Expert consensus on breastfeeding in case of maternal infections

After completing this article, readers should be able to: Over the past 50 to 60 years, human milk has been described and recognized as the best first food for human infants; breast is best! Human milk provides substantial nutritional, cognitive, emotional, and immunologic benefits for the infant. Such ongoing acclamation is based on the observations and experiences of mothers, families, midwives, doulas, nutritionists, nurses, physicians, and scientists.Over the past 30 years, scientific study and research have accumulated and now constitute a large body of evidence documenting the actual benefits of breastfeeding for the infant and the mother. This article examines and references much of this evidence-based data in describing human milk and how it contributes to the health and well-being of infants and mothers.The Agency for Healthcare Research and Quality (AHRQ) Report on Breastfeeding in Developed Countries summarizes evidence (published in English through May 2006) on breastfeeding in maternal and infant health. (1) More than 9,000 abstracts were considered, and data from more than 400 individual studies were included after evidence-based review of meta-analyses, updated systematic review of the data, and newly performed systematic reviews. It is important to emphasize that this report included data from developed countries only. Table 1presents definitions of breastfeeding that are particularly useful in "quantification" as standard definitions used in clinical studies.Nineteen specific outcomes were reviewed by the AHRQ research team, including 13 for term infants and six for mothers. The outcomes for infants were: incidence of acute otitis media, atopic dermatitis, gastrointestinal (GI) infections, lower respiratory tract infections, asthma, obesity, type 1 and 2 diabetes, childhood leukemia, infant mortality, and sudden infant death syndrome as well as cognitive development and the risk of cardiovascular disease. Factors studied in mothers were: return to prepregnancy weight and incidence of type 2 diabetes, osteoporosis, postpartum depression, breast cancer, and ovarian cancer.For infants, the meta-analyses or systematic reviews strongly favored breastfeeding over not breastfeeding for a reduced risk of acute otitis media, GI infections, asthma (regardless of whether there was a family history of asthma), type 2 diabetes, leukemia, and sudden infant death syndrome. The meta-analysis of GI infections reported a crude odds ratio for 14 cohort studies of 0.36 (95% confidence interval [CI] 0.32 to 0.41) strongly favoring breastfeeding (ever) in reducing the risk of GI infection in infants younger than 1 year of age (Fig. 1). Another analysis reported on two case-control studies demonstrating a summary odds ratio of 0.54 (95% CI 0.36 to 0.80) again favoring breastfeeding. A separate analysis demonstrated that infants breastfeeding exclusively for greater than 3 months' or greater than 6 months' duration had significant reductions in the risk of acute otitis media compared with infants who were never breastfed. The analysis of infants developing atopic dermatitis (who had a family history of atopic disease) demonstrated that the risk for atopic dermatitis was lower in infants breastfed exclusively for longer than 3 months compared with children who were breastfed for less than 3 months. An analysis examining lower respiratory tract infections showed an overall reduced risk of hospitalization due to lower respiratory tract infections in infants (<1 year of age) who were breastfed exclusively for 4 months or longer compared with infants who were never breastfed (Fig. 1).The report presented two meta-analyses and a systematic review demonstrating a reduced risk of breast cancer associated with breastfeeding primarily in premenopausal women. One meta-analysis that included 45 studies showed a 4.3% reduction in risk for each year of breastfeeding. A second meta-analysis that included 23 studies demonstrated a 28% reduced risk of breast cancer for 12 months or more of breastfeeding. The AHRQ team performed a meta-analysis of 9 "fair" quality studies that included 4,387 cases of ovarian cancer and more than 10,000 controls. This new meta-analysis showed an association between breastfeeding and a reduced risk of ovarian cancer. Cumulative lifetime breastfeeding duration of more than 12 months was associated significantly with a decreased risk of ovarian cancer compared with never breastfeeding. This benefit was not seen for cumulative duration of breastfeeding of less than 12 months (Fig. 2). Additional data are needed to confirm a dose-response relationship between breastfeeding and a reduced risk of ovarian cancer.The analysis for type 2 diabetes, involving two very large cohort studies, showed that breastfeeding was associated with a reduced risk of developing type 2 diabetes in women who did not have a