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1% of patients with P. falciparum infection die of the disease; the mortality in non-immune travellers with untreated falciparum infection is significantly higher. The initial symptoms, which may be mild, may not be easy to recognize as being due to malaria. It is important that the possibility of falciparum malaria is considered in all cases of unexplained fever starting at any time between the seventh day of first possible exposure to malaria and three months or, rarely, later ; after the last possible exposure. Any individual who experiences a fever in this interval should immediately seek diagnosis and effective treatment, and inform medical personnel of the possible exposure to malaria infection. Early diagnosis and appropriate treatment can be life-saving. Falciparum malaria may be fatal if treatment is delayed beyond 24 hours. A blood sample should be examined for malaria parasites. If no parasites are found in the first blood film while there is clinical suspicion of malaria, a series of blood samples should be taken at 612-hour intervals and examined very carefully. Pregnant women, young children and elderly travellers are particularly at risk. Malaria in pregnant travellers increases the risk of maternal death, miscarriage, stillbirth and neonatal death. The forms of malaria caused by other Plasmodium species are less severe and rarely life-threatening. Chemoprophylaxis and treatment of falciparum malaria are becoming more difficult because P. falciparum is increasingly resistant to various antimalarial drugs. Chloroauine resistance of P. vivax is rare and was first reported in the late 1980s in Papua New Guinea and Indonesia. Focal "true" chloroquine resistance i.e. in patients with adequate blood levels at day of failure ; or prophylactic and or treatment failure have later also been observed in Brazil, Columbia, Ethiopia, Guatemala, Guyana, India, Myanmar, Peru, the Republic of Korea, Solomon Islands, Thailand and Turkey. P. malariae resistant to chloroquine has been reported from Indonesia.
The development of chloroquine as an antimalarial drug and the subsequent evolution of drug-resistant Plasmodium strains had major impacts on global public health in the 20th century. In P falciparum, the cause of the most lethal human malaria, chloroquine resistance . is linked to multiple mutations in PfCRT, a protein that likely functions as a transporter in the parasite's digestive vacuole membrane. Rapid diagnostic assays for PfCRT mutations are already employed as surveillance tools for drug resistance. Here, we review recent field studies that support the central role of PfCRT mutations in chloroquine resistance. These studies suggest chloroquine resistance arose in 4 distinct geographic foci and substantiate an important role of immunity in the outcomes of resistant infections after chloroquine treatment. P vivax, which also causes human malaria, appears to differ from P falciparum in its mecha nism of chloroquine resistance. Investigation of the resistance mechanisms and of the role of immunity in therapeutic outcomes will support new approaches to drugs that can take the place of chloroquine or augment its efficiency.
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Acknowledgements This research was supported by Grant Agency of the Czech Republic Grants No. 521 2002 04000 and 526 02 0293, and by the grant MSMT LN00B030. We thank Drs. I. Schubert Gatersleben, Germany ; , S. Knasmller Vienna, Austria ; and A. Mukherjee Calcutta, India ; for discussions and assistance with this manuscript.
The first phase of the largest MILCON project in Air Force history. The project ultimately demolishes the repaired homes and 1, 067 new twostory units are constructed in their place. The new units have an average of 77 more square feet than previous homes, and each unit has at least a one-car garage. All homes are expected to be at least 18 feet above sea level to ensure maximum protection from future damage, and all existing utilities -- natural gas, water, storm and sewer -- are replaced. The contract to build the homes will be awarded in mid-April, and the reconstruction is expected to take about two years.
Malaria parasite infection during pregnancy and at delivery in mother, placenta, and newborn: efficacy of chloroquine and mefloquine in rural malawi.
The first study included in the review evaluated the effectiveness of Fansidar compared to chloroquine with respect to parasite resistance. A quasi-experimental design was used. Chl9roquine was used as a control treatment due to the P. falciparum parasite's known resistance to it. A placebo was not used. Resistance to treatment was measured using a scale similar to one established by WHO, where minimal resistance is classified as RI, somewhat resistant as RII, and highly resistant as RIII. The results of the study indicated that parasites are much less resistant to Fansidar than to chloroquine Bloland et al., 1993 and amantadine.
