Gallium-67 citrate scanning for noninvasive detection of inflammation in pericardial diseases

The treatment of acute nonspecific pericarditis is controversial. No study is available that confirms the efficacy of the administration of corticosteroids or nonsteroid anti-inflammatory agents in this condition. There is no reliable invasive marker for pericardial inflammation, because echocardigraphy demonstrates only the presence of fluid. In four patients with pericarditis, gallium-67 citrate scanning was performed, and the isotope was localized to the cardiac silhouette in all. In one patient with effusion the gallium scan was positive and then reverted to negative with corticosteroid therapy. In another, the gallium scan remained positive despite resolution of the pericardial effusion with corticosteroid therapy. This patient eventually required pericardial stripping. Pericardial localization of gallium was useful in detecting the cause of fever in a patient after aortocoronary bypass grafting and in detecting pericardial involvement in a patient with multisystem viral disease. Pericardial localization of gallium-67 may be diagnostically useful and may provide a proper control for the study of the efficacy of corticosteroids versus nonsteroid anti-inflammatory agents in pericarditis.     

1例Q热肺炎诊治报告北大核心CSCD

Q热是一种重要的人兽共患病,病原体为贝氏柯克斯体(Coxiella burnetii),其经呼吸道吸入进入体内,引起急性Q热,严重急性Q热可出现肺炎、肝炎或心肌炎并发症。部分患者治疗不彻底转为慢性Q热。慢性Q热为贝氏柯克斯体在机体局部持续感染,常需要外科手术及数年抗感染治疗,其严重危害患者身体健康及加重家庭经济负担;。追其原因是临床医生对该病认识不足,导致延误治疗所致。本文旨在报告1例Q热肺炎的诊治和体会,以提高临床医生对该病认识。     

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.     

Q fever 1985-1998. Clinical and epidemiologic features of 1,383 infections

In order to describe the clinical features and the epidemiologic findings of 1,383 patients hospitalized in France for acute or chronic Q fever, we conducted a retrospective analysis based on 74,702 sera tested in our diagnostic center, National Reference Center and World Health Organization Collaborative Center for Rickettsial Diseases. The physicians in charge of all patients with evidence of acute Q fever (seroconversion and/or presence of IgM) or chronic Q fever (prolonged disease and/or IgG antibody titer to phase I of Coxiella burnetii > or = 800) were asked to complete a questionnaire, which was computerized. A total of 1,070 cases of acute Q fever was recorded. Males were more frequently diagnosed, and most cases were identified in the spring. Cases were observed more frequently in patients between the ages of 30 and 69 years. We classified patients according to the different clinical forms of acute Q fever, hepatitis (40%), pneumonia and hepatitis (20%), pneumonia (17%), isolated fever (17%), meningoencephalitis (1%), myocarditis (1%), pericarditis (1%), and meningitis (0.7%). We showed for the first time, to our knowledge, that different clinical forms of acute Q fever are associated with significantly different patient status. Hepatitis occurred in younger patients, pneumonia in older and more immunocompromised patients, and isolated fever was more common in female patients. Risk factors were not specifically associated with a clinical form except meningoencephalitis and contact with animals. The prognosis was usually good except for those with myocarditis or meningoencephalitis as 13 patients died who were significantly older than others. For chronic Q fever, antibody titers to C. burnetii phase I above 800 and IgA above 50 were predictive in 94% of cases. Among 313 patients with chronic Q fever, 259 had endocarditis, mainly patients with previous valvulopathy; 25 had an infection of vascular aneurysm or prosthesis. Patients with endocarditis or vascular infection were more frequently immunocompromised and older than those with acute Q fever. Fifteen women were infected during pregnancy; they were significantly more exposed to animals and gave birth to only 5 babies, only 2 with a normal birth weight. More rare manifestations observed were chronic hepatitis (8 cases), osteoarticular infection (7 cases), and chronic pericarditis (3 cases). Nineteen patients were observed who experienced first a documented acute infection, then, due to underlying conditions, a chronic infection. To our knowledge, we report the largest series of Q fever to date. Our results indicate that Q fever is a protean disease, grossly underestimated, with some of the clinical manifestations being only recently reported, such as Q fever during pregnancy, chronic vascular infection, osteomyelitis, pericarditis, and myocarditis. Our data confirm that chronic Q fever is mainly determined by host factors and demonstrate for the first time that host factors may also play a role in the clinical expression of acute Q fever.     

