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Journal articles on the topic 'Pulmonary and cerebral malaria'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Milner, Danny, Rachel Factor, Rich Whitten, Richard A. Carr, Steve Kamiza, Geraldine Pinkus, Malcolm Molyneux, and Terrie Taylor. "Pulmonary pathology in pediatric cerebral malaria." Human Pathology 44, no. 12 (December 2013): 2719–26. http://dx.doi.org/10.1016/j.humpath.2013.07.018.

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2

Torre, Sabrina, Sebastien P. Faucher, Nassima Fodil, Silayuv E. Bongfen, Joanne Berghout, Jeremy A. Schwartzentruber, Jacek Majewski, et al. "THEMIS Is Required for Pathogenesis of Cerebral Malaria and Protection against Pulmonary Tuberculosis." Infection and Immunity 83, no. 2 (December 1, 2014): 759–68. http://dx.doi.org/10.1128/iai.02586-14.

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We identify anN-ethyl-N-nitrosourea (ENU)-induced I23N mutation in the THEMIS protein that causes protection against experimental cerebral malaria (ECM) caused by infection withPlasmodium bergheiANKA.ThemisI23Nhomozygous mice show reduced CD4+and CD8+T lymphocyte numbers. ECM resistance inP. bergheiANKA-infectedThemisI23Nmice is associated with decreased cerebral cellular infiltration, retention of blood-brain barrier integrity, and reduced proinflammatory cytokine production. THEMISI23Nprotein expression is absent from mutant mice, concurrent with the decreased THEMISI23Nstability observedin vitro. Biochemical studiesin vitroand functional complementationin vivoinThemisI23N/+:Lck−/+doubly heterozygous mice demonstrate that functional coupling of THEMIS to LCK tyrosine kinase is required for ECM pathogenesis. Damping of proinflammatory responses inThemisI23Nmice causes susceptibility to pulmonary tuberculosis. Thus, THEMIS is required for the development and ultimately the function of proinflammatory T cells.ThemisI23Nmice can be used to study the newly discovered association ofTHEMIS(6p22.33) with inflammatory bowel disease and multiple sclerosis.

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3

Punnath, Kishore, Kiran K. Dayanand, Valleesha N. Chandrashekar, Rajeshwara N. Achur, Srinivas B. Kakkilaya, Susanta K. Ghosh, Suchetha N. Kumari, and D. Channe Gowda. "Association between Inflammatory Cytokine Levels and Thrombocytopenia during Plasmodium falciparum and P. vivax Infections in South-Western Coastal Region of India." Malaria Research and Treatment 2019 (April 11, 2019): 1–10. http://dx.doi.org/10.1155/2019/4296523.

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Background. Thrombocytopenia is a most commonly observed complication during malaria infections. Inflammatory cytokines such as IL-1, IL-6, and IL-10 have been documented in malaria induced thrombocytopaenia. This study was aimed to understand the possible relationship between inflammatory cytokines across varying degrees of thrombocytopenia during P. vivax, P. falciparum, and mixed infections. Methods. A hospital-based cross sectional study was conducted at District Wenlock Hospital in Mangaluru, a city situated along the south-western coastal region of Arabian Sea in India. In this study, blood samples from 627 malaria patients were analyzed for infected parasite species, clinical conditions, platelet levels, and key cytokines that are produced in response to infection; samples from 176 uninfected healthy individuals were used as controls. Results. The results of our study showed a high prevalence of malarial thrombocytopenia (platelets <150 ×103/μl) in this endemic settings. About 62.7% patients had mild-to-moderate levels of thrombocytopenia and 16% patients had severe thrombocytopenia (platelets <50 × 103/μl). Upon comparison of cytokines across varying degrees of thrombocytopenia, irrespective of infecting species, the levels of TNF-α and IL-10 were significantly higher during thrombocytopenia, whereas IL-6 levels were considerably lower in severe thrombocytopenia patients suffering from P. vivax or P. falciparum infections. The severe clinical complications observed in patients with malarial thrombocytopenia included severe anemia (17.5%), acute renal failure (12.7%), jaundice (27.0%), metabolic acidosis (36.5%), spontaneous bleeding (3.2%), hypoglycemia (25.4%), hyperparasitemia (4.8%), acute respiratory distress syndrome (1.6%), pulmonary edema (19.0%), and cerebral malaria (1.6%) in various combinations. Conclusion. Overall, the results of our study suggest that inflammatory cytokines influence the transformation of mild forms of thrombocytopenia into severe forms during malarial infections. Further studies are needed to understand the association of inflammatory cytokine responses with severe malaria complications and thrombocytopenia.

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Mathur, Arvind, Mohit Kackar, Indu Thanvi, and Harish Agarwal. "STUDY OF CLINICAL FEATURES AND EPIDEMIOLOGY OF COMPLICATED VIVAX MALARIA." International Journal of Research -GRANTHAALAYAH 7, no. 9 (September 30, 2019): 47–51. http://dx.doi.org/10.29121/granthaalayah.v7.i9.2019.556.

