Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eight new strains of Coxiella burnetii were isolated from chronic Q fever patients using centrifugationashell vial technique. Seven patients had endocarditis (including one patient with an immunodeficiency syndrome), and one had a vascular prosthesis infection. Three prototype strains, Nine Mile phase II, Q212 and Priscilla and eight new isolates were cultured in L 929 cells. Heterogeneity of their cytopathic effect was observed. DNAs of the eleven strains have been isolated and purified by standard procedures. Plasmid DNA was separated from chromosomal DNA by a low melting point gel. Electrophoresis in agarose gel showed that seven of the eight new strains had plasmids which were about 40 kb (plasmid V517 was used as size marker). Endonuclease-restriction analysis of the 8 human isolates is currently under investigation.
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PMID:Phenotypic and genotypic heterogeneity of 8 new human Coxiella burnetti isolates. 135 Jan 76

The major agents responsible for atypical pneumonia in children include a wide variety of organisms, one Mycoplasma species, two Chlamydia species, a rickettsia, and one fastidious bacterium. Mycoplasma pneumoniae and C. pneumoniae together may be responsible for over 40% of these infections. Recognition of the role that these agents play in pneumonia is important since many of the diagnostic methods used to detect these organisms are not available in most hospital microbiology laboratories. If you don't look, you won't find. Epidemiologic factors can provide valuable clues, especially with the less frequently encountered infections, since it is almost impossible to make a clinical diagnosis on which to base treatment. A reliable history of avian exposure should suggest psittacosis, exposure to sheep or pregnant cats suggests Q fever, and children with underlying malignancy or immunodeficiency or those receiving systemic steroids may have legionnaires' disease. None of these organisms are susceptible to beta-lactam antibiotics. Sometimes the diagnosis is not considered until after the child has failed to respond to a penicillin or a cephalosporin and routine bacteriology is negative. In view of the role played by M. pneumoniae and C. pneumoniae, a macrolide may be the first-line antibiotic for atypical pneumonia in children.
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PMID:Atypical pneumonias in children. 771 3

We describe a 37-year-old farmer with a 3-week history of fevers and hepatitis, in whom Q fever was diagnosed. The diagnosis was based on the findings of characteristic "ring" granulomas on a bone marrow biopsy specimen and confirmed by complement-fixation antibody tests to Coxiella burnetii. Unusual aspects of this case included (1) relatively low complement-fixation antibody titers, (2) prolonged prothrombin time, (3) false-positive results of a serologic test for the human immunodeficiency virus (HIV), and (4) ring granulomas that progressed to atypical granulomas in biopsy specimens.
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PMID:Unusual aspects of acute Q fever-associated hepatitis. 803 34

The first case of Q fever endocarditis that has been diagnosed in Mexico is presented. A 10-year-old girl with discrete subaortic stenosis (SAS) and patent ductus arteriosus (PDA) was seen in December of 1996 with fever, hepatomegaly and splenomegaly. She presented also anemia, leukopenia, hypergammaglobulinemia, positive rheumatoid factor, cryoglobulinemia, antinuclear and anticytoplasmic antibodies (anti-RNA-proteins and anti-DNA). An aortic valve vegetation was seen by echocardiogram. Blood-cultures were negative. Antibody test for Coxiella burnetii was positive. Treatment with doxicyclin was initiated as soon the diagnosis was done. PDA was closed, SAS was liberated and two aortic vegetations were resected. Endocarditis in Q fever occurs when there is predisposing heart disease and/or immunodeficiency. Effective therapy has not yet been established. The diagnosis of Q fever endocarditis is difficult; it should be considered, in case of clinical suspicion of endocarditis with negative blood-cultures.
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PMID:[Coxiella burnetii endocarditis. A report of the first case diagnosed in Mexico]. 981 Mar 69

Following biosynthesis, class II MHC molecules are transported through a lysosome-like compartment, where they acquire antigenic peptides for presentation to T cells at the cell surface. This compartment is characterized by the presence of HLA-DM, which catalyzes the peptide loading process. Here we report that the morphology and function of the class II loading compartment is affected in diseases with a phenotypic change in lysosome morphology. Swollen lysosomes are observed in cells from patients with the hereditary immunodeficiency Chediak-Higashi syndrome and in cells infected with Coxiella burnetii, the rickettsial organism that causes Q fever. In both disease states, we observed that HLA-DR and HLA-DM accumulate in enlarged intracellular compartments, which label with the lysosomal marker LAMP-1. The distribution of class I MHC molecules was not affected, localizing disease effects to the endocytic pathway. Thus, cellular mechanisms controlling lysosome biogenesis also affect formation of the class II loading compartment. Analysis of cell surface class II molecules revealed that their steady-state levels were not reduced on diseased cells. However, in both disease states, enhanced interaction between HLA-DR and HLA-DM was detected. In the Chediak-Higashi syndrome cells, this correlated with more efficient removal of the CLIP peptide. These findings suggest a mechanism for perturbation of Ag presentation by class II molecules and consequent immune deficiencies in both diseases.
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PMID:Enhanced interaction of HLA-DM with HLA-DR in enlarged vacuoles of hereditary and infectious lysosomal diseases. 988 29

