Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021311 (Infection)
38,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Often, a child is referred for evaluation to a pediatric rheumatologist and found to have a nonrheumatologic disorder. Infections constitute an important group of disorders with potential musculoskeletal system involvement. Reactive arthritis subsequent to infection with Yersinia is discussed, as well as reactive arthritis seen in the course of cystic fibrosis. Musculoskeletal manifestations of tuberculosis and brucellosis are reviewed. The continued presence of acute rheumatic fever in the United States has been documented, but the clinical spectrum of the disease appears to be changing over time. A variety of inherited syndromes may involve the musculoskeletal system, either primarily or as a minor manifestation. The bony dysplasias, another group of disorders, result from abnormal collagen structure and affect musculoskeletal development; clinical findings and new genetic information is reviewed. Descriptions of several rare syndromes (eg, hyaline fibromatosis and hypertrophic osteoarthropathy) also are reviewed here.
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PMID:Nonrheumatic conditions in children including infectious diseases and syndromes. 851 15

Clinical features of infantile diarrhea were studied among 603 infants from birth to 12 months of age to determine the predominant clinical feature(s) seen in infantile diarrhea associated with a specific enteric pathogen. Among the major clinical features, fever was most often seen in diarrhea due to Yersinia spp. (61.5%) followed by that in rotavirus (26.1%). Vomiting was mostly associated with Vibrio cholerae infection (90.9%) and shigellosis (64.6%). Dehydration was predominant in Vibrio cholerae (90.9%) and Salmonella (84.9%) infections. Bloody diarrhea was mostly due to Shigella infection (74.3%). As regards diarrhea with multiple pathogens, vomiting and dehydration were most frequent with Campylobacter+Enteropathogenic Escherichia coli (EPEC) (88.9% and 77.8%, respectively), while fever was more common with rotavirus+Shigella+Escherichia coli and rotavirus+Giardia. Infection with invasive organisms lead to vomiting, 4-10 stools per day and dehydration significantly more often as compared to infections with non-invasive organisms. Similarly more stools of patients infected with invasive organisms showed presence of blood and more than 5 leukocytes/HPF as compared to those infected with non-invasive organisms.
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PMID:Clinical features of infantile diarrhea associated with single or multiple enteric pathogens. 871 22

A case of appendicitis followed by reactive arthritis in an HLA B27-positive, 29-year-old man after infection with Yersinia enterocolitica is reported. Infection with Y. enterocolitica was diagnosed by determination of serotype specific antibodies and antibodies to Yersinia outer membrane proteins. Bacteriological cultures from the appendix were not made. Although reactive arthritis is a well-known complication of Yersinia-associated enteric disease, there are only few reports of patients with Y. enterocolitica pseudo-appendicitis complicated by arthritis during follow-up.
Infection
PMID:Appendicitis followed by reactive arthritis in an HLA B27-positive man after infection with Yersinia enterocolitica, diagnosed by serotype specific antibodies and antibodies to Yersinia outer membrane proteins. 933 70

A 78-year-old-man was hospitalized for surgical treatment of a Yersinia enterocolitica serotype O:9 infected primary aortoabdominal aneurysm which ruptured soon after admission. Infection of aneurysm is an unusual manifestation of yersiniosis, especially in patients with no predisposing underlying condition. This case, and review of the literature, highlights that serotype O:9 has a predilection for vascular tissue. Cross reaction with Brucella spp. may be responsible for misdiagnosis of Y. enterocolitica O:9 infected aneurysms.
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PMID:Aortoabdominal aneurysm infected by Yersinia enterocolitica serotype O:9. 945 12

Denmark has in recent years experienced a rise in the number of bacterial gastrointestinal infections. We have reviewed patients hospitalized with culture confirmed bacterial gastroenteritis in Roskilde County during 1991-1993. Two hundred and seven patients were included, 68 were children (< 15 years). The microorganism isolated was Salmonella in 61% of the cases. Campylobacter in 20% and Yersinia enterocolitica in 13%. Ninety-three percent of the patients had diarrhoea, 74% had fever (> 38 degrees C), and 66% abdominal pain. Blood in the stools was most frequent in patients infected with Campylobacter. Leucocytosis was rare. Twenty-four patients had bacteraemia. Reactive arthritis occurred in 4.8%. Three patients died, all infected with zoonotic Salmonella types. Three stool cultures were made for 115 patients, and all three cultures were positive in 73% of these patients. Bacterial gastroenteritis requiring hospitalization in Roskilde County, 1991-1993 affected mainly children and young adults. Infections due to zoonotic Salmonella types were more severe than Campylobacter and Yersinia enterocolitica gastroenteritis. It seems necessary to collect at least three stool cultures to secure a bacteriological diagnosis.
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PMID:[Bacterial gastroenteritis in hospitalized patients in Roskilde county 1991-1993]. 946 56

