scholarly journals Q Fever: An Old but Still a Poorly Understood Disease

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Hamidreza Honarmand

Q fever is a bacterial infection affecting mainly the lungs, liver, and heart. It is found around the world and is caused by the bacteriaCoxiella burnetii.The bacteria affects sheep, goats, cattle, dogs, cats, birds, rodents, and ticks. Infected animals shed this bacteria in birth products, feces, milk, and urine. Humans usually get Q fever by breathing in contaminated droplets released by infected animals and drinking raw milk. People at highest risk for this infection are farmers, laboratory workers, sheep and dairy workers, and veterinarians. Chronic Q fever develops in people who have been infected for more than 6 months. It usually takes about 20 days after exposure to the bacteria for symptoms to occur. Most cases are mild, yet some severe cases have been reported. Symptoms of acute Q fever may include: chest pain with breathing, cough, fever, headache, jaundice, muscle pains, and shortness of breath. Symptoms of chronic Q fever may include chills, fatigue, night sweats, prolonged fever, and shortness of breath. Q fever is diagnosed with a blood antibody test. The main treatment for the disease is with antibiotics. For acute Q fever, doxycycline is recommended. For chronic Q fever, a combination of doxycycline and hydroxychloroquine is often used long term. Complications are cirrhosis, hepatitis, encephalitis, endocarditis, pericarditis, myocarditis, interstitial pulmonary fibrosis, meningitis, and pneumonia. People at risk should always: carefully dispose of animal products that may be infected, disinfect any contaminated areas, and thoroughly wash their hands. Pasteurizing milk can also help prevent Q fever.

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Matteo Boattini ◽  
André Almeida ◽  
Rita Barata Moura ◽  
João Abreu ◽  
Ana Sofia Santos ◽  
...  

We describe the case of a 55-year-old man with a biological prosthetic aortic valve who suffered from epigastrium and right hypochondrium pain associated with intermittent night sweats. Liver biopsy showed infectious hepatitis pattern without pathognomonic features.Coxiella burnetiiserology was suggestive of chronic Q fever, and modified Duke's criteria for endocarditis were also fulfilled. The authors present a brief literature review concerning chronic Q fever, emphasizing absent previous reports of chronic Q fever with hepatitis and endocarditis and no increase in inflammatory markers.


1998 ◽  
Vol 5 (6) ◽  
pp. 814-816 ◽  
Author(s):  
Christian Capo ◽  
Ioana Iorgulescu ◽  
Maryse Mutillod ◽  
Jean-Louis Mege ◽  
Didier Raoult

ABSTRACT A detailed analysis of the humoral response to Coxiella burnetii may provide insight into the pathogenesis of Q fever, a zoonosis caused by C. burnetii. The subclasses of C. burnetii-specific antibodies were determined by immunofluorescence in 20 patients with acute Q fever and 20 patients with chronic Q fever. Although immunoglobulin G1 (IgG1) and IgG3 antibodies were found in acute and chronic Q fever, neither IgG2 nor IgG4 was detected. The detection of IgG1 and IgG3 antibodies was not due to an increase of the IgG1 and IgG3 subclasses. Moreover, IgG1 and IgG3 antibodies were not correlated, suggesting that they may play different roles in Q fever.


2012 ◽  
Vol 141 (4) ◽  
pp. 847-851 ◽  
Author(s):  
L. M. KAMPSCHREUR ◽  
J. C. J. P. HAGENAARS ◽  
C. C. H. WIELDERS ◽  
P. ELSMAN ◽  
P. J. LESTRADE ◽  
...  

SUMMARYThe Netherlands experienced an unprecedented outbreak of Q fever between 2007 and 2010. The Jeroen Bosch Hospital (JBH) in 's-Hertogenbosch is located in the centre of the epidemic area. Based on Q fever screening programmes, seroprevalence of IgG phase II antibodies to Coxiella burnetii in the JBH catchment area was 10·7% [785 tested, 84 seropositive, 95% confidence interval (CI) 8·5–12·9]. Seroprevalence appeared not to be influenced by age, gender or area of residence. Extrapolating these data, an estimated 40 600 persons (95% CI 32 200–48 900) in the JBH catchment area have been infected by C. burnetii and are, therefore, potentially at risk for chronic Q fever. This figure by far exceeds the nationwide number of notified symptomatic acute Q fever patients and illustrates the magnitude of the Dutch Q fever outbreak. Clinicians in epidemic Q fever areas should be alert for chronic Q fever, even if no acute Q fever is reported.


2012 ◽  
Vol 17 (3) ◽  
Author(s):  
W van der Hoek ◽  
P M Schneeberger ◽  
T Oomen ◽  
M C Wegdam-Blans ◽  
F Dijkstra ◽  
...  

