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PubMed1992

World malaria situation 1990. Division of Control of Tropical Diseases. World Health Organization, Geneva.

Malaria risk of varying degree exists in 99 countries or areas. However, falciparum malaria does not exist or its relative prevalence is less than 1% in 13 of these countries. Accurate information on the global incidence of malaria is difficult to obtain because reporting is particularly incomplete in areas known to be highly endemic. The global incidence of malaria is estimated to be nearly 120 million clinical cases each year, with nearly 300 million people carrying the parasite. 90% of the total number of cases reported annually to WHO are from 19 countries only. This does not include the WHO African Region where reporting of cases remains fragmentary and irregular despite improvements in recent years. Some 75% of cases are concentrated in 9 countries (in decreasing order): India, Brazil, Afghanistan, Sri Lanka, Thailand, Indonesia, Viet Nam, Cambodia and China. Furthermore, within these countries malaria is concentrated in certain areas. Of a total world population of about 5.3 billion people, 3.1 billion (59%) live in areas free of malaria (it never existed, disappeared or was eliminated by antimalaria campaigns and the malaria-free status has been maintained). 1.7 billion people (32%) live in areas where endemic malaria was considerably reduced or even eliminated but transmission was reinstated and the situation is unstable or deteriorating. These latter areas include zones with the most severe malaria problems which developed following major ecological or social changes, such as agricultural or other economic exploitation of jungle areas, sociopolitical unrest, etc.; these zones comprise only about 1% of the world population. Areas where endemic malaria remains basically unchanged, and no national antimalaria programme was ever implemented, are inhabited by 500 million people (9%), mainly in tropical Africa. Severe malaria and mortality are caused by Plasmodium falciparum which is the predominant species of malaria in tropical Africa. In the rest of the world it is far less common. WHO receives very limited and irregular reports on malaria deaths. The vast majority of malaria deaths occur in Africa; estimates vary greatly: a figure of 800,000 deaths per year in African children has been quoted in 1991 by the WHO African Region. There are indications that mortality in children has fallen in some areas because of the widespread use of antimalarials, of social development and of better education. Countries in tropical Africa are estimated to have more than 80% of all clinical cases and more than 90% of all parasite carriers.(ABSTRACT TRUNCATED AT 400 WORDS)

Africa↗
PubMed1992

Altered plasma lipid pattern in falciparum malaria.

Plasma levels of HDL, LDL, total cholesterol and triglycerides were measured in 60 patients with falciparum malaria (37 severe cases and 23 mild) and in 83 healthy individuals, to study malaria-induced changes in plasma lipids. Triglyceride levels were lower in the patients than in the controls but the difference was significant only for those with severe malaria (P < 0.001). In contrast, the levels of all the other plasma lipids were significantly higher (P < 0.001) in those with severe malaria than in those with mild malaria, and in the mild malaria cases compared with the controls. Initially LDL cholesterol was estimated by the Friedwald formula, but this gave negative values in a few cases of severe malaria. Plasma lipoproteins were therefore also measured by nephelometry; the estimated levels of S particles, corresponding to LDL, were then found to be lower in all malaria cases than in the controls (P < 0.001) but never negative. Interestingly, levels of L particles in the patients with severe malaria were significantly elevated compared with the other patients and controls (P < 0.001), indicating impaired metabolism of chylomicrons. Plasma albumin, considered a negative acute phase protein (i.e. its level decreases as a consequence of the acute phase response), was reduced significantly and was directly correlated to HDL cholesterol levels (r = 0.715 and r = 0.895, respectively) in both mild and severe malaria. Follow-up of 22 of the severe malaria cases three weeks after treatment indicated that, while triglycerides had returned to similar levels to those in the controls, total cholesterol levels were still elevated and could give misleading results if lipid profiles were used, immediately after malaria infection, to assess an individual's risk of developing atherosclerosis.

Cholesterol↗
PubMed1992

The importance of T cell homing and the spleen in reaching a balance between malaria immunity and immunopathology: the moulding of immunity by early exposure to cross-reactive organisms.

