Acute urinary tract infection and Q fever as causes of FUO in the same patient. A case history plus brief review of Q fever.
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Acute Disease↗
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Q fever studies. XII. Certain observations on the relationships between serologic tests for brucellosis; syphilis and Q fever.
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Brucellosis↗
Prolonged fever and pyuria: an uncommon manifestation of Q fever.
A patient with Q fever is described who had been ill for a year before the diagnosis was made on the basis of serological data. In addition it was possible to isolate Coxiella burnetii, the causative agent by culture from the urine. This is very exceptional and is to our knowledge only the second case in which this has been achieved. The patient made a full recovery after lengthy treatment with tetracycline. Q fever should be considered in patients with pyrexia of unknown origin, particularly in travellers.
Adult↗
Acute hepatitis with or without jaundice: a predominant presentation of acute Q fever in southern Taiwan.
Acute Q fever was previously regarded as an uncommon infectious disease in Taiwan but has been increasingly recognized recently. Acute febrile illness, hepatitis, and pneumonia are the 3 most common manifestations of this condition, whereas jaundice is rarely reported among patients with acute Q fever. We report 2 cases of acute Q fever with jaundice and multi-organ involvement. The first patient presented with fever, severe headache, and acute abdomen necessitating laparotomy and was complicated with acute cholestatic hepatitis, acute non-oliguric renal failure and disseminated intravascular coagulation. The second patient had acute cholestatic hepatitis and thrombocytopenia, and the latter was likely related to the infection of bone marrow by Coxiella burnetii, as evidenced by the presence of C. burnetii DNA detected by nested polymerase chain reaction. The incidence and clinical significance of hyperbilirubinemia was also determined by review of medical records of 35 cases of acute Q fever cases diagnosed serologically at National Cheng Kung University Hospital from 1994 to 2001. All had biochemical hepatitis and 23% had hyperbilirubinemia (serum bilirubin > or =2 mg/dL). The febrile course before admission and the period between the initiation of effective medication to defervescence were longer in patients with hyperbilirubinemia than in patients without hyperbilirubinemia, although this difference was not significant. Our results suggest that the predominant presentation of acute Q fever in southern Taiwan is acute febrile illness with hepatitis and that jaundice is not uncommon. Due to the clinical polymorphism of acute Q fever, the threshold of surveys for C. burnetii infections should be low for febrile patients with elevated transaminases or hyperbilirubinemia of unknown cause.
Abdominal Pain↗
Serological diagnosis of Q fever endocarditis.
The diagnosis of Q fever endocarditis cannot be made by bacterial cultures and necessitates serological identification of specific antibodies to Coxiella burnetii which stimulates mainly the production of anti-phase II antibodies during the acute disease, but primarily anti-phase I antibodies in endocarditis. Indirect microimmunofluorescence allows rapid detection of specific IgA, IgG and IgM. The results of serological analyses of 191 acute cases of Q fever were compared with those of 8 cases of Coxiella burnetii endocarditis. All sera were evaluated by complement fixation and microimmunofluorescence tests. The highest titre differences between primary Q fever and Q fever endocarditis were observed with anti-phase I IgA and IgG antibodies measured by microimmunofluorescence followed by anti-phase I antibodies measured by complement fixation tests. Antiphase I IgG and IgM titres were consistently higher than anti-phase II titres in endocarditis. The reverse is true in acute Q fever. In addition, anti-phase I IgA appeared to be diagnostic for Coxiella burnetii endocarditis. Accordingly we recommend the testing of these specific IgA, IgG, and IgM by microimmunofluorescence in cases of culture-negative endocarditis. These tests could also prove useful for following the development of Coxiella burnetii endocarditis in patients under treatment.
Antibodies, Bacterial↗
Q fever: current concepts.
Persons with Q fever usually present with severe retrobulbar headache, a fever to 104 degrees F or higher with shaking chills, general malaise, myalgia, chest pain, and sometimes pneumonia and hepatitis. Cattle, sheep, goats, and ticks are the primary reservoirs of the etiologic agent, Coxiella burnetii. Humans are usually infected by inhaling infectious aerosols. Because C. burnetii can survive for long periods in the environment, it poses a continuing health hazard once it is disseminated. Q fever usually occurs sporadically, but large outbreaks are frequently observed throughout the world, particularly among abattoir workers and personnel working in research centers. Q fever endocarditis follows a chronic course and is frequently fatal. Tests for antibodies to C. burnetii are required for confirmation of the diagnosis. Tetracyclines remain the mainstay of treatment for acute Q fever, and tetracyclines in combination with other antibiotics have been advocated for patients with Q fever endocarditis. Vaccines for Q fever have been proven effective in clinical trials.
Animals↗
[Q fever in the Ukraine].