Yield PFU ; Cell type No-drug control 15 mM NH4Cl % of control ; 5.0 mM chloroquine % of control.
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NaHCO3INa2CO3 50 mmol L, pH isotonic saline with bovine serum albumin PBS BSA ; contained 10 mmol of NaH2PO4 Na2HPO4, 150 mmol of NaC1, and 1 g of bovine serum albumin Cohn Fraction V powder; Sigma, Poole, U.K. ; per liter. Buffered pH 6.0 ; substrate for measurement of peroxidase contained, per liter, 0.2 mol of potassium acetate, 5 mmol of citric acid, 8.3 mmol of o-phenylenediamine, and 5.9 mmol of H202. All buffers contained 100 mg of thimerosal per liter as a preservative and were stored at 4# C. The wash-solution concentrate contained, per liter, 1.5 mol of NaCl and 5 ml of Tween-20 surfactant and was diluted 10fold before use. All solvents and buffer components were of high quality analytical grade ; and were obtained from Reidel-de Ha# n, Hanover, F.R.G. Horseradish peroxidase EC 1.11.1.7, Type VI ; , and some steroids see Table 1 ; were obtained from Sigma, Poole, Dorset, England. Estrone 3glucuronide sodium salt ; , estrone, and all other steroids were obtained from Steraloids, Wilton, NH. Estrone stock standard solution 18.5 mmol L in ethanol ; was stored at 4# C. Working standard solutions 37 to 1850 pmolJL ; were prepared in PBS BSA and stored at -20 # C. Antisera: Primary antiserum, rabbit anti-estrone 3-glucuronide-BSA R21 73 ; , was purchased from the Courtauld Institute of Steroid Biochemistry, University College, London. Donkey anti-rabbit IgG was supplied by Guildhay Antisera, Guildford, Surrey, U.K. The IgG fraction of the latter antiserum was purified before use 13 ; . Steroid-enzyme conjugate: Estrone 3-glucuronide was covalently linked to horseradish peroxidase EC 1.11.1.7 ; by the mixed anhydride method of Erlanger et al. 14 ; as modified by Dawson et al. 15 ; . The conjugate is stable for at least two years when stored in an equivolume mixture of phosphate-buffered saline and glycerol containing 1 mg of cytochrome c per milliliter, and working solutions 2 mg L ; may be stored for at least three months at 4# C without loss of enzymatic or immunological activity. Microtiter plates: We used only the inner 60 wells of 96well enzymoimmunoassay plates code no. 5390; Costar, Broadway, MA ; . Quality-control plasma: We used plasma, separated from three 500-ml units of blood which had low 200 pmol L ; endogenous estrone concentrations, to prepare three qualiCoating buffer was 9.6 ; . Phosphate-buffered.
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1.2. Health Center 1.2.1 Diagnosis At this level, diagnosis should be based on clinical assessment and microscopic examination of blood films. Patients referred from health posts and other sites and those with symptoms of severity or danger signs should get priority for microscopic diagnosis. As different drugs are used to treat malaria caused by different species, a microscopic examination of blood films should guide treatment. However, it should be noted that in some cases a blood slide may be negative even when the patient has malaria. Therefore, the health worker's judgment should dictate the decision to treat or not to treat the patient for malaria under such condition. On the other hand, malaria parasitaemia may not be the only cause of the presenting illness. Thus, the health worker has to treat the patient for malaria and then look for other causes of illness. 1.2.2 Treatment a ; First-line treatment The first-line treatment of P. falciparum malaria is artemether-lumefantrine administered 2 times a day for 3 days. For infants less than five kg of body weight and pregnant women, oral quinine administered 3 times a day for 7 days is the first line treatment. For the treatment of malaria caused due to P.vivax, P.malariae or P. ovale, the first-line drug of choice is chloroquine. In malaria-free areas and where compliance can be insured, in order to eliminate hypnozoite forms relapsing stages ; of P.vivax from the liver and to bring about radical cure, primaquine may be administered daily for 14 days starting after chloroquine treatment is completed. However, in malarious areas where there is a high risk of re-infection, and where the main purpose of treatment should be to bring about clinical cure rather than radical cure, administration of primaquine is not recommended. See Annex IIe for primaquine dosage according to age and body weight. b ; Second-line treatment If a P. falciparum positive patient returns back to facility with fever or history of fever between the 4th day and 14th day after treatment with ArtemetherLumefantrine, do blood examination for malaria parasites. In addition, ask the patient if he she has vomited the drug or had diarrhea after treatment. Check also whether the drug taken is of reliable brand and is not expired. If the blood film is positive for asexual malaria parasites and other conditions are excluded, administer oral quinine if condition of the patient permits.
