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Biomedical subjects

R D Horstmann

Publications and source records attributed to R D Horstmann.

At least 73 records · Page 4Linked to original sources
PubMed1991

Renal failure is a common complication in non-immune Europeans with Plasmodium falciparum malaria.

Renal failure in malaria appears to be a complication less well known than anaemia and cerebral malaria. Thirty-one non-immune patients treated for Plasmodium falciparum malaria at Hannover Medical School were reviewed. Nine patients (29%) had acute renal failure, seven of whom required dialysis, and five patients needed mechanical ventilation. Cerebral symptoms were seen in nine patients, and three of the patients died. In a second series, information about patients who died of malaria in Germany and Austria was gathered. Thirty-six reports were obtained and analysed retrospectively. Thirty-four patients (94%) had acute renal failure. Eighteen patients received dialysis while five other patients with high central venous pressure or hyperkalaemia would have benefitted from dialysis. Cerebral involvement was seen in 34 patients, and 20 patients showed respiratory failure. It was concluded that renal failure in P. falciparum malaria is as common in non-immune adults as cerebral malaria. As untreated renal failure may have a deleterious influence on cerebral and respiratory functions, early dialysis-treatment in patients with severe P. falciparum malaria and signs of deteriorating renal function is recommended.

Acute Kidney Injury↗
PubMed1989

Genomic DNA differences between pathogenic and nonpathogenic Entamoeba histolytica.

cDNA libraries were constructed from pathogenic (HM-1:IMSS) and nonpathogenic (SAW 1734) isolates of Entamoeba histolytica. A cDNA clone (cEH-P1) specific for pathogenic amoebae was identified by screening with a pool of sera from patients with invasive amoebiasis that had been absorbed with nonpathogenic amoebae. This clone was used for the identification of a homologous clone (cEH-NP1) in the cDNA from nonpathogenic amoebae. Sequence analysis and comparison of the predicted amino acid sequences for both clones disclosed 12% evolutionary divergence in structure. Hybridization of both cDNA probes to genomic DNA from four pathogenic and five nonpathogenic E. histolytica isolates revealed two distinct Southern blot patterns, one characteristic for pathogenic amoebae and the other for nonpathogenic amoebae. Further, the complex pattern of restriction fragments hybridizing to an actin cDNA probe was also different between pathogenic and nonpathogenic isolates but was conserved within each group of amoebae. The results indicate that pathogenic isolates of E. histolytica are genetically distinct from nonpathogenic isolates.

Amino Acid Sequence↗
PubMed1988

Antiphagocytic activity of streptococcal M protein: selective binding of complement control protein factor H.

Isolated complement components were used to study the regulation of the alternative complement pathway C3 convertase (EC 3.4.21.47), also called C3b,Bb, on M protein-carrying (M+) and M protein-lacking (M-) streptococci. Neither M- nor M+ streptococci directly affected the formation or dissociation of the surface-bound C3b,Bb or the inactivation of surface-bound C3b by factor I. However, the activity of the serum control protein of the alternative complement pathway, factor H, in controlling streptococcus-bound C3b and C3b,Bb was 6-8 times stronger on M+ organisms than on M- organisms. Furthermore, M+ streptococci of different serotypes and purified streptococcal M6 protein were shown to selectively bind factor H, the dissociation constants ranging from 4.5 X 10(-6) M to 6 X 10(-7) M. We conclude that the antiphagocytic activity of streptococcal M protein may be due to complement inhibition mediated by the binding of factor H. Binding of a regulatory protein appears to be a previously unrecognized route by which a pathogen is able to evade alternative pathway activation.

Antigens, Bacterial↗
PubMed1987

Regulation of the alternative pathway of complement by pH.

Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired hemolytic anemia. The abnormal PNH erythrocytes are highly susceptible to complement-mediated lysis in vitro, especially at pH 6.4. Lysis has been shown to be due to alternative pathway activation. The purpose of this study was to determine why lysis of PNH erythrocytes is increased at acidic pH. The results presented demonstrate that at pH 6.4: binding of C5 and Factor B to C3b deposited on human erythrocytes is markedly enhanced; generation of the two C3 convertases, C3(H2O), Bb and C3b,Bb is increased; and control of C3b on human erythrocytes by CR1 and Factor I is diminished. In addition, it was found that rabbit erythrocytes, which activate the human alternative pathway, are also lysed much better at pH 6.4 than at pH 7.4. These results indicate that the optimal pH for the initiation and amplification of the alternative complement pathway, and probably also for the activation of the membrane attack complex, is 6.4.

Complement Activation↗
PubMed1987

Eosinophil production in human bone-marrow cultures induced by 80-85 kDa serum component(s) of patients with eosinophilia.

Eosinophil production from normal human bone-marrow cells was induced by plasma or serum of patients with eosinophilia. After 10-12 d of liquid suspension culture, 14-42% of bone-marrow cells were identified as maturing eosinophil granulocytes. Upon molecular sieve chromatography, the activity eluted in a single peak corresponding to a substance of 80-85 kDa molecular weight. The activity did not stimulate colony formation in semi-solid agar media, but was detected in liquid suspension cultures only. Furthermore, addition of exogenous colony-stimulating factor (CSF) had a differential effect depending on the culture system used. In semi-solid media, predominance of eosinophil colonies was only observed when CSF was added at a low concentration. In liquid suspension cultures, however, 30-40% of cultured cells were eosinophils independent of the CSF concentration used. These findings extend recent studies in an animal model and support the hypothesis that a differentiation factor is involved in the regulation of eosinophil production in man.

Bone Marrow↗
PubMed1986

Demonstration of C3b receptor-like activity and of decay-accelerating factor-like activity on rabbit erythrocytes.

C3b receptor activity and decay-accelerating activity for the C3 convertase, C3b,Bb, were demonstrated on rabbit erythrocytes (ERAB). Particles bearing C3b agglutinated ERAB if the C3b was of rabbit origin, but not if it was of human origin. The reactivity of rabbit C3b was abolished by enzymatic conversion of C3b to C3bi. Deposited on ERAB, rabbit C3b, but not human C3b, was cleaved by factor I in the absence of factor H. Similarly, decay acceleration of the C3b,Bb complex on ERAB occurred when the complex was of rabbit origin, but not when it was of human origin. Soluble immune complexes in the presence of rabbit serum were bound to and then released from the ERAB. Binding of the complexes is presumed to be mediated by immune complex-bound C3b and release to be the consequence of degradation of C3b by Factor I. These findings suggest that ERAB, like human erythrocytes, are endowed with membrane-associated complement regulators that protect these cells against homologous complement attack and participate in the clearing mechanism of circulating immune complexes.

Animals↗
PubMed1985

[Fatal complications of tropical malaria in non-immune patients. A retrospective clinico-pathologic analysis of 25 cases].

Clinical and pathological data on 25 fatal cases of tropical malaria were obtained from several hospitals in a retrospective survey. The patients originated, without exception, from non-malaria endemic regions (non-immunes). Death occurred in nine patients despite elimination of the parasitaemia with schizontocides. Life threatening complications were complex and apparently interacting. Manifestations of the disease included (1) initial acute renal failure, (2) disturbance of water and electrolyte balance, (3) cerebral oedema resulting in microhaemorrhages, (4) lung oedema, and increasing respiratory insufficiency even after elimination of the parasitaemia (in 4 cases there was histological evidence of shock lung), (5) myocarditis (histological evidence of cellular myocardial infiltration obtained in 4 cases), (6) hepatocellular damage, (7) complications associated with intensive-care treatment in 2 cases. The data allow no conclusions on the intensity and nature of blood clotting disturbances. According to this analysis the clinical manifestations of advanced malaria resemble protracted shock conditions having other aetiologies. However, specific cerebral and cardiac complications and homeostatic disturbances do apparently occur, the treatment of which requires experience with the clinical syndrome.