Q fever occurs in all geographical landscape zones and in most administrative regions of the Ukrainian SSR. The disease was diagnosed in those areas where no such cases had ever been registered. In the Kharkov region the examination of 425 fever patients with unclear diagnosis resulted in diagnosing 5 cases of Q fever. The proportion of seropositive persons among different professional groups of the population in the eastern part of the republic was determined (6.9% among workers of meat-packing factories, 8.7% among workers of fur- and wool-treating establishments, 5.2% among stock breeders). At the farms of the Kharkov, Poltava and Sumy regions the spread of infection among large cattle was 2.3% and among small cattle 5.6%. Rickettsial carriership revealed in hard ticks collected in the Kharkov region indicated the possibility of the existence of the natural focus of Q fever in this zone and increased the available information on the presence of the territories with the natural foci of this infection in the Ukraine.
Agricultural Workers' Diseases↗
Q fever.
An outbreak of Q fever occurred in Scotland during this summer and was reported in news headlines. Despite these newsworthy headlines, Q fever remains poorly understood. The causative organism, Coxiella burnetii, has a worldwide distribution, with the notable exception of New Zealand. Even with its ubiquitous nature, Q fever is rarely reported. We explore some of the underlying reasons for this apparent under diagnosis together with some of the diagnostic challenges posed by this obligate intracellular pathogen. The host range for this microbe spans arthropods, through to birds and a diverse range of mammals including livestock, companion animals and man. In most, infection remains sub-clinical, however, in some, infection can cause severe and life-threatening complications. Furthermore, possible long-term persistence within those infected, may result in long-term sequelae disassociated from initial risk factors or acute clinical presentation. We review current thinking on C. burnetii, and identify some of our current knowledge gaps.
Adult↗
[Q-fever imported into Norway].
Q fever is an important zoonosis that occurs throughout the world. In contrast to most other European countries, there has been no evidence of endemic Q fever in Norway up to now. The disease is caused by Coxiella burnetii, a rickettsia-like bacterium. Humans are infected mainly by inhalation of contaminated aerosols from cattle, sheep and goats. Clinical manifestations are protean, ranging from asymptomatic infection to life-threatening endocarditis. In this article we present the first four cases of serological proven acute Q fever imported into Norway. The patients were Norwegian tourists who had visited Bhutan, the Canary Islands, and Morocco. Two patients had fever with maculopapular exanthema, one had pneumonia, and one had biopsy-proven granulomatous hepatitis. Three were treated with tetracyclines. All four patients recovered well.
Aged↗
Q fever in Israel.
BACKGROUND: Q fever was first described over fifty years ago. While in a proportion of cases there is a clear etiologic link to farm animals, their products, and fomites, in the majority of cases no such association is apparent, and the mode of infection is a mystery. METHODS: In this paper, we examine the reported incidence of Q fever in Israel since it was made notifiable in 1951, and in particular for the period 1981-1985, when special surveillance at national reference laboratories was carried out. RESULTS: Age and sex as well as urban-rural distributions suggest the influence of occupation, but in the large majority of cases mode of transmission was unknown. CONCLUSIONS: If our knowledge concerning the etiology of Q fever in Israel, and the means of preventing it, is to be advanced, each case should be investigated assiduously to uncover risk factors for exposure, and sero-epidemiologic studies carried out to identify geographic or occupational groups differentially infected.
Adolescent↗
Q fever serology: cutoff determination for microimmunofluorescence.
Q fever, a worldwide zoonosis caused by Coxiella burnetii, lacks clinical specificity and may present as acute or chronic disease. Because of this polymorphism, serological confirmation is necessary to assess the diagnosis. Although microimmunofluorescence is our reference technique, the cutoff titers that are currently used to make a diagnosis of active or chronic Q fever were determined years ago with limited series of patients and sera. We determined the titers of immunoglobulin G (IgG), IgM, and IgA against both phases (I and II) of Coxiella burnetii. Rheumatoid factor was removed before testing IgM and IgA. We report here the various cutoff titers and the kinetics of antibody development from 2,218 first serum samples of patients, among whom 208 suffered from acute Q fever and 53 had chronic Q fever. In active Q fever, we have defined a low cutoff (phase II IgG titer < or = 100) below which the diagnosis cannot be made and would need further confirmation and confirmed a high cutoff (phase II IgG titer > or = 200 and phase II IgM titer > or = 50) over which the diagnosis can be made. For chronic Q fever diagnosis, phase I IgA titers are not contributive despite previous works claiming their usefulness; a phase I IgG titer of > or = 800 is highly predictive (98%) and sensitive (100%). We have also studied the possibility of rejecting or evoking the diagnosis of chronic Q fever by phase II IgG and IgA titers. This method is useful when phase I testing is not available, but the sensitivity remains low (57%).
Acute Disease↗
Serological diagnosis and follow-up of asymptomatic and acute Q fever infections.
