- Top of page
- Limitations and strengths
The vast majority of HIV-infected children acquire the infection through mother-to-child transmission (MTCT) in utero, around the time of labour and delivery, or postnatally through breast feeding [1, 2]. Approximately 70% of all perinatally acquired HIV transmission occurs early (i.e. in utero, intra-partum or within 6 weeks of birth) in an exposed infant's life . Previous investigations have identified several factors associated with early HIV transmission, including maternal (low CD4 cell count, high viral load and lack of antiretroviral therapy during pregnancy, mastitis and breast abscess), delivery (noncesarean section birth and absence of prophylactic nevirapine use) and child (low birth weight and prematurity) factors [2-4].
HIV and malaria infections represent the most important health problems in sub-Saharan Africa (SSA), where these infections overlap and coinfection is common . An estimated 24.3 to 37% of HIV-positive pregnant women in the malaria-endemic regions of SSA are coinfected with malaria [6-8]. Malaria infection up-regulates the expression of chemokine (C-C motif) receptor 5 (CCR5) receptors in placental macrophages , increases peripheral and placental HIV-1 viral load , and thereby increases the risk of HIV MTCT for infants of pregnant HIV-positive women.
Nevertheless, there is little research on the potential contribution of coincident infections, such as malaria in pregnancy (MIP), to early HIV MTCT among HIV-exposed infants of HIV-infected women in SSA; when available, results have been inconclusive [6-8, 10-16]. In a short-term prospective study of infants born to 277 HIV-positive Kenyan women and 372 HIV-negative hospital-based controls, Inion et al. found no association between placental malaria and in utero or peripartal transmission of HIV-1 by 6 weeks . Maternal placental malaria was associated with a lower risk of child HIV-positive status at 1 month of life among 207 pregnant HIV-positive women, each provided with a long-lasting insecticide-treated bed net with randomization to either intermittent preventive malaria therapy with sulfadoxyl-pyrimethamine or a placebo . Another study of 512 HIV-positive mothers from Kenya found complex associations between maternal placental malaria and perinatal HIV MTCT . On the one hand, low-density placental malaria was an independent protective risk factor for HIV MTCT. This association varied by maternal viral load such that, among mothers with low HIV viral load, low-density placental malaria protected against HIV MTCT, whereas, among mothers with high HIV viral loads, high-density placental parasitemia was associated with an elevated risk of HIV MTCT . Further, a large, multi-site, randomized, placebo-controlled trial of antibiotics for reduction of chorioamnionitis that included pregnant HIV-positive women from three SSA countries, Malawi, Zambia and Tanzania, found no association between placental malaria and MTCT at birth . However, among women with low baseline viral load, placental malaria was positively associated with HIV MTCT at birth . On the other hand, a study of HIV-positive mothers from the Rakai District in Uganda found a twofold higher risk of HIV MTCT for HIV-positive mothers with placental malaria relative to those without placental malaria [7, 10]. Most recently, a small case−control study of the placentas of 40 HIV-infected mother−child pairs, which included 20 pairs in which the infants were perinatally HIV infected and 20 in which the infants were HIV-exposed but uninfected, as well as 20 HIV-uninfected mother−child pairs, reported sixfold higher odds of child perinatal HIV infection for mothers with placental malaria . Both studies that found significant positive associations between in-pregnancy malaria and HIV MTCT were implemented prior to the availability of antiretroviral therapy for pregnant HIV-infected African women [10, 11].
In the light of these mixed findings and the persisting need to understand the potential role of maternal malarial morbidity during pregnancy in early HIV MTCT in the post-highly active antiretroviral therapy (HAART) era , we undertook this prospective cohort study to re-examine the hypothesis that maternal malarial morbidity during pregnancy is positively associated with MTCT. To this end, we used data collected between 2004 and 2008 among HIV-positive mothers whose children were enrolled in a trial of micronutrient supplementation in Dar es Salaam, Tanzania.
