Home HOMEPAGE   Tue, 10/15/2024 GMT + 7
    Q & A   Site map Forum   Site map Sitemap   E-mali Contact   Vietnamese Vietnamese
IMPE-QN
Finance & Retail News - Events
Home
International
IMPE
Scientific research
World Malaria Day 25 April
Web Sites & Commerce Introduction
Web Sites & Commerce Collaborative activities
Web Sites & Commerce Training
Web Sites & Commerce Specific research studies
Web Sites & Commerce Publications
Web Sites & Commerce Mass organization activities
Web Sites & Commerce Legal documents
Web Sites & Commerce Statistical data
Web Sites & Commerce Work safety
Web Sites & Commerce Vietnam`s Physicians
Web Sites & Commerce Malariology
Web Sites & Commerce Helminthology
Web Sites & Commerce Other vector-borne diseases

SEARCH

LOGIN
Username
Password

WEBLINKS
Other links

Visiting users: 204
5 4 1 0 2 9 0 0
Online
2 0 4
 News - Events International
Up-to-date in severe malaria with pulmonary complication: world english medical literature review

By the case report of severe malaria with pulmonary form and other complications in Vietnam. We would like to share with colleagues o­n pulmonary complication in pernicious-severe malaria via medical literature review.

1. Pulmonary edema in severe falciparum malaria. Hemodynamic study and clinicophysiologic correlation (Charoenpan P et al., 1990)

This study was performed to extend the knowledge of the pathogenesis of PE in severe falciparum malaria. Sequential hemodynamic studies were conducted in 13 patients with severe falciparum malaria. Seven patients developed PE, while the other six patients had NPE. Two patients died, o­ne in each group. Hemodynamic changes were found in both groups, including an initial reduction in SVR and PVR, along with an increased CI and variable values (normal and increased) of PCWP. All abnormalities persisted for at least two days; changes in PVR lasted especially longer (throughout five days). The initial hemodynamic changes cannot predict the development of PE; however, heavy parasitemia of more than 60 percent and severe hypoalbuminemia were found to be more common in PE than NPE. Of three patients with PE who had normal PCWP, o­ne died, with postmortem findings of increased pulmonary capillary permeability. The increased PCWP which was found in the other four cases of PE was proven to be volume overload without evidence of CHF. It was concluded that the pathophysiologic changes in severe falciparum malaria were systemic and pulmonary vasodilation. The abnormal pulmonary vascular change was found to be the cause of PE. Volume overload and hypoalbuminemia could aggravate further pulmonary capillary leakage in these cases.

2. Pulmonary manifestations of malaria (Rauber K, 1987)

We report o­n the two different types of pulmonary manifestations in acute plasmodium falciparum malaria. The more severe variant shows long standing interstitial pulmonary infiltrates, whereas in the more benign courses o­nly short-term pulmonary edemas are visible.

3. Pulmonary damage associated with falciparum malaria: a report of ten cases (James MF et al., 1985)

Ten cases of pulmonary involvement associated with falciparum malaria are described. Measurements of pulmonary capillary wedge pressure were made in five of the ten cases, and no evidence of raised hydrostatic pressure in the pulmonary microcirculation was found which could account for the pulmonary oedema observed. All cases were treated with oxygen and positive end expiratory pressure (PEEP), and there were six survivors. The evidence to support the presence of an Adult Respiratory Distress Syndrome (ARDS)-type lesion in malaria is discussed.

4. Acute respiratory distress syndrome (ARDS) in cerebral malaria (Blanloeil Y, 1980)

Non hemodynamic pulmonary edemas included by some authors in the acute respiratory distress syndrome (ARDS) had been reported in cerebral malaria. We describe a new case. Clinical data, hemodynamic studies with PWP measurement, and anatomic findings are coherent with the diagnosis of ARDS. Although the underlying causal mechanisms--the marked parasitemia and its consequence o­n permeability of the pulmonary capillary remain speculative, they seem credible. The pulmonary lesions are provoked by these main factors and worsened by hypoprotidemia and surinfection. Prevention of all these factors can stop the evolution towards refractory hypoxemia but the precocity of quinine treatment remains the most important point.

5. Cytoadherence in human falciparum malaria as a cause of respiratory distress (Corbett CE et al, 1989).

The ultrastructure of three cases of fatal human falciparum malaria was studied in order to identify the cytoadherence of the endothelial cells in relation to parasitized red blood cells and septal interstitial changes which could be related to respiratory distress. Two cases showed marked endothelial oedema narrowing the capillary lumen with areas of adherence preferentially related to knobs, accompanied by septal interstitial oedema. o­ne case showed no endothelial cells oedema, no knobs in parasitized red blood cells with no cytoadherence, no septal interstitial oedema and no respiratory distress. Cytoadherence seems to be the mechanism responsible for the septal pulmonary changes in severe falciparum malaria.

6. Cytoadherence of knobless Plasmodium falciparum-infected erythrocytes and its inhibition by a human monoclonal antibody (Udomsangpetch R, 1989).

Red blood cells infected with mature stages of the malaria parasite Plasmodium falciparum bind to the endothelial lining of capillaries and venules. This sequestration is important for the survival of the parasite but may have severe consequences for the host. For example, it is involved in the causation of cerebral malaria which carries 25% mortality. Knob-like protrusions present o­n the surface of infected erythrocytes have been considered necessary but not sufficient for this cytoadherence. Here we describe the adhesion to endothelial cells of infected erythrocytes which do not have knobs. A human monoclonal antibody (33G2) which was specific for an epitope containing regularly spaced dimers of glutamic acid present in the repeated amino-acid sequences of some defined P. falciparum antigens was found to inhibit cyto-adherence and may therefore be an important reagent for elucidating the molecular basis of parasite sequestration.

7. Plasmodium falciparum: analysis of the cytoadherence inhibition of the human monoclonal antibody 33G2 and of antibodies reactive with antigen Pf332 (Iqbal J, 1993)

The capacity of a human monoclonal antibody (MAb 33G2) to interfere in vitro both with Plasmodium falciparum merozoite invasion and cytoadherence of infected erythrocytes to melanoma cells has been reported. MAb 33G2 cross-reacts with several P. falciparum antigens but shows highest reactivity with repeated sequences in the asexual blood stage antigen Pf332. This study was conducted in order to further analyze the cytoadherence inhibition mediated by MAb 33G2 and to evaluate the relative contribution of antibodies to Pf332 in the inhibitory activity of immunoglobulins from P. falciparum immune donors. We show here that MAb 33G2 inhibits cytoadherence of infected erythrocytes (PRBCs) with similar efficiency independently of the strain of parasite, while the inhibitory capacity of immunoglobulin fractions from Liberian immune donors was restricted to some strains o­nly. There appears to be no correlation between the reactivity with Pf332 of immunoglobulin preparations from different donors and their capacity to inhibit cytoadherence of PRBCs to melanoma cells. In contrast to MAb 33G2, polyclonal antibodies affinity purified o­n the Pf332 peptide containing the epitope seen by the MAb showed little or no inhibition of cytoadherence of infected erythrocytes.

