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PubMed1993

Plasmodium vivax malaria in Sri Lanka: transmission, disease and immunity.

We have established a study site in a malaria endemic region around Kataragama in the south of Sri Lanka. A population of about 3,000 individuals in a group of villages around Kataragama have been provided with access to a small field clinic enabling us to monitor aspects of malarial infection under conditions of natural transmission. At the present time, both Plasmodium falciparum and Plasmodium vivax are prevalent to a similar degree although prior to about five years ago P. falciparum had been virtually absent for most of the previous ten years.

Animals↗
PubMed1993

The role of the host during the development of Plasmodium berghei hepatic schizonts.

Immature exoerythrocytic stages of Plasmodium berghei are immunogenic and produce antigens with protective capacities. Immunization experiments show a strong dependency of the responses on the host species and strain. To study this dependency a potential natural host of Plasmodium berghei, Thamnomys gazellae, was introduced, a species which is very susceptible for infection. Young liver stages were produced in different hosts after inoculation with irradiated sporozoites or after treatment with difluoromethylornithine.

Animals↗
PubMed1993

[Plasmodium prevalence and parasitic burden in blood donors of Brazzaville, Congo].

To assess the frequency of malaria-infected blood donations in Brazzaville (Congo) thick films from all blood donors (n = 12,375, minimum per month: 857, maximum per month: 1,295; sex ratio: 9.6) at the Brazzaville University Hospital were examined quantitatively for Plasmodium (screening threshold: 20/microliters of blood) over one year (1989). The overall prevalence rate for all species of Plasmodium was 8.5%. It varied according with age but not with sex. P. falciparum predominated (92%), followed by P. malariae (7%) and P. ovale (3%). For P. falciparum: 1--the prevalence rate was 7.8% but varied over the year from 4.8% in August (6.2% for the dry season on the whole) to 11.5% in March (9.6% for the rainy season); 2--the parasitic load, also variable according to the season, was over 600/microliters in 24% of the cases (i.e. 1.9% of all donations) and over 6,000/microliters in 15 cases (i.e. 1.6% of the cases). In conclusion the proportion of blood donations infected with P. falciparum (with a parasitic load > or = 20/microliters) varied in Brazzaville from 6% in the dry season to 10% in the rainy season.

Adolescent↗
PubMed1993

Pathogenicity and chemotherapy of Plasmodium durae in experimentally infected domestic turkeys.

Only 3 out of 8 South African isolates of Plasmodium durae used in 524 turkeys in 161 passages caused approximately 50% mortality, a further 3 produced approximately 10% mortality while 2 were found to be apathogenic. Exoerythrocytic schizonts were the main pathogenic stage. In most survivors the effect on mass gains was minimal. Twelve drugs currently available for use in poultry, as well as chloroquin phosphate, were tested for their activity against experimental infections with Plasmodium durae in domestic turkeys. While chloroquin phosphate showed a certain degree of effectivity, Amprolium, Amprolium + Ethopabate, Maduramycin, Toltrazuril, Metronidazole, Furazolidone, Enrofloxacin and Sulfamethoxypyridazine + Trimethoprim were ineffective. Halofuginone and Penta-Sulfa at a high dose had some protective effect. At high doses Sulfachloropyrazine protected from mortality without affecting the parasitaemia, while Sulfamonomethoxine suppressed parasitaemia without entirely protecting from mortality. From these data it is concluded that Halofuginone has a potential as possible chemoprophylactic. While a combination of Sulfamonomethoxine and Sulfachloropyrazine could be used in the treatment of outbreaks in the field.

Animals↗
PubMed1977

Lipids of Plasmodium lophurae, and of erythrocytes and plasma of normal and P. lophurae-infected Pekin ducklings.

