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

This report, presents a case of congenital malaria in an 8-hour-old female neonate. She responded well to oral chloroquine at a dose of 25 mg/kg in divided doses over a period of three days and was discharged home for follow-up, 24 hours after completion of the course of chloroquine. This case emphasized the need for routine screening for malaria in sick newborn infants in malaria endemic regions. This is particularly important in situations where clear evidence of sepsis cannot be established, either from history or physical examination of the sick newborn. Malaria and sepsis have similar clinical features in newborn infants.
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PMID:Congenital malaria in 8 hours old newborn: case report. 1222 66

The Lady Dufferin Fund, founded in 1885 in India, had by 1940 established 400 hospitals to alleviate diseases and mortality related to childbirth. After independence 2328 community health centers and 21254 primary health centers were created in the country. During 1974-94 more than 131,000 subcenters were set up and about 620,000 auxiliary nurse midwives (ANMs) had been trained. The Ministry of Health introduced four health prevention schemes in 1969: 1) immunization of children against diphtheria, pertussis, and tetanus; 2) immunization of pregnant women against tetanus; 3) prophylaxis of mothers and children against nutritional anemia; and 4) prophylaxis of children against blindness caused by vitamin A deficiency. As a result, infant mortality declined from 146/1000 live births to 74/1000 in 1993; but maternal mortality still stayed around 4-5/1000. In 1993 an estimated 117,356 maternal deaths occurred out of a total of 26,057,000 births, equalling 4.5 deaths per 1000 live births. The main causes of maternal deaths are hemorrhage, anemia, abortion, toxemia, and puerperal sepsis. Only about 411 first referral units in community health centers are functioning properly. Prenatal care of mothers includes the administration of tetanus toxoid and iron-folic acid tablets. However, the prenatal coverage reached only about 50% of mothers; and the coverage was only 21.4% in Bihar, 23.8% in Nagaland, 29.3% in Rajasthan, and 29.6% in Uttar Pradesh. In these areas administrative inefficiency is widespread with nonavailability of essential drugs for malaria, infections, sepsis, dysentery, and colds. During 1992-93 the rate of hospital deliveries ranged from 6.1% in Nagaland to 88.4% in Kerala, with a national average of only 25.6%. 71% of deliveries in rural areas and 30% in urban areas were conducted by untrained assistants. Although there are 450 ANM training schools in the country, the level of training has deteriorated. The major causes of infant deaths are respiratory infections and diarrhea, responsible for 13.5% and 6.9% of mortality, respectively. Severe malnutrition and inadequate vaccination are other major causes of child deaths and morbidity.
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PMID:Maternal and child health in India: a critical review. 1229 Sep 61

The host response to microbial infection is associated with the release of inflammatory mediators. We hypothesized that the type and degree of the systemic response as reflected by levels of circulating mediators predict morbidity and mortality, according to the invasiveness of microbial infection. We prospectively studied 133 medical patients with fever and culture-proven microbial infection. For 3 days after inclusion, the circulating levels of activated complement C3a, interleukin (IL)-6, and secretory phospholipase A(2) (sPLA(2)) were determined daily. Based on results of microbiological studies performed for up to 7 days, patients were classified as having local infections (Group 1, n = 80 positive local cultures or specific stains for fungal or tuberculous infections) or bacteremia (Group 2, n = 52 plus 1 patient with malaria parasitemia). Outcome was assessed as the development of septic shock and as mortality up to 28 days after inclusion. Fifteen patients (11%) developed septic shock and overall mortality was 18% (n = 24). Bacteremia was associated with shock and shock predisposed to death. Circulating mediator levels were generally higher in Group 2 than in Group 1. Circulating levels of IL-6 and sPLA(2) were higher in patients developing septic shock and in nonsurvivors, particularly in Group 1. High C3a was particularly associated with nonsurvival in Group 2. In Group 1, the area under the curve (AUC) of the receiver operating characteristic (ROC) curve for the peak sPLA(2) for shock development was 0.79 (P < 0.05). The AUC of the ROC curve of the peak IL-6 and sPLA(2) for mortality was 0.69 and 0.68 (P < 0.05), respectively. In Group 2, the AUC of the ROC for peak C3a predicting mortality was 0.73 (P < 0.05). In conclusion, in medical patients with fever and microbial infection, the systemic inflammatory host response predicts shock and death, at an early stage, dependent on the invasiveness of microbial infection. The results suggest a differential pathogenetic role of complement activation on the one hand and release of cytokine and lipid mediators on the other in bacteremic and local microbial infections, respectively. They may partly explain the failure of strategies blocking proinflammatory cytokines or sPLA(2) in human sepsis and may extend the basis for attempts to inhibit complement activation at an early stage in patients at risk of dying from invasive microbial infections.
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PMID:Circulating inflammatory mediators predict shock and mortality in febrile patients with microbial infection. 1267 1

