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Memórias do Instituto Oswaldo Cruz

Print version ISSN 0074-0276On-line version ISSN 1678-8060

Mem. Inst. Oswaldo Cruz vol.102  suppl.1 Rio de Janeiro Oct. 2007  Epub Aug 31, 2007

http://dx.doi.org/10.1590/S0074-02762007005000093 

Epidemiology of Chagas disease in non endemic countries: the role of international migration

 

 

Gabriel A Schmunis+

Pan American Health Organization/World Health Organization, 525 23rd Street, NW Washington, DC 20037, US

 

 


ABSTRACT

Human infection with the protozoa Trypanosoma cruzi extends through North, Central, and South America, affecting 21 countries. Most human infections in the Western Hemisphere occur through contact with infected bloodsucking insects of the triatomine species. As T. cruzi can be detected in the blood of untreated infected individuals, decades after infection took place; the infection can be also transmitted through blood transfusion and organ transplant, which is considered the second most common mode of transmission for T. cruzi. The third mode of transmission is congenital infection.
Economic hardship, political problems, or both, have spurred migration from Chagas endemic countries to developed countries. The main destination of this immigration is Australia, Canada, Spain, and the United States. In fact, human infection through blood or organ transplantation, as well as confirmed or potential cases of congenital infections has been described in Spain and in the United States.
Estimates reported here indicates that in Australia in 2005-2006, 1067 of the 65,255 Latin American immigrants (16 per 1000) may be infected with T. cruzi, and in Canada, in 2001, 1218 of the 131,135 immigrants (9 per 1000) whose country of origin was identified may have been also infected. In Spain, a magnet for Latin American immigrants since the 2000, 5125 of 241,866 legal immigrants in 2003 (25 per 1000), could be infected. In the United States, 56,028 to 357,205 of the 7,20 million, legal immigrants (8 to 50 per 1000), depending on the scenario, from the period 1981-2005 may be infected with T. cruzi. On the other hand, 33,193 to 336,097 of the estimated 5,6 million undocumented immigrants in 2000 (6 to 59 per 1000) could be infected. Non endemic countries receiving immigrants from the endemic ones should develop policies to protect organ recipients from T. cruzi infection, prevent tainting the blood supply with T. cruzi, and implement secondary prevention of congenital Chagas disease.

Key words: Chagas disease - immigration - non endemic countries - blood supply - prevention - transfusion and congenital transmission


 

 

American trypanosomiasis or Chagas disease is caused by the protozoa Trypanosoma cruzi. Human infection extends through North, Central, and South America, from Mexico in the north to Argentina and Chile in the south, affecting 21 countries (WHO 1991, 2002, OPS 2006).

Most human infections in the Western Hemisphere still occur when the skin or mucous membranes come into contact with the stool or urine of T. cruzi infected bloodsucking insects of the triatomine species (WHO 1991). However, significant advances have been made on this front. Strengthening vector control of the main domiciliary vector in the Southern Cone of South America, Triatoma infestans, interrupted vector transmission of T. cruzi by that triatomine in Uruguay in 1997, Chile in 1999 (WHO 2002), and Brazil in 2006. That success stimulated countries in Central America to attempt control of their intradomiciliary vector, Rhodnius prolixus. Up to now, significant success has been achieved in El Salvador and Guatemala.

As T. cruzi can be detected in the blood of untreated infected individuals, or of those with treatment failure (WHO 1991), decades after infection took place, said infection can be transmitted to an uninfected individual through blood transfusion. As long as blood from infected donors is not discarded, the possibility of transmitting infections through transfusion remains. Transfusion of whole blood, packed red blood cells, platelets, leukocytes, frozen fresh plasma, and cryoprecipitate is dangerous. In contrast, the use of lyophilized products appears to be safe (Schmunis 1991).

Transfusion can be considered the second most common mode of transmission for T. cruzi. Fortunately, only a fraction of infected blood recipients will become infected, e.g., between 12 and 20% in Argentina, Brazil, and Chile, and up to 48% in Bolivia (Schmunis 1991). However, this risk might be even less; in the United States, it was shown that 11 individuals who had received blood units positive for T. cruzi serology remained seronegative (Leiby et al.1997).

In the last 15 years, most Latin American countries have implemented policies to prevent transmission of Chagas disease by transfusion. Four countries screened 100% of donors for T.cruzi in 1993-1995; 5, in 1997; 7, in 2001-2002 (Schmunis et al. 1998, and 2001, Schmunis & Cruz 2005); and 8, in 2004 (PAHO 2006). Another four countries screened > 99% of donors in 2004 (PAHO 2006) (Table I). In fact, the only common mode of transmission of T. cruzi to which not enough attention has been paid in most endemic countries is the transplacental route. Although infection rates of congenital infection vary widely, it is accepted in the Southern Cone countries of South America that 1 to 12% of newborns from infected mothers could be infected (Carlier & Torrico 2003).

The estimated number of individuals infected with T. cruzi in endemic areas of Latin America decreased steadily since the 1980s, from 16-18 million cases in the middle of that decade and early 1990s (WHO 1991) to 11 million in the mid to late 1990s (Schmunis 2004); and to 7.6 million in 2006 (OPS 2006). This decrease may also be observed by comparing the burden of disease caused by several infectious diseases in 1990 with the equivalent data for 2001.

In Latin America, the disease burden produced by Chagas disease was surpassed only by acute respiratory infections, diarrheal diseases, and AIDS (World Bank 1993). Chagas disease had a higher disease burden than tuberculosis in 1990 (Fig. 1). At that time, the disease burden produced by the so called tropical diseases, malaria, schistosomiasis, leishmaniasis, and leprosy together equaled 25% of the disease burden caused by Chagas disease (Schmunis 1994).

 

 

In 2001, the disease burden decreased for all the aforementioned diseases, except for tuberculosis; nevertheless, Chagas disease had the greatest decrease when measured in disability adjusted life years (DALYs): 2.7 million to 867,000 DALYs (World Bank 2006) (Fig. 1). The number of deaths attributed to T. cruzi infection also decreased, from 45,000 deaths a year in the 1980s (Moncayo 1993) to 14,000 in 2001 (World Bank 2006 a). Indeed Chagas disease is in retreat in Latin America.

