Leishmaniasis in Arabia: an annotated bibliography.
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Humans↗
Biomedical subjects
W Peters
Publications and source records attributed to W Peters.
Platelets acquire a secretion defect after high-dose chemotherapy.
Patients receiving high-dose chemotherapy (HDC) and autologous bone marrow transplantation (ABMT) may experience life-threatening hemorrhagic myocarditis. The authors investigated whether HDC was associated with an acquired platelet defect. Platelet aggregation and release were evaluated after HDC in ten patients with either metastatic breast carcinoma or melanoma. Platelets underwent shape change and a primary wave of aggregation. High-dose chemotherapy was associated with the inhibition of secondary aggregation of platelets induced by adenosine diphosphate (ADP), arachidonic acid, prostaglandin H2 (PGH2) analog (U44619), and collagen. Although electron microscopic study of the platelets revealed normal morphologic features with an adequate number of dense bodies and alpha-granules, release of adenosine triphosphate (ATP) from dense granules was less than 20% of normal. The acquired platelet defect occurred before development of thrombocytopenia. Aggregation of platelets from normal volunteers was not inhibited by either the addition of the chemotherapeutic agents, chemotherapy metabolites, or the patients' sera. In conclusion, HDC induces an acquired abnormality in platelet secretion and aggregation which may contribute to the development of hemorrhagic complications after ABMT.
Adenosine Triphosphate↗
The hard parts (trophi) of the rotifer mastax do contain chitin: evidence from studies on Brachionus plicatilis.
The jaws (trophi) of the rotifer Brachionus plicatilis are soluble in strong acids but are resistant to long treatments by strong alkali. They show the same buoyant density as chitin and also as the chitin-containing layers of rotifer egg-shells. The presence of chitin in these structures was confirmed using the following techniques: chitosan-tests, thin-layer chromatography of trophi-hydrolysates which revealed glucosamine, by dissolving trophi with chitinase and electron microscopic WGA/gold-labelling. The content of chitin in the trophi was estimated by two different methods to be approx. 64% (50-75%).
Animals↗
The prevention of antimalarial drug resistance.
The deployment of antiprotozoal drugs on a large scale for prophylaxis or monotherapy inevitably results in the selection of drug-resistance. The use of appropriately selected drug combinations may impede this process. Point mutations underlie resistance to dihydrofolate reductase inhibitors such as pyrimethamine. Potentiating combinations of such compounds with sulfonamides or sulfones have effectively delayed resistance to them. The use of triple combinations may be of value in protecting such compounds as chloroquine and mefloquine, resistance to which is associated in some cases with gene amplification. It is essential to seek partner compounds for any new antimalarials, e.g. artemisinin. Past experience with existing compounds is discussed and the need to make use of all available means of interrupting malaria transmission is stressed, rather than depending entirely on drugs.
Animals↗
A new species of Leishmania isolated from the great gerbil Rhombomys opimus.
Leishmania turanica n.sp., found infecting the desert rodent Rhombomys opimus in the southern territories of the USSR and the Mongolian People's Republic, is described. This parasite exists sympatrically with L. major and L. gerbilli in R. opimus and is the predominant species. A total of 284 isolates of L. turanica from R. opimus, 3 from naturally infected Phlebotomus andrejevi and 1 from P. papatasi were characterized and found to be clearly distinguishable on isoenzyme and nuclear DNA characteristics from all other Old World taxa of Leishmania.
Animals↗
Plasmodium: resistance to antimalarial drugs.
Quinine-resistant Plasmodium falciparum was first reported in 1910 from Brazil. Today this parasite is resistant in most endemic areas to the widely used blood schizonticide, chloroquine. Many strains are resistant also to antifols (e.g. pyrimethamine, proguanil) and some are also no longer eliminated by quinine. These polyresistant parasites have an enhanced ability to resist also new drugs such as mefloquine and halofantrine. There are indications that P. vivax is also becoming resistant to chloroquine in Papua-New Guinea where primaquine resistance of the hypnozoites also exists. The modes of action of antimalarials and mechanisms by which parasites become resistant to them are discussed. Future developments include the search for radically new compounds, for drugs that reverse chloroquine resistance and for new strategies to impede the progress of this problem.