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Severe and complicated malaria is defined by the World Health Organization Malaria Action Programme in June 19851 as the presence of one or more of the following conditions in a slide confirmed diagnosed case of malaria cerebral malaria, severe anemia, renal failure, pulmonary edema or adult respiratory distress syndrome, hypoglycemia, circulatory collapse or shock, spontaneous bleeding, repeated generalized convulsions, acidemia or acidosis, macroscopic hemoglobinuria, impairment of consciousness less marked than unarousable coma,, hyperparasitemia, jaundice, hyperpyrexia, and the presence of complicating or associated infections. However, severe anemia and thrombocytopenia that causes bleeding diatesis is produced by hemolysis, reduced cell deformity of parasitized and non-parasitized erythrocytes, increased splenic clearance, reduction of platelet survival, decreased platelet production, and increased splenic uptake of platelets. Though these changes can be produced by P. vivax and P. falciparum infection yet the complicated malaria has commonly been associated with P. falciparum infections.

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5

Sianti, Eka, and Jose Meky Mandei. "Confusions and dilemma around hepatic dysfunction associated falciparum malaria: A case report and brief review of the literature." Paediatrica Indonesiana 49, no. 4 (August 31, 2009): 244. http://dx.doi.org/10.14238/pi49.4.2009.244-8.

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Malaria remains a big burden in East Indonesia. Severe malaria assaults children in endemic area and leads toenormous morbidities and mortalities.According to the World Health Organization's criteria,recognition of one or more of the following clinicalfeatures should raise the suspicion of severe malariai.e, cerebral malaria (unrousable coma), severe anemia(hemoglobin <5 g/dl), renal failure (creatinine serum> 3 mg/dl), pulmonary edema or adult respiratory distresssyndrome (ARDS), hypoglycemia (glucose < 40 mg/dl),circulatory collapse or shock, disseminated intravascularcoagulation (DIC), repeated generalized convulsions,acidosis (pH < 7 .25), macroscopic hemoglobinuria,hyperparasitaemia ( > 5% of the erythrocytes infested byparasites), or jaundice (bilirubin> 3 mg/dl).l-3Jaundice in malaria due to hepatic dysfunction isa classical case, nevertheless, there are some confusionsand dilemmas in managing it.1 We report a case withjaundice due to hepatic dysfunction and hemolysisassociated falciparum malaria that we treated inGeneral Hospital of Fakfak, West Papua, and providea brief literature review on the matter.

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6

Hansen, Diana S., Krystal J. Evans, Marthe C. D'Ombrain, Nicholas J. Bernard, Adrienne C. Sexton, Lynn Buckingham, Anthony A. Scalzo, and Louis Schofield. "The Natural Killer Complex Regulates Severe Malarial Pathogenesis and Influences Acquired Immune Responses to Plasmodium berghei ANKA." Infection and Immunity 73, no. 4 (April 2005): 2288–97. http://dx.doi.org/10.1128/iai.73.4.2288-2297.2005.

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ABSTRACT The natural killer complex (NKC) is a genetic region of highly linked genes encoding several receptors involved in the control of NK cell function. The NKC is highly polymorphic, and allelic variability of various NKC loci has been demonstrated in inbred mice. Making use of BALB.B6-Cmv1r congenic mice, in which the NKC from disease-susceptible C57BL/6 mice has been introduced into the disease-resistant BALB/c background, we show here that during murine malaria infection, the NKC regulates a range of pathophysiological syndromes such as cerebral malaria, pulmonary edema, and severe anemia, which contribute to morbidity and mortality in human malaria. Parasitemia levels were not affected by the NKC genotype, indicating that control of malarial fatalities by the NKC cells does not operate through effects on parasite growth rate. Parasite-specific antibody responses and the proinflammatory gene transcription profile, as well as the TH1/TH2 balance, also appeared to be influenced by NKC genotype, providing evidence that this region, known to control innate immune responses via NK and/or NK T-cell activation, can also significantly regulate acquired immunity to infection. To date, NKC-encoded innate system receptors have been shown mainly to regulate viral infections. Our data provide evidence for critical NKC involvement in the broad immunological responses to a protozoan parasite.

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7

IOANNIDIS, LISA J., CATHERINE Q. NIE, and DIANA S. HANSEN. "The role of chemokines in severe malaria: more than meets the eye." Parasitology 141, no. 5 (December 13, 2013): 602–13. http://dx.doi.org/10.1017/s0031182013001984.

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SUMMARYPlasmodium falciparummalaria is responsible for over 250 million clinical cases every year worldwide. Severe malaria cases might present with a range of disease syndromes including acute respiratory distress, metabolic acidosis, hypoglycaemia, renal failure, anaemia, pulmonary oedema, cerebral malaria (CM) and placental malaria (PM) in pregnant women. Two main determinants of severe malaria have been identified: sequestration of parasitized red blood cells and strong pro-inflammatory responses. Increasing evidence from human studies and malaria infection animal models revealed the presence of host leucocytes at the site of parasite sequestration in brain blood vessels as well as placental tissue in complicated malaria cases. These observations suggested that apart from secreting cytokines, leucocytes might also contribute to disease by migrating to the site of parasite sequestration thereby exacerbating organ-specific inflammation. This evidence attracted substantial interest in identifying trafficking pathways by which inflammatory leucocytes are recruited to target organs during severe malaria syndromes. Chemo-attractant cytokines or chemokines are the key regulators of leucocyte trafficking and their potential contribution to disease has recently received considerable attention. This review summarizes the main findings to date, investigating the role of chemokines in severe malaria and the implication of these responses for the induction of pathogenesis and immunity to infection.

