Blood examination and prognosis in acute falciparum malaria

Field, J. W.

doi:10.1016/0035-9203(49)90022-x

Cited by 98 publications

(50 citation statements)

References 7 publications

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“…19 It has been shown that HbS heterozygotes, particularly young children, have lower parasite rates and densities. 20,21 Since the mortality from falciparum malaria was related to parasite densities, 22 these children had a lower mortality rate from malaria. [23][24][25][26] Similar protection is provided by the G-6-PD deficiency, 27,28 and thus an increased frequency of these genes is encountered in most of the areas of the world that are or have been malaria endemic.…”

mentioning

confidence: 99%

The Frequency of Glucose-6-Phosphate Dehydrogenase Phenotypes and Sickle Cell Genes in Al-Qatif Oasis

El‐Hazmi¹,

Warsy²

1994

Annals of Saudi Medicine

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mentioning

confidence: 99%

The Frequency of Glucose-6-Phosphate Dehydrogenase Phenotypes and Sickle Cell Genes in Al-Qatif Oasis

El‐Hazmi¹,

Warsy²

1994

Annals of Saudi Medicine

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“…Furthermore, more episodes of severe malarial anaemia (Hb <6g/dl), hypoglycaemia, and high parasitaemia (>10000parasites/μl) were more evident in well nourished G6PD non-deficient subjects compared to G6PD deficient ones. Our results also revealed lower morbidity and mortality rates caused by P. falciparum since both factors are related to Hb concentration and parasite densities in malaria infection (Field, 1949). However, since severe malaria may occur in the face of occult malaria infection when the parasites are sequestered and their growth cycle is tightly synchronized, the use of parasitaemia may be an unreliable guide to malaria severity.…”

Section: Discussionmentioning

confidence: 59%

Malaria Protection In Glucose-6-Phosphate Dehydrogenase Deficient Individuals In Bamenda Population Of Cameroon

Awah¹,

Uzoegwu²

2008

Glo Jnl Pure Appl Sci

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The high frequency of glucose-6-phosphate dehydrogenase (G6PD) deficiency gene in malaria endemic regions is believed to be due to the enzyme deficiency advantage against fatal malaria. However, the mechanism of this protection is not well understood and therefore was investigated by comparing differences in plasmodial parasitaemia, full blood count profile and the severity of clinical malarial symptoms of G6PD deficient and G6PD non-deficient cohort groups in the population. Our results showed that 10.4% (63/606) of those tested carried the G6PD deficiency gene. G6PD deficient heterozygous females and hemizygous males manifested significantly reduced (P<0.05) parasitaemia, less severe malarial anaemia, less severe clinical malarial symptoms and elevated haematological profile during the progress of malaria when compared with G6PD non-deficient subjects. The results seem to suggest that G6PD deficiency gene could be among the factors that confer malaria protection in the hosts through reduction of severe malarial anaemia, density parasitaemia and clinical malarial symptoms while having less effect on frequency of infection perse.

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“…29 Many factors confound the relationship between parasitemia and disease, 41 but there is generally a loose positive correlation between circulating parasite load and clinical status. 44 It seems likely that one primary factor that lowers the correlation is that only a fraction of P. falciparum parasites appear in the peripheral circulation, and that total parasite density (as considered in our model) is more closely correlated. Thus, overall our model suggests that P. vivax-P. falciparum interactions in mixed infections can have profound clinical effects in both uncomplicated malaria (perhaps by maintaining P. falciparum densities below fever threshold) and severe cases.…”

Section: Discussionmentioning

confidence: 86%

Blood-stage dynamics and clinical implications of mixed Plasmodium vivax-Plasmodium falciparum infections.

Mason

McKenzie²

1999

Am J Trop Med Hyg

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Abstract. We present a mathematical model of the blood-stage dynamics of mixed Plasmodium vivax-Plasmodium falciparum malaria infections in humans. The model reproduces features of such infections found in nature and suggests several phenomena that may merit clinical attention, including the potential recrudescence of a long-standing, low-level P. falciparum infection following a P. vivax infection or relapse and the capacity of an existing P. vivax infection to reduce the peak parasitemia of a P. falciparum superinfection. We simulate the administration of antimalarial drugs, and illustrate some potential complications in treating mixed-species malaria infections. Notably, our model indicates that when a mixed-species infection is misdiagnosed as a single-species P. vivax infection, treatment for P. vivax can lead to a surge in P. falciparum parasitemia.Plasmodium vivax and P. falciparum are the most widespread and commonly studied of the four species that cause human malaria. Dual infections are common and frequently recorded in field surveys, but there has been little research on the within-host interactions or clinical impacts of coinfecting species. Cohen 1 reviewed prevalence surveys and concluded that in general, fewer mixed-species infections are observed than would be expected from the prevalences of the constituent species. Richie 2 reviewed prevalence surveys and concluded that there is no general pattern in the frequencies of mixed-species infections in humans. Our reviews of more recent cross-sectional studies 3,4 found that lower-than-expected frequencies of dual P. vivax-P. falciparum infections correspond to higher overall malaria prevalence, and, in general, that the frequencies of mixed-species Plasmodium infections detected in humans may depend upon the particular combinations of Plasmodium species present. We have also found mixed-species Plasmodium infections common in vector Anopheles species. 5Longitudinal studies of mixed-species infections are extremely rare. Several neurosyphilis malariatherapy charts published by Boyd and Kitchen 6,7 suggest that P. falciparum suppressed P. vivax parasitemia in these patients. Interspecies inhibition was also suggested by other such studies. [8][9][10][11] Shute 12 reported that P. vivax often failed to thrive if inoculated simultaneously with P. falciparum, but could reach patent levels if inoculated a few days before P. falciparum. More recently, clinical studies 13,14 have found high rates of P. vivax infection following treatment of patients previously assumed to be infected only with P. falciparum. Studies with non-human malarias have also suggested interspecific suppression. [15][16][17][18][19] The pathologic consequences of mixed-species infections are of particular interest to clinicians. Jeffrey 20 noted that prior infection with P. ovale could alter the clinical course of subsequent P. falciparum infection. Other studies have noted relationships between mixed-species infections and enlarged spleen size, 10 decreased spleen size, 1 and depres...

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Blood examination and prognosis in acute falciparum malaria

Cited by 98 publications

References 7 publications

The Frequency of Glucose-6-Phosphate Dehydrogenase Phenotypes and Sickle Cell Genes in Al-Qatif Oasis

The Frequency of Glucose-6-Phosphate Dehydrogenase Phenotypes and Sickle Cell Genes in Al-Qatif Oasis

Malaria Protection In Glucose-6-Phosphate Dehydrogenase Deficient Individuals In Bamenda Population Of Cameroon

Blood-stage dynamics and clinical implications of mixed Plasmodium vivax-Plasmodium falciparum infections.

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