On the other hand, the potential for transfusing T. cruzi-infected blood or blood products is not exclusive to Latin America. Economic hardship, political problems, or both, have spurred migration from Chagas endemic countries to developed countries. For example, it was estimated that in the United States between 100,000 (Skolnick 1989) and 370,000 people (Milei et al. 1992) had chronic T. cruzi infection, and that 75,000 of those suffered from chronic myocardiopathy of that etiology (Milei et al. 1992). In Canada, in a recent survey of 102 Latin American refugees and immigrants, the prevalence of Chagas disease was found to be at 1% (Steel et al. 2007). Surprisingly, a similar survey conducted among immigrants in Germany showed 2% prevalence (Hegenscheid et al. 1997). Also as a result of migration, a case of congenital Chagas disease was diagnosed in Sweden (Pehrson et al. 1981).

In the late in 1980s, the number of documented Latin American immigrants in the United States from countries endemic for T. cruzi was 2,24 million, 1,55 million of whom were from Mexico (Statistical abstract of the United States 1989). The potential for finding T. cruzi infected individuals also existed in Europe, Australia, and Japan, where in the late 1980s, 250,000, 80,000, and 200,000 immigrants from Latin America, respectively, were living (Schmunis 1991). Immigrants in Japan were mainly Brazilians of Japanese ancestry whose living conditions in Brazil made them unlikely to have been infected with T. cruzi. In the United States, more than 7 million people from T. cruzi endemic countries become legal residents between 1981 and 2005 (US Census Bureau 2007). In Europe, Spain has become a magnet for immigrants from Latin America.

We report here, estimates of the number of T. cruzi infected individuals in non endemic countries i.e., Australia, Canada, Spain, and the United States, with immigrant populations from Latin American endemic countries. We discuss as well the public health implications of said immigration.

 

 

METHOD

Data on the number of immigrants, regardless of their legal status, were obtained from official sources from Australia (Australia Bureau of Statistics 2007), Canada (Canadian Statistics 2005), Spain (General Police Directorate, Interior Ministry (2002), Eurostat Europa, (2006), and the United States (Statistical Abstract of the United States 1989; US Department of Homeland Security 2003 and 2004; US Bureau of Census 2006, 2007; and information from newspapers.

The possibility of getting and infected transfusion from immigrant blood donors depends on the prevalence of infection in the country of origin. Taking into account that serology in blood donors correlated well with serological surveys among the general population (Schmunis 1994), we used the prevalence of T. cruzi infection per 1000 blood donors at the time when it was first officially reported by the countries of Latin America (around 1993-1995), as proxy for that prevalence: Argentina, 49 per 1000 donors; Bolivia, 148; Chile and Colombia, 12; Costa Rica, 8; Ecuador, 2; El Salvador, 15; Guatemala, 14; Honduras, 12; Nicaragua, 2; Panama, 1; Paraguay, 45; Uruguay 6; and Venezuela, 13 (Schmunis & Cruz 2005). Two countries, Brazil and Peru, reported country-wide prevalence of T. cruzi serology in blood donors for the first time in 1999 and 1997, respectively (8 per 1000 in Brazil, and 2 per 1000 Peru) (Schmunis & Cruz 2005). In Mexico, prevalence of T. cruzi infection in blood banks of the public health services in 12 of the 34 Mexican states ranged from 1,7/1000 (Chihuahua) to 17/1000 (in Morelos) from 1978 to 2004 (Cruz Reyes & Pickering Lopez 2006). On the other hand, 1999 was the first year for which data from Mexico on the prevalence of infectious disease markers in blood donors were officially provided; at that time, the prevalence rate for T. cruzi (4 per 1000) was based on the screening of only 13% of the total number of donors (Schmunis & Cruz 2005). In 2004 however, screening coverage increased to 34%, and the prevalence for T. cruzi also increased to 5 per 1000 (PAHO 2006), the same prevalence found in the state of Veracruz (Ramos-Lingonio et al. 2006). In some instances, information on rates of T. cruzi infection among blood donors from non endemic Mexican states (where there is no transmission) indicated high positive rates; such is the case of Puebla in 2001-2002 with a rate of 77 per 1000 (Sanchez Guillen et al. 2002), or Mexico City in 1998-2000 with a rate of 68 per 1000 (Cabrera et al. 2004). It was considered that the latter were mostly low income donors from 28 out of the 31 states of the country.

Taking into account the variations in prevalence rates among Mexican blood donors and the large numbers of Mexican immigrants in the United States, two scenarios were used for calculations. The first one used the prevalence found in the overall donor pool in 2004 (5 per 1000), and the other, the prevalence found among donors in Mexico City hospitals in Mexico City (68 per 1000). The latter was assumed to be a better estimate of the prevalence among low income populations likely to migrate to the United States.

It was also assumed that blood donors in immigrants' host countries would have been born at least 18-20 years before 2006 in their country of origin (in 1986-1988 or earlier) at a time when the overall T. cruzi prevalence rate in the latter country would have been higher (Schmunis 1991). Therefore, immigrant rates shown here are conservative estimates of the potential rate of infection of the immigrant population in the receiving country. All data were rounded to the nearest tenth of a unit by conventional methods.

 

RESULTS

Australia

Information was available on permanent arrivals from Argentina, Brazil, Chile, El Salvador, and Uruguay from 1975 to 2005. For Colombia and Peru, the information available was the estimated resident population in 2006 (Australian Bureau of Statistics 2007). Overall, the total number of immigrants was 65, 255, and the overall potential number of infected individuals could have been 1067 (Table II) when combining both permanent arrivals and resident population or 16 per 1000 of Latino immigrants in Australia (Table II).