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8

Jha, Sanjeev, and Mohd Khateebullah Ansari. "Leptospirosis presenting as acute meningoencephalitis." Journal of Infection in Developing Countries 4, no. 03 (January 25, 2010): 179–82. http://dx.doi.org/10.3855/jidc.646.

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Leptospirosis in humans is a common zoonotic disease. It is often under-diagnosed, especially when associated with neurological features, resulting in significant morbidity and mortality. This subgroup of patients with neurological manifestations is often empirically treated for cerebral malaria, dengue fever, tuberculous meningitis, hepatic encephalopathy, viral encephalitis, etc. Hence it is important to be aware of uncommon manifestations of this disease. We report one such patient, which highlights the importance of considering leptospirosis as the diagnostic possibility with hepato-renal, pulmonary and nervous system involvement, particularly where diagnostic supports and resources are limited.

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9

RYG-CORNEJO, VICTORIA, ANN LY, and DIANA S. HANSEN. "Immunological processes underlying the slow acquisition of humoral immunity to malaria." Parasitology 143, no. 2 (January 8, 2016): 199–207. http://dx.doi.org/10.1017/s0031182015001705.

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SUMMARYMalaria is one of the most serious infectious diseases with ~250 million clinical cases annually. Most cases of severe disease are caused by Plasmodium falciparum. The blood stage of Plasmodium parasite is entirely responsible for malaria-associated pathology. Disease syndromes range from fever to more severe complications, including respiratory distress, metabolic acidosis, renal failure, pulmonary oedema and cerebral malaria. The most susceptible population to severe malaria is children under the age of 5, with low levels of immunity. It is only after many years of repeated exposure, that individuals living in endemic areas develop clinical immunity. This form of protection does not result in sterilizing immunity but prevents clinical episodes by substantially reducing parasite burden. Naturally acquired immunity predominantly targets blood-stage parasites and it is known to require antibody responses. A large body of epidemiological evidence suggests that antibodies to Plasmodium antigens are inefficiently generated and rapidly lost in the absence of ongoing exposure, which suggests a defect in the development of B cell immunological memory. This review summarizes the main findings to date contributing to our understanding on cellular processes underlying the slow acquisition of humoral immunity to malaria. Some of the key outstanding questions in the field are discussed.

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10

El-Assaad, Fatima, Julie Wheway, Andrew John Mitchell, Jinning Lou, Nicholas Henry Hunt, Valery Combes, and Georges Emile Raymond Grau. "Cytoadherence of Plasmodium berghei-Infected Red Blood Cells to Murine Brain and Lung Microvascular Endothelial CellsIn Vitro." Infection and Immunity 81, no. 11 (August 12, 2013): 3984–91. http://dx.doi.org/10.1128/iai.00428-13.

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ABSTRACTSequestration of infected red blood cells (iRBC) within the cerebral and pulmonary microvasculature is a hallmark of human cerebral malaria (hCM). The interaction between iRBC and the endothelium in hCM has been studied extensively and is linked to the severity of malaria. Experimental CM (eCM) caused byPlasmodium bergheiANKA reproduces most features of hCM, although the sequestration of RBC infected byP. bergheiANKA (PbA-iRBC) has not been completely delineated. The role of PbA-iRBC sequestration in the severity of eCM is not well characterized. Using static and flow cytoadherence assays, we provide the first directin vitroevidence for the binding of PbA-iRBC to murine brain and lung microvascular endothelial cells (MVEC). We found that basal PbA-iRBC cytoadherence to MVECs was significantly higher than that of normal red blood cells (NRBC) and of RBC infected withP. bergheiK173 (PbK173-iRBC), a strain that causes noncerebral malaria (NCM). MVEC prestimulation with tumor necrosis factor (TNF) failed to promote any further significant increase in mixed-stage iRBC adherence. Interestingly, enrichment of the blood for mature parasites significantly increased PbA-iRBC binding to the MVECs prestimulated with TNF, while blockade of VCAM-1 reduced this adhesion. Our study provides evidence for the firm, flow-resistant binding to endothelial cells of iRBC from strain ANKA-infected mice, which develop CM, and for less binding of iRBC from strain K173-infected mice, which develop NCM. An understanding ofP. bergheicytoadherence may help elucidate the importance of sequestration in the development of CM and aid the development of antibinding therapies to help reduce the burden of this syndrome.

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11

Gajović, Olgica, Marijana Stanojevic-Pirkovic, Biljana Popovska-Jovicic, Ljiljana Nesic, Zeljko Mijailovic, Ivan Cekerevac, Romana Susa, and Jagoda Gavrilovic. "Life-Threatening Plasmodium Falciparum Malaria in Patient after Visiting Angola-Case Report." Serbian Journal of Experimental and Clinical Research 18, no. 1 (March 1, 2017): 81–84. http://dx.doi.org/10.1515/sjecr-2016-0039.

