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$F:\Jprfeb 2010\2010\NOV 2010\Ac$ Review Article Pramod Kumar et al. / Journal of Pharmacy Research 2010, 3(11),2700-2705 ISSN: 0974-6943 Available online through www.jpronline.info An awareness towards the chagas disease: A review Pramod Kumar1*, Peeyush Kumar1, Devendra Singh Thakur1, Champal Lal 1, Vinod Kumar Swami 2 1SLT Institute of Pharmaceutical sciences, Guru Ghasidas Vishwavidyalaya, Bilaspur, (C.G.) India, 495001. 2Lachoo Memorial College of sciences & Technology, Jodhpur, (Rajasthan), India 342003. Received on: 15-06-2010; Revised on: 18-08-2010; Accepted on:13-09-2010 ABSTRACT American trypanosomiasis (Chagas disease) is an important cause of heart disease, megaesophagus and megacolon among people in Mexico, Central and South America. Many mammals can be infected with the parasite that causes this disease; however, among animals, clinical cases have been reported mainly in dogs. Chagas disease is transmitted by the bites of triatomine insects, or “kissing bugs.” Some infected insects occur in sylvatic environments, where humans are exposed only occasionally. These “sylvatic cycles” are found from the U.S. through South America. From Mexico through South America, triatomine insects have also become adapted to human dwellings, particularly substandard housing where the insects hide in cracks during the day and emerge to feed on humans and animals at night. Most human cases are acquired from insects in these “domestic cycles,” and campaigns to eliminate the bugs, together with testing to prevent congenital cases and transmission in blood transfusions, have significantly reduced the incidence of Chagas disease. Antiparasitic treatment is most effective early, before irreversible damage occurs to the heart or gastrointestinal tract. Key words: Chagas disease, Trypanosoma cruzi, ELISA, Prevention INTRODUCTION The discovery of American trypanosomiasis by Carlos Chagas was one of the Chagas disease is an autochthonous disease of 22 countries in the continental most successful and completes findings in the whole history of tropical medi- Western Hemisphere caused by the protozoa Trypanosoma cruzi (T. cruzi). cine. The natural history of Chagas disease began millions of years ago as an Human infection is primarily transmitted by domestic and sylvatic insects of enzootic disease among wild animals, and this still persists in enzootic areas the subfamily Triatominae (Hemiptera, Reduviidae), the kissing bug, whose such as the Amazon region. When mankind ventured into the natural ecotopes habitat in the Americas ranges from the US and Mexico in the north to of the infection, it began to be transmitted accidentally to humans as an Argentina and Chile in the south. T. cruzi infection may be also transmitted to anthropozoonosis. Because of the extensive deforestation for agriculture and humans congenitally, by blood transfusion and organ transplant and by the oral 3 livestock rearing over the last 200–300 years in Latin America, triatomines route. The possibility that vector transmission may occur in Europe or in that were left without their food sources due to the removal of wild animals other continents by autochthonous triatominae is considered remote. More started to colonize areas surrounding human dwellings, and the dwellings them- feasible however, is the risk of accidental transport of domestic Latin Ameri- can species of triatominae to other regions or continents (i.e. in the baggage selves. They adapted to this new niche, including feeding on the blood of of airline passengers). In the US, the social conditions in the rural areas are not humans and domestic animals. Fig. 1 shows the domestic and wild cycles of 1,2 usually adequate for the intimate contact between vectors and humans. There- Chagas disease discovered by Carlos Chagas. fore, the probability of vector transmission is low and few autochthonous Chagas disease cases have been documented in the US.4,5 Currently, Chagas’ disease affects 10 to 12 million individuals worldwide.6 Its geographic distribution extends from the 40th parallel north, in the southern part of North America, to 45th parallel south, in Argentina and Chile.7 Latin American urbanization, which intensified in the second half of the 20th cen- tury, has altered the epidemiologic profile of the disease, and migratorymovements from endemic countries have led to the diagnosis of Chagas’ disease in regions in which it is not endemic.8,7 Spain has become one of the European countries that receive the largest number of immigrants from Latin American. As of December 31, 2005 close to a million individuals from Latin America were included in the records of foreign nationals holding a Spanish resident’sidentity card,10 although mu- nicipal census records for the year 2005 indicated higher figures (1445796 