Antipyretics, including acetaminophen (paracetamol), are prescribed commonly in children with pyrexia, despite minimal evidence of a clinical benefit. A literature review was performed by searching Medline and the Cochrane databases for research papers on the efficacy of paracetamol in febrile illnesses in children and adverse outcomes related to the use of paracetamol. No studies showed any clear benefit for the use of paracetamol in therapeutic doses in febrile children with viral or bacterial infections or with malaria. Some studies suggested that fever may have a beneficial role in infection, although no definitive prospective studies in children have been done to prove this. The use of paracetamol in therapeutic doses generally is safe, although hepatotoxicity has occurred with recommended dosages in children. In developing countries where malnutrition is common, data on the safety of paracetamol are lacking. The cost of paracetamol for poor families is substantial. No evidence shows that it is beneficial to treat febrile children with paracetamol. Treatment should be given only to children who are in obvious discomfort and those with conditions known to be painful. The role of paracetamol in children with severe malaria or sepsis and in malnourished, febrile children needs to be clarified.
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PMID:Evidence on the use of paracetamol in febrile children. 1285 56

Falciparum malaria is a complex disease with no simple explanation, affecting organs where the parasite is rare as well as those organs where it is more common. We continue to argue that it can best be understood in terms of excessive stimulation of normally useful pathways mediated by inflammatory cytokines, the prototype being tumor necrosis factor (TNF). These pathways involve downstream mediators, such as nitric oxide (NO) that the host normally uses to control parasites, but which, when uncontrolled, have bioenergetic failure of patient tissues as their predictable end point. Falciparum malaria is no different from many other infectious diseases that are clinically confused with it. The sequestration of parasitized red blood cells, prominent in some tissues but absent in others with equal functional loss, exacerbates, but does not change, these overriding principles. Recent opportunities to stain a wide range of tissues from African pediatric cases of falciparum malaria and sepsis for the inducible NO synthase (iNOS) and migration inhibitory factor (MIF) have strengthened these arguments considerably. The recent demonstration of bioenergetic failure in tissue removed from sepsis patients being able to predict a fatal outcome fulfils a prediction of these principles, and it is plausible that this will be demonstrable in severe falciparum malaria. Understanding the disease caused by falciparum malaria at a molecular level requires an appreciation of the universality of poly(ADP-ribose) polymerase-1 (PARP-1) and Na(+)/K(+)-ATPase and the protean effects of activation by inflammation of the former that include inactivation of the latter.
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PMID:The pathophysiology of falciparum malaria. 1288 13

Tanzania's health policy is to improve the health of all Tanzanians with a focus on those most at risk. One of the major objectives is to reduce infant and maternal morbidity and mortality and increase life expectancy. The life expectancy in Tanzania is 49 years for males and 53 years for females. Maternal mortality is recorded at 300-400 deaths per 100,000 women. The main causes are haemorrhage, sepsis, rupture of the uterus, anaemia, and others. The risk factors associated with the above causes include maternal height, age, child spacing, and number of births per woman; malaria and anaemia; imbalance of energy and food intake; HIV/AIDS; women's workload; and female genital mutilation (FGM). To address issues of women's health, the government has put in place many strategies, for example, a ministry to look after women's issues, the safe motherhood initiatives, improvement of the knowledge and skill of health care providers, as well as collaboration with nongovernmental organizations (NGOs) and private agencies. The health sector reform is important because it has negatively affected women's access to health care. To improve the health of women in Tanzania, health and health-related sectors should cooperate and collaborate in order to empower women in the areas of education, social status, and technology. Policies must also address poverty, nutrition, adolescent health, and violence and sexual abuse.
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PMID:Major factors that impact on women's health in Tanzania: the way forward. 1295 70