Adolescent↗
PubMed1985

Haemostatic alterations in malaria correlate to parasitaemia.

Fibrin(ogen) degradation products, platelet counts, antithrombin III, and the components of the Factor VIII complex were studied in a total of 80 patients with Plasmodium falciparum, Plasmodium vivax or Plasmodium ovale infections. The haemostatic findings were correlated to the numbers of parasitized erythrocytes and to each other. The results indicate that haemostatic changes in malaria correlate with the degree of parasitaemia. Evidence for moderate hyperfibrinolysis was found in patients with high P. falciparum parasitaemias only. Thrombocytopenia closely corresponded to parasitaemia and to von Willebrand factor levels, but appeared not to be linked to a consumption of coagulation factors. It was concluded that thrombocytopenia in malaria is not indicative of disseminated intravascular coagulation (DIC) but may relate to endothelial damage.

Erythrocytes↗
PubMed1985

Isolation of rabbit C3, Factor B, and Factor H and comparison of their properties with those of the human analog.

The rabbit complement components C3, Factor B, and Factor H were isolated and characterized and were compared to the corresponding proteins of human serum. Chromatographic behavior, chemical properties, and functional interactions show great similarities between the components in both species. By SDS polyacrylamide gel electrophoresis, the m.w. were estimated to be 195,000 for C3, 86,000 for Factor B, and 155,000 for Factor H. The amino acid compositions of the rabbit proteins resembled those of the human analog. The total carbohydrate content of rabbit C3 and Factor H was approximately one-half that of the human proteins. In addition, a qualitative difference in the carbohydrate moieties of the C3 proteins was observed. The serum concentration of the rabbit proteins was markedly lower than that of the human proteins. The rabbit C3b,Bb enzyme resembled the human analog with respect to half-life, control by Factor H, and stabilization by nickel ions.

Amino Acids↗
PubMed1985

Species specificity of recognition by the alternative pathway of complement.

The recognition function of the alternative complement pathway was studied with isolated human and rabbit components. Zymosan and homologous and heterologous erythrocytes were used as representative activators or nonactivators. The binding affinity of Factor B and Factor H for particle-bound C3b was measured. In both species, the average affinity of Factor H for bound C3b on homologous cells (nonactivators) was eight to 10 times higher than on zymosan particles (activators). The interaction between Factor H and C3b on rabbit erythrocytes was species-specific: rabbit Factor H bound strongly to rabbit C3b on rabbit erythrocytes and also on human erythrocytes, which are nonactivators for the rabbit alternative pathway. Human Factor H bound strongly to human C3b on human erythrocytes but seven times weaker on rabbit erythrocytes, which are activators of the human alternative pathway. No substantial differences were found in the binding of Factor B to bound C3b regardless of the nature of the particle to which C3b was bound. The results indicate that in the two species studied, the molecular mechanism of recognition is analogous and that recognition is species-specific.

Animals↗
PubMed1985

Origin of proteinuria in human malaria.

The prevalence and pathogenesis of renal involvement was investigated in 74 patients with malarial infections. A rise in proteinuria of 150 to 5,000 mg per day was seen in 12 out of 27 patients with Plasmodium falciparum infections. SDS-polyacrylamide gel electrophoresis revealed either an increase in albumin and high molecular weight proteins alone or an increase in low and high molecular weight proteins. Serum creatinine and urea were increased in 5 patients. In P. vivax infections, 8 out of 46 patients developed a proteinuria level of up to 462 mg per day. Low and, to a lesser degree, high molecular weight proteins were increased. In one patient with quartan malaria infection, proteinuria rose as far as 432 mg per day. There was a correlation between the appearance of proteinuria and fever; however, there was no correlation between the amount of proteinuria and the height of fever. It is therefore unlikely that a rise in temperature is the only cause of proteinuria in malarial infections. The electrophoretic analyses of proteinuria indicate that in malarial infections, glomerular as well as tubular lesions may cause reversible proteinuria.