Canada

Among the 29,639,035 individuals that populated Canada in 2001, 216,975 were classified as of Latin American origin. For 131,235 of those, there is information about country of origin. Most came from Mexico, followed, in decreasing order by Chile, El Salvador, Peru, and Colombia (Table II). Another 41,620 were from Central and South America; no information was available on the country of origin. There were also 44,120 individuals considered Latinos born in Canada (Canadian Statistics 2005). Estimates on the number of individuals potentially infected with T. cruzi from each country are shown in Table II. In Canada, the rate used to calculate the infection rate among immigrants from Mexico was 5 per 1000. Overall 9 per 1000 immigrants whose country of origin was identified may have been infected with T. cruzi (Table II).

Spain

In Europe, Spain is the country with the largest number of immigrants from Latin America. According to the General Police Directorate of the Ministry of the Interior 2002, there were 297,171 legal immigrants from Argentina, Brazil, Chile, Colombia, Ecuador, Peru, Uruguay, and Venezuela in 2002. At that time, there was no information on the number of immigrants from other endemic countries such as Bolivia, Costa Rica, El Salvador, Guatemala, Honduras, Nicaragua, Panama, and Paraguay. In 2003 (Table III), 241,866 immigrants were reported, including those from two countries where Chagas disease was highly prevalent, i.e., Bolivia and Paraguay (Eurostat 2006). It was estimated that 6125 or 25 per 1000 of those immigrants could have been infected.

 

 

The Ministry of the Interior (2005) indicated that of the approximate 2 million legal immigrants in Spain, 640,000 (32%) were from Latin America (Gazcon 2006). Of those, 11% were from Ecuador (70,400), 7% from Colombia (44,800); 3.5% from Peru (22,400), and 3% from Argentina (19,200). Following the same estimation method as above, the number of infected individuals would have been 141 from Ecuador, 538 from Colombia, 45 from Peru, and 941 from Argentina. Taking into account only those legal immigrants from those four countries, it can be estimated that there were 1665 individuals infected with T. cruzi in Spain. There are indications that illegal immigration is even greater than legal immigration. For example, 550,000 tourists from 17 Latin American countries entered Spain in 2002, but only 86,000 have a registered departure. Ecuador is at the extreme of this situation, with 101,432 Ecuadorian tourists entering Spain and only 874 returning to their country of origin. Among those who stayed, there could be 203 estimated cases of T. cruzi infected individuals. In addition, it was recently estimated that there were 400,000 Bolivian immigrants in Spain (El Deber Santa Cruz 2007). Given the prevalence of T. cruzi positive serology in blood banks in Bolivia, it could be expected that 59,200 of Bolivian immigrants in Spain may also turn out to have positive serology for T. cruzi. A survey done for the Interamerican Development Bank, estimated that in Spain there were 1,820,000 Latin American immigrants; including 262,000 from Argentina, 269,000 from Colombia, 414,000 from Ecuador, 126,000 from Peru (Ultima Hora 2007), and 37,000 from Paraguay (La Nacion 2007). Estimates of those infected were 12,838, 3228, 828, 252, and 1665 respectively.

United States

Up to late 1980s, the United States was by far the main destination for immigrants from Latin America, mostly from Mexico. At the time, of a total of 2439 million legal immigrants, 1,55 million were from Mexico (Statistical Abstract of the United States 1989). Since then, these numbers have increased significantly. In 1990, there were 7 million legal immigrants from Latin America (Schmunis 1994). According to data from the 2000 Census, 35 million Hispanics lived in the United States, and in 2004, that number was estimated at 41 million. A significant number of these immigrants came from countries endemic for T. cruzi infection (US Department of Homeland Security 2003, US Census Bureau 2006).

In the United States, the potential number of infected Latinos who could transmit T. cruzi infection through blood transfusion cannot be estimated based on the total Latino population, whose members were mostly born in that country. Also, the social and economic conditions of the rural population are not such as to allow intimate contact between the sylvatic vector of T. cruzi and humans. In consequence, only five cases of vector transmission of the infection have been reported (Herwald et al. 2000). Nevertheless, an approximation of the number of potentially infected Latinos may be based on the number of legal immigrants from the period 1981 to 2005, i.e., 7,200,493 (Table IV); estimates of the number of undocumented immigrants arriving in the United States from T. cruzi endemic countries in Latin America (5.6 million in 2000) (Table IV) (Department of Homeland Security 2003 & 2004, US Census Bureau 2006), and the prevalence of infection in the respective country of origin, as mentioned in the method section. As a result, it could be estimated that 56,028 to 357,205 legal immigrants or 8 to 50 per 1000 populations might be expected to have T. cruzi infection, depending on the scenario used to estimate the infection rate among Mexican immigrants. On the other hand, 33,193 to 336,097 undocumented immigrants or between 6 and 59 per 1000 population might also be infected.

In 2006, it was estimated that there were 11 million undocumented immigrants in the United States, of which 57% (6,270,000) came from Mexico, 24% (2,640,000) from other Latin American countries, and the rest, from Africa, Asia, Canada, and Europe (The Wall Street Journal 2006). By applying the same method as above, one might expect to find between 31,350 and 426,360 T. cruzi infected individuals among those undocumented Mexican immigrants. Documented or undocumented, the real number of those infected from Mexico may lie somewhere between the aforementioned numbers.

In summary, there is ample evidence that non endemic countries harbor a population of individuals infected with T. cruzi, and that, sooner or later, nations should have to confront the prevention of transfusion or organ-acquired infection, as well as secondary prevention of congenital infection.

 

DISCUSSION

Migration from Latin America has occurred for economic and/or political reasons. As of the 1970s, the country receiving the largest number of immigrants was the United States (Schmunis 1991, 1994). In the late 1990s, and early in the new century, immigration to Spain grew exponentially.

Since the 1980s, there have been several signs warning that, in time, non endemic countries would have to face the problem of transfusion T. cruzi infection (Schmunis 1985, Kirhoff et al. 1987). In Spain, a case of infection was reported in a bone marrow transplant recipient in 1992 (Villalba et al.1992), but worries about T. cruzi tainting the blood supply coincided with the increase in the number of immigrants around 2000. A survey conducted in Valencia among 705 blood donors at potential risk of infection because of their ethnic Latin American origin or residence in Latin America, found a positive infection rate for T. cruzi of 1.56% by indirect hemagglutination test, and 0.85% positive rate by indirect immunofluorescence (IIF). Of the six positive blood donors, two were from Bolivia and one each from Chile, Ecuador, Mexico, and Nicaragua (Parada et al. 2005).

