[Spreading of Q fever in the USSR (Q fever in Chkalov region)].
Explore the source record for details and available documents.
Humans↗
SEARCH · PubMed Health
Results for “Q fever”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Variation in immune response genes and chronic Q fever. Concepts: preliminary test with post-Q fever fatigue syndrome.
Acute primary Q fever is followed by various chronic sequelae. These include subacute Q fever endocarditis, granulomatous reactions in various organs or a prolonged debilitating post-infection fatigue syndrome (QFS). The causative organism, Coxiella burnetii, persists after an initial infection. The differing chronic outcomes may reflect variations within cytokine and accessory immune control genes which affect regulation of the level of persistence. As a preliminary test of the concept we have genotyped QFS patients and controls for gene variants spanning 15 genes and also examined HLA-B and DR frequencies. QFS patients exhibited a significantly increased frequency of HLA-DR-11 compared with controls and also significant differences in allelic variant frequencies within the NRAMP, and IFNgamma genes. These results indicate a possible genetic role in the expression of overt chronic Q fever. Further studies will be undertaken to increase sample sizes, to survey other forms of chronic Q fever and to examine Q fever patients who have recovered without sequelae.
Cation Transport Proteins↗
Circulating cytokine balance and activation markers of leucocytes in Q fever.
As Q fever is associated with an inflammatory syndrome, we determined circulating levels of inflammatory cytokines, cytokine antagonists, and activation markers of leucocytes in patients with acute Q fever and Q fever endocarditis. Tumour necrosis factor (TNF) and IL-6, but not IL-1beta, were markedly increased compared with controls. Cytokine antagonists and activation markers of leucocytes were profoundly different in acute and chronic Q fever. IL-1 receptor antagonist and TNF receptor type II were significantly increased in patients with acute Q fever, suggesting a shift of cytokine balance towards cytokine antagonists. The activation marker of B cells, sCD23, was significantly increased in Q fever endocarditis compared with controls and patients with acute Q fever. In a 2-year follow-up study of patients with Q fever endocarditis, sCD23 and specific IgG levels slowly decreased in patients whose symptoms resolved, but remained high in those who required prolonged treatment.
Adult↗
[Experience in mass vaccination against Q fever. I. Capacity of Q fever vaccine to produce reactivity and immunity].
Explore the source record for details and available documents.
Bacterial Vaccines↗
Antibody responses in acute and chronic Q fever and in subjects vaccinated against Q fever.
An analysis is made of the antibody response to Coxiella burnettii Phase-1 and Phase-2 antigens, as measured by immunofluorescence in the IgM, IgG or IgA immunoglobulin classes, or by complement-fixation, in patients with acute and chronic Q fever and in vaccinated or skin-tested subjects. In acute (primary) Q fever, IgM specific antibodies to Phase-1 antigen are present in early convalescence together with IgM, IgG, IgA and CF antibodies to Phase-2 antigen. IgM specific antibody may persist for at least 678 days after onset of the acute illness. Patients with chronic Q fever have no IgM specific antibody to Phase-1 or -2 antigens, or only at very low levels; high levels of specific antibody in the IgG and IgA classes, together with CF antibody to both antigenic phases, appear to be characteristic. The serological response in initially seronegative, vaccinated subjects is mainly to Phase-1 antigen in the IgM fraction, and to a lesser degree to Phase-2 antigen by CF and in IgM and IgG classes. Subjects who were equivocally seropositive before vaccination showed IgA and IgG specific antibody responses to Phase-1 antigen and CF and IgG class responses to Phase-2 antigen. Similar antibody profiles were observed in patients who seroconverted after a positive skin-test. Data are also presented on the suitability of C. burnettii antigens for use in immunofluorescence and on the binding of IgM specific antibody by Phase-1 antigen but its failure to fix complement.
Acute Disease↗
Coxiella burnetii blood cultures from acute and chronic Q-fever patients.
Q fever, a worldwide zoonosis caused by Coxiella burnetii, may present as either an acute or a chronic disease. We correlated the results of 844 C. burnetii blood cultures with serological, clinical, and therapeutic data. C. burnetii was isolated from 17% of untreated patients with acute Q fever and from 53% of untreated patients with chronic Q fever. C. burnetii was not isolated from patients who were receiving antibiotics active against C. burnetii. For seven culture-positive patients with acute Q fever, serology was negative when C. burnetii was isolated. One patient with acute Q fever had a positive blood culture 25 days after the discontinuation of specific antibiotic therapy, and another had a positive blood culture after the resolution of symptoms. In one case of chronic Q fever, a positive blood culture resulted from noncompliance with treatment. The culture method described in this report is suitable for all laboratories with cell culture facilities. Our findings suggest that blood samples must be collected prior to the initiation of an antibiotic regimen if C. burnetii is to be successfully isolated.
Acute Disease↗
The 75-kD tumour necrosis factor (TNF) receptor is specifically up-regulated in monocytes during Q fever endocarditis.
