Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chlamydiae are Gram-negative bacteria with obligate intracellular reproduction and disability to synthesize high-energy compounds such as ATP. Their cycle of development is unique among the prokaryotes: the host cells, mainly epithelial cells, are infected by so-called elementary bodies (EB) which undergo reorganization to form metabolically active reticulate bodies (RB). These RB multiply by binary fission, and after transition into infectious EB they are released within 48-72 hours. Chlamydiae cause prolonged subclinical infections of the conjunctiva, lung, cervix, and urethra. Complications in newborns are inclusion conjunctivitis, nasopharyngitis and pneumonia; in females, salpingitis, infertility, and perihepatitis; in male patients, epididymitis and prostatitis; and in both sexes, Chlamydiae-induced arthritis. Identification of the pathogenic agent confirms clinical diagnosis; tissue culture identification remains the diagnostic method of choice. Therapeutical drugs are tetracycline, erythromycin, josamycin, and in certain cases quinolone derivatives.
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PMID:Chlamydiae as pathogens--an overview of diagnostic techniques, clinical features, and therapy of human infections. 192 Dec 29

During an outbreak of a disease in a swine insemination centre in Bavaria, Fed. Rep. of Germany, characterized by conjunctivitis, severe polyarthritis and infertility mycoplasmas have been isolated from the joint fluids of the three boars investigated. Two of the isolate could be typed as Mycoplasma (M.) arthritidis which causes arthritis in rats, mice and rabbits, the third as M. collis, a probably apathogenic rodent mycoplasma species. One of the two isolated M. arthritidis strains (strain D 263) was injected intravenously in rats and mice, which developed mild to severe polyarthritis or even died, depending on the numbers of organisms inoculated. Since the bacteriological and virological investigations of the joints of boars did not yield a causative agent, it is to suppose that M. arthritidis played the substantial role in the production of the disease of the boars. It is very likely that the boars caught the mycoplasmas from rodents infected with the isolated species.
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PMID:Isolation of Mycoplasma arthritidis from the joint fluid of boars. 222 Jan 96

Chlamydia trachomatis infection of humans is commonly a localized inflammation that can result in infertility, blindness, and perhaps arthritis. The pathogenic process(es) that cause these sequelae are thought to be immunological. A 57-kD protein that is common among Chlamydia elicits ocular inflammation when introduced onto the conjunctivae of guinea pigs or nonhuman primates previously sensitized by chlamydial infection. This protein is thought to mediate the immunopathology that follows chlamydial infection. To more thoroughly characterize this chlamydial component, we cloned its gene from a C. psittaci strain and identified a particular recombinant that produced the 57-kD polypeptide. The recombinant gene product was immunoreactive with a monospecific anti-57-kD serum, and elicited an ocular inflammation similar to that produced by the 57-kD antigen isolated from chlamydiae. Sequencing identified two ORFs that encode polypeptides of 11.2 and 58.1 kD and are co-transcribed. These two polypeptides show homology with Escherichia coli groE and Coxiella burnetii htp heat-shock proteins. Striking homology (greater than 50%) was found between the 57-kD protein and the HtpB, GroEL, 65-k Mycobacterium tuberculosis and Hsp60 proteins. Thus, the 57-kD chlamydial protein, previously implicated as mediating a deleterious immunologic response to chlamydial infections, is a stress-induced protein similar to those that occur universally in both prokaryotic and eukaryotic organisms.
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PMID:Chlamydial disease pathogenesis. The 57-kD chlamydial hypersensitivity antigen is a stress response protein. 257 68

The serovares D-K of Chlamydia trachomatis (CT) are associated with inclusion conjunctivits, non-gonoccoccal urethritis (NGU), post-gonoccoccal urethritis (PGU), epididymitis, and ensuing male infertility. CT can be isolated from testicular tissue, in sexually acquired reactive arthritis (SARA) and in proctitis. Female partner infection primarily involves the cervix with ascending infection and ensuing infertility. Asymptomatic CT infection of the urogenital tract does not only present epidemiological problems, but also calls for smear examination in the asympotomatic partner. Double infection with CT and Neisseria gonorrhoeae is not necessarily followed by PGU. Incomplete detection of CT must be taken into account especially after application of penicillin and in the isolation procedures from sperm. The serovares L1-L3 are the infectious agents in venereal lymphogranuloma. Tetracyclines and erythromycin are usually recommended as the therapy of choice in CT infection. Sulfonamides should be applied with caution, since resistent CT isolates have been made known. There is still further clinical study required regarding the efficacy of quinolines in urogenital infections with chlamydiae.
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PMID:[Chlamydia infections in dermatology]. 266 68