- Top of page
- Limitations and strengths
Enrolled in the parent study were 2387 HIV-positive mothers and their HIV-exposed infants. The average gestational age at enrolment was 22 weeks. Of the 2387 mother−child pairs, detailed maternal pregnancy health history and HIV status data at 6 weeks were available for the 2367 pairs who formed the study base for this nested longitudinal study. Eighty-four per cent of mothers breast fed their infants post-delivery. By the infant's 6th week of life, 262 (11.1%) were HIV positive (Table 1). The prevalences of fever symptoms and ever doctor-diagnosed clinical malaria during pregnancy were 16.6% (n = 394) and 15.9% (n = 376), respectively. Clinical malaria was also diagnosed in 54% of women with fever symptoms in pregnancy. Among women with clinical MIP, 1.6, 27.5 and 47.2% of all diagnoses occurred in the first, second and third trimesters, respectively. As many as 30.7% (n = 122) of women were clinically diagnosed with at least two episodes of MIP within the same trimester or across multiple trimesters. The vast majority (96%) of clinical MIP diagnoses were classified as uncomplicated malaria, but a laboratory test to confirm parasitaemia was ordered in 38% of women only. Test results, however, were available for only 19 women, of whom 18 were positive for the malaria parasite (data not shown).
Table 1. Sociodemographic, obstetric history and at-birth description of HIV-infected mothers and their newborns from Dar es Salaam, Tanzania
| ||Overall||Child HIV-positive at 6 weeks||Child HIV-negative at 6 Weeks||P-value|
|(n = 262; 11.1%)||(n = 2105; 88.9%)|
|Mother's age (years) [mean (SD)]||28.5 (4.9)||28.8 (4.94)||28.6 (4.95)||0.5170|
|Mother's years of education [mean (SD)]||7.2 (2.7)||7.2 (2.33)||7.19 (2.79)||0.6195|
|GA at enrolment (weeks) [mean (SD)]||22.2 (5.30)||22.2 (5.39)||22.1 (5.29)||0.7276|
|Married/cohabiting||1996 (85.0)||213 (80.7)||1783 (85.6)||0.1782|
|Mother has own income||809 (34.5)||79 (29.9)||730 (35.0)||0.1001|
|Post-PEPFAR enrollee||1449 (61.2)||154 (58.8)||1295 (61.5)||0.3955|
|Obstetric history|| || || || |
|Neonatal deaths in prior pregnancies||351 (15)||60 (22.7)||291 (14.0)||0.0008|
|Spontaneous abortions (prior pregnancies)||437 (18.5)||52 (19.9)||385 (18.3)||0.5377|
|Gravidity (including current pregnancy)|| || || || |
|1||531 (23.6)||56 (21.5)||475 (23.0)||Ref|
|2||772 (32.9)||83 (31.4)||689 (33.0)||0.9619|
|3||524 (22.3)||67 (25.4)||457 (21.9)||0.2805|
|≥ 4||499 (21.3)||55 (20.8)||444 (21.3)||0.8541|
|Malaria during pregnancy|| || || || |
|Ever||513 (21.6)||64 (24.1)||450 (25.1)||0.3210|
|Number of malaria episodes|| || || || |
|0||1855 (78.3)||180 (76.0)||1537 (78.6)||0.0178|
|1||391 (16.5)||39 (14.9)||352 (16.7)|| |
|2||101 (4.3)||18 (6.9)||83 (3.3)|| |
|≥ 3||21 (0.9)||6 (2.3)||15 (0.7)|| |
|Delivery details and infant characteristics|| || || || |
|Mothers who took nevirapine at labour onset||711 (30.0)||66 (25.2)||645 (30.6)||0.0703|
|In-hospital delivery||2011 (85.7)||214 (81.8)||1797 (86.2)||0.0241|
|Vaginal tears||351 (15.0)||49 (18.6)||396 (19.0)||0.8632|
|Female sex||1083 (45.7)||131 (50.0)||952 (45.2)||0.1417|
|Cesarean section||275 (11.7)||23 (8.7)||252 (12.1)||0.1076|
|Full-term birth||1774 (75)||1578 (75.7)||186 (70.5)||0.0623|
|Low birth weight||157 (6.7)||42 (15.9)||115 (5.5)||< 0.0001|
|Infant received nevirapine within 72 h||1691 (71.4)||170 (64.9)||1521 (72.2)||0.0132|
|Breast fed between delivery and 6 weeks||1989 (84.0)||230 (87.8)||1759 (83.5)||0.0759|
|Maternal health; immunological/laboratory details|| || || || |
|Anaemia at enrolment||643 (27.2)||89 (34.0)||554 (26.3)||0.0085|
|Breast pain/inflammation, or cracked or bleeding nipple by 6 weeks||32 (1.4)||6 (2.4)||26 (1.2)||0.1629|
|CD4 count < 350 cells/uL at enrolment||774 (34.0)||102 (45.6)||672 (32.9)||< 0.0001|
|HIV disease stage > 1 at enrolment||383 (16.2)||43 (16.4)||340 (16.1)||0.9116|
|On antiretrovirals at any time during pregnancy||166 (7.1)||5 (1.9)||161 (7.6)||0.0006|
Sociodemographic, obstetric and at-birth information for the mother−child pairs is presented in Table 1. Mothers of children who were HIV positive at 6 weeks did not differ from mothers of children who were HIV negative at 6 weeks with respect to age, educational status, gestational age at study enrolment, gravidity or marital status. A greater proportion of mothers whose children were HIV negative at 6 weeks, however, delivered in hospitals and received antiretroviral therapy during pregnancy. Similarly, the proportion of mothers who took nevirapine prophylaxis at the onset of labour and the proportion of infants who received nevirapine prophylaxis within 72 h of birth were higher among infants who were HIV negative at 6 weeks. In addition, a lower percentage of mothers with HIV-negative children at 6 weeks had low-birth-weight infants, a prior history of early neonatal deaths, and CD4 cell counts < 350 cells/uL at enrolment. However, infants whose mothers had multiple episodes of malaria during pregnancy were over-represented among infants who were HIV-infected at 6 weeks (Table 1).
