Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Only nine cases of Q fever were recorded in Canada in the 20 years prior to 1978. In the 18 months from August 1979 to January 1981 the disease was diagnosed serologically in six patients from the Maritime provinces. All were epidemiologically unrelated and none had been exposed to animals. Five had pneumonia and one had chronic Q fever with probable prosthetic valve endocarditis. Three of the five pneumonia patients presented with signs and symptoms of an acute lower respiratory tract infection and were indistinguishable clinically from other patients with atypical pneumonias. The other two with pneumonia presented with nonresolving pulmonary infiltrates and complained of decreased energy. Four of the five pneumonia patients responded well to treatment with erythromycin; the fifth required two courses of tetracycline. The patient with chronic Q fever had a large amount of cryoglobulins in his serum and evidence of immune complex disease. These cases indicate that Q fever should be considered as a possible cause of atypical pneumonia in Canada.
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PMID:Q fever in maritime Canada. 707 57

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

Q fever is a worldwide zoonosis caused by the strictly intracellular bacterium Coxiella burnetii. Among symptomatic patients (one-half of patients remain asymptomatic), acute Q fever most frequently manifests as a self-limited febrile illness, pneumonia, or hepatitis. Endocarditis is the predominant form of chronic Q fever. All the classical techniques of bacteriology may be used for diagnosis of C burnetii infection. Nonetheless, because of the risk of contamination, isolation must be performed in biosafety level 3 laboratories. Moreover, to date no diagnostic tests for detection by polymerase chain reaction or specific antibodies for immunochemistry are available commercially. Hence, Q fever is diagnosed in most cases by serology. The most reliable technique appears to be micro-immunofluorescence, which exhibits both good sensitivity and specificity. A wider use of this serology in cases of blood culture-negative endocarditis, atypical pneumonia, unexplained fever, and hepatitis should lead to an increase of diagnosed cases.
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PMID:Current laboratory diagnosis of Q fever. 1249 Dec 31

Coxiella burnetii, the causative agent of Q fever, is a Gram negative coccobacillus. It resides and replicates in the host s monocytes and macrophages. The developmental cycle of C. burnetii includes macrocellular and microcellular forms and the formation of spore-like bodies. It undergoes a phase variation of outer cell surface antigens from virulent phase I to avirulent phase II after passaging in the yolk sac of embryonated chicken eggs or in cell cultures. C. burnetii belongs to the most resistant bacteria. The main reservoirs of C. burnetii are cattle, sheep and goats. Human Q fever usually results from inhalation of contaminated aerosols. Acute infection mostly takes the course of a flu-like disease, atypical pneumonia or hepatitis, the chronic form resembles endocarditis. Laboratory examinations are based on the presence of antibodies. The drugs of choice are broad-spectrum antibiotics.
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PMID:[Q fever]. 1770 1

Coxiella burnetii is the agent of Q fever , an emergent worldwide zoonosis of wide clinical spectrum. Although C. burnetii infection is typically associated with acute infection, atypical pneumonia and flu-like symptoms, endocarditis, osteoarticular manifestations and severe disease are possible, especially when the patient has a suppressed immune system; however, these severe complications are typically neglected. This study reports the sequencing of the repetitive element IS1111 of the transposase gene of C. burnetii from blood and bronchoalveolar lavage (BAL) samples from a patient with severe pneumonia following methotrexate therapy, resulting in the molecular diagnosis of Q fever in a patient who had been diagnosed with active seronegative polyarthritis two years earlier. To the best of our knowledge, this represents the first documented case of the isolation of C. burnetii DNA from a BAL sample.
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PMID:Coxiella burnetii, the agent of Q fever in Brazil: its hidden role in seronegative arthritis and the importance of molecular diagnosis based on the repetitive element IS1111 associated with the transposase gene. 2285 Sep 65

Q fever is a zoonosis caused by an intracellular Gram-negative bacteria, Coxiella burnetii. Animals are the main reservoir and transmission to men generally is occurring by inhalation of contaminated aerosols. Acute Q fever generally is benign and usually resolves spontaneously. When symptomatic, the clinical presentation typically includes one of the following three syndromes: a flu-like illness, a granulomatous hepatitis or an atypical pneumonia. Individuals presenting risk factors such as patients with valvular heart diseases and vascular prostheses, as well as pregnant women and immuno-suppressed patients represent a population at risk of chronic infection, with endocarditis as the most common clinical form.
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PMID:[Q fever, a zoonosis often overlooked]. 2369 82

