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M. T. GALáN-PUCHADES and A. OSUNA cruzi. Hemos revisado la literatura buscando evidencias sobre la interacción entre helmintos y T. cruzi para establecer si esta coinfección pudiera alterar parámetros como: i) la susceptibilidad para adquirir la enfermedad de Chagas; ii) la progresión de la enfermedad; y iii) la probabilidad de la transmisión congénita. Según un estudio realizado en autopsias humanas, personas que presentaron coinfección entre cisticercosis y T. cruzi tuvieron una mayor expectativa de vida que aquellas que presentaron sólo uno de los dos parásitos, o ninguno de ellos. Perros solo chagásicos mostraron más daños cardíacos comparados con aquellos que presentaban coinfección con Dirofilaria immitis. Las helmintiasis crónicas en ratones alteraron la susceptibilidad hacia T. cruzi. Primates coinfectados con Chagas y helmintos también mostraron diferencias tanto en la seroprevalencia de T. cruzi y como en las características de la infección, siendo los mismos tipos de T. cruzi los implicados. La coinfección con helmintos puede ser capaz de interferir de una manera significativa en la enfermedad de Chagas, por lo que es un potencial factor modulador no explorado ni a nivel humano ni en modelos experimentales. Palabras clave: Enfermedad de Chagas, Trypanosoma cruzi, poliparasitismo, helmintos, coinfección. 6 INTRODUCTION Host-parasite interactions are rarely one-onone. Most hosts, including humans, are often infected with more than one parasite species (Telfer et al., 2010). Thus, multiple species parasitic infections seem to be the norm rather than the exception (Raso et al., 2004). However, polyparasitism is a neglected phenomenom. Despite the ubiquity of polyparasitism, its public health significance has been inadequately studied (Pullan and Brooker, 2008). In this context, the current disease-by-disease approach to modelling and treating infectious diseases, such as Chagas Disease (CD), may be inadequate. CD is caused by the protozoan Trypanosoma cruzi affecting some 18 million people in Latin America. The World Health Organization estimates that over 300,000 new cases of American Trypanosomiasis and 15,000 deaths are reported annually in countries where 75 million people live at risk of infection. CD is neither a unique pathological entity nor a uniform disease with the same pattern in all patients. The existence of a wide range of clinical manifestations varying from asymptomatic to severe cardiac and/or digestive (megaesophagus and megacolon) pathologies during the chronic phase stresses the necessity to define the factors related with the clinical aspects of the disease. What mechanisms are involved in producing such severe pathologies? Helminths are among the most common parasites of free-living animals (Poulin, 2007). Worms have been shown to induce immune hyporesponsiveness in their hosts, which might affect the immune reaction to concomitant species since the modulation of this immune response is not only directed at helminths, but also at non-related antigens (Riet et al., 2007). In most areas where CD is endemic, helminth infections are highly prevalent, and evolution of the host’s immune responses to both types of parasites may have adapted Chagas immunology to the presence of helminths. The aim of this review is to gather information on the effect of co-infection between helminths and intracellular protozoan parasites, and, in particular, between worms and Trypanosoma cruzi, to ascertain if this co-infection could alter: i) the susceptibility to acquire CD; ii) the progression of the disease; and iii) the probability of congenital transmission. INTRACELLULAR PROTOzOAN AND HELMINTH CO-INFECTIONS The characteristics of the immune response to infection depend on the type of pathogen. Intracellular protozoan organisms such as Plasmodium sp., Toxoplasma gondii, Leishamania sp., and Trypanosoma cruzi stimulate a Th1-like response associated with the production of IL-12, IFN-g, IL-2, and TNF-a and the classical activation of macrophages. In contrast, extracellular helminths induce aTh2like response with the production of IL-4, IL-5, IL- 10 and the alternative activation of macrophages. Rev. Ibero-Latinoam. Parasitol. (2012); 71 (1): 5-13