Animals↗
The chemotherapy of rodent malaria. XLV. Reversal of chloroquine resistance in rodent and human Plasmodium by antihistaminic agents.
The inherent blood schizontocidal activities of five antihistaminic compounds, cyproheptadine hydrochloride (CYP), ketotifen hydrogen fumarate (KET), pizotyline hydrogen maleate (PIZ), azatadine maleate (AZAT) and loratadine (LOR) were examined against the following organisms: chloroquine-sensitive (CS) Plasmodium berghei and chloroquine-resistant (CR) P. yoelii ssp. NS in mice; and CS Tak 9 clone 96 and CR K1 strain of P. falciparum in vitro. Chloroquine, verapamil and desipramine were used as comparison standards. CYP, KET, PIZ were active against the CS strain in vivo with ED90 levels between 20 and 30 mg kg-1 (given sc daily for four days). They were slightly more active against the CR strain. AZA was active, but much less so than the other compounds. LOR, verapamil and desipramine were inactive in vivo at the doses tested. Against CS P. falciparum in vitro, all five antihistaminics and desipramine were active at EC50 concentrations ranging from about 50-80 mumol l-1, while verapamil was only active at 175 mumol l-1. Against the CR strain of this parasite, CYP, PIZ and LOR were slightly more active than against the CS strain, but KET, AZAT, desipramine and verapamil were significantly less active. The action of all these compounds in combination with chloroquine was then examined both in vivo and in vitro. The ability of verapamil and desipramine to reverse chloroquine resistance in vitro was confirmed, but only a low level of reversal was seen with these compounds in vivo. However, CYP, KET, PIZ and AZAT produced a marked reversal of chloroquine resistance both in vivo and in vitro. The implications of these observations in relation to further laboratory and clinical research are discussed.
Animals↗
Nonhomogeneous local atrial activity during acute atrial fibrillation: spectral and dynamic analysis.
Atrial fibrillation (A Fib) has been categorized into four different types (I-IV) based on the morphology of the epicardial bipolar electrogram. In the present study, we hypothesized that these same types of A Fib also exist at endocardial sites. Simultaneous high, mid, and low right atrial endocardial bipolar electrograms were analyzed during acute A Fib induced by a rapid train of stimuli (20-40 Hz) for 1-3 seconds in anesthetized closed-chest dogs (N = 7, total of 72 episodes). A Fib lasted between 3 seconds and a few minutes (22.3 +/- 22.8 sec). During A Fib, bipolar electrograms (0.5-500 Hz) were both discrete (types I and II) on electrograms recorded at one site and at the same time irregular (type III) on electrograms recorded at another site. The three simultaneously recorded electrograms encompassed all combinations of the four types of A Fib. When A Fib had a discrete electrogram morphology (types I and/or II), the mean rate of the A Fib was 494 +/- 93 beats/min. At a given site, electrogram morphology also changed type over time. Fast Fourier transform (FFT) of the digitized electrograms (8-10 sec, 800 Hz digitization) showed peaks mostly below 15 Hz (range 0-30 Hz), that were either discrete (narrow band) with clear harmonic components, or had continuous (broad band) spectra, that changed in a time and site dependent manner. Phase plane plots (PPP), a plot of voltage versus rate of change of voltage, varied with respect to time and location. However, the morphology of these PPP often inscribed well defined structure suggesting dynamics compatible with deterministic chaos, rather than random dynamics.(ABSTRACT TRUNCATED AT 250 WORDS)
Acute Disease↗
Effects of converting-enzyme inhibition on barrier function in diabetic glomerulopathy.
Differential solute clearances were used to examine the effects of a 90-day course of enalapril on glomerular barrier function in 16 proteinuric patients with diabetic glomerulopathy. By day 90, plasma renin and prorenin became elevated, and arterial pressure declined. Transglomerular passage of dextrans of broad size distribution (radii 28-60 A) was lowered significantly. In a subset of 8 patients, withdrawal of enalapril was followed after an additional 30 days by a return of renin levels and arterial pressure to pretreatment levels. The dextran-sieving profile also returned to baseline, becoming uniformly elevated above treated day-90 levels. A theoretical analysis of the serial dextran-sieving profiles indicated that enalapril shifted glomerular pore size distribution to smaller size. These changes in barrier size selectivity were associated with a reduction in fractional albumin and IgG clearances during enalapril therapy and a subsequent rise in these quantities after its withdrawal; urinary protein excretion rate tended to vary in parallel. We conclude that inhibition of converting enzyme in humans with established diabetic glomerulopathy diminishes glomerular permeability to proteins by enhancing barrier size selectivity. Because neither enalapril therapy nor its withdrawal influenced the glomerular filtration or renal plasma flow rates significantly, we propose that the primary action of enalapril may be to modulate the intrinsic membrane properties of the glomerular barrier.