From 2007 to 2009, the Netherlands faced large seasonal outbreaks of Q fever, in which infected dairy goat farms were identified as the primary sources. Veterinary measures including vaccination of goats and sheep and culling of pregnant animals on infected farms seem to have brought the Q fever problem under control. However, the epidemic is expected to result in more cases of chronic Q fever among risk groups in the coming years. In the most affected area, in the south of the country, more than 12% of the population now have antibodies against Coxiella burnetii. Questions remain about the follow-up of acute Q fever patients, screening of groups at risk for chronic Q fever, screening of donors of blood and tissue, and human vaccination. There is a considerable ongoing research effort as well as enhanced veterinary and human surveillance.


1999 ◽  
Vol 6 (2) ◽  
pp. 173-177 ◽  
Author(s):  
Pierre-Edouard Fournier ◽  
Didier Raoult

ABSTRACT Diagnosis of acute Q fever is usually confirmed by serology, on the basis of anti-phase II antigen immunoglobulin M (IgM) titers of ≥1:50 and IgG titers of ≥1:200. Phase I antibodies, especially IgG and IgA, are predominant in chronic forms of the disease. However, between January 1982 and June 1998, we observed anti-phase II antigen IgA titers of ≥1:200 as the sole or main antibody response in 10 of 1,034 (0.96%) patients with acute Q fever for whom information was available. In order to determine whether specific epidemiological or clinical factors were associated with these serological profiles, we conducted a retrospective case-control study that included completion of a standardized questionnaire, which was given to 40 matched controls who also suffered from acute Q fever. The mean age of patients with elevated phase II IgA titers was significantly higher than that usually observed for patients with acute Q fever (P = 0.026); the patients were also more likely than controls to live in rural areas (P = 0.026) and to have increased levels of transaminase in blood (P = 0.03). Elevated IgA titers are usually associated with chronic Q fever and are directed mainly at phase I antigens. Although the significance of our findings is unexplained, we herein emphasize the fact that IgA antibodies are not specific for chronic forms of Q fever and that they may occasionally be observed in patients with acute disease. Moreover, as such antibody profiles may not be determined by most laboratories, which test only for total antibody titers to phase I and II antigens, the three isotype-specific Ig titers should be determined as the first step in diagnosing Q fever.


1999 ◽  
Vol 12 (4) ◽  
pp. 518-553 ◽  
Author(s):  
M. Maurin ◽  
D. Raoult

SUMMARY Q fever is a zoonosis with a worldwide distribution with the exception of New Zealand. The disease is caused by Coxiella burnetii, a strictly intracellular, gram-negative bacterium. Many species of mammals, birds, and ticks are reservoirs of C. burnetii in nature. C. burnetii infection is most often latent in animals, with persistent shedding of bacteria into the environment. However, in females intermittent high-level shedding occurs at the time of parturition, with millions of bacteria being released per gram of placenta. Humans are usually infected by contaminated aerosols from domestic animals, particularly after contact with parturient females and their birth products. Although often asymptomatic, Q fever may manifest in humans as an acute disease (mainly as a self-limited febrile illness, pneumonia, or hepatitis) or as a chronic disease (mainly endocarditis), especially in patients with previous valvulopathy and to a lesser extent in immunocompromised hosts and in pregnant women. Specific diagnosis of Q fever remains based upon serology. Immunoglobulin M (IgM) and IgG antiphase II antibodies are detected 2 to 3 weeks after infection with C. burnetii, whereas the presence of IgG antiphase I C. burnetii antibodies at titers of ≥1:800 by microimmunofluorescence is indicative of chronic Q fever. The tetracyclines are still considered the mainstay of antibiotic therapy of acute Q fever, whereas antibiotic combinations administered over prolonged periods are necessary to prevent relapses in Q fever endocarditis patients. Although the protective role of Q fever vaccination with whole-cell extracts has been established, the population which should be primarily vaccinated remains to be clearly identified. Vaccination should probably be considered in the population at high risk for Q fever endocarditis.


1990 ◽  
Vol 36 (4) ◽  
pp. 292-296 ◽  
Author(s):  
J. Embil ◽  
J. C. Williams ◽  
T. J. Marrie

The isotypic immune response of 16 individuals who developed Q fever pneumonia following exposure to an infected parturient cat was studied. The enzyme-linked immunosorbent (ELISA) test was used to detect IgM, IgA, and IgG antibodies to phase I and phase II Coxiella burnetii whole-cell antigens and to the phase I lipopolysaccharide. The indirect immunofluorescent antibody (IFA) test was also used to detect antibodies to phase I and phase II whole cells. None of the 16 subjects developed antibodies to the phase I lipopoly saccharide. The ELISA was more sensitive than the IFA test. IgM antibodies to phase II antigen were detectable by ELISA in 80% of the subjects at the time of onset of symptoms and were still present in 7 of the 8 tested at 32 weeks following the onset of symptoms. In all instances (ELISA: IgG, IgM; IFA: IgG, IgM) phase II antibodies developed earlier and reached higher levels than did phase I antibodies. The absence of antibodies to phase I lipopolysaccharide in acute Q fever combined with our unpublished findings of antibodies to phase I lipopoly saccharide in chronic Q fever suggests that this test may be used to distinguish acute from chronic Q fever. Key words: Q fever, immune response, ELISA.