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This feeding method is employed in five broad categories of patients- cerebrovascular disease, neurodegenerative conditions, malignancy primarily ropharyngeal oesophageal ; , dementia with anorexia and head injuries and parlodel.
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| Chloroquine tabsVERY HIGH RISK OF THERAPEUTIC FAILURE WITH CHLOROQUINE FOR UNCOMPLICATED PLASMODIUM FALCIPARUM AND P. VIVAX MALARIA IN INDONESIAN PAPUA.
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We wish thank to thank our funding agencies, FAPESP; CNPq, CAPES, PADC FCF; FINEP; FUNDUNESP, for financial support. List of abbreviations used 5-FC: 5-fluorocytosine 5-FU: ADEPT: antibody-directed enzyme prodrug therapy AN-10: butylidene dibutyrate apoL-I: apolopoprotein L1 BA: butyric acid CD-CS: recombinant fusion protein consisting of CS protein as a ligand and bacterial CD: cytosine deaminase CL: cutaneous leishmaniasis CMD-P: CpG ODN: CpG oligodeoxynucleotides CpG: a dinucleotide constituted by a cytosine followed by guanine separated by a phosphate CQ: chloroquine CS: malaria circunsporozoite DFMO: eflornithine DHA: dihydroartemisinin DHFR: dihydrofolate reductase DHFR-TS: dihydrofolate reductase thymidilate synthase dNTPs: deoxyribonucleotides DOXP: 1-deoxy-D-xylulose 5-phosphate EB: ethambutol ETA: ethionamide EthA: a flavin monooxygenase found to catalyze the Baeyer-Villiger reaction Et-NIPOx: ethyl ester of N-isopropyl oxamate fma: 2- N-formyl-N-methyl ; aminoethyl GI: gastrointestinal GR: glutathione reductase GSH: glutatione HADH-isozyme: -hydroxyacid dehydrogenase-isozyme HAT: Human African Trypanosomiasis Hb: hemoglobin Hb F: fetal hemoglobin Hb S: hemoglobin S HU: hydroxyurea INH: isoniazid and dilantin.
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Hope that the addition of neurotrophic factors provided by en bloc fetal spinal tissue might result in behavioral improvement. In the case of posttraumatic syringomyelia, outcomes that do not worsen over time, perhaps by inhibiting the progressive neural degeneration, are desirable. These trials demonstrated that the cells survived and some patients demonstrated improved recovery 44, 128, 143 ; . Implants into the gap composed of Schwann cells, which form the myelin in the peripheral nervous system in which regeneration does occur 22 ; , or multiple grafting of intracostal nerves 31 ; in rodent models of spinal injury are both approaches in which some regenerating nerve cell axons have been able to grow across the gap, but penetration into the host tissue was not impressive. Some functional recovery was demonstrated in both approaches. Clinical trials in which peripheral nerves are used as bridges are in progress at the University of Sao Paulo, and in Taiwan, where more than 20 patients have received nerve bridges : carecure tgers Lectures SCIHope. htm ; . Similarly, implanted olfactory ensheathing cells have been shown to align, migrate long distances, and promote functional recovery and regeneration through the lesion site in rodents 106 ; . Human neural progenitor cells and embryonic stem cells have been used in rodent spinal injury models and have demonstrated functional recovery 86, 154 ; . Although considerable work in the field of stem cell biology remains 147 ; , there are some clinical trials in Russia in which fetal stem cells are used as transplant sources for chronic SCI or in combination with olfactory ensheathing glial cells. Other transplant sources include transposition of the omentum Cuba, China, and Italy ; and transplantation of embryonic shark cells in Tijuana, Mexico : carecure tgers Lecutres SCIHope ; . These latter two approaches lack support from both clinical practitioners and researchers in the United States and are generally thought to lack scientific merit. Advances in the field of biomatrix material have provided opportunities to bridge the gap with artificial material, such as biodegradable hydrogels or combinations of hydrogels and cells 22 ; , that may promote regeneration. Desired properties of a synthetic bridge are to provide simultaneously a physical substrate for axonal attachment and growth without triggering an and docusate and Cheap chloroquine online.