Helminth infection can bias the human immune response towards a Th2 type over a Th1 and a Th17 response (Walsh et al., 2009), thus impairing the host’s ability to control concurrent intracellular microparasite infections (Ezenwa et al., 2010), such as T. cruzi, and potentially modify disease dynamics. Hence, helminths are likely to make hosts more resistant to pathogens in which protection is mediated by the Th2-like response and more susceptible to pathogens in which protection is mediated by the Th1-like response. In the last five years, several interesting review articles dealing with the immunomodulation of helminths in their hosts and its consequences on coinfections with intracellular protozoans have been published (van Riet et al., 2007; Graham, 2008; Pullan and Brooker, 2008; Helmby, 2009; Moreau and Chauvin, 2010; Supali et al., 2010; Ezenwa and Jolles, 2011, among others), coinciding on the ability of helminths to alter host immune responses. This ability could be of detriment to the host if it negatively interferes in protective immune responses against other infections or may have a beneficial role in controlling autoimmune or other excessive inflammatory responses provoked by other pathogens. Considering intracellular protozoan parasites, the effects of helminth co-infection have been studied mainly in malaria and secondarily in leishmaniosis and toxoplasmosis. There are two main aspects to elucidate as a consequence of the interaction. First, if the susceptibility to acquire the protozoan infection is higher or lower in wormy hosts, and if these hosts present better or worse clinical signs compared with those free of helminths. Malaria and helminths Although interest in the subject of the interaction between worms and malaria has recently increased, there are still no large-scale studies in humans dealing with the real consequences of this interaction, i. e. to determine whether worms increase or decrease incidence and whether they protect or not from different presentations of severe malaria. An early study performed more than 30 years ago described that anthelminthic treatment of severe ascariasis in a high-transmission area was followed by an increase in symptomatic malaria Rev. Ibero-Latinoam. Parasitol. (2012); 71 (1): 5-13 CHAGAS DISEASE IN A WORMY WORLD (Murray et al., 1978). However, several decades later, the notion that infection with helminths increases the susceptibility to malaria infection was backed (Hartgers and Yazdanbakhsh, 2006). Concerning the course of the disease, deworming malaria patients would be like ‘robbing Peter to pay Paul’ since evidence suggests that helminth co-infection leads to higher plasmodium loads being less harmful, as helminth infection protects from acute renal failure and cerebral malaria (Specht and Hoerauf, 2007). In a murine model, Schistosoma mansoni infection reduced the incidence of cerebral malaria (Waknine-Grinberg et al., 2010). Recently, a survey carried out in Nigeria provided evidence that asymptomatic falciparum malaria and intestinal helminth infections do co-exist without clinical symptoms (Ojurongbe et al., 2011). However, in filarial/malaria co-infection, the presence of filarial infection may lead to a profound inability to mount an effective response to provide protection against severe malaria and also dampens the success of malaria vaccination schemes in filaria-endemic regions of the world (Metenou et al., 2011). These analyses of helminth and malaria coinfections seem controversial depending on the helminth species involved, the intensity of duration of worm infection, and the age of the individual under study. Nevertheless, helminths may be a missing link in the understanding not only a number of facts about malaria but also the failures of certain anti-malaria vaccine strategies (Nacher, 2001; Noland et al., 2010). Leishmaniosis and helminths Just as in CD, a Th1-type immune response is crucial in the control of leishmania infection. However, excessive inflammation caused by Th1 cytokine release has also been implicated in the pathogenesis of cutaneous leishmaniosis. Two first studies examining the interplay between schistosomiasis and Leishmania major (Yoshida et al., 1999; La Flamme et al., 2002) showed not only a delay in lesion resolution but also in its development (La Flamme et al., 2002) in mice. Later, the co-infection between a filarial nematode and also L. major in mice was studied (Lamb et al., 2005) and the results obtained were similar to those previously observed (La Flamme 7
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