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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In severe falciparum malaria there is a pathophysiological cascade beginning with changes in the parasitized red blood cells which induce intermediate effects, in turn contributing to dysfunction of several organs. A low serum albumin is a common but often unrecognized finding which may contribute to oedema especially in the lung and brain. The only irreversible complication in falciparum malaria is the acute respiratory distress syndrome, manifested by cyanosis and rapid breathing, basically distinct from acute pulmonary oedema caused by therapeutic overhydration. The pathophysiology of falciparum malaria may be complex but the treatment is simple. Drugs, other than antimalarials, are rarely needed. Guidelines for cholorquine or quinine dosage in severe disease are proposed; each drug is given at a dose of 5 to 10 mg/kg in 10 ml/kg of fluid as an intravenous infusion in four hours at a frequency of dosing every 12 to 24 hours. When the disease has been brought under control the treatment should be changed from the intravenous to the oral route.
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PMID:The treatment of severe falciparum malaria. 33 21

The anamnestic antibody response of CBA mice to bovine serum albumin was characterized by a rapid production of high-avidity antibody. After 3 weeks both the total amount of antibody and its avidity declined but still remained above those seen in the primary response for at least 6 weeks. The effects of acute Plasmodium berghei and Plasmodium yoelii yoelii infections upon the induction and the expression of this anamnestic response were studied. Mice infected with these malaria parasites responded poorly to primary immunization and the immunological memory generated was quantitatively subnormal. In addition, presence of the infection during a period between approximately the second and third weeks of the primary response prejudiced the development of high-avidity memory. Optimally primed mice, challenged during a subsequent acute infection, responded well initially, but were unable to maintain the secondary response at a normal level in terms of both quantity and avidity of the antibody. However, if challenge was delayed until after recovery from the infection, a normal secondary response ensued. Antibody concentrations in the sera of primed animals declined rapidly during infection. This was at least partly due to increased catabolism.
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PMID:Immunosuppression in murine malaria. IV. The secondary response to bovine serum albumin. 39 34

The primary antibody response to alumadsorbed bovine serum albumin was depressed in CBA mice infected with Plasmodium yoelii yoelii. Responses initiated within approximately 3 weeks of this malaria infection were reduced in quantity, but not in avidity. Responses initated later were normal. A depressed primary response was also seen in infected compared to control splenectomized mice; this was accompanied by impaired priming for a secondary response.
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PMID:Immunosuppression in murine malaria. II. The primary response to bovine serum albumin. 60 88

The binding of quinine to human serum albumin (HSA), alpha 1-acid glycoprotein (AAG) and plasma obtained from healthy subjects (10 caucasians and 15 Thais) and from Thai patients with falciparum malaria (n = 20) has been investigated. In healthy volunteers, plasma protein binding expressed as the percentage of unbound quinine was 7.9-31.0% (69-92.1% bound). The mean percentage of unbound quinine found with essentially fatty acid-free HSA (40 g L-1) was 65.4 +/- 1.5% (mean +/- s.d.) and was comparable with the value (66.3 +/- 3.8%, mean +/- s.d.) for Fraction V HSA (40 g L-1). This suggests that fatty acids do not influence the plasma protein binding of quinine. Binding of quinine to 0.7 g L-1 AAG was high (mean unbound 61.0 +/- 5.0%), indicating that quinine is bound primarily to AAG and albumin, although other plasma proteins such as lipoproteins may be involved. The mean percentage of unbound quinine was slightly less in caucasians (14.8 +/- 6.7% unbound), compared with healthy Thai subjects (17.0 +/- 6.7% unbound). The higher binding of quinine in caucasian subjects was associated with a higher plasma AAG concentration observed in caucasians. Mean percentage of unbound quinine was significantly lower in Thai patients with malaria (10.9 +/- 4.0%) than in the healthy Thai subjects. The increase in the extent of quinine binding corresponded with the increase in the acute-phase reactant protein, AAG in the patients with malaria. Overall, when the data were combined there was a significant correlation (r = 0.846, P < 0.005) between the binding ratio (bound/unbound) of quinine and the plasma AAG concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma protein binding of quinine: binding to human serum albumin, alpha 1-acid glycoprotein and plasma from patients with malaria. 136 May 5