history of gestational diabetes. Each additional year of lifelong breastfeeding was associated with a 4% to 12% risk reduction in the two different cohorts. Breastfeeding did not appear to lead to a reduced risk of developing type 2 diabetes in women who had gestational diabetes. The studies on return to prepregnancy weight, osteoporosis, and postpartum depression were unable to demonstrate an association between breastfeeding and these specific maternal health outcomes due to methodologic issues and the effect of other contributing factors or confounders.These high-quality, evidence-based data from the AHRQ Report support breastfeeding as providing significant health benefits to both the mother and infant, even in developed countries. A larger body of evidence from developing countries examines the benefits of breastfeeding in locales where the risk of infection in infants and children is high due to poor sanitation, low water quality, contaminated food sources, and other variables. This benefit is well documented for diarrheal disease, respiratory infections, and otitis media.Beyond the evidence-based medicine measures is the realm of attachment and bonding between infant and mother and the psychological and developmental benefits of breastfeeding for the mother and infant. How these spheres are influenced by breastfeeding has been studied extensively in many different countries and cultures. Close and frequent contact between the mother and infant, especially skin-to-skin contact, affects the mother's attachment to the infant positively. The positive feelings affected by the close (skin-to-skin) and frequent early contact facilitate successful breastfeeding, longer duration of breastfeeding, and more attachment behavior (fondling, kissing, and caressing the infant). Recognition of these effects has led to more direct contact between the infant and his or her parents in the delivery and postpartum areas. Such recognition has supported the recommendation to allow placement of the infant in direct skin-to-skin contact with the mother in the first hour after birth to encourage successful breastfeeding. The multiple contributory factors to infant development makes it difficult to demonstrate a causative connection between early skin-to-skin contact or breastfeeding and overall infant and child development, emotional stability, personality, attachment, or person-to-person interactions.The impact of different methods of feeding infants on the onset of allergy has been researched. A meta-analysis of 18 prospective studies involving term infants who had a family history of atopy found a reduction of 42% (95% CI, 8% to 59%) in the risk of atopic dermatitis for infants breastfed for at least 3 months compared with those who were breastfed for less than 3 months. (1)Studies on asthma were less definitive. The AHRQ reported that breastfeeding for at least 3 months was calculated to provide a 27% (95% CI, 8% to 41%) reduction in the risk of asthma in children who had no family history of asthma compared with children who were not breastfed. Children who had a family history of asthma had a 40% risk (95% CI, 18% to 57%) reduction in the occurrence of asthma before 10 years of age if breastfed for 3 months compared with those not breastfed. The risk for children older than 10 years is less clear. Exclusive breastfeeding for the first 6 months is recommended by the American Academy of Pediatrics (AAP) for many reasons, including reducing the risk of allergy. Further if supplementation is necessary, an amino acid-based formula is recommended (hypoallergenic formula).The milk available in the breast after 16 weeks' gestation is called prepartum milk. When the infant delivers and is placed at the breast (or is allowed to find his or her way) to suckle, the milk is colostrum for the next few days. A gradual change from this transition milk to mature milk usually occurs by 14 days. Postpartum colostrum is called "the first immunization" because it contains high concentrations of antibodies and other infection-protective elements, including cells. Colostrum is high in total protein, low in carbohydrate, and lower in fat than mature milk. The amount of milk produced in the first 24 hours after birth is approximately 50 g, with 190 g produced by the second 24 hours, 400 g by the third 24 hours, and 1,100 g/24 hours by the fourteenth day (800 to 1,000 mL). Human milk and cow milk differ substantially in their composition (Table 2).The proteins differ in quality and quantity. In its unaltered form, cow milk contains too much protein, too much casein, too much sodium, and too much phosphorus and has too high a solute load for a human infant. Formulas have been designed to improve these issues. Cow milk does not contain any taurine, an amino acid that has high concentrations in human milk and is essential to infant brain growth. The profile of amino acids in cow milk differs significantly from