It takes a number of years to develop clinical immunity to malaria and malaria pathology is also most evident a number of years after birth. T cells are known to play an important role in defence from malaria parasites but may also contribute to the disease symptoms associated with malaria. T cells which react against malaria parasites have arisen through stimulation with organisms which cross-react with malaria or through exposure to the malaria parasites themselves and express a memory phenotype (CD45Ro+, CD45Ra-, CD4+). T clones which have arisen through exposure to cross-reactive organisms may be expected to home to the tissues where initial exposure occurred as determined by tissue-specific adhesion molecules on the lymphocyte surface. Such tissues may not be appropriate to parasite killing and localization of T cells in such sites may contribute to the immunopathology of malaria. The sharp increase in immunity and decline in pathology observed in later childhood in malaria endemic areas may result from an increase in the number of T cells induced by the parasite itself (as opposed to cross-reactive organisms). Such T cells may not have a preferential trafficking to other organs and may be more likely to circulate through the spleen. Splenic changes may also allow more malaria-specific T cells to concentrate in the spleen and may facilitate interactions between T cells, monocytes, neutrophils and parasites resulting in parasite death. Whereas cytokines secreted by parasite-reactive T cells in all locations may contribute to cerebral malaria and other forms of pathology, cytokines in the spleen at least, should directly contribute to parasite death.

Age Factors↗
PubMed1992

Artemether in the treatment of multiple drug resistant falciparum malaria.

Artemether has the potential to be an alternative antimalarial for multiple drug resistant falciparum malaria. However, it has been associated with high recrudescent rates which may be due to incorrect dosage regimens. The dosage regimens are varied from country to contry. We have carried out a comparative study of two dosage regimens, ie 480 mg and 600 mg total dose given over 5 days in uncomplicated and severe falciparum malaria. 167 patients were included in the study, 61 with acute uncomplicated falciparum malaria and 106 with severe malaria. All patients showed a good initial response. The difference in total dose had no effect on the parasite or fever clearance time (PCT or FCT). However, the severity of the disease did have some influence of these times. The PCT and FCT from either regimen of uncomplicated malaria were significantly faster than those of severe malaria (p < 0.005 and = 0.05, respectively). The cure rate seems to have some correlation with the amount of drug given and severity of the disease. The cure rates in uncomplicated malaria were 84 and 92%, respectively, for 480 mg and 600 mg. In severe malaria the cure rates dropped to 65 and 76%, respectively, for 480 and 600 mg. We conclude that artemether can be considered as an alternative antimalarial for multiple drug resistant falciparum malaria. However, the cure rate of severe falciparum malaria in this study is not considered satisfactory in areas with multiple drug resistant falciparum malaria. Further studies are needed to assess the curative efficacy with different dosage regimens.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2026

Malaria driven mechanisms shaping cancer risk and aggressiveness in African populations.

Malaria and cancer represent intersecting public health challenges in sub-Saharan Africa, where malaria remains endemic and cancer incidence is rapidly increasing. Emerging evidence indicates that chronic or recurrent malaria infection may influence carcinogenesis and tumour aggressiveness through complex biological mechanisms. This narrative review critically synthesizes data from PubMed, Scopus, and Web of Science to elucidate the mechanistic intersections between malaria and cancer risk, progression, and therapeutic response. The review highlights five principal axes linking malaria to oncogenesis: malaria-induced oxidative stress and chronic inflammation driving genomic instability; gut microbiome dysbiosis altering systemic immunity and tumour microenvironment; exploitation of shared molecular targets such as the endothelial protein C receptor (EPCR) and oncofetal chondroitin sulfate by Plasmodium parasites and cancer cells; cooperative interactions between malaria and oncogenic viruses like Epstein-Barr virus in lymphomagenesis; and malaria-associated vitamin D deficiency impairing immune surveillance. Furthermore, pharmacological evidence reveals that several antimalarial agents, including artemisinin derivatives, chloroquine, and quinacrine, possess anticancer properties, while some anticancer drugs exhibit antimalarial activity, underscoring opportunities for dual-action or repurposed therapeutics. The convergence of malaria and cancer biology underscores the urgent need for integrative, multidisciplinary research spanning molecular epidemiology, immunology, and pharmacology. Unveiling these mechanisms may unveil novel biomarkers and therapeutic targets, guiding context-specific interventions to reduce the disproportionate cancer burden in malaria-endemic African populations.

Humans↗
PubMed1992

Malaria in a rural area of eastern Thailand: baseline epidemiological studies at Bo Thong.

