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PubMed1996

Carboxylic ionophores in malaria chemotherapy: the effects of monensin and nigericin on Plasmodium falciparum in vitro and Plasmodium vinckei petteri in vivo.

Chloroquine is widely used in malaria chemotherapy. Due to its weak base properties, this drug accumulates in the parasite food vacuole where it acts initially by raising the pH of this organelle, thereby reducing the digestion of hemoglobin by the parasite and preventing its growth. Nevertheless, alkalinization of the food vacuole and inhibition of lysosomal protein degradation could also be achieved by means of carboxylic ionophores such as monensin and nigericin. These drugs intercalate into intracellular organelle membranes and exchange protons for K+ or Na+. In the present study, we show that monensin and nigericin exhibit in vitro intrinsic antimalarial activities at nanomolar and picomolar range, respectively, on P.falciparum and thereby appear 25 fold and 30,000 fold more potent than chloroquine. The very low IC50 values exhibited by these two ionophores prompted us to test their antimalarial activities in vivo on Plasmodium vinckei petteri. We found that the ED50 and ED90 values were respectively 1.1mg/kg and 3.5 mg/kg for monensin; 1.8 mg/kg and 4.6 mg/kg for nigericin. In addition, when treated with monensin at 10 mg/kg, 100% of the infected mice were cured. Interestingly, nigericin can be combined with monensin and we show that this combination is synergic. Thus, this finding would allow the use of lower doses of these ionophores and prevent occurrence of drug resistance. Carboxylic ionophores can be viewed as a new strategy in malaria chemotherapy.

Animals↗
PubMedDate not supplied

Malaria parasites of rodents of the Congo (Brazzaville): Plasmodium chabaudi adami subsp. nov. and Plasmodium vinckei lentum Landau, Michel, Adam and Boulard, 1970.

Descriptions are given of the blood forms, sporogonic stages and enzyme forms of Plasmodium chabaudi adami subsp.-nov. and P. vinckei lentum, malaria parasites of the thicket-rat Thamnomys rutilans of the Brazzaville region. The two species differ from each other in both morphological and enzymic characters. P.c. adami and P. v. lentum differ from the other subspecies of P. chabaudi and P. vinckei principally by their enzyme forms.

Animals↗
PubMed2001

Plasmodium kentropyxi n.sp. (Apicomplexa: Haemosporina: Plasmodiidae) and a Plasmodium tropiduri-like parasite in the lizard Kentropyx calcarata (Lacertilia: Teiidae) in north Brazil.

Plasmodium kentropyxi n.sp. is described in the teiid lizard Kentropyx calcarata from north Brazil. Young asexual stages and gametocytes are at first polar in the erythrocyte but with elongation, move to a lateral position. Largest meronts seen contained from 30-40 nuclei and conspicuous greenish-black pigment granules located in a distinct vacuole. With growth the gametocytes eventually assume a smooth, curved cylindrical shape, with evenly rounded ends. Pigment is scattered or concentrated around a conspicuous vacuole which is slowly developed as the gametocytes mature. Mature male parasites measured 11.8 x 4.0 microns (9.6 x 4.2 - 13.2 x 3.6 microns), shape-index 2.9 (2.2 - 5.0), and females 13.5 x 4.5 microns (12.0 x 4.5 - 15.0 x 4.8 microns), shape-index 3.0 (2.2 - 3.8). Some larger meronts may slightly enlarge the erythrocyte, but most asexual stages and the mature gametocytes rarely do so. A second, P. tropiduri-like parasite encountered in K. calcarata possessed small rounded or fan-shaped meronts producing from 4-14 merozoites, and spherical to subspherical gametocytes of approximately 6.0 x 5.0 microns. The parasite was consistently polar in its position in the erythrocyte.

Animals↗
PubMed1991

Inability of Plasmodium vinckei-immune spleen cells to transfer protection to recipient mice exposed to vaccine 'vectors' or heterologous species of plasmodium.