Based on multivariable models (Table 2), the RR of HIV infection at 6 weeks was elevated by 24%, but not statistically different, for infants whose mothers were ever vs. never (95% CI 0.94−1.64) diagnosed with clinical malaria and for infants whose mothers were diagnosed with a single vs. no malaria episodes (RR 1.07; 95% CI 0.77–1.48) during pregnancy. The RR of HIV MTCT, however, rose significantly per malaria episode increment during pregnancy (RR 1.29; 95% CI 1.04–1.58), and infants of HIV-positive women with at least two malaria diagnoses in pregnancy were more than twice as likely as infants of HIV-positive women not diagnosed with MIP to be HIV-infected at 6 weeks (RR 2.12; 95% CI 1.31–3.45). These malaria-associated estimated risks of HIV MTCT were robust to adjustment for variations in infant-related factors, maternal sociodemographic factors, delivery factors, maternal health status in pregnancy, and seasonality. Additional adjustment for potential mediators, including maternal immunological status at enrolment, use vs. non-use of HAART in pregnancy, and maternal WHO HIV disease stage, slightly attenuated but did not materially change the malaria-associated high risk of HIV MTCT (Table 2). Similarly, the adjustment of multivariable models for number of nonspecific fever symptoms reported in pregnancy slightly attenuated but did not ablate the positive association between early HIV MTCT and (i) number of clinical MIP diagnoses in pregnancy (RR 1.25; 95% CI 1.00−1.57) and (ii) multiple vs. no MIP diagnosis (RR 1.92; 95% CI 1.13−3.25).
Table 2. Mother-to-child HIV transmission by 6 weeks in relation to clinical malaria diagnosis by a doctor during pregnancy among HIV-positive mothers and their HIV-exposed infants from Dar es Salaam, Tanzania
| || ||Univariate association||Adjusted model 1a||Adjusted model 2b|
|Maternal malaria in pregnancy||n/N||RR (95% CI)||RR (95% CI)||RR (95% CI)|
| || || || || |
|Per episode increment in clinical malaria||n/a||1.31 (1.08−1.61)||1.29 (1.04−1.58)||1.29 (1.05−1.59)|
|Number of doctor-diagnosed clinical malaria episodes|| || || || |
|1 vs. 0||38/332||1.08 (0.78−1.50)||1.07 (0.77−1.48)||1.09 (0.80−1.48)|
|≥ 2 vs. 0||15/62||2.27 (1.39−3.71)||2.12 (1.31−3.45)||1.99 (1.20−3.27)|
Nonmalaria predictors of HIV MTCT at 6 weeks are presented in Table 3. The ever vs. never maternal report of fever symptoms was strongly and significantly associated with clinical MIP diagnosis (RR 5.80; 95% CI 4.91−6.93) but not with early HIV MTCT in multivariate models mutually adjusted for clinical MIP diagnosis (RR 1.04; 95% CI 0.87−1.29). However, maternal baseline immune-deficiency status, the presence of nipple lesions/inflammation at or before 6 weeks after birth, and infant low birth weight each predicted elevated risks of HIV MTCT at 6 weeks of life. Conversely, the receipt of HAART at any time during pregnancy, maternal possession of own income, and cohabiting or married status were significant protective risk factors for early HIV MTCT (Table 3). The relationship between clinical MIP and the factors identified above was generally invariant within levels of maternal CD4 count at enrolment, maternal WHO HIV disease stage at enrolment, child sex, and prematurity. However, the relationship between MIP (per episode increment) and HIV MTCT was heterogeneous within strata of maternal education (P-value for interaction term = 0.05). Specifically, each unit increment in maternal malaria episode was associated with a 3.2-fold (95% CI 1.49–6.71) RR of HIV MTCT among mothers with fewer than 7 years of education, whereas the risk of HIV MTCT by 6 weeks was nonsignificantly elevated among mothers with 7 or more years of education (RR 1.2; 95% CI 0.94–1.53).