Malaria is still a serious health problem in Thailand. Present attempts at controlling the disease by drug treatment and other means remain unsatisfactory. Thus, development of vaccination against malaria is a major research goal of malaria immunology. The objective of this study was to acquire epidemiological base line data for subsequent vaccine trials. A cross-sectional descriptive survey was conducted among 253 local inhabitants during the beginning of the transmission season in July 1989 at Bo Thong District, Chonburi Province, Eastern Thailand where malaria transmission was likely to be moderately high. Following the cross-sectional survey weekly morbidity surveillance was started to detect new cases of malaria by using active and passive case detection at the district hospital, local health centers and at neighboring malaria clinics. Fifty-four percent of the population were male and forty-six percent female: nearly a half (48.3%) were under the age of 15 and 17% under the age of 5 years. Eighty percent of the adults were married. Seventy percent of the subjects interviewed gave a history of malarial illness in the past. Malaria, malnutrition, anemia abnormal hemoglobin diseases and parasitic infestations were the main health problems in the study area. The annual parasite incidence of malaria was 169.4/1,000 population and 77% of parasitemic individuals were asymptomatic, indicating the existence of a semi-immune condition among these subjects. Antibody level to crude parasite antigen increased with age. It is hoped that the information obtained from these field studies may be useful in malaria vaccine trials in the near future.

Adolescent↗
PubMed1976

Seroepidemiologic investigations of malaria in Guyana.

The results of longitudinal seroepidemiologic malaria surveys with the indirect haemagglutination test in four sectors in the interior of Guyana did not suggest recent malaria transmission. Indigenous malaria cases had not been detected in these sectors since 1968 but malaria surveillance here had been incomplete. The multi-stage cluster sampling method used proved to be efficient and permitted the survey of a large and sparsely populated area to be concentrated in relatively few localities. Observation of a group of 147 seropositive and seronegative persons after one year showed a four-fold or greater decline of antibody titres in five per cent of the cohort population and no such titre increases were seen, thus confirming the absence of recent malaria infections. Seropositivity rates were higher in persons with a history of malaria than in those without such a history. Collecting blood on filter paper facilitated obtaining material for serologic testing especially in the younger age group and no refusals were encountered. This advantage compensates for the slight loss in sensitivity when filter paper eluates are titrated instead of sera. The difference between the past infection probabilities of the age groups over and under 20 years old suggests that the disappearance of malaria from the interior was related more to the elimination of malaria transmission along the coast than to the specific malaria campaign in the interior.

Adolescent↗
PubMed1992

Neurological complications of malaria.

This paper reviews the neurological complications of malaria. Cerebral malaria, the acute encephalopathy which complicates exclusively the infection by Plasmodium falciparum commonly affects children and adolescents in hyperendemic areas. Plugging of cerebral capillaries and venules by clumped, parasitized red blood cells causing blood sludging in the capillary circulation is one hypothesis to explain its pathogenesis. The other is a humoral hypothesis which proposes a nonspecific, immune-mediated, inflammatory response with release of vasoactive substances capable of producing endothelial damage and alterations of permeability. Cerebral malaria has a mortality rate up to 50%, and also a considerable longterm morbidity, particularly in children. Hypoglycemia, largely in patients treated with quinine, may complicate the cerebral symptomatology. Other central nervous manifestations of malaria include intracranial hemorrhage, cerebral arterial occlusion, and transient extrapyramidal and neuropsychiatric manifestations. A self-limiting, isolated cerebellar ataxia, presumably caused by immunological mechanisms, in patients recovering from falciparum malaria has been recognized in Sri Lanka. Malaria is a common cause of febrile seizures in the tropics, and it also contributes to the development of epilepsy in later life. Several reports of spinal cord and peripheral nerve involvement are also available. A transient muscle paralysis resembling periodic paralysis during febrile episodes of malaria has been described in some patients. The pathogenesis of these neurological manifestations in malaria remains unexplored, but offers excellent perspectives for research at clinical as well as experimental level.

Adolescent↗
PubMed1992

Pathology of fatal and resolving Plasmodium berghei cerebral malaria in mice.