BACKGROUND: As well as being inducible by haem, haemoxygenase -1 (HO-1) is also induced by interleukin-10 and an anti-inflammatory prostaglandin, 15d PGJ2, the carbon monoxide thus produced mediating the anti-inflammatory effects of these molecules. The cellular distribution of HO-1, by immunohistochemistry, in brain, lung and liver in fatal falciparum malaria, and in sepsis, is reported. METHODS: Wax sections were stained, at a 1:1000 dilution of primary antibody, for HO-1 in tissues collected during paediatric autopsies in Blantyre, Malawi. These comprised 37 acutely ill comatose patients, 32 of whom were diagnosed clinically as cerebral malaria and the other 5 as bacterial diseases with coma. Another 3 died unexpectedly from an alert state. Other control tissues were from Australian adults. RESULTS: Apart from its presence in splenic red pulp macrophages and microhaemorrhages, staining for HO-1 was confined to intravascular monocytes and certain tissue macrophages. Of the 32 clinically diagnosed cerebral malaria cases, 11 (category A) cases had negligible histological change in the brain and absence of or scanty intravascular sequestration of parasitized erythrocytes. Of these 11 cases, eight proved at autopsy to have other pathological changes as well, and none of these eight showed HO-1 staining within the brain apart from isolated moderate staining in one case. Two of the three without another pathological diagnosis showed moderate staining of scattered monocytes in brain vessels. Six of these 11 (category A) cases exhibited strong lung staining, and the Kupffer cells of nine of them were intensely stained. Of the seven (category B) cases with no histological changes in the brain, but appreciable sequestered parasitised erythrocytes present, one was without staining, and the other six showed strongly staining, rare or scattered monocytes in cerebral vessels. All six lung sections not obscured by neutrophils showed strong staining of monocytes and alveolar macrophages, and all six available liver sections showed moderate or strong staining of Kupffer cells. Of the 14 (category C) cases, in which brains showed micro-haemorrhages and intravascular mononuclear cell accumulations, plus sequestered parasitised erythrocytes, all exhibited strong monocyte HO-1 staining in cells forming accumulations and scattered singly within cerebral blood vessels. Eleven of the available and readable 13 lung sections showed strongly staining monocytes and alveolar macrophages, and one stained moderately. All of the 14 livers had strongly stained Kupffer cells. Of five cases of comatose culture-defined bacterial infection, three showed a scattering of stained monocytes in vessels within the brain parenchyma, three had stained cells in lung sections, and all five demonstrated moderately or strongly staining Kupffer cells. Brain sections from all three African controls, lung sections from two of them, and liver from one, showed no staining for HO-1, and other control lung and liver sections showed few, palely stained cells only. Australian-origin adult brains exhibited no staining, whether the patients had died from coronary artery disease or from non-infectious, non-cerebral conditions CONCLUSIONS: Clinically diagnosed 'cerebral malaria' in children includes some cases in whom malaria is not the only diagnosis with the hindsight afforded by autopsy. In these patients there is widespread systemic inflammation, judged by HO-1 induction, at the time of death, but minimal intracerebral inflammation. In other cases with no pathological diagnosis except malaria, there is evidence of widespread inflammatory responses both in the brain and in other major organs. The relative contributions of intracerebral and systemic host inflammatory responses in the pathogenesis of coma and death in malaria deserve further investigation.
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PMID:Induction of HO-1 in tissue macrophages and monocytes in fatal falciparum malaria and sepsis. 1462 2