A mouse model was developed to evaluate the efficacy of antibiotic treatment of pneumonic plague; streptomycin was compared to antibiotics with which there is little or no clinical experience. Infection was induced by inhalation of aerosolized Yersinia pestis organisms. Antibiotics were administered by intraperitoneal injection every 6 hours for 5 days, at doses that produced levels of drug in serum comparable to those observed in humans treated for other serious infections. These studies compared in vitro to in vivo activity and evaluated the efficacy of antibiotics started at different times after exposure. Early treatment (started 24 h after challenge, when 0 of 10 mice tested had positive blood cultures) with netilmicin, ciprofloxacin, ofloxacin, ceftriaxone, ceftazidime, aztreonam, ampicillin, and rifampin (but not cefazolin, cefotetan, or ceftizoxime) demonstrated efficacy comparable to streptomycin. Late treatment (started 42 h after exposure, when five of five mice tested had positive blood cultures) with netilmicin, ciprofloxacin, ofloxacin, and a high dose (20 mg/kg of body weight every 6 h) of gentamicin produced survival rates comparable to that with streptomycin, while all of the beta-lactam antibiotics (cefazolin, cefotetan, ceftriaxone, ceftazidime, aztreonam, and ampicillin) and rifampin were significantly inferior to streptomycin. In fact, all groups of mice treated late with beta-lactam antibiotics experienced accelerated mortality rates compared to normal-saline-treated control mice. These studies indicate that netilmicin, gentamicin, ciprofloxacin, and ofloxacin may be alternatives for the treatment of pneumonic plague in humans. However, the beta-lactam antibiotics are not recommended, based upon poor efficacy in this mouse model of pneumonic plague, particularly when pneumonic plague may be associated with bacteremia.
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PMID:Antibiotic treatment of experimental pneumonic plague in mice. 951 50

The Yersinia plasmid-encoded Yop virulon enables extracellular adhering bacteria to deliver toxic effector proteins inside their target cells. It includes a type III secretion system (Ysc), at least two translocator proteins (YopB, YopD), and a set of intracellular Yop effectors (YopE, YopH, YopO, YopM, and YopP). Infection of macrophages with a wild-type strain leads to low levels of tumor necrosis factor alpha (TNF-alpha) release compared to infection with plasmid-cured strains, suggesting that the virulence plasmid encodes a factor impairing the normal TNF-alpha response of infected macrophages. This effect is correlated with the inhibition of the macrophage mitogen-activated protein kinase (MAPK) activities. To identify the Yop protein responsible for the suppression of TNF-alpha release, we infected J774A.1 and PU5-1.8 macrophages with a battery of knockout Yersinia enterocolitica mutants and we quantified the TNF-alpha released. Mutants affected in secretion (yscN), in translocation (yopB and yopD), or in synthesis of all the known Yop effectors (yopH, yopO, yopP, yopE, and yopM polymutants) were unable to block the TNF-alpha response of the macrophages. In contrast, single yopE, yopH, yopO, and yopM mutants behaved like the wild-type strain. A yopP mutant elicited elevated TNF-alpha release, and complementation of the yopP mutant or the yop effector polymutant strain with yopP alone led to a drop in TNF-alpha release. In addition, YopP was also responsible for the inhibition of the extracellular signal-regulated kinase2 (ERK2) and p38 MAPK activities. These results show that YopP is the Yop effector responsible for the Yersinia-induced suppression of TNF-alpha release by infected macrophages.
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PMID:Role of YopP in suppression of tumor necrosis factor alpha release by macrophages during Yersinia infection. 957 64