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RESULTS A total of 64 Cameroonian isolates were used to characterize the in vitro drug sensitivity pattern and analyze the pfmdr1 polymorphisms. The complete in vitro drug sensitivity pattern for chloroquine, quinine, mefloquine, halofantrine, and artemisinin derivatives was characterized for 31 clinical isolates. For 33 additional isolates, the in vitro response data were available for chloroquine and quinine. Of 64 isolates, 26 41% ; were chloroquine-sensitive geometric mean IC50 33.4 nM, range 14.661.1 nM ; , and 38 59% ; were chloroquine-resistant geometric mean 246 nM, range 111586 nM ; . All isolates were sensitive to quinine n 64; geometric IC50 166 nM, range 31.6591 nM ; , mefloquine n 31; geometric mean IC50 9.81 nM, range 2.9029.8 nM ; , and halofantrine n 31; geometric mean IC50 1.40 nM, range 0.5605.35 nM ; . The IC50 values for artemether n 8 ; , artesunate n 14 ; , and dihydroartemisinin n 9 ; ranged from 0.290 to 6.60 nM, with geometric means of 1.81 nM, 0.940 nM, and 1.07 nM, respectively. The IC50 values for individual isolates n 31 ; tested against the complete panel of antimalarial drugs are shown in Table 1. The in vitro responses between chloroquine and quinine r 0.407 ; , quinine and mefloquine r 0.405 ; , mefloquine and halofantrine r 0.704 ; , mefloquine and artemisinin derivatives r 0.368 ; , and halofantrine and artemisinin derivatives r 0.504 ; were significantly correlated P 0.05 ; . The majority of isolates displayed mutant codons Tyr-86 and Phe-184. Fifty-six of 64 isolates 88% ; carried the mutant codon Tyr-86, while seven 11% ; carried the wild-type codon Asn-86 and one had mixed codons. Fifty-eight of 64 had the mutant codon Phe-184, five had the wild-type codon Tyr-184, and one isolate no. 70 00 ; had mixed codons. The geometric mean IC50 values for chloroquine were 83.4 nM range 14.6279 nM ; in parasites carrying Asn-86 allele n 7 ; and 115.6 nM 20.8586 nM ; in those carrying Tyr-86 allele n 56; one mixed isolate was excluded from this analysis ; P 0.05 ; . Taken individually, Tyr-86 and Phe-184 were not associated with in vitro resistance to chloroquine P 0.05 ; . For quinine, the geometric mean IC50 values were 107 nM range 31.6369 nM ; in parasites with Asn-86 allele n 7 ; and and zometa.
Around one-third of persons with unipolar depression major depressive or dysthymic disorder ; receive treatment from a mental health professional each year Wang et al., 2005 ; . In addition, many other people in therapy experience depressed feelings as part of another disorder, such as an eating disorder, or in association with general problems that they are encountering in life.Thus much of the therapy being administered today is for unipolar depression. A variety of treatment approaches are currently in widespread use for unipolar depression.We shall look first at the psychological approaches, focusing on the psychodynamic, behavioral, and cognitive therapies. We will then turn to the sociocultural approaches, including a highly regarded intervention called interpersonal psychotherapy. Last, we will consider two effective biological approaches--electroconvulsive therapy and antidepressant drugs. In the process, it will become evident that unipolar patterns of depression are indeed among the most successfully treated of all psychological disorders.
