Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024530 (malaria)
44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:An outbreak of introduced malaria in California possibly involving secondary transmission. 32 Aug 91

Hepatic function of 80 children aged under 3 years with Plasmodium vivax malaria were studied during the acute attack and 6 weeks after antimalarial treatment. Raised levels of serum aspartate transaminase (serum AST; SGOT), serum alanine transaminase (serum ALT; SGPT), and alkaline phosphatase were observed in 68%, 39% and 46% of cases respectively. AST levels were higher than ALT ones and the mean level of both enzymes was much higher in patients with hepatomegaly. The hepatic dysfunction which these observations reflect is transient, as these enzymes were found to be at their normal levels 6 weeks after treatment. A transient derangement of liver function is thus a common feature of childhood malaria, and hepatic dysfunction takes place to a significant degree even in P. vivax malaria.
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PMID:Hepatic dysfunction in childhood malaria. 37 43

An outbreak of Plasmodium vivax malaria occurred in Trinidad some 25 years after a successful eradication programme. The 'index case' was infected while visiting Perdaneles, Venezuela, and was responsible for the renewal of malaria transmission by indigenous Anopheles aquasalis mosquitoes in Icacos, Trinidad, W.I. Nine cases (four females and five males) of P. vivax malaria were locally transmitted in Icacos. Most of the cases (70%) were in the 15-24 or 25-44 year age groups. In Granville/Chatham, another, unrelated case of locally transmitted P. vivax malaria was discovered through active surveillance. The intervention measures adopted, which successfully eradicated P. vivax malaria from Trinidad, are described. The need to maintain malaria surveillance is emphasized.
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PMID:An outbreak of Plasmodium vivax malaria in Trinidad, W.I. 130 99

Demonstration of parasite associated antigen in blood by inhibition ELISA in malaria patients and controls is described. The test was negative in all the healthy controls and positive in 90 per cent of the Plasmodium vivax malaria cases. The test was found to be quite sensitive, being able to detect 5 parasites/10(6) RBC in a case of natural P. falciparum infection. There was 95.3 per cent agreement between the results of this test and IgM-IIF test.
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PMID:Detection of malaria antigen in blood by inhibition ELISA. 134 43

Plasmodium vivax malaria infections in non-immune individuals manifest as periodic clinical episodes of fever with chills and rigors known as paroxysms. We have demonstrated that in non-immune patients the period of paroxysm is associated with the transient presence of plasma factors which kill gametocytes, the intra-erythrocytic sexual stages of the malaria parasite which transmit the infection from humans to mosquito, rendering them non-infectious to mosquitoes. Gametocyte killing in paroxysm plasma is mediated by tumour necrosis factor (TNF) acting in conjunction with other essential serum factor(s). Plasma TNF levels were elevated during a paroxysm. In semi-immune individuals from a P. vivax-endemic area clinical symptoms of malaria are mild and the parasite killing factors are not induced during paroxysm. Serum TNF levels were correspondingly lower in endemic patients during a paroxysm. Human peripheral blood mononuclear cells (PBMC) can be stimulated in vitro by extracts of P. vivax blood stage parasites to produce TNF and associated parasite killing factor(s), thus simulating in vitro the events that occur during a paroxysm, this being the release of parasite exo-antigens by rupturing schizonts and the subsequent induction of PBMC to produce TNF and other parasite-killing factors. We were able to show that convalescent serum from P. vivax semi-immune individuals block the induction of TNF and parasite-killing factors by malaria antigens in vitro, presumably through antibodies that neutralize parasite exo-antigens. Thus, individuals living in malaria-endemic areas appear to acquire clinical immunity to malaria by avoiding their induction during infection; we have shown that one such mechanism is the neutralization of parasite exo-antigens that induce the production of parasite killing factors.
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PMID:Tumour necrosis factor-dependent parasite-killing effects during paroxysms in non-immune Plasmodium vivax malaria patients. 135 32

All 110 patients seen in North East Scotland after contracting malaria from foreign travel were treated in the Regional Infection Unit in Aberdeen. Those patients managed there from January 1980 to March 1991 are described. There were 54 episodes of Plasmodium falciparum malaria (49%) and 26 episodes (23%) of Plasmodium vivax malaria. The remainder had either mixed infection or were diagnosed as malaria on high clinical probability. The majority of the patients were male (80%) and under 40 years of age (84%). Most patients were either caucasians born in the UK (69%) or native Africans (23%) who were students recently arrived for further education or who had returned from visiting their country of origin for summer holidays. The British residents acquired infection either while on oil related business in West or Central Africa (46%) or after travelling on holiday (30%). The peak incidence of presentation was August and September. 93.5% of patients with falciparum malaria had returned or originated from Africa. 42% with vivax malaria had visited Africa and 27% Papua New Guinea. 70% had been prescribed antimalarial prophylaxis but less than half of these took their medication correctly. The majority of patients with falciparum malaria presented within two weeks of arrival in Britain while patients with vivax malaria presented at varying (but generally longer) intervals, 42% being diagnosed more than three months after exposure. Falciparum infection was more severe although there have been no deaths in the unit from malaria. Our experience seemed of interest and worth reporting because of the number of patients whose infection reflected travel related to the off shore oil industry, which is centred in Aberdeen.
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PMID:Malaria in Aberdeen: an audit of 110 patients admitted between 1980-1991. 141 77