Another survey was conducted in Cataluña in 2005 among 1770 blood donors, 1524 (86%) of them born in endemic areas of Latin America. The screening used was the ID-PaGIA antibody test (Rabello et al. 1999), and confirmation of positive samples was done by two different ELISA tests. The results yielded 21 positive samples by screening (1.2%), of which 11 were confirmed by ELISA (0.62%). Most positive samples came from Bolivian blood donors (Piron et al. 2007). In 1996, and also in Cataluña, testing for T. cruzi was conducted among 70 children 0-14 years of age and 98 women of child bearing age. In this survey, 18 of 168 (10.65%) samples were positive (Soriano et al. 2007), when serology was done using the Stat-Pak screening test (Chembio Diagnostic Systems 2000, Ponce et al. 2005). However, when tested for confirmation with two different ELISA tests, five positive samples from children and four from the women tested turned out to be false positive. The prevalence rate among the women tested was 4% (Soriano et al. 2007). Therefore, when a case of congenital Chagas disease was detected in Barcelona (Guarro et al. 2007), it was not an unexpected event.

In the late 1980s in the United States there were reports of transfusion-transmitted infection among immunosuppressed patients who had received blood or platelets in Canada and the United States (Geiseler et al.1987, Grant et al.1989, Nickerson et al.1989). Two other cases were detected later (Cimo et al. 1993, Leiby et al. 1999). Five of the seven cases identified were reported in the United States and two in Canada (Nickerson et al. 1989, Lane et al. 2000). There probably are many more undiagnosed cases among immunocompetent hosts, whose onset of symptoms is four or five weeks after transfusion, whose symptoms are mild and may disappear after symptomatic treatment, or whose infection is indeed completely asymptomatic (Bergoglio 1984). Detectable parasitemia is uncommon. In most cases, diagnosis is made because serology for T. cruzi becomes positive. Transfusional T. cruzi infections in immunocompromised hosts may present with fever, hepatosplenomegaly, global signs of heart failure and detectable parasitemia.

A case of transmission of T. cruzi through solid organ transplantation, in which three organ recipients were infected from one donor, has been also documented (CDC 2002). Another two patients who received heart transplant were also infected, but in both cases recipients of other organs from the same donor were apparently not infected (Mascola et al. 2006).

In the United States, blood donors more likely to harbor T. cruzi are in areas with the largest Latino populations. In Los Angeles, California, 1.1% of 988 donors were found to have positive serology for T. cruzi; 0.1% of the total were positive by two diagnostic techniques in 1987 (Kerndt et al. 1991). A questionnaire to identify high-risk donors in California, found that 543 of 3492 donors (15.5%) came from areas endemic for T. cruzi in 1989-1990. Seventy-two were regarded as high-risk donors, and T. cruzi serology was performed on 45 of them; of those, two (4.4%) were positive when tested by two serological techniques (Appleman et al. 1993). Using another risk assesment questionaire, 988 donors were tested by EIA beginning in 1993. One in 299 eligible donors were seroreactive, and one in 524 appeared infected with T. cruzi. Of the donors who admitted to birth or travel history to endemic areas for Chagas disease one in 141 had a positive serology, and one in 247 were apparently infected (Shulman 1995). In another study of 13,309 donors living in California, New Mexico, and Texas, including 7835 of Hispanic origin, 0.10% tested positive for T. cruzi (Brashear et al.1995). And of 49,465 donors tested in Miami and California in 1994-1995, 105 (0.21%) were seroreactive. After conducting a second test using a different technique, only 34 of the 49,465 samples (0.06%) remained positive (Leiby et al. 1997). Positive samples were also detected among blood donors from the Southwestern United States considered to be at moderate risk (0.14% was considered repeatable reactive and 0.003% of 100,089 donors was confirmed positive (Leiby et al. 1999a). Nationwide estimates suggest that 1 in 25,000 blood donors are infected with T. cruzi. However, when a risk screening questionnaire was applied to more than 1.1 million donors in Los Angeles and 181,000 in Miami, 7.3 and 14.3% of respondent, respectively, reported risk. Serology indicated that one per 7500 donors were positive in Los Angeles and one per 9000 in Miami. In addition, the donors showed an increase in the positive rates for T. cruzi from 1996 to 1998 (Leiby et al. 2002).

When ELISA testing for T. cruzi antibodies was conducted in Houston, Texas, among 3765pregnant women (2107 Hispanic and 1658 non Hispanic), 22 women (0.6%) were reactive. Eleven were also positive by indirect hemagglutination (IHA) (0.3%); nine of the latter (0.4%) came from the Hispanic group, and two (0.1%) were non Hispanic (Di Pentima et al. 1999). This is further indication that congenital Chagas disease, which in endemic countries is mostly asymptomatic, has the potential of going undiagnosed and, consequently, untreated in the United States. In fact, two potential cases of congenital Chagas disease have been detected in the United States (Leiby et al. 1999a).

Prevention

Regarding T.cruzi infection in countries at the receiving end of migration, the riskier blood or organ donors are those who come from areas where the prevalence of infection is high; there is also an increased risk in places with a great number of immigrants. Such is the case, with immigrants from Mexico, Chile, and El Salvador in Canada; those from Argentina, Bolivia, Colombia, Ecuador, and Peru in Spain; and those from Argentina, Colombia, El Salvador, Guatemala, and Mexico, in the United States.

