Maternal HIV Infection and Vertical Transmission of Pathogenic Bacteria

Cutland, Clare; Schrag, Stephanie J.; Zell, Elizabeth R.; Kuwanda, Locadiah; Buchmann, Eckhardt; Velaphi, Sithembiso; Groome, Michelle; Adrian, Peter V.; Madhi, Shabir А.

doi:10.1542/peds.2011-1548

Cited by 46 publications

(45 citation statements)

References 23 publications

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“…Cutland et al performed the largest study published so far including more than 5000 pregnant women, of which 1347 were HIV-infected pregnant women in South Africa. This study found a significantly lower prevalence of GBS carriage in HIV-infected compared to HIV-uninfected pregnant women (17 vs. 23%; P = 0.0002) (24). …”

Section: Maternal Gbs Colonization In Hiv-infected Pregnant Womenmentioning

confidence: 72%

“…On the other hand, HIV-infected women with low CD4 cell count are known to have increased prevalence of bacterial vaginosis that could compete with GBS and are more likely to take cotrimoxazole prophylaxis resulting in lower GBS carriage rates (27–29). In the Cutland et al’s study, CD4 cell count was only available in a limited proportion of HIV-infected women but the majority had a CD4 count >350/mm 3 (24). …”

Section: Maternal Gbs Colonization In Hiv-infected Pregnant Womenmentioning

confidence: 99%

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Increased Risk of Group B Streptococcus Invasive Infection in HIV-Exposed but Uninfected Infants: A Review of the Evidence and Possible Mechanisms

et al. 2016

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Group B Streptococcus (GBS) is a major cause of neonatal sepsis and mortality worldwide. Studies from both developed and developing countries have shown that HIV-exposed but uninfected (HEU) infants are at increased risk of infectious morbidity, as compared to HIV-unexposed uninfected infants (HUU). A higher susceptibility to GBS infections has been reported in HEU infants, particularly late-onset diseases and more severe manifestations of GBS diseases. We review here the possible explanations for increased susceptibility to GBS infection. Maternal GBS colonization during pregnancy is a major risk factor for early-onset GBS invasive disease, but colonization rates are not higher in HIV-infected compared to HIV-uninfected pregnant women, while selective colonization with more virulent strains in HIV-infected women is suggested in some studies. Lower serotype-specific GBS maternal antibody transfer and quantitative and qualitative defects of innate immune responses in HEU infants may play a role in the increased risk of GBS invasive disease. The impact of maternal antiretroviral treatment and its consequences on immune activation in HEU newborns are important to study. Maternal immunization presents a promising intervention to reduce GBS burden in the growing HEU population.

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Section: Maternal Gbs Colonization In Hiv-infected Pregnant Womenmentioning

confidence: 72%

Section: Maternal Gbs Colonization In Hiv-infected Pregnant Womenmentioning

confidence: 99%

Increased Risk of Group B Streptococcus Invasive Infection in HIV-Exposed but Uninfected Infants: A Review of the Evidence and Possible Mechanisms

et al. 2016

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“…Previously reported conflicting findings,17,18 may depend on the frequency of antimicrobial use (and provision of anti-retroviral therapy). In contrast, neonatal GBS disease is increased with HIV-exposure,40 with reduced maternal GBS capsular antibody in HIV-1 infection,41,42 and/or because, as shown here, the most virulent clone, CC17, is more frequently found in HIV-infected GBS colonised women, compared to other non-CC17 types.…”

Section: Discussionmentioning

confidence: 95%

“…Data from sSA are limited, but are also conflicting for potentially important risk factors such as HIV-infection. In South Africa, maternal GBS colonisation was lower in HIV-infected mothers17 but in Malawi, only amongst HIV-infected mothers with lower CD4 counts 18. In the USA15 and Zimbabwe19 no association with HIV was found.…”