Despite the availability of effective antimicrobial agents and aggressive public health programmes, gonococcal infections, including salpingitis, remain a major worldwide problem resulting in significant rates of morbidity and infertility. Using an experimental model of gonococcal-infected human fallopian tubes in organ culture which are examined by light microscopy and scanning and transmission electron microscopy, basic pathogenic interactions between the gonococcus and the fallopian tube have been elucidated. The major steps in the pathogenic process include attachment, damage and invasion. Attachment appears to result from interaction of gonococcal pili with the tips of microvilli of non-ciliated cells of the fallopian tube mucosa. After gonococcal attachment occurs, fallopian tube damage is evident with loss of ciliary activity and sloughing of ciliated cells. The 2 compounds most likely to be mediators of this damage appear to be gonococcal lipopolysaccharide, which is released from the surface of the organism in the form of outer membrane blebs, as well as monomeric units of peptidoglycan, which are elaborated by the organism. Gonococcal attachment and perhaps elaboration of some molecule appear to initiate phagocytosis by non-ciliated epithelial cells. Gonococci are transported to the base of the non-ciliated cells and are released into the subepithelial space. This may lead to local disease (salpingitis) or disseminated disease (dermatitis-arthritis). Understanding the molecular mechanisms by which gonococci attach to, damage or invade the fallopian tube mucosa may result in identification of ways of preventing gonococcal infections and their sequelae.
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PMID:Molecular mechanisms of pathogenicity of gonococcal salpingitis. 287 17

Chlamydia trachomatis, the causative agent of trachoma, affecting hundreds of millions of people, is now recognized as a major cause of sexually transmitted disease. In many countries chlamydial infection now outstrips gonorrhoea as the major cause of genital tract infection. Chlamydial urethritis and cervicitis are frequently complicated by ascending infection involving the endometrium, the fallopian tubes and epididymis. This often results in serious reproductive sequelae, e.g., infertility in the female and ectopic pregnancy. Extra-genital manifestations of chlamydial infection may occur involving the eyes (follicular conjunctivitis), joints (arthritis), and distal intestinal tract. Infection of the newborn child during birth may result in ocular or lung disease.There is need for further research on chlamydial infection, with the involvement of a number of different fields including medicine, epidemiology, microbiology, immunology, molecular genetics and operational research. The role of chlamydia has also to be defined in a variety of clinical syndromes for the development of improved diagnostic reagents and vaccine and the production of improved control and intervention strategies.
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PMID:Extra-ocular chlamydial infection. WHO Working Group. 349 Sep 21

Prophylactic colchicine remains an efficacious drug in preventing recurrent attacks of acute gouty arthritis. Its use is indicated especially in those patients with frequent and severe attacks, and in those with coexisting medical complications. In the present study which reviews the experience of 540 patients, 518 males and 22 females over a period of more than 20 yr, excellent results were obtained in approximately 82% of the patients, the response was satisfactory in 12%, and unsatisfactory in 5%. Hyperuricemia per se did not offset the efficacy of the prophylactic regimen. Factors affecting the failure of the regimen were most frequently related to associated uncontrolled medical complications or intemperate habits of food or alcoholic beverages. Few patients were colchicine intolerant. No hematologic or renal toxic effects were observed with extended and regular ingestion of colchicine. At the dosage employed for prophylaxis 0.5 or 1.0 mg, colchicine was most likely involved in the suppression of chemotactic factors involving the synovial lining cells. There is no evidence of chromosomal aberration or infertility. Discontinuance of the prophylactic program may be attempted in any patient who has been free from recurrent attacks for several years, particularly in older patients with no medical complications.
Semin Arthritis Rheum 1982 Nov
PMID:The efficacy of colchicine prophylaxis in articular gout--a reappraisal after 20 years. 610 Dec 17