individuals). Units and services specialized in tropical medicine and interna- tional health in Spain have already begun to diagnose and treat individuals with the disease.9 The recent meeting of the Pan-American Health Organization in Montevideo discussed this situation and in its final report mentioned the needs of countries receiving immigrants from endemic areas in order to deal with Chagas’disease and to be able to provide appropriate treatment to affected individuals, as well as to prevent vertical and blood borne transmission of T cruzi.10 1. TRYPANOSOMA CRUZI LIFE CYCLE AND MODE OF TRNSMISSION The life cycle of T cruzi involves four distinct forms in insect vectors and mammalian hosts: (1) the epimastigote, present in the intestinal tract of the insect, that replicates; (2) the infective metacyclic trypomastigote in the vector’s hindgut; (3) a blood stage form (trypomastigote) that penetrates Fig. 1. Domestic and wild cycles of Chagas disease discovered by Carlos Chagas mammalian cells; and (4) an intracellular form (amastigote) that replicates. *Corresponding author. Infection occurs when an infected bloodsucking bug bites and it defecates on Pramod Kumar the skin of a susceptible host. The metacyclic trypomastigotes in the feces SLT Institute of Pharmaceutical sciences produce a local infection when it is rubbed into the site of the bite (chagoma) G. G.V. Bilaspur(C.G.) India, 495001 Tel.: + 91-9770765502 E-mail:[email protected] Journal of Pharmacy Research Vol.3.Issue 11.November 2010 2700-2705 Pramod Kumar et al. / Journal of Pharmacy Research 2010, 3(11),2700-2705 or by penetrating the intact mucous membrane of the eye (Romaiia’s sign). disease, with myocarditis or encephamomyelitis; without treatment, around Once inside the local reticuloendotelial and connective cells, the infective 5–10% of these patients die.15 cruzi differentiates into amastigotes that begin replicating. When the cell is full of amastigotes, they transform once more and become trypomastigotes Detection of antibodies to T. cruzi has been and is the main method for the by growing flagellae. The trypomastigotes lyse the cells, infect adjacent tis- diagnosis of Chagas’ disease. Antibodies are detected by an array of available sue, and enter the bloodstream. Circulating trypomastigotes disseminate the commercial tests; among them, the most employed are indirect hemagglutina- infection by penetrating muscle cells (cardiac, smooth, and skeletal), neurons, tion (IHA), indirect immunofluorescence (IFA), and ELISA. The antigens lymph nodes, liver, and spleen. The cycle is completed when areduviid bug employed in these tests are whole or semipurified antigenic fractions of T. becomes infected by ingesting the blood from an infected human or animal. cruzi epimastigote forms, giving rise to unspecific reactions (false positives) Most Trypanosoma cruzi infections in humans are acquired from the insect and a sensitivity that is far from ideal. Thus, two or three tests must be vector, but may occur by transfusion of blood from an infected donor, even in employed to reach a definitive conclusion. The WHO recommends using at nonendemic countries.11 Congenital transmission, accidental contamination, least two tests in parallel. Variation in the reproducibility and reliability of the and transmission by organ transplantation are other possible routes of infec- results has been reported and it could be explained by poor standardization of tion. the reagents.16,17 1.1. ACUTE AND CHRONIC INFECTION There are three methods for diagnosis of chagas disease Trypanosoma cruzi produces disease during the initial infection (acute phase) 1.Conventional serologic tests and again decades later.12 Acute Chagas’ disease usually affects children or 2.ELISA young adults in endemic areas. It produces local inflammation at the parasite 3.TESA blot entry site, as well as malaise; fever; enlargement of the liver, spleen, and lymph nodes; and subcutaneous edema. Mortality in the acute phase occasion- 3.1.Conventional serologic tests ally occurs (< 5% of cases) due to acute myocarditis and or meningoencepha- The epi-ELISA, IFA, and IHA for Chagas’ disease diagnosis were carried out at litis. In most infected persons, the illness is not diagnosed because of the the Faculty of Medicine of Goiania, Federal University of Goia´s (Goia´s, nonspecific nature of the signs and symptoms and the lack of access of poor Brazil). The epi-ELISA was performed using a crude extract of epimastigote patients to medical care. In this phase, treatment with an antiparasitic drug, forms of T. cruzi (Y strain).18 The results were expressed as an index obtained such as benznidazole, will usually cure the infectied and prevent the chronic by division of the values of absorbance read at 492 nm (A492nm) of

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