Fabian Mwanyumba

Vulnerability of women in an African setting: lessons for mother-to-child HIV transmission prevention programmes.

After discussing advantages and risks, only a third of the 290 HIV-infected women included in an intervention study to reduce mother-to-child transmission of HIV in Mombasa, Kenya, informed their partners of their results. Despite careful counselling, 10% subsequently experienced violence or disruption of their relationship. To increase the uptake of interventions to reduce perinatal HIV transmission safely, we recommend the involvement of partners in HIV testing. In addition, the counselling of women has to address methods and skills to deal with violence.

Vaginal lavage with chlorhexidine during labour to reduce mother-to-child HIV transmission: clinical trial in Mombasa Kenya.

ObjectivesTo evaluate the effect of vaginal lavage with diluted chlorhexidine on mother-to child transmission of HIV (MTCT) in a breastfeeding population. MethodsThis prospective clinical trial was conducted in a governmental hospital in Mombasa, Kenya. On alternating weeks, women were allocated to non-intervention or to intervention consisting of vaginal lavage with 120 ml 0.2% chlorhexidine, later increased to 0.4%, repeated every 3 h from admission to delivery. Infants were tested for HIV by DNA polymerase chain reaction within 48 h and at 6 and 14 weeks of life. ResultsEnrolment and follow-up data were available for 297 and 309 HIV-positive women, respectively, in the non-lavage and the lavage groups. There was no evidence of a difference in intrapartum MTCT (17.2 versus 15.9%, OR 0.9, 95% CI 0.6–1.4) between the groups. Lavage solely before rupture of the membranes tended towards lower MTCT with chlorhexidine 0.2% (OR O.6, 95% CI 0.3–1.1), and even more with chlorhexidine 0.4% (OR 0.1, 95% CI 0.0–0.9). ConclusionThe need remains for interventions reducing MTCT without HIV testing, often unavailable in countries with a high prevalence of HIV. Vaginal lavage with diluted chlorhexidine during delivery did not show a global effect on MTCT in our study. However, the data suggest that lavage before the membranes are ruptured might be associated with a reduction of MTCT, especially with higher concentrations of chlorhexidine.

Diversity of the Human Immunodeficiency Virus Type 1 (HIV-1) env Sequence after Vertical Transmission in Mother-Child Pairs Infected with HIV-1 Subtype A

ABSTRACT Although several virologic and immunologic factors associated with an increased risk of perinatal human immunodeficiency virus type 1 (HIV-1) transmission have been described, the mechanism of mother-to-child transmission is still unclear. More specifically, the question of whether selective pressures influence the transmission remains unanswered. The aim of this study was to assess the genetic diversity of the transmitted virus after in utero transmission and after peripartum transmission and to compare the viral heterogeneity in the child with the viral heterogeneity in the mother. To allow a very accurate characterization of the viral heterogeneity in a single sample, limiting-dilution sequencing of a 1,016-bp fragment of the env gene was performed. Thirteen children were tested, including 6 with in utero infections and 7 with peripartum infections. Samples were taken the day after birth and at the ages of 6 and 14 weeks. A homogeneous virus population was seen in six (46.2%) infants, of whom two were infected in utero and four were infected peripartum. A more heterogeneous virus population was detected in seven infants (53.8%), four infected in utero and three infected peripartum. The phylogenetic trees of the mother-child pairs presented a whole range of different tree topologies and showed infection of the child by one or more maternal variants. In conclusion, after HIV-1 transmission from mother to child a heterogeneous virus population was detected in approximately one-half of the children examined. Heterogeneous virus populations were found after peripartum infection as well as after in utero infection. Phylogenetic tree topologies argue against selection processes as the major mechanism driving mother-to-child transmission but support the hypothesis that virus variability is mainly driven by the inoculum level and/or exposure time.

Placental Malaria and Perinatal Transmission of Human Immunodeficiency Virus Type 1

Prevalence of placental malaria in human immunodeficiency virus (HIV) type 1-infected and -uninfected women and the effect of placental malaria on genital shedding and perinatal transmission of HIV-1 were examined. Genital samples for HIV-1 DNA RNA were collected during labor. Infants were tested for HIV-1 at 1 day and 6 weeks postpartum. Placental malaria was diagnosed by histopathological examination: 372 placentas of HIV-1-infected women and 277 of HIV-1-uninfected women were processed. A higher prevalence of placental malaria was seen in HIV-1-infected women. No association was found between placental malaria and either maternal virus load, genital HIV-1 DNA, or HIV-1 RNA. Placental malaria did not correlate with in utero or peripartal transmission of HIV-1.

