Abstract
ObjectiveWe evaluated the effect of Trypanosoma cruzi infection on fertility, gestation outcome, and maternal-fetal transmission in guinea pigs (Cavia porcellus).MethodsAnimals were infected with T. cruzi H4 strain (TcI lineage) before gestation (IBG) or during gestation (IDG). Tissue and sera samples of dams and fetuses were obtained near parturition.ResultsAll IBG and IDG dams were seropositive by two tests, and exhibited blood parasite load of 1.62±2.2 and 50.1±62 parasites/μl, respectively, by quantitative PCR. Histological evaluation showed muscle fiber degeneration and cellular necrosis in all infected dams. Parasite nests were not detected in infected dams by histology. However, qPCR analysis detected parasites-eq/g heart tissue of 153±104.7 and 169.3±129.4 in IBG and IDG dams, respectively. All fetuses of infected dams were positive for anti-parasite IgG antibodies and tissue parasites by qPCR, but presented a low level of tissue inflammatory infiltrate. Fetuses of IDG (vs. IBG) dams exhibited higher degree of muscle fiber degeneration and cellular necrosis in the heart and skeletal tissues. The placental tissue exhibited no inflammatory lesions and amastigote nests, yet parasites-eq/g of 381.2±34.3 and 79.2±84.9 were detected in IDG and IBG placentas, respectively. Fetal development was compromised, and evidenced by a decline in weight, crow-rump length, and abdominal width in both groups.ConclusionsT. cruzi TcI has a high capacity of congenital transmission even when it was inoculated at a very low dose before or during gestation. Tissue lesions, parasite load, and fetal under development provide evidence for high virulence of the parasite during pregnancy. Despite finding of high parasite burden by qPCR, placentas were protected from cellular damage. Our studies offer an experimental model to study the efficacy of vaccines and drugs against congenital transmission of T. cruzi. These results also call for T. cruzi screening in pregnant women and adequate follow up of the newborns in endemic areas.
Highlights
American trypanosomiasis, known as Chagas disease, is caused by a flagellate protozoan Trypanosoma cruzi (T. cruzi)
All infected before gestation (IBG) and Infection during gestation (IDG) dams were seropositive by two tests, and exhibited blood parasite load of 1.62±2.2 and 50.1±62 parasites/μl, respectively, by quantitative PCR
T. cruzi TcI has a high capacity of congenital transmission even when it was inoculated at a very low dose before or during gestation
Summary
Known as Chagas disease, is caused by a flagellate protozoan Trypanosoma cruzi (T. cruzi). The clinical course of Chagas disease is divided into the acute and chronic phases. The acute infection is presented with blood parasitemia and is often mildly symptomatic. While many remain in an indeterminate phase without any clinical symptoms, ~30% progress to develop clinically relevant Chagas disease. Chronic Chagasic Cardiomyopathy is a complex disease that includes a wide-spectrum of manifestations, ranging from minor myocardium involvement to left ventricular (LV) systolic dysfunction, dilated cardiomyopathy, arrhythmias, thromboembolic events, and terminal cardiac failure [1]. Gastrointestinal (GI) manifestations, such as megasyndromes involving tubular structures of the GI tract, though not commonly recorded, are frequent in certain geographic areas [2]
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