam administration because the illness often takes a natural course.

Animals↗
PubMed2006

Questing one Brazilian query: reporting 16 cases of Q fever from Minas Gerais, Brazil.

Q fever has been considered non-existing in Brazil where reports of clinical cases still cannot be found. This case-series of 16 patients is a result of a systematic search for such illness by means of clinical and serologic criteria. Serologic testing was performed by the indirect microimmunofluorescence technique using phase I/II C. burnetii antigens. Influenza-like syndrome was the most frequent clinical form (eight cases--50%), followed by pneumonia, FUO (fever of unknown origin), mono-like syndrome (two cases--12.5% each), lymphadenitis (one case--6.3%) and spondylodiscitis associated with osteomyelitis (one case--6.3%). The ages varied from four to 67 years old with a median of 43.5. All but one patient had positive serologic tests for phase II IgG whether or not associated with IgM positivity compatible with acute infection. One patient had both phase I and phase II IgG antibodies compatible with chronic Q fever. Seroconvertion was detected in 10 patients. Despite the known limitations of serologic diagnosis, the cases here reported should encourage Brazilian doctors to include Q fever as an indigenous cause of febrile illness.

Adult↗
PubMedDate not supplied

[Incidence and characteristics of Q fever in a community habitat].

Q fever is more common in our country than is usually thought, as shown by the diagnostic incidence curve, which approached an exponential rather than lineal function. Sixty cases were diagnosed between 1985 and October 1989. The disease predominated in middle aged males. The suspect epidemiologic contacts did not have any significance. Q fever was more frequent during autumn. Its usual clinical presentation was pneumonia (75%), commonly associated with a flu-like syndrome. Liver was commonly involved (66.6%), although in a mild degree. One of the patients had chronic Q fever, with granulomatous and hepatic, but not endocardial, involvement. The diagnosis was based on seroconversion detected by indirect immunofluorescence. As a rule, the course of the disease was favorable independently from therapy.

Adolescent↗
PubMed1996

Production of interleukin-10 and transforming growth factor beta by peripheral blood mononuclear cells in Q fever endocarditis.

The pathophysiology of Q fever endocarditis is characterized by the suppression of antigen-specific cell-mediated immune responses. We investigated the production of interleukin-10 (IL-10) and transforming growth factor beta (TGF-beta), known to interfere with the development of protective cell immunity. IL-10 was markedly released by unstimulated peripheral blood mononuclear cells (PBMC) from patients with Q fever endocarditis. This release resulted from the upregulation of IL-10 gene transcription. Similarly, the release of TGF-beta1 and TGF-beta2 was significantly higher in patient PBMC than in control cells, but the expression of their respective mRNA was not enhanced in patient cells. In contrast, lipopolysaccharide-stimulated transcription and release of IL-10 and TGF-beta were similar in patients and controls. The release of IL-10 by PBMC but not that of TGF-beta was correlated with the clinical status of the patients. First, IL-10 production was correlated with specific antibody levels. Second, IL-10 release remained elevated in patients prone to relapse. Taken together, our results suggest that the release of IL-10 and TGF-beta is upregulated in Q fever endocarditis. IL-10 might be considered as a marker of disease relapses and might be instrumental in monitoring the efficiency of the treatment.

Adult↗