During an outbreak of Q fever at a farmer's market in Soest (North Rhine-Westphalia, Germany) in 2003, we examined 263 serum samples of presumably infected persons for Q fever antibodies. One hundred and seventy-one of these patients were tested positive for acute Q fever infection. Furthermore, 29 persons of certain risk groups like pregnant women (n=11) or patients with valvular heart disease (n=18) were examined. Among these, in four pregnant women and two heart patients an acute but asymptomatic infection could be diagnosed. With 30 patients we performed a serological follow-up for 8-60 weeks. In our study, phase 2 (PH2)-IgM antibodies as a marker for acute infection were present in all 30 patients 3-4 weeks after onset of clinical signs and disappeared 3-4 months later. Six weeks to three months after clinical manifestation, all patients developed PH1-IgG antibodies in low levels with no clinical signs of chronic Q fever. Three patients, including one pregnant woman showed high-level titres and were treated for chronic Q fever. Eleven patients with low PH1-IgG antibodies and all three patients with high titres developed IgA antibodies from 10 weeks after clinical manifestation; therefore PH1-IgA cannot be used as the only serological marker for chronic Q fever. Chronic infections were indicated only by a continuous increase of PH1 antibodies and a high persistence of PH2-IgG. We therefore conclude that the exclusion of chronic Q fever infection by a single serological examination cannot be done. At least three consecutive tests should be performed, that is 3, 6, and 9 months after initial Q fever infection.
Acute Disease↗
A review of Q fever in Australia 1991-1994.
Q fever continues to be an important disease in Australia. Despite the development of an effective vaccine that has been commercially available since 1989, the number of cases notified has continued to increase. This study reviewed national notifications of Q fever between 1991 and 1994, together with demographic, socioeconomic and occupational information, to investigate temporal and spatial disease patterns. Based on notification data, Q fever can be considered primarily a disease of adult males that occurs in eastern Australia: southern Queensland and northern New South Wales have the highest levels of activity. A significant association between Q fever activity of areas and the presence of livestock was found. A strong association with the meat industry was also confirmed. Q fever is conservatively estimated to cost Australia around A$1 million and more than 1700 weeks of work time annually. There is a need to increase awareness of this disease and its prevention. An extension program in rural communities and provision of vaccine to all abattoir workers would appear to be sensible public health approaches.
Adolescent↗
[Q fever endocarditis and bicuspid aortic valve].
Q fever is caused by the rickettsia Coxiella burnetti, an obligate intracellular bacterium acquired by inhalation of infected dust from subclinically infected animals. Q fever may be acute or chronic; the chronic form mostly presents as endocarditis. Immunocompromised states and underlying heart disease are the most important risk factors. Usually the symptoms of Q fever endocarditis are nonspecific and diagnosis is often established very late. New criteria for diagnosis include a single blood culture positive for Coxiella burnetti, positive Q fever serology and characteristic echocardiographic studies. We describe a 49-year-old man with bicuspid aortic valve admitted with fever, weight loss and a new heart murmur. The diagnosis of Q fever endocarditis was established by positive Q fever serology, and an echocardiogram showing vegetations and valvular dysfunction. This case suggests that Q fever endocarditis should be considered in patients with "sterile" endocarditis.
Aortic Valve↗
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↗
Q fever in Taiwan.
BACKGROUND: Although Q fever, a rickettsial disease caused by Coxiella burnetii, is supposed to occur sporadically worldwide, there is only one case report of this disease in Taiwan. We examined the antibody of Q fever to evaluate the status of Q fever in Taiwan. METHODS: In total, 579 paired serum specimens of suspected febrile patients sent by several hospitals and sanitary stations to this Institute in 1991 and 1992 were tested according to the technique of indirect fluorescent antibody (IFA). RESULTS: In total 48 serologically acute Q fever cases were found, mostly from Tainan, Pingtung and Kaohsiung. There was only one female, and the age of most patients was 40-50 years. The high season is in June and July. CONCLUSIONS: The antibody titer of all 48 positive cases reached 1:320 or higher on the 13th day after onset of the disease. IFA as a diagnostic tool to detect acute and convalescent serum antibody titer is discussed.
Adult↗
Acute and chronic Q fever in patients with cancer.
Q fever is caused by Coxiella burnetii, a strictly intracellular bacterium that lives within the phagolysosome of infected cells. We report here five cases of Q fever in patients with cancer. Three of them had a solid tumor, one had a B cell lymphoma, and one had chronic myeloid leukemia. One patient had acute Q fever, and the four others had chronic Q fever endocarditis. Two patients with endocarditis had no previous history of valvulopathy. C. burnetii was isolated from the valves of two patients. One of the patients with endocarditis died. Patients with cancer who have unexplained fever and live in areas in which C. burnetii is endemic should undergo serological testing for infection with this microorganism.
Acute Disease↗
An outbreak of cat-associated Q fever in the United States.
Q fever is usually acquired by contact with aerosols generated during parturition of domestic ungulates (e.g., sheep, cows, goats). In the maritime provinces of Canada, parturient cats have also been implicated in its transmission. A 66-year-old woman from eastern Maine developed high fever, rigors, headache, myalgias, pulmonary infiltrates, and elevated hepatocellular enzymes, and the diagnosis of acute Q fever was confirmed serologically. She and 14 other family members had attended a family reunion in Maine 2 weeks earlier, when they were exposed to a parturient cat. All 11 adults and older children attending the reunion developed symptoms consistent with acute Q fever. Serum samples were obtained from 10 who attended the reunion and 8 who did not attend. Titers greater than or equal to 1:64 to Coxiella burnetii were present in all who attended the reunion but in none of those who did not. Cat-associated Q fever should be considered when sporadic cases of the disease occur in the United States.
Adolescent↗