We have developed a multi-state mathematical model to describe the transmission of Plasmodium vivax malaria; the model accommodates variable transmission-blocking/enhancing immunity during the course of a blood infection, a short memory for boosting immunity, and relapses. Using the model, we simulated the incidence of human malaria, sporozoite rates in the vector population, and the level of transmission-blocking immunity for the infected population over a period of time. Field data from an epidemiological study conducted in Kataragama in the south of Sri Lanka were used to test the results obtained. The incidence of malaria during the study period was simulated satisfactorily. The impact of naturally-acquired transmission-blocking immunity on malaria transmission under different vectorial capacities was also simulated. The results show that at low vectorial capacities, e.g., just above the threshold for transmission, the effect of transmission-blocking immunity is very significant; however, the effect is lower at higher vectorial capacities.
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PMID:A mathematical model for Plasmodium vivax malaria transmission: estimation of the impact of transmission-blocking immunity in an endemic area. 178 21

We have found polymorphism in the repetitive and nonrepetitive regions of the sporozoite vaccine antigen, the circumsporozoite (CS) protein, in Plasmodium vivax malaria parasites from two geographically distant malaria endemic regions of the world. Like the recently described variant repeat sequence of P. vivax from Thailand, the CS protein repeat sequence of the variant P. vivax parasites from Papua New Guinea and Brazil is ANGA(G/D)(N/D)QPG, which differs from the previously identified CS repeat sequence, GDRA(D/A)GQPA, of P. vivax parasites from South America, Central America, and North Korea. Comparison of the P. vivax CS protein outside the repeat region revealed restricted polymorphism in regions that have exhibited T-cell immune function and sequence heterogeneity in the CS protein of Plasmodium falciparum. Our results show that P. vivax malaria parasites with the variant CS repeat sequences are widespread in nature and that the polymorphism in the CS protein of P. vivax is also present in the nonrepeat region.
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PMID:Wide distribution of the variant form of the human malaria parasite Plasmodium vivax. 188 63

Between 18 June and 20 September 1986, 28 cases of Plasmodium vivax malaria were documented in Carlsbad, California, a coastal town north of San Diego. Malaria occurred in 1 local resident who had no risk factors, a second local resident who had traveled to a malarious area 9 months earlier, and 26 Mexican migrant workers (MWs). Among the 28 cases, 27 lived in a square mile marshy area where Anopheles hermsi, a newly described American species of the Anopheles maculipennis group, was known to be breeding. An investigation of MWs residing in the affected area was done to determine the extent of the outbreak and to identify risk factors for acquiring malaria. We interviewed and drew blood from 304 healthy MWs and 17 (65%) of the MWs with malaria. Fluorescent antibody titers to P. vivax greater than or equal to 1:256 occurred in 14 (82%) of the 17 MWs with malaria tested and 9 (3%) of the healthy MWs. The principal risk factor identified for contracting malaria was sleeping outside on a hillside adjacent to the marshy area. Malaria in a local resident with no malaria risk factors and the clustering in time and place of 26 cases suggest that P. vivax malaria was introduced and local transmission was sustained through several generations, producing the largest outbreak of introduced malaria in the United States since 1952.
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PMID:Transmission of Plasmodium vivax malaria in San Diego County, California, 1986. 196 16

Eighteen patients with Plasmodium vivax malaria were prospectively evaluated to assess the time of onset and extent of upper gastrointestinal mucosal injury caused by oral administration of four tablets (600-mg base) of chloroquine. Endoscopy was performed in the group of three separate patients. Each patient underwent endoscopy, both before the drug was given, and at intervals of 1, 2, 4, 12, 24, and 36 h. Before the drug was given, endoscopy was normal in all of the patients. However, mucosal erosions developed in four of 18 patients who were endoscoped 24 and 36 h after chloroquine ingestion (gastric, four; duodenal, two; esophageal, one). The same doses of chloroquine failed to produce any mucosal lesions when given to these four patients while they were afebrile and when given to 11 healthy individuals who served as controls. Poor correlation was noted between subjective symptoms and endoscopic findings. In conclusion, neither malaria alone nor chloroquine alone causes mucosal lesions. However, chloroquine administered during malarial fever causes mucosal damage in susceptible individuals.
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PMID:Endoscopic assessment of chloroquine phosphate-induced damage to esophageal, gastric, and duodenal mucosa. 201 45


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