A lipid analysis was performed on the avian malaria parasite Plasmodium lophurae, freed from duckling erythrocytes by immune hemolysis, and on the erythrocytes and plasmas of normal and P. lophurae-infected ducklings. Major lipids of normal erythrocytes were: phosphatidylcholine (40% of total lipids), phosphatidylethanolamine (20%), cholesterol (20%), sphingomyelin (11%), and glycosphingolipids (5%). Major fatty acids of erythrocyte total phospholipids (74% of total lipids) were 16:0 (22%), 18:2 (n-6) (21%), 18.1 (n-7, n-9) (18%), 18:0 (9%), 20:4 (n-6) (9%), 22:6 (n-3) (5%). Erythrocyte phosphatidylcholine was greater than 90% the diacyl form, while phosphatidylethanolamine was approximately 44% alkoxy forms and phosphatidylinositol approximately 11% alkoxy forms. Major fatty aldehydes of phosphatidylethanolamine were 16:0 (47%), 18:1 (23%), 18:0 (14%), and 14:0 (12%). The lipid composition of P. lophurae (plus the parasitophorous vacuole membrane) was qualitatively and quantitatively different from that of the duckling erythrocyte in a number of respects. Major lipids were phosphatidylcholine (40%), phosphatidylethanolamine (36%), cholesterol (8%), phosphatidylinostol (4%), 1,2-diacylglycerols (3%), sphingomyelin (2%), and glycosphingolipids (2%). Diphosphatidylglycerol (approximately 1%) was also detected. The major fatty acids of parasite total phospholipids (86% of total lipids) were more saturated than those of the erythrocyte, and octadecenoic acids were notably elevated: 18:1 (33%), 16:0 (26%), 18:0 (16%), 18:2 (12%), 20:4 (3%), and 22:6 (3%). Parasite phosphatidylcholine and phosphatidylethanolamine were greater than 93% the diacyl form and phosphatidylinositol was approximately 25% alkoxy forms. Major fatty aldehydes of the phosphatidylethanolamine were 14:0 (62%), unidentified long chain forms (24%), 16:0 (7%), 18:0 (4%), 18:1 (3%). The lipid composition of the infected erythrocyte reflected the separate contributions of the erythrocyte and parasite. The major lipids of normal duckling plasma were phosphatidylcholine (33%), triacylglycerols (22%), cholesterol esters (20%), cholesterol (12%), phosphatidylethanolamine (5%), and sphingomyelin (2%). The fatty acids of plasma total lipids were 18:1 (26%), 16:0 (26%), 18:2 (12%), 20:4 (12%), 18:0 (9%), 22:6 (3%). Plasma phosphoglycerides were remarkably lower in C18 unsaturated fatty acids and higher in 20:4 than the erythrocyte phosphoglycerides. Infection of ducklings with P. lophurae caused increases in plasma unesterified fatty acids, triacylglycerols and cholesterol esters, and a notable rise in the 18:1 content of all fatty acid-containing plasma neutral lipids. These findings are compared with those reported for other species of Plasmodium infecting other avian and mammalian hosts.

Animals↗
PubMed1995

[The inhibitory effects of immune sera against two recombinant hybrid antigens on the growth of Plasmodium falciparum in vitro].

The inhibitory effects of rabbit immune sera against two recombinant hybrid antigens (C and CAC) of Plasmodium falciparum to the multiplication and development of in vitro cultured P. falciparum parasites were tested. Although both of anti-C and anti-CAC immune sera had inhibitory effect on parasites, the anti-CAC serum showed much greater effect than that of anti-C serum (P < 0.05). The inhibitory capacities in the sera to parasites were enhanced with the increase in the serum concentration as well as with the prolongation of the incubation time of the sera with the parasites. It was shown that after 72 h incubation of the anti-CAC serum with the parasites at the concentration of 1%, 10% and 20%, the inhibition rates were 15%, 54% and 82%, respectively. The immune sera caused the dispersion of parasite cytoplasm, atrophy of parasites, agglutination of free merozoites and degeneration of schizonts, suggesting that the hybrid antigen could produce multi-functional protective antibodies against antigens of Plasmodium falciparum.

Animals↗
PubMed1996

Reduced invasion and growth of Plasmodium falciparum into elliptocytic red blood cells with a combined deficiency of protein 4.1, glycophorin C, and p55.

