Disseminated herpes simplex type 2 and systemic Candida infection in a patient with previous asymptomatic human immunodeficiency virus infection.
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Biomedical subjects
Publications and source records attributed to F Gudat.
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We report the case of a 58-year-old renal transplant patient who developed oral hairy leukoplakia. Examination for HIV-1 and HIV-2 infection was negative. Biopsy of the lateral tongue showed ballooned prickle cells and electron microscopy revealed herpes-type viruses. In situ hybridization and examinations with the Southern blot technique yielded Epstein-Barr virus. Serology for Epstein-Barr virus was reactive. Immunological investigation of the patient showed a marked decrease of T-helper and T-suppressor cells as the result of immunosuppressive regimen. Oral hairy leukoplakia may be a marker for severe immunosuppression but is not necessarily associated with HIV infection.
This study was conceived to identify specific morphological characteristics associated with cytomegalovirus (CMV) infection of the kidney. 33 patients with manifest CMV infection at autopsy and 32 biopsies of kidney transplants with active or inactive CMV infection were studied. In 8 patients of the autopsy group a CMV infection of the kidney was detected (CMV cells in 3 cases, positive viral tissue culture in 4 cases, positive in-situ hybridization in one case), which was associated with severe dissemination into different organs. In situ hybridization was not superior to ordinary light microscopy in the detection of CMV cells. The biopsies were screened for the presence of glomerulopathy. No association of glomerulopathy with CMV could be found by light microscopy, whereas a significant correlation of glomerulopathy with vascular rejection was demonstrated. No differences as to the incidence of glomerulopathy were found, when non-transplant patients with manifest CMV infection at autopsy were compared with matched controls. With active infection electron microscopy revealed no osmiophilic deposits, but in immunofluorescence tiny IgG deposits were identified within the glomeruli (p less than 0.01). IgM or C3 deposition in the glomeruli was not specifically associated with either CMV infection or vascular rejection. Thus morphological identification of CMV infection of the kidney is difficult, necessitating the detection of CMV cells, positive viral tissue culture or positive in-situ hybridization. Glomerulopathy in light microscopy is associated with vascular rejection and is therefore termed transplant glomerulitis. Tiny IgG deposits may be indicative of CMV infection, although these are not always present.
The epitope recognized by the murine monoclonal antibody (mAB lu-5) recently described as a formaldehyde-resistant, "pan-epithelial marker" of great value in tumour diagnosis is located on the surface of cytokeratin filaments. It has been preserved during vertebrate evolution from amphibia to man. As this epitope is not reactive after SDS-polyacrylamide gel electrophoresis (SDS-PAGE), the epitope-bearing protein has been identified by a dot-blot antibody binding assay, using purified proteins in which the epitope is reconstituted. We show that the epitope is present in most cytokeratin polypeptides of both the acidic (type I) and basic (type II) subfamily but does not occur in other cytoskeletal proteins. The location of this widespread epitope is discussed with respect to homologies of amino acid sequences of cytokeratins and their conformations.
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The method described below combines an immunoreaction with Papanicolaou's stain on cytological smears. For the immunoreaction, the avidin-biotin-complex (ABC) method was used. The method was tested on various cytological material with the monoclonal antibody lu-5 and two polyclonal antibodies (anti-keratin and anti-chymotrypsin). Wet fixation of the smears with a modified Delaunay's solution is recommended. Drying of the material impairs immunoreactivity. The main advantages of the technique are the clear-cut permanent immunostaining and the preservation of the nuclear structure, permitting a combined immuncytological characterization of cellular products and conventional cyto-diagnosis.