CBA/T6 and Balb/c mice inoculated with Plasmodium berghei ANKA strain (PbA) died from cerebral malaria 6-8 days post-inoculation. DBA/2J mice similarly inoculated developed a non-fatal cerebral malaria, with mild temporary cerebral symptoms, and died between days 15 and 22 from other malaria-related complications. When inoculated with P. berghei K173 (Pb) these mouse strains did not develop a cerebral malaria but died between days 15 and 22 from other malaria-related complications. These mouse strain/parasite strain combinations allow for detailed examination of factors critical in the pathology of murine cerebral malaria. Monastral Blue, a colloid dye, when injected intravascularly between days 0 and 2 into PbA-inoculated CBA (PbA-CBA) or Balb/c (PbA-Balb/c) mice prevented death from cerebral malaria. There was no evidence of increased vascular permeability at this stage. When Monastral Blue was injected between days 5 and 8, there was increased vascular permeability in the kidney, liver, lung, spleen and brain of PbA-CBA and PbA-Balb/c mice. Injection of Monastral Blue into these animals at this time also precipitated cerebral symptoms and death, but not in Pb-infected mice. Endothelial and mononuclear cells phagocytosed, and were coated with, the Monastral Blue particles when the dye was injected between days 5 and 8 into PbA-CBA and PbA-Balb/c mice. Control, uninfected mice did not demonstrate either of these features. Pb-infected mice only demonstrated coated mononuclear cells. Mononuclear cell attachment to the endothelium, increased vascular permeability and increased association of Monastral Blue particles with monocytes and endothelial cells were correlated with cerebral symptoms and death. Monastral Blue is thus a useful agent for studying the roles of mononuclear cells and endothelium in murine cerebral malaria.

Animals↗
PubMed1977

Malaria in the Republic of the Philippines. A review.

Malaria in the Republic of the Philippines is caused principally by P. falciparum and P. vivax, with the former as predominant species. P. malariae is occasionally reported, while P. ovale is very rare and has been reported only in the island of Palawan. Malaria is widespread in distribution with prevalence varying from one area to the other. In 1970, the malaria morbidity rate was reported to be 77.6 per 100,000 while the mortality rate was 1.8 per 100,000. Case detection activities revealed that, in 1973, the slide parasite rate was 7.2%, the annual parasite index was 6.1% and the annual blood examination rate was 8.4%. The principal vector of malaria in the Philippines is An. minimus flavirostris which breeds in clear, fresh-water streams in foothills and mountain slopes. An. mangyanus and An. maculatus appear to play a secondary role. The vectorial capacity of the former appears to be confined only where conditions are primitive, while the latter is associated with malaria transmission in high altitudes. In the absence of fresh-water streams, the salt-water breeder mosquito, An. litoralis, assumes the vectorial role. The epidemiology of malaria in the Philippines is discussed. Emergence of strains of P. falciparum with diminished sensitivity to the commonly used antimalarial drugs is reported in Palawan and Rizal provinces. The development of malaria control activities in the Philippines are presented. As of 1972, Cagayan Valley, Palawan, Mindoro, Sulu and circumscribed areas in Mindanao are still considered hard-core malarious areas with on-going persistent transmission.

Animals↗
PubMed1992

Malaria epidemic in Baniyani village, District Farrukhabad (U.P.).

Many deaths were recorded in village Baniyani of Talgram PHC of District Farrukhabad, U.P. during August to November 1991, which is the malaria transmission season in this area. Integrated measures, like one-round spraying of DDT and HCH, six-round fogging of malathion and six-time application of Baytex in mosquito breeding sites, were adopted by the Health Department of the U.P. government to avert an epidemic. Investigations carried out by the Malaria Research Centre during November and December 1991 showed low mosquito densities and larval positivity but very high incidence of malaria in the village. No malaria case was recorded by the surveillance worker of the Health Department of the state government before the outbreak of the disease. However, high slide falciparum rate (51.57), child parasite rate (40.0), infant parasite rate (66.66) and spleen rate (82.90) in the village clearly indicated hyperendemic conditions in the area and hence deaths recorded in the village during the malaria transmission period could be due to malaria only. Major factors responsible for the deaths due to malaria in the village were poor surveillance, faulty diagnosis, and low literacy and socio-economic status of the villagers.

Animals↗
PubMed1979

Immunity to malaria.