Adult↗
Converting enzyme inhibition and glomerular size selectivity in diabetic nephropathy.
Differential solute clearances were used to examine the effects of enalapril on glomerular barrier function in 16 proteinuria patients with diabetic glomerulopathy. In these patients, a 90-day course of enalapril reduced arterial pressure without lowering renal plasma flow or glomerular filtration rate. Glomerular clearances of dextrans of broad size distribution (28 to 60 A) were lowered significantly. Theoretical analysis of the dextran clearance profiles revealed that enalapril shifted glomerular pore size distribution to a smaller size. This change in barrier size selectivity was associated with a reduction in fractional albumin and immunoglobulin G clearances during enalapril therapy; urinary protein excretion tended to decrease in parallel. These results indicate that converting enzyme inhibition diminishes glomerular permeability to proteins in diabetic nephropathy by enhancing barrier size selectivity. Because enalapril therapy did not alter the renal plasma flow rate or glomerular filtration rate, these results further suggest that the primary action of enalapril may be to modulate the intrinsic membrane properties of the glomerular barrier.
Adolescent↗
Drug resistance in malaria.
Half of the world's population live in regions where malaria is still endemic and about 2 million are killed by the disease every year. There is an exponential increase in the number of non-immune travellers who visit such areas and thousands develop malaria after they return home. The few drugs currently available for the prevention or treatment of malaria are discussed and the history of the emergence of multiple drug resistance in the malignant tertian parasite, Plasmodium falciparum, is traced from its origins in the late 1950s to the present time when it is found in the endemic regions of all continents. These are indications that chloroquine resistance is beginning to appear now also in P. vivax in the Southwest Pacific. The few new drugs under development and the uncertain future that they face are discussed.
Animals↗
[A case of congenital malaria with atypical expression of Plasmodium vivax originating from Madagascar].
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Animals↗
Antihistaminic drugs that reverse chloroquine resistance in Plasmodium falciparum.
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Animals↗
Binding of lectin-gold conjugates by two Trypanosoma cruzi strains in ampullae and rectum of Triatoma infestans.
The ampullae and recta of Triatoma infestans infected with Trypanosoma cruzi were incubated with lectin-gold conjugates of wheat germ agglutinin (WGA) and soy bean agglutinin (SBA) and investigated by electron microscopy. T. cruzi colonized the whole lumen of the ampullae. The rectal pads with their intensive intracellular membrane system and thin cuticle were often covered by a compact layer of flagellates, whereas the remaining rectal sac- recognizable by a thick layered cuticle - was colonized less densely. All freely accessible stages of T. cruzi strain 'Chile 5' (Zymodeme 1) showed a reaction with SBA-gold complexes but not with WGA, revealing that N-acetyl-galactosamine and/or galactose but no N-acetyl-glucosamine residues were present on the surface. T. cruzi strain 'Chile 7' (Zymodeme 2) also reacted with SBA. WGA-bovine serum albumin-gold conjugates bound strongly to the surface of epimastigotes of this strain, in variable amounts to stages in transition to trypomastigotes, but not to metacyclic trypomastigotes.
Animals↗
[A new Plasmodium species from a lemur: Plasmodium coulangesi n. sp].
The splenectomy of a female Lemur macaco macaco, showing a scanty blood infection by Haemosporidians and a Trypanosome was followed by a dramatic increase of the rate of intra-erythrocytic parasitaemia. Three species of Plasmodium where then identified. The first species was unknown; it is described in this paper and named Plasmodium coulangesi n. sp. It is characterised by--the low (6). constant number of merozoites in mature schizonts,--the disposition of the pigment, well apart from the parasitic mass to which it is linked by a tiny wisp of cytoplasm,--the normal host erythrocyte, the shape, size and colour of which are unaltered. The second species was provisionaly designated as Plasmodium sp.; it was previously seen in the same host by Garnham and Uilenberg in 1975 and designated by these authors as Plasmodium girardi Buck, Coudurier et Quesnel, 1952. Only gametocytes of the last species were found; they are similar to those of Plasmodium lemuris Huff and Hoogstraal, 1963.