The in vitro study of TNF promoter polymorphism (SNP) function was stimulated by the numerous case-control (association) studies of the polymorphisms in relation to human disease and the appearance of several studies claiming to show a functional role for these SNPs provided a further impetus to researchers interested in the role of TNF in their disease of interest. In this review we consider case-control studies, concentrating on the autoimmune and inflammatory diseases rheumatoid arthritis, multiple sclerosis, ankylosing spondylitis, and asthma, and on infectious diseases including malaria, hepatitis B and C infection, leprosy and sepsis/septic shock. We also review the available evidence on the functional role of the various TNF promoter polymorphisms. In general, case-control studies have produced mixed results, with little consensus in most cases on whether any TNF polymorphisms are actually associated with disease, although results have been more consistent in the case of infectious diseases, particularly malaria. Functional studies have also produced mixed results but recent work suggests that the much studied -308G/A polymorphism is not functional, while the function of other TNF polymorphisms remains controversial. Studies of the TNF region are increasingly using extended haplotypes that can better capture the variation of the MHC region.
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PMID:Is there a future for TNF promoter polymorphisms? 1497 48

Bacterial DNA (bDNA) and lipopolysaccharide (LPS) are potent activators of immune cells such as monocytes and macrophages, which contribute to systemic inflammatory response syndrome (SIRS) and sepsis. To date, no effective anti-sepsis drugs have been developed for clinical use. Chloroquine (CQ), a diprotic weak base traditionally used for treating malaria, was recently shown to decrease cytokine release from macrophages induced by LPS and CpG oligonucleotide (CpG ODN). In the present study, Escherichia coli DNA (EC DNA), CpG ODN and LPS were used to induce SIRS/sepsis in animal models. We found that 30 mg/kg of CQ could protect mice from lethal challenge by CpG ODN and LPS, and 25 mg/kg of CQ could decrease serum TNF-alpha and IL-6 in rats injected with sublethal doses of CpG ODN and LPS. In addition, treatment of murine macrophage ANA-1 cells with 2 mM CQ potently inhibited the release of TNF-alpha, IL-6 and IL-12 induced by CpG ODN and LPS. In human peripheral blood mononuclear cells (hPBMC), 100-200 microM CQ almost completely abrogated release of both TNF-alpha and IL-6 induced by CpG ODN and LPS, whereas IL-6 release induced by EC DNA was not significantly affected by 50 microM CQ. Furthermore, CQ reduced the expression of TLR9 and TLR4 mRNA and the activation of NFkappaB and AP-1 stimulated by CpG ODN and LPS in ANA-1 cells. Flow cytometry and confocal microscopy revealed that CQ increased the accumulation of CpG ODN within ANA-1 cells without influence on its uptake, suggesting that the delayed degradation of CpG ODN was associated with the reduction of proinflammatory cytokine release from the cells. Our results demonstrated that CQ-mediated protection of lethal challenge by CpG ODN and LPS was associated with the reduction of proinflammatory cytokine release.
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PMID:Chloroquine protects mice from challenge with CpG ODN and LPS by decreasing proinflammatory cytokine release. 1499 14

Malaria is thought to be rare among neonates in malaria-endemic regions. Consequently, blood film for malaria parasite is not routinely included in the sepsis screening protocol for neonates. We examined the role of malaria in perinatal morbidity among neonates admitted into our unit with a view to determining the need or otherwise of including malaria parasitaemia in the sepsis work-up in suspected neonatal septicaemia. Fourteen babies who met our preset criteria were screened for malaria parasitaemia out of which five (35.71 per cent) had positive blood smears for Plasmodium falciparum. Eighty per cent of the neonates presenting with fever had positive blood films (Yates corrected chi2 = 3.9822; p = 0.04). All the babies responded to an oral course of chloroquine. These data have further highlighted the importance of malaria in perinatal morbidity in our environment. We recommend a multi-centred study to define clearly the role of malaria in perinatal and neonatal morbidity and mortality in malaria endemic areas.
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PMID:Malaria parasitaemia in neonates in Port Harcourt, Nigeria. 1508 2


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