Depression in pregnant Hispanic women: Risk factors, pregnancy outcomes and plasma cytokines.

Background: Maternal depression is considered a major contributor to morbidity and mortality in pregnancy. A population at risk are U.S. born or immigrant Hispanic women, and few prenatal depression or immune studies have focused on this population. Objective: The research questions for the study were 1) What are the occurrences, risk factors and outcomes associated with depression in Hispanic pregnant women in the United States and 2) What are the associations of plasma immune cytokines and prenatal depression in this population. Study design: Women of self-reported Hispanic ethnicity were born in the continental United States or foreign-born. Screening of potential participants (n = 690) at a first prenatal clinic visit consisted of antibody testing for Toxoplasma gondii antibodies in a larger grant, and only the women with antibody levels below the cutoff for T. gondii positivity (N = 536) were included in the present study. All participants completed a health and demographic questionnaire, the Edinburgh Postpartum Depression (EPDS) scale, the Perceived Stress Scale (PSS), and the Medical Outcomes Study Social Support (MOS) scale. We surveyed electronic health records (EHR) for risk factors and adverse pregnancy outcomes in the sample. We further measured physical and mental health and seven plasma immune cytokines at four study visits during pregnancy in a longitudinal subsample (N = 128). Results: The frequency of EPDS scores of 10 (depression risk) or above was 18.6 % at the time of enrollment. Socioeconomic factors such as less education, greater unemployment, and U.S. born nativity were associated with greater depression risk, but these relationships became insignificant when we corrected for false discovery rate. Depression scores were not associated with adverse birth and pregnancy outcomes. The inflammatory cytokine TNF-α was significantly higher across pregnancy in women with depression risk (p < 0.03). Other inflammatory cytokines were higher in depressed women, but only at one time point in mid-pregnancy. Conclusions: Prenatal depression occurs in early pregnancy and then declines in Hispanic women. The frequency of depression and stress were higher in U.S. born compared to immigrant Hispanic women. There was an elevation in plasma levels of TNF-α through the pregnancy in depressed women, and elevations in other cytokines, at midpregnancy. The adverse pregnancy outcomes, including preterm delivery, known to be associated with prenatal depression were not present in this cohort.

Diabetic Retinopathy during pregnancy in Hispanic women with latent Toxoplasma gondii infection.

BACKGROUND: Retinal photography was performed in pregnancy and postpartum in pregnant Hispanic women with latent Toxoplasma gondii (TG) infection in order to screen for characteristic retinal lesions or the particular scars found in people with active T. gondii infection. A comparison group of TG negative women was included in the study but they did not have retinal photography. OBJECTIVE: The goal of the parent study was to assess for adverse pregnancy events and evidence for parasite reactivation in TG positive (TG + ) women, through examination of the eyes for characteristic lesions. Retinal photography, usually at prenatal visits 2 (17 +/- 3.35 weeks) and 3 (26.3+/-1.75) weeks, was done on TG + women. Fifty-six of these women also (43 %) had retinal photography at the postpartum visit. Health and demographic data were obtained at the first prenatal visit for all women. STUDY DESIGN: From the 690 recruited at the first prenatal visit, 128 TG- women and 158 TG + women were enrolled in a prospective study through pregnancy and the postpartum. All TG- women (n = 532) provided data at the first prenatal visit and throughout their pregnancy and birth through the EHR. This allowed comparison of health and outcome data for the TG + compared to a larger number of TG- Hispanic pregnant women. RESULTS: While there was no evidence of ocular toxoplasmosis during pregnancy, there was a surprisingly large number (42 %) of TG + women with diabetic retinopathy (DR). We also observed that TG + women had a 20 % incidence of gestational diabetes mellitus (GDM) compared to 11.3 % in the TG- women (p = 0.01). At postpartum (mean 5.6 weeks), 23 of 30 women with pregnancy DR showed no DR in the postpartum. CONCLUSIONS: No characteristic T. gondii lesions were discovered. Retinal photography serendipitously revealed DR in these T. gondii positive women. It was also found that latent TG infection was associated with increased incidence of GDM. Hispanic pregnant women's increased risk for latent TG infection, GDM and DR are underappreciated. Retinal photography may need to be considered an innovative approach to screening.

Tryptophan metabolism and immune alterations in pregnant Hispanic women with chronic Toxoplasma gondii infection.

PROBLEM: Pregnancy markedly modifies women's metabolism and immune functions. We hypothesized that pregnancy might alter the immune and metabolic responses to chronic Toxoplasma gondii infection in pregnancy. METHOD OF STUDY: A population of 690 pregnant Hispanic women were screened for antibodies to T. gondii and 158 women were positive (23% positivity) with 83% showing high avidity indices. These seropositive women were followed through their pregnancies with four data collection time points and a postpartum collection at two clinics in Tampa, Florida. A T. gondii seronegative group (N = 128) was randomly selected to serve as a control group and measured along pregnancy in the same way. Serum levels of tryptophan, kynurenine, and their ratio, phenylalanine, tyrosine and their ratio, neopterin, and nitrite were measured through pregnancy and the postpartum. A plasma cytokine panel (IFN-γ, TNFα, IL-2, IL-10, IL-12, IL-6, IL-17) was analyzed in parallel. RESULTS: The major findings suggest that indoleamine 2,3-dioxygenase (IDO-1) was less activated in T. gondii seropositive pregnant Hispanic women with chronic infection. Evidence for IDO-1 suppression was that tryptophan catabolism was less pronounced and there were lower levels of multiple inflammatory cytokines including IFN-γ, which is the major inducer of IDO-1, and higher nitrite concentration, a surrogate marker for nitric oxide, an inhibitor of IDO. CONCLUSIONS: Latent T. gondii infection was associated with higher plasma tryptophan levels, and lower inflammatory cytokines across pregnancy, suggesting suppression of the IDO-1 enzyme, and possible T cell exhaustion during pregnancy.