Placental inflammation and perinatal transmission of HIV-1.

&NA; The effect of placental membrane inflammation on mother‐to‐child transmission (MTCT) of HIV‐1 is reported. Placentas from HIV‐1‐infected women were examined as part of a perinatal HIV‐1 project in Mombasa. Kenya. Polymerase chain reaction analysis was used to test for HIV‐1 in the infants at birth and at 6 weeks. The maternal HIV‐1 seroprevalence was 13.3% (298 of 2,235). The overall rate of MTCT of HIV‐1 was 25.4%; polymerase chain reaction analysis revealed that of the 201 infants 6.0% (12) were already HIV‐1‐positive at birth (intrauterine transmission) and 19.4% (39) were infected during the peripartum period or in early neonatal life (perinatal transmission). The prevalence of acute chorioamnionitis was 8.8%, that of deciduitis was 10.8%, and that of villitis was 1.6%. Acute chorioamnionitis was independently associated with peripartum HIV‐1 transmission but not with in utero MTCT (17.9% vs. 6.7%, respectively; adjusted odds ratio, 3.9; 95% confidence interval, 1.2‐12.5; p = .025). Other correlates of perinatal MTCT were presence of HIV in the genital tract and in the babys oral cavity and a high maternal viral load in peripheral blood. The adjusted population attributable fraction of 12.8% (95% confidence interval, 1.5%‐22.8%) indicated that approximately 3% of MTCT could be prevented if acute chorioamnionitis was eliminated. We suggest that further research on the role of antimicrobial treatment in the prevention of chorioamnionitis and the reduction of peripartum MTCT needs to be performed.

Exposure to HIV-1 during delivery and mother-to-child transmission.

BackgroundThe correlation between the presence of HIV-1 in maternal cervico-vaginal secretions and in the infants oro-pharyngal secretions at birth, and mother-to-child HIV transmission (MTCT) were examined to obtain a better understanding of its mechanism. MethodsWomen without medical and obstetrical complications, living within a reasonable distance of the government hospital in Mombasa, Kenya, were recruited after informed consent. Maternal and infant characteristics were collected. Polymerase chain reaction was used to detect HIV-1 in cervico-vaginal and oro-pharyngal secretions. Infants were tested for HIV-1 by polymerase chain reaction within 48 h and at 6 weeks after delivery. ResultsBetween April 1998 and April 1999, 228 woman–infant pairs were included in the study. HIV-1 DNA in cervico-vaginal secretions was independently associated with HIV-1 maternal viral load and with infant birth-weight, whereas HIV-1 RNA was associated with maternal viral load and maternal age. HIV-1 DNA in the oro-pharyngal secretions was also independently associated with maternal viral load. MTCT rate at the age of 6 weeks was 23.6%. Intrapartum and early postpartum HIV transmission was independently associated with maternal viral load [adjusted odds ratio (OR), 1.6; 95% confidence interval (CI),1.0–2.7], detection of HIV-1 RNA in cervico-vaginal secretions (adjusted OR, 3.2; 95% CI, 1.5–7.3) and of HIV-1 DNA in oro-pharyngal secretions (adjusted OR, 3.2; 95% CI, 1.1–9.0). DiscussionAs far as is known, this is the first study showing that infant exposure to HIV-1 in the birth canal and the presence of HIV-infected cells in the infants oro-pharyngal cavity are independently associated with intrapartum and early postpartum MTCT. It supports the hypothesis that MTCT could occur through the oral route.

Low efficacy of nevirapine (HIVNET012) in preventing perinatal HIV-1 transmission in a real-life situation.

Since 2001, the unrestricted use of HIVNET012 has been recommended for the prevention of mother-to-child transmission in low-resource settings, despite the lack of validated efficacy data outside research settings. We implemented the nevirapine regimen in a real-life situation in Kenya. The perinatal HIV-1 transmission rate at 14 weeks was 18.1%, similar to the 21.7% before the intervention. These data call for further evaluation of the simple nevirapine regimen in field conditions, and underline the need for alter-native strategies.