8. Pulmonary edema in cerebral malaria patients in Thailand (Aursudkij B,1998)

Pulmonary edema is a serious complication of falciparum malaria that usually occurs in association with cerebral malaria, acute renal failure, high parasitemias, or delayed antimalarial treatment. From 1993 to 1996, 120 adult patients admitted to the intensive care unit of the Bangkok Hospital for Tropical Diseases were enrolled in a prospective study to assess the combination of artesunate and mefloquine for the treatment of cerebral malaria. Twenty-five patients (21%) presented with pulmonary edema and a majority developed complications in other organs as well, especially acute renal failure. In most patients (19 of 25), pulmonary edema was noted o­n the first day of admission and was associated with higher parasitemias and levels of acidemia, than in patients without pulmonary edema.

Ten of the 25 patients diagnosed with pulmonary edema developed signs consistent with adult respiratory distress syndrome (ARDS). The mean central venous pressure when pulmonary edema was diagnosed was markedly lower in ARDS than in non-ARDS patients, supporting the argument that fluid imbalance is not essential for malaria-induced lung injury. Seven of 10 patients with ARDS died, 5 within 24 hours of admission, but there were no deaths in the 15 pulmonary edema patients without ARDS. Early diagnosis and prompt treatment remain important principles to reduce the morbidity and mortality associated with complicated falciparum malaria. This report emphasizes that ARDS, when concurrently occurs, is a poor prognostic clinical indicator in cerebral malaria.

Treat Respir Med. 2006;5(6):419-28.

Pulmonary manifestations of malaria : recognition and management.

Taylor WR1, Cañon V, White NJ.

Lung involvement in malaria has been recognized for more than 200 hundred years, yet our knowledge of its pathogenesis and management is limited. Pulmonary edema is the most severe form of lung involvement. Increased alveolar capillary permeability leading to intravascular fluid loss into the lungs is the main pathophysiologic mechanism. This defines malaria as another cause of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS).Pulmonary edema has been described most often in non-immune individuals with Plasmodium falciparum infections as part of a severe systemic illness or as the main feature of acute malaria. P.vivax and P.ovale have also rarely caused pulmonary edema.Clinically, patients usually present with acute breathlessness that can rapidly progress to respiratory failure either at disease presentation or, interestingly, after treatment when clinical improvement is taking place and the parasitemia is falling. Pregnant women are particularly prone to developing pulmonary edema. Optimal management of malaria-induced ALI/ARDS includes early recognition and diagnosis. Malaria must always be suspected in a returning traveler or a visitor from a malaria-endemic country with an acute febrile illness. Slide microscopy and/or the use of rapid antigen tests are standard diagnostic tools. Malaria must be treated with effective drugs, but current choices are few: e.g. parenteral artemisinins, intravenous quinine or quinidine (in the US o­nly). A recent trial in adults has shown that intravenous artesunate reduces severe malaria mortality by a third compared with adults treated with intravenous quinine. Respiratory compromise should be managed o­n its merits and may require mechanical ventilation.Patients should be managed in an intensive care unit and particular attention should be paid to the energetic management of other severe malaria complications, notably coma and acute renal failure. ALI/ARDS may also be related to a coincidental bacterial sepsis that may not be clinically obvious. Clinicians should employ a low threshold for starting broad spectrum antibacterials in such patients, after taking pertinent microbiologic specimens. Despite optimal management, the prognosis of severe malaria with ARDS is poor.ALI/ARDS in pediatric malaria appears to be rare. However, falciparum malaria with severe metabolic acidosis or acute pulmonary edema may present with a clinical picture of pneumonia, i.e. with tachypnea, intercostal recession, wheeze or inspiratory crepitations. This results in diagnostic confusion and suboptimal treatment. Whilst this is increasingly being recognized in malaria-endemic countries, clinicians in temperate zones should be aware that malaria may be a possible cause of 'pneumonia' in a visiting or returning child.

Braz J Infect Dis. 2005 Oct;9(5):425-30. Epub 2006 Jan 6.

Acute respiratory distress syndrome due to vivax malaria: case report and literature review.

Lomar AV1, Vidal JE, Lomar FP, Barbas CV, de Matos GJ, Boulos M.

Severe pulmonary involvement in malaria has been frequently reported in cases of Plasmodium falciparum infection, but rarely in vivax malaria. Among the 11 previous cases of vivax-related severe respiratory involvement described in the literature, all except o­ne developed it after the beginning of anti-malarial treatment; these appear to correspond to an exacerbation of the inflammatory response. We report the case of a 43-year-old Brazilian woman living in a malaria-endemic area, who presented acute respiratory distress syndrome (ARDS) caused by P. vivax before starting anti-malarial treatment. The diagnosis was made based o­n microscopic methods. A negative rapid immunochromatographic assay, based o­n the detection of Histidine Rich Protein-2 (HRP-2) of P. falciparum, indicated that falciparum malaria was unlikely. After specific anti-plasmodial therapy and intensive supportive care, the patient was discharged from the hospital. We conclude that vivax malaria-associated ARDS can develop before anti-malarial therapy.

Trop Doct. 2013 Apr;43(2):83-5. doi: 10.1177/0049475513485733. Epub 2013 May 24.

Plasmodium vivax malaria presenting as acute respiratory distress syndrome: a case report.

Rahman AK1, Sulaiman FN.

Severe pulmonary involvement in malaria has been frequently reported in cases of Plasmodium falciparum infection but rarely in vivax malaria. We look at a case of a 38-year-old man living in a malaria endemic area who presented with acute respiratory distress syndrome (ARDS) caused by P. vivax. DNA polymerase chain reaction (PCR) confirmed that it was not a mixed infection. After specific antimalarial therapy and intensive supportive care, the patient was discharged from the hospital. This case illustrates that P. vivax-induced ARDS is not uncommon and should be readily recognized by the treating physicians. A confirmatory test with PCR is required in order to exclude P. falciparum co-infection.

J Infect Dev Ctries. 2015 Aug 29;9(8):910-3. doi: 10.3855/jidc.6813.

Plasmodium vivax infection causes acute respiratory distress syndrome: a case report.

Gupta H1, Afsal MP, Shetty SM, Satyamoorthy K, Umakanth S.

Plasmodium falciparum (Pf) is associated with numerous complications and high mortality, whereas Plasmodium vivax (Pv) infection is generally considered to be benign. However, severe complications, such as acute respiratory distress syndrome (ARDS) in Pv infection, are emerging. This case report highlights the complication of ARDS during the course of Pv infection in a 60-year-old woman. The diagnosis of the patient was made using microscopy, immunochromatography, and polymerase chain reaction assays for Pf and Pv species. The data indicated the presence of mono-Pv infection in the patient's blood, and Pf infection was specifically ruled out. The patient was discharged after intensive supportive care and antimalarial treatment. Pv infection is associated with ARDS and other complications such as sepsis and multi-organ dysfunction syndrome; this enhanced severity of Pv infection, if unrecognized, can lead to more deaths in malaria-endemic areas.

ARDS (Srinivas, 2015)

Acute pulmonary edema is a grave and usually fatal complication of severe falciparum malaria with more than 50% mortality. Acute lung injury is defined as the acute o­nset of bilateral pulmonary infiltrates with an arterial oxygen tension/fractional inspired oxygen ratio of 300 mmHg or less, a pulmonary artery wedge pressure of 18 mmHg or less, and no evidence of left atrial hypertension. ARDS is defined as acute lung injury and an arterial oxygen tension/fractional inspired oxygen ratio of 200 mmHg or less. Volume overload and hypoalbuminemia may aggravate pulmonary capillary leakage. Chest radiograph abnormalities range from confluent nodules to basilar and/or diffuse bilateral pulmonary infiltrates. Noncardiogenic pulmonary edema rarely occurs with P. vivax and P. ovale malaria.

