Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0348321 (Haemophilus)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A report is presented on the findings in what is to our knowledge the first described case of glomerulonephritis resulting from Haemophilus aphrophilus endocarditis. After an insidious onset, serious renal failure developed which subsided with antibiotic therapy. Cardiac damage was minimal and the patient recovered his usual state of health, an outcome which has not been so satisfactory in other reported cases of endocarditis due to Haemophilus aphrophilus. The case is discussed with reference to the clinical course of the disease and the microbiologic properties of Haemophilus aphrophilus.
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PMID:[A case of glomerulonephritis and subacute endocarditis associated to Hemophilus aphrophilus septiciemia]. 24 46

A 65 year old man developed endocarditis and septicemia due to Hemophilus aphrophilus, a Gram-negative coccobacillus. Renal rather than cardiac failure was the principal feature of his illness and renal biopsy was compatible with glomerulonephritis secondary to septicemia. Rapid recovery of renal function and improvement of the glomerular lesion followed antibiotic treatment of the septicemia. This case illustrates the renal damage that can occur in association with septicemia due to rarer infectious agents. As with more common organisms, specific antimicrobial therapy leads to rapid improvement of the nephropathy.
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PMID:Glomerulonephritis associated with Hemophilus aphrophilus endocarditis. 63 69

Recurrent group A beta-hemolytic streptococcus (GABHS) pharyngotonsillitis related to penicillin failure presents a serious clinical problem. Failure to eradicate streptococci from patients can occasionally lead to rheumatic fever and rarely to glomerulonephritis. beta-lactamase-producing strains of aerobic and anaerobic bacteria in inflamed tonsils have been associated with increased failure rates of penicillins in the eradication of these infections. These organisms include Staphylococcus aureus, Haemophilus influenzae and H parainfluenzae, Moraxella catarrhalis, Fusobacterium sp, and pigmented Prevotella and Porphyromonas spp. The indirect pathogenicity of these organisms is apparent in their ability not only to survive penicillin therapy but also to protect penicillin-susceptible pathogens from that drug. These organisms have demonstrated the ability to protect GABHS in vitro and in vivo from penicillin. Numerous reports have described the successful therapy of recurrent GABHS tonsillitis with antimicrobials directed at both GABHS and the beta-lactamase-producing organisms.
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PMID:Penicillin failure and copathogenicity in streptococcal pharyngotonsillitis. 830 10

IgA nephropathy is characterized by IgA deposits, predominantly in the glomerular mesangium and mesangial proliferative glomerulonephritis. Concerning its pathogenesis, several investigators suggest that the deposited IgA is an antibody to viral, bacterial, or dietary antigens. Such reports strengthen the possibility of a relationship between mucosal immunity and the pathogenesis of IgA nephropathy. We previously observed that Haemophilus parainfluenzae (HP) is more commonly isolated from the pharynx of patients with IgA nephropathy than from those with other diseases. We have also identified the glomerular deposition of the outer membranes of HP antigens (OMHP) and an increased serum concentration of IgA antibodies against OMHP in patients with IgA nephropathy. These findings suggest that HP has a role in the etiology of IgA nephropathy.
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PMID:[Pathogenesis of IgA nephropathy: role of outer membranes of Haemophilus parainfluenzae antigens]. 920 Sep 51

IgA nephropathy (IgAN), a common glomerular disease, is characterized by the presence of IgA deposits, predominantly in the glomerular mesangium, and by mesangial proliferative glomerulonephritis (GN). Concerning its pathogenesis, several investigators suggest that the deposited IgA is an antibody to viral, bacterial, or dietary antigens. Thus the antibody is probably produced as part of the specific host immune response to various environmental antigens. Such reports strengthen the possibility of a relationship between mucosal immunity and the pathogenesis of IgAN. Nevertheless, attempts to isolate a specific IgA-circulating immune complex associated antigen in patients with IgAN have been unsuccessful. We have showed that such mucosal infections as pharyngitis are often associated with the acute onset of IgAN. Then IgAN is an immune complex disease that is caused by a poor mucosal immune response to environmental antigens to which the patient has been chronically exposed. We observed that Haemophilus parainfluenzae (HP) is more commonly isolated from the pharynx of patients with IgAN than from those with other diseases. We have also identified the glomerular deposition of outer membranes of HP antigens (OMHP) and an increased serum concentration of IgA antibodies against OMHP in patients with IgAN. Further studies will be necessary to determine whether the association of OMHP antigens in the glomeruli and IgA antibody against OMHP antigens in the sera of patients with IgAN can be confirmed in other parts of the world and whether this association is important in the pathogenesis of IgAN. Nevertheless, the demonstration of glomerular deposition of OMHP antigens and of IgA antibody against OMHP in sera indicates a potential new avenue of investigation into the elusive cause of IgAN.
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PMID:[Haemophilus parainfluenzae antigens in IgA nephropathy]. 949 34