In this investigation, we have measured the invasion and growth of the malaria parasite Plasmodium falciparum into elliptocytic red blood cells (RBCs) obtained from subjects with homozygous hereditary elliptocytosis. These elliptocytic RBCs have been previously characterized to possess molecular defects in protein 4.1 and glycophorin C. Our results show that the invasion of Plasmodium falciparum into these protein 4.1 (-) RBCs is significantly reduced. Glycophorin C (-) Leach RBCs were similarly resistant to parasite invasion in vitro. The intracellular development of parasites that invaded protein 4.1 (-) RBCs was also dramatically reduced. In contrast, no such reduction of intracellular parasite growth was observed in the glycophorin C (-) Leach RBCs. In conjunction with our recent finding that a third protein termed p55 is also deficient in protein 4.1 (-) and glycophorin C (-) RBCs, the present data underscore the importance of the membrane-associated ternary complex between protein 4.1, glycophorin C, and p55 during the invasion and growth of malaria parasites into human RBCs.

Animals↗
PubMed1996

Exacerbation of Plasmodium chabaudi malaria in mice by depletion of TCR alpha beta+ T cells, but not TCR gamma delta+ T cells.

Although gamma delta T cells are found in increased numbers in the spleens of humans and mice infected with malaria, it is not known if these cells are necessary components of an effective immune response. The surface phenotype of spleen cells obtained from mice infected with avirulent Plasmodium chabaudi adami or virulent Plasmodium chabaudi chabaudi were examined using anti-delta or anti-alpha beta T-cell-specific reagents and flow cytometry. Levels of parasitaemia, red blood cell (RBC) counts, and survival times were followed in mice depleted of tumour necrosis factor (TCR)gamma delta+ or TCR alpha beta+ T cells. Numbers of gamma delta T cells increased in the spleens of control antibody-treated infected mice, but not in mice depleted of TCR gamma delta+ or TCR alpha beta+ T cells. Mice depleted of gamma delta T cells had levels of parasitaemia, RBCs, and survival rates similar to control antibody-treated mice. However, mice depleted of TCR alpha beta+ T cells had higher levels of parasitaemia, lower RBC counts, and decreased survival rates. These results indicate that TCR alpha beta+ but not TCR gamma delta+ T cells play an essential role in host defense against P. chabaudi infection in mice.

Anemia↗
PubMed1996

Inhibition of hemozoin formation in Plasmodium falciparum trophozoite extracts by heme analogs: possible implication in the resistance to malaria conferred by the beta-thalassemia trait.

BACKGROUND: Human falciparum malaria, caused by the intracellular protozoa Plasmodium falciparum, results in 1-2 million deaths per year. P. falciparum digests host erythrocyte hemoglobin within its food vacuole, resulting in the release of potentially toxic free heme. A parasite-specific heme polymerization activity detoxifies the free heme by cross-linking the heme monomers to form hemozoin or malaria pigment. This biochemical process is the target of the widely successful antimalarial drug chloroquine, which is rapidly losing its effectiveness due to the spread of chloroquine resistance. We have shown that chloroquine resistance is not due to changes in the overall catalytic activity of heme polymerization or its chloroquine sensitivity. Therefore, the heme polymerization activity remains a potential target for novel antimalarials. In this study, we investigated the ability of heme analogs to inhibit heme polymerization and parasite growth in erythrocytes. MATERIALS AND METHODS: Incorporation of radioactive hemin substrate into an insoluble hemozoin pellet was used to determine heme polymerization. Incorporation of radioactive hypoxanthine into the nucleic acid of dividing parasites was used to determine the effects of heme analogs on parasite growth. Microscopic and biochemical measurements were made to determine the extent of heme analog entry into infected erythrocytes. RESULTS: The heme analogs tin protoporphyrin IX (SnPP), zinc protoporphyrin IX (ZnPP), and zinc deuteroporphyrin IX, 2,4 bisglycol (ZnBG) inhibited polymerization at micromolar concentrations (ZnPP << SnPP < ZnBG). However, they did not inhibit parasite growth since they failed to gain access to the site of polymerization, the parasite's food vacuole. Finally, we observed high ZnPP levels in erythrocytes from two patients with beta-thalassemia trait, which may inhibit heme polymerization. CONCLUSIONS: The heme analogs tested were able to inhibit hemozoin formation in Plasmodium falciparum trophozite extracts. The increased ZnPP levels found in thalassemic erythrocytes suggest that these may contribute, at least in part, to the observed antimalarial protection conferred by the beta-thalassemia trait. This finding may lead to the development of new forms of antimalarial therapy.