human milk, especially phenylalanine and tyrosine, which are at high concentrations in cow milk and formula and contribute to problems in phenylketonuria.The effect of higher protein in infant formula recently has been questioned by investigators of the obesity epidemic. It has been suggested that a constant intake of high protein in infancy stimulates the metabolic rate and contributes to the long-term obesity of formula-fed infants. After processing, cow milk and infant formulas contain no cells, no enzymes, and no antibodies or other active protective agents and do not support the maintenance of physiologic flora of the infant's GI tract.Docosahexaenoic acid (DHA) has received considerable attention because studies in preterm infants have demonstrated improved visual acuity and auditory acuity in those fed human milk compared with those fed regular preterm formula. When DHA was added to formula, the acuity improved but did not reach the scores achieved by breastfed infants. DHA and omega-3 fatty acids derived from bacterial culture are added to many formulas, although a benefit has not been proven.Vitamin concentrations in human and cow milk are comparable, except for vitamin C, which is significantly higher in human milk (100 mg/d). Vitamins in infant formula exceed the concentrations found naturally. Vitamin D has become an important issue because the vitamin D generated in human skin from exposure to sunshine has diminished through the use of sunscreen, wearing of clothing to shade from the sun, pollution of the air by industrial waste, and migration of dark-skinned populations to climates with less sun. Pregnant women have been documented in recent decades to pass less vitamin D to the fetus, so newborns lack sufficient stores at birth. As a result, breastfed infants now are given 400 U daily from birth. Investigative work continues on the benefits of providing pregnant and lactating women with 1,000 U of vitamin D daily. Most, but not all, infant formulas contain 400 U of vitamin D in 26 to 32 oz of reconstituted formula.Vitamin K content presents an important issue for the newborn who is born with low concentrations, even when the mother receives extra doses at the time of delivery. Hemorrhagic disease of the newborn, with GI or intracranial hemorrhage and generalized bleeding, can present early or up to several weeks after birth and is due to relative deficiencies of vitamin K-dependent coagulation factors. Such deficiency has resulted in all newborns receiving 1 mg of vitamin K intramuscularly at birth, regardless of the proposed mode of feeding. If vitamin K is administered orally, multiple doses should be provided. Formula has extra vitamin K, so an infant who receives 26 to 32 oz per day of formula receives 4 mg of vitamin K orally daily. Concentrations in human milk and cow milk are lower.Neonates and infants are immunologically immature and at increased risk for infection. Such developmental immune defects are only some of the factors that place infants at greater risk of infection. In the first 6 postnatal months, phagocyte function is immature, with limited ability to migrate to the site of infection, and reserve production of phagocytes in response to infection is limited. Cell-mediated immunity develops throughout childhood. Defects are particularly apparent in the first 6 months after birth, including decreased cytokine production, decreased natural killer cell function, poor stimulation of B cells for antibody production, and limited numbers of mature functioning T cells. In addition, function of the classical and alternative pathways of complement formation and activation is decreased. Immunoglobulin (Ig) production is limited in amount and repertoire, including poor isotype switching, limited IgG subclass production, and low serum IgA concentrations through 7 to 8 years of age.Human milk not only bolsters the infant's immature immune response by providing numerous bioactive factors that dynamically affect the innate, adaptive, and mucosal immunity against specific infectious agents but also by influencing immune system development and maturation of the mucosal barrier. A very clear dose-response relationship has been documented between the amount (full [exclusive], partial, token) and duration of breastfeeding and the benefits gained by the infant and mother. (See Table 1 for the definitions.) Most bioactive factors exert their effects at the level of the mucosal immune system. Igs are the best recognized and studied bioactive components in human milk. Igs in human milk are predominantly secretory IgA, with much smaller amounts of IgM and IgG. Colostrum contains higher amounts of Igs and immunologically competent mononuclear cells than transitional or mature milk. The Igs function by binding directly to specific microbial antigens, blocking binding and adhesion to host cells, enhancing phagocytosis, and modulating local immune response. Table 3 in