Discussion
Chagas disease is endemic in much of Central and South America, where the risk of congenital infection is recognised and routine antenatal screening is well established.2, 5 Increasing migration from Latin America to Europe (and laterally to northern Europe) and the trend towards increased numbers of female migrants has increased the risk of congenital transmission from infected mothers in non-endemic countries; the highest incidence is reported in Spain.3 Murcia et. al. documented a transmission rate of 13.8% among pregnant seropositive Bolivian women in Spain.6
The UK is now home to around 250,000 people of Latin American origin. Approximately half live in London.7 While numbers of migrants from Latin America to Ireland are smaller in comparison, they are increasing; the Brazilian population in Ireland has more than trebled in size since 2006.8 Pooled prevalence of CD among Latin American migrants living in Europe is estimated to be 4% but the burden of disease is largely hidden.3,4 It is estimated that > 95% of migrants to Europe infected with CD are undiagnosed.2,9 This report confirms the long held suspicion that changes in traditional migration patterns have increased the risk of cCD in Ireland and the UK.1
Both infants were born in 2020 to immunocompetent women from Bolivia, where seroprevalence rates are highest (40% in some rural areas).2,3,6 Both women gave a history of asymptomatic chronic CD. Case 2 was complicated by IUGR, not surprising given the high parasitic burden observed in the placenta.10Chagas disease increases the risk of preterm birth, low-birth weight and stillbirth - but otherwise there was little apparent cause for concern, and, as is commonly the case, both newborns were asymptomatic at birth.6,11 A minority of newborns with cCD have findings similar to those of congenital infection caused by classic TORCH (Toxoplasma gondii , Rubella , CMV andHerpes simplex ) organisms. Recognition of the increased risk of cCD in Latin American migrants and the asymptomatic nature of maternal and neonatal infection has led Spain, France, Germany, Italy, and Switzerland to establish cost-effective targeted antenatal screening programs.4 In the continued absence of such initiatives in Ireland and the UK, diagnosis of cCD requires increased awareness to perform specific testing of mothers and infants in a timely manner with the assistance of specialised diagnostic centres. In the first case, notwithstanding a high index of suspicion based on positive antenatal serology and serial testing of the infant, congenital infection was not confirmed until 3 months of age. In the second case, despite a history of chronic maternal infection and IUGR, the diagnosis of cCD was unexpected; follow-up testing of the infant was triggered by findings on placental histology.
The consequences of a missed diagnosis of cCD can be severe. Left untreated, 40% of infants with cCD progress to chronic infection with symptomatic cardiac, neurological or gastrointestinal disease later in life and untreated female infants may perpetuate vertical transmission from one generation to the next.2 The gold standard for diagnosis of cCD is identification of parasites in cord or venous blood of the newborn or at any time in infancy, or positive T. cruzi specific serology in infants > 8 months of age.5 Negative serology > 8 months of age indicates the absence of congenital infection. PCR for T. cruziis available in specialised centres and has higher sensitivity than microscopy.2,11 As in Case 1, tests may be inconclusive in early congenital infection due to low initial parasite replication as parasitaemia peaks beyond 1 month of life and thus may need to be repeated serially in suspected cases.5,10
Congenital CD should be treated as soon as the diagnosis is confirmed.2 The teratogenic risks are unknown and adverse drug reactions are relatively common in adults, thus it is not possible to prevent congenital infection in established pregnancy. Whilst efficacy and safety of available anti-trypanosomal treatment (Benznidazole and Nifurtimox) in adult populations is far from ideal, treatment in early infancy is almost 100% effective and adverse drug reactions are rare.2,5,11 While the infants tolerated Benznidazole treatment well, both mothers had concerns related to breast-feeding. One mother discontinued her Benznidazole treatment because of concerns that it might reduce lactation and quality of breast milk, and the other discontinued breast-feeding because of concerns for ongoing T. cruzi transmission from mother to child via breast milk. Risk of transmission of T. cruzi in breast-milk is considered low and interruption of breast-feeding is generally not recommended but published studies are scarce.12Pasteurisation or microwaving expressed breast milk is considered a safe alternative. Temporary interruption of breast-feeding is recommended if the mother has fissured or bleeding nipples.
The consequences of a missed or delayed diagnosis of cCD in infancy can be severe, but reliable tests for cCD are available and the condition is curable. In Ireland and the UK, structures exist for antenatal screening for other infectious diseases and capture of maternal demographics. Targeted testing of women who give a clear history of CD is a potential method for early diagnosis of cCD. In the absence of targeted screening programs, education of health care providers in Ireland and the UK regarding the potential risk of cCD in pregnant Latin American women would be a useful first step toward early detection and treatment of cCD.