Mice can be immunized to Plasmodium vinckei by repeated infections followed by cure. Such immunity is dependent on CD4 T cells and an architecturally modified spleen, but has little requirement for antibody. Thus, athymic mice can be exposed to P. vinckei and cured, but do not develop immunity. They are resistant to challenge with parasites, however, if they are then given spleen cells from euthymic immunized animals. Such immune spleen cells, however, cannot transfer resistance to normal mice which have been exposed to BCG, Salmonella typhimurium, or vaccinia virus, and are only partially effective in transferring resistance to mice which have been previously immunized with heterologous plasmodia, P. yoelii, P. chabaudi and P. berghei. Mice exposed to varying numbers of irradiated P. vinckei-pRBC do not develop immunity and nor are such animals protected following adoptive transfer of immune spleen cells. Cellular immunity to malaria may not only be dependent on a population of immune CD4 T cells, but may require a specifically architecturally modified spleen which may not occur following either exposure to candidate vaccine vectors, heterologous plasmodia or non-viable homologous plasmodia.

Animals↗
PubMed1996

Expression of a Plasmodium gene introduced into subtelomeric regions of Plasmodium berghei chromosomes.

Targeted integration of exogenous DNA into the genome of malaria parasites will allow their phenotype to be modulated by means of gene disruption or the stable expression of foreign and mutated genes. Described here is the site-specific integration through reciprocal exchange, and subsequent expression, of a selectable marker gene into the genome of the pathogenic, bloodstage forms of the rodent malaria parasite Plasmodium berghei. Stable integration of a single copy of the marker gene (retained for more than 70 generations in the absence of drug pressure) into a nontranscribed subtelomeric repeat array of different chromosomes was observed. Expression of the gene within the subtelomeres indicated that the previously recorded absence of transcription in these regions could be due to a corresponding absence of genes rather than active silencing mechanisms.

Animals↗
PubMed2003

[Internal validity of clinical trials for Plasmodium vivax malaria treatment: analysis of evaluation study of in vivo Plasmodium vivax emergence of resistance to standard doses of primaquine].

Parasite resistance can be defined as the ability of a parasite strain to survive and/or to multiply despite the administration and absorption of a drug given in doses equal or higher than those usually recommended, but within the limits of tolerance of the patients. Therefore, the ideal study design to be used to monitor emergence of parasite resistance would use historical controls or any valid baseline data. Moreover, it is desirable to have some control of remaining determinants of therapeutic failure, not related to biological parasite resistance, which could vary over time and would have potential to distort the analysis for detecting emergence of parasite resistance. Here we comment on the internal validity of studies, which aim to assess the in vivo Plasmodium vivax emergence of resistance to standard doses of primaquine used routinely by health services. Few studies have paid attention to the need to control for other determinant factors of therapeutic failures or made any attempt to compare current findings with cure failure rates of historical controls from a given geographical area. Therefore, attention to the internal validity (and limitations) of study conclusions in these types of study is strongly advised.

Animals↗
PubMed1987

Antimalarial activity of a riboflavin analog against Plasmodium vinckei in vivo and Plasmodium falciparum in vitro.

The riboflavin analog 10-(4'-chlorophenyl)-3-methylflavin was found to have significant activity against Plasmodium vinckei vinckei when administered orally and parenterally; it was active against P. falciparum in culture. It inhibited mouse erythrocyte glutathione reductase in a dose-dependent manner. When administered orally, 5-deazariboflavin was not active in vivo although it has been shown to have activity against P. falciparum in vitro.

Administration, Oral↗
PubMed1994

Lymphocyte responses to Plasmodium falciparum ring-infected erythrocyte surface antigen (Pf155/RESA) peptides in individuals with naturally acquired Plasmodium falciparum malaria.