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Abstract Malaria is a potentially life-threatening disease, especially when complicated by a septic shock. It is caused by infection of erythrocytes with protozoan parasites of the genus Plasmodium that are inoculated into the humans by a feeding female anopheline mosquito. Of the four Plasmodia species, infection with Plasmodium (P.) falciparum is often associated with different types of complications and significant mortality. Most imported cases of malaria are not in tourists but in immigrants and their children who have returned to the country of their family’s origin to visit friends and relatives (so-called VFR travelers) and have forgone chemoprophylaxis.We described a case of a 52 year old patient who came from Angola, an African country with endemic malaria before the occurrence of the first symptoms of the disease. The first symptoms were not recognized by the presence of nonspecific symptoms. Very soon the patient was gone under the hemodynamic unstability that eas followed by shock and high percentage parasitemia of 25%. A global health disorder was developed accompanied with hemodynamic instability and cerebral dysfunction. He performs pulmonary ventilation disorder and renal failure. Only data from social epidemiological survey of travel to the African country, was sufficient to cast doubt on malaria. The diagnosis was conducted using the standard method - peripheral blood smear. After turning antimalarial drugs, improvement of health status with complete recovery within 10 days was noticed. The only consequence of the disease is persistent hypertension that is sensitive to standard antihypertensive therapy.

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12

Cserti-Gazdewich, Christine, Aggrey Dhabangi, Charles Musoke, Nicolette Nabukeera-Barungi, Henry Ddungu, Arthur Mpimbaza, Isaac Ssewanyana, and Walter H. Dzik. "Hematologic Findings and Transfusion Therapy in Severe Pediatric Plasmodium Falciparum Malaria: Results from a Prospective Observational Study in Uganda." Blood 112, no. 11 (November 16, 2008): 3041. http://dx.doi.org/10.1182/blood.v112.11.3041.3041.

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Abstract Background: Plasmodium falciparum malaria is a leading global killer of children and cause for transfusion in endemic areas. Sequestration cytopenias and microvascular insufficiency are pathologic consequences of the acquired cytoadhesivity of P falciparum-infected red blood cells (iRBC). Parasite-derived surface knobs (PfEMP1) expressed on iRBC promote their binding to blood group ligands on non-infected blood cells and the microvascular endothelium. The purpose of the Cytoadherence in Pediatric Malaria Study (clinicaltrials.gov, NCT 00707200) is to study the association between malaria outcomes and host markers of cytoadhesion. Methods: This prospective observational study of children with malaria (age 6 m–12 y, HIV-neg) was launched in October 2007 at Mulago Hospital, Uganda. Patients with severe malaria syndromes, as defined by the WHO, were compared with uncomplicated malaria (UM) patients for presenting hematologic features and transfusion practices. Associations between severe malaria syndromes and mortality were also explored. Results: Over the study’s 1st 7 months, 785 patients were screened, 492 enrolled, and 44 excluded (40 malaria false positives, 4 HIV+). A total of 448 were analyzed (199 severe, 249 UM), including 16 deaths (severe malaria case fatality rate: 8%). Patients were 55% male/45% female. Severe malaria patients were significantly younger than those with UM (2.3 ± 1.9 y, 93% ≤ 5 y, vs 3.5 ± 2.7 y, 76% <5 y), p < 2×10−7. Hematologic features of the patients are summarized in Table 1, illustrating significantly greater derangements in the CBC of severe cases versus UM. In contrast, both groups had a similar sickle trait prevalence and level of parasitemia: Table 1: Hematologic Features in Uncomplicated Malaria (UM) vs Severe Malaria UM (n = 249) Severe (n = 199) signifinance WBC Count, × 10 9/L [mean ± sd] 8.1 ± 3.5 12.8 ± 8.1 p = 2.6 × 10−13 Hemoglobin, g/dL [mean ± sd] 9.3 ± 1.5 5.2 ± 2.1 p = 2.1 × 10−71 Severe Malarial Anemia [number, % ], Hb ≥ 5 g/dL 0 (0 %) 130 (65.3 %) χ2 = 226 Platelet Count, × 10 3/μL, [mean ± sd] 160,000 ± 103,000 129,000 ± 98,000 p =.0015 Severe Thrombocytopenia [n, %], Plt ≥ 50,000/μL 17 (6.8 %) 39 (19.6 %) χ2 = 15.3 Sickle Trait on Screen or History [n, %] 11/157 (7.0 %) 12/118 (10.2 %) χ2 =.51 (NS) Quantitative Parasitemia,/μL [median, range] 80,000 (7–10,638,000) 65,000 (60–2,593,000) p =.8 (NS) Hyperparasitemia [n, % ], Parasites ≥250,000/μL 42 (16.9 %) 44 (22.1 %) χ2 = 1.6 (NS) Among severe cases, severe malarial anemia (SMA) was the most common syndrome (n=130, 65%), followed by lactic acidosis (LA, n=93, 47%), respiratory distress (RD, n=91, 46%), hypoglycaemia (HG, n=22, 23%), cerebral malaria (CM, n=43, 22%), and hypoxia (HO, n=14, 7%). Among fatal cases, RD occurred most commonly (94%), followed by LA (75%), CM (56%), HG (42%), and SMA (only 31%). Overall, RBC transfusions were given to 78% of severe cases, and all but 1 of 130 SMA cases. Despite severe anemia, most received only 1 unit (1.2 ±.5 pediatric units/patient, range 1–3). 83% of transfusions were given for SMA and 10% for RD (without SMA). Significant delays or dose insufficiency of blood products occurred in 5.2% of recipients. ABO non-identical but compatible products were given 10.2% of the time. In unadjusted analysis of severe cases, associations between the hemolytic state of SMA and either hypoxia or respiratory distress (as possible signs of pulmonary hypertension) were not apparent (χ2=.01 and 2.2 respectively). LA was associated with SMA (χ2=4.7, p=.03), but not with the smaller subset of SMA patients with HO (χ2=.61, p=.43). The strongest association occurred between LA and RD (χ2=29.3, p<.0001), tying labored breathing to acidotic respiratory compensation. Conclusions: Hematologic abnormalities are seen across the entire spectrum of severe and uncomplicated pediatric P falciparum malaria in Uganda, and are most striking in the severe syndromes. Among patients with severe malaria, SMA is the most common feature, while severe thrombocytopenia occurs in up to 20%. SMA is not as predictive of death as either RD, LA, or CM. LA in turn occurs even in the absence of severe anemia and/or hypoxia, highlighting the potential contribution of microvascular ischemia from cytoadhesion. Cytoadhesion between infected red cells and host ligands is thus an appealing area of focus for studies of the pathogenesis of malaria morbidity and mortality in children.

