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Arch Dis Child Fetal Neonatal Ed 89:F468-F469 doi:10.1136/adc.2003.041335
  • LETTER

In utero HIV infection in pregnancies complicated by tuberculosis in Durban, South Africa

  1. T Pillay1,
  2. M Adhikari1,
  3. H M Coovadia1,
  4. J Moodley2,3,
  5. M Khan3,
  6. J L Sullivan4
  1. 1Department of Paediatrics and Child Health, University of Natal Medical School, South Africa
  2. 2Department of Obstetrics and Gynaecology University of Natal Medical School
  3. 3Medical Research Council Pregnancy and Hypertension Unit, Durban, South Africa
  4. 4University of Massachusetts Medical School, Worcester, MA, USA
  1. Correspondence to:
    Dr Pillay
    Peter Medawar Building for Pathogen Research, Room 305.40.24, South Parks Road, University of Oxford, Oxford OX1 3SY, UK; tpillaygwmail.jr2.ox.ac.uk

    At the core of the HIV-1 and tuberculosis (TB) epidemics, a defined effect of these combined pathogens on maternal and child health has been observed at King Edward VIII Hospital in Durban South Africa.1,2 Here we report on the adverse effect of maternal HIV-1 infection with TB disease on fetal acquisition of HIV-1.

    In a prospective cohort study conducted at the hospital between April 1997 and July 1999, 42 HIV-1 infected pregnant women with active TB disease were investigated for intrauterine transmission of HIV-1. Intrauterine infection was diagnosed by a positive HIV-1 RNA polymerase chain reaction (PCR) (Amplicor; Roche Molecular Diagnostic Systems, Branchburg, New Jersey, USA; limits of detection 50 copies/ml) detected on a neonatal sample obtained within the first 72 hours of birth, with a subsequent positive HIV-1 PCR or clinical progression of disease. Assays were performed in a single laboratory which was participating in a continuing quality certification programme for HIV-1 RNA quantitation sponsored by the National Institutes of Health.

    Eight newborns were HIV-1 RNA PCR positive by 72 hours of birth resulting in a 19% in utero transmission rate of HIV-1 for singleton live births exposed to maternal HIV-1 infection and TB disease in Durban. The rate of intrauterine transfer of HIV-1 in this category of ill women was much higher than the overall 5–10%3 in utero transmission rates recorded in resource poor countries. Maternal CD4 (427 (278) v 318 (289) cells/mm3 (mean (SD)); p  =  0.37), plasma viral burden (median log 5.0 v 4.7), extrapulmonary sites of TB disease, and sputum smear or culture positive rates for Mycobacterium tuberculosis were no different between in utero transmitting and non-transmitting mothers. A further nine babies were HIV-1 PCR positive on follow up (intrapartum or postpartum transmission), resulting in an overall HIV-1 mother to child transmission rate of 40.4% (17/42).

    This observation augments current knowledge on the impact of perinatal infections on mother to child transmission of HIV-1. High maternal viral burden and CD4 suppression, which are characteristic of advancing AIDS, have been associated with higher overall vertical transmission of HIV-1 and greater risk of rapidly progressive infant HIV-1.4 Here we quantify this intrauterine risk in HIV-1 infected pregnant women ill with TB disease, and suggest that, in these situations, regimens of antiretroviral therapy which are likely to reduce fetal acquisition of HIV-1 will need to be considered. These should supplement public health programmes to detect and prevent TB disease in HIV-1 infected pregnancies in endemic regions.

    References