Antibody titers and lymphocyte responses to synthetic peptides corresponding to repeated amino acid sequences of the 3' and 5' regions of Pf155/ring-infected erythrocyte surface antigen (RESA) were studied in two groups of Thai subjects, soldiers (Rangers), and villagers who differed in their history of malaria exposure. The frequency of Pf155/RESA seropositivity was similar in the two groups while the frequency of high titer antibody was significantly greater in villagers than in Rangers. Lymphocyte responsiveness in vitro to all Pf155/RESA peptides was infrequent for both groups although half of the subjects studied responded to crude Plasmodium falciparum asexual blood stage malaria antigen (MA). Among responders, Pf155/RESA peptides elicited lymphocyte responses in which proliferation and interferon-gamma (IFN-gamma) production were not associated, whereas with MA, the two responses were associated. The MA-stimulated lymphocyte proliferation and IFN-gamma production for both groups of volunteers appeared to be independent of antibody titer. In this study, antibody, but not lymphocyte, responses to Pf155/RESA peptides were shown to reflect differences in prior exposure and levels of acquired immunity to falciparum malaria.

Adult↗
PubMed1975

Immunological studies in rodent malaria. I: Protective immunity induced in mice by mild strains of Plasmodium berghei yoelii against a virulent and fatal line of this plasmodium.

Mild and virulent lines of Plasmodium berghei yoelii are readily distinguished both by their course of infection and by the preference of the virulent line for mature red blood cells. Mice given either mild line were fully protected against the virulent P.b. yoelii one week after they had become negative. Mice given the mild line of P.b. yoelii 17X were fully protected against a challenge by the virulent line on the third day of infection (D+3). Mice given the mild and virulent lines of P.b. yoelii 17X concomitantly showed only slight protection, all eventually succumbing. Mice given the virulent P.b. yoelii 17X and challenged with P.b. yoelii 17X mild on D+1 showed 2/6 with virulent-like infections and 4/6 infections which resembled the mild controls. Five out of eleven animals challenged with P.b. berghei after immunization with mild P.b. yoelii had infections which resembled the P.b. berghei control group and were dead by D+23. The other six mice became negative, but all of them relapsed and three of them subsequently died. In mice challenged four weeks after their mild P.b. yoelii 17X infections had become negative, 5/6 succumbed to a P.b. berghei infection. Mice immunized with P.b. yoelii 17X mild and challenged with P.v. vinckei one week after becoming negative had a survival rate of 2/10.

Animals↗
PubMed2000

[The synergistic action of guanghuoxiang volatile oil and sodium artesunate against Plasmodium berghei and reversal of SA-resistant Plasmodium berghei].

OBJECTIVE: To study the synergistic action of a combination of guanghuoxiang volatile oil (B) and sodium artesunate (SA) against Plasmodium berghei (P. b) and the resistance-reversal activity against SA-resistant P. b (P. b SA-R). METHODS: Mice infected with P. b N or P. b R were treated with a combination of B and SA respectively by 4-day suppressive test method and linear regression to calculate the SD50 of B and SA for each drug alone and in combination (equally effective dose compatibility). RESULTS: B alone, N:SD50 = 87.64 +/- 19.58(GKD), R:SD50 = 43.24 +/- 7.71(GKD); SA alone, N:SD50 = 0.88 +/- 0.01(MGKD), R:SD50 = 27.69 +/- 0.93(MGKD). B and SA combination, N:B SD50 = 36.89 +/- 4.57(GKD), SA SD50 = 0.39 +/- 0.05 (MGKD); R:B SD50 = 7.40 +/- 1.30(GKD), SA SD50 = 4.21 +/- 0.74(MGKD). The synergistic indexes of B and SA in combination were 2.2 for N and 6.6 for R, respectivly. The multiple of resistance reversal of B vs SA was 6.6. The relative reversal rate was 87.6%. CONCLUSION: A combination of B and SA may enhance the antimalarial effect against P. b and reverse the SA-resistance of P. b and delay the occurrence of resistance to SA in N.

Animals↗
PubMed1989

[A preliminary study on detecting Plasmodium falciparum in blood by Plasmodium falciparum DNA probe].

