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)

The author has reviewed different aspects of the role of immunocompetence in the development of Q fever. Coxiella burnetii lives within the phagolysosomes of infected cells. In animals, the immunosuppression caused by either cortisone or X-irradiation reactivates Q fever. In humans, cases of Q fever are reported in immunocompromised hosts suffering from leukemia, cancer, and human immunodeficiency virus infection (AIDS). Similar data are reported with strict or facultative intracellular parasites living within the phagolysosome. Sporadic publications reported the appearance of auto-antibodies during Q fever which may change the clinical picture of the disease. The pathological findings of hepatitis diagnosed during acute Q fever and those with C. burnetii chronic endocarditis are quite different and may reflect a different immunological response to C. burnetii. These facts emphasize the importance of host factors in the clinical expression and outcome of Q fever.
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PMID:Host factors in the severity of Q fever. 219 33

Human infection with the rickettsia Coxiella burnetii presents as an acute flulike primary Q fever, as a subacute granulomatous hepatitis, or, rarely, as chronic endocarditis. We have previously described lymphocyte unresponsiveness to Coxiella antigen in patients with Q fever endocarditis. This unresponsiveness was antigen specific and was mediated in part by adherent suppressor cells. In this report we show that the adherent suppressor cells work via prostaglandin E2 (PGE2)4 production. Addition of the cyclooxygenase inhibitor indomethacin to cultures of PBMC from patients with endocarditis or chronic laboratory exposure resulted in consistent increases in Coxiella-specific lymphocyte proliferation. The degree of increase in proliferation induced by indomethacin correlated strongly with the amount of PGE2 produced in a 4-hr culture stimulated by Coxiella antigen, but it also correlated with the sensitivity to inhibition of mitogenesis by PGE2. The suppressor mechanism was antigen nonspecific, because induction of suppression in vitro by Coxiella antigen also suppressed Candida-induced proliferation when both antigens were present in the same culture. Addition of indomethacin to these antigen cocultures totally reversed the Coxiella-induced suppression, confirming the evidence above that the nonspecific effector mechanism of suppression was prostaglandin (PG)-mediated. Elicitation of suppression, however, was antigen specific and involved a T cell-monocyte suppressor circuit. Supernatants from Coxiella-stimulated immune T cells and from the suppressor subset (OKT8+-enriched) of those T cells, but not unstimulated immune cells, induced augmented PGE2 production by unrelated nonimmune PBMC. We conclude that the lymphocyte unresponsiveness characterizing patients with Q fever endocarditis is modulated in part by an antigen-specific T suppressor cell which secretes a lymphokine to stimulate PGE2 production by adherent cells.
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PMID:Cellular immunity in Q fever: modulation of responsiveness by a suppressor T cell-monocyte circuit. 240 35

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.
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PMID:Cellular immunity in Q fever: specific lymphocyte unresponsiveness in Q fever endocarditis. 241 42

Acute infection with Coxiella burnetii usually results in a self-limited illness, but it can occasionally cause chronic endocarditis or hepatitis. Headache is a common presenting symptom of acute infection with this agent, but specific neurological abnormalities are rare. We report the case of a patient with acute Q fever that caused frank encephalitis. We also review the literature on central nervous system disease attributable to C. burnetii.
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PMID:Encephalitis caused by Coxiella burnetii. 374 Aug 16

Q fever is a zoonosis caused by Coxiella burnetii. The infection is transmitted to humans mainly through aerosols generated from products of delivery of cows and other animals. Generally the disease presents acutely with fever, pneumonitis and hepatitis. But chronic endocarditis is also a possible occurrence. Diagnosis is usually made by serology. The acute form of the infection responds well to tetracyclines and other antibiotics. But endocarditis is difficult to treat, and its prognosis is grim.
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PMID:[Q fever]. 1827 68

Q fever, caused by Coxiella burnetii, can present as an outbreak of acute disease ranging from asymptomatic disease, pneumonia, hepatitis or fever of unknown origin, which can progress to a chronic disease, most frequently endocarditis. The occurrence of Q fever within families is rarely described, and in most cases presents with uniform acute disease manifestations. Here we present a familial cluster of Q fever presenting as highly variable synchronous manifestations in four of five family members, including prolonged fever of unknown origin, asymptomatic carrier state, hepatitis, and chronic endocarditis developing in the absence of previous symptoms. This case series highlights the possibility of Q fever developing in cohabitated individuals with highly variable symptoms masking the common disease etiology. Screening of all exposed individuals, even those not clinically suspected to be infected, may enable to better identify, treat and prevent progression to chronic disease.
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PMID:Familial Q fever clustering with variable manifestations imitating infectious and autoimmune disease. 2577 Jul 47