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)

Attributes of Chlamydia pneumoniae of potential importance to a relationship with atherosclerosis are described. Among these are that C. pneumoniae is not new. It is unique. It is a pathogen with which everyone is infected, and it is difficult to treat. It causes immunopathology, myocarditis, and endocarditis and chronicity is a hallmark of Chlamydia infection. Current knowledge of the relation of C. pneumoniae and atherosclerosis comes from observational (e.g., seroepidemiology and tissue studies) and experimental studies. The limitations of the serologic studies of chronic infection are noted as is the conclusive demonstration of an association of C. pneumoniae and atherosclerosis by the repeated and frequent finding of the organism in atherosclerotic tissue. Experimental studies are needed to determine if the association is causal. Such studies should include animal models, basic mechanisms, and secondary prevention antibiotic treatment trials.
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PMID:Background and current knowledge of Chlamydia pneumoniae and atherosclerosis. 1083 24

Bartonella species are important emerging zoonotic pathogens. Transmission of these organisms in nature may be much more complex than is currently appreciated. Cats can be infected with five Bartonella species, including, Bartonella henselae, Bartonella clarridgeae, Bartonella bovis, Bartonella koehlerae and Bartonella quintana. In addition to cats, numerous domestic and wild animals, including bovine, canine, human, and rodent species can serve as chronically infected reservoir hosts for various intra-erythrocytic Bartonella species. In addition, an increasing number of arthropod vectors, including biting flies, fleas, keds, lice, sandflys and potentially ticks have been implicated in the transmission of various Bartonella species to animals or human beings. In the reservoir host, Bartonella species cause chronic intra-erythrocytic and vascular endothelial infections, with a relapsing bacteremia documented in experimentally infected cats. Although the immunopathology induced by Bartonella infection requires additional study, the organisms can localize to the heart valve (endocarditis), cause granulomatous inflammation in lymph nodes, liver or spleen, induce central nervous system dysfunction with or without cerebrospinal fluid changes, and may contribute to inflammatory polyarthritis. Hematological abnormalities are infrequent, but thrombocytopenia, lymphocytosis, neutropenia, and eosinophilia have been reported in B. henselae-infected cats. Serology, PCR and culture can be used to support a diagnosis of feline bartonellosis, however, due to the high rate of sub-clinical infections among various cat populations, documenting causation in an individual cat is difficult, if not impossible. Response to treatment can be used in conjunction with serology or organism isolation to support a clinical diagnosis of feline bartonellosis. As fleas are involved in the transmission among cats, the use of acaracide products to eliminate fleas from the environment is of critical importance to decrease the risk of B. henselae transmission among cats and to humans.
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PMID:Feline bartonellosis and cat scratch disease. 1829 47

Toxic shock syndrome toxin-1 (TSST-1) is a potent superantigen produced by Staphylococcus aureus. In addition to menstrual and nonmenstrual toxic shock syndromes, TSST-1 is also implicated in the immunopathogenesis of pneumonia, infective endocarditis, neonatal exanthematous disease, and atopic dermatitis among others. Superantigens first bind to major histocompatibility complex (MHC) class II molecules and then activate a large proportion of T cells by cross-linking their T cell receptor. As binding to MHC class II molecules is a critical step in the robust activation of the immune system by TSST-1 and other superantigens, polymorphic variations between different HLA-DR alleles could potentially influence the magnitude of immune activation and immunopathology caused by TSST-1. As TSST-1 is highly toxic to humans and given that multiple variations of alleles of HLA-DR and HLA-DQ are expressed in each individual, it is difficult to determine how HLA-DR polymorphisms quantitatively and qualitatively impact immune activation caused by TSST-1 in humans. However, such investigations can be conducted on transgenic mice lacking all endogenous MHC class II molecules and expressing specific HLA class II alleles. Therefore, transgenic mice expressing different HLA-DRB1 alleles (HLA-DRB1*15:01, HLA-DRB1*15:02, HLA-DRB1*03:01, HLA-DRB1*04:01), and sharing HLA-A1*01:01 chain, were systemically challenged with purified TSST-1 and multiple immune parameters were assessed. Among the HLA-DR alleles, mice expressing HLA-DRB1*15:01 allele elicited a significantly higher serum cytokine/chemokine response; greater splenic T cell expansion and most severe organ pathology. Our study highlights the potential utility of human leukocyte antigen (HLA) transgenic mice in understanding the impact of HLA polymorphisms on the outcomes of diseases caused by TSST-1 and other superantigens.
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PMID:HLA-DR polymorphisms influence in vivo responses to staphylococcal toxic shock syndrome toxin-1 in a transgenic mouse model. 2786 61