Dysregulation of cytokines in acute Q fever: role of interleukin-10 and tumor necrosis factor in chronic evolution of Q fever

Q fever manifests as primary infection or acute Q fever and may become chronic in patients with underlying valvulopathy. Because Coxiella burnetii infection depends on host response, we measured tumor necrosis factor (TNF), interleukin (IL)-6, IL-12, and IL-10 in patients with different clinical presentations of acute Q fever. Compared with control subjects, patients with uncomplicated acute Q fever exhibited increased release of the 4 cytokines. Their amounts were higher in patients with hepatitis than in patients with fever or pneumonia. In patients with valvulopathy, who exhibited the highest risk of chronic evolution, the amounts of TNF and IL-10 were higher than in patients without valvulopathy. TNF production was specifically enhanced in patients who developed Q fever endocarditis. These results show that acute Q fever is associated with cytokine overproduction. Persistent TNF amounts were associated with the occurrence of endocarditis in patients with valvulopathy, and that may be a marker of chronic evolution of Q fever.     

Q fever bioprosthetic aortic valve endocarditis (PVE) successfully treated with doxycycline monotherapy

Q fever is a zoonotic infection caused by Coxiella burnetii. The most common clinical manifestation of acute Q fever infection is as an atypical community-acquired pneumonia. The pulmonary findings are accompanied by extrapulmonary findings, most typically an increase in serum transaminases and splenomegaly. Because C. burnetii is difficult to culture, the diagnosis of Q fever is usually made serologically. The diagnosis of acute Q fever atypical community-acquired pneumonia is made by demonstrating a fourfold or greater increase in titer between acute and convalescent specimens or by demonstrating elevated immunoglobulin (IgM) (phase II) titers. Chronic Q fever is manifested as granulomatous hepatitis or more commonly as culture-negative endocarditis (CNE). Chronic Q fever (CNE) is a difficult diagnosis because of difficulty in culturing the organism from the blood and the vegetations with Q fever CNE are small or absent. The diagnosis of chronic Q fever CNE is based on serology. Such patients commonly have highly elevated IgM and IgG titers (phase I/II) titers. Chronic Q fever CNE may involve native or prosthetic heart valves. Q fever prosthetic valve endocarditis is rare compared with native valve Q fever endocarditis. Q fever prosthetic valve endocarditis usually requires valve replacement for cure. We present a case of chronic Q fever bioprosthetic aortic valve endocarditis that was successfully treated with doxycycline monotherapy that did not require aortic valve replacement.     

Coxiella burnetii and acute exacerbations/infections in patients with chronic lung disease

The aim of the present study was to determine the incidence of Q fever in patients with an acute exacerbation of a chronic lower respiratory tract infection. Eighty patients treated for acute exacerbation of chronic lower respiratory tract infections during a 30-month period were studied. Q fever was diagnosed by ELISA. Two elderly woman with pre-existing bronchiectasis (2.5%) were diagnosed as having an acute infection by Coxiella burnetii. The acute illness was considered to be a result of mixed infection with Pseudomonas aeruginosa and Haemophilus influenzae with C. burnetii. Co-infection with C. burnetii can occur during a bacterial exacerbation of a chronic lower respiratory tract infection.     

Two rare severe and fulminant presentations of Q fever in patients with minimal risk factors for this disease

We described two rare severe and fulminant clinical presentations of acute Q fever. The first patient had severe multiorgan failure. The second patient had fever and severe cholera-like diarrhoea. Coxiella burnetii polymerase chain reaction on blood or serum can be clinically useful in the diagnosis of acute Q fever before seroconversion.     

Seroepidemiology of Coxiella burnetii infection and its frequency as a cause of community-acquired pneumonia in Canada

The present study tested acute and convalescent serum samples from 788 patients hospitalized for community-acquired pneumonia in seven Canadian provinces for antibodies to Coxiella burnetii. One hundred nine patients (13.8%) had antibodies to this microorganism, and seven patients had acute Q fever. Serological evidence of infection with C burnetii was present in patients from all seven provinces. Three of the seven cases of acute Q fever were from Manitoba, suggesting that there may be unrecognized cases of Q fever in this province. In addition, a case of acute Q fever in Newfoundland, where there had previously been no reported cases, was noted, although subsequently, an outbreak of Q fever on goat farms has been reported.     

