The increased seroprevalence of toxoplasmosis in victims of traffic accidents suggested that the subjects with latent toxoplasmosis had significantly higher risk of traffic accidents than non-infected subjects. Relative risk of traffic accidents was highest in subjects with supposedly relatively recent or massive T. gondii infection and decreased with the decrease of anti-toxoplasma immunity, i.e. with duration of Toxoplasma infection.
Retrospective case-control study cannot reveal why a higher seroprevalence of latent toxoplasmosis occurs among victims of traffic accidents. Theoretically, toxoplasmosis can either increase the probability of traffic accident or decrease the probability that the subject visits a physician and therefore enters the control set. Results of independent recent studies on prevalence of toxoplasmosis in Prague, however, suggest that the former possibility is more probable. After taking into account the differences in age and gender composition of particular sets, the differences between seroprevalence measured in the multipurpose immunological surveys and in the set of 857 conscripts or in the set of 723 pregnant women were not significant (conscripts: p = 0.12, women: p = 0.78) [16
]. It is also possible that some unknown confounding factor, such as the socioeconomic status of a person, can influence the probability of both Toxoplasma
infection and a traffic accident. The most parsimonious explanation, however, seems to be that the Toxoplasma
-infected individuals have increased risk of traffic accidents due to their worse psychomotor performance. Previously published results suggest that the effect of latent toxoplasmosis on human reaction times is rather moderate, accounting for only 8% of the total variance [11
]. However, the comparison of psychomotor performance in the first, second, and third minutes of the test indicates that Toxoplasma
-infected subjects have reasonably good reaction times in the first minute of the test but lose concentration more quickly than the controls. It has been reported in literature that older drivers are able to compensate for the prolongation of their reaction times [17
]. It suggests that other behavioural factors, like the capacity for long-term concentration, are more critical with respect to the risk of a traffic accident [19
]. It is difficult to quantify capacity for long-term concentration under natural conditions using laboratory test. However, it is possible that the risk of traffic accident is in fact more strongly influenced by the toxoplasmosis-associated decrease of capacity of concentration than by the moderate increase of reaction time.
The existence of positive correlation between concentration of antibodies and relative risk of traffic accident contrasts with previously reported negative correlation between concentration of antibodies and increase of reaction times of infected subjects [11
]. Possibly, the positive correlation between the concentration of antibody and the risk of traffic accident observed in the present study reflects a positive correlation between intensity of infection and its behavioural effect rather than a negative correlation between duration of infection and its behavioural effects. It is also possible that the long-term infected subjects with low antibody concentration already successfully reduced the risk of accident by adjusting their behaviour to the decrease of their psychomotor performance. In both studies, we eliminated all subjects with acute toxoplasmosis from the data set by screening the subjects for IgM antibodies. Moreover, in the present study, a positive correlation existed even within the subset of subjects with low titres (8–32) (p = 0.032). Therefore, the effect of latent toxoplasmosis, rather than transient effect of acute toxoplasmosis disease seems to be more probable candidate for explanation of increased risk of traffic accident in Toxoplasma
The dormant stages of Toxoplasma
, the tissue cysts, are located mainly in brain and muscular tissues of infected animals [18
]. In rodents, these cysts usually survive in an infectious form until the death of the host. The low rate of decrease of specific antibodies in an infected individual [19
], extremely low frequency of seroconversion (loss of specific antibodies) among seropositive subjects [14
], and high frequency of reactivation of toxoplasmosis in seropositive AIDS patients [20
] suggest the existence of life-long Toxoplasma
infections in humans as well. The slowing of reaction times and other behavioural changes that can increase the risk of predation in Toxoplasma
-infected rodents are probably mediated by production or induction of production of a neurotransmitter, possibly dopamine, [22
] in the brain of infected animals. In humans, such manipulative activity is non-productive for Toxoplasma
. It must be considered here "an evolutionary constraint," as it arises as a side effect of selection in different host species, with no apparent direct adaptive significance in humans [23
]. Indeed, the difference in behavioural alterations induced by Toxoplasma
in various animal species might help to reveal the neurophysiological mechanism(s) of the manipulation activity of the parasite.