Joseph Bastien - The Kiss of Death

Chagas’ disease is no longer restricted to Latin America. Immigrants from El Salvador and Nicaragua in Washington, D.C., have tested positive for T. cruzi infection. In 1985, estimates were that 100,000 individuals living in the United States were infected with T. cruzi (Kirchhoff, Gam, and Gillian 1987). I now estimate that number to be more than one million people because of increased immigration from Latin America, increased travel back and forth between countries in Latin America, increased numbers of blood transfusions and organ transplants, and transmission of the disease through birth. [18] 5. Although the potential problem of the blood supply in the United States has been recognized for some time (Schmuñis 1985), the recent diagnosis of Chagas’ disease acquired through blood transfusion in the United States (Grant et al. 1989) and Canada (Nickerson et al. 1989) has significantly highlighted the seriousness of this problem (Skolnick 1989, Kirchhoff 1989).

T. cruzi can travel through the placenta, birth canal, and maternal milk. Infected mothers pass Chagas’ disease to their children, but in lesser percentages than might be expected. Some unknown immunologic process often protects the infant (Calvo et al. 1978:80). In general, the incidence of congenital T. cruzi transmission is under 10 percent, although this rate is much higher in endemic areas such as Bolivia (Mufioz and Acevedo 1994). In Punata, Bolivia, the mortality rate for children infected congenitally was 47 percent (SOH/CCH 1994). Rates of congenital transmission have increased over the years (Azogue, La Fuente, and Darras 1985:176). [19] 6. In Brazil in 1911 Carlos Chagas considered the possibility of congenital transmission of T. cruzi when he found trypomastigotes in the blood-smear of a two-month-old child whose mother was also infected (quoted in Howard and Rubio 1968). In Venezuela in 1949 Dao reported other cases of congenital Chagas’ disease in Latin America (quoted in Bittencourt 1976). In Chile, Howard (1962) observed that 0.5 percent of premature babies weighing less than 2,000 grams (4.4 pounds) suffered from congenital Chagas’ disease. In Salvador, Bahia, and Brazil, Bittencourt and colleagues (Bittencourt and Barbosa 1972, Bittencourt, Barbosa, et al. 1972) found that 2 percent of stillborn babies were infected with T. cruzi ; and, in Argentina, Salem and colleagues found slightly higher rates, 2.35 percent among stillborn infants (quoted in Bittencourt 1975). By 1979 the number of described cases had reached 100, giving the impression that congenital transmission of Chagas’ disease is infrequent. However, this impression is misleading, because the registered cases are only of fetuses and premature stillborns and do not include congenital Chagas’ disease in newborns delivered at term (Bittencourt et al. 1974). The varying degrees of fetal and neonatal pathology in such countries as Argentina, Brazil, and Chile may be related to inherent characteristics of the parasite (Moya 1994). The fact that the incidence of infection remains the same in each of these countries and geographic regions suggests that population-related factors are not involved. Various factors having to do with the mother, the fetus, and the parasite are more likely implicated in transplacental transmission.

In Bolivia, congenital transmission rates were 7 percent in La Paz and 43 percent in Cochabamba (Brénière et al. 1983). Antibodies were detected in the serum of the mother and in the umbilical cord, with the concentration and quality of the antibodies similar. In Santa Cruz, Bolivia, 329 newborn babies were examined from 1979 to 1980; T. cruzi was found in twenty-five cases (Azogue, La Fuente, and Darras 1985:176-80). [20] 7. The newborns were delivered at the Percy Boland Maternity Hospital in the city of Santa Cruz and observed from August 1979 until July 1980. Blood samples from newborns and mothers were used to investigate the presence of T. cruzi by means of the modified Strout concentration, which has the highest sensitivity (95.2 percent; but only for acute cases) when compared to other direct parasitological testing methods (Flores et al. 1966; Cerisola 1972:97-100). (See Appendix 12.) Some 51 percent of the mothers and 13 percent of the infants tested positive for Chagas’ disease. Twenty-one (80 percent) of the infected infants weighed less than 2,500 grams (5.5 pounds). It is not clear whether nutrition is an independent or dependent variable; that is, whether the immune system of nutritionally healthy babies resists Chagas’ disease or whether babies infected with Chagas’ disease lose weight. Also, not one case was found before the sixth month of gestation. Although the mother is infected from conception, transmission of T. cruzi from her to the fetus takes time. [21] 8. Fetal infection can occur when the mother is in acute, indeterminate, and chronic phases of infection. Most infected pregnant women experience the chronic, or inapparent, form of the disease during their pregnancy, although cases of acute infection have been reported (Moya 1994). The fetus of an infected pregnant woman is usually unaffected, with no observed alterations in the growth or viability of the fetus, nor is the newborn predisposed to exhibit specific disorders. Chagas’ disease in the mother poses little risk to the baby during the perinatal period, which is after the twenty-eighth week of pregnancy through twenty-eight days following birth (Moya 1977, 1994; Moya and Barousse 1984; Castilho and Da Silva 1976). If the fetus is infected, the outcome of pregnancy may be spontaneous abortion, fetal death, premature birth, low birth weight for gestational age, and even full-term delivery (Moya 1994). Congenitally infected infants present a broad spectrum of clinical manifestationsfrom grave illness with multisystem compromise (usually in premature neonates) to a total absence of symptoms at birth. Some infants remain asymptomatic; others present manifestations of the disease several weeks or months later. Clinical manifestations are encephalitis, meningoencephalitis, lesions in the retina or choroid, and elevated protein levels and cell counts in cerebrospinal fluid (Mufioz and Acevedo 1994).

The delayed infection of fetuses raises the possibility of treating infected mothers during pregnancy to reduce transmission of the disease to the fetus. The high toxicity levels of nifurtimox and benznidazole used pose serious threats to unborn infants. Moreover, congenitally infected fetuses have been delivered from mothers both positive and negative for parasitemia, and infants have been born uninfected from pregnant women with acute infections and positive parasitemia. Intrauterine T. cruzi infection can cause abortions and premature births (WHO 1991:5).

Mechanisms of transmission of the disease from mother to fetus have not been determined. Possibilities include through the extra-embryonic membranes by diffusion of the parasites, or through progressive migration of the parasite throughout the stroma of the umbilical cord towards the blood vessels, provoking fetal infection by way of the blood (Azogue, La Fuente, and Darras 1985:180). [22] 9. Another route for T. cruzi is through the blood, by hematogenous spread, and through crossing of the placenta, with multiplication of the parasite in the Hofbauer cells (Bittencourt 1975). The amniotic fluid may provide another vehicle for T. cruzi to travel to fetuses as well as to obstetricians and gynecologists (Apt, Tejada, and Atrozz 1968; Bittencourt et al. 1981; Nattan-Larrier 1921). Contact of the skin with infected amniotic fluid could allow penetration of the skin, and T. cruzi has been found in the skin (Bittencourt 1976). Research is needed to evaluate the exact mechanisms of congenital transmission.