Animals↗
PubMed1996

Lactate dehydrogenase as a marker of Plasmodium infection in malaria vector Anopheles.

Lactate dehydrogenase (Ldh) electrophoresis showed the presence of Plasmodium yoelii yoelii in Anopheles stephensi and An. gambiae. The Ldh appeared as an additional band (pLdh) whose activity was more intense with 3-acetyl pyridine adenine dinucleotide as coenzyme than with beta nicotin-amide adenine dinucleotide. Several allelic forms occurred both in the vector and the host. The isoelectric point of Ldh, similar in the vector and host, differed from those of Ldh from mosquito and mouse. The presence of pLdh was detected from the 2nd to the 28th day of infection. The pLdh appeared to be proportional to the number of sporozoites present in infected salivary glands. However, pLdh was not found in salivary glands or midguts, but it was detected in the rest of the corresponding mosquito. The origin and use of pLdh as a marker of Plasmodium in its vector is discussed.

Animals↗
PubMed1996

Protection against malaria by Plasmodium yoelii sporozoite surface protein 2 linear peptide induction of CD4+ T cell- and IFN-gamma-dependent elimination of infected hepatocytes.

Plasmodium falciparum sporozoite surface protein 2 (SSP2), also known as TRAP, is included in experimental human malaria vaccines because Plasmodium yoelii SSP2 is the target of protective CD8+ CTL that eliminate P. yoelii-infected hepatocytes in mice. We now report that immunization with a synthetic branched-chain peptide including four copies of a PySSP2 sequence, NPNEPS, and two tetanus toxin T helper epitopes in the adjuvant TiterMax, or with an 18 amino acid peptide (NPNEPS)3 in the adjuvant protects A/J, but not BALB/c or C57BL/6 mice. Transfer of T lymphocyte-enriched immune splenocytes protects naive mice; in vivo depletion of CD4+ T cells eliminates vaccine-induced protection; and in vivo treatment with anti-IFN-gamma reverses vaccine-induced activity against infected hepatocytes. Lymph node cells from immunized A/J, BALB/c, and C57BL/6 mice recognize the (NPNEPS)3 peptide in vitro. However, the protected A/J mice respond with a predominantly Th1 pattern of lymphocyte response, and the non-protected strains of mice respond with a Th2 pattern. There are many examples of CD4+ T cells transferring protection against infectious organisms. However, to our knowledge, this is the first formal demonstration that immunization with a linear synthetic peptide induces CD4+ T cell-dependent, IFN-gamma dependent, genetically restricted sterile protective immunity against an infectious agent.

Adoptive Transfer↗
PubMed1996

[In vitro sensitivity of 85 Plasmodium falciparum isolates in the Fatick region, Senegal].

Increasing resistance of Plasmodium falciparum to chloroquine and other antimalarials has been reported in Africa. Only fragmentary data are available for Senegal. Although combined chloroquine-proguanil is soon scheduled for released on the market, few studies have been published concerning the susceptibility of isolates to either drug. The in vitro susceptibility of 85 Plasmodium falciparum isolates obtained between October 24 and December 2, 1995 from malaria-infected patients living in the Fatick Region of Senegal to five classical antimalarial drugs (chloroquine, cycloguanil, quinine, mefloquine, and halofantrine) was evaluated using an isotopic, semi-microtest. Twenty-nine percent of isolates were resistant to chloroquine (IC50 > 100 nM), 22% to cycloguanil (IC50 > 500 nM), 1% to quinine (IC50 > 500 nM), 22% to mefloquine (IC50 > 20 nM), and 8% to halofantrine (IC50 > 5 nM). Five percent of isolates were resistant to both chloroquine and cycloguanil. Positive correlation was observed between quinine and halofantrine activity and between mefloquine and halofantrine activity. These findings suggest cross resistance or reduced susceptibility between these antimalarial agents which all exhibit a methanolic function.

Animals↗
PubMed1996

Enhanced gametocyte formation by Plasmodium chabaudi in immature erythrocytes: pattern of production, sequestration, and infectivity to mosquitoes.