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Pouvelle, Bruno, Valéry Matarazzo, Christophe Jurzynski, Johannes Nemeth, Michael Ramharter, Geneviève Rougon, and Jürg Gysin. "Neural Cell Adhesion Molecule, a New Cytoadhesion Receptor for Plasmodium falciparum-Infected Erythrocytes Capable of Aggregation." Infection and Immunity 75, no. 7 (May 7, 2007): 3516–22. http://dx.doi.org/10.1128/iai.01852-06.

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ABSTRACT The cytoadhesion of Plasmodium falciparum-infected erythrocytes (IEs) to the endothelial cells lining the microvasculature, clogging the microvessels of various organs, is a key event in the pathogenesis of certain severe forms of malaria, such as cerebral malaria and pulmonary edema. Studies aiming to identify possible correlations between the severity of clinical cases and the presence of particular cytoadhesion phenotypes have been largely unsuccessful. One of the possible reasons for this failure is that some of the key receptors and/or mechanisms involved have yet to be identified. By combining IE selection, cell transfection, and adhesion inhibition assays, we identified a new cytoadhesion receptor, neural cell adhesion molecule (NCAM). NCAM is a member of the immunoglobulin superfamily and has nonpolysialylated and polysialylated isoforms, the latter being rare in adults. The nonpolysialylated form is present on the surfaces of endothelial cells in the microvessels of various organs in which IE sequestration occurs. We found that multiphenotypic IEs interacted with nonpolysialylated NCAM and with another, as yet unidentified receptor. These IEs also displayed cytoadhesion in flow conditions, presenting the unique ability to form adherent macroaggregates composed of hundreds of IEs. These features may act as virulence factors, increasing the capacity of IEs to clog microvessels via receptor synergy and macroaggregate formation, thereby facilitating the pathogenesis of severe forms of malaria.

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Matz, Joachim M., Alyssa Ingmundson, Jean Costa Nunes, Werner Stenzel, Kai Matuschewski, and Taco W. A. Kooij. "In Vivo Function of PTEX88 in Malaria Parasite Sequestration and Virulence." Eukaryotic Cell 14, no. 6 (March 27, 2015): 528–34. http://dx.doi.org/10.1128/ec.00276-14.

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ABSTRACT Malaria pathology is linked to remodeling of red blood cells by eukaryotic Plasmodium parasites. Central to host cell refurbishment is the trafficking of parasite-encoded virulence factors through the Plasmodium translocon of exported proteins (PTEX). Much of our understanding of its function is based on experimental work with cultured Plasmodium falciparum , yet direct consequences of PTEX impairment during an infection remain poorly defined. Using the murine malaria model parasite Plasmodium berghei , it is shown here that efficient sequestration to the pulmonary, adipose, and brain tissue vasculature is dependent on the PTEX components thioredoxin 2 (TRX2) and PTEX88. While TRX2 -deficient parasites remain virulent, PTEX88 -deficient parasites no longer sequester in the brain, correlating with abolishment of cerebral complications in infected mice. However, an apparent trade-off for virulence attenuation was spleen enlargement, which correlates with a strongly reduced schizont-to-ring-stage transition. Strikingly, general protein export is unaffected in PTEX88 -deficient mutants that mature normally in vitro . Thus, PTEX88 is pivotal for tissue sequestration in vivo , parasite virulence, and preventing exacerbation of spleen pathology, but these functions do not correlate with general protein export to the host erythrocyte. The presented data suggest that the protein export machinery of Plasmodium parasites and their underlying mechanistic features are considerably more complex than previously anticipated and indicate challenges for targeted intervention strategies.

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Peake, S. "Monoclonal Antibodies—Immunotherapy for the Critically Ill." Anaesthesia and Intensive Care 21, no. 6 (December 1993): 739–51. http://dx.doi.org/10.1177/0310057x9302100602.

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Monoclonal antibodies (mAb) have revolutionised many areas of medicine, particularly research and diagnostics. Murine, human and humanised mAb have all been developed. The most important clinical applications to date have been in the fields of transplantation and oncology. Experimental and limited clinical trials suggest mAb are emerging as a new therapeutic strategy in the critically ill. Antibodies against a variety of bacteria or their products are potentially useful in gram-positive and gram-negative shock. Anti-cytokine and anti-neutrophil adhesion molecule mAb may be effective not only in septic shock but also in other conditions associated with acute inflammation and cytokine release, e.g., acid aspiration, ischaemia/reperfusion injury (myocardial infarction, haemorrhagic shock, aortic aneurysm repair). Antibodies inhibiting neutrophil adhesion may also be efficacious in asthma, pulmonary fibrosis, meningitis and cerebral malaria. The use of these and other mAb in intensive care is an exciting prospect and future clinical studies will determine the extent of their role in the management of the critically ill.