Q fever is an infectious disease caused by Coxiella burnetii, an obligate intracellular microorganism that inhabits monocytes/macrophages. The dysregulated production of TNF-alpha in Q fever endocarditis has been associated with defective killing of C. burnetii by patient monocytes. As soluble receptors for TNF-alpha (TNF-R55 and TNF-R75) regulate TNF-alpha activity, we investigated their release by monocytes in Q fever. Spontaneous and C. burnetii-stimulated release of TNF-R75, but not of TNF-R55, was up-regulated in patients with ongoing endocarditis compared with controls. The increase in TNF-R75 release was related to the activity of Q fever endocarditis, since TNF-R75 release was similar in patients with cured endocarditis and controls. While spontaneous release of TNF-R75 by monocytes from patients with ongoing Q fever endocarditis occurred without changes in its membrane expression, C. burnetii increased the surface expression of TNF-R75. In addition, TNF-R75 transcripts were increased in resting and C. burnetii-stimulated monocytes from patients with ongoing endocarditis. On the other hand, TNF-R75 release was not related to TNF-alpha secretion. These results indicate that the modulation of TNF-R75 is a critical feature of the pathophysiology of Q fever endocarditis.
Adult↗
[Q fever pericarditis].
Q fever is a zoonotic disease caused by Coxiella burnetii--an obligate, gram negative, intracellular bacteria. The term Q (Query) was first used because at the time the disease was named its etiology was unknown. Q fever is divided into acute and chronic infections characterized by different evolution, serological profiles and treatment. Pericarditis, as a manifestation of Q fever is rare and difficult to diagnose. This is due to the following: firstly, the clinical presentation of acute Q fever is pleomorphic, nonspecific and self limited, and secondly, the diagnosis relies on the physician's interest and the presence of a reliable diagnostic laboratory. The objective of that review is to increase the physician's awareness of the clinical presentation of Q fever, to discuss the importance of the diagnosis and laboratory tests and to guide the physician as to when to provide treatment and the relevant patient population to be treated.
Humans↗
Atypical manifestations of chronic Q fever.
Chronic Q fever is uncommon, with the majority of cases manifesting as culture-negative endocarditis. In this report, we describe 3 patients who present with atypical manifestations of chronic Q fever. These were a 43-year-old man whose site of chronic Q fever was the central nervous system, a 53-year-old woman who underwent coronary angioplasty 6 days before the onset of symptoms of acute Q fever and within 4 months had serologic evidence consistent with chronic Q fever, and a 66-year-old man with fever of unknown origin, a pancreatic mass, and aorto-bifemoral grafts.
Adult↗
Q fever endocarditis.
Q fever is a widespread disease caused by the rickettsia Coxiella burnetii, an obligate intracellular bacteria which man usually acquires through the inhalation of infected dust from subclinically infected animals. Q fever may be acute or chronic. The chronic form mostly presents as endocarditis, which is difficult to diagnose and may ultimately be fatal. Immunocompromised conditions and underlying heart disease are the most important risk factors to consider in cases of Q fever endocarditis. The ultimate diagnosis is based on specific diagnostic tests which include serology, demonstration of C. burnetii in valvular material, isolation of C. burnetii from blood and tissue samples by cell-culture techniques as well as amplification and detection of the bacterial DNA by polymerase chain reaction. Treatment of chronic Q fever endocarditis is complex and requires long-term antibiotic therapy, sometimes associated with heart valve replacement. At the present time neither an optimal antibiotic combination nor the duration of treatment is known and patients with Q fever endocarditis require prolonged follow-up because of the possibility of later relapses.
Coxiella burnetii↗
Infection in renal transplantation: a case of acute Q fever.
Acute Q fever is a zoonotic infection that most often occurs as an asymptomatic or very mild febrile illness. A small percentage of patients go on to develop chronic Q fever months or even years after the acute infection. We present a case of acute Q fever occurring in a renal transplant recipient who developed severe systemic disease with renal involvement. Serological diagnosis was carried out, and the patient was treated successfully with antibiotic therapy. This case emphasizes Q fever as one of the atypical infectious agents that may have serious consequences in immunocompromised renal transplant recipients and reminds us of the importance of careful inquiry regarding personal or occupational activities that could lead to exposure to specific organisms.
Humans↗
Clinical and pathologic changes in a guinea pig aerosol challenge model of acute Q fever.
Acute Q fever is a zoonotic disease caused by the obligate intracellular bacterium Coxiella burnetii and can manifest as a flu-like illness, pneumonia, or hepatitis. A need exists in Q fever research for animal models mimicking both the typical route of infection (inhalation) and the clinical illness seen in human cases of Q fever. A guinea pig aerosol challenge model was developed using C. burnetii Nine Mile phase I (RSA 493), administered using a specialized chamber designed to deliver droplet nuclei directly to the alveolar spaces. Guinea pigs were given 10(1) to 10(6) organisms and evaluated for 28 days postinfection. Clinical signs included fever, weight loss, respiratory difficulty, and death, with the degree and duration of response corresponding to the dose of organism delivered. Histopathologic evaluation of the lungs of animals infected with a high dose showed coalescing panleukocytic bronchointerstitial pneumonia at 7 days postinfection that resolved to multifocal lymphohistiocytic interstitial pneumonia by 28 days. Guinea pigs receiving a killed whole-cell vaccine prior to challenge with the highest dose of C. burnetii were protected against lethal infection and did not develop fever. Clinical signs and pathological changes noted for these guinea pigs were comparable to those seen in human acute Q fever, making this an accurate and valuable animal model of human disease.