The only effective form of prevention is to avoid the use blood from donors from countries where Chagas disease is endemic, or to perform serological screening for T. cruzi exclusively on donors from these countries. In endemic countries, the administration of a questionnaire prior to donation to determine place of birth (rural area), housing characteristics (unsanitary), and/or familiarity with the vector (positive identification in a picture) yields warning signs to rule out donors. Such questionnaires could also be employed in non endemic countries. However, even when experts implement the questionnaire, some infected individuals will not be detected, and only through serology will it be possible to determine whether a potential donor for whom the questionnaire yielded no warning sign is infected or not. On the other hand, one could question the need for blood from donors from areas where the prevalence of T. cruzi infection is high, such as the departments of Santa Cruz de la Sierra, Tarija, Sucre or Cochabamba, in Bolivia (prevalence between 29 and 51% in blood donors) (Carrasco et al. 1990), or may be not as high, but still much higher than in the rest of the country, as is the case the Argentinean provinces of El Chaco, Jujuy, La Rioja, Salta, and Santiago del Estero (prevalence between 16 and 21% in blood donors) (Perez & Segura 1989).

In Latin America, the most commonly tests for screening, and sometimes for confirmation, are the enzyme immunoassays using conventional (crude antigens) or non conventional reagents (mixture of peptides or recombinant antigens) (Luquetti 1990, Ferreira et al. 2001, Umezawa et al. 2003). The IHA is also used for screening and, on occasions, as a second test for confirmation. However, sensitivity and specificity of commercial reagents available varies widely (Saez-Alquezar et al. 1997) other non conventional tests that has been used for confirmation are an Immunoblot (Umezawa et al. 1996), the TESA (Silveira-Lacerda et al. 2004), the INNOLIA Chagas (Saez-Alquezar et al. 2000), and the RIPA (Leiby et al. 2000), all aimed at replacing the IIF as the gold standard.

The Ministry of Health of Brazil tested several reagents used for T. cruzi antibody testing in that country (Tables V, VI). The recommendation was to use screening reagents that have a 99% or higher sensitivity, and 97% or higher specificity (Ministry of Health, Brazil, 2006). Up to now, the perfect reagent for the perfect high sensitivity and high specificity test, that is easy to use and inexpensive, has yet to be developed.

 

 

 

 

Chagas disease among immigrant populations, most of whose members do not know they are infected, represents a challenge for non endemic countries. First, this is a disease that the health services in non endemic countries are not accustomed to manage, so that specialized services with appropriate infrastructure and trained staff would need to be developed. For countries at the receiving end of migration that offer free medical care, services for Chagas are going to be expensive, and should be planned for. If immigrants are going to be allowed to become blood donors, blood donor screening policies should be adjusted to prevent tainting the blood supply. In fact, several European governments have already begun implementing such policies. For instance, the French Government has halted blood collection in the overseas territory of French Guyana, and implemented T. cruzi screening among French blood donors at risk, such as those born in an endemic area or from a mother from an endemic area; and donors traveling in endemic areas, regardless of the length of stay. When returning from those areas, donors are deferred for four months.

In addition, a performance evaluation of different ELISA tests was done. Two of them were selected for further testing. One was made from a crude antigen and another from a recombinant antigen, both to be used simultaneously in routine blood screenings. An IIF test will be used as a confirmatory test (Assal & Aznar 2007).

In Spain, Royal Decree 1088 (Real Decreto 2005) on hemodonation, automatically and permanently deferred donors with Chagas disease. If screening tests were not available, donors born in the endemic area, those born from mothers born in endemic areas, and persons who received transfusions in endemic areas are excluded from donating blood labile components (red cells and platelets). However, if these donors have a negative screening test, they may donate blood.

In the United States, the Food and Drug Administration for the first time approved a test (ELISA) to screen for Chagas disease (US Food and Drug Administration 2007). Although the use of this test to screen for T. cruzi antibodies in blood donation centers is not required, organizations responsible for collecting approximately 65% of the country's blood supply began screening donors in January 2007. The American Association of Blood Banks (AABB) recommended that blood donations that are repeatedly reactive by ELISA should be removed from distribution, and its donor deferred (Stramer et al. 2007). Recipients of blood from positive donors (repeat positive by ELISA and RIPA positive) collected previously should be investigated. Moreover, deferred donors, at risk family members, and infected recipients that received components from infected donors should be referred to health services for medical care.

The tests use as antigen a lysate of epimastigotes (Tobler et al. 2007). In 2005, 40,000 blood samples were tested; only one sample turned out positive, but the same was negative by RIPA. Further testing by ELISA conducted by the American Red Cross in 146, 969 samples, detected 63 positive from 61 positive donors (Stramer et al. 2007). Thirty two of these samples were positive by RIPA. Overall, the test is considered to have a sensitivity of >99% detecting 198 out of 199 positive samples from individuals believed to be infected. Field trials of more than 70,000 donor samples revealed that the likelihood of obtaining a false positive result was small (2 to 3 per 100,000 tests) (US Food and Drug Administration 2007).

Last, but not least, legislation might have to be modified so that immigrants are not discriminated against at their places of employment due to their infection.

 

ACKNOWLEDGMENT

To Ms Roxane Salvatierra for editing the manuscript and to Ms Carmen Chand and Vivien Lewis for collecting and reviewing the references.

 

REFERENCES

Assal A, Aznar C 2007. Chagas disease screening in the French blood donor population. Screening assays and donor selection. Enfermedades Emergentes 9: 38-40.         [ Links ]

Appleman MD, Shulman IA, Saxema S, Kirhoff LV 1993. Use of a questionaire to identify potential blood donors at risk for infection with Trypanososma cruzi.Transfusion 33: 61-64.         [ Links ]

Australian Bureau of Statistics, 2007.         [ Links ]

Bergoglio RM 1984. Enfermedad de Chagas postransfusional; experiencia clínica de 48 casos. Prensa Med Argent 71: 49-52.         [ Links ]

Brashear RJ, Winkler MA, Schur JD, Lee H, Burczrck JD, Hall HJ, Pan AA 1995. Detection of antibodies to Trypanososma cruzi among blood donors in the Southwestern United States. I. Evaluation of the sensitiviuty and specificity of an enzyme immunoassay for detecting antibodies to T. cruzi. Transfusion 35:186-188.         [ Links ]

