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

In 1989 there were 71 cases of imported malaria admitted to the hospital in Bordeaux. This is 16.5% and 29% lower than in 1988 and 1987 respectively, thanks to the widespread use in Africa of mefloquine chemoprophylaxis. Sub-Saharan Africa is involved in 95% of cases, mainly West Africa (70% of cases), unlike the situation in 1987, and the first cases of paludism despite mefloquine chemoprophylaxis appeared during the second semester from the seasonal mid-summer recrudescence onwards, in travellers returning from this region. The most frequent species is still Plasmodium falciparum (80% of declared cases). This imported disease especially affects young adults despite regular prophylaxis in 59% of cases. It is therefore important to recommend rigorous protection against anopheles. Male predominance (sex ratio: 5.5) was greater in 1989 than in the previous two years, and French nationals represented 85% of the population. Falciparum malaria presents symptoms in 95% of cases before the end of the month following the patient's return to France, while for P. ovale the time for symptoms to appear is between 39 days and two years after return. Management of patients on their return poses a problem of information, since in 40% of cases diagnosis is made more than a week after the first symptoms. Attacks are mild in most cases (93%); among the serious cases death occurred in a 3-year-old child. Thrombopenia is the most frequent biological sign (22.5% of cases), followed to a lesser degree by anaemia and leukopenia. Mild attacks respond well to classical treatment (halofantrine, mefloquine, quinine, chloroquine), while two cases of more complicated symptoms required exchange transfusion.
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PMID:[Imported malaria in Bordeaux in 1989. Epidemiologic, clinical and therapeutic study of 71 cases]. 208 18

From 1986 until 1988 chloroquine sensitivity of Plasmodium falciparum malaria was monitored in 515 hospital patients in Nchelenge district, northeastern Zambia. After treatment with chloroquine 30 mg base/kg, bloodslides were examined on day 2, 4, 6 and 7. The overall resistance rate was 21.4%, of which 29% was R1-, 30% R2-, 18% R3- and 23% R2-3 resistance. Resistance rates were negatively correlated with age and positively with the initial parasitemia. It is suggested that in vivo tests of chloroquine sensitivity also reflect the host's immune status for malaria. In rural areas with chloroquine resistance in vivo testing should be performed on all malaria patients.
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PMID:Chloroquine-resistant Plasmodium falciparum malaria at Nchelenge, northeastern Zambia. Follow-up on 515 hospital patients. 210 73

59 cases of Plasmodium falciparum malaria fever occurring in non-immune Caucasian subjects having got a correct chemoprophylaxis by chloroquine were treated by halofantrine (HALFAN). They were given 1500 mg divided in 3 doses of 500 mg every 6 hours from D1 to D8. All them were back from a malarial highly endemic zone with chloroquine resistance. Analysis of the main biological and clinical efficiency parameters displayed very satisfactory results: disappearances of fever (mean 22 H) and parasitemia (mean 36 H) are short. After two months of monitoring, no malaria recrudescence was noted. With an efficacy of 10 p.c. associated to a noticeable clinical and biological tolerance Halofantrine is a first-class treatment of chloroquine resistant malaria fever.
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PMID:[The treatment of imported Plasmodium falciparum malaria with halofantrine. Apropos of 59 case reports (corrected and republished article orginally printed in Med Trop (Mars) 1990 Jan-Mar;50(1):113-7)]. 210 May 12