Adolescent↗
PubMed1984

Plasmodium falciparum-malaria: resistance to chloroquine, but sensitivity to mefloquine in the Gabon. A prospective in-vitro study.

A determination of the sensitivity to chloroquine and to mefloquine was carried out in malaria patients of the Albert Schweitzer Hospital, Lambarene, Gabon, by using the schizont maturation test. The chloroquine testing showed in 6 of 31 cases a schizont maturation at 1.14 pmol/microliter of blood and more; this means an in-vitro resistance in 19% of the cases. The evaluation of the effective concentrations (i.e. concentrations producing the appropriate inhibition of schizont maturation) with the probit analysis yielded for chloroquine an EC50 of 0.2537 X 10(-6) mol/l of blood and an EC90 of 0.8317 X 10(-6) mol/l of blood. In the testing of mefloquine, schizont maturation was found in 3 of 31 cases in concentrations of 1.6 pmol/microliter of blood, the probit analysis, however, showed effective doses in the normal range with an EC50 of 0.2192 X 10(-6) mol/l of blood and an EC90 of 0.7863 X 10(-6) mol/l of blood. These results demonstrate the alarming observation of Plasmodium falciparum strains resistant in-vitro to chloroquine in a region where in vivo resistance has not been observed hitherto.

Adolescent↗
PubMed1983

Ineffective erythropoiesis in acute human P. falciparum malaria.

An analysis of erythroblast cell kinetics utilizing quantitative 14C-autoradiography has been performed in five cases of acute Plasmodium falciparum malaria prior to and, in four patients, 3 or 6 days after the onset of antimalarial therapy. Associated with no or only moderate anemia were changes of erythroblast morphology, a considerable shift in the frequency of red and white blood cell precursors in the bone marrow, and a reduced rate of erythroblast proliferation. There was a marked loss of polychromatic erythroblasts, which was smaller but still detectable during the therapeutic phase. The results provide some quantitative data on the extent of "parenchymal damage" of bone marrow and stress the impact of ineffective erythropoiesis and reduced rate of erythropoietic proliferation on the emergence of anemia in Plasmodium falciparum malaria.

Acute Disease↗
PubMed1982

Observations on mebendazole vs. thiabendazole in the treatment of human trichinellosis.

Six patients with acute trichinellosis were studied. Three patients were treated with mebendazole and the other three with thiabendazole. Both drugs were given at a daily dose of 50 mg per kg body weight for seven consecutive days. No substantial differences were evident in the efficacy of the two drugs when symptoms, clinical findings, and laboratory data were followed for three months. However, mebendazole was better tolerated than thiabendazole. The diagnosis was based on epidemiological data and positive antibody tests. In two cases, diagnosis was confirmed by isolation of trichinella larvae from 10 ml blood samples filtered through polycarbonate membranes.

Adolescent↗
PubMed1981

Malaria-induced thrombocytopenia.

Platelet counts were investigated in 26 patients with P. falciparum malaria and 39 patients with P. vivax malaria before and after treatment. Before schizontocidal treatment 22 of 26 (85%) patients with P. falciparum malaria and 30 of 39 (72%) patients with P. vivax malaria had depressed platelet counts below 150,000/microliters blood. There was a correlation between low platelet counts and high counts of malarial plasmodia (parasitized red blood cells) in P. falciparum and P. vivax infections (p less than 0.001). Platelet survival, studied by malonaldehyde formation in three patients during the period of decreasing parasitaemia, revealed a shortened life span to 2--3 days in comparison to 7--10 days in normal controls. In all patients platelet counts rose to threefold the initial values within 5 days after clearance of parasites. The results demonstrate that, first, thrombocytopenia is a common feature in human malaria, second, thrombocytopenia induced by malaria is due to shortened life span in the peripheral blood and, third, some interaction is present between platelets and malaria plasmodia or parasitized red cells.

Blood Platelets↗