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.