We describe herein a case of nephrotic syndrome (NS) following allogeneic bone marrow transplantation (allo-BMT) for natural killer cell leukemia/lymphoma. Histologic studies defined the diagnosis as crescentic glomerulonephritis with massive immunoglobulin A (IgA) deposition, which has never been reported in NS cases following allo-BMT. Most of the massive infiltrated cells in the interstice were CD3(+)CD4(-)CD8(+) T cells derived from the donor. We observed mesangial deposition of Haemophilus parainfluenza outer membrane (OMHP) antigen and decreased glycosylation of the IgA1 hinge in the recipient's samples is consistent with the recently reported pathogenesis of IgA nephropathy. Further, the titer of IgA antibody against the donor serum was as high as other IgA nephropathy cases. These findings suggest that NS and crescentic glomerulonephritis in this case occurred as one of the forms of chronic graft-versus-host disease (GVHD), and that IgA deposition was associated with H parainfluenza and decreased glycosylation of the IgA1 hinge.
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PMID:Nephrotic syndrome with crescent formation and massive IgA deposition following allogeneic bone marrow transplantation for natural killer cell leukemia/lymphoma. 1254 67

IgA nephropathy (IgAN), the most common form of primary glomerulonephritis, is recognized as a disease that often becomes worse during acute tonsillitis. Although many reports have shown that tonsillectomy is an effective treatment for IgAN patients, the immunological evidence has not yet been investigated fully. In this study, we compared the expression of T cell receptor (TCR) V beta families in tonsillar T cells of IgAN patients to those of non-IgAN patients. The reverse transcription-polymerase chain reaction (RT-PCR) and flow cytometric analyses showed that the TCR V beta 6 was used more frequently in tonsillar T cells of IgAN patients than in those of non-IgAN patients (P < 0.01 each). Similarly, the proportions of TCR V beta 6-positive cells in peripheral blood T cells were significantly higher in IgAN patients than in non-IgAN patients (P < 0.05). After tonsillectomy, the proportions decreased in IgAN patients (P < 0.05), but did not in non-IgAN patients. Furthermore, in vitro stimulation with Haemophilus parainfluenzae antigen, which is reported to deposit in the glomerular mesangium of IgAN, enhanced expression of TCR V beta 6 in tonsillar T cells from both IgAN and non-IgAN patients. These results suggest that TCR V beta 6-positive tonsillar T cells might be activated by H. parainfluenzae, move into the kidney through blood circulation and induce glomerulonephritis.
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PMID:Selective expansion of T cell receptor (TCR) V beta 6 in tonsillar and peripheral blood T cells and its induction by in vitro stimulation with Haemophilus parainfluenzae in patients with IgA nephropathy. 1798 47

Infective endocarditis is a life threatening condition with a high mortality rate. Intravenous Drug Abusers (IVDA) are more likely to acquire endocarditis. Most of the cases of infective endocarditis are caused by a single pathogen; cases of polymicrobial endocarditis are rare and they are associated with a reported mortality rate of more than 30%. Only 21 cases of N. sicca endocarditis have been described in the literature since 1918, and only 15 reported cases of endocarditis which involved Actinomyces species have been reported since 1939. We are reporting a case of a 49-year-old male with intravenous heroin and fentanyl abuse, who presented with infective endocarditis caused by Neisseria sicca/subflava(N. sicca), Actinomyces, Streptococcus mitis, and Haemophilus parainfluenzae, complicated by septic emboli to the lungs and skin, ARDS , splenic infarct and immunocomplex mediated proliferative glomerulonephritis.
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PMID:Polymicrobial endocarditis in intravenous heroin and fentanyl abuse. 2455 99