The aim of the present investigation was to localize cyclosporine (CSA) in the rat kidney. The experimental approaches included autoradiography after i.v. injection of 3H-CSA, immunofluorescence after i.v. injection of fluorochrome labeled CSA and immunohistochemistry using the rabbit-alpha-CSA antibody. It was not possible to localize CSA in specific structures of the rat kidney. Finally, immunohistochemistry of human renal tissue gave only an unspecific staining of proximal tubular cells, which was lost when the antibody was absorbed on renal tissue homogenate. In vitro binding of 3H-CSA on renal homogenate indicated only unspecific absorption of the highly lipophilic compound; no specific binding was detected on cytosolic renal fractions. The failure to demonstrate CSA in tubular or arteriolar lesions might have been due to the fact that the affinity of binding is too low for detection, or that CSA does not accumulate within these structures.
The beta-adrenergic effect on the release of immunoregulatory cells from the spleen was investigated by physical stress testing (bicycle ergometry up to submaximal work capacity) in 19 normal subjects (15 males, median 21 years) and in 10 male patients splenectomized for trauma (median 29 years). It was repeated in 6 subjects of each group during beta-blockade with 80 mg oxprenolol. Blood samples for leucocyte analysis were taken before and at the end of the test. Leucocyte subpopulations were analyzed in a cytofluorograph after staining of buffy coat cells by direct (B cells) or indirect immunofluorescence with monoclonal antibodies directed against the phenotypes of T- (Leu-1), T helper- (Leu-3a), T suppressor/cytotoxic (Leu-2a) cells and natural killer (OKM1+ lymphocytes) cells. In the controls all leucocyte subsets increased at ergometry, but B-, Leu-2a- and OKM1-cells increased more than Leu-3a cells. During beta-blockade the leucocyte changes reached only 50% of the value without treatment; the B- and Leu-2a cell mobilization was reduced more than the Leu-3a-, OKM1 cell- and monocyte changes. In splenectomized patients the proportional cellular changes were only half of those found in normal subjects, except for the Leu-3a cells which were not released. Beta-blockade during ergometry had no effect on Leu-3a cells, a similar effect on B- and Leu-2a cells as in normal subjects and a stronger effect on granulocytes, monocytes and OKM1 cells than in controls. In conclusion, the B- and Leu-2a cell mobilization from the spleen (50%) was beta-adrenoceptor dependent, while the one from other lymphoid organs was beta-adrenoceptor independent. The strongly spleen dependent Leu-3a cell changes were not beta-adrenoceptor mediated. Granulocyte-, monocyte- and OKM1 cell changes were only partly spleen dependent. The spleen independent changes however were strongly beta-adrenoceptor dependent.
A mouse monoclonal antibody (mAB lu-5) was prepared using a lung cancer cell line as an antigen. The selected clone produces an IgG with a gamma-1 heavy chain and a kappa-light-chain. Immunohistochemical testing of mAB lu-5 on 117 normal tissue biopsies and 474 tumours revealed reactivity with an intracytoplasmic, formaldehyderesistant antigen present in most epithelial and mesothelial cells, but absent in mesenchymal cells. The antibody can therefore be used as a first order, pan-epithelial marker. It proved also useful for fast tumour diagnosis on frozen sections.