In addition to severe falciparum parasitemia and sequestration, secondary infections, severe anemia, hyperpyrexia, dehydration/fluid overload, metabolic acidosis, hypoxia and disseminated intravascular coagulation can also contribute to the cardiovascular problems in malaria. Although myocardial function is generally well preserved in severe falciparum malaria, malaria can complicate pre-existing cardiac decompensation and may even prove fatal for patients with compromised heart. Cardiac arrhythmias are uncommon.

Pathology of Acute Pulmonary Oedema: In a few patients it could be due to fluid overload as a result of enthusiastic fluid therapy. In others it develops even with normal or negative fluid balance. Pulmonary oedema develops later compared to other complications and it may even appear several days after treatment for malaria, when the patient is otherwise improving with a reduction in peripheral parasitemia.

The mechanism of pulmonary oedema is not clearly understood. It has a close resemblance to adult respiratory distress syndrome. While over-hydration may be the cause in some cases of pulmonary oedema, it can also develop in patients with normal capillary wedge pressures. Such cases may be due to increased permeability of pulmonary capillaries. Sequestration of red cells and clogging of pulmonary microcirculation and disseminated intravascular coagulation may also play their role. Pulmonary oedema is more common in patients with hyperparasitemia, renal failure and pregnancy and it is commonly associated with hypoglycemia and metabolic acidosis. It may develop suddenly after delivery, due to fluid overload. Pulmonary oedema may be the terminal event in many cases of fatal falciparum infection.

The first sign of impending pulmonary oedema is an increase in the respiratory rate. Tachypnoea may also be the first indicator of aspiration bronchopneumonia and metabolic acidosis and a chest X-ray will help in differentiating these conditions. Then patient develops signs of pulmonary oedema like basal crackles, cyanosis, tachycardia etc. The breathlessness worsens rapidly and the patient may die within a few hours. Hypoxia can cause convulsions and deterioration in the level of sensorium.


Management:

Pulmonary oedema is the most fatal of the complications of falciparum malaria and therefore calls for careful and energetic management.

Fluid overload should be avoided at all costs, especially in pregnant women. The central venous pressure should be maintained between 0-5 cm of H2O by regulating fluid intake and nursing the patient propped up at 450. All intravenous fluids should be stopped immediately and diuretics may have to be administered.

Initial management of pulmonary oedema includes treatment with oxygen, back-rest and diuretics if there is evidence of fluid overload. Inj. Furoscemide 40 mg should be given intravenously and if there is no desired response, the dose can be progressively increased up to 200 mg. Fluid volume can be further reduced by venesection and letting of 250 ml of blood initially. This blood or its packed cells can be re-transfused o­nce the problem settles down. The procedure can be repeated carefully if needed.

If the patient deteriorates with conservative treatment, mechanical ventilation is indicated. Positive end expiratory pressure ventilation may also be needed. Drugs like corticosteroids are not of any proven benefit in the management of these cases.

Overall, pulmonary oedema carries a poor prognosis.



17. Enhancing blockade of Plasmodium falciparum erythrocyte invasion: assessing combinations of antibodies against PfRH5 and other merozoite antigens.

Williams AR, Douglas AD, Miura K, Illingworth JJ, Choudhary P, Murungi LM, Furze JM, Diouf A, Miotto O, Crosnier C, Wright GJ, Kwiatkowski DP, Fairhurst RM, Long CA, Draper SJ.

PLoS Pathog. 2012;8(11):e1002991. doi: 10.1371/journal.ppat.1002991. Epub 2012 Nov 8.

PMID: 23144611, Free PMC Article, Similar articles



18. Plasmodium falciparum variant STEVOR antigens are expressed in merozoites and possibly associated with erythrocyte invasion.

Khattab A, Bonow I, Schreiber N, Petter M, Schmetz C, Klinkert MQ.

Malar J. 2008 Jul 23;7:137. doi: 10.1186/1475-2875-7-137.

PMID: 18651957, Free PMC Article, Similar articles

19. Antibodies raised against receptor-binding domain of Plasmodium knowlesi Duffy binding protein inhibit erythrocyte invasion.

Singh AP, Puri SK, Chitnis CE.

Mol Biochem Parasitol. 2002 Apr 30;121(1):21-31.

PMID: 11985860, Similar articles

20. Correlation of high levels of antibodies to multiple pre-erythrocytic Plasmodium falciparum antigens and protection from infection.

John CC, Moormann AM, Pregibon DC, Sumba PO, McHugh MM, Narum DL, Lanar DE, Schluchter MD, Kazura JW.

Am J Trop Med Hyg. 2005 Jul;73(1):222-8.

Acta Trop. 2009 Dec;112(3):295-302. doi: 10.1016/j.actatropica.2009.08.017. Epub 2009 Aug 18.

PMID: 19695213, Similar articles



25. High-level expression of the malaria blood-stage vaccine candidate Plasmodium falciparum apical membrane antigen 1 and induction of antibodies that inhibit erythrocyte invasion.

Kocken CH, Withers-Martinez C, Dubbeld MA, van der Wel A, Hackett F, Valderrama A, Blackman MJ, Thomas AW.

Infect Immun. 2002 Aug;70(8):4471-6. Erratum in: Infect Immun 2002 Oct;70(10):5901.

PMID: 12117958, Free PMC Article, Similar articles

27. Antibodies to ring-infected erythrocyte surface antigen (Pf155/RESA) protect against P. falciparum parasitemia in highly exposed multigravidas women in Malawi.

Astagneau P, Steketee RW, Wirima JJ, Khoromana CO, Millet P.

Acta Trop. 1994 Sep;57(4):317-25.

PMID: 7528968, Similar articles

28. Erythrocyte rosetting in Plasmodium falciparum malaria-with special reference to the pathogenesis of cerebral malaria.

Carlson J.

Scand J Infect Dis Suppl. 1993;86:1-79.

PMID: 8493454, Similar articles



29. Specificities of antibodies that inhibit merozoite dispersal from malaria-infected erythrocytes.

Lyon JA, Thomas AW, Hall T, Chulay JD.

Mol Biochem Parasitol. 1989 Aug;36(1):77-85.

PMID: 2509909, Similar articles

30. Band 3 clustering promotes the exposure of neoantigens in Plasmodium falciparum-infected erythrocytes.

Winograd E, Prudhomme JG, Sherman IW.

Mol Biochem Parasitol. 2005 Jul;142(1):98-105. Epub 2005 Apr 7.

PMID: 15907563, Similar articles

31. Induction of biologically active antibodies in mice, rabbits, and monkeys by Plasmodium falciparum EBA-175 region II DNA vaccine.

Sim BK, Narum DL, Liang H, Fuhrmann SR, Obaldia N 3rd, Gramzinski R, Aguiar J, Haynes JD, Moch JK, Hoffman SL.

Mol Med. 2001 Apr;7(4):247-54.

PMID: 11471569, Free PMC Article, Similar articles

32. Transmission-blocking immunity against malaria and other vector-borne diseases.

Kaslow DC.

Curr Opin Immunol. 1993 Aug;5(4):557-65. Review.

PMID: 8216932, Similar articles



33. Immunogenicity of a recombinant malaria vaccine candidate, domain I+II of AMA-1 ectodomain, from Indian P. falciparum alleles.

