TY - JOUR
T1 - Effects of Acute and Chronic Trypanosoma cruzi Infection on Pregnancy Outcomes in Mice
T2 - Parasite Transmission, Mortality, Delayed Growth, and Organ Damage in Pups
AU - Rios, Lizette E.
AU - Lokugamage, Nandadeva
AU - Garg, Nisha J.
N1 - Publisher Copyright:
© 2023 American Society for Investigative Pathology
PY - 2023/3
Y1 - 2023/3
N2 - Chagas disease is caused by Trypanosoma cruzi. This study aimed to determine the effects of T. cruzi infection on fertility rate and health of the newborn pups in pregnant mice. Female mice were challenged with T. cruzi and mated at 21 days (acute parasitemic phase) or 90 days (chronic parasite persistence phase) after infection. Pups were examined for growth up to 20 days after birth; and parasite burden in brain, heart, skeletal muscle, and intestine was measured by real-time quantitative PCR. The inflammatory infiltrate, necrosis, and fibrosis in pups' heart and brain tissues were evaluated by histology. T. cruzi infection in dams delayed the onset of pregnancy, decreased the fertility rate, and led to vertical transmission of parasite to the pups. Furthermore, infected dams delivered pups that exhibited decreased survival rate, decreased birth weight, and decreased growth rate. Significantly increased inflammation, necrosis, and fibrosis of cardiac and brain tissues were noted in pups born to infected dams. Initial challenge with higher parasite dose had more detrimental effects on fertility rate and pups' health in both acutely and chronically infected dams. In conclusion, mice offer a promising model to evaluate the efficacy of new vaccines and therapeutic drugs in controlling the acute and chronic maternal T. cruzi infection and congenital transmission to newborns, and in improving the fertility rate and pups' health outcomes.
AB - Chagas disease is caused by Trypanosoma cruzi. This study aimed to determine the effects of T. cruzi infection on fertility rate and health of the newborn pups in pregnant mice. Female mice were challenged with T. cruzi and mated at 21 days (acute parasitemic phase) or 90 days (chronic parasite persistence phase) after infection. Pups were examined for growth up to 20 days after birth; and parasite burden in brain, heart, skeletal muscle, and intestine was measured by real-time quantitative PCR. The inflammatory infiltrate, necrosis, and fibrosis in pups' heart and brain tissues were evaluated by histology. T. cruzi infection in dams delayed the onset of pregnancy, decreased the fertility rate, and led to vertical transmission of parasite to the pups. Furthermore, infected dams delivered pups that exhibited decreased survival rate, decreased birth weight, and decreased growth rate. Significantly increased inflammation, necrosis, and fibrosis of cardiac and brain tissues were noted in pups born to infected dams. Initial challenge with higher parasite dose had more detrimental effects on fertility rate and pups' health in both acutely and chronically infected dams. In conclusion, mice offer a promising model to evaluate the efficacy of new vaccines and therapeutic drugs in controlling the acute and chronic maternal T. cruzi infection and congenital transmission to newborns, and in improving the fertility rate and pups' health outcomes.
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U2 - 10.1016/j.ajpath.2022.11.010
DO - 10.1016/j.ajpath.2022.11.010
M3 - Article
C2 - 36565805
AN - SCOPUS:85149227956
SN - 0002-9440
VL - 193
SP - 313
EP - 331
JO - American Journal of Pathology
JF - American Journal of Pathology
IS - 3
ER -