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. 2008 May 21;3(5):e2196. doi: 10.1371/journal.pone.0002196

Table 2. Factors associated with children being ‘more susceptible’ than others.

Factor Normal ‘More Susceptible’ Crude Odds ratio
N = 295 (79.1%) N = 78 (20.9%) (95% confidence intervals)
Female 143 (48.5%) 31 (40%) 1.42 (0.86–2.37), p = 0.2
Bednets (N = 342)Ω 140 (52.6%) 40 (52.6%) 1.0 (0.6–1.7), p = 1.0
Transmission* 105 (35.6%) 38 (48.7%) 1.71 (1.03–2.85), p = 0.03
Parasitological cross-sectional survey (n = 238).
>5,000 par/µl of blood§ 13 (7.3%) 13 (22%) 3.6 (1.5–8.48), p = 0.002
Always –veβ 70 (39.1%) 7 (11.9%) 0.21 (0.08–0.5), p<0.001
Genetic markers
Sickle trait (N = 352) 36 (13%) 4 (5.4%) 0.38 (0.13–1.12), p = 0.07
Thalassaemia (N = 284)φ 148 (67.9%) 47 (71.2%) 1.17 (0.6–2.14), p = 0.6
Incidence of clinical disease [Episodes/child/year and 95% confidence intervals]
Normal ‘More Susceptible’
Malaria fevers 0.56 (0.51–0.61) 2.35 (2.17–2.53)
Non-malarial fevers 0.91 (0.85–0.97) 0.93 (0.81–1.04)

Note:

Ω

Bednets either untreated or treated that were in good condition.

*Transmission: This reflects the household level of transmission and shows the proportion of children in the two groups that came from homes with above average parasite rate (≥50%) compared to those below average (<50%).

§

These are geometric mean parasite densities in those cross-sectional surveys were the slide was positive. The cut-off for high geometric mean parasite density was set arbitrarily at >5,000 parasites/µl of blood compared to those with less

β

Compares those who were always negative at all six cross-sectional surveys with those who were positive at least once.

φ

α Thalassaemia genotype: Homozygous (-α/-α) and heterozygous (αα/-α) compared to normal (αα/αα). Comparing homozygous and heterozygous alone did not make a difference to these associations.