Alcohol overuse increases susceptibility to malaria and its complications: a pilot study
https://dx.doi.org/10.4314/njpar.v42i2.2
Keywords:
malaria, alcohol, dyslipidemia, hematological indices, hepatic dysfunction, renal damageAbstract
Malaria has remained a dangerous disease that has been posing great burden to man and his wellbeing. Several factors influence the susceptibility to this disease including genetic and environmental determinants. The role of alcohol on malaria parasite infection and its complications is not well-defined. It is established that malaria infection and alcohol independently influence the immune system of man and other animals. Therefore, it is logical to reason that their combined influence may be additive. The aim of this study was to investigate the effect of alcohol on determinants of malaria infection in mice. Nine groups of mice (n = 5) were used with group one serving as normal control, group 2 (alcohol control) received 12 g/kg b.w/d. of 50% absolute ethanol p.o only for 7 days and group 3 was parasitized only (parasite control). Groups 4-6 received 12 g/kg b.w/d. of 10, 30 and 50% ethanol, respectively for 7 days prior to parasite inoculation. Similarly, groups 7-9 were parasitized and thereafter received 12 g/kg b.w/d. of 10, 30 and 50 % ethanol, respectively 24-h after parasite inoculation till the next 7 days. In each case, malaria infection was confirmed 72-h post-inoculation. Thereafter, overnight fasted blood samples were analyzed for malaria parasitemia (malaria parasite density), hematological indices (hemoglobin concentration, packed cell volume and erythrocyte and leukocyte counts), lipid profile (total cholesterol, triacylglycerol, low and high density lipoproteins), and liver (alanine and aspartate aminotransferases and total bilirubin) and kidney (urea and creatinine) status using standard methods. The results of various analyzed parameters in alcohol exposed mice infected with malaria parasite were compared with mice exposed to alcohol and malaria parasite alone using one-way analyses of variance. The result showed that parasitized alcohol-treated mice had higher malaria parasitemia (34.33 ± 2.53, 39.49 ± 1.71 and 54.12 ± 2.76 x104 parasites/μL, respectively for 10, 30 and 50 % ethanol) relative to parasitized mice not treated with alcohol (22.01 ± 1.35 x104 parasites/μL). In addition, concentration-based reduction in hematological status (packed cell volume, hemoglobin concentration, and erythrocyte and leukocyte counts) was observed in alcohol-fed parasitized mice relative to parasite only and alcohol only controls. Furthermore, biochemical status indicating dyslipidemia as characterized by the elevation in total cholesterol, low density lipoprotein and triacylglycerol concentrations and decrease in high density lipoprotein level, hypoglycemia, renal and hepatic dysfunctions as indicated by increase in liver function markers as well as creatinine and urea levels in serum were observed in infected mice treated with alcohol relative to parasite only and alcohol only controls. In conclusion, this observation suggests that alcohol overuse exacerbates malaria parasitemia and suppresses immune response to malaria parasites, in a concentration-dependent manner, thereby promoting the progression and severity of complications associated with malaria. Further study to investigate the mechanism behind this preliminary observation is warranted.
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