Extracellular Yersinia disarm the immune system of their host by injecting effector Yop proteins into the cytosol of target cells. Five effectors have been described: YopE, YopH, YpkA/YopO, YopP and YopM. Delivery of these effectors by Yersinia adhering at the cell surface requires other Yops (translocators) including YopB. Effector and translocator Yops are secreted by the type III Ysc secretion apparatus, and some Yops also need a specific cytosolic chaperone, called Syc. In this paper, we describe a new Yop, which we have called YopT (35.5kDa). Its secretion required an intact Ysc apparatus and SycT (15.0kDa, pl4.4), a new chaperone resembling SycE. Infection of macrophages with a Yersinia, producing a hybrid YopT-adenylate cyclase, led to the accumulation of intracellular cAMP, indicating that YopT is delivered into the cytosol of eukaryotic cells. Infection of HeLa cells with a mutant strain devoid of the five known Yop effectors (deltaHOPEM strain) but producing YopT resulted in the alteration of the cell cytoskeleton and the disruption of the actin filament structure. This cytotoxic effect was caused by YopT and dependent on YopB. YopT is thus a new effector Yop and a new bacterial toxin affecting the cytoskeleton of eukaryotic cells.
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PMID:YopT, a new Yersinia Yop effector protein, affects the cytoskeleton of host cells. 972 29

Human intestinal epithelial cells up-regulate the expression of an inflammatory gene program in response to infection with a spectrum of different strains of enteroinvasive bacteria. The conserved nature of this program suggested that diverse signals, which are activated by enteroinvasive bacteria, can be integrated into a common signaling pathway that activates a set of proinflammatory genes in infected host cells. Human intestinal epithelial cell lines, HT-29, Caco-2, and T84, were infected with invasive bacteria that use different strategies to induce their uptake and have different intracellular localizations (i.e., Salmonella dublin, enteroinvasive Escherichia coli, or Yersinia enterocolitica). Infection with each of these bacteria resulted in the activation of TNF receptor associated factors, two recently described serine kinases, I kappa B kinase (IKK) alpha and IKK beta, and increased NF-kappa B DNA binding activity. This was paralleled by partial degradation of I kappa B alpha and I kappa B epsilon in bacteria-infected Caco-2 cells. Mutant proteins that act as superrepressors of IKK beta and I kappa B alpha inhibited the up-regulated transcription and expression of downstream targets genes of NF-kappa B that are key components of the epithelial inflammatory gene program (i.e., IL-8, growth-related oncogene-alpha, monocyte chemoattractant protein-1, TNF-alpha, cyclooxygenase-2, nitric oxide synthase-2, ICAM-1) activated by those enteroinvasive bacteria. These studies position NF-kappa B as a central regulator of the epithelial cell innate immune response to infection with enteroinvasive bacteria.
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PMID:NF-kappa B is a central regulator of the intestinal epithelial cell innate immune response induced by infection with enteroinvasive bacteria. 1041 47

Yersinia-induced reactive arthritis is highly associated with HLA-B27, the role of which in defense against the triggering bacteria remains unclear. The aim of this study was to examine the capacity of rats transgenic for HLA-B27 to mount a cytotoxic T-lymphocyte (CTL) response against Y. pseudotuberculosis and to determine the influence of the HLA-B27 transgene on this response. Rats transgenic for HLA-B*2705 and human beta(2)-microglobulin of the 21-4L line, which do not spontaneously develop disease, and nontransgenic syngeneic Lewis (LEW) rats were infected with Y. pseudotuberculosis. Lymph node cells were restimulated in vitro, and the presence of for Y. pseudotuberculosis-specific CTLs against infected targets was determined. Infection of 21-4L rats triggered a CD8(+) T cell-mediated cytotoxic response specific for Y. pseudotuberculosis. Analysis of this response demonstrated restriction by an endogenous major histocompatibility complex molecule. However, no restriction by HLA-B27 was detected. In addition, kinetics studies revealed a weaker anti-Yersinia CTL response in 21-4L rats than in nontransgenic LEW rats, and the level of cytotoxicity against 21-4L lymphoblast targets sensitized with Y. pseudotuberculosis was lower than that against nontransgenic LEW targets. We conclude that HLA-B27 transgenic rats mount a CTL response against Y. pseudotuberculosis that is not restricted by HLA-B27. Yet, HLA-B27 exerts a negative effect on the level of this response, which could contribute to impaired defense against Yersinia.
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PMID:Cytotoxic T-cell-mediated response against Yersinia pseudotuberculosis in HLA-B27 transgenic rat. 1041 37


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