The objective of this study was to investigate the chronobiology and infectivity of the gametocytes of Plasmodium chabaudi chabaudi. In order to increase the production of gametocytes, mice were treated with phenylhydrazine to induce a hyper-reticulocytosis. The authors observed an important stimulation of gametocytogenesis. Gametocytes were seen as soon as the second day postinoculation and were produced periodically at each schizogony, every 24 hr. The gametocytic developmental cycle lasted 60 hr and consisted of 4 successive stages: stage 0 at 36 hr, from merozoite invasion, stage I at 42 hr, stage II at 48 hr, and stage III at 54 hr. An important fraction of stage II was sequestered in small peripheral capillaries. The numbers of oocysts in the mosquitoes fed on phenylhydrazine-treated mice were larger than in controls. When mosquitoes were fed at different times of the day, circadian differences in the oocyst counts were not statistically significant. However, stage II was considered to be probably the most infective stage because, like the infective gametocyte stage of other species of murine malaria, it is sequestered in the peripheral capillaries. In contrast with Plasmodium vinckei, there is no peak of infectivity at the time of sequestration of the infective stage; this is probably due to the inhibitory effect of the schizogony occurring at this time.

Animals↗
PubMed1995

Monoclonal antibodies against lactate dehydrogenase of Plasmodium knowlesi.

Lactate dehydrogenase (LDH) of malarial parasites has been demonstrated to be biochemically and immunochemically distinct from the equivalent host enzyme. The polyclonal antibodies raised against the purified plasmodial LDH showed specificity to Plasmodium spp. Six hybridoma cell lines secreting monoclonal antibodies specific to Plasmodium knowlesi LDH have been obtained. The two monoclonal antibodies (2A3B7 and 4A6A7) showed high reactivity with LDH from simian (P. knowlesi. P. cynomolgi), human (P. falciparum, P. vivax) and rodent (P. berghei, P. yoelii) malarial parasites and did not cross-react with red cell LDH as well as with isoenzymic forms of mammalian LDH (A4, B4 and C4). One monoclonal antibody (4A6A7) strongly inhibited the enzyme activity specifically of plasmodial LDH and did not have any effect on the activity of red cell LDH. The other monoclonal (2A3B7) did not show inhibitory effect on parasite LDH. These findings as well as competitive immunoassay studies suggest the presence of at least two parasite specific epitopes on plasmodial LDH.

Animals↗
PubMed1997

Efficacy of artemisinin and mefloquine combinations against Plasmodium falciparum. In vitro simulation of in vivo pharmacokinetics.

The activity of artemisinin in combination with mefloquine was tested in vitro against a chloroquine-sensitive (F32) strain of Plasmodium falciparum. A method of repetitive dosing and extending the culture observation period to 28-30 days was used to mimic the in vivo pharmacokinetic situation. Plasmodium falciparum was exposed to artemisinin from 10(-8) to 10(-5) M, mefloquine from 3 x 10(-9) to 10(-5) M and their combinations. The exposure time for artemisinin was 3 hours twice daily and for mefloquine 24 hours. The drug-dosing duration was 3 days. Neither artemisinin nor mefloquine alone provided radical clearance of P. falciparum, even when maximum concentrations (10(-5) M) were applied. The antiparasitic activity of artemisinin and mefloquine were significantly higher when dosed alone. Effective concentrations for different degrees of inhibition (EC 50, 90 and 99) of both artemisinin and mefloquine respectively were significantly lower when used in combination. At concentrations normally reached in vivo, this effect was clearly synergistic (P = 0.016) Our in vitro model of intermittent dosing of artemisinin and mefloquine combinations for 3 days provides significant evidence of positive interaction between the two compounds. Lower combination concentrations around the MIC-values for the individual compounds showed synergistic effect, and high concentrations showed additive effect. This indicates that such drug combinations may provide radical clearance at concentrations lower than those required for single-drug treatment.

Animals↗
PubMed1996

Small GTP-binding proteins in Plasmodium falciparum.