Lalitha PV, Biswas S, Pillai CR, Saxena RK.

Vaccine. 2008 Aug 18;26(35):4526-35. doi: 10.1016/j.vaccine.2008.06.031. Epub 2008 Jun 30.

PMID: 18590786, Similar articles

34. Molecular characterisation of Plasmodium reichenowi apical membrane antigen-1 (AMA-1), comparison with P. falciparum AMA-1, and antibody-mediated inhibition of red cell invasion.

Kocken CH, Narum1 DL, Massougbodji A, Ayivi B, Dubbeld MA, van der Wel A, Conway DJ, Sanni A, Thomas AW.

Hum Immunol. 2008 Dec;69(12):856-60. doi: 10.1016/j.humimm.2008.08.294. Epub 2008 Sep 25. Review.

PMID: 18824049, Similar articles



38. Affinity-purified antibodies to ring-infected erythrocyte surface antigen do not correlate with merozoite invasion inhibition in Plasmodium falciparum.

Coleman JP, Jensen JB.

Infect Immun. 1988 Feb;56(2):457-61.

PMID: 3276626, Free PMC Article, Similar articles

39. Analysis of human antibodies to erythrocyte binding antigen 175 of Plasmodium falciparum.

Okenu DM, Riley EM, Bickle QD, Agomo PU, Barbosa A, Daugherty JR, Lanar DE, Conway DJ.

Infect Immun. 2000 Oct;68(10):5559-66.

PMID: 10992454 Free PMC Article, Similar articles

40. Immunization with recombinant duffy binding-like-gamma3 induces pan-reactive and adhesion-blocking antibodies against placental chondroitin sulfate A-binding Plasmodium falciparum parasites.

Costa FT, Fusaï T, Parzy D, Sterkers Y, Torrentino M, Douki JB, Traoré B, Petres S, Scherf A, Gysin J.

J Infect Dis. 2003 Jul 1;188(1):153-64. Epub 2003 Jun 23.

PMID: 12825185, Similar articles

41. Emerging rules for subunit-based, multiantigenic, multistage chemically synthesized vaccines.

Patarroyo ME, Patarroyo MA.

Acc Chem Res. 2008 Mar;41(3):377-86. doi: 10.1021/ar700120t. Epub 2008 Feb 12. Review.

PMID: 18266328, Similar articles



42. Protection against Plasmodium falciparum malaria in chimpanzees by immunization with the conserved pre-erythrocytic liver-stage antigen 3.

Daubersies P, Thomas AW, Millet P, Brahimi K, Langermans JA, Ollomo B, BenMohamed L, Slierendregt B, Eling W, Van Belkum A, Dubreuil G, Meis JF, Guérin-Marchand C, Cayphas S, Cohen J, Gras-Masse H, Druilhe P.

Exp Parasitol. 2007 Jul;116(3):214-24. Epub 2007 Jan 27.

PMID: 17336297, Similar articles



45. Acquisition of antibodies to variant antigens o­n the surface of Plasmodium falciparum-infected erythrocytes during pregnancy.

Fievet N, Le Hesran JY, Cottrell G, Doucoure S, Diouf I, Ndiaye JL, Bertin G, Gaye O, Sow S, Deloron P.

Infect Genet Evol. 2006 Nov;6(6):459-63. Epub 2006 Apr 18.

PMID: 16621725, Similar articles

46. Identification of a conserved region of Plasmodium falciparum MSP3 targeted by biologically active antibodies to improve vaccine design.

Singh S, Soe S, Mejia JP, Roussilhon C, Theisen M, Corradin G, Druilhe P.

J Infect Dis. 2004 Sep 1;190(5):1010-8. Epub 2004 Jul 27.

PMID: 15295710, Similar articles.

47. Measuring Plasmodium falciparum Erythrocyte Invasion Phenotypes Using Flow Cytometry.

Bei AK, Duraisingh MT.

Methods Mol Biol. 2015;1325:167-86. doi: 10.1007/978-1-4939-2815-6_14.

PMID: 26450388, Similar articles



Blood. 1994 Sep 1;84(5):1594-602.

PMID: 8068948, Free Article, Similar articles



51. Mode of action of invasion-inhibitory antibodies directed against apical membrane antigen 1 of Plasmodium falciparum.

Dutta S, Haynes JD, Barbosa A, Ware LA, Snavely JD, Moch JK, Thomas AW, Lanar DE.

Infect Immun. 2005 Apr;73(4):2116-22.

PMID: 15784553, Free PMC Article, Similar articles

52. Plasmodium falciparum: Rosettes do not protect merozoites from invasion-inhibitory antibodies.

Deans AM, Rowe JA.

Exp Parasitol. 2006 Apr;112(4):269-73. Epub 2005 Dec 20.

PMID: 16364300, Free PMC Article, Similar articles



53. Development and optimization of high-throughput methods to measure Plasmodium falciparum-specific growth inhibitory antibodies.

Persson KE, Lee CT, Marsh K, Beeson JG.

J Clin Microbiol. 2006 May;44(5):1665-73.

PMID: 16672391, Free PMC Article, Similar articles

54. A single fragment of a malaria merozoite surface protein remains o­n the parasite during red cell invasion and is the target of invasion-inhibiting antibodies.

Blackman MJ, Heidrich HG, Donachie S, McBride JS, Holder AA.

J Exp Med. 1990 Jul 1;172(1):379-82.

PMID: 1694225, Free PMC Article, Similar articles

55. Antibody-Dependent Cell-Mediated Inhibition (ADCI) of Plasmodium falciparum: o­ne- and Two-Step ADCI Assays.

Bouharoun-Tayoun H, Druilhe P.

Methods Mol Biol. 2015;1325:131-44. doi: 10.1007/978-1-4939-2815-6_11.

PMID: 26450385, Similar articles



56. The apical organelles of malaria merozoites: host cell selection, invasion, host immunity and immune evasion.

Anti-self phosphatidylserine antibodies recognize uninfected erythrocytes promoting malarial anemia.

Fernandez-Arias C, Rivera-Correa J, Gallego-Delgado J, Rudlaff R, Fernandez C, Roussel C, Götz A, Gonzalez S, Mohanty A, Mohanty S, Wassmer S, Buffet P, Ndour PA, Rodriguez A.

Cell Host Microbe. 2016 Feb 10;19(2):194-203. doi: 10.1016/j.chom.2016.01.009.

PMID: 26867178, Free PMC Article, Similar articles



61. PfRH5 as a candidate vaccine for Plasmodium falciparum malaria.

Drew DR, Beeson JG.

Trends Parasitol. 2015 Mar;31(3):87-8. doi: 10.1016/j.pt.2015.02.001. Epub 2015 Feb 19.

PMID: 25704640, Similar articles

62. New approaches to studying Plasmodium falciparum merozoite invasion and insights into invasion biology.

Boyle MJ, Wilson DW, Beeson JG.

Int J Parasitol. 2013 Jan;43(1):1-10. doi: 10.1016/j.ijpara.2012.11.002. Epub 2012 Dec 5. Review.

PMID: 23220090, Free Article, Similar articles



63. Invasion of red blood cells by malaria parasites-what are the components that determine specificity?

van Schravendijk MR, Wilson RJ, Pasvol G.

Ann Inst Pasteur Microbiol (1985). 1986 May-Jun;137A(3):342-7. Review. No abstract available.