Cabrera M, Bucio M, Rojo J, Bonifaz R, Guevara Y, Salazar-Schettino 2004. Detection of antibodies against Trypanosoma cruzi in blood donors in the General hospital of Mexico city. Rev Patol Trop 33: 71-80.         [ Links ]

Carlier Y, Torrico F 2003. Congenital infection with Trypanosoma cruzi: from mechanisms of transmission to strategies for diagnosis and control. Rev Soc Brasil Med Trop 36: 767-771.         [ Links ]

Canadian Statistics 2005. Ethno-cultural portrait of Canada. www.statcan.ca.         [ Links ]

Carrasco R, Miguez H, Camacho C, Echalar L, Revollo S, Ampuero T, Dedet JP 1990. Prevalence of Trypanosoma cruzi infection in blood banks of seven departments of Bolivia. Mem Inst Oswaldo Cruz 85: 69-73.         [ Links ]

CDC 2002. Chagas disease after organ transplantation - United States, 2001. MMWR 51: 210-212.         [ Links ]

Cimo PL, Luper WE, Scouros MA 1993. Transfusion-associated Chagas' disease in Texas: report of a case. Texas Med J 89: 48-50.         [ Links ]

Chembio diagnostic Systems 2000. Instructions for use of Chagas Stat-Pak. CG101-20 test Kit.         [ Links ]

Cruz Reyes A, Pickering-Lopez JM 2006. Chagas disease in Mexico: an analysis of gegraphical distribution during the past 76 years- A review. Mem Inst Oswaldo Cruz 101: 345-354.         [ Links ]

Di Pentima MC, Hwang LY, Skeeter CM, Edwards MS 1999. Prevalence of antibodies to Trypanasoma cruzi in pregnant Hispanic women in Houston. Clin Infect Dis 28: 1281-1285.         [ Links ]

El Deber. Santa Cruz 2007. Miles de niños quedaron `sin sus padres'. Santa Cruz de la Sierra, 12 Abril, p. 8.         [ Links ]

Eurostat. Europa 2006. Inmigration by sex and citizenship. Last update Jan 26.         [ Links ]

Ferreira AW, Belem AZ, Lemos EA, Reed SG, Campos Neto A 2001. Enzime-linked immunoabsorbent assay for serological diagnosis of Chagas disease employing a Tripanosoma cruzi recombinant antigen that consist of four different peptides. J Clin Microbiol 39: 4390-4395.         [ Links ]

Gazcon J 2006. Diagnostico y tratamiento de la enfermedad de Chagas importada. Med Clin (Barc) 125: 230-235.         [ Links ]

Geiseler PJ, Ito JI, Tegtmeier BR, Kerndt PR, Krance R 1987. Fulminant Chagas' disease (CD) in bone marrow transplantation (BMT) [abstract 418]. In Program and abastracts of the 27th Interscience Conference onAntimicrobial Agents and Chemotherapy (New York), American Society for Microbiology, Washington, DC, p. 169.         [ Links ]

Grant IH, Gold JW, Wittner M, et al 1989. Transfusion-associated acute Chagas' disease acquired in the United States. Ann Intern Med 111: 849-851.         [ Links ]

Guarro A, El-Kassab H, Jorba JM, Lobato A, Castro M, Martin C, Angrill R, Corcoy F, Riera C 2007. Un caso de transmision congenita de la enfermedad de Chagas en Cataluña. Enfermedades Emergentes 9: 28-35.         [ Links ]

Hegenscheid FM, Janitschke K, Weinke T 1997. Prevalence and epidemiological significance of Trypanosoma cruzi infection among Latin American immigrants in Berlin, Germany. Infection 25: 355-358.         [ Links ]

Herwaldt BL, Grijalva MJ, Newsome AL, et al 2000. Use of the polymerase chain reaction to diagnose the fifth reported US case of of autochthonous transmission of Trypanosoma cruzi, in Tennessee, 1998. J Infect Dis 181: 395-399.         [ Links ]

Kerndt PR, Waskin HA, Kirchhooff LV, Steurer F, Waterman SH, Nelson JM, Gellert GA, Shullman IA 1991. Prevalence of antibody to Trypanosoma cruzi among blood donors in Los Angeles, California. Transfusion 31: 814-818.         [ Links ]

Kirchhoff LV, Gam AA, Gillian AA 1987. American trypanosomiasis (Chagas'disease) in Central American immigrants. Am J Med 82: 915-920.         [ Links ]

La Nacion 2007. El 60% de las personas que piden pasaporte son mujeres. Paraguay, 9 Junio, p.31         [ Links ]

Lane DJ, Sher G, Ward B, Ndao M, Leiby D, Hewlett B 2000. Investigation of the second case of transfusion transmitted Chagas disease in Canada. 2nd Annual Meeting of the American Society of Hematology, San Francisco, California; December 1-5.         [ Links ]

Leiby DA, Read EJ, Lenes BA, Yund AJ, Stumpf RJ, Kirchhoff R, Dodd YR 1997. Seroepidemiology of Trypanosoma cruzi, etiologic agent of Chagas' disease in US blood donors. J Infect Dis 176: 1047-1052.         [ Links ]

Leiby DA, Lenes BA, Tibbals MA, Tames-Olmedo MT 1999. Prospective evaluation of a patient with Trypanososma cruzi infection transmitted by transfusion. N Engl J Med 341: 1237-1239.         [ Links ]

Leiby DA, Fucci MH, Stumpf RJ 1999a. Trypanososma cruzi in a low-to moderate-risk blood donor population: seroprevalence and possible congenital transmission. Transfusion 39: 310-317.         [ Links ]

Leiby DA, Wendell S. Takaoka DT, Fachini RM, Oliveira LC, Tibbals MA 2000. Serologic testing for Trypanososma cruzi: Comparison of radioimmunoprecipitation assay with commercially available indirect immunofluorescence assay, indirect hemagglutination assay, and enzyme-linked immunosorbent assay kits. J Clin Microbiol 38: 639-642.         [ Links ]

