Transmission route
-
Vector-borne: contact with the feces of an infected triatomine bug (or "kissing bug")
-
Non vector-borne: mother-to-child transmission (congenital), contaminated blood
transfusions, transplantation
Epidemiology
-
Endemic: Mexico, Central America, South America (8 million infected people)
-
Non-endemic: North America (Canada & US), Western Pacific Region (Australia & Japan),
Europe (due to migration)
Clinical presentation
-
Acute phase (parasites circulate in the blood): 2 months after infection, asymptomatic or
mild symptoms: skin lesion or swelling of an eye-lid (purple), fever, headache,
swollen lymph glands, muscle pain, abdominal & chest pain, pallor -
Chronic phase (parasites hide in the heart and digestive muscles): cardiac disorders (arrhythmias),
digestive problems (colon/oesophagus enlargement), neurological alterations
Curable?
-
Yes, if treatment is started in an early (acute) stage
-
10.000 deaths yearly
Pregnant women
-
Serological testing of pregnant women recommended for: (a) women living in endemic areas, (b) receivers of blood transfusion in endemic areas, (c) women born (or that have lived) in endemic areas, (d) women whose mothers were born in endemic areas.
-
Seropositive pregnant women: anti-parasitic treatment (benznidazole and nifurtimox) is not recommended during pregnancy (teratogenic risks insufficiently known).
-
In case Anti-T.cruzi antibodies are present in maternal serum, the fetus might be infected. Microscopical examination of cord/peripheral blood of the neonate on the presence of mobile T. cruzi trypomastigotes (microhematocrit test) is necessary.
-
Early diagnosis of acute congenital infection in newborns and treatment with anti-parasitic therapy is key to reduce side-effects, to obtain high cure rates and to avoid lifelong chronic infections.
Maternal-foetal transmission
-
An average of 5% vertical transmission in case of chronically infected mothers in endemic areas (huge variation in numbers between different endemic regions).
-
Probably no transmission via breast milk and amniotic fluid or transuterine.
-
Probable route of transmission: transplacental (during second-third trimester and perinatal)
-
Congenital infection gives an increased risk of premature delivery, low birth weight, premature ruptures of membranes.
-
20 to 183 cases of congenital Chagas disease in Europe annually.
Factors that can play a role in transmission
1) Parasite: parasitic load, virulency, genotype (strain), capacity to invade placental cells.
2) Mother:
-
Parasitaemia increases during pregnancy (especially in the second and third trimester) and is associated with congenital transmission.
-
Immune status of the pregnant women (reactivated infection has a higher transmission risk than an acute infection, a chronic infection often has a low parasitaemia).
-
Co-infection with HIV/malaria/plasmodium vivax increases the risk of transmission.
3) Placenta
-
T. Cruzi can infect and multiply within villous trophoblastic cells.
-
Via the placental marginal zone and placental breaches/tears, parasites can enter and multiply in the chorionic plate and reach the umbilical cord and the fetus.
4) Foetus
-
Most neonates of infected mothers are asymptomatic, 2 - 10% present with respiratory distress, meningoencephalitis, myocarditis, hepatosplenomegaly, etc.
Ultrasound markers to look out for
There are various possible signs of intrauterine infections, among which:
Biometrics
-
Growth restriction
Amniotic Fluid Index
-
Polyhydramnion
Skull/brain
-
(Unilateral) ventriculomegaly
-
Microcephaly
-
Colpocephaly
-
Mega-Cisterna Magna
Heart
-
Ventricular hypertrophy
Organs
-
Hepatosplenomegaly (hyperechogenic)
Fetal hydrops
-
Cord edema
-
Ascites
-
Pleural effusion
-
Pericardial effusion
Differential Diagnosis
- TORCH infections (Toxoplasmosis, Rubella, CMV, Herpes)
- Congenital Hepatitis
- Syphilis
- Leptospirosis
Hint
A proper anamnesis can put you on track of Chagas Disease.
* * *
Resources
American Trypanosomiasis
https://web.stanford.edu/class/humbio103/ParaSites2006/T_cruzi/
WHO Fact Sheet
http://www.who.int/mediacentre/factsheets/fs340/en/
Centres for Disease Control and Prevention
https://www.cdc.gov/parasites/chagas/
Congenital Transmission of Chagas Disease — Virginia, 2010 Weekly, July 6, 2012 / 61(26);477-479. See: https://www.cdc.gov/mmwr/preview/mmwrhtml/mm6126a1.htm
Carlier, Y. et al. (2011). Congenital Chagas Disease: Recommendations for Diagnosis, Treatment and Control of Newborns, Siblings and Pregnant Women. PloS Negl Trop Dis., 5(10): e1250. Doi: 10.1371/journal.pntd.0001250
Carlier, Y. et al. (2015). Congenital Chagas disease: an update. Mem. Inst. Oswaldo Cruz., 110(3): 363–368. Doi: 10.1590/0074-02760140405 See: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4489473/
Cevallos, A. & Hernandez, R. (2014). Chagas’ Disease: Pregnancy and Congenital Transmission. BioMed Research International. Doi: 10.1155/2014/401864
Flores-Chavez, M. et al. (2008) Fatal congenital Chagas' disease in a non-endemic area: a case report. Cases J., 1: 302. Doi: 10.1186/1757-1626-1-302
Chagas Disease
Named after
Brazilian physician Carlos Chagas (1909)
Also known as
American trypanosomiasis
Culprit
protozoan parasite Trypanosoma cruzi (T. cruzi)