PMID: 2447821, Similar articles

64. Antibodies and DNA probes used to analyze variant populations of the Indochina-1 strain of Plasmodium falciparum.

Hommel M, Hughes M, Bond P, Crampton JM.

Infect Immun. 1991 Nov;59(11):3975-81.

PMID: 1937756, Free PMC Article, Similar articles

65. Association of malaria with inactivation of alpha1,3-galactosyl transferase in catarrhines.

Ramasamy R, Rajakaruna R.



Tài li?u tham kh?o

1.Charoenpan P1, Indraprasit S, Kiatboonsri S, Suvachittanont O, Tanomsup S. Pulmonary edema in severe falciparum malaria. Hemodynamic study and clinicophysiologic correlation. Chest. 1990 May;97(5):1190-7.

2.Charoenpan P1, Indraprasit S, Kiatboonsri S, Suvachittanont O, Tanomsup S. (1987). Pulmonary edema in severe falciparum malaria. Hemodynamic study and clinicophysiologic correlation. Rofo. 1987 May;146(5):507-10.

3.Rauber K, Enkerlin HL, Riemann H, Schoeppe W. Pulmonary manifestations of malaria.

4.James MF. Pulmonary damage associated with falciparum malaria: a report of ten cases. Ann Trop Med Parasitol. 1985 Apr;79(2):123-38.

5.Blanloeil Y, Baron D, de Lajartre AY, Nicolas F. Acute respiratory distress syndrome (ARDS) in cerebral malaria. Sem Hop. 1980 Jun 8-15;56(21-24):1088-90.

6.Corbett CE, Duarte MI, Lancellotti CL, Silva MA, Andrade Júnior HF (1989). Cytoadherence in human falciparum malaria as a cause of respiratory distress. J Trop Med Hyg. 1989 Apr;92(2):112-20.

7.Udomsangpetch R1, Aikawa M, Berzins K, Wahlgren M, Perlmann P (1989). Cytoadherence of knobless Plasmodium falciparum-infected erythrocytes and its inhibition by a human monoclonal antibody. Nature. 1989 Apr 27;338(6218):763-5.

8.Iqbal J, Perlmann P, Berzins K (1993). Plasmodium falciparum: Analysis of the cytoadherence inhibition of the human monoclonal antibody 33G2 and of antibodies reactive with antigen Pf332. Exp Parasitol. 1993 Aug;77(1):79-87.

9.Aursudkij B, Wilairatana P, Vannaphan S, Walsh DS, Gordeux VR, Looareesuwan S (1998). Pulmonary edema in cerebral malaria patients in Thailand. Southeast Asian J Trop Med Public Health. 1998 Sep;29(3):541-5.

10.Taylor WR, Cañon V, White NJ (20060. Pulmonary manifestations of malaria: Recognition and management. Treat Respir Med. 2006;5(6):419-28.

11.Lomar AV, Vidal JE, Lomar FP, Barbas CV, de Matos GJ, Boulos M (2005). Acute respiratory distress syndrome due to vivax malaria: case report and literature review. Braz J Infect Dis. 2005 Oct;9(5):425-30. Epub 2006 Jan 6.

12.Rahman AK, Sulaiman FN. Plasmodium vivax malaria presenting as acute respiratory distress syndrome: A case report. Trop Doct. 2013 Apr;43(2):83-5. doi: 10.1177/0049475513485733. Epub 2013 May 24.

13.Gupta H, Afsal MP, Shetty SM, Satyamoorthy K, Umakanth S. (2015). Plasmodium vivax infection causes acute respiratory distress syndrome: a case report. J Infect Dev Ctries. 2015 Aug 29;9(8):910-3. doi: 10.3855/jidc.6813.

14.  Srinivas | February 27, 2015 | Complications. ARDS

15.Andrej Trampuz, Matjaz Jereb, Igor Muzlovic, Rajesh M Prabhu. Clinical review: Severe malaria Critical Care 2003;7:315-323 Available at http://ccforum.com/content/7/4/315.

16.Persson KE.Erythrocyte invasion and functionally inhibitory antibodies in Plasmodium falciparum malaria. Acta Trop. 2010 Jun;114(3):138-43.

17.Ramasamy R, Ramasamy M, Yasawardena S. (2001). Antibodies and Plasmodium falciparum merozoites. Trends Parasitol. 2001 Apr;17(4):194-7.

18.Sim BK (1998). Delineation of functional regions o­n Plasmodium falciparum EBA-175 by antibodies eluted from immune complexes. Mol Biochem Parasitol. 1998 Sep 15;95(2):183-92.

19.Bull PC, Marsh K (2002). The role of antibodies to Plasmodium falciparum-infected-erythrocyte surface antigens in naturally acquired immunity to malaria. Trends Microbiol. 2002 Feb;10(2):55-8.

20.Pandey KC, Singh S, Pattnaik P, Pillai CR, Pillai U, Lynn A, Jain SK, Chitnis CE (2002). Bacterially expressed and refolded receptor binding domain of Plasmodium falciparum EBA-175 elicits invasion inhibitory antibodies. Mol Biochem Parasitol. 2002 Aug 7;123(1):23-33.

21.Sjöberg K, Hosein Z, Wåhlin B, Carlsson J, Wahlgren M, Troye-Blomberg M, Berzins K (1991). Plasmodium falciparum: an invasion inhibitory human monoclonal antibody is directed against a malarial glycolipid antigen. Exp Parasitol. 1991 Oct;73(3):317-25.

22.John CC, O'Donnell RA, Sumba PO, Moormann AM, de Koning-Ward TF, King CL, Kazura JW, Crabb BS (2004). Evidence that invasion-inhibitory antibodies specific for the 19-kDa fragment of merozoite surface protein-1 (MSP-1 19) can play a protective role against blood-stage Plasmodium falciparum infection in individuals in a malaria endemic area of Africa. J Immunol. 2004 Jul 1;173(1):666-72.

23.Sharling L, Enevold A, Sowa KM, Staalsoe T, Arnot DE (2004). Antibodies from malaria-exposed pregnant women recognize trypsin resistant epitopes o­n the surface of Plasmodium falciparum-infected erythrocytes selected for adhesion to chondroitin sulphate A. Malar J. 2004 Sep 6;3:31.

24.Nielsen MA, Staalsoe T, Kurtzhals JA, Goka BQ, Dodoo D, Alifrangis M, Theander TG (2002). Plasmodium falciparum variant surface antigen expression varies between isolates causing severe and nonsevere malaria and is modified by acquired immunity. J Immunol. 2002 Apr 1;168(7):3444-50.

25.Murhandarwati EE, Black CG, Wang L, Weisman S, Koning-Ward TF, Baird JK, Tjitra E, Richie TL, Crabb BS, Coppel RL (2008). Acquisition of invasion-inhibitory antibodies specific for the 19-kDa fragment of merozoite surface protein 1 in a transmigrant population requires multiple infections. J Infect Dis. 2008 Oct 15;198(8):1212-8.

26.Wickramarachchi T, Cabrera AL, Sinha D, Dhawan S, Chandran T, Devi YS, Kono M, Spielmann T, Gilberger TW, Chauhan VS, Mohmmed A (2009). A novel Plasmodium falciparum erythrocyte binding protein associated with the merozoite surface, PfDBLMSP. Int J Parasitol. 2009 Jun;39(7):763-73.

