Timing of breast milk HIV-1 transmission: a meta-analysis.

OBJECTIVE: To define the frequency and timing of breast milk transmission of HIV-1. DESIGN: Meta-analysis of data abstracted from published literature. SUBJECTS: Participants in prospective cohort studies of MTCT of HIV-1. Cohorts were separated on the basis of breast feeding duration. INTERVENTIONS: None. MAIN OUTCOME MEASURES: HIV-1 transmission rates. RESULTS: Two thousand three hundred and seventy five HIV-1 infected women and their infants, 499 of whom breast fed, the estimated risk of breast milk HIV-1 transmission was 16% (95% CI: 9, 22%). Among breastfeeding infants, forty seven per cent of HIV-1 infections were attributable to breast feeding. Breast milk transmission risk was 21% (95% CI: 10, 33%) in cohorts with mean/median duration of breast feeding > or = 3 months and 13% (95% CI: 4, 21%) in cohorts with median duration of breast feeding < 2 months. In a separate analysis of 702 infants with prolonged duration of breast feeding, the risk of late postnatal transmission (infection occurring later than three to six months of age) was four per cent (95% CI 2, 5%). CONCLUSIONS: This analysis suggests that breast milk transmission of HIV-1 is substantial and continues throughout the postnatal period. Early cessation of breast feeding at six months would avert some but not most infant HIV-1 infections due to breast feeding. While recently published studies showing some effectiveness of antiretrovirals early during the breast feeding period are encouraging, prevention of breast milk HIV-1 transmission needs to remain a high research priority.

Effect of breastfeeding on mortality among HIV-1 infected women: a randomised trial.

BACKGROUND: We have completed a randomised clinical trial of breastfeeding and formula feeding to identify the frequency of breastmilk transmission of HIV-1 to infants. However, we also analysed data from this trial to examine the effect of breastfeeding on maternal death rates during 2 years after delivery. We report our findings from this secondary analysis. METHODS: Pregnant women attending four Nairobi city council clinics were offered HIVtests. At about 32 weeks' gestation, 425 HIV-1 seropositive women were randomly allocated to either breastfeed or formula feed their infants. After delivery, mother-infant pairs were followed up monthly during the first year and quarterly during the second year until death, or 2 years after delivery, or end of study. FINDINGS: Mortality among mothers was higher in the breastfeeding group than in the formula group (18 vs 6 deaths, log rank test, p=0.009). The cumulative probability of maternal death at 24 months after delivery was 10.5% in the breastfeeding group and 3.8% in the formula group (p=0.02). The relative risk of death for breastfeeding mothers versus formula feeding mothers was 3.2 (95% CI 1.3-8.1, p=0.01). The attributable risk of maternal death due to breastfeeding was 69%. There was an association between maternal death and subsequent infant death, even after infant HIV-1 infection status was controlled for (relative risk 7.9, 95% CI 3.3-18.6, p<0.001). INTERPRETATION: Our findings suggest that breastfeeding by HIV-1 infected women might result in adverse outcomes for both mother and infant.

Postpartum endometritis caused by herpes simplex virus.

BACKGROUND: Herpes simplex virus (HSV) is rarely the causative agent of endometritis and is usually found in association with pelvic inflammatory disease. Only one case of postpartum HSV endometritis has been reported. CASES: We describe two cases of herpes simplex postpartum endometritis. Neither patient had genital HSV lesions noted at the time of delivery. The first case developed after a preterm cesarean delivery in an 18-year-old primipara. She had persistent puerperal fever despite broad-spectrum anti-microbial treatment. The second case was a 16-year-old primipara whose vaginal delivery was complicated by severe postpartum endometritis. Vulvar and endometrial cultures were positive for HSV alone in both patients. Both infants died from disseminated HSV infection. CONCLUSION: Herpes simplex virus can cause clinical postpartum endometritis.

Iatrogenic epidemics of puerperal fever in the 18th and 19th centuries.

The epidemics of puerperal fever in the 18th and 19th centuries began soon after the creation of Lying-in hospitals in the mid-18th century. The primary purpose of these hospitals was to provide physicians with training in obstetrics in general and in forceps deliveries in particular. The first reports describing epidemics of puerperal fever, its contagiousness and control were made by British physicians in the latter half of the 18th century. Alexander Gordon provided epidemiological evidence of contagion in 1792, and Oliver Wendell Holmes in the USA reviewed these reports in his paper on outbreaks of puerperal fever around Boston in 1843. Ignaz Semmelweis in Vienna, unaware of previous work on this disease, re-discovered the actions required to control the contagion in 1847, but published his paper much later in 1861. A few enlightened doctors struggled to prove that puerperal fever was contagious and could be spread by doctors and midwives. Their peers and colleagues predominantly displayed apathy and ignorance until forced to act by the weight of evidence. However, it was the multitude of parturient women who paid the ultimate price for these iatrogenic epidemics.

