Obstet Gynecol. 2013 Feb;121(2 Pt 2 Suppl 1):452-4. doi: http://10.1097/AOG.0b013e31827566ca.
Intra-amniotic fluconazole therapy for Candida albicans intra-amniotic infection.
Bean LM1, Jackson JR, Dobak WJ, Beiswenger TR, Thorp JA.
The consequences of intra-amniotic Candida infection can be devastating. Currently, standard management includes delivery. We identified only one previous case reporting intrauterine antifungal therapy, which used transcervical amphotericin B. We present two cases of intra-amniotic Candida infection treated with intra-amniotic fluconazole instilled before membrane rupture.
Two patients presented with intra-amniotic Candida albicans infection that was diagnosed during previability. Both underwent cerclage placement before culture results were available. Aggressive antifungal therapy was instituted using oral, vaginal, and intra-amniotic fluconazole instilled through serial amniocenteses. Both fetuses survived without sequelae.
Intra-amniotic Candida infection is associated with preterm rupture of membranes, preterm labor, severe neonatal infection, and fetal death. Early diagnosis and treatment is essential.
[Show abstract][Hide abstract] ABSTRACT: Background:
Preventing preterm birth and subsequent adverse neonatal sequelae is among the greatest clinical challenges of our time. Recent studies suggest a role for Candida spp. in preterm birth and fetal injury, as a result of their colonization of either the vagina and/or the amniotic cavity. We hypothesized that intraamniotic Candida albicans would cause a vigorous, acute fetal inflammatory response.
Sheep carrying singleton pregnancies received single intraamniotic injections of either saline (control) or 10(7) colony-forming units C. albicans 1 or 2 d prior to surgical delivery and euthanasia at 124 ± 2 d gestation.
Colonization of the amniotic cavity by C. albicans resulted in a modest inflammatory response at 1 d and florid inflammation at 2 d, characterized by fetal thrombocytopenia, lymphopenia, and significant increases of inflammatory cytokines/chemokines in the fetal membranes skin, lung, and the amniotic fluid.
Acute colonization of the amniotic cavity by C. albicans causes severe intrauterine inflammation and fetal injury. C. albicans is a potent fetal pathogen that can contribute to adverse pregnancy outcomes.
Pediatric Research 03/2014; 75(6). DOI:10.1038/pr.2014.35 · 2.31 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Preterm birth (PTB) (delivery before 37 weeks' gestation) is a leading cause of neonatal death and disease in industrialized and developing countries alike. Infection (most notably in high-risk deliveries occurring before 28 weeks' gestation) is hypothesized to initiate an intrauterine inflammatory response that plays a key role in the premature initiation of labor as well as a host of the pathologies associated with prematurity. As such, a better understanding of intrauterine inflammation in pregnancy is critical to our understanding of preterm labor and fetal injury, as well as on-going efforts to prevent PTB. Focusing on the fetal innate immune system responses to intrauterine infection, the present paper will review clinical and experimental studies to discuss the capacity for a fetal contribution to the intrauterine inflammation associated with PTB. Evidence from experimental studies to suggest that the fetus has the capacity to elicit a pro-inflammatory response to intrauterine infection is highlighted, with reference to the contribution of the lung, skin, and gastrointestinal tract. The paper will conclude that pathological intrauterine inflammation is a complex process that is modified by multiple factors including time, type of agonist, host genetics, and tissue.
Frontiers in Immunology 12/2014; 5:574. DOI:10.3389/fimmu.2014.00574
[Show abstract][Hide abstract] ABSTRACT: Prevalence studies indicate that Candida species colonize the vagina in at least 20 % of all women, rising to 30 % in pregnancy. Although, some studies concluded that pregnant women were more likely to have symptomatic vaginal infections caused by Candida, yet other studies found a high prevalence of asymptomatic infection only during pregnancy. Most episodes of symptomatic vulvovaginal candidiasis (VVC) occur during the second and third trimesters. The increased risk of VVC in pregnancy is likely sustained by pregnancy-related factors, such as immunologic alterations, increased estrogen levels, and increased vaginal glycogen production. Although evidence is incomplete, there is some emerging data which suggests that candidiasis in pregnancy may be associated with increased risk of pregnancy complications, such as premature rupture of membranes, preterm labor, chorioamnionitis, and congenital cutaneous candidiasis. In contrast to nonpregnant women, there are no formal studies, evaluating the use of long-term suppressive maintenance oral azoles in the treatment of recurrent VVC (RVVC) in pregnancy. Most clinicians do not offer suppressive therapy in pregnancy and prefer to treat individual symptomatic episodes only utilizing a topical imidazole vaginally for 7 days to minimize systemic exposure to medications.
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