A simple and rapid method for detecting Plasmodium falciparum in human blood was used in this study. The assay is based on DNA-DNA spot hybridization. For this purpose, the total genomic DNA of P. falciparum was isolated and purified from the parasite cultured in vitro. Then the total genomic DNA was used as a probe and labelled with [alpha-32P]-dATP by nick-translation. Twenty-five test samples, ten-microliter lysed infected blood each, were spotted onto dry nitrocellulose paper and hybridized with labelled genomic DNA. After hybridization, the paper was exposed to X-ray film for autoradiography, resulting in an image in places where hybridization occurred. The result shows that the assay appears to be sensitive enough to detect parasitaemia up to 0.0009%. No visible hybridization was detected in normal human blood or human leukocytes. Many samples can be processed simultaneously. This may be applicable to mass survey for detecting P. falciparum in epidemiological study (Fig. 2).

Animals↗
PubMedDate not supplied

[Study of gametocytes from the Plasmodium "vivax" group: morphology, development in Anopheles and infectivity of Plasmodium yoelii microgametocytes].

The study of the gametocytes of Plasmodium yoelii enabled the differentiation of 4 morphological types: O, I, II and III (in a chronological order) and amongst each of these types the differentiation of healthy and altered gametocytes. These morphological data represent a tool for investigations on the biology of the gametocytes of the "vivax" group. Preliminary experiments bring informations on the evolution of gametocytes and the mechanisms of their infectivity. 1--In experimentaly infected white mice gametocytes of P.y. nigeriensis are infective up to the 3rd-4th day, those of P. y. yoelii until the 5th-6th days. These periods can be shorter when the infection is very virulent or longer when chronical. 2--The drop in infectivity coincides with the increase in number of the altered gametocytes. 3--The loss of infectivity is connected with the condition of the blood: when parasitaemiae are high, it becomes rapidly unsuitable to a normal evolution of the gametocytes: thus, non infective gametocytes acquire a good infectivity in less than two hours when transfered to a clean mouse. 4--The gametocytic composition of the blood taken up by the Anopheles in the capillaries can be very different from that taken at the tail of a Rodent. In the young parasitaemiae, when the Rodents are most infective to the Mosquitoes, there is a considerable enrichment in gametocytes O-I of the blood ingested by the Anopheles as compared to that taken from the Rodents by the usual techniques. This phenomenon could perhaps be explained by the larger size of gametocytes O and I and their retention in the capillaries of the host. 5--The strong infectivity of gametocytes O and I is confirmed by the fact that no infection develops in the Mosquitoes when no such gametocytes are present in the ingested blood. 6--The ageeing of gametocytes appears to be very rapid for gametocytes arising from exo-erythrocytic schizontes reach stage II, 29 hours and stage III, 35 hours, after the rupture of the very first schizonts.

Animals↗
PubMed1997

[Infection of Anopheles (Kerteszia) cruzii by Plasmodium vivax and Plasmodium vivax variant VK247 in the municipalities of São Vicente and Juquitiba, São Paulo].

Sporadic cases of autochthonous malaria have been recorded in São Paulo State, located in the Southeast region of Brazil. These cases are characterized by their benign course, low parasitemia, and mild symptomatology and have been identified as vivax malaria. Little is known about the symptoms and immune response elicited in humans by the variants Plasmodium vivax VK247 and P. vivax-like human malaria parasites. These variants are transmitted by Anopheles (Kerteszia) cruzii, one of the most common species of mosquitoes in the Southeast of Brazil. The objective of the study described in this paper was to investigate infection in anophelines using ELISA immunoenzymatic assay with specific monoclonal antibodies directed against the repetitive regions of the circumsporozoite protein in classic P. vivax, P. brasilianum/P. malariae, and P. vivax VK247. Between 1991 and 1993, mosquitoes were collected in São Vicente and Juquitiba, municipalites located in a remnant of the Brazilian Atlantic forest in São Paulo State, an ecosystem rich in plants of the Bromeliaceae family. These plants function as nurseries for immature forms of anophelines of the subgenus Kerteszia. Of 1,117 An. (Ker.) cruzii captured in São Vicente, 0.179% were positive for classic P. vivax. In Juquitiba, of 1,161 An. (Ker.) cruzii, 0.086% were positive for P. vivax VK247, confirming the presence of this variant in the region. Although the infection rate is low, the high density of these mosquitoes and their voracity (they exhibit 24-h biting activity) could compensate for the low percentage of infected specimens.

Animals↗