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The forensic background of the FCNS is one that includes multidisciplinary teamwork and collaboration on a regular basis, with members of law enforcement, the criminal justice system, emergency departments, and other first responders. Forensic nurses are experts in the principles and practice of chain-of-custody. They are accustomed to troubleshooting gaps in knowledge and experience and at creative problem solving to achieve pragmatic solutions that can be tailored for an individual "fit." Likewise, the forensic experience crosses all geographical boundaries, i.e., urban, rural, state, regional, national, and global. Forensic investigations parallel the process of disease surveillance. Most forensic nurses are versed at working in highly stressful clinical situations; thus they understand the implications of catastrophic events on both staff and vulnerable populations. The forensic clinical nurse specialist should be able to draw on forensic experiences to plan and implement training modules, exercises and drills, and to develop just-intime training for exigent situations. Moreover, as a nurse, the FCNS can identify with, and better employ, creative solutions to the training of public health nursing personnel. Disaster Nursing, Forensic Nurse, Public Health Nursing.
Administered in a single dose. Paracetamol 30 mg kg body weight day ; was administered to all patients. The patients were followed on days 1, 2, 3, and 14 at either health centers or home. Parents whose children developed fever or required other medical attention between days 4 and 6 and between days 8 and 13 were strongly advised to return to the health care center. Clinical and parasitological examinations were performed during each follow-up visit. Likewise, each dose was administered under supervision during the visits. Patients were observed for at least 30 minutes. If vomiting occurred within 30 minutes, another dose was administered. Patients with repeated vomiting were excluded from the study and treated with parenteral quinine followed by oral quinine. Patients who failed to respond to the assigned drug were treated with oral quinine 25 mg kg body weight day for 5 days ; . Data interpretation. The lot quality assurance sampling LQAS ; method was used to calculate the sample size for studies between 1999 and 2001, which included the assessment of chloroquine.15 The sample size was calculated to be 63, with the confidence level 1- ; and power 1- ; set at 95% and 80%, respectively. The lower and upper limits for treatment failure rates were fixed at 12.5% i.e., acceptable therapeutic efficacy if failure rate is 12.5% ; and 25% i.e., unacceptable therapeutic efficacy if the failure rate is 25% ; , respectively. A major advantage of the LQAS method is that it allowed an early termination of the study if a high proportion of patients failed to respond to chloroquine. This ethical consideration was important for studies conducted in southern and central Cameroon, where previous studies have suggested that chloroquine is ineffective. In the studies on amodiaquine and sulfadoxine-pyrimethamine between 2002 and 2004, the minimum sample size was set at 50, with the anticipated prevalence of therapeutic failure of 15%, confidence level of 95%, and precision of the estimated prevalence of 10%.16 The expected prevalence of clinical failure was based on an earlier study.20 The clinical and parasitological response of each patient was classified according to the 2003 WHO protocol: 16 i ; early treatment failure ETF ; , danger signs or severe and complicated malaria on days 13 with positive smear, parasitemia on day 2 parasitemia on day 0, parasitemia on day 3 25% of parasitemia on day 0, or positive smear and fever on day 3; ii ; late clinical failure LCF ; , danger signs, or severe and complicated malaria on days 414 with positive smear, or positive smear and fever on days 414; iii ; late parasitological failure LPF ; , positive smear on day 14 without fever; and iv ; adequate clinical and parasitological response ACPR ; , negative smear on day 14, with or without fever. Results were expressed as the percentage of patients' response corresponding to one of the 4 possible responses. It is generally considered that failure rates ETF + LCF + LPF ; should be 15% for a drug to be a viable option. Drugs with failure rates 25% may be said to be ineffective. Such high failure rates are a strong indication for a change in drug policy. However, it must be emphasized that a single study performed at a sentinel site may not warrant a change in drug policy. A sufficient amount of clinical and parasitological data collected over several sites and over a period of time is required before a rational decision can be made. Part of the results on amodiaquine N 62 enrolled patients ; and sulfadoxine-pyrimethamine N 64 ; in Hvcam in 2001 was.