There is reluctance by some to regard ureaplasmas as a cause of nongonococcal urethritis in men largely because the organisms may also be found in healthy persons. Could they be no more than passengers in disease? A review of past work suggests that this is not likely, a notion supported by the results of more recent studies. In certain other human diseases, such as urethritis and arthritis in hypogammaglobulinemic patients, the pathogenicity of ureaplasmas appears beyond question. In a variety of other conditions, such as the urethral syndrome in women, infertility, various pregnancy-related problems, and respiratory distress in infants, the situation is confused. It is possible that ureaplasmas have some part to play in all these conditions. However, both old and new information indicates that they do not have a major role in most of them, and that assertions to the contrary are fanciful. In the veterinary field, it is easier to come to conclusions about the role of these organisms, although their involvement in genital tract disease is least well validated. Finally, the occurrence of ureaplasmas in a colony of male and female chimpanzees, some with infertility problems, is presented, and the possible value of this situation in attempting to define the role of ureaplasmas in the human condition is mentioned.
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PMID:Ureaplasmas as a cause of disease in man and animals: fact or fancy? 651 61

Tripterygium wilfordii Hook F (TWHF) is a kind of Chinese herbal medicine used for 2000 years. It was applied externally for treatment of arthritis and inflammatory tissue swelling in early years. Recently, this drug has been found to have immunosuppressive effects which could successfully induce remission of some autoimmune disorders without obvious adverse effects. Although there are side effects of gastrointestinal upset, infertility and suppression of lymphocyte proliferation, little information about lethal toxicities has been reported. A case is presented here of a previously healthy young man who developed profuse vomiting and diarrhea, leukopenia, renal failure, profound hypotension and shock after ingestion of an extract of TWHF. In addition to his hypovolemic shock, serial electrocardiograms (ECG), cardiac enzyme studies, and echocardiography also showed some evidence of coexisting cardiac damage. He died of intractable shock 3 days after the abuse of TWHF. Further studies of the pathogenesis of peripheral collapse and possible cardiac toxicity, and determination of the therapeutic range of this drug are necessary before it is used extensively.
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PMID:Hypovolemic shock and mortality after ingestion of Tripterygium wilfordii hook F.: a case report. 762 89

Chlamydia trachomatis is a major cause of sexually transmitted disease, infertility and reactive arthritis in the Western world, and of trachoma in the developing world. There is evidence that the chronic inflammatory reaction seen in diseases associated with chlamydiae represents a delayed-type hypersensitivity response to chlamydial antigens. Little is known about which chlamydial antigens elicit T-cell responses yet such information could have important implications in terms of both immunopathological understanding of these diseases and immunoprophylaxis design. In this study, 61 chlamydia-specific T-cell clones have been produced from the synovial fluid of an individual with sexually acquired reactive arthritis (SARA). Ten clones have been characterized in detail and used to identify T-cell stimulatory antigens of chlamydiae by means of T-cell immunoblotting. Two distinct antigenic fractions have been identified, one recognized by three of the clones (molecular weight 18,000), the other recognized by six of the clones (molecular weight 30,000). The fractions are distinct from the major outer membrane protein, the 57,000 MW stress protein and the 60,000 MW cysteine-rich membrane protein of chlamydiae. The major histocompatibility complex (MHC) restriction of the response to these antigens differed: clones recognizing the 18,000 MW antigen required antigen-presenting cells expressing DR1 subtype DRB1*0101 or DRB1*0102 which only differ at amino acids 85 and 86 on the DR beta-chain; by contrast clones recognizing the 30,000 MW antigen were presented to only by antigen-presenting cells from DRB1*0101 individuals, reflecting extreme sensitivity of these clones to the polymorphism at positions 85 and 86 on the DR beta-chain.
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PMID:Identification of T-cell stimulatory antigens of Chlamydia trachomatis using synovial fluid-derived T-cell clones. 769 30


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