Two cases of acute lupus peritonitis]

We report two cases of systemic lupus erythematosus (SLE) diagnosed when acute peritonitis was appeared. Case 1 was a 20 year-old woman suffering from stomachache and right lower abdominal pain. Case 2 was a 40 year-old woman with diarrhea, epigastralgia, pollakisuria. In both cases, their peritoneal fluids were exudative with positive autoantibodies. After high dose steroid therapy, abdominal symptoms and ascites improved promptly. However, due to the complication of lupus nephritis, additional therapy was necessary. To characterize the feature of lupus peritonitis (LP), we examined the clinical and laboratory findings of LP from the literature. In patients with acute LP, abdominal pain, vomiting, diarrhea were significantly more common compared with chronic LP patients (P < 0.05), and fever, arthritis, central nervous system involvement and cystitis were more common. In patients with chronic LP, pleural effusion and pericardial effusion were more common compared with acute LP patients. Gastrointestinal manifestations such as abdominal pain, vomiting and diarrhea were more common in patients with acute LP compared with patients with chronic LP. Most patients with chronic LP were asymptomatic, ascites and serositis being the only clinical findings. The response to steroid therapy was better in acute LP.     

Travel-associated Coxiella burnetii infections: three cases of Q fever with different clinical manifestation

BACKGROUND: Certain activities expose travellers to Coxiella burnetii, the causative agent of acute human Q fever. Awareness of Q fever must be improved, also as a potential imported disease, but delayed seroconversion and serological cross-reactivity complicate the diagnosis. Granulomatous inflammation of liver and bone marrow can be typical histopathological findings. CASE PRESENTATIONS: We present three imported cases of Q fever with different clinical presentations, in which the travel history identified the sources of infection. CONCLUSIONS: Q fever should be suspected in any imported febrile disease of unknown origin. Clinical manifestations are variable and repeated serological testing is mandatory. In some cases diagnostic biopsies might help to establish early diagnosis.     

Q fever in children

Q fever is a zoonosis caused by Coxiella burnetii. Farm animals and pets are the main reservoirs of infection, and transmission to human beings is mainly accomplished through inhalation of contaminated aerosols. This illness is associated with a wide clinical spectrum, from asymptomatic or mildly symptomatic seroconversion to fatal disease. Q fever in children has been rarely reported. We reviewed published work on this topic. Seroepidemiological studies show that children are frequently exposed to C burnetii. However, children are less frequently symptomatic than adults following infection, and may have milder diseases. Using the standard diagnostic criteria, we identified 46 published paediatric cases only. Self-limited febrile illness and pneumonia were the most common manifestations of acute Q fever. Chronic disease manifested as endocarditis and osteomyelitis. A history of exposure to possible sources of infection with C burnetii in a child with a compatible infectious syndrome should prompt testing for Q fever. Studies are required to determine the spectrum of morbidity associated with Q fever during childhood.     

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.     

Granulomatous hepatitis caused by Q fever: a differential diagnosis of fever of unknown origin

The differential diagnosis of fever of unknown origin (FUO) includes infectious, neoplastic, rheumatic-inflammatory and miscellaneous diseases. We report the case of a 35-year-old man with FUO caused by Q fever. A liver biopsy showed the characteristic fibrin-ring lipogranulomas compatible with Q fever. The serologic tests confirmed the diagnosis of acute infection by Coxiella burnetii. The therapeutic response was excellent. In conclusion, we described a patient with acute Q fever and granulomatous hepatitis.     

Epidemiologic features and clinical presentation of acute Q fever in hospitalized patients: 323 French cases.