Because subunit vaccines may create artificial epitopes, the goal of this study was to concentrate the immune response toward protective epitopes contained in a peptide, [(NAGG)5]Y. This peptide consisted of five repeat sequences of the immunodominant epitope of the circumsporozoite protein of the simian malaria parasite Plasmodium cynomolgi and a terminal tyrosine. It was conjugated to bovine serum albumin and mixed with various adjuvant formulations, including block copolymers L121, L141, L180.5 and a lipopolysaccharide (LPS). Outbred mice were vaccinated with seven vaccine formulations. Postvaccination sera from each group of mice were then pooled, and antibody responses against peptide [(NAGG)5]Y or (NAGG)5 were tested in an enzyme-linked immunosorbent assay and against sporozoites of P. cynomolgi in an indirect fluorescent antibody assay. Although all groups elicited a high antibody response to the peptide [(NAGG)5Y], the presence of the tyrosine induced a different antibody response to the peptide (NAGG)5, and formulations containing LPS alone did not induce an antibody response to either (NAGG)5 or P. cynomolgi sporozoites. The formulation including both LPS and the copolymer L121 was the only one to inhibit the development of P. cynomolgi sporozoites in rhesus monkey hepatocytes by 50%. These results suggest that vaccine formulations influence B-cell epitope selection.
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PMID:Effect of adjuvant formulations on the selection of B-cell epitopes expressed by a malaria peptide vaccine. 137 51

Renal specimens from Aotus monkeys were studied by light microscopy and immunohistochemistry to examine pathologic changes following vaccination with synthetic peptides corresponding to the 35-kD, 55-kD, and 83-kD asexual blood stage antigens of Plasmodium falciparum. The monkeys were vaccinated and later challenged with P. falciparum. In the monkeys vaccinated with Centers for Disease Control peptides (group I), specimens from four of six postvaccinated animals had mild to severe mesangial proliferation and two had diffuse interstitial nephritis. Specimens from three monkeys vaccinated with Colombia peptides (group II) had mild to severe mesangial proliferation and one had interstitial nephritis. In the hybrid polymer-vaccinated monkeys (group III), specimens from three animals had mild to moderate mesangial proliferation and one had severe interstitial nephritis. On the other hand, the control group immunized with bovine serum albumin (group IV) showed that specimens from three animals had mild to severe mesangial proliferation and two had severe interstitial nephritis. In the nonimmunized group (group V), specimens from three animals had moderate to severe mesangial proliferation and two had severe and mild interstitial nephritis. Immunohistochemical analysis using the peroxidase-antiperoxidase method revealed mesangial deposits of P. falciparum antigens in 11 of 14 vaccinated monkeys and in five of 10 unvaccinated controls. These results show that treatment of monkeys with prospective malaria vaccines does not increase the frequency of occurrence or of the severity of renal lesions. These data thus provide a baseline for assessing the safety of synthetic malarial vaccines in the future.
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PMID:Renal pathology in owl monkeys vaccinated with Plasmodium falciparum asexual blood-stage synthetic peptide antigens. 144 2

In this paper we seek evidence for the participation of the idiotype-anti-idiotype network in the polyclonal B-cell activation (PBA) associated to malaria. For this purpose we tested by an immunoradiometric assay a panel of nine monoclonal antibodies (including seven anti-idiotype antibodies) against three different (plasmodial or non plasmodial) heteroantigens: the 307 synthetic peptide (an epitope of a P. falciparum hepatic stage specific antigen) the (NANP)4 synthetic peptide (a repetitive epitope of the circumsporozoite protein of the P. falciparum sporozoite surface), and dinitrophenyl (DNP) molecule coupled to bovine serum albumin (BSA). Besides the anti-TNP-DNP antibody, the ABPC48 idiotype (directed against beta polyfructosan a fragment of levan molecule) and one anti-idiotype antibody reacted with DNP-BSA. Two other anti-idiotype antibodies (directed against idiotypes of antibodies specific of beta poly-fructosan and phosphorylcholine) were positive against the (NANP)4 antigen. Three antibodies reacted with the 307 antigen which was also recognized by the ABPC48. One of these antibodies was positive to both P. falciparum peptides tested. These preliminary results suggest the existence of crossreactions between plasmodial antigens and idiotypes of antibodies directed against other heterologous antigens. Thus, malaria induced cross-reactive antibodies could act as hetero and/or auto-antibodies explaining, at least partially, the malaria associated PBA phenomenon and modulating the specific immune response during the course of the infection.
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PMID:Cross-reactions between idiotypes, Plasmodium falciparum derived peptides, dinitrophenyl and beta(2-->6) polyfructosan. 166 57