Section: Introductionmentioning

confidence: 93%

Maternal colonization with Streptococcus agalactiae and associated stillbirth and neonatal disease in coastal Kenya

et al. 2016

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Streptococcus agalactiae (Group B Streptococcus, GBS) causes neonatal disease and stillbirth, but its burden in sub-Saharan Africa is uncertain. We assessed maternal recto-vaginal GBS colonisation (7967 women), stillbirth and neonatal disease. Whole genome sequencing was used to determine serotypes, sequence types (ST), and phylogeny. We found low maternal GBS colonisation prevalence (934/7967, 12%), but comparatively high incidence of GBS-associated stillbirth and early onset neonatal disease (EOD) in hospital (0.91(0.25-2.3)/1000 births; 0.76(0.25-1.77)/1000 live-births respectively). However, using a population denominator, EOD incidence was considerably reduced (0.13(0.07-0.21)/1000 live-births). Treated cases of EOD had very high case fatality (17/36, 47%), especially within 24 hours of birth, making under-ascertainment of community-born cases highly likely, both here and in similar facility-based studies. Maternal GBS colonisation was less common in women with low socio-economic status, HIV infection and undernutrition, but when GBS-colonised, they were more likely colonised by the most virulent clone, CC17. CC17 accounted for 267/915(29%) of maternal colonising (265/267(99%) serotype III, 2/267(0.7%) serotype IV), and 51/73(70%) of neonatal disease cases (all serotype III). Trivalent (Ia/II/III) and pentavalent (Ia/Ib/II/III/V) vaccines would cover 71/73(97%) and 72/73(99%) of disease-causing serotypes respectively. Serotype IV should be considered for inclusion, with evidence of capsular switching in CC17 strains.

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“…Extrapolating from studies in endemic settings, they may translate into an increased susceptibility to infectious diseases. HEU infants born to severely immunocompromised mothers (CD4 < 200 cells/mm 3 ) in a South African cohort were found to be at higher risk of developing early- and late-onset sepsis than those born to mothers with CD4 > 350 cells/mm 3 [49]. Data from the Ban trial in Malawi further demonstrated that low total white blood cell counts at birth are a significant predictor of serious morbidity and mortality among HEU infants [50].…”

Section: Discussionmentioning

confidence: 99%

Impact of maternal HIV-1 viremia on lymphocyte subsets among HIV-exposed uninfected infants: protective mechanism or immunodeficiency

et al. 2014

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BackgroundReports of increased morbidity and mortality from infectious diseases among HIV Exposed Uninfected (HEU) infants have raised concern about a possible underlying immunodeficiency among them. The objective of this study was to assess the immunological profile of HEU infants born to mothers exhibiting different levels of HIV-1 viremia at the time of delivery.MethodsStudy subjects were enrolled in the Centre maternel et infantile sur le SIDA (CMIS) mother-child cohort between 1997 and 2010 (n =585). Infant CD4+ T cell, CD8+ T cell and CD19+ B cell counts were assessed at 2 and 6 months of age, and compared among HEU infants in groups defined by maternal viral load (VL) at the time of delivery (VL < 50 copies/ml, VL 50–1000 copies/ml, and VL > 1000 copies/ml) in a multivariable analysis.ResultsAt 2 months of age, infants born to mothers with VL > 1000 copies/ml had lower CD4+ T cell counts compared to those born to mothers with VL < 50 copies/ml at the time of delivery (44.3% versus 48.3%, p = 0.007, and 2884 vs. 2432 cells/mm3, p = 0.02). These differences remained significant after adjusting for maternal and infant antiretroviral drug use, gender, race and gestational age, and persisted at 6 months of age. There were no differences in CD8+ T cell count or absolute CD19+ B cell count between groups, though higher CD19+ B cell percentage was seen among infants born to mothers with VL > 1000 copies/ml.ConclusionsThese results suggest that exposure to high levels of HIV-1 viremia in utero, even in the absence of perinatal transmission, may affect the infant’s developing immune system. While further work needs to be done to confirm these findings, they reinforce the need for optimal treatment of HIV infected pregnant women, and careful follow-up of HEU infants.

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Maternal HIV Infection and Vertical Transmission of Pathogenic Bacteria

Abstract: Maternal HIV infection was not associated with increased risk of maternal bacterial colonization, vertical transmission, EOS, or LOS. HIV-infected neonates, however, were at increased risk of EOS and LOS.

Cited by 46 publications

References 23 publications

Increased Risk of Group B Streptococcus Invasive Infection in HIV-Exposed but Uninfected Infants: A Review of the Evidence and Possible Mechanisms

Increased Risk of Group B Streptococcus Invasive Infection in HIV-Exposed but Uninfected Infants: A Review of the Evidence and Possible Mechanisms

Maternal colonization with Streptococcus agalactiae and associated stillbirth and neonatal disease in coastal Kenya

Impact of maternal HIV-1 viremia on lymphocyte subsets among HIV-exposed uninfected infants: protective mechanism or immunodeficiency

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