PURPOSE: To contribute to the knowledge of epidemiologic and clinical features of patients hospitalized with Q fever in France. METHODS: We conducted a retrospective analysis of 22,496 sera submitted between 1982 and 1990 to the French National Reference Center for Rickettsial Diseases (NRC). The diagnosis of acute Q fever was based on an IgG titer greater than or equal to 1:200 and an IgM titer greater than or equal to 1:25 against phase II Coxiella burnetii antigen on an indirect immunofluorescence test (IFA). Fifteen cases prior to 1985 were diagnosed on the basis of a complement fixation titer greater than or equal to 1:8. A serosurvey of blood donors from Marseille was also conducted in 1988 on 924 sera, using IFA with a cutoff titer of 1:25. RESULTS: The serosurvey conducted in 1988 showed a seroprevalence of 4.03%, without age or sex prediction. The incidence rate of acute Q fever detection at the NRC was 0.58 per 100,000 inhabitants over the 9-year period. Three hundred twenty-three clinical cases were diagnosed, rising from 1 in 1982 to 107 in 1990. In patients hospitalized for acute Q fever, there was a significantly higher sex ratio of males to females (2.3), which, coupled with the age distribution, indicated that elder males, who are overrepresented due to our recruitment bias, are more susceptible to C. burnetii infections. The mean age of the patients was 45.5 years, while the risk was increased in the 30 to 39 age group as well as in the 60 to 69 age group. Usual epidemiologic risk factors were found in 20.1% of the cases. Hepatitis (61.9%) was a more common clinical presentation in our patients with Q fever than pneumonia (45.8%). This might reflect differences in strains of C. burnetii or the biology of the host. However, French farmers and stock breeders commonly drink unpasteurized raw milk from their cattle, which might indicate a relationship between hepatitis and infection via the digestive tract. CONCLUSION: Our results indicate that many cases of acute Q fever are undiagnosed. A greater awareness of the disease and more extensive serologic testing of patients with symptoms compatible with Q fever may improve the situation.     

Spontaneous splenic rupture complicating acute Q fever.

Q fever is usually a self-limited febrile illness that involves the lungs and the liver. Acute complications are rare. We present the case of a 30-yr-old patient with spontaneous splenic rupture during the course of acute Q fever infection. He was admitted to the hospital with high temperature and the radiological signs of an atypical pneumonia. Forty-eight hours after admission, he developed shock. Because of free intraabdominal liquid, a laparatomy was performed that revealed a tear in the enlarged spleen. A splenectomy was performed. The diagnosis of Q fever was established by a significant titer increase in complement fixation test and IgM-ELISA. Serological investigations into the patient's surroundings revealed evidence of Q fever infection in 10 additional persons. Q fever should be taken into account as a possible differential diagnosis in patients with unexplained febrile illness and symptoms of pneumonia. The acute course of Q fever infection can be complicated by splenic rupture. The diagnosis of an acute infection with Coxiella burnetii often requires serologic testing of a second serum sample obtained at least 10 days after the onset of symptoms. Q fever should be ruled out in cases of unexplained splenic rupture particularly in Q fever endemic areas.     

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.     

Q fever in acute exacerbation of chronic lower respiratory tract infection]

We studied the effect of Q fever in acute exacerbation of chronic lower respiratory tract infection. The subjects consisted of 80 cases with acute exacerbation of chronic lower respiratory tract infection treated during the period from March 2002 till October 2004. Q fever was diagnosed using a PanBio Coxiella burnetii ELISA test kit. Two cases (2.5%) were positive for IgM in the acute stage, and were diagnosed as having acute infection by C. burnetii. They were elderly women with bronchiectasis, aged 76 and 82. They had no history of keeping cats or dogs, but the onset of acute exacerbation of chronic lower respiratory tract infection was June and March which is the breeding seasons for cats and dogs. Acute exacerbation of chronic lower respiratory tract infection were considerd to be a mixed infection with Pseudomonas aeruginosa (the 76-year-case) and Haemophilus influenzae (the 82-year-case). It is concluded that C. burnetii can induce exacerbation of chronic lower respiratory tract infection, their cases were considerd to be mixed infection with C. burnetii and other bacteria.     

Epstein-Barr virus-associated pericarditis and pericardial effusion: case report and diagnostic aspects

We report the case of a 39-year-old patient suffering from acute pericarditis accompanied by considerable pericardial effusion, most probably secondary to acute Epstein-Barr virus infection, an etiology uncommonly reported with pericardial inflammation and effusion. Diagnostic aspects and the approach to etiologic evaluation are discussed.     

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.