2021 ◽  
Vol 15 (6) ◽  
pp. e0009467
Author(s):  
Yong Chan Kim ◽  
Hye Won Jeong ◽  
Dong-Min Kim ◽  
Kyungmin Huh ◽  
Sang-Ho Choi ◽  
...  

Background In South Korea, the number of Q fever cases has rapidly increased since 2015. Therefore, this study aimed to characterize the epidemiological and clinical features of Q fever in South Korea between 2011 and 2017. Methods/Principal findings We analyzed the epidemiological investigations and reviewed the medical records from all hospitals that had reported at least one case of Q fever from 2011 to 2017. We also conducted an online survey to investigate physicians’ awareness regarding how to appropriately diagnose and manage Q fever. The nationwide incidence rate of Q fever was annually 0.07 cases per 100,000 persons annually. However, there has been a sharp increase in its incidence, reaching up to 0.19 cases per 100,000 persons in 2017. Q fever sporadically occurred across the country, with the highest incidences in Chungbuk (0.53 cases per 100,000 persons per year) and Chungnam (0.27 cases per 100,000 persons per year) areas. Patients with acute Q fever primarily presented with mild illnesses such as hepatitis (64.5%) and isolated febrile illness (24.0%), whereas those with chronic Q fever were likely to undergo surgery (41.2%) and had a high mortality rate (23.5%). Follow-up for 6 months after acute Q fever was performed by 24.0% of the physician respondents, and only 22.3% of them reported that clinical and serological evaluations were required after acute Q fever diagnosis. Conclusions Q fever is becoming an endemic disease in the midwestern area of South Korea. Given the clinical severity and mortality of chronic Q fever, physicians should be made aware of appropriate diagnosis and management strategies for Q fever.


2015 ◽  
Vol 22 (6) ◽  
pp. 664-671 ◽  
Author(s):  
Jeroen L. A. Pennings ◽  
Marjolein N. T. Kremers ◽  
Hennie M. Hodemaekers ◽  
Julia C. J. P. Hagenaars ◽  
Olivier H. J. Koning ◽  
...  

ABSTRACTA large community outbreak of Q fever occurred in the Netherlands in the period 2007 to 2010. Some of the infected patients developed chronic Q fever, which typically includes pathogen dissemination to predisposed cardiovascular sites, with potentially fatal consequences. To identify the immune mechanisms responsible for ineffective clearance ofCoxiella burnetiiin patients who developed chronic Q fever, we compared serum concentrations of 47 inflammation-associated markers among patients with acute Q fever, vascular chronic Q fever, and past resolved Q fever. Serum levels of gamma interferon were strongly increased in acute but not in vascular chronic Q fever patients, compared to past resolved Q fever patients. Interleukin-18 levels showed a comparable increase in acute as well as vascular chronic Q fever patients. Additionally, vascular chronic Q fever patients had lower serum levels of gamma interferon-inducible protein 10 (IP-10) and transforming growth factor β (TGF-β) than did acute Q fever patients. Serum responses for these and other markers indicate that type I immune responses toC. burnetiiare affected in chronic Q fever patients. This may be attributed to an affected immune system in cardiovascular patients, which enables localC. burnetiireplication at affected cardiovascular sites.


1956 ◽  
Vol 54 (4) ◽  
pp. 533-546 ◽  
Author(s):  
B. P. Marmion ◽  
M. S. Harvey

An investigation in an urban area of south-east Kent of 160 patients who had had either pneumonia or unexplained fever during the period from the end of 1948 to the beginning of 1954 revealed that twenty-three (14%) had probably had Q fever.A comparison of the epidemiological histories of patients who had had Q fever with those of the remainder showed that the use of a household supply of raw milk was commoner among the former.Occupational exposure to animals (or animal products), visits to potentially infectious places, or residence near potential sources of infection were not significantly more frequent among the Q-fever cases as compared with the controls.The isolation ofRickettsia burnetifrom the bulked milk of some local herds supplying retail dairies in the towns, together with the general epidemiological evidence, suggested that Q fever in the towns was predominantly milk-borne.


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