27.Persson KE, McCallum FJ, Reiling L, Lister NA, Stubbs J, Cowman AF, Marsh K, Beeson JG (2008). Variation in use of erythrocyte invasion pathways by Plasmodium falciparum mediates evasion of human inhibitory antibodies. J Clin Invest. 2008 Jan;118(1):342-51.

28.Narum DL, Haynes JD, Fuhrmann S, Moch K, Liang H, Hoffman SL, Sim BK (2000). Antibodies against the Plasmodium falciparum receptor binding domain of EBA-175 block invasion pathways that do not involve sialic acids. Infect Immun. 2000 Apr;68(4):1964-6.

29.Rogerson SJ, Beck HP, Al-Yaman F, Currie B, Alpers MP, Brown GV (1996). Disruption of erythrocyte rosettes and agglutination of erythrocytes infected with Plasmodium falciparum by the sera of Papua New Guineans. Trans R Soc Trop Med Hyg. 1996 Jan-Feb;90(1):80-4.

30.Cowman AF, Baldi DL, Duraisingh M, Healer J, Mills KE, O'Donnell RA, Thompson J, Triglia T, Wickham ME, Crabb BS (2002). Functional analysis of Plasmodium falciparum merozoite antigens: implications for erythrocyte invasion and vaccine development. Philos Trans R Soc Lond B Biol Sci. 2002 Jan 29;357(1417):25-33.

31.Nikodem D, Davidson E (2000). Identification of a novel antigenic domain of Plasmodium falciparum merozoite surface protein-1 that specifically binds to human erythrocytes and inhibits parasite invasion, in vitro. Mol Biochem Parasitol. 2000 Apr 30;108(1):79-91.

32.Williams AR, Douglas AD, Miura K, Illingworth JJ, Choudhary P, Murungi LM, Furze JM, Diouf A, Miotto O, Crosnier C, Wright GJ, Kwiatkowski DP, Fairhurst RM, Long CA, Draper SJ (2012). Enhancing blockade of Plasmodium falciparum erythrocyte invasion: assessing combinations of antibodies against PfRH5 and other merozoite antigens. PLoS Pathog. 2012;8(11):e1002991.

33.Khattab A, Bonow I, Schreiber N, Petter M, Schmetz C, Klinkert MQ (2008). Plasmodium falciparum variant STEVOR antigens are expressed in merozoites and possibly associated with erythrocyte invasion. Malar J. 2008 Jul 23;7:137.

34.Singh AP, Puri SK, Chitnis CE. (2002). Antibodies raised against receptor-binding domain of Plasmodium knowlesi Duffy binding protein inhibit erythrocyte invasion. Mol Biochem Parasitol. 2002 Apr 30;121(1):21-31.

35.John CC, Moormann AM, Pregibon DC, Sumba PO, McHugh MM, Narum DL, Lanar DE, Schluchter MD, Kazura JW (2005). Correlation of high levels of antibodies to multiple pre-erythrocytic Plasmodium falciparum antigens and protection from infection. Am J Trop Med Hyg. 2005 Jul;73(1):222-8.

36.Iqbal J, Perlmann P, Berzins K (1993). Plasmodium falciparum: analysis of the cytoadherence inhibition of the human monoclonal antibody 33G2 and of antibodies reactive with antigen Pf332. Exp Parasitol. 1993 Aug;77(1):79-87.

37.Akum AE, Minang JT, Kuoh AJ, Ahmadou MJ, Troye-Blomberg M (2005). Plasmodium falciparum inhibitory capacities of paired maternal-cord sera from south-west province, Cameroon. J Trop Pediatr. 2005 Jun;51(3):182-90.

38.Miller LH, Good MF, Milon G (1994). Malaria pathogenesis. Science. 1994 Jun 24;264(5167):1878-83.

39.Awah NW, Troye-Blomberg M, Berzins K, Gysin J (2009). Mechanisms of malarial anaemia: potential involvement of the Plasmodium falciparum low molecular weight rhoptry-associated proteins. Acta Trop. 2009 Dec;112(3):295-302.

40.Kocken CH, Withers-Martinez C, Dubbeld MA, van der Wel A, Hackett F, Valderrama A, Blackman MJ, Thomas AW (2002). High-level expression of the malaria blood-stage vaccine candidate Plasmodium falciparum apical membrane antigen 1 and induction of antibodies that inhibit erythrocyte invasion. Infect Immun. 2002 Aug;70(8):4471-6.

41.Astagneau P, Steketee RW, Wirima JJ, Khoromana CO, Millet P (1994). Antibodies to ring-infected erythrocyte surface antigen (Pf155/RESA) protect against P. falciparum parasitemia in highly exposed multigravidas women in Malawi. Acta Trop. 1994 Sep;57(4):317-25.

42.Carlson J. (1993). Erythrocyte rosetting in Plasmodium falciparum malaria-with special reference to the pathogenesis of cerebral malaria. Scand J Infect Dis Suppl. 1993;86:1-79.

43.Lyon JA, Thomas AW, Hall T, Chulay JD (1989). Specificities of antibodies that inhibit merozoite dispersal from malaria-infected erythrocytes. Mol Biochem Parasitol. 1989 Aug;36(1):77-85.

44.Winograd E, Prudhomme JG, Sherman IW (2005). Band 3 clustering promotes the exposure of neoantigens in Plasmodium falciparum-infected erythrocytes. Mol Biochem Parasitol. 2005 Jul;142(1):98-105. Epub 2005 Apr 7.

45.Sim BK, Narum DL, Liang H, Fuhrmann SR, Obaldia N 3rd, Gramzinski R, Aguiar J, Haynes JD, Moch JK, Hoffman SL (2001). Induction of biologically active antibodies in mice, rabbits, and monkeys by Plasmodium falciparum EBA-175 region II DNA vaccine. Mol Med. 2001 Apr;7(4):247-54.

46.Kaslow DC (1993). Transmission-blocking immunity against malaria and other vector-borne diseases. Curr Opin Immunol. 1993 Aug;5(4):557-65.

47.Lalitha PV, Biswas S, Pillai CR, Saxena RK. (2008). Immunogenicity of a recombinant malaria vaccine candidate, domain I+II of AMA-1 ectodomain, from Indian P. falciparum alleles. Vaccine. 2008 Aug 18;26(35):4526-35.

48.Kocken CH, Narum1 DL, Massougbodji A, Ayivi B, Dubbeld MA, van der Wel A, Conway DJ, Sanni A, Thomas AW (2000). Molecular characterisation of Plasmodium reichenowi apical membrane antigen-1 (AMA-1), comparison with P. falciparum AMA-1, and antibody-mediated inhibition of red cell invasion. Mol Biochem Parasitol. 2000 Jul;109(2):147-56.

49.Zhang D, Pan W (2005). Evaluation of three Pichia pastoris-expressed Plasmodium falciparum merozoite proteins as a combination vaccine against infection with blood-stage parasites. Infect Immun. 2005 Oct;73(10):6530-6.

50.Flyg BW, Perlmann H, Perlmann P, Esposito F, Berzins K (1997). Wild isolates of Plasmodium falciparum malaria show decreased sensitivity to in vitro inhibition of parasite growth mediated by autologous host antibodies. Clin Exp Immunol. 1997 Feb;107(2):321-7.

51.Ghosh K (2008). Evolution and selection of human leukocyte antigen alleles by Plasmodium falciparum infection. Hum Immunol. 2008 Dec;69(12):856-60.