Leiby DA, Herron RM Jr, Read EJ, Lenes BA, Stumpf RJ 2002. Trypanosoma cruzi in Los Angeles and Miami blood donors: impact of evolving donor demographics on seroprevalence and implications for transfusion transmission. Transfusion 42: 549-555.         [ Links ]

Luquetti AO 1990. Use of Trypanosoma defined proteins for diagnosis-multicenter trial. Serological and technical aspects. Mem Inst Oswaldo Cruz 85: 497-505.         [ Links ]

Mascola L, Kuba B, Radhakrishna S, Mone T, Hunter R, Leiby DA, Kuehnert M, Moore A, Steurer F, Kun H 2006. Chagas Disease After Organ Transplantation. Los Angeles, California. MMWR 55: 798-800.         [ Links ]

Milei J, Mantner B. Storino R, Sánchez JA, Ferrans VJ 1992. Does Chagas'disease exist as an undiagnosed form of cadiomiopathy in the United States? Am Heart J 123:1732-1735.         [ Links ]

Ministry of Health, May 2006. Technical Note no. 03/06. Results off the evolution of kits for diagnosis of Chagas disease.         [ Links ]

Moncayo A 1993. Chagas'disease. In Tropical Disease Research: Progress 1991-92. Eleventh programme report of the UNDP/World Bank/WHO Special Programme for Research and Training in Tropical Diseases. Geneva: World Health Organization, 67-75.         [ Links ]

Nickerson P, Orr P, Schroeder JL, Sekla L, Johnston JB 1989. Transfusion-associated Trypanosoma cruzi infection in a non-endemic area. Ann Intern Med 111: 851-831.         [ Links ]

Organización Panamericana de la Salud. Estimación cuantitativa de la enfermedad de Chagas en las Américas. Organización Panamericana de la Salud OPS/.HDM/CD/425-06.         [ Links ]

Pan American Health Organization 2006. National Blood Systems in the Caribbean and Latin American countries: Basic indicators of their status in 2004. THS/EV-2006/002.         [ Links ]

Parada C. Vila E, Villaba J, Alvarez M, Puig N, Ample I, Chavez A, Sarrion A, Montoso JA, Roig R 2005. Determinacion de Trypanososma cruzi: estudio preliminar de prevalencia en donantes de sangre. Centro de Transfusión, Comunidad Valenciana,. Resumen del Congreso SETS, San Sebastian, p. 339.         [ Links ]

Pehrson PO, Wahlgren M, Bengtsson E 1981. Asymptomatic congenital Chagas'disease in a five-year-old child. Scand J Infec Dis 13: 307-308.         [ Links ]

Perez A, Segura E 1989. Blood transfusion and transmission of Chagas' infection Rev Argent Transfus 15: 127-132.         [ Links ]

Piron M, Maymo RM, Hernandez JM, Verges M, Muñoz J, Portus M, Casamitjana N, Puig L, Gazcon J, Sauleda S 2007. Resultados preliminares del estudio en banco de sangre, Cataluña. Enfermedades Emergentes 9 (Suppl. 1): 36-40.         [ Links ]

Piron C, Ponce E, Vinelli E, Montoya A, de Aguilar V, Gonzalez A, Zingales B, Rangel-Alado R, Levin MJ, Esfandiari J, Umezawa ES, Luquetti AO, Franco da Silveira J 2005. Validation of a rapid and reliable test for diagnosis of Chagas' disease by detection of Trypanosoma cruzi-specific antibodies in blood of donors and patients in Central America. J Clin Microbiol 43: 5065-5068.         [ Links ]

Rabello A, Luquetti AO, Moreira EF, Gadelha MF, Dos Santos JA, de Melo L, Schwind P 1999. Serodiagnosis of Trypanosoma cruzi infection using the new particle gel immunoassay – ID-PaGia Chagas. Mem Inst Oswaldo Cruz 94:77-82.         [ Links ]

Ramos-Lingonio A, Ramirez-Sanchez ME, Gonzalez-Hernandez JC, Rosales-Encina JL, Lopez-Monteon A 2006. Prevalencia de anticuerpos contra Tripanosoma cruzi en donadores de sangre del IMSS, Orizaba, Veracruz, Mexico. Salud Publica de México 48: 13-21.         [ Links ]

Real Decreto 1088/2005. Boletín Oficial del estado del 20 de septiembre 2005, nº 225, 31288-31304.         [ Links ]

Saez-Alquezar A, Luquetti AO, Borges Pereira J, Moreira EF, Gadelha MFS, Garcia Zapata MT, Arruda AHS 1997. Estudo multicentrico. Avaliação do desempenho de conjuntos diagnósticos de HHHh, emaglutinação indireta disponíveis no Brasil, para o diagnóstico sorológico da infecção pelo Trypanosoma cruzi. Rev Patol Tropical 26: 343-374.         [ Links ]

Saez-Alquezar A, Sabino EC, Salles N, Chamone DF, Hulstaert F, npotel H, Stoops E, Zrein M 2000. Serological confirmation of Chagas disease by a recombinant and peptide antigen line immunoassay: INNO-LIA Chagas. J Clin Microbiol 38: 851-854.         [ Links ]

Sanchez Guillen MC, Barnabe C, Cuegan JF, Tibairenc M, Velazquez Rojas M, Martinez-Munguia J, Salgado-Rosas H, Torres-Rasgado E, Rosas-Ramirez MI, Perez -Fuentes R 2002. High prevalence anti-trypanosoma cruzi antibodies, among blood donors in the State of Puebla, a non endemic area of Mexico. Mem Inst Oswaldo Cruz 97: 947-952.         [ Links ]

Schmunis GA 1985. Chagas'disease and blood transfusion. In RV Dodd, LF Barker, Infection Immunity and Blood Transfusion, AR Liss, New York, p. 127-145.         [ Links ]

Schmunis GA 1991. Trypanosoma cruzi, the etiologic agent of Chagas disease: status in the blood supply in endemic and non endemic countries. Transfusion 31: 547-557.         [ Links ]