Streptococcus pneumoniae invasive disease in the neonatal period: an increasing problem?

UNLABELLED: A series of 11 cases of invasive infection with Streptococcus pneumoniae, occurring over an 11-year period, is reported. Eight of the 11 cases occurred during the final 2 years of the study suggesting that the incidence of infection may be increasing. Infection carries a high mortality (3/11). Morbidity includes meningitis, convulsions and respiratory failure. In one case S. pneumoniae meningitis occurred in both mother and newborn. Most mothers who carried the organism were asymptomatic at the time of delivery. CONCLUSION: S. pneumoniae should be specifically sought in swabs taken from the pregnant mother and newborn and if isolated, even in the absence of symptoms, antibiotic therapy against the organism should be strongly considered.

[Puerperal infections. From Semmelweis to current problems]. / Infeksjoner i tilslutning til fødsel. Fra Semmelweis til aktuell problematikk.

Maternity hospitals began to be established in the middle of the 18th century to relieve the distress of the poor. As the number of lying-in hospitals increased, so did the cases of puerperal sepsis. The death rate from puerperal sepsis in Norway was high and remained so until 1934. Semmelweis studied the maternal mortality rates in two obstetric clinics in Vienna for the years 1841-46. He declared that puerperal fever was transmitted by the doctors who taught in the dissecting room and went straight from there into the labour wards. I 1847 he instructed all doctors or students to scrub their hands in a solution of chloride of lime before they delivered, examined or touched any patient. The haemolytic streptococcus was finally proved to be the cause of puerperal sepsis by Louis Pasteur in 1879. There was a significant drop in mortality rates in maternity hospitals after the introduction of antiseptic and aseptic techniques around 1880. Deaths from puerperal fever paralleled deaths from erysipelas, and both conditions declined after 1934. Puerperal fever and pelvic inflammation is still a clinical problem. The author discusses sexually transmitted diseases and multibacterial causes.

Breast-feeding during primary maternal human immunodeficiency virus infection and risk of transmission from mother to infant.

Examination of breast-fed infants of the complete cohort of Australian women whose primary human immunodeficiency virus (HIV) infection occurred postpartum allows for an estimate of risk of transmission of HIV. Ten women with no other risk factors were infected via blood transfusion postpartum. They breast-fed for up to 9 months; 2 of their infants were infected. Another woman, who shared needles for intravenous drug use, seroconverted 6-10 months post-partum. She breast-fed for 14 months. Retrovirus was visualized in the cellular and cell-free fraction of her milk by electron microscopy. Infection in her infant was confirmed at 12 months. Thus, 3 of the 11 babies at risk became infected, providing an estimate of risk of 27% for breast-feeding during primary maternal infection (95% confidence interval, 6-61%). These data establish the association of primary maternal HIV infection and breast-feeding with a high risk of transmission to infants.

Recurrent group A streptococcal carriage in a health care worker associated with widely separated nosocomial outbreaks.

Nine postpartum infections (five bacteremias, three cases of endometritis without bacteremia, and one infected episiotomy site) caused by an M-nontypable, T-28 strain of group A Streptococcus occurred during a 9-week period in 1987. Seven cases were cared for by one obstetrician, who was also present in the delivery suite when the remaining patients delivered. This individual was found to be an anal carrier of group A Streptococcus with the same M and T types. During the cluster, the attack rate for vaginal deliveries performed by this individual was 18% (6 of 34 patients). The individual was treated with penicillin V (500 mg four times a day for 10 days), rifampin (600 mg twice a day for 5 days), and hexachlorophene showers. Surveillance cultures of the physician were negative 1 week, 1 month, and 3 months after completion of therapy. No additional cases were identified among the next 210 vaginal deliveries performed by this individual. Fourteen months after therapy, four new cases occurred during 2 days. The physician was found to be heavily colonized once again with the original strain of group A Streptococcus and was treated with rifampin (600 mg twice a day) and oral vancomycin (250 mg four times a day) for 7 days. An open-ended regimen of penicillin V (250 mg/day) and periodic surveillance cultures was begun. During the next 19 months, this physician performed 275 vaginal deliveries, one of which resulted in an M-nontypable, T-28 group A streptococcal infection, at a time when the physician's surveillance cultures were negative. It is unclear how long a colonized health care worker who causes nosocomial group A streptococcal disease must be treated or monitored, but there is some risk after more than a year. Long-term surveillance or prophylaxis may be useful in some circumstances.

An outbreak of puerperal fever caused by group C streptococci.

Between 19 February and 18 April 1987, 33 confirmed cases of puerperal fever caused by Streptococcus equisimilis serotype T204 occurred at three hospitals in and around Chelmsford. Most of the cases (70%) occurred on one ward, in which toilet seats and a shower are believed to have aided transmission, although insufficient data were obtained to exclude a role for person-to-person spread. Possession of M-protein antigen was demonstrated in the outbreak strain.