Acute Disease↗
Immunogenicity and reactogenicity of a Q fever chemovaccine in persons professionally exposed to Q fever in Czechoslovakia.
An immunization trial carried out on 1310 persons professionally exposed to Q fever confirmed the suitability of a chemovaccine for field use. Its immunogenicity and reactogenicity differed in three groups of subjects who differed in their previous experience of Q fever and who were given different lots of the vaccine. There was some correlation between reactogenicity of the vaccine and pre-immunization positivity in the microagglutination and skin tests as indicators of a previous exposure. The skin test was more reliable for predicting post-immunization reactions.
Animals↗
An economic evaluation of increased uptake in Q fever vaccination among meat and agricultural industry workers following implementation of the National Q Fever Management Program.
INTRODUCTION: Q fever is a serious but vaccine-preventable infectious disease that predominantly affects those working in the meat and agricultural industries. In October 2000, the Commonwealth Government introduced the National Q Fever Management Program. This economic evaluation assesses the cost-effectiveness and cost-utility of improved vaccine uptake among meat and agricultural industry workers. METHODS: Separate analyses were conducted for meat and agricultural industry workers. Clinical and epidemiological data used to create the models were obtained from published sources. Markov modelling was used to estimate the impact of Q fever vaccination uptake on the direct costs and outcomes of Q fever over a 20-year period. RESULTS: Increasing vaccine uptake from 65% to 100% among meat industry workers results in an incremental cost per life year gained of $20,002, and a cost per QALY of $6,294. Increasing vaccine uptake from zero to 20% among agricultural industry workers results in an incremental cost per life year gained of $24,950, and a cost per QALY of $7,984. Including some indirect costs in the form of Workcover payments results in cost savings for both industry groups. CONCLUSION: The results of this evaluation indicate that public health strategies to enhance the uptake of Q fever vaccine among high-risk workers potentially provides excellent value for the money invested.
Adult↗
[Epidemiology of Q fever in Plovdiv; two epidemics of Q fever].
Explore the source record for details and available documents.
Epidemics↗
Q fever endocarditis.
Q fever endocarditis, which is seen most often in Great Britain and Australia, has been rarely observed in the United States. A patient with an eight month febrile illness who had signs and symptoms of endocarditis and serologic studies diagnostic of Q fever endocarditis is reported. A history of extensive travel makes it unclear where he originally contracted the disease. Q fever endocarditis is probably underdiagnosed and should be looked for in any case of culture negative endocarditis or chronic fever of unknown origin.
Aged↗
Pigeon pneumonia in provence: a bird-borne Q fever outbreak.
Q fever is a widespread zoonosis caused by Coxiella burnetii, an obligate intracellular bacterium, which humans usually acquire through the inhalation of infected dust from subclinically infected mammals. Human infection commonly takes place when an infected mammal gives birth, since high concentrations of the organism are found in the products of conception. Worldwide, cattle, sheep, and goats are the most common reservoirs for C. burnetii. A few investigators have also reported parturient cats and dogs as the sources of human outbreaks of Q fever. During a 10-day period in May 1996, all five members of one family living on a farm in Provence, in the south of France, became ill with fever, general malaise, and cough. All of them had acute Q fever. An epidemiological investigation suggested that this outbreak resulted from exposure to contaminated pigeon feces and ticks.
Adult↗
Q fever vaccine uptake in South Australian meat processors prior to the introduction of the National Q Fever Management Program.
Despite the availability of a vaccine, the incidence of Q fever disease among populations at risk continues to be high. Q fever is an important cause of morbidity for workers, particularly in the meat and agricultural industries. Following an increase in 1998 in the number of Q fever notifications among meat processors to the Communicable Disease Control Branch, South Australia, a survey was conducted in the same year to assess the uptake of Q fever immunisation programs in meat processors and to identify barriers to offering these programs. This survey was conducted prior to the introduction of the National Q Fever Management Program in 2001 that provided a targeted vaccination program to specific at-risk occupations. The results of the survey highlighted that very few meat processors in South Australia offered a Q fever immunisation program to their workers. More importantly, this article highlights that there was a wide variety of attitudes and beliefs about Q fever disease and its prevention. These attitudes and beliefs have the potential to impact on whether workers at risk are offered or seek Q fever vaccination. Previous attitudes may return and levels of protection in at-risk occupations will decrease without a concerted effort at a state level. A replication of this study should benchmark the prevailing attitudes about Q fever programs. In response to the 1998 survey a number of strategies and initiatives were developed to address the barriers to Q fever vaccination in South Australian meat processors. The National Q Fever Management Program (2001-2005) further enhanced the ability to address barriers such as vaccine cost.
Abattoirs↗