Table 3. Nonmalaria predictors of mother-to-child HIV transmission by 6 weeks among HIV-positive mothers and their HIV-exposed infants from Dar es Salaam, Tanzania
| ||With exposure||Without exposure||Univariate model ||Adjusted modelb|
|(n/N)||(n/N)||RR (95% CI)||RR (95% CI)|
|Maternal health indicators|| || || || |
|Maternal CD4 count < 350 cells/μL at enrolment||94/607||168/1761||1.83 (1.42, 2.35)||1.84 (1.44, 2.36)|
|Ever vs. never maternal fever during pregnancy||53/376||209/1992||1.34 (1.01, 1.78)||1.04 (0.78, 1.38)|
|Maternal anaemia at Enrolment|| || || || |
|Moderate anaemia (Hgb 8.5 to < 11 vs. ≥ 11 g/dL)||79/587||183/1781||1.38 (1.00, 3.24)||1.25 (0.97, 1.62)|
|Severe anaemia (Hgb < 8.5 vs. ≥ 11 g/dL)||10/56||252/2312||1.77 (1.07, 1.79)||1.61(0.93, 2.81)|
|On antiretrovirals in pregnancy||5/166||257/2202||0.30 (0.13, 0.73)||0.20 (0.08, 0.50)|
|Maternal obstetric history in prior pregnancies/deliveries|| || || || |
|≥ 1 vs. 0 early child deathsa/spontaneous abortions||96/771||166/1597||1.25 (0.97, 1.61)||1.19 (0.92, 1.54)|
|Breast feeding and maternal breast/nipple health|| || || || |
|Any vs. no breast feeding (birth to 6 weeks of life)||230/1989||32/379||1.40 (0.94, 2.10)||1.27 (0.85, 1.90)|
|Any vs. no breast lesions/pain/inflammation, or cracked or bleeding nipple (birth to 6 weeks post-partum)||6/32||256/2336||1.69 (0.81, 3.51)||1.90 (1.02, 3.55)|
|Delivery factors/infant characteristics|| || || || |
|Nevirapine prophylaxis given to:|| || || || |
|Both mother at labour onset and baby within 72 h of birth||60/644||202/1724||0.66 (0.49, 0.90)||0.75 (0.53, 1.08)|
|Baby only within 72 h of birth||110/1047||152/1321||0.74 (0.57, 0.97)||0.84 (0.60, 1.17)|
|Mother at labour onset only||5/60||257/2308||0.59 (0.25, 1.40)||0.67 (0.29, 1.53)|
|Cesarean section vs. other type of birth||23/275||239/2093||0.74 (0.49, 1.12)||0.83 (0.55, 1.25)|
|Premature birth (< 37 vs. ≥ 37 weeks)||49/348||213/2020||1.35 (1.02, 1.81)||1.01 (0.75, 1.35)|
|Female vs. male sex||131/1083||131/1285||1.19 (0.94, 1.49)||1.13 (0.91, 1.41)|
|Low (< 2500 g) vs. normal (≥ 2500 g) birth weight||40/156||222/2212||2.65 (1.96, 3.57)||2.30 (1.71, 3.07)|
|In hospital vs. home/other location of delivery||212/2026||50/342||0.70 (0.50, 0.98)||0.99 (0.66, 1.48)|
|Economic/sociodemographic/temporal factors|| || || || |
|Married/cohabiting vs. single/divorced/widowed/separated||222/2060||40/308||0.82 (0.60, 1.13)||0.73 (0.54, 1.00)|
|Has own income vs. no income||78/813||184/1555||0.81 (0.63, 1.04)||0.76 (0.59, 0.98)|
|Maternal education (≥ 7 vs. < 7 years)||234/2046||28/322||1.32 (0.90, 1.92)||1.31(0.91, 1.92)|
- Top of page
- Limitations and strengths
In this cohort of HIV-positive mothers from Dar es Salaam, Tanzania, enrolled in the study during pregnancy and followed through delivery, 11% of HIV-exposed infants contracted HIV in utero, intra-partum or within the first 6 weeks of life. The 11% HIV MTCT rate observed in this study is 45 to 62% lower than the typically reported 20 to 29% rate of new HIV infections among HIV-positive treatment-naïve pregnant women [21-23] but comparable to the MTCT rates observed in other malaria-endemic African settings where nevirapine prophylaxis was used for prevention of MTCT in the absence of HAART [24, 25]. We found no difference in the risk of HIV MTCT for infants of women with one vs. no malaria episodes in pregnancy and women with and without fever symptoms during pregnancy. However, there was a significant elevation of HIV MTCT risk per malaria episode increment. MIP diagnosis was an independent predictor of HIV MTCT at 6 weeks for infants of mothers with two or more malaria episodes, compared with infants whose mothers were not diagnosed with malaria during the pregnancy. These associations were strongest for infants born to women with fewer than 7 years of education. We found no evidence that the positive relationship between MIP diagnosis and HIV MTCT was mediated by fever symptoms.
