A clinical audit of maternal syphilis in a regional hospital in KwaZulu-Natal, South Africa.

BACKGROUND: Despite the availability of screening guidelines and effective treatment for maternal syphilis (MS), its prevalence remains high and is re-emerging in many parts of the world. This might be because of varying screening tests and algorithms for the laboratory diagnosis and treatment of syphilis. In addition, HIV co-infection may compromise the elimination of MS. The present study is a clinical audit of the prevalence of MS in KwaZulu-Natal, South Africa, using the 'Traditional Algorithm' screening. METHODS: This was a retrospective audit in which data on syphilis testing were obtained over a 1-year period (2016) at a large regional hospital in South Africa. The standard screening test at the study site was the non-treponemal antigen, rapid plasma reagin (RPR). Data on the prevalence of MS and comorbidity with HIV infection were analysed. RESULTS: There were 10 680 deliveries in the study period of which 118 were RPR reactive, giving an MS prevalence of 1.1%. MS occurred predominantly in the age groups < 18 and > 35 years (p = 0.001). The prevalence of HIV infection was 41.2% (n = 4451). Seventy-two (61.0%) had both HIV and MS infection, whilst 46 (39.0%) had discordant results (p = 0.001). CONCLUSION: We report an increase in the prevalence of MS compared to previous South African National Antenatal Syphilis Surveillance studies. This may be because of the prozone effect caused by HIV infection on the sensitivity of the RPR. We propose a change in MS screening, using a Rapid DUO (Dual HIV and syphilis point of care test) and Reverse Algorithm for screening that could improve the sensitivity, detection and management of both diseases.

Angiogenesis, Lymphangiogenesis, and the Immune Response in South African Preeclamptic Women Receiving HAART.

Purpose of the review: This review highlights the role of angiogenesis, lymphangiogenesis, and immune markers in human immunodeficiency virus (HIV)-associated preeclamptic (PE) pregnancies in an attempt to unravel the mysteries underlying the duality of both conditions in South Africa. Recent findings: Studies demonstrate that HIV-infected pregnant women develop PE at a lower frequency than uninfected women. In contrast, women receiving highly active anti-retroviral therapy (HAART) are more inclined to develop PE, stemming from an imbalance of angiogenesis, lymphangiogenesis, and immune response. Summary: In view of the paradoxical effect of HIV infection on PE development, this study examines angiogenesis, lymphangiogenesis, and immune markers in the highly HIV endemic area of KwaZulu-Natal. We believe that HAART re-constitutes the immune response in PE, thereby predisposing women to PE development. This susceptibility is due to an imbalance in the angiogenic/lymphangiogenic/immune response as compared to normotensive pregnant women. Further large-scale studies are urgently required to investigate the effect of the duration of HAART on PE development.

Morphometric image analysis of placental C-type lectin domain family 2, member D (CLEC2D) immuno-expression in HIV associated pre-eclampsia.

OBJECTIVE: C-type lectin domain family 2, member D (CLEC2D) is implicated in the immune response. Pre-eclampsia and HIV infection have opposing immune responses. In view of the high prevalence of HIV infection and pre-eclampsia in South Africa, this study assessed the placental immuno-expression of CLEC2D in HIV associated pre-eclampsia. METHOD: Placental tissue was obtained from 60 pregnancies which were categorized according to pregnancy type (pre-eclamptic or normotensive) and HIV status (positive or negative). Immunohistochemistry and morphometric image analysis were used to evaluate placental CLEC2D immuno-expression. RESULTS: CLEC2D expression was significantly decreased in the conducting villi of pre-eclamptic vs normotensive placentae (p = 0.0418) but was increased in the exchange villi, albeit non-significant (p = 0.4948). HIV positive status intensified placental CLEC2D immuno-expression in conducting (p = 0.0312) and exchange (p = 0.0025) villi. CLEC2D expression was significantly different in exchange vs conducting villi (p < 0.0001) and across study groups (p = 0.0003). Normotensive; HIV negative placentae (control) had a non-significant difference in CLEC2D expression across villi types, however significant difference was noted within the remaining groups: normotensive; HIV positive (p < 0.05), pre-eclamptic; HIV positive (p < 0.01 and pre-eclamptic; HIV negative (p < 0.001). CONCLUSION: The contrasting expression of CLEC2D in HIV infection and pre-eclampsia is demonstrative of the immunosuppressive and pro-inflammatory roles of the respective pathologies. However, this implication may be confounded by highly active anti-retroviral treatment (HAART).

Lymphatic vascular endothelial hyaluronan receptor-1 immunoexpression in placenta of HIV infected pre-eclamptic women.

INTRODUCTION: Lymphangiogenesis is the formation of new vessels from pre-existing lymphatic vessels. Data on lymphangiogenesis in the placenta of HIV-infected pre-eclamptics are sparse and the findings are conflicting. The aim of this novel study was to evaluate LYVE-1 immunoexpression in the placenta of HIV infected normotensive versus pre-eclamptic women. METHODS: Placental tissue was obtained from normotensive and pre-eclamptic women stratified according to their HIV status. The pre-eclamptic group was divided into early (<34 weeks) and late (>34 weeks) onset. Immunohistochemistry utilized mouse anti-human LYVE-1 antibody and was morphometrically evaluated. RESULTS: LYVE-1 immunostaining was localized within endothelium of the arterial supply and venous drainage of both conducting and exchange villi as well as within medial cells of arteries. LYVE-1 immunostained macrophage-like cells were observed within the fetal and maternal circulation. LYVE-1 immunoexpression was higher (p=0.0001) in HIV positive cohort, regardless of pregnancy and villous type. Irrespective of HIV status and pregnancy type, LYVE-1 immunoexpression was significantly elevated in the conducting compared to the exchange villi (p=0.01). LYVE-1 immunoexpression was higher in N and LOPE compared to EOPE groups for both conducting and exchange villi types respectively (p=0.0001 and p=0.006). There is a decrease of LYVE-1 expression in EOPE+ (conducting villi) and EOPE- (exchange villi) compared to N and LOPE subgroups. CONCLUSION: This study provides a novel insight into an up-regulation of LYVE-1 expression in the fetal circulation of conducting and exchange villi of HIV-infected pre-eclamptics.