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A series of 610 consecutive liver biopsies collected from Jan. 1980 to Oct. 1983 in two Swiss gastro-enterological centers was studied by immunohistology for the presence of delta-antigen, HBsAg and HBcAg in frozen sections. This led to the identification of 46 tissue and 45 serum samples of 28 patients, including 5 with follow-up biopsies. All had ongoing hepatitis B (HB) with delta-superinfection, representing 13.3% of all patients with HB. The sera were studied for HBsAg, anti-HBs, anti-HBc and HBe-markers by RIA, for anti-delta by indirect immunofluorescence on delta-positive test sections and for Dane particles by immune electromicroscopy. 18 of the 21 native Swiss patients were i.v. drug users between 20 and 28 years of age (30% of all drug users in this series). The other patients were residents from Mediterranean countries (n = 5), Eastern Europe (n = 1) and Asia (n = 1). Female patients (n = 5) were seen only among i.v. drug users. The most frequent histological type of HB was chronic active (aggressive) hepatitis (CAH) (26 of 46 biopsies or 13 of 28 patients, respectively), followed by acute HB with histological signs of possible transition to chronicity (8 of 46 biopsies or 6 of 28 patients), and acute lobular HB (6 of 46 biopsies or 5 of 28 patients). Chronic persistent HB (CPH) was rare (5 of 46 biopsies, final diagnosis in 3 patients). The delta-infection was found to persist in sequential biopsies when a chronic HB was established, the longest documented period being 72 months.(ABSTRACT TRUNCATED AT 250 WORDS)
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In the present work a minibead method has been employed to study human hepatocyte receptors for albumin-coupled latex particles. The cell-latex reaction was observed in both phase contrast and scanning electron microscopy. It has been demonstrated that human hepatocytes exhibit bindings sites for different forms of glutaraldehyde-treated albumin, and the ligand has proved to be species-nonspecific. The albumin binding activity is temperature-dependent and can be only partially blocked by preincubation with free, glutaraldehyde-treated protein, unless hepatocytes are pretreated with vinblastine sulfate. The possible biological role of these receptors as regards the infection due to the hepatitis B virus (that shares common, but not identical binding sites) is also discussed.
The present state of the art in non-A, non-B hepatitis is reviewed. Eight years of world-wide efforts in research have not yielded a definite characterization of agent(s) and markers of this viral infection. Diagnosis is therefore established mainly by exclusion of the hepatitis viruses A and B, Epstein-Barr virus and cytomegalovirus, and drug-induced liver disease. Currently available serological, electron microscopic, immune electron microscopic and clinical information on non-A, non-B hepatitis in chimpanzee and man is briefly reviewed. Some light microscopic features provisionally regarded as suggestive of non-A, non-B hepatitis in man are presented. In daily practice the diagnostic tools in the near future will largely depend upon progress in the elaboration of suitable serological test systems and on further confirmation of microscopic findings, unless an unexpected breakthrough occurs through identification and characterization of the virus(es) in non-A, non-B infection.
36 patients with acute sporadic non-A, non-B viral hepatitis were prospectively followed up. Study parameters included biochemical and immunological (hepatitis A/B) data, histology of the acute and chronic stage of the disease and immunohistology for hepatitis B markers. The mean follow-up period for the patients with complete remission was 8.5 months, and 30.5 months for the patients with progression to chronic liver disease. 13 (36%) patients developed histologically confirmed chronic hepatitis (6 CPH, 7 CAH). In the chronic stage of the disease, the transaminases showed a markedly fluctuating course in 8 of the 13 patients. Two of the 6 patients with CPH showed complete remission after 25 and 58 months respectively; in the 4 others the disease remained unchanged. In the 7 patients with CAH no remission occurred, but in 2 patients complete cirrhotic transformation of the liver was demonstrated after 36 and 38 months respectively. Hence the prognosis of chronic sporadic non-A, non-B hepatitis seems to be worse than the prognosis of chronic posttransfusion non-A, non-B hepatitis.
Report is given on a 68-year-old man who suffered primarily from progressive weight loss and repeated episodes of fever and arthralgia. Later, liver dysfunction and renal insufficiency developed. Liver and kidney biopsies disclosed granulomatous hepatitis and nephritis. Because of the morphologic and clinical findings, the diagnosis of Boeck's disease was made. Shortly before death, diarrhea developed. Autopsy revealed a massive systemic involvement in Whipple's disease proven by light and electron microscopy and immunofluorescence. Tuberculoid and epitheloid cell granulomas and isolated giant cells were found in addition to the biopsy findings in skeleton muscles, the small intestine, lymphnodes and bronchi. At autopsy, the kidney showed chronic interstitial nephritis. The literature of kidney involvement in Whipple's disease is reviewed. This is the first case with granulomatous interstitial nephritis and chronic renal insufficiency in an inadequately treated Whipple's disease.