Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:[Q-fever imported into Norway]. 944 20

The recent discovery of the bacterium Bartonella henselae was mainly due to the development of molecular biology techniques adapted to microbial diagnosis and to the description of new human diseases linked to Aids. About 10% of pet cats and 33% of stray cats harbour that bacterium in their blood. In immunocompetent patients, that bacterium is responsible for human cat scratch disease, characterized essentially by a localized lymph nodes enlargement in the vicinity of the entry site of the bacteria. This disease occurs more likely in pet cats less than 1-year-old and infested with fleas. The bacterium is transmitted to humans by scratches or bites; the role of fleas is possible, but is not yet documented. In 5 to 13% of cases, the cat scratch disease appears as more severe, including health impairment, hepatitis, Parinaud's oculo-glandular syndrome, neurological complications or stellate retinitis. In immunocompromised patients, B. henselae is responsible for various clinical presentations: bacillary angiomatosis, bacillary peliosis, recurrent or persistent bacteremia or endocarditis. Diagnosis of infections due to B. henselae can be performed by serological specific testing with sensitivity and specificity values ranging from 75 to 100%. Cultivation of the bacterium is fastidious, particularly in cases of cat scratch disease. The most efficient diagnostic test is the in vitro DNA amplification which has the drawback to require a lymph node sample. Antibiotics are usually inefficient for the treatment of cat scratch disease. By contrast, in immunocompromised patients, these infections are successfully treated for a more or less long time by macrolides or tetracyclines or rifampin.
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PMID:[Bartonellosis: I. Bartonella henselae]. 985 27

Pseudomonas luteola is an aerobic, Gram negative rod, formerly classified as CDC group Ve-1 and Chryseomonas luteola. It is an uncommon clinical isolate. A previously healthy 59-year-old homosexual man with facial cellulitis and Pseudomonas luteola bacteremia is reported. Previously reported cases of P. luteola bacteremia have occurred in association with pancreatic abscess, prosthetic valve endocarditis, cardiac surgery, granulomatous hepatitis, peritonitis, and indwelling vascular catheters. This case suggests that the spectrum of disease caused by this bacteria may continue to expand.
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PMID:Facial cellulitis and Pseudomonas luteola bacteremia in an otherwise healthy patient. 993 47

Chronic Q fever is most commonly associated with culture-negative endocarditis and less frequently with infection of vascular grafts, infection of aneurysms, hepatitis, pulmonary disease, osteomyelitis, and neurological abnormalities. We report a case of chronic sternal wound infection, polyclonal gammopathy, and mixed cryoglobulinemia in which Q fever endocarditis was subsequently diagnosed. Polymerase chain reaction analysis of the wound tissue was positive for Coxiella burnetii DNA, and treatment of the endocarditis resulted in prompt healing of the wound. Chronic Q fever can occur without epidemiological risk factors for C. burnetii exposure and can produce multisystem inflammatory dysfunction, aberrations of the immune system, and persistent wound infections.
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PMID:Chronic sternal wound infection and endocarditis with Coxiella burnetii. 1045 Nov 61

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.
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PMID:Q fever. 1051 1

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.
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PMID:Q fever 1985-1998. Clinical and epidemiologic features of 1,383 infections. 1077 10

Q fever is a zoonosis caused by Coxiella burnetii, an obligate intracellular bacterium. Domestic ungulates and parturient cats are the primary reservoirs of infection. The animals excrete the bacterium in urine, faeces, milk and amniotic fluid. After desiccation the micro-organism spreads via aerosols. After inhalation or ingestion and an incubation period of 2-6 weeks acute Q fever may develop with atypical pneumonia and hepatitis as major clinical symptoms. The infection also may present as a flu-like illness or remain asymptomatic. Generally, the prognosis is favourable. However, endocarditis or another chronic form of Q fever occasionally develops with possibly fatal outcome. Diagnosis relies upon serologic testing with an indirect immunofluorescence method. Doxycycline is the antibiotic of choice in the treatment of Q fever. Endocarditis needs therapy for years with the addition of rifampin or hydroxychloroquine. Q fever is poorly recognised due to the variety of clinical presentations.
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PMID:[Acute and chronic Q fever; epidemiology, symptoms, diagnosis and therapy of infection caused by Coxiella burnetii]. 1091 6

Listeria monocytogenes has long been known as a pathogen of immunocompromised hosts, including solid organ and bone marrow transplant recipients. Its principal manifestations include bacteremia and meningitis. Endocarditis due to Listeria is far less common and in general affects the left side of the heart. We here report an unusual case of Listeria tricuspid valve endocarditis and septic pulmonary emboli in a sulfa-intolerant liver transplant recipient with a history of relapsing cytomegalovirus (CMV) hepatitis and an indwelling Hickman catheter. The literature on Listeria endocarditis and infections in transplant recipients is reviewed. The possible relationship between susceptibility to Listeria infection and the discontinuation of trimethoprim-sulfamethoxazole prophylaxis is of interest.
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PMID:Listeria monocytogenes tricuspid valve endocarditis with septic pulmonary emboli in a liver transplant recipient. 1142 99

Cat-scratch disease (CSD) is a clinical syndrome that usually presents as a self-limiting lymphadenopathy associated with a cat scratch or bite. Commonly affecting children and young adults, it has a worldwide distribution. In temperate climates, higher rates are reported in the autumn and winter, which can be attributed to the seasonal breeding of the domestic cat. The organism responsible was identified in 1983, having eluded detection for 50 years. Initially, Afipia felis was thought to be the cause; however, subsequent study failed to confirm a link. During the 1990s, it was demonstrated conclusively that Rochalimaea henselae, later reclassified as Bartonella henselae, was the cause of CSD. B. henselae has been isolated from bacteraemic cats, with transmission among cats thought to be via the cat flea. Although other Bartonella species are transmitted by arthropod vectors, it is unlikely that the cat flea is involved directly in human infection, but plays a role in amplifying the reservoir. B. henselae is difficult to culture, and either serology or the polymerase chain reaction are considered to be the best methods of detection. Genetic variation occurs amongst B. henselae strains, perhaps explaining the inconsistency of some diagnostic techniques. A separate serogroup (Marseilles) has been reported in a seronegative patient with CSD, and B. clarridgeiae has the potential to cause the disease. Atypical presentation is seen in up to 25% of cases, and manifests itself as ocular involvement, encephalopathy, granulomatous hepatitis, hepatosplenic infection, endocarditis and osteomyelitis. The majority of CSD cases resolve spontaneously and do not require antibiotic treatment. In complicated CSD, treatment with trimethoprim-sulphamethoxazole, ciprofloxacin or azithromycin is recommended, with gentamicin being reserved for the severely ill patient.
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PMID:Cat-scratch disease: epidemiology, aetiology and treatment. 1144 Feb 2

Q fever is a zoonosis caused by Coxiella burnetii. The acute Q fever is usually characterized by a self-limited flu-like syndrome, fever, pneumonia and hepatitis. Symptoms of the chronic Q fever (evolution>3 months) mainly consist of endocarditis with negative culture. Focal neurological symptoms are rarely observed. Neurological symptoms of acute Q fever consist of meningitis or meningo-encephalitis. Neurological symptoms of chronic Q fever are cerebral embolisms from Coxiella burnetii infected heart valves. We herein report two patients with meningoencephalitis revealing acute Q fever.
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PMID:[Meningo encephalitis revealing Q fever: two cases and a review of the literature]. 1193 27


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