Animals↗
[Plasmodia of lemurs in Madagascar].
Lemur macaco macaco from Ambanja region was found polyparasitized by four different species of Plasmodium: --Plasmodium coulangesi recently described by lepers et al. (1989). --P. bucki n. sp.: its main differential characterisitics are the large numvber (32) of merozoites produced in mature schizonts and the stippling, resembling Maurer's dots, in an hypertrophied pinkish erythrocyte. --P. percygarnhami n. sp. (= P. girardi sensu Uilenberg, 1970 pro parte and sensu Garnham et Uilenberg, 1975 pro parte) producing 20 merozoites in mature schizonts and developing inside a deformed corpuscle (holly leaf-shaped or sometimes sea-urchin-shaped) which may also become decolourized when parasitized by older stages. --(?) Plasmodium lemuris: gametocytes are very large (11 microns x 7 micron); the parasitized erythrocyte is much hypertrophied (+/- 10 microns), distored and of a pinkish colour; one schizont only, possibly exo-erythrocytic, was found. The authors hypothesized this parasite to be a Haemoproteid. The analysis of published data led the authors to make the following modifications to the nomenclature previously established: --Plasmodium girardi Buck et al., 1952, sensu Garnham, 1966, sensu Uilenberg, 1970 parte and sensu Garnham and Uilenberg, 1975 pro parte, is refered to as Plasmodium sp., for stages developing in the blood of Lemur fulvus fulvus. The taxon P. percygarnhami is to be employed for stages developing in L. m. macaco and P. girardi Buck et al., 1952 for those developing in Lemur fulvus rufus. --Plasmodium foleyi Buck et al., 1952, sensu Garnham and Uilenberg, 1975 in L. f. fulvus is named Plasmodium uilenbergi n. sp., P. folleyi being a parasite of L.f. rufus. Excluding P. lemuris which probably does not belong to the genus Plasmodium, the morphological analysis led to individualize 7 species, in the three species of Lemurs studied. A phenomenon of "vicariance" thus appears, similar to what is known for the african Rodent Plasmodia, but with a more pronounced speciation. The vicariant species form a pair constituted of: --on the one hand a small species developing in a red blood cell of normal size, P. girardi in L.f. rufus, P. sp. in L.f. fulvus, P. percygarnhami, with also, P. coulangesi, in L. m. macaco; --on the other hand a large species determining an hypertrophy of the erythrocyte, P. foleyi in L.f. rufus, P. uilenbergi in L.f. fulvus and P. bucki in L.m. macaco.
Animals↗
Hydrazide antidepressants possess novel antileishmanial activity in vitro and in vivo.
The hydrazide monoamine oxidase inhibitor antidepressants possess a novel antiparasitic action against visceral and cutaneous strains of Leishmania. In vitro, phenelzine was the most active compound tested, while in vivo, nialamide was more potent, and was also effective when applied topically to cutaneous lesions. Despite the coincidence of tricyclic antidepressants also possessing antileishmanial activity, the evidence suggests that the antiparasitic action of the hydrazides is unrelated to either monoamine oxidase inhibition or CNS effects.
Animals↗
Antileishmanial effects of clofazimine and other antimycobacterial agents.
In the search for more effective alternatives to the presently-used antileishmanial drugs, the activity of the major groups of antimycobacterial compounds has been examined, both in vitro and in animal models of infection. In vitro, clofazimine was the most active compound tested, with a mean ED50 of 2.3 mg l-1 against Leishmania mexicana amazonensis, 1.4 mg l-1 against L. donovani and 0.5 mg l-1 against L. major. Other active compounds were the thiosemicarbazone, thiambutosine, and salinazid, a derivative of isoniazid. Isoniazid itself was inactive, and rifampicin only partially active. In vivo, only clofazimine displayed significant activity, and it was most effective against the cutaneous infections. It is concluded that antimycobacterial activity is in general a poor predictor of antileishmanial potency.
Administration, Topical↗