Chagas Disease: Increased Parasitemia during Pregnancy Detected by Hemoculture

Siriano, Liliane da Rocha; Luquetti, Alejandro Ostermayer; Avelar, Juliana Boaventura; Marra, Neusa Leal; Castro, Ana Maria de

doi:10.4269/ajtmh.2011.10-0015

Cited by 31 publications

(20 citation statements)

References 12 publications

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“…This is in line with previous reports in chronically infected pregnant women displaying higher parasitemia than non-pregnant ones [60]–[64]. This limited effect on chronic parasitemias might be associated with some degree of gestation-associated immune depression (imbalance of types 1 and 2 immune responses and increased amounts of Treg cells; [62], [65]), probably insufficient enough to modify significantly the high parasite levels produced in acute infection.…”

Section: Discussionsupporting

confidence: 92%

Fertility, Gestation Outcome and Parasite Congenital Transmissibility in Mice Infected with TcI, TcII and TcVI Genotypes of Trypanosoma cruzi

et al. 2013

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This work aims to compare the effects of acute or chronic infections with the T. cruzi genotypes TcI (X10 strain), TcII (Y strain) and TcVI (Tulahuen strain) on fertility, gestation, pup growth and the possible vertical transmission of parasites in BALB/c mice. The occurrence of congenital infection was evaluated by microscopic examination of blood and/or qPCR on blood and heart in newborn pups and/or older offspring submitted to cyclophosphamide-induced immunosuppression in order to detect possible cryptic congenital infection. Altogether, the results show that: i) for the three strains tested, acute infection occurring after the embryo implantation in the uterus (parasite inoculation 4 days before mating), or close to delivery (parasite inoculation on day 13 of gestation), prevents or severely jeopardizes gestation outcome (inducing pup mortality and intra-uterine growth retardation); ii) for the three strains tested, gestation during chronic infection results in intra-uterine growth retardation, whereas re-inoculation of TcVI parasites during gestation in such chronically infected mice, in addition, strongly increases pup mortality; iii) congenital infection remains a rare consequence of infection (occurring in approximately 4% of living pups born to acutely infected dams); iv) PCR, detecting parasitic DNA and not living parasites, is not convenient to detect congenial infection close to delivery; v) transmission of parasites by breast milk is unlikely. This study should encourage further investigations using other parasite strains and genotypes to explore the role of virulence and other factors, as well as the mechanisms of such effects on gestation and on the establishment of congenital infection.

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Section: Discussionsupporting

confidence: 92%

Fertility, Gestation Outcome and Parasite Congenital Transmissibility in Mice Infected with TcI, TcII and TcVI Genotypes of Trypanosoma cruzi

et al. 2013

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“…The primary drawback associated with parasite isolation is selection bias for particular subpopulations, initially by preferential outgrowth due to faster dividing rates and/or culture media [55,119,120] and subsequently by loss of clonal diversity from serial maintenance in axenic culture or animals [121–126] . Hemoculturing is laborious; recovery rates are usually less than 30% among chronic patients [127] and almost entirely determined by parasite load and distribution within the starting sample. Xenodiagnosis, which can facilitate greater parasite recovery, has also been shown to vary depending on vector permissibility to local strains [128–130] .…”

Section: T Cruzi Clinical Genotyping: Perils and Pitfallsmentioning

confidence: 99%

Between a bug and a hard place:Trypanosoma cruzigenetic diversity and the clinical outcomes of Chagas disease

Messenger

Miles

Bern

2015

Expert Review of Anti-infective Therapy

166

170

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Over the last 30 years, concomitant with successful transnational disease control programs across Latin America, Chagas disease has expanded from a neglected, endemic parasitic infection of the rural poor to an urbanized chronic disease, and now a potentially emergent global health problem. Trypanosoma cruzi infection has a highly variable clinical course, ranging from complete absence of symptoms to severe and often fatal cardiovascular and/or gastrointestinal manifestations. To date, few correlates of clinical disease progression have been identified. Elucidating a putative role for T. cruzi strain diversity in Chagas disease pathogenesis is complicated by the scarcity of parasites in clinical specimens and the limitations of our contemporary genotyping techniques. This article systematically reviews the historical literature, given our current understanding of parasite genetic diversity, to evaluate the evidence for any association between T. cruzi genotype and chronic clinical outcome, risk of congenital transmission or reactivation and orally transmitted outbreaks.

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“…Congenital transmission of T . cruzi is suggested to occur when the phagocytic capacity of the placenta is compromised [ 43 ] and a significant amount of blood parasites are present in the infected women [ 44 ]. Others have suggested that the maternal-fetal transmission of T .…”

Section: Discussionmentioning

confidence: 99%

Quantitative and histological assessment of maternal-fetal transmission of Trypanosoma cruzi in guinea pigs: An experimental model of congenital Chagas disease

et al. 2018

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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.

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Chagas Disease: Increased Parasitemia during Pregnancy Detected by Hemoculture

Cited by 31 publications

References 12 publications

Fertility, Gestation Outcome and Parasite Congenital Transmissibility in Mice Infected with TcI, TcII and TcVI Genotypes of Trypanosoma cruzi

Fertility, Gestation Outcome and Parasite Congenital Transmissibility in Mice Infected with TcI, TcII and TcVI Genotypes of Trypanosoma cruzi

Between a bug and a hard place:Trypanosoma cruzigenetic diversity and the clinical outcomes of Chagas disease

Quantitative and histological assessment of maternal-fetal transmission of Trypanosoma cruzi in guinea pigs: An experimental model of congenital Chagas disease

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