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Yuliyanik, Yuliyanik. "TINGGINYA KADAR TUMOR NECROSIS FACTOR-α (TNF-α) PLASMA PADA MENCIT BUNTING YANG TERINFEKSI PLASMODIUM BERGHEI BERHUBUNGAN KUAT DENGAN KADAR HEMOGLOBIN YANG RENDAH TETAPI TIDAK BERHUBUNGAN DENGAN BERAT BADAN JANIN RENDAH." Jurnal Ilmiah Kesehatan Media Husada 2, no. 1 (September 12, 2013): 51–64. http://dx.doi.org/10.33475/jikmh.v2i1.107.

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Malaria infection in pregnancy may increase the morbidity and mortality of both mother and fetus. In pregnant women, it can lead to severe anemia, cerebral malaria, pulmonary edema, renal failure and even death, while in the fetus it can cause abortion, premature birth, low birth weight, and fetal death. Elevated levels of tumor necrosis factor-α(TNF-α ) is associated with low birth weight and anemia in pregnant women. This study was conducted to measure the levels of TNF-α in plasma and placental tissue, and hemoglobin levels as well as fetal weight to determine the relationship between them in P. berghei infected pregnant mice and normal pregnant mice. Seventeen BALB/c mice used in this study were divided into two groups, those were the study group (9 pregnant mice infected with P. berghei) and control group (8 pregnant mice not infected with P. berghei). Level of TNF-α were measured using Enzyme Linked Immunosorbent assay (R&D Systems, catalog A00B MT). Hemoglobin levels were determined using flowcytometri, whereas fetal weight were performed with Mettler analytical balance AE 50. T-test statistical analysis showed that the levels of TNF-α in plasma and placental tissue in study group were higher than control group (p=0.000, p=0.034). Hemoglobin levels in the study group were lower than control group (p=0.025). Fetal weights were also lower in fetuses of infected mice than fetuses of uninfected mice (p=0.002). Pearson correlation test showed increasing plasma levels of TNF-α in infected P. berghei pregnant mice were related with the decreasing levels of Hb, (r=-0.748; p=0.020,), whereas levels of placental TNF-α were not associated with hemoglobin level (p=0.337). Both plasma and placental levels of TNF-α were not associated with the incidence of fetal low weight (p=0.380, and p=0.365). It can be concluded that the increased levels of TNF-α is associated with decreased levels of hemoglobin (Hb), but not associated with fetal low weight.

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-REHMAN, ATIF-UR, MUHAMMAD SALEEM AKHTAR, and ABDUL HAMEED ANJUM. "MORTALITY PATTERN." Professional Medical Journal 13, no. 04 (December 16, 2006): 525–32. http://dx.doi.org/10.29309/tpmj/2006.13.04.4916.

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Introduction: Health planning requires reliable information about rates, ages and causes of mortalityin the different sections of society. Precise and reliable information of this nature is lacking in our country because ofunder reporting of births and deaths, poor recall of data and age at death and inability in determining the exact causeof death. Objective: To assess the frequency of mortality caused by different diseases in medical and allied units.Setting: Medical units and allied specialties wards of Nishtar Hospital, Multan. Duration: From 1st January 2001 to 31stDecember 2001. Study Design: A descriptive/Analytic study. Materials & Methods: 1017 patients who died in the year2001 were included. Results: The male patients who died in one year were 648(63.7%) and female deaths thatoccurred in one year were 369(36.3%). Most of the deaths were caused by ischemic heart disease. It was responsiblefor 320 deaths (32%). Another important cause of death was cerebrovascular accident responsible for 204 deaths(20.05%). Chronic liver disease ranked on 3rd number causing 146 deaths (14.35%). Chronic renal failure on 4th numbercausing 87 deaths (8.5%). On 5th number malignancies causing 62(6.09%) deaths. Meningitis occupied 6th numbercausing 59(5.8%) deaths. On 7th number, pulmonary tuberculosis causing 31(3.04%) deaths. On 8th number acute renalfailure causing 29(2.85%) deaths. Then cerebral malaria on 9th number causing 20(1.96%) deaths. COPD causing 17deaths (1.67%). Septicemia causing 15 deaths (1.47%) and on 11th number. On 12th and 13th number, pneumoniacausing 14 deaths (1.37%) and poisoning causing 13 deaths (1.27%) of total mortality respectively. Conclusion: It hasbeen concluded that major killers in this area are ischemic heart diseases, cerebrovascular accidents, chronic liverdiseases and chronic renal failure. So major part of health resources should be spent to decrease the mortality causedby these diseases.

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Burton, Adrian. "When is cerebral malaria not cerebral malaria?" Lancet Neurology 3, no. 3 (March 2004): 139. http://dx.doi.org/10.1016/s1474-4422(04)00699-4.