Falciparum malaria cannot be eradicated from sub-Saharan Africa with present technology. The mainstay of malaria control in this situation is treatment of fever cases with chloroquine, aiming principally at reduction of mortality. The efficacy of this policy is now endangered because of the appearance and spread of chloroquine-resistance on the African continent. The present review examines laboratory and field research on the resistance of African P.falciparum to chloroquine, amodiaquine, pyrimethamine, proguanil, chlorproguanil and the combination sulfadoxine-pyrimethamine. Drug-resistance in malaria may be assessed with in vivo and in vitro technology. In vivo tests are simple, but the results are difficult to compare because of the influence of immunity. In vitro tests provide a more precise epidemiological tool, but their analysis should be undertaken with consideration of their technical limitations. For parasitological, immunological and epidemiological reasons, a one-to-one correlation between in vivo and in vivo grading of resistance is usually not found. Extended in vivo tests may be at least as sensitive as in vitro tests for detecting rare resistant parasites. On the other hand, the standardized grading of higher levels of in vivo resistance is arbitrary, and it is doubtful, whether such distinction has any clinical relevance. The 4-aminoquinolines (chloroquine and amodiaquine) presumably act by interfering with vital functions in the acid vesicles of parasites. Recent experiments indicate that resistance may be related to an increased rate of efflux of chloroquine from the parasite. It is caused by mutation, and at least three genetic levels of resistance have been identified. The blood stages of resistant plasmodia seem to have a biological advantage over sensitive ones, an observation that raises some hitherto unanswered questions. In the 1970s, a low degree of resistance to chloroquine was found in African P. falciparum in several localities. Resistance to the standard dose of chloroquine of 25 mg/kg was found in 1978 in tourists, who had sojourned in Kenya and Tanzania. Since then, chloroquine-resistance has spread centrifugally with increasing rapidity from an original focus in Northern Tanzania or Southern Kenya. The rate of increase in the proportion of resistant infections has generally been more rapid in the areas, where resistance has been introduced recently than in the original epifocus. The rate of increase is also generally more rapid in urban than in rural areas, an observation that can be ascribed to differences in drug pressure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The resistance of falciparum malaria in Africa to 4-aminoquinolines and antifolates. 210 Aug 81

With an increasing movement towards cost saving in the health sector, preventive medicine must also be judged according to its economic viability. The fact that prevention can autofinance itself is suggested by the results of a cost/benefit analysis of chemoprophylaxis of Falciparum malaria with Mefloquin among travellers in Kenya. Out of the whole group of travellers analysed by means of an interview-based test (Malpro-Study), the costs in the case of both Switzerland and the Federal German Republic were lower for those people who had undergone Mefloquin-prophylaxis than for those who had not. In this way the prophylaxis not only compensates the required outlay but also results in an overall benefit in macroeconomic terms. Therefore economically based opposition to the prophylaxis of malaria with Mefloquin for short stays in high-risk countries is not justified.
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PMID:[Cost-benefit analysis of malaria prophylaxis with mefloquine in travelers to Kenya]. 212 79

1. Anopheles arabiensis Patton and An. funestus Giles were identified as vectors of Plasmodium falciparum malaria in the Mwea-Tebere irrigation scheme, Kenya. An. arabiensis was the only member of the An. gambiae complex identified from chromosome characteristics. Other Anopheles species found included An. pharoensis Theobald, An. rufipes Gough and An. coustani Laveran. Survival rates per gonotrophic cycle for An. arabiensis averaged 0.37 during the short rains (October-November), 0.49 during the dry season (February) and 0.78 during the long rains (May-June). Vectorial capacities were correspondingly low due to low survival rates and a high degree of zoophily. The average duration of infective life for P. falciparum was 0.2 days for both An. arabiensis and An. funestus. In contrast, entomological inoculation rates were comparatively high: 6-8 infective bites/man/month. An. pharoensis averaged 110 bites/man/night during the short rains; 1/999 (0.1%) was positive by ELISA for P. falciparum circumsporozoite antigen, but the ELISA evidence is not conclusive for vector incrimination. In correspondence with clinical observations, the transmission of P. malariae and P. ovale is unlikely due to the low vector survival rates. The observed anomaly between low vectorial capacities and high entomological inoculation rates demonstrates the importance of accurately estimating vector sporozoite rates to monitor unstable malaria transmission in irrigated areas.
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PMID:Malaria transmission potential of Anopheles mosquitoes in the Mwea-Tebere irrigation scheme, Kenya. 213 10

