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M. T. GALáN-PUCHADES and A. OSUNA et al., 2002), i.e. both helminths are capable of altering the progression of leishmaniosis. A preexisting filarial infection enhanced the immune response mounted against L. major. Co-infected mice also exhibited a lower pathology during the course of the experiment compared to mice singly infected with L. major. Additionally, there was a trend toward a larger L. major parasite load in the co-infected mice. Therefore, the pre-existing helminth infection may explain the elevated number of parasites and delayed lesion size. However, co-infection with tapeworm Taenia crassiceps led to increased lesion sizes upon subsequent L. major and L. mexicana infection in mice (Roderiguez-Sosa et al., 2006). On the other hand, comparison of the general course of Leishmania infection in L. major singly and L. major ⁄ Strongyloides ratti co-infected mice revealed no difference in first and second L. major infection (Kolbaum et al., 2011). It seems clear that the results of co-infection are not always consistent without taking into account the helminth- and Leishmania species, the local or systemic nature of the infections, and the timing and the sequence of exposure to parasites. Only one study carried out in human´s analysed co-infection between helminths and L. braziliensis (O’Neil et al., 2007). The authors concluded that helminths influence both the clinical outcome and the immune response of patients with leishmaniosis. Patients with helminths tend to have smaller main lesions whose healing takes longer than those in their helminth-negative counterparts. Toxoplasmosis and helminths More than 30 years ago the concomitant infection Schistosoma-Toxoplasma in albino mice was studied (Kloetzel et al., 1977). The results depended on the time-course evolution of the initial infection. When toxoplasmic mice were infected with S. mansoni few notable effects were observed. However, S. mansoni infection was much more severe in mice previously infected with the helminth and subsequently by T. gondii. The same results were obtained years later (Marshall et al., 1999), since the mortality rate was higher when mice with schistosomiasis were infected with the protozoan. In other helminth infections such as Nip- 8 postrongylus brasiliensis and Fasciola hepatica, potent immune responses to T. gondii were capable of suppressing the responses to helminth infections (Liesenfeld et al., 2004; Miller et al., 2009). However, infection of mice with N. brasiliensis did not alter immune responses to subsequent infection with T. gondii and did not alleviate gut pathology or prevent death of mice, while prior infection with Heligmosomoides polygyrus led to the development of suboptimal adaptive immunity against T. gondii, essential for long-term protection against this parasite (Khan et al., 2008). Once more, the results of co-infection are not always consistent, thus highlighting the importance of the species involved and the sequence of exposure to parasites. Concerning susceptibility, it has been found that persons infected with Toxocara spp. were more likely to be infected with T. gondii, and similarly, persons infected with T. gondii were more likely to be infected with Toxocara spp. (Jones et al., 2008). CHAGAS DISEASE AND HELMINTHS In humans To our knowledge there is only one published paper that deals with co-infection between CD and helminths in humans. An epidemiological analysis in patients co-infected with CD and cysticercosis was conducted by means of data obtained from autopsies performed in 1501 corpses (Faleiros et al., 2009). The authors found that CD was 10 times more frequent in patients co-infected with cysticercosis. Intriguingly, the authors also found that co-infected patients had a longer survivorship compared to those suffering from CD only or those with cysticercosis only and even those persons without any infection. The impact of co-infection between CD and concomitant helminth infections has been analysed in some other hosts such as mice, dogs and primates. In mice Almost 40 years ago, albino mice were exposed concomitantly to S. mansoni and T. cruzi (Kloetzel et al., 1973). The findings were very similar to those obtained in the interaction between S. mansoni Rev. Ibero-Latinoam. Parasitol. (2012); 71 (1): 5-13
and Toxoplasma mentioned above. The authors observed an enhanced and more persistent T. cruzi parasitaemia in mixed infections. It has also been found that the presence of Taenia crassiceps cysticerci in mice modified the immune response and the susceptibility to T. cruzi (Rodriguez et al., 1999). These modifications also depended on the time-course evolution of the initial infection, since co-infection with the protozoan in the early stages of the helminth infection induced a delay in the onset of parasitaemia. However, a significant increase in susceptibility to T. cruzi was observed only when mice were co-infected in the late stages, i.e. when the helminth load is heavier and a Th2 type response against it is predominant. Thus, in late co-infection, parasitaemia presented an early increase, leading to a fourfold parasite load over the singly infected mice at the peak of parasitaemia. In dogs Natural Dirofilaria immitis and T. cruzi coinfection was recently studied in dogs from Mexico (Cruz-Chan et al., 2010). The authors observed a relatively high prevalence of D. immitis and T. cruzi co-infection as well as a decreased inflammatory reaction in the heart of D. immitis and T. cruzi co-infected dogs compared to those only affected by CD. The authors suggested that D. immitis infection may modulate T. cruzi immunopathology by decreasing the inflammatory immune response induced by T. cruzi and also suggested that great care should be taken in the interpretation of immunological and pathological data from naturally infected animals, as co-infection may significantly interfere with host responses and should be taken into account by researchers and clinicians. In primates A study on the parasite community interactions between T. cruzi and intestinal helminths was performed in wild primates (the golden lion tamarin Leontopithecus rosalia and the golden-headed lion tamarin L. chrysomelas) in Brazil (Monteiro et al., 2007). According to the authors, a better understanding of the epidemiology of T. cruzi in the wild may improve knowledge on the risk of new cases and the clinical course of CD in humans and Rev. Ibero-Latinoam. Parasitol. (2012); 71 (1): 5-13 CHAGAS DISEASE IN A WORMY WORLD other mammal species. The authors stated that the differences found in T. cruzi seroprevalence and the infection profile of the studied primate populations are the result of concomitant helminth infections. The authors found significantly higher helminth prevalences in T. cruzi infected tamarins than in T. cruzi seronegative ones. T. cruzi parasitaemia also varied depending on the helminth species, which is the reason why the authors stated that these distinct T. cruzi infection profiles could not be explained by the T. cruzi genotype as all typed isolates were the same. The obtained data suggested to the authors that T. cruzi infection could have both beneficial and detrimental effects on the hosts: not only lowering helminth-linked death rates but also lowering their ability to rid themselves of helminth infection. T. cruzi and helminths would both benefit from these effects, through increased transmission rates to new hosts, thanks to the longer persistence of infected hosts in the population. Concerning the health status, those tamarins coinfected with helminths and T. cruzi, were healthier than those only harbouring helminths (Monteiro et al., 2010). Could co-infection with chronic helminthiases increase the risk of mother-child transmission of CD? Parasitaemia in pregnant women seems to be an important factor contributing to congenital transmission of T. cruzi. Pregnant women displaying high parasitaemia present a higher transmission risk than chronically infected women in whom blood parasites are hardly detectable (Carlier and Truyens, 2010; Brutus et al., 2010). Maternal co-infection with T. cruzi and HIV results in increasing frequency and severity of congenital CD, highlighting the important role of maternal immunity and high parasitaemia in favoring parasite transmission to the fetus (Scapellato et al., 2009; Carlier and Truyens, 2010). Mothers transmitting T. cruzi to their fetuses display lower T-cell mediated immune responses to parasites and produce less IFN-g, which probably contributes to an increase in parasitaemia (Carlier and Truyens, 2010). All the co-infection cases between CD and chronic helminth infections analyzed resulted 9
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