Two large outbreaks of Q fever occurred in 1987 and 1988 in an agricultural community for the rehabilitation of drug users. Approximately 40% of the residents were human immunodeficiency virus (HIV)-positive. Two hundred thirty-five residents presented with clinical evidence of a flulike syndrome that was confirmed to be Q fever; moreover, a large proportion of residents developed an asymptomatic infection. Clinical signs and symptoms were rather nonspecific: fever, malaise, and muscle pain that were often associated with pulmonary symptoms. Single or multiple opacities were detected, with mild interstitial inflammation evident on chest roentgenograms. The source of infection was the sheepfold, which is part of the stock-farming activity of the community. Both outbreaks occurred just after lambing had begun. Residents who were exposed during the first epidemic were protected in the second one. The attack rate among HIV-positive residents was significantly higher than that among HIV-negative residents in the first outbreak, whereas only a slight, marginally significant difference was observed in the second outbreak. The clinical features of Q fever did not differ between HIV-positive and HIV-negative individuals. No cases of relapse or chronic disease were observed.
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PMID:Consecutive epidemics of Q fever in a residential facility for drug abusers: impact on persons with human immunodeficiency virus infection. 1082 52

Q fever, a worldwide zoonosis caused by Coxiella burnetii, has many manifestations in humans. Endocarditis is the most serious complication of Q fever. Animal models are limited to acute pulmonary or hepatic disease and reproductive disorders. An appropriate experimental animal model for Q fever endocarditis does not yet exist. In this study, severe combined immunodeficient (SCID) mice infected with C. burnetii showed persistent clinical symptoms and died, whereas immunocompetent mice similarly infected became asymptomatic and survived. The SCID mice examined in this study had severe chronic lesions in their primary organs: the heart, lung, spleen, liver, and kidney. The heart lesions of the SCID mice were similar to those in humans with chronic Q fever endocarditis: they had focal calcification and expanded macrophages containing C. burnetii. The 50% lethal dose of C. burnetii in SCID mice was at least 10(8) times less than that in immunocompetent mice. The SCID mouse is highly susceptible to C. burnetii, and the immunodeficiency of the host enhances the severity of Q fever. This animal model could provide a new tool for the study of chronic Q fever and Q fever in immunodeficient hosts.
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PMID:SCID mouse model for lethal Q fever. 1287 53

Chloroquine (CQ) and its hydroxyl analogue hydroxychloroquine (HCQ) are weak bases with a half-century long use as antimalarial agents. Apart from this antimalarial activity, CQ and HCQ have gained interest in the field of other infectious diseases. One of the most interesting mechanisms of action is that CQ leads to alkalinisation of acid vesicles that inhibit the growth of several intracellular bacteria and fungi. The proof of concept of this effect was first used to restore intracellular pH allowing antibiotic efficacy for Coxiella burnetii, the agent of Q fever, and doxycycline plus HCQ is now the reference treatment for chronic Q fever. There is also strong evidence of a similar effect in vitro against Tropheryma whipplei, the agent of Whipple's disease, and a clinical trial is in progress. Other bacteria and fungi multiply in an acidic environment and encouraging in vitro data suggest that this concept may be generalised for all intracellular organisms that multiply in an acidic environment. For viruses, CQ led to inhibition of uncoating and/or alteration of post-translational modifications of newly synthesised proteins, especially inhibition of glycosylation. These effects have been well described in vitro for many viruses, with human immunodeficiency virus (HIV) being the most studied. Preliminary in vivo clinical trials suggest that CQ alone or in combination with antiretroviral drugs might represent an interesting way to treat HIV infection. In conclusion, our review re-emphasises the paradigm that activities mediated by lysosomotropic agents may offer an interesting weapon to face present and future infectious diseases worldwide.
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PMID:Recycling of chloroquine and its hydroxyl analogue to face bacterial, fungal and viral infections in the 21st century. 1762 79

Q fever is a zoonotic disease caused by the ubiquitous pathogen Coxiella burnetii responsible for acute and chronic clinical manifestations. Its geographically heterogeneous prevalence seems mainly related to the clinician interest and the availability of a reference center. Its polymorphic clinical expression imposes reference to diagnosis in presence of pneumonia, hepatitis, prolonged fever or endocarditis with no proof of its etiology. The diagnosis is mainly serological. If acute Q fever is most often benign, endocarditis is constantly fatal without treatment. The treatment is effective and well tolerated, but must be adapted to the acute or chronic pattern, the presence of a heart valve disease, an aneurysm or a vascular prosthesis, an immunodeficiency and the specific problem of pregnancy.
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PMID:[Q fever: current diagnosis and treatment options]. 1901 34

Of veterans from the U.S. Global War on Terrorism who have sought care in the Department of Veterans Affairs, approximately 12% have an infectious disease diagnosis. Infections in those veterans with traumatic brain injury (TBI) include infections associated with blast injuries and burns, such as skin and soft tissue infections; infections as a result of retained bullet or shrapnel fragments; pulmonary infections resulting from lung injury, intubation, or resultant tracheostomy; hospital-acquired infections, such as those associated with methicillin-resistant Staphylococcus aureus and other antimicrobial resistant organisms such as Acinetobacter baumannii; and infections from implanted prosthetic devices, such as metal hardware or skull flaps. Longer-term cognitive impairment may result in behaviors that place veterans with TBI at risk for human immunodeficiency virus or hepatitis C virus infections. Finally, chronic infections acquired abroad, such as cutaneous leishmaniasis or Q-fever, may be diagnosed after veterans return to the United States. These infections present challenges in terms of added morbidity and costs associated with complex antimicrobial management; isolation requirements; and surgical procedures, such as those to remove infected retained fragments or prosthetic devices. In this review, providers will become more familiar with the scope and complexity of infectious disease management in veterans with TBI.
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PMID:Infectious complications in OIF/OEF veterans with traumatic brain injury. 2010 97


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