52.Coleman JP, Jensen JB (1988). Affinity-purified antibodies to ring-infected erythrocyte surface antigen do not correlate with merozoite invasion inhibition in Plasmodium falciparum. Infect Immun. 1988 Feb;56(2):457-61.

53.Okenu DM, Riley EM, Bickle QD, Agomo PU, Barbosa A, Daugherty JR, Lanar DE, Conway DJ (2000). Analysis of human antibodies to erythrocyte binding antigen 175 of Plasmodium falciparum. Infect Immun. 2000 Oct;68(10):5559-66.

54.Costa FT, Fusaï T, Parzy D, Sterkers Y, Torrentino M, Douki JB, Traoré B, Petres S, Scherf A, Gysin J (2003). Immunization with recombinant duffy binding-like-gamma3 induces pan-reactive and adhesion-blocking antibodies against placental chondroitin sulfate A-binding Plasmodium falciparum parasites. J Infect Dis. 2003 Jul 1;188(1):153-64.

55.Patarroyo ME, Patarroyo MA (2008). Emerging rules for subunit-based, multiantigenic, multistage chemically synthesized vaccines. Acc Chem Res. 2008 Mar;41(3):377-86.

56.Daubersies P, Thomas AW, Millet P, Brahimi K, Langermans JA, Ollomo B, BenMohamed L, Slierendregt B, Eling W, Van Belkum A, Dubreuil G, Meis JF, Guérin-Marchand C, Cayphas S, Cohen J, Gras-Masse H, Druilhe P (2000). Protection against Plasmodium falciparum malaria in chimpanzees by immunization with the conserved pre-erythrocytic liver-stage antigen 3. Nat Med. 2000 Nov;6(11):1258-63.

57.Vernes A, Haynes JD, Tapchaisri P, Williams JL, Dutoit E, Diggs CL (1984). Plasmodium falciparum strain-specific human antibody inhibits merozoite invasion of erythrocytes. Am J Trop Med Hyg. 1984 Mar;33(2):197-203.

58.Xu L, Pei X, Berzins K, Chaudhuri A (2007). Plasmodium yoelii: experimental evidences for the conserved epitopes between mouse and human malaria parasite, Plasmodium falciparum. Exp Parasitol. 2007 Jul;116(3):214-24.

59.Fievet N, Le Hesran JY, Cottrell G, Doucoure S, Diouf I, Ndiaye JL, Bertin G, Gaye O, Sow S, Deloron P (2006). Acquisition of antibodies to variant antigens o­n the surface of Plasmodium falciparum-infected erythrocytes during pregnancy. Infect Genet Evol. 2006 Nov;6(6):459-63. Epub 2006 Apr 18.

60.Singh S, Soe S, Mejia JP, Roussilhon C, Theisen M, Corradin G, Druilhe P (2004). Identification of a conserved region of Plasmodium falciparum MSP3 targeted by biologically active antibodies to improve vaccine design. J Infect Dis. 2004 Sep 1;190(5):1010-8..

61.Bei AK, Duraisingh MT (2015). Measuring Plasmodium falciparum Erythrocyte Invasion Phenotypes Using Flow Cytometry. Methods Mol Biol. 2015;1325:167-86.

62.Dent A, Malhotra I, Mungai P, Muchiri E, Crabb BS, Kazura JW, King CL (2006). Prenatal malaria immune experience affects acquisition of Plasmodium falciparum merozoite surface protein-1 invasion inhibitory antibodies during infancy. J Immunol. 2006 Nov 15;177(10):7139-45.

63.Bongfen SE, Ntsama PM, Offner S, Smith T, Felger I, Tanner M, Alonso P, Nebie I, Romero JF, Silvie O, Torgler R, Corradin G (2009). The N-terminal domain of Plasmodium falciparum circumsporozoite protein represents a target of protective immunity. Vaccine. 2009 Jan 7;27(2):328-35.

64.Oeuvray C, Bouharoun-Tayoun H, Gras-Masse H, Bottius E, Kaidoh T, Aikawa M, Filgueira MC, Tartar A, Druilhe P (1994). Merozoite surface protein-3: a malaria protein inducing antibodies that promote Plasmodium falciparum killing by cooperation with blood monocytes. Blood. 1994 Sep 1;84(5):1594-602.

65.Dutta S, Haynes JD, Barbosa A, Ware LA, Snavely JD, Moch JK, Thomas AW, Lanar DE (2005). Mode of action of invasion-inhibitory antibodies directed against apical membrane antigen 1 of Plasmodium falciparum. Infect Immun. 2005 Apr;73(4):2116-22.

66.Deans AM, Rowe JA (2006). Plasmodium falciparum: Rosettes do not protect merozoites from invasion-inhibitory antibodies. Exp Parasitol. 2006 Apr;112(4):269-73.

67.Persson KE, Lee CT, Marsh K, Beeson JG (2006)..Development and optimization of high-throughput methods to measure Plasmodium falciparum-specific growth inhibitory antibodies. J Clin Microbiol. 2006 May;44(5):1665-73.

68.Blackman MJ, Heidrich HG, Donachie S, McBride JS, Holder AA (1990). A single fragment of a malaria merozoite surface protein remains o­n the parasite during red cell invasion and is the target of invasion-inhibiting antibodies. J Exp Med. 1990 Jul 1;172(1):379-82.

69.Bouharoun-Tayoun H, Druilhe P. (2015). Antibody-Dependent Cell-Mediated Inhibition (ADCI) of Plasmodium falciparum: o­ne- and Two-Step ADCI Assays. Methods Mol Biol. 2015;1325:131-44.

70.Preiser P, Kaviratne M, Khan S, Bannister L, Jarra W. (2000). The apical organelles of malaria merozoites: host cell selection, invasion, host immunity and immune evasion.

71.Microbes Infect. 2000 Oct;2(12):1461-77.

72.Duncan EH, Bergmann-Leitner ES (2015). Miniaturized Growth Inhibition Assay to Assess the Anti-blood Stage Activity of Antibodies. Methods Mol Biol. 2015;1325:153-65.

73.Ahouidi AD, Amambua-Ngwa A, Awandare GA, Bei AK, Conway DJ, Diakite M, Duraisingh MT, Rayner JC, Zenonos ZA (2016). Malaria Vaccine Development: Focusing Field Erythrocyte Invasion Studies o­n Phenotypic Diversity: The West African Merozoite Invasion Network (WAMIN). Trends Parasitol. 2016 Apr;32(4):274-83.

74.Boyle MJ, Wilson DW, Richards JS, Riglar DT, Tetteh KK, Conway DJ, Ralph SA, Baum J, Beeson JG (2010). Isolation of viable Plasmodium falciparum merozoites to define erythrocyte invasion events and advance vaccine and drug development. Proc Natl Acad Sci U S A. 2010 Aug 10;107(32):14378-83.

75.Fernandez-Arias C, Rivera-Correa J, Gallego-Delgado J, Rudlaff R, Fernandez C, Roussel C, Götz A, Gonzalez S, Mohanty A, Mohanty S, Wassmer S, Buffet P, Ndour PA, Rodriguez A (2016). Anti-self phosphatidylserine antibodies recognize uninfected erythrocytes promoting malarial anemia. Cell Host Microbe. 2016 Feb 10;19(2):194-203.

