Comunicaciones Breves                   

Fidias E. León-Sarmiento,^1,3 Jaime Bayona-Prieto,^1,2 Hernan G. Hernández^2,3

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Resumen

La infección por Trypanosoma cruzi esta aún lejos de haberse resuelto en latinoamérica. Investigaciones recientes sobre este germen están fuertemente sesgadas hacia la investigación de ciencias básicas, principalmente a nivel molecular, dejando de lado importantes hallazgos clínicos y epidemiológicos. Presentamos aquí evidencias científicas que demuestran como el Trypanosoma cruzi afecta diferentes sistemas neurales  incluyendo el autónomo. Las rutas de trasmisión oral y genital relacionadas con este parásito, así como las reacciones cruzadas y falsos positivos descritas durante la realización de diferentes tests serológicos que investigan la posible presencia del Trypanosoma  cruzi, incluyendo los utilizados para investigar el VIH, deben todas ellas ser tomadas muy en cuenta antes de rotular a los pacientes con el, casi siempre, fatal diagnóstico de enfermedad de Chagas.

Abstract

Trypanosoma cruzi infection is far for being solved in Latin America. Recent research is strongly biased to basic investigations mostly at molecular levels putting aside important clinical involvement and epidemiological findings. Here, we present evidence that Trypansoma cruzi affect neural systems including the autonomous one. Oral and genital routes of transmission of this parasite as well  as the cross-reactions and false-positives described with different serological tests including those used to test HIV must be checked out before putting the almost always fatal diagnoses of Chagas disease.

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Introduction

Trypanosoma cruzi (T. cruzi) infection is still a challenge to scientists working in basic and/or clinical grounds; some of these problems, mainly the basic ones, have been addressed by different groups in different Latin- American countries and commented in some recent publications as supplements; however, the basic - clinical  gap seems to remain in current investigations.1,2 In order to help in closing such a gap on this international health public problem we consider timely to go further looking for probable clinical, epidemiological and laboratory  advances unaddressed in those previous scientific communications that may influence patient’s intervention in clinical practice. We concentrate our efforts in knowing neural  structures involvement because the neurotropism of this parasite is clearly established.

Material and Methods

Following methodologies described in previous research published on this topic3 we identified references by searches of Medline/PubMed from 1966 until December 2006 and of Scielo from 1997 until December 2006 with the terms “trypanosoma cruzi” “chagas” “central nervous  system” “epidemiology” “spinal cord” “peripheral nervous system” “neuromuscular junction” “muscle” “muscle disorders” “neuromuscular diseases and disorders”  “synapticopathies” “pathophysiology” “clinical neurophysiology” “functional neurology” “clinical neurosciences” “transmission route” “laboratory.” Articles were also identified through searches of the authors’ own files. Papers published  in English, Spanish and Portuguese were analyzed. Inclusion and exclusion criteria were similar to those chosen in a previous research; however, we consider at this time publications reporting serological tests  using polymerase chain reaction as well.3

Results and Discussion

In clinical grounds, besides T. cruzi infection-associated dysautonomy widely recognized and investigated,4 it was noteworthy to find a good number of acute and chronic disorders including cerebrovascular disease (CVD), meningitis, cognitive disorders, peripheral neuropathies, synapticopathies such as myastenia gravis, myopathies including polymiositis, pupilopathies and impotence.

We highlight here CVD because it is a very common complication of T. cruzi infection with a high morbimortality as well as an increasing trend in social and personal costs.5-7 It should be remarked that T cruzi infection itself, without a clinically established disease including cardiopathy, is more than enough to trigger CVD in humans.6,8,9

Regarding routes of transmission, it was interesting to find that the parasite colonizes human body by means other than bites including oral route thru breast feeding and sugar cane juices.10-12 Genital route seems to be another way of transmission not well characterized yet in countries where this problem is endemic.13

On the other hand, T. cruzi generates one of the seventy six cross reactions described so far while looking for HIV antibodies14-16 making this germen much more dangerous to humans than previously thought. Thus, immunosuppressants given as regular treatments to patients harboring unisolated HIV viruses17,18 may increase immunosuppression in patients infected by T. cruzi worsening clinical complications produced by this parasite as the ones commented above, and would allow to T cruzi to act more aggressively than usual with devastating consequences to infected people.

These facts call the attention on what might be the true cause of possible complications found in seropositive patients to both T. cruzi and HIV including the deterioration of syncopal reactions.19

All the aforementioned comments support the continued interest in researching and publishing supplementary scientific issues on Chagas disease to complement and up date the knowledge of the complex disorders produced by T. Cruzi. However, we want to go further and stress that the “new” routes of infection, the “infrequent” systemic complications that are very far from being included in  level I of epidemiological evidence statistically speaking, and the “new” crossed reactions described in the present report can be, all of them, the first evidence of a serious health problem that is still far from being solved in, at least, some Latin-American countries.