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In this sense, then, the refusal to accept particular information as `evidence' can be seen as an act of resistance. This suggests that there are no easy or value-free ways in which `evidence' can be defined separately from the context of its use. Such judgements involve a deployment of complex technical expertise and positional power dressed up in the guise of disinterested rationality. Despite such inevitably political concerns, many of the initiatives developed as part of reformed decision making processes seem to assume relatively unproblematic, rational and linear relationships between research, evidence and policy. Much effort has been expended on improving the supply of research: ensuring that the right questions get investigated; supporting rigorous synthesis of existing research studies; and providing for a degree of translation of research findings so that they are accessible both literally and intellectually. All of these have to some extent ramped up the availability of concise research-based evidence. However, supply alone is clearly insufficient, and attention has been given in parallel to the demand side. Encouraging the policy demand for research evidence has also been a central feature of reformed processes. Departmental spending bids are now required to be supported by evidence, and the evidence underpinning key policy decisions is increasingly being cited and published. Moreover, staff training and support for evidence use has received much greater attention than hitherto; and the expectation that policies and programmes will be piloted and evaluated is now increasingly the norm. Formal evaluation of these ways of increasing the demand for evidence is rather thin on the ground but nonetheless some positive experiences are reported.
1. Bloland PB, Lackritz EM, Kazembe PN, Were JBO, Steketee R, Campbell CC, 1993. Beyond chloroquine: implications of drug resistance for evaluating malaria therapy efficacy and treatment policy in Africa. J Infect Dis 167: 932937. 2. Trape JF, Pison G, Preziosi MP, Enel C, Desgrees du Lou A, Delaunay V, Samb B, Lagarde E, Molez JF, Simondon F, 1998. Impact of chloroquine resistance on malaria mortality. C R Acad Sci Paris Serie III 321: 689697. 3. Charmot G, Amat-Roze JM, Rodhain F, Le Bras J, Coulaud JP, 1991. Abord geographique de l'epidemiologie de la chloro quino-resistance de Plasmodium falciparum en Afrique trop icale. Ann Soc Belge Med Trop 71: 187197. 4. Sokhna C, Molez JF, Ndiaye P, Sane B, Trape JF, 1997. Tests in vivo de chimiosensibilite de Plasmodium falciparum a la chlo ` roquine au Senegal: evolution de la resistance et estimation de l'efficacite therapeutique. Bull Soc Pathol Exot 90: 8389. 5. Mtango FDE, Neuvians D, 1986. Acute respiratory infections in children under five years. Control project in Bagamoyo District, Tanzania. Trans R Soc Trop Med Hyg 80: 851858. 6. Kilama WL, Kihamia CM, 1991. Malaria. Mwaluko GMP, Kilama WL, Mandara MP, Muru M, Macpherson CNL, eds. Health and Disease in Tanzania. London: Harper Collins Academic, 117132. 7. Premji Z, Ndayanga P, Shiff C, Minjas J, Lubega P, MacLeod J, 1997. Community based studies on childhood mortality in a malaria holoendemic area on the Tanzanian coast. Acta Trop 63: 101109. 8. Khoromana CO, Campbell CC, Wirima JJ, Heyman DL, 1986. In vivo efficacy of chloroquine treatment for Plasmodium falciparum in Malawian children under five years of age. J Trop Med Hyg 35: 465471. 9. Overbosch D, Vandenwall Bake AWL, Stuiver PC, Van der Kay HJ, 1984. Chloroquine-resistant falciparum malaria from Malawi. Trop Geogr Med 36: 7172. 