Schmunis GA 1994. La tripanosomiasis americana como problema de salud pública. En: La enfermedad de Chagas y el sistema nervioso. Org Panam Salud Pub Sci. 547: 3-31.         [ Links ]

Schmunis GA 2004. Southern Cone initiative. In C Schofield , C Ponce, Proceedings of the second international workshop on population genetics and control of triatominae, p. 26-31.         [ Links ]

Schmunis GA, Cruz R 2005. Safety of the blood supply in Latin America. Clin Microbiol Rev 18: 12-29.         [ Links ]

Schmunis GA, Zicker F, Pinheiro F, Brandling-Bennett D 1998. Risk for transfusion-transmitted infectious diseases in Central and South America. Emerging Dis 4: 5-11.         [ Links ]

Schmunis GA, Zicker F, Cruz FR, Cuchi P 2001. Infectious diseases transmitted by blood in Latin America. Safety of blood supply for infectious diseases in Latin American countries, 1994-1997. Am J Trop Med Hyg 65: 924-930.         [ Links ]

Shulman IA 1995. Preventing transfusion-transmitted Chagas' disease: the Los Angeles county/university of Southern California experience. Program and abstracts of the National Institutes of Health. Development Conference on infectious diseases testing for blood transfusion: National Institutes of Health, p. 95-99.         [ Links ]

Silveira-Lacerda ER, Silva AG, Junior SF, Souza MA, Kasper N, Botelha Filho A, Umezaua ES 2004. Chagas disease: application of TESA-blot in inconclusive sera from a Brazilian blood bank. Vox Sanguinis 87: 204-207.         [ Links ]

Skolnick A 1989. Does influx from endemic areas mean more transfusion-associated Chagas' disease? JAMA 262: 1433.         [ Links ]

Spain, Ministry of the Interior 2002. General Police Directorate.         [ Links ]

Soriano A, Verges M, Muñoz J,Castells M, Portus M, Gascon J 2007. Prevalencia de la infeccion por el Trypanososma cruzi en la poblacion infentil y en mujeres de edad fertil inmigrantes procedentes de America Central y del Sur (Resultados preliminares). Enfermedades Emergentes 9: 28-35.         [ Links ]

Statistical abstract of the United States, Washington, 1989. 109 th ed., Bureau of the Census document. US Department of Commerce.         [ Links ]

Steele LS, MacPherson DW, Kim J, Keystone JS, Gushulak BD 2007. The sero-prevalence of antibodies to Trypanosoma cruzi in Latin American refugees and immigrants to Canada. J Immigr Minor Health 9: 43-47.         [ Links ]

Stramer SL, Dodd RY, Leiby DA, Herron RM, Mascola L. Rosemberg LJ, Lawaczeck E, Sunenshine RH, Kuehnert MJ, Montgomery S, Bern C, Moore A, Herwaldt B, Kun H, Verani JR 2007. Blood donor screening for Chagas disease-United States, 2006-2007. MMWR 56: 141-143.         [ Links ]

The Wall Street Journal. Population Boom. March 2, 2006.         [ Links ]

Tobler LH, Contestable P. Pitina L 2007. Evaluation of a new enzyme-linked immunoabsorbent assay for detection of Chagas antibody in US blood donors. Transfusion 47: 90-96.         [ Links ]

Ultima Hora, 2007. Remesas y trabajadores latinos en España en 2006. Asuncion, 7 Junio, p.40.         [ Links ]

Umezawa ES, Nascimento MS, Kasper Jr N, Coura JR, Borges Pereira, Junqueira AC, Camargo ME 1996. Immunoblot assay using excreted-secreted antigens of Trypanosoma cruzi in serodiagnosis of congenital acute and chronic Chagas'disease. J Clin Microbiol 34: 2143-2147.         [ Links ]

Umezawa Es, Bastos S, Coura JR, Levin MJ, Gonzalez A, Rangel-Aladao R, Zingales B, Luquetti AO, da Silveira JF 2003. Improved serodiagnosis test for Chagas disease employing a mixture of Trypanosoma cruzi recombinant antigens. Transfusion 43: 91-97.         [ Links ]

US Department of Homeland Security 2003. Office of Immigration Statistics, Earbook of Immigration Statistics.         [ Links ]

US Department of Homeland Security. Office of Immigration Statistics, 2004. Earbook of Immigration Statistics. See also http://www.uscis.gov/graphics/shared/statistics/yearbook/index.htm         [ Links ]

US Census 2006. Bureau, Statistical abstract of the United States. pag.11.         [ Links ]

US Census Bureau. The 2007 Statistical Abstract. See also Http://www.census.gov/compendia/statab/population/immigration/         [ Links ]

US Food and Drug Administration 2006. FDA Approves first test to screen blood donors for Chagas disease. http://www.fda.gov/bbs/topics/NEWS/2006/NEW01524.html         [ Links ]

Villalba R, Fornes G, Alvarez MA, Roman I, Rubio V, Fernandez M, Garcia JM, Vinal M, Torres A 1992. Acute Chagas' disease in a recipient of a bone marrow transplant in Spain: Case report. Clin Infect Dis 14: 594-595.         [ Links ]

World Bank. World Development Report 1993. Investing in Health. The World Bank, Oxford University Press, p. 216-224.         [ Links ]

World Bank 2006. Global burden of disease and risk factors. In AD Lopez, CD Mathers, M Ezzati, DT Jamison, CJL Murray, Oxford University Press and the World Bank, p. 228.         [ Links ]

World Bank 2006a. Global burden of disease and risk factors. In AD Lopez, CD Mathers, M Ezzati, DT Jamison, CJL Murray, Oxford University Press and the World Bank, p. 144.         [ Links ]

World Health Organization 1991. Control of Chagas' disease. WHO Tech Rep Ser 811.         [ Links ]

World Health Organization 2002. Control of Chagas' disease. WHO Tech Rep Ser. 905.         [ Links ]

World Health Organization 2002a. The World Health Report 2002. Reducing risks, promoting healthy life, Geneva, p. 172.         [ Links ]

 

 

Received 4 June 2007
Accepted 2 July 2007

 

 

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