During its erythrocytic life cycle Plasmodium falciparum exchanges compounds with host cells through phagocytosis and exocytosis. In eucaryotic cells, small GTP-binding proteins of the Ras superfamily appear to be involved in different steps of membrane trafficking and in intracellular signals. In this paper, we investigate the Rab4, Rab6 and Ras-related proteins in P falciparum infected red cells. We report that P falciparum Rab and Ras-related proteins could be distinguished from their counterparts by iso-electrofocusing and immunoblotting. The localization of P falciparum Rab 4 and Rab 6 was studied by immunogold electron microscopy on ultrathin frozen sections of infected red blood cells. Rab4 parasite-related protein was found associated with the membranes of early endosome-like structures near the parasite plasma membrane. Rab6-related protein was associated with the Golgi/trans Golgi network, as already suggested by immunofluorescence microscopy studies and Ras-related protein was cytoplasmic and plasma membrane-associated. These results are in accordance with their mammalian counterparts and support the implication of Rab-related proteins in vesicular trafficking in Plasmodium.

Animals↗
PubMed1997

Plasmodium yoelii sporozoite infectivity varies as a function of sporozoite loads in Anopheles stephensi mosquitoes.

Mechanisms by which Plasmodium sporozoites survive and maintain their infectivity within the salivary glands of mosquitoes are unknown. In this study we establish a relationship between the number of sporozoites present in the salivary glands of individual mosquitoes (sporozoite load) and sporozoite infectiousness (or "quality") as measured by infections in BALB/c or ICR mice. When Plasmodium yoelii-infected Anopheles stephensi mosquitoes were each allowed to feed on a single mouse, we noted that sporozoites from mosquitoes with higher sporozoite loads were more infectious in 13 of 30 (43%) mice. In a second experiment, we inoculated mice with known numbers of sporozoites from individual mosquitoes. Eleven of 18 (61%) and 16 of 18 (89%) mice that received 25 and 100 sporozoites, respectively, became infected. For inoculations using 100 sporozoites, again we noted that sporozoites from mosquitoes with higher sporozoite loads were more infectious to mice. In a third and final experiment, the overall infectiousness of sporozoites from individual mosquitoes was evaluated first by allowing individual mosquitoes to feed on individual mice and then by intravenous inoculations of 100 sporozoites in a second mouse. There was a significant difference in host infections as a function of sporozoite loads in 14 of 19 (74%) mice. Analysis of the feeding times for infected versus noninfected mosquitoes did not show a significant difference between the 2 groups. The mean total feeding times for 50 infected and 45 noninfected An. stephensi mosquitoes were 306 (standard deviation [SD] = +/-230) and 441 (SD = +/-273) sec, respectively. Further, among infected An. stephensi mosquitoes there was no difference in probing times between cohorts that transmitted infectious sporozoites to mice and cohorts that failed to transmit infectious sporozoites. Our findings that sporozoite load influences sporozoite infectiousness or quality suggest that this may be an important factor in malaria parasite transmission.

Animals↗
PubMed1996

[Experimental study of immunity in anti-plasmodium infection on preserved spleen and splenectomized mice].

OBJECTIVE: To investigate the function of the spleen as well as the changes of splenic function after hemisplenectomy and hemisplenic autotransplanted in plasmodium yoelili infected mice (first and second infection). METHODS: 336 mice were divided into six groups: 1. total splenectomy, 2. hemisplenectomy, 3. hemisplenic autotransplanted, 4. sham-operation, 5. total splenectomy of 2nd infection, 6. sham-operation of the 2nd infection. 3 months after operation (1-4) or 15 day after 1st infection and operation (5-6) in mice intraperitoneal inoculations were initiated. RESULTS: 1. First infection: in total splenectomy group the antiplasmodium antibody reduced, the remanent rate of 51Cr-RBC in circulation was high, RBC count continously decreased, parasitized erytrocytes still were seen after 1 month. These changes were mild in the preserved spleen. But the production of antiplasmodium antibody and spleen uptake rate of 51Cr-RBC of the hemisplenic autotrans aplaned were rather lower than those of the shamoperate group. 2. Second lethal yoelli infection: in the mice of shamoperation of 2nd yoelii infection the parasitized erytrocyte was lower than that of shamoperated group, but the higher level antiplasmodium antibody and uptake rates of 51Cr-RBC of unit weight splenic tissue. CONCLUSIONS: Under the plasmodium infection preserved hemispleen alternate normal spleen to play the immunologic role, splenic tissue autotransplantation can fairly restore the partial function of spleen. Different preserved spleen method is a useful operation for clinic.

Animals↗