We confirm the overall trend of lower HIV MTCT with greater access to HAART in pregnancy  and the positive associations between HIV MTCT risk and maternal immune deficiency [20, 27], child low birth weight [28, 29], and the presence of breast inflammation and nipple lesions in breast-feeding HIV-positive women [20, 30, 31]. Similar to prior reports [32, 33], we found protective associations between indicators of superior socioeconomic position and early HIV MTCT .
Our finding of a statistically significant positive association between MIP and MTCT is corroborated by findings of a twofold higher risk of HIV MTCT among HIV-positive mothers with MIP in the Rakai District of Uganda [7, 10] and the recently reported sixfold elevated odds of early HIV MTCT for infants of Rwandan HIV-positive women with MIP . Our results are further supported by the finding of a higher risk of MTCT among HIV-positive pregnant women with high-density placental malaria in western Kenya  and the recent finding of a MIP associated increased risk of HIV MTCT by Msamanga et al. in a subset of their sample of pregnant HIV-positive women – specifically, those with low viral load .
The above notwithstanding, findings from at least three other epidemiological studies either do not support our findings, with respect to the relationship of maternal MIP to HIV MTCT [13, 14], or are in direct conflict with ours . Specifically, our results are not supported by the overall finding of no association reported by Msamanga et al.  In addition, our finding of a higher risk of HIV MTCT among pregnant HIV-positive women with malarial morbidity stands in contrast to the findings from a Mozambican cohort of 207 HIV-positive mothers enrolled in a trial of intermittent malaria preventive treatment with two doses of SP vs. a placebo .
We note that salient differences between our study and some of the above studies may be partly responsible for these disparate findings. Naniche et al.'s  study included fewer subjects than did ours (n = 207 vs. 2367, respectively), involved very few cases of HIV MTCT (n = 19 vs. 262, respectively), and had complete data on malaria and HIV MTCT for fewer mother−child pairs (n = 153 vs. 2367, respectively), all of which contribute to lower statistical power relative to the present study. These limitations make it difficult to determine whether their findings were true effects or the result of random variation with respect to placental malaria rates and their relationship to HIV MTCT. The findings also may be different when the same question is investigated in the context of a larger, adequately powered sample that includes more mother−child pairs and MTCT events. Despite these potential explanations for the differences in results, rigorously designed large studies using gold-standard malaria diagnostic criteria will be necessary to confirm or refute our findings.
According to the most recent UNAIDS (Joint United Nations Programme on HIV/AIDS) report, there has been an overall 24% reduction in MTCT between 2001 and 2009 . This encouraging trend has contributed to the belief that the virtual elimination of MTCT is achievable with the implementation of proven strategies for prevention of HIV transmission . Yet, the 22% prevalence of clinical malarial morbidity in this cohort is comparable to estimates from other investigations among HIV-positive women from the region prior to widespread access to antiretroviral drugs in pregnancy [6, 7, 10, 13]. Of note, the rate of malarial morbidity has been assessed using varied approaches, including clinical diagnoses and rapid diagnostic and malaria parasitaemia tests. All methods suggest that the incidence of malaria has been on the decline in certain regions of Tanzania, particularly in the island of Zanzibar, since 2000 . Nevertheless, a significant malaria burden remains, particularly for noncoastal regions in the Republic of Tanzania. Hence, the results of this study provide an impetus to provide more comprehensive malaria prevention measures.