10. Fogh S, Jepsen S, Mataya RH, 1984. R-III chloroquine-resistant Plasmodium falciparum malaria from northern Malawi. Trans R Soc Trop Med Hyg 78: 282. 11. Kihamia CM, Gill HS, 1982. Chloroquine-resistant falciparum malaria in semi-immune native African Tanzanians. Lancet 2: 43. 12. Schwartz IK, Campbell CC, Payne E, Khatib OJ, 1983. In vivo and in vitro assessment of chloroquine-resistant Plasmodium falciparum malaria in Zanzibar. Lancet 2: 10031005. 13. Greenberg AE, Ntumbanzondo M, Ntula N, Mawa L, Howell J, Davichi F, 1989. Hospital-based surveillance of malariarelated paediatric morbidity and mortality in Kinshasa, Zaire. Bull World Health Organ 67: 189196. 14. Nguyen-Dinh P, Schwartz IK, Sexton JD, Bomboto, Egumb, Botomwito B, Kalisa R, Ngimbi NP, Wery M, 1985. In vivo and in vitro susceptibility to chloroquine of Plasmodium falciparum in Kinshasa and Mbuji-Mayi, Zaire. Bull World Health Organ 63: 325330. 15. Ngimbi NP, Wery M, Henry MC, Mulumba MP, 1985. Reponse in vivo a la chloroquine au cours du traitement du paludisme ` a Plasmodium falciparum en region suburbaine de Kinshasa, ` Zaire. Ann Soc Belge Med Trop 65 suppl 2 ; : 123135. 16. Paluku KM, Breman JG, Moore M, Ngimbi NP, Sexton JD, Roy J, Steketee RW, Weinman JM, Kalisa-Ruti, Mambu ma-Disu, 1988. Response of children with Plasmodium falciparum to chloroquine and development of a national malaria treatment policy in Zaire. Trans R Soc Trop Med Hyg 82: 353357. 17. Nguyen-Dinh P, Greenberg AE, Kabote N, Davachi F, Groussard B, Embonga B, 1987. Plasmodium falciparum in Kinshasa, Zaire: in vitro drug susceptibility studies. J Trop Med Hyg 37: 217219. 18. Carme B, Moudzeo H, Mbitsi A, Sathounkasi C, Ndounga O, Brandicourt F, Gay F, Le Bras J, Gentilini M, 1990. La resis tance de Plasmodium falciparum au Congo. Bilan des enque tes realisees de 1985 a 1989. Bull Soc Pathol Exot 83: 228 ` 241. 19. Carme B, Yombi B, Bouquety JC, Plassard H, Nzingoula S, Senga J, Akani I, 1992. Child morbidity and mortality due to.
Introduction Vhloroquine CHQ ; , primaquine PRQ ; and amodiaquine AMQ ; are the quinoline derivatives used in medicine as antimalarial drugs Henry, 1973 ; . CHQ is the most commonly used antimalarial drug at present in different parts of the world. CHQ is reported to induce teratogenic effects in rats Sharma and Rawat, 1989 ; . It is deposited in tissues and can cross the placenta McChesney and McAnliff, 1961; McChesney et al., 1967; Linquist, 1973 ; . CHQ forms intercalated complexes with DNA Cohen.S.N. and Yielding, 1965; Sternglanz etal., 1969; Waring, 1970 ; and acts as an inhibitor of DNA synthesis and repair Yielding et al., 1970; Wichard et al, 1972; Michael and William, 1974; Field et al., 1978 ; . PRQ has a limited use because of its toxic effects. PRQ is known to produce methemoglobinaemia Cohen.R.J. et al., 1986 ; and to cause acute haemolysis in patients deficient in glucose 6-phosphate dehydrogenase Reever et al., 1992 ; . AMQ has an action similar to CHQ. It is as effective as CHQ against CHQsensitive and some CHQ-resistant strains of Plasmodium falciparum. CHQ and PRQ have been reported to be weakly mutagenic in Salmonella typhimurium Ames and Whitfield, 1966; ObaseikiEbor and Obasi, 1986; Marrs et al., 1987; Thomas et al., 1987 ; and in Bacillus subtilis Kadotani et al., 1984 ; . Mutagenic effects of CHQ were also reported in Salmonella strains using the fluctuation assay by Schupbach 1979 ; and Cortinas de Nava et al. 1983 ; and in strains TA1537, TA1538, TA98 and TA100 by Espinosa-Aguirre et al. 1989 ; . Marrs et al. 1987 ; observed weak mutagenic effects of PRQ in TA1537 with or without S9 and no mutagenic effects in TA100, regardless of the presence or absence of S9. PRQ was reported.
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