Peripheral blood lymphocytes from healthy, Epstein-Barr virus (EB-virus)-seropositive donors and from patients with acute Plasmodium falciparum malaria were tested for their cytotoxicity towards autologous EB-virus-infected B-cells using an in vitro regression assay. Of the 18 cultures from control donors, 88.8% showed the normal pattern of regression. Of the 20 malaria patients in the study, 40% failed to exhibit the normal pattern observed in the control group. Analysis of the lymphocyte subsets showed a high incidence of inverted CD4:CD8 ratios in the patient group due to an absolute rise in the CD8 population. This data suggests that the immunosuppressive effects of acute malaria extend to defective control over EB-virus. The relevance of the observations to the aetiology of EB-virus-associated, endemic Burkitt's lymphoma (eBL) is discussed.
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PMID:In vitro analysis of Epstein-Barr virus: host balance in patients with acute Plasmodium falciparum malaria. I. Defective T-cell control. 216 84

Serum antibody response to plasmodial antigens was investigated in 97 Thai patients with Plasmodium falciparum malaria. No difference in immunoglobulin G (IgG) antibody levels was detected between groups without or with cerebral manifestations of malaria (n = 40). In patients with the most severe form of the disease, i.e., those who died despite adequate therapy (n = 12), antibody detected in the immunofluorescent-antibody test was found at lower levels than in those who recovered (geometric means: IgG = 1/420 versus 1/3,800; IgM = 1/15 versus 1/70); similarly, precipitating malarial antibodies were present in only 1 of these 12 patients, while they were detectable in 65 of the remaining 85 patients (76.5%). In contrast, anticytomegalovirus antibody levels were similar in the different groups of patients. Results show that depression of antibody response may extend to antiplasmodial responses during severe malaria. The link between fatality and a low level of antibody production suggests that an appropriate immune response to malarial antigens may be required to achieve recovery with drug treatment and provides a new direction for malaria therapy research.
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PMID:Impairment of Plasmodium falciparum-specific antibody response in severe malaria. 217 59

To determine splenic Fc receptor function in patients with acute Plasmodium falciparum malaria, the clearance of IgG-coated autologous 51Cr-labeled erythrocytes in 20 patients and 10 normal controls was studied. Clearance half-times were directly correlated with both the absolute parasite count (r = .635, P less than .005) and hematocrit (r = .791, P less than .001). Clearance half-times in patients varied from 1.0 to 96.3 h (median, 14.8 h) while those of controls ranged from 8.0 to 80.3 h (median, 23.1 h) (P = .10). Nine of the 20 patients had clearance half-times shorter than the lower 95% confidence limit of controls (less than 12.4 h). The clearance of IgG-coated erythrocytes was accelerated after parasites were eliminated from the circulation (P less than .05) and returned toward normal 6-8 weeks after the acute infection. Although circulating immune complexes were detectable, there was no correlation between immune complex levels and clearance half-times (P greater than .05). The failure to increase Fc receptor-mediated red cell clearance in patients with high parasitemias suggests inadequate splenic phagocytic activity in the face of considerable antigenic challenge. These findings indicate that splenic Fc receptor function may be important both in the control of infection and the development of anemia in P. falciparum malaria.
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PMID:Splenic Fc receptor function in host defense and anemia in acute Plasmodium falciparum malaria. 217 26

A 24-year-old man with severe Plasmodium falciparum malaria died after 77 h of treatment with full parenteral doses of quinine. His peripheral parasitemia at death exceeded the level on admission. Plasma concentrations of quinine were abnormally low throughout. This case emphasizes the importance of pharmacokinetic factors in determining the therapeutic response in severe P. falciparum malaria.
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PMID:Fatal Plasmodium falciparum malaria after an inadequate response to quinine treatment. 217 27


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