Malaria remains prevalent throughout tropical and subtropical regions and almost a third of the World's population is exposed to the risk of infection. There is currently a serious resurgence of the disease in Asia and Central America. The failure of global eradication measures based upon the use of insecticides and chemotherapy has resulted from difficulties of practical implementation compounded by the spread of insecticide and drug resistance. Repeated natural infection does not produce detectable resistance to the exo-erythrocytic cycle of malaria in man. Irradiated sporzoite vaccines do, however, induce stage specific immunity in murine malaria and in a proportion of human subjects. Vaccinated individuals remain susceptible to blood stage infection which causes clinical malaria. In addition the vaccine is unstable and must be administered by intravenous inoculation. Since neither sporogonic nor exo-erythrocytic parasite development is cyclical in human malarias, there is little prospect for vaccine production through cultivation of these stages. The inhabitants of hyperendaemic areas become increasingly resistant to malaria during childhood and adolescence, through the slow development of specific, acquired immunity to asexual blood stage parasites. Immunity is mediated by antibody, which blocks merozoite invasion of red cells, as well as by cell mediated mechanisms and non-specific cytotoxic agents. Vaccination with merozoites induces long lasting immunity of broad serological specificity active against the blood-stage of the parasite. Merozoite vaccines can be preserved by freeze drying and harvested from continuous cultures of blood stage parasites. The major problem in development of a human merozoite vaccine concerns the requirement for Freund's complete adjuvant which is not acceptable for man. The effective immunity induced by vaccination contrasts with the slow development of incomplete resistance which follows repeated natural infection. The latter is associated with the generation of immune suppressor cells, lymphoid cell mitogens and soluble antigens, and in some species by the occurrence of antigenic variation--all of which may favour parasite survival. It is probable that vaccination with non-viable antigen of appropriate composition, induces immune effector processes without activating mechanisms which allow parasites to escape the consequences of immunity. Many effective vaccines such as those against measles, poliomyelitis, tetanus and rabies are commercially available but barely used in the developing world. The affected nations cannot afford their purchase, nor do the means exist for their distribution. It follows that if a safe and effective malaria vaccine were to be developed, its bulk manufacture and administration would require massive international support and cooperation.

Animals↗
PubMed1992

Neurological manifestations of malaria.

The involvement of the nervous system in malaria is reviewed in this paper. Cerebral malaria, the acute encephalopathy which complicates exclusively the infection by Plasmodium falciparum commonly affects children and adolescents in hyperendemic areas. Plugging of cerebral capillaries and venules by clumped, parasitized red cells causing sludging in the capillary circulation is one hypothesis to explain its pathogenesis. The other is a humoral hypothesis which proposes nonspecific, immune-mediated, inflammatory responses with release of vasoactive substances capable of producing endothelial damage and alterations of permeability. Cerebral malaria has a mortality rate up to 50%, and also a considerable longterm morbidity, particularly in children. Hypoglycemia, largely in patients treated with quinine, may complicate the cerebral symptomatology. Other central nervous manifestations of malaria include intracranial hemorrhage, cerebral arterial occlusion, and transient extrapyramidal and neuropsychiatric manifestations. A self-limiting, isolated cerebellar ataxia, presumably caused by immunological mechanisms, in patients recovering from falciparum malaria has been recognized in Sri Lanka. Malaria is a common cause of febrile seizures in the tropics, and it also contributes to the development of epilepsy in later life. Several reports of spinal cord and peripheral nerve involvement are also available. A transient muscle paralysis resembling periodic paralysis during febrile episodes of malaria has been described in some patients. The pathogenesis of these neurological manifestations remains unexplored, but offers excellent perspectives for research at a clinical as well as experimental level.

Adult↗
PubMed1977

An outbreak of introduced malaria in California possibly involving secondary transmission.

During 1974, 12 cases of Plasmodium vivax malaria were reported from an agricultural area in California's Sacramento Valley. At least three of these cases resulted from local mosquito transmission. The imported cases were in Punjabi immigrants except for one in an American-born visitor to the Punjab. This is the 11th reported outbreak of introduced malaria in the United States since 1952, and the first in California since 1957. A unique aspect of this outbreak is the likelihood that secondary transmission occurred. Extensive surveillance activities, including a house-to-house case-finding survey in a 15-square-kilometer area of suspected transmission, yielded no new malaria cases, but the activities may have increased awareness of malaria among both the medical community and the public, and thus facilitated the detection of later cases. The occurrence of local malaria transmission coincided with unusually high numbers of Anopheles freeborni. The increase in imported malaria cases probably reflects a resurgence of malaria in Punjab State, India.

Adolescent↗