A meta-analysis of changes in cholinesterase activity among experimental animals infected with Toxoplasma gondii

The zoonotic disease toxoplasmosis, caused by the protozoan parasite Toxoplasma gondii, is prevalent in about one third of human population. The disease modulates blood and tissue cholinesterase (ChE) activity in laboratory animals. The present meta-analysis examines changes in ChE activity in experimental animals infected with T. gondii as laboratory animal models of toxoplasmosis. Experimental studies on toxoplasmosis in laboratory animals, showing blood or tissue ChE activity were selected for the meta-analysis according to guidelines of the Preferred Reporting Items for Systematic Reviews and Meta-Analysis. Nine records were finally identified and selected from seven studies on mice (n= 54 versus 54 controls) and rats (n=12 versus 12 control). Values of ChE activity were extracted from tables and figures of the selected studies. Thereafter, each mean ± SD of ChE activity of the toxoplasmosis group was unified as the percentage of respective mean control value in the blood (or its constituents), liver or brain. One-group randomised effects meta-analysis model was applied to construct the forest plot and assess effect size, subgroup analysis, heterogeneity, publication bias-funnel plot as well as the risk of bias. Meta-analysis of the records showed an overall significant increase in effect size (% ChE activity of the toxoplasmosis group versus control) by 18.23%. The combined effect size was 118.23, with SE of 23.63; 95% C.I. lower and upper limits of 63.73 and 172.72, respectively, and Z value of 5 at two-tailed p-value= 0.0001. The data were highly heterogeneous, with significant Cochrane Q-test (Q=140.13, p<0.0001) and high I2 -heterogeneity index (94.29%). Subgroup analysis according to tissue/blood ChE activities revealed that brain ChE activity in toxoplasmosis was high and significant with an effect size of 174.51 and no heterogeneity (I2= 0%, Q=0.21, p=0.899). Those of the liver and blood were 43.9 and 104.66, respectively, with significant and high heterogeneities (I2 = 89.05% and 76.55%; Q=9.13 and 12.79%; p=0.003 and 0.005, respectively). The funnel plot did not show any publication bias and Egger’s regression analysis confirmed it (t=1.62, p=0.149). The overall risk of bias was moderate (unclear), however, the score (14 out of 20) of each record approached the low bias level. In conclusion, the present meta-analysis suggests differential tissue-specific changes in ChE activity following toxoplasmosis in experimental animals. Reduced liver ChE activity could be a biomarker of liver injury along with other liver function tests in experimental animals infected with T. gondii. Blood ChE activity should be evaluated according to its various constituents as they differ considerably in toxoplasmosis. Concomitant animal behavioural changes in relation to increases in brain ChE activity and their clinical implications are worth of pursuing after toxoplasmosis.