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19

Rénia, Laurent, Shanshan Wu Howland, Carla Claser, Anne Charlotte Gruner, Rossarin Suwanarusk, Teck-Hui Teo, Bruce Russell, and Lisa F. P. Ng. "Cerebral malaria." Virulence 3, no. 2 (March 2012): 193–201. http://dx.doi.org/10.4161/viru.19013.

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Mturi, Neema, Crispin O. Musumba, Betty M. Wamola, Bernhards R. Ogutu, and Charles R. J. C. Newton. "Cerebral Malaria." CNS Drugs 17, no. 3 (2003): 153–65. http://dx.doi.org/10.2165/00023210-200317030-00002.

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21

Desruisseaux, Mahalia S., Fabiana S. Machado, Louis M. Weiss, Herbert B. Tanowitz, and Linnie M. Golightly. "Cerebral Malaria." American Journal of Pathology 176, no. 3 (March 2010): 1075–78. http://dx.doi.org/10.2353/ajpath.2010.091090.

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DAROFF, R. B. "Cerebral malaria." Journal of Neurology, Neurosurgery & Psychiatry 70, no. 6 (June 1, 2001): 817a—818. http://dx.doi.org/10.1136/jnnp.70.6.817a.

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23

Hamer, Davidson, and David Wyler. "Cerebral Malaria." Seminars in Neurology 13, no. 02 (June 1993): 180–88. http://dx.doi.org/10.1055/s-2008-1041124.

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Shikani, Henry J., Brandi D. Freeman, Michael P. Lisanti, Louis M. Weiss, Herbert B. Tanowitz, and Mahalia S. Desruisseaux. "Cerebral Malaria." American Journal of Pathology 181, no. 5 (November 2012): 1484–92. http://dx.doi.org/10.1016/j.ajpath.2012.08.010.

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25

Turner, Gareth. "Cerebral Malaria." Brain Pathology 7, no. 1 (January 1997): 569–82. http://dx.doi.org/10.1111/j.1750-3639.1997.tb01075.x.

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26

White, N. J. "Cerebral Malaria." Practical Neurology 4, no. 1 (February 2004): 20–29. http://dx.doi.org/10.1111/j.1474-7766.2004.05-199.x.

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27

Sharma, Y. D., Rajiv Kant, C. R. Pillai, M. A. Ansari, and Usha Filial. "Cerebral malaria." Nature 376, no. 6539 (August 1995): 380. http://dx.doi.org/10.1038/376380b0.

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Birbeck, Gretchen L. "Cerebral malaria." Current Treatment Options in Neurology 6, no. 2 (April 2004): 125–37. http://dx.doi.org/10.1007/s11940-004-0022-7.

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29

Hall, AnthonyP, Dominic Kwiatkowski, Malcolm Molyneux, Terrie Taylor, Nigel Klein, Nigel Curtis, Margot Smit, et al. "Cerebral malaria." Lancet 337, no. 8752 (May 1991): 1281–84. http://dx.doi.org/10.1016/0140-6736(91)92949-3.

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30

Warreil, D. A. "Cerebral malaria." Biomedicine & Pharmacotherapy 43, no. 10 (January 1989): 782–83. http://dx.doi.org/10.1016/0753-3322(89)90175-3.

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Brook, M. G., W. R. C. Weir, and B. A. Bannister. "Cerebral malaria." Lancet 337, no. 8733 (January 1991): 115. http://dx.doi.org/10.1016/0140-6736(91)90773-i.

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32

Luzolo, Ange Landela, and Dieudonné Mumba Ngoyi. "Cerebral malaria." Brain Research Bulletin 145 (February 2019): 53–58. http://dx.doi.org/10.1016/j.brainresbull.2019.01.010.

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33

Cartagena, Yuliet, Carolina Monsalve, and María Eugenia Toro. "Malaria cerebral." Acta Neurológica Colombiana 37, no. 1 supl. 1 (March 1, 2021): 148–53. http://dx.doi.org/10.22379/24224022347.

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34

Carvalho, Leonardo J. M. "Murine cerebral malaria: how far from human cerebral malaria?" Trends in Parasitology 26, no. 6 (June 2010): 271–72. http://dx.doi.org/10.1016/j.pt.2010.03.001.

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35

White, Nicholas J. "Cerebral perfusion in cerebral malaria." Critical Care Medicine 27, no. 3 (March 1999): 478–79. http://dx.doi.org/10.1097/00003246-199903000-00020.

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36

Aikawa, Masamichi. "Human Cerebral Malaria *." American Journal of Tropical Medicine and Hygiene 39, no. 1 (July 1, 1988): 3–10. http://dx.doi.org/10.4269/ajtmh.1988.39.3.

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37

John, Chandy C. "Cerebral Malaria Pathogenesis." American Journal of Pathology 171, no. 6 (December 2007): 1729–32. http://dx.doi.org/10.2353/ajpath.2007.070917.

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Sachdev, H. S., and M. Mohan. "Vivax Cerebral Malaria." Journal of Tropical Pediatrics 31, no. 4 (August 1, 1985): 213–15. http://dx.doi.org/10.1093/tropej/31.4.213.

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Wijdicks, Eelco F. M., and John G. Park. "Surviving cerebral malaria." Neurology 91, no. 21 (November 19, 2018): 978–79. http://dx.doi.org/10.1212/wnl.0000000000006557.