Linear B- and T-cell epitopes have been identified in the Plasmodium falciparum clustered-asparagine-rich-protein (CARP). Twenty-six synthetic peptides, 15-25 amino acids in length, were assayed for their ability to stimulate purified, human T-cells primed to P.falciparum by natural infection to proliferate and/or secrete gamma-interferon (IFN gamma). The plasma of malaria exposed individuals were tested for antibody reactivity with peptides coupled to bovine serum albumin in a semiquantitative ELISA. Two of the peptides (NNFMNRNMKNKNMN/NAKNVNDMYRDGEMS) induced T-cells from many malaria exposed donors to proliferate and/or secrete-IFN gamma. Six peptides bound antibodies from a large number of the plasma samples, the amounts ranging from ten to more than 200 micrograms specific antibody/ml. T-cell activation was most pronounced when the T-cells were from highly immune donors. In contrast, high anti-peptide specific antibody levels were usually detected in the plasma of less immune donors, recently exposed to infection. One short sequence (NAKNVNDMYRDGEMS) was found to contain both T- and B-cell epitopes. Thus, CARP includes both T- and B-cell reactive elements recognized by the human immune system following exposure to the parasite by natural infection.
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PMID:Epitopes of the Plasmodium falciparum clustered-asparagine-rich protein (CARP) recognized by human T-cells and antibodies. 172 21

Anthropometric measurements were made and serum iron and ferritin levels determined in a group of Gambian children at the beginning of the rainy season and these findings were related to the malaria experience of the children during the following malaria transmission season. Susceptibility to malaria was not correlated with prior weight-for-age, height-for-age, weight-for-height or serum albumin, or with serum iron, serum iron binding capacity nor serum ferritin. Thus, our findings do not provide any support for the view that poor nutritional status, as assessed by anthropometric measurements, or iron deficiency protect against malaria infection. Children who developed a clinical attack of malaria accompanied by a high level of parasitaemia tended to have a higher mean weight-for-age at the beginning of the rainy season than did children who had a clinical attack accompanied by a low level of parasitaemia, but the difference between groups was not statistically significant. However, they had a significantly higher mean serum ferritin level (P less than 0.01).
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PMID:The relationship between anthropometric measurements and measurements of iron status and susceptibility to malaria in Gambian children. 178 Sep 80

The levels of DDT and metabolites in serum of 23 applicators involved in malaria control operations in Natal were determined using gas chromatography with electron capture detection. The mean levels (microgram/l, ppb) were 61.7 DDT, 129.3 DDE, 11.0 DDD and 202.0 sigma DDT. Percentage DDT was 33.4%. These levels were higher than for an age matched sample of the general population in KwaZulu, who are protected by DDT against malaria. Percentage DDT correlated negatively with age (P less than 0.05) for the applicators, suggesting a change in pharmacodynamics with age. Mean serum albumin, alkaline phosphatase, aspartate transferase and gamma-glutamyltransferase (GGT) levels did not differ significantly from an age-matched control group, but the mean GGT value for the applicators was higher than the maximum of the laboratory normal range. Although not clinically significant, the alanine transferase was significantly higher in the applicators than in the control group. These higher levels suggest a possible risk to the health of the sprayers, but uncertainties remain.
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PMID:Serum levels of DDT and liver function of malaria control personnel. 201 43


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