Tularemia is a potentially severe zoonotic disease caused by Francisella tularensis. A lack of awareness about tularemia can be embarrassing and could result in delayed treatment because of improper diagnosis. The diagnosis of tularemia is difficult, because the infections are rare and the clinical spectrum is broad. As only 1 adult case has been reported in Korea thus far, pediatricians in Korea may be unfamiliar with tularemia. We report our experience with a 14-year-old male adolescent with tularemia who presented with atypical pneumonia and possible infective endocarditis. Although the infectivity and mortality rates for tularemia are very high if left untreated, we did not suspect tularemia in this case until the incidental isolation of F. tularensis. The present case suggests that clinicians in Korea should be more aware of tularemia. This case also suggests that tularemia should be considered in undetermined cases of atypical pneumonia or acute febrile illness without local signs.
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PMID:The first pediatric case of tularemia in Korea: manifested with pneumonia and possible infective endocarditis. 2657 85

Coxiella burnetii, the etiological agent of Q fever, is a Gram-negative bacterium transmitted to humans by inhalation of contaminated aerosols. Acute Q fever is often self-limiting, presenting as a febrile illness that can result in atypical pneumonia. In some cases, Q fever becomes chronic, leading to endocarditis that can be life threatening. The formalin-inactivated whole-cell vaccine (WCV) confers long-term protection but has significant side effects when administered to presensitized individuals. Designing new vaccines against C. burnetii remains a challenge and requires the use of clinically relevant modes of transmission in appropriate animal models. We have developed a safe and reproducible C. burnetii aerosol challenge in three different animal models to evaluate the effects of pulmonary acquired infection. Using a MicroSprayer aerosolizer, BL/6 mice and Hartley guinea pigs were infected intratracheally with C. burnetii Nine Mile phase I (NMI) and demonstrated susceptibility as determined by measuring bacterial growth in the lungs and subsequent dissemination to the spleen. Histological analysis of lung tissue showed significant pathology associated with disease, which was more severe in guinea pigs. Infection using large-particle aerosol (LPA) delivery was further confirmed in nonhuman primates, which developed fever and pneumonia. We also demonstrate that vaccinating mice and guinea pigs with WCV prior to LPA challenge is capable of eliciting protective immunity that significantly reduces splenomegaly and the bacterial burden in spleen and lung tissues. These data suggest that these models can have appreciable value in using the LPA delivery system to study pulmonary Q fever pathogenesis as well as designing vaccine countermeasures to C. burnetii aerosol transmission.
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PMID:Coxiella burnetii Intratracheal Aerosol Infection Model in Mice, Guinea Pigs, and Nonhuman Primates. 3150 Dec 49

Q fever is a zoonotic disease that is caused by Coxiella burnetii, a gram-negative coccobacillary bacterium. Human infection primarily occurs following the inhalation of aerosols containing C. burnetii. The infection can either present in an acute or chronic form. The three main presentations are flu-like syndrome, atypical pneumonia, and hepatitis. Chronic Q fever mainly affects the heart where the disease manifests as endocarditis. In this case report, the patient was born at term with congenital heart defects, namely double outlet right ventricle (DORV), ventricular septal defects (VSD), and coarctation of the aorta. He underwent coarctation repair and pulmonary artery binding. At the age of three years, he presented with palpitation, sudden high-grade fever, myalgia, and dyspnea. Endocarditis was suspected due to a history of a surgical repair of congenital heart defects. Blood cultures were negative, however, a diagnosis of Q fever endocarditis was confirmed based on serologic titers. Q fever endocarditis is a challenging diagnosis since the echocardiography findings are often nonspecific. Moreover, Q fever can present as negative-culture endocarditis with low sensitivity of blood and tissue polymerase chain reaction (PCR) for C. burnetii. Hence, the modified Duke criteria has considered phase 1 immunoglobulin G (IgG) titers of 1:800 or more as diagnostic for infective endocarditis. Although uncommon, physicians should maintain a high index of suspicion for Q fever endocarditis, especially among patients with pre-existing structural heart disease and associated symptoms and risk factors such as animal exposure.
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PMID:Q Fever Endocarditis in a Saudi Child: A Case Report and Literature Review. 3193 13