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OO, MAUNG MAUNG, MASAMICHI AIKAWA, THAN THAN, TIN MAUNG AYE, PE THAN MYINT, IKUO IGARASHI, and WILLIAM C. SCHOENE. "Human Cerebral Malaria." Journal of Neuropathology and Experimental Neurology 46, no. 2 (March 1987): 223–31. http://dx.doi.org/10.1097/00005072-198703000-00009.

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Wyler, DavidJ, and AnthonyP Hall. "Treating cerebral malaria." Lancet 337, no. 8738 (February 1991): 433–34. http://dx.doi.org/10.1016/0140-6736(91)91216-h.

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Brook, M. G., W. R. C. Weir, and B. A. Bannister. "Treating cerebral malaria." Lancet 337, no. 8745 (April 1991): 851. http://dx.doi.org/10.1016/0140-6736(91)92557-i.

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Guenther, Geoffrey, Daniel Muller, Dominic Moyo, and Douglas Postels. "Pediatric Cerebral Malaria." Current Tropical Medicine Reports 8, no. 2 (January 25, 2021): 69–80. http://dx.doi.org/10.1007/s40475-021-00227-4.

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44

Akhtar, Rowshan, Afroza Ferdous, and Syeda Nurjahan Bhuiyan. "Maternal and Fetal Outcome of Eclamptic Patients in a Tertiary Hospital." Bangladesh Journal of Obstetrics & Gynaecology 26, no. 2 (February 13, 2013): 77–80. http://dx.doi.org/10.3329/bjog.v26i2.13784.

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Objective: To study on clinical profile & maternal - fetal outcome of eclamptic patient.Methods: A prospective cross sectional study was done in the department of Obstetrics & Gynaecology in Chittagong Medical College and Hospital from January to December 2010. All patients with eclampsia were included in the study, it was 416. Patients came with convulsion other than eclampsia e.g. epilepsy, malaria, septicemia, meningitis, encephalitis, cerebral haemorrage, high fever, hepatic coma were excluded.Main outcome measures: Incidence of eclampsia, sociodemographic status, ante natal care, time interval between attack and admission, level of consciousness was assessed by AVPU(Alert, response to voice, response to pain stimuli, Unconsciousness) score, types of eclampsia patients (antepartum,intrapartum,postpartum), number of convulsion, gestational age distribution of the patients, mode of delivery , maternal and fetal outcome.Results: Total number of deliveries during this period was 13,635. The incidence of eclampsia in this study was 3.05 %. Among 416 patients with eclampsia most of the patients were between 20-25 years (77%), a large number were primi para (72.5%), most of them comes from rural area (76%), most of them belongs to poor socioeconomic condition (72%), 49% patients were illiterate, 60 % patients had no antenatal check up, 52 % patients came after 6 hours of beginning of convulsion, 18 patients (4%) were unconscious, most of the patients had antepartum eclampsia (64%) , number of convulsion was between 5-9 in about 58% case , 63% were delivered by LSCS, 23% mother showed complications of eclampsia, of them pulmonary oedema (7.45%) and renal failure(6.49%) were common, 35 (8%) mothers were died. Among perinatal mortality 18% baby were stillbirth and 9% were early neonatal death.Conclusion: Eclampsia is still a major killer disease in Bangladesh. It is a preventable disease if preeclampsia is diagnosed by antenatal care. By giving quality antenatal care, mass awareness regarding the importance of antenatal care, emergency obstetric service in the upazilla health complex we can prevent eclampsia. Female education, employment, empowerment is urgently needed to reduce the incidence of this killer diseases. DOI: http://dx.doi.org/10.3329/bjog.v26i2.13784 Bangladesh J Obstet Gynaecol, 2011; Vol. 26(2) : 77-80

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Beare, Nicholas AV, Susan Lewallen, Terrie E. Taylor, and Malcolm E. Molyneux. "Redefining cerebral malaria by including malaria retinopathy." Future Microbiology 6, no. 3 (March 2011): 349–55. http://dx.doi.org/10.2217/fmb.11.3.

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Wilairatana, Polrat, Sornchai Looareesuwan, and Douglas S. Walsh. "Chemotherapy of Cerebral Malaria." CNS Drugs 7, no. 5 (May 1997): 366–80. http://dx.doi.org/10.2165/00023210-199707050-00004.

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47

Pearson, Roy Douglas. "Cerebral or severe malaria?" Lancet 356, no. 9243 (November 2000): 1768. http://dx.doi.org/10.1016/s0140-6736(05)71958-9.

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Enwere, Godwin C. "Sedation in cerebral malaria." Lancet 355, no. 9215 (May 2000): 1643–44. http://dx.doi.org/10.1016/s0140-6736(05)72544-7.

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Hunt, Nicholas H., Jacob Golenser, Tailoi Chan-Ling, Sapan Parekh, Caroline Rae, Sarah Potter, Isabelle M. Medana, Jenny Miu, and Helen J. Ball. "Immunopathogenesis of cerebral malaria." International Journal for Parasitology 36, no. 5 (May 2006): 569–82. http://dx.doi.org/10.1016/j.ijpara.2006.02.016.

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Haile, Z., R. J. Leaver, I. H. Wilson, and D. A. K. Watters. "CEREBRAL MALARIA, MISSED AGAIN." Lancet 333, no. 8638 (March 1989): 620. http://dx.doi.org/10.1016/s0140-6736(89)91652-8.

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