Acknowledgments

We dedicate this manuscript to Eugenio Leon, father of one of us (FEL-S). He stated ten years before being diagnosed as T. cruzi carrier at the UIS laboratory of parasitology, in Bucaramanga, Colombia, that he acquired the parasite after eating contaminated beef and that never ever he had been bitten by any possible parasite’s reservoir. Unfortunately he already died of chagasic myocardiopathy when he was 77 years-old and he took away with him all of the evidence.

Bibliografía

1. Moncayo A. La enfermedad de Chagas en 1909 y 2006. Biomedica 2007; 27 (suppl 1): 5-8.

2. Arias, AR, Dias JCP. Working group: social, epidemiological, and control determinants of Chagas disease in American southern cone. Mem Inst Oswaldo Cruz. Epub ahead [citado 2007-10-20].

3. Leon-Sarmiento FE, Prada D, Valderrama V, Bayona J. Neurotripanosomiasis: conceptos básicos de un problema clínico. Biomedica 2003; 23: 462-475.

4. Kaufmann H. Disautonomias mas comunes. Rev Neurol 2003; 36: 93-96.

5. Pradilla G, Vesga BE, Leon-Sarmiento FE & Grupo Geneco. Estudio neuroepidemiologico en Colombia. Boletin OPS 2003; 14: 104 -111.

6. Leon-Sarmiento FE, Mendoza E, Torres-Hillera M, Pinto N, Prada J, Silva CA, Vera SJ, Castillo E, Valderrama V, Prada DG, Bayona-Prieto J, Garcia I. Tripanosoma cruzi-associated cerebrovascular disease: a case-control study in eastern colombia. J Neurol Sci 2004; 217: 61-64.

7. Perez G. Marcadores de inflamación y enfermedad cerebrovascular en Colombia. Acta Neurol Col 2006;22: 1-2.

8. Carod-Artal FJ, Vargas AP, Horan TA, Nadal Nunes LG. Chagasic cardiomyopathy is independently associated with ischemic stroke in Chagas disease. Stroke 2005; 36: 965-970.

9. Oliveira-Filho J, Viana LC, Vieira-de-Melo RM, Facial F, Torreão JA, Villar FAGA, Reis FJFB. Chagas disease is an independent risk factor for stroke. Baseline characteristics of a Chagas disease cohort. Stroke 2005; 36: 2015-2017.

10. Ferrerira CS, Martinho PC, Amato Neto V, Cruz RR. Pasteurizacion of human milk to prevent transmisión of Chagas disease. Rev Inst Med Trop Sao Paulo 2001; 43:161-162.

11. Camandaroba EL, Pinheiro Lima CM, Andrade SG. Oral transmission of Chagas disease: importance of Trypanosoma cruzi biodeme in the intragastric experimental infection. Rev Inst Med Trop Sao Paulo 2002; 44: 97-103.

12. Cardoso AVN, Lescano SAZ, Amado Neto V, Gakiya E, Santos SV. Survival of Trypanosome cruzi in sugar cane used to prepare juice. Rev Inst Med Trop Sao Paulo 2006; 48: 287-289.

13. Herrera L, Urdaneta-Morales S. Experimental transmission of Trypanosoma cruzi through the genitalia of albino mice. Mem Ist Oswaldo Cruz 2001; 96: 713-717.

14. Gonzales CI, Thomas MC, Martin F, Alcami J, Alonso C, Lopez MC. Reverse transcriptase-like activity in Trypanosoma cruzi. Acta Trop 1997; 63: 117-126.

15. Leon-Sarmiento FE (ed). ViH & Los virus de la imaginación humana. Bogota: Celsus, 2001.

16. Parra-Piñeros JE, Valderrama V, Leon-Sarmiento FE, Daza N, Ramirez-Diaz H, Leon-Sarmiento ME, Bayona J. False-positive human immunodeficiency virus tests and Trypanosoma cruzi infection in eastern Colombia. South Med J 2004; 97: 423-424

17. Papadopulos-Eleopulos E, Turner VF, Papdimitriou JM, Causer D, Page BA. HIV antibodies tests and antiviral load: more unanswered questions and a further plea for clarificacion. Curr Med Res Op 1998; 14: 185-186.

18. Leon-Sarmiento FE, Carpintero M. Retrovirus, micotoxinas, inmunosupresion and neurodegeneration. Rev Neurol 2002; 35: 562-571.