Placental inflammation and perinatal outcome.

OBJECTIVE To examine the role of placental inflammation in adverse obstetrical outcome (AOO). METHODS Analysis of perinatal data of 701 randomly selected mothers of singleton infants, Mombasa, Kenya. RESULTS There were 661 (94.3%) live infants and 40 (5.7%) stillbirths. Out of the live born infants, 78 (12.4%) had a low birth weight (LBW < 2500g); 33 of them were preterm and 41 small for gestational age (SGA). The incidence of neonatal sepsis and post partum endometritis was 3.6 and 19.8%, respectively. The perinatal death rate was estimated to be 7.3% (51/701). The prevalence of acute placental inflammation was 19.6%. Acute placental inflammation was independently associated with preterm low birth weight (ARR=3.8, 95% CI=1.7-8.9, P<0.01), stillbirth (ARR=2.3, 95% CI=1.1-5.0, P=0.03) and perinatal death (ARR=2.8, 95% CI=1.4-5.4, P<0.01). Women with acute placental inflammation had a two-fold higher risk for AOO (32.6 versus 15.2%, respectively, ARR=2.5, 95% CI=1.3-4.8, P<0.01). Other risk factors for AOO were bad obstetrical history, low haemoglobin level and leucocytosis. CONCLUSIONS The incidence of adverse obstetrical outcome defined as low birth weight, low Apgar score, perinatal mortality and post partum endometritis, was high in this population. Acute placental inflammation was associated with preterm birth, stillbirth and perinatal death. More research is needed to study the role of infection in adverse obstetrical outcome, and to design interventions to decrease infectious morbidity and mortality in pregnancy.

Correlation between maternal and infant HIV infection and low birth weight: a study in Mombasa, Kenya.

This article aimed to examine the association between maternal and infant HIV infection and low birth weight (LBW <2500 grams). Data from 8563 singleton liveborns in Mombasa, Kenya, were analysed. Maternal HIV infection was found in 14.1% of the women and 9.6% of neonates had a birth weight of <2500 grams. In multivariate analysis, maternal HIV infection was independently associated with LBW (RR=1.46, 95% CI=1.20-1.79, P =0.0002). Maternal age, primiparity, sex of the baby, religion, syphilis infection, anaemia and previous history of stillbirth were also independently associated with LBW (RR: 1.32, 2.19, 1.44, 1.56, 1.61, 1.31 and 1.69, respectively). The rate of intra-uterine HIV transmission was 5.1% and 20.1% of the exposed infants were infected during the intrapartum period. Intrapartum infected infants had a relative risk of LBW of 1.95 (95% CI=1.18-2.87, P <0.01) compared to uninfected children, whereas the birth weight of infants infected in utero was not different from uninfected infants (RR=1.18, 95% CI=0.56-2.60, P=0.630). HIV infected mothers are more likely to have small babies, even after controlling for possible confounding factors. Low birth weight babies were more at risk for peripartum HIV transmission, but further research is needed to study mechanisms of transmission in relation to birth weight.This article aimed to examine the association between maternal and infant HIV infection and low birth weight (LBW <2500 grams). Datafrom 8563 singleton liveborns in Mombasa, Kenya, were analysed. Maternal HIV infection was found in 14·1% of the women and 9·6% of neonates had a birth weight of <2500 grams. In multivariate analysis, maternal HIV infection was independently associated with LBW (RR=1·46, 95% CI=1·20-1·79, P =0·0002). Maternal age, primiparity, sex of the baby, religion, syphilis infection, anaemia and previous history of stillbirth were also independently associated with LBW (RR: 1·32, 2·19, 1·44, 1·56, 1·61, 1·31 and 1·69, respectively). The rate of intra-uterine HIV transmission was 5·1% and 20·1% of the exposed infants were infected during the intrapartum period. Intrapartum infected infants had a relative risk of LBW of 1·95 (95% CI=1·18-2·87, P <0·01) compared to uninfected children, whereas the birth weight of infants infected in utero was not different from uninfected infants (RR=1·18, 95% CI=0·56-2·60, P=0·630). HIV infected mothers are more likely to have small babies, even after controlling for possible confounding factors. Low birth weight babies were more at risk for peripartum HIV transmission, but further research is needed to study mechanisms of transmission in relation to birth weight.