Vol 27 No 2 December - The Indian Society for Parasitology

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100 Red cell genetic defects and malaria JPD : Vol. 27 (2), 2003 solubility test whereas fetal haemoglobin, Hb-F was confirmed by alkali denaturation technique as malarial and non-malarial subjects were also analysed described elsewhere (Dacie and Lewis, 1986). statistically and found to be non-significant. Methaemoglobin reduction test (MRT) was followed 3 Plasmodium parasite density (per mm ) was for rapid screening of large number of blood samples determined in the subjects who had heterozygous for the evidence of G-6-PD enzyme deficiency (Brewer et al., 1960). The number of blood samples forms of Hb-S and β-thal. as well as in G-6-PD enzyme studied for P. falciparum, P. vivax and normal (control deficients and was found to be relatively low in these group) individuals belonging to different ethnic individuals as compared to normal subjects. However, groups viz., scheduled tribes (S.T.), scheduled castes P. vivax parasite counts were relatively higher than (S.C.), and general castes (G.C.) has been depicted in subjects infected with P. falciparum. Data pertaining Table I. The basic sources for sampling were General to parasite density in subjects having these red cell Hospitals, Primary Health Centres, and hostels located genetic defects relation to different genetic defects in the study areas. have been analysed and found relatively highly significant in the case of P. falciparum (Table II) as During blood sampling, peripheral thin and thick compared to P. vivax (Table III). blood smears of malarial and non-malaria (control) individuals were also prepared, stained by Giemsa It is obvious that in the malaria endemic provinces Hb- d stain and examined under high power and oil S, β-thal. and G genes are more prevalent. 'In fact, immersion lens of microscope for the evidence of any heterozygous forms of these red cell defective genes red cell (erythrocyte) abnormalities and malaria are reported to provide a selective advantage against P. parasite (Plasmodium spp.). The initial parasite counts falciparum infection. In the present study falciparum were also done by counting the number of parasitized infection was not found in homozygotes of Hb-S and cells per 1000 erythrocytes in the smears. The red β-thal. but was found in heterozygotes with less severe 3 blood cells count per mm was also determined and the parasitaemia (Table II). It has also been observed that 3 number of parasites per mm were then calculated. The heterozygotes can become infected with P. falciparum data of the present study was analysed statistically. A but high parasitaemia and subsequent mortality is few individuals with Hb-D and Hb-E were excluded relatively low amongst such individuals (Raper, 1956; from the study. Fleming et al., 1979). These findings suggest that RESULTS AND DISCUSSION Plasmodium parasites can infect or invade the erythrocytes (red cell) with any of these defects (Hb-S, Out of 3205 malaria suspected individuals, 1914 d β-thal. and G ) but their further development or (59.71%) were found to be infected with Plasmodium multiplication is restricted or not enhanced. This is parasites with varying parasitaemia. Of these 1264 also supported by many in vitro studies which showed (66.03%) showed P. falciparum whereas 650 (33.96%) that P. falciparum does not easily invade and grow well were infected with P. vivax. Amongst these malaria d in the erythrocytes with Hb-S, β-thal. and G . The d positive cases, the incidence of Hb-S, β-thal. and G suggested reasons for this include defective genes was found to be 1.51% (29 cases), 2.24% (43 erythrocyte membranes, oxygen stress, increased cases), and 5.64% (108 cases) respectively which is sickling and low Hb content (Pasvol and Wilson, 1982; lower than that observed in non-malarials (3.50%, Roth et al., 1983; Nagel and Roth, 1989). Therefore, it 5.08% and 10.45% respectively). However, subjects has been concluded that the abnormal erythrocytes of having falciparum malaria did not show the evidence d individuals with Hb-S, β-thal. and G genetic defects of homozygous state of Hb-S and β-thal. genes are less easily parasitised by P. falciparum than the (Table I). The relative distribution and occurrence of genetically normal erythrocytes (normal subjects) and these red cell defective (mutant) genes in different this provided a considerable degree of protection types of malaria cases (falciparum and vivax) as well against lethal malaria (P. falciparum) which is also in as in normal individuals belonging to different ethnic support of Darwin theory of "natural selection". groups have been shown in Table I. Data pertaining to d the occurrence of Hb-S, β-thal. and G genes in
JPD : Vol. 27 (2), 2003 Red cell genetic defects and malaria 101 Table I : Relative distribution and incidence of sickle cell Hb, β-thalassaemia and G-6-PD enzyme deficiency d (G ) in malarial and non-malarial (normal) subjects of each ethnic groups Red cell genetic defects Ethnic group Type of No. of Sickle cell Hb β-thalassaemia G-6-PD Malaria tested Hb-AS Hb-SS Minor Major deficiency d (trait) (G ) Scheduled falciparum 584 11 - 16 - 47 Tribes (S.T.) (1.88) (0.00) (2.74) (0.00) (8.05) vivax 260 9 1 11 1 19 (3.46) (0.38) (4.23) (0.38) (7.31) Normal 3163 146 22 202 18 443 (4.62) (0.70) (6.39) (0.57) (14.00) Scheduled falciparum 331 3 - 5 - 18 Castes (S.C.) (0.91) (0.00) (1.51) (0.00) (5.43) vivax 180 2 - 5 - 15 (1.11) (0.00) (2.77) (0.00) (8.33) Normal 1155 20 2 40 2 95 (1.73) (0.17) (3.46) (0.17) (8.23) General falciparum 349 2 - 4 - 9 Castes (G.C.) (0.57) (0.00) (1.15) (0.00) (2.58) vivax 210 - 1 - 1 - (0.00) (0.48) (0.00) (0.48) (0.00) Normal 1585 17 - 37 1 79 (1.07) (0.00) (2.33) (0.06) (4.98) Total falciparum 1264 16 - 25 - 74 (1.27) (0.00) (1.98) (0.00) (5.85) vivax 650 11 2 16 2 34 (1.69) (0.31) (2.46) (0.31) (5.23) Normal 5903 183 24 279 21 617 (3.10) (0.41) (4.73) (0.36) (10.45) Figures in parentheses represent percentage Differences between infected and controls was statistically non-significant (p > 0.05) for all genetic defects.
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