Relationships of the very low birth weight infant microbiome with neurodevelopment at 2 and 4 years of age.

Very low birth weight (VLBW) infants (<1500 g) are at risk for poor neurodevelopmental outcomes depending on gestational age (GA), birth weight (BW), and morbidity in early life. The contribution of the gut microbiome is not well understood. Stool samples were collected weekly in the neonatal intensive care unit (NICU) from 24 VLBW infants for 6 weeks after admission and then again at 2 and 4 years of age. The Battelle Development Inventory-2 Screening Test (BDI-2 ST) was administered at 2- and 4-year time points. VLBW infants had dysbiotic microbiota in the NICU that progressed for most to an adult-type microbiota by 4 years of age. The BDI-2 ST results at age of 2 years triggered referral for further testing in 14 toddlers (70%), and by 4 years of age only seven of these 14 continued to require referral. Both NICU infant stool diversity and particular microbial amplicon sequence variants were associated with BDI-2 ST subscales, particularly for cognition, adaptive, and communication subscales, when controlled for GA, BW, and antibiotic exposure. Network analysis of the NICU infant stool microbial ecology showed differences in children needing neurodevelopmental referral. The results of this preliminary study indicate that the neonatal gut microbiome plays a role in early cognitive and behavioral neurodevelopment.

Conflicts Within the Discipline of Nursing: Is There a Looming Paradigm War?

This paper presents a view of the current sources of potential conflicts in the academic discipline of nursing. It suggests that these conflicts could lead, in the Kuhnian sense, to a paradigm war. The differing paradigms underlying the education and traditions of the PhD prepared nurse scientist/researcher/scholar and the DNP prepared nurse practitioner are a challenge for the discipline. DNP programs are swelling and faculty are needed to teach in these programs, and their position with regard to the usual rank and tenure structures of academe are not yet clear. Concern arises when the tenured PhD nurse scientist faculty numbers drop as the DNP faculty numbers increase. The body of nursing science is threatened as fewer students enter PhD programs and faculty retire. The DNP faculty paradigm does not provide for the rigor and preparation need to carry forward the disciplinary scientific knowledge mission. Rather than a fruitless war between the two paradigms, ways are suggested to fully embrace the differences as important to nursing, and to increase the number of PhD prepared nurse scientists.

Immune changes and dysphoric moods across the postpartum.

PROBLEM: Little is known about postpartum immune recovery and relationships of common dysphoric moods, stress, immunology, and endocrinology. METHOD OF STUDY: Healthy women (n = 72) were followed for six postpartum months with immune and hormone measures and dysphoric moods and stress scales. A panel of cytokines produced in mitogen-stimulated whole blood assays were measured at each time, along with plasma levels of hsC-reactive protein (hsCRP), Interleukin-6 (IL-6), and a panel of hormones. RESULTS: Cellular immunity, measured by production of Interferon-gamma (IFNγ) and (Interleukin-2 (IL-2) from stimulated whole blood culture, was low in the early postpartum with changes by 3 months. Tumor necrosis factor alpha (TNFα) showed a similar pattern. Plasma levels of CRP and Interleukin-6 (IL-6) showed higher levels in the early postpartum. Mood disturbance scores dropped across the postpartum with a change in slope at 3 months. No significant relationships were found between immune, endocrine, and psychosocial measures. CONCLUSION: Return to normal cellular immune function may take 3-4 months in the postpartum. Some aspects of early immunology (hsCRP and IL-6) probably reflect the latter stage of pregnancy, the stress of birth and the inflammation associated with involution. Dysphoric moods are higher in the early postpartum but are not related to immune factors or hormones.

Role of chronic stress and depression in periodontal diseases.

An extensive body of experimental and clinical evidence documents the negative impact of chronic psychological stress and depression on the immune system and health. Chronic stress and depression can result in general dysregulation of the immune system, of both cellular and humoral pathways, which may contribute to pathogenic infection and concomitant periodontal tissue destruction. In general, the evidence is consistent with the hypothesis that stress can modify the host defense and progression of periodontal infections in patients susceptible to periodontitis. However, substantial evidence also indicates that these conditions can mediate risk for disease, including periodontitis, through changes in health-related behaviors, such as oral hygiene, smoking and diet. The unequivocal interpretation of studies has also been hampered, in part, by issues related to conceptualization of stress and depression, as well as commonly associated comorbidities, such as diabetes, that can modify the onset and progression of periodontal disease. In addition, stress and depression appear to fall into a spectrum, ranging from mild to severe, involving a complex interaction of genetic background, coping strategies and environment. Differences in the conceptualization of stress and depression are probably important in assessing associations with other biologic and clinical measures. Future studies are necessary to clarify the complex interactions of chronic stress and depression in periodontal diseases.