A recent review article suggested that coinfections, including malaria, tuberculosis and herpes simplex virus type 2, in high HIV-prevalence areas could be important, persistent drivers of HIV transmission  in the HAART era. The results reported herein, and the recently reported elevated risk of postnatal HIV infection for breast-feeding infants of HIV-positive women with malaria compared with those without malaria, provide empirical evidence in support of this position . That the association between MIP diagnosis and HIV infection at birth was slightly attenuated but still statistically significant after controlling for nonspecific fever symptoms suggests that the observed relationship may reflect malaria-parasite-induced immune suppression and HIV viral load amplification. Malarial morbidity is associated with lower immune fitness in HIV-positive persons [8, 9, 37]. The ubiquity of malarial morbidity among pregnant women in SSA may directly counteract the health benefits of increased HAART access for pregnant HIV-positive women and thus has real potential to limit the effectiveness of prevention of MTCT programmes in this population. Our results suggest that maternal malarial morbidity in pregnancy is likely to remain an important independent risk factor for HIV MTCT in malaria-endemic regions of SSA, even when multiple confounders, including maternal immunological status, nonspecific fever symptoms, and the expected beneficial impact of maternal access to HAART during pregnancy, are accounted for.
Limitations and strengths
- Top of page
- Limitations and strengths
The most important limitation of this study is the use of a clinically defined malaria diagnosis as a surrogate for malarial morbidity. This may have resulted in over-diagnosis of malaria in this study. The extent of over-diagnosis of malaria is unclear, as our cumulative 16.6% prevalence of clinical MIP is lower than the 20.4% clinical malaria prevalence reported among pregnant women from Moshi, Tanzania , the 23% prevalence found among pregnant HIV-positive women from Uganda , and the 21% malaria prevalence among pregnant HIV-positive women from Rwanda, where more rigorous diagnostic criteria were employed . We acknowledge this limitation of our data and stress the utility of rapid diagnostic assays that are increasingly available at reasonable cost to facilitate accurate diagnosis of malaria, whenever possible, even in the most resource-limited settings. This limitation notwithstanding, our study represents the largest prospective investigation of whether newborns of HIV-infected pregnant women with diagnosed MIP are at elevated risk of HIV infection within 6 weeks of birth in an area of high malaria endemicity, with control for an extensive array of relevant confounders − including number of fever symptoms in pregnancy, maternal HAART use in pregnancy and baseline immunological status, maternal and child nevirapine prophylaxis, and differences in sociodemographic and child-related characteristics.
Our results suggest that malarial morbidity in pregnant HIV-positive women might be an independent risk factor for HIV MTCT in SSA. Our finding that the association between MIP diagnosis and HIV MTCT was not explained by fever symptoms suggests that MIP in HIV-positive women may elevate the incidence of HIV infection in co-endemic regions independent of nonspecific fever symptoms. Hence, the risk of HIV transmission may remain elevated in HIV-positive women in spite of the increasing HAART availability and improved coverage of prevention of MTCT services. Attainment of the expressed goal of zero MTCT by 2015, as noted in the most recent UNAIDS report in malaria and HIV co-endemic settings, will be enhanced by understanding the contribution of malaria and other coinfections to HIV transmission and by ramping up control efforts to mitigate such risks. Given the limitations described above, further studies on this subject, with more rigorous malaria definitions, are warranted to further elucidate the relationship of laboratory-confirmed malarial morbidity in pregnancy and MTCT.
In the light of the grave health risks associated with MIP, the special vulnerability of HIV-positive women to malaria, and its potential contribution to elevated risk of HIV MTCT, we believe that large-scale adoption and consistent implementation of malaria prevention measures, including universal access to insecticide-treated bed nets, among HIV-positive pregnant women are warranted. An additional prevention strategy that might improve patient compliance with malaria prevention measures is large-scale dissemination of information regarding the possible malaria-associated higher risk of HIV MTCT. Further, all HIV-positive adults may benefit from active, rather than passive, clinical assessment for malaria and its treatment when indicated as part of routine health care as asymptomatic malaria parasitaemia is likely to be common among HIV-positive adults.
Conflicts of interest: The authors do not have commercial (e.g. pharmaceutical stock ownership or consultancy) or other associations that pose a conflict of interest in the collection, analysis, presentation and interpretation of these data.
Funding: This work was supported by the National Institute of Child Health and Human Development, grant number R01HD043688. CD was supported in part by K24 HD058795. The funder of this study had no role in the design, data collection, analysis, interpretation or writing of this report.
Authorship: The corresponding author had full access to all the data in the study and the final responsibility for the decision to submit for publication.