76.Drew DR, Beeson JG (2015). PfRH5 as a candidate vaccine for Plasmodium falciparum malaria. Trends Parasitol. 2015 Mar;31(3):87-8.

77.Boyle MJ, Wilson DW, Beeson JG (2013). New approaches to studying Plasmodium falciparum merozoite invasion and insights into invasion biology. Int J Parasitol. 2013 Jan;43(1):1-10. doi: 10.1016/j.ijpara.2012.11.002.

78.van Schravendijk MR, Wilson RJ, Pasvol G (1985). Invasion of red blood cells by malaria parasites-what are the components that determine specificity? Ann Inst Pasteur Microbiol (1985). 1986 May-Jun;137A(3):342-7.

79.Hommel M, Hughes M, Bond P, Crampton JM (1991). Antibodies and DNA probes used to analyze variant populations of the Indochina-1 strain of Plasmodium falciparum. Infect Immun. 1991 Nov;59(11):3975-81.

80.Ramasamy R, Rajakaruna R (1997). Association of malaria with inactivation of alpha1,3-galactosyl transferase in catarrhines. Biochim Biophys Acta. 1997 May 24;1360(3):241-6.

81.Chen L, Xu Y, Wong W, Thompson JK, Healer J, Goddard-Borger ED, Lawrence MC, Cowman AF (2017). Structural basis for inhibition of erythrocyte invasion by antibodies to Plasmodium falciparum protein CyRPA. Elife. 2017 Feb 14;6. pii: e21347.

82.Brattig NW, Kowalsky K, Liu X, Burchard GD, Kamena F, Seeberger PH (2008). Plasmodium falciparum glycosylphosphatidylinositol toxin interacts with the membrane of non-parasitized red blood cells: a putative mechanism contributing to malaria anemia. Microbes Infect. 2008 Jul;10(8):885-91.

83.Eisenhut M (2010). Auto-antibodies and glomerulonephritis in Plasmodium falciparum malaria. Autoimmunity. 2010 Dec;43(8):640-1.

84.Boyle MJ, Reiling L, Beeson JG (20160. Evaluating Complement-Mediated Humoral Immunity to P. falciparum Blood Stages. EBioMedicine. 2016 Dec;14:9-10.

85.Clark MA, Goheen MM, Fulford A, Prentice AM, Elnagheeb MA, Patel J, Fisher N, Taylor SM, Kasthuri RS, Cerami C (2014). Host iron status and iron supplementation mediate susceptibility to erythrocytic stage Plasmodium falciparum. Nat Commun. 2014 Jul 25;5:4446.

86.Debierre-Grockiego F, Schofield L, Azzouz N, Schmidt J, Santos de Macedo C, Ferguson MA, Schwarz RT. Fatty acids from Plasmodium falciparum down-regulate the toxic activity of malaria glycosylphosphatidylinositols. Infect Immun. 2006 Oct;74(10):5487-96.

87.Du Toit A (2015). Parasite biology: an anchor for Plasmodium spp. invasion. Nat Rev Microbiol. 2015 Mar;13(3):128-9.

88.Cowman AF, Tonkin CJ, Tham WH, Duraisingh MT. The Molecular Basis of Erythrocyte Invasion by Malaria Parasites. Cell Host Microbe. 2017 Aug 9;22(2):232-245.

89.Jacobs HR (1947). A consideration of the antierythrocytic factors in resistance to malaria. Q Bull Northwest Univ Med Sch. 1947 Spring;21(1):52-7.

90.Fowler RE, Fookes RE, Mitchell GH, Bannister LH. Malaria, microtubules and merozoite invasion: reply. Parasitol Today. 1998 Jan;14(1):41.

91.Hommel M, Schrével J. (1998). Malaria, microtubules and merozoite invasion. Parasitol Today. 1998 Jan;14(1):6-7.

92.Charoenpan P, Indraprasit S, Kiatboonsri S, Suvachittanont O, Tanomsup S.

93.Pulmonary edema in severe falciparum malaria. Hemodynamic study and clinicophysiologic correlation. Chest. 1990 May;97(5):1190-7.

94.Rauber K, Enkerlin HL, Riemann H, Schoeppe W. [Pulmonary manifestations of malaria. Rofo. 1987 May;146(5):507-10.

95.James MF. Pulmonary damage associated with falciparum malaria: a report of ten cases. Ann Trop Med Parasitol. 1985 Apr;79(2):123-38.

96.Blanloeil Y, Baron D, de Lajartre AY, Nicolas F. Acute respiratory distress syndrome (ARDS) in cerebral malaria (author's transl. Sem Hop. 1980 Jun 8-15;56(21-24):1088-90.

97.Corbett CE, Duarte MI, Lancellotti CL, Silva MA, Andrade Júnior HF. Cytoadherence in human falciparum malaria as a cause of respiratory distress. J Trop Med Hyg. 1989 Apr;92(2):112-20.

98.Udomsangpetch R, Aikawa M, Berzins K, Wahlgren M, Perlmann P. Cytoadherence of knobless Plasmodium falciparum-infected erythrocytes and its inhibition by a human monoclonal antibody. Nature. 1989 Apr 27;338(6218):763-5.

99.Iqbal J, Perlmann P, Berzins K. Plasmodium falciparum: analysis of the cytoadherence inhibition of the human monoclonal antibody 33G2 and of antibodies reactive with antigen Pf332. Exp Parasitol. 1993 Aug;77(1):79-87.

100.Aursudkij B, Wilairatana P, Vannaphan S, Walsh DS, Gordeux VR, Looareesuwan S. Pulmonary edema in cerebral malaria patients in Thailand. Southeast Asian J Trop Med Public Health. 1998 Sep;29(3):541-5.

101.Taylor WR, Cañon V, White NJ. Pulmonary manifestations of malaria : recognition and management. Treat Respir Med. 2006;5(6):419-28.

102.Lomar AV, Vidal JE, Lomar FP, Barbas CV, de Matos GJ, Boulos M. Acute respiratory distress syndrome due to vivax malaria: case report and literature review. Braz J Infect Dis. 2005 Oct;9(5):425-30. Epub 2006 Jan 6.

103.Rahman AK, Sulaiman FN. Plasmodium vivax malaria presenting as acute respiratory distress syndrome: a case report. J Infect Dev Ctries. 2015 Aug 29;9(8):910-3. doi: 10.3855/jidc.6813.

104.Gupta H, Afsal MP, Shetty SM, Satyamoorthy K, Umakanth S. Plasmodium vivax infection causes acute respiratory distress syndrome: a case report.

11/02/2018
Dr. Huynh Hong Quang
Institute of Malariology, Parasitology, and Entomology Quy Nhon
 

Announcement

LIBRARY
Book
Magazine
Document
Photos
Thesis
Documentary form
Research studies
PROFFESSIONAL SOFTWARE
Malaria forecast & management
Document management
Personel management
LEGAL DOCUMENTS
Law
Decision
Decree
Instruction
Circular
Official document
Reports
Others
SPECIFIED IMFORMATION
Malaria facts
Malaria epidemic
Petechial fever
HEALTH SERVICES
Hospital & medical centre
Drugstore
Surgery
Your doctor

Institue of Malariology Parastology and Entomology Quy Nhon
Address: 611B Nguyen Thai Hoc Str,. Quy Nhon City
Tel: (84) 056 846571 Fax: (84) 056 846755
• Designed by Quang Ich JSC