the online edition of this article lists specific antibodies that have been identified in human milk.The actual antibodies against specific microbial agents present in an individual woman's milk depends on her exposure and response to the particular agents. Not every mother has antibodies in her milk against every microbe. The predominant action of Igs in human milk is seen at the mucosal level of the infant's mouth, nasopharynx, and GI tract, where they bind to and block the infectious entry of microbial agents through the mucosal barrier. Although best recognized and remembered in association with "specific" protection against individual infectious agents, Igs provide only a small portion of the overall immunologic benefit of human milk.Other important individual bioactive proteins include lactoferrin, lysozyme, alpha-lactalbumin, and casein. Lactoferrin exerts its effects via iron chelation, which contributes to limiting bacterial growth, blocking adsorption and penetration of viruses and adhesion of bacteria, and enhancing intestinal cell growth and repair. Lysozyme binds to endotoxin, increases macrophage activation, and contributes to bacterial cell wall lysis. Lactalbumin transports calcium and enhances the growth of Bifidobacterium, and a modified lactalbumin (in the gut) affects immune modulation. Casein limits adhesion of bacteria and facilitates the growth of Bifidobacterium. Carbohydrates are an important nutritional component in human milk, and the specific carbohydrates lactose, oligosaccharides, and glycoconjugates act as bioactive factors. Oligosaccharides act as prebiotics, enhancing the growth of specific probiotic bacteria in breastfed infants, and both oligosaccharides and glycoconjugates bind specific microbial antigens.Lipids in the form of triglycerides, long-chain polyunsaturated fatty acids, and free fatty acids (FFAs) have a lytic effect on many viruses and are active against Giardia as well. Nucleotides, nucleosides, and nucleic acids comprise more than 15% of the nonprotein nitrogen in human milk. Nucleotides serve many crucial roles in energy metabolism, nucleic acid production, and signal transduction, processes of increased importance during the cellular activation and replication related to an active immune response. Research related to the "essential" nature of nucleotides in protection against infection has led to the addition of nucleotides to some infant formulas. Cytokines and soluble receptors of cytokines are other examples of bioactive factors that serve several functions. Cytokines can act as functional growth factors and have both inflammatory and anti-inflammatory effects in different situations.Hormones and growth factors, including erythropoietin, epidermal growth factor, insulin, insulin-like growth factor, nerve growth factor, and transforming growth factor-alpha, stimulate the growth and maturation of the GI tract and, to a degree, systemic growth. These bioactive factors are less specific than Igs, but by acting in concert with multiple factors, they provide the major portion of protective effects from human milk.The concept of immune protection without an extensive and potentially damaging inflammatory response is gaining in significance in general medicine and in breastfeeding medicine. Many of the same protective bioactive factors act at the mucosal level without stimulating a significant inflammatory response, which indirectly decreases inflammation and possible local tissue damage. Certain factors limit further inflammatory stimulation: lactoferrin blocks activation of complement, and lysozyme inhibits neutrophil chemotaxis and limits formation of toxic oxygen radicals. Various enzymes in human milk break down inflammatory molecules: catalase destroys hydrogen peroxide, histaminase destroys histamine, and arylsulfatase degrades leukotrienes. Various soluble receptors in human milk (IL-1Ra, STNF-alpha R1 and R2) bind to specific cytokines, blocking their inflammatory action.Vitamins A, C, and E, which are present in higher concentrations in human milk than in cow milk, scavenge oxygen radicals. Catalase and glutathione peroxidase as well as lactoferrin serve multiple purposes and have antioxidant properties. Prostaglandins in human milk limit superoxide production. The sum total of these anti-inflammatory effects of human milk occurring at the mucosal level limits damage to the mucosal barrier and facilitates its ongoing growth and development to further enhance human milk's protection of the infant.The concept that "normal" intestinal microflora influence the development of the local mucosal immunity and even "prime" systemic immunity is being supported by new research. Pathogen-associated molecular patterns in the microflora are recognized by toll-like receptors and may contribute to the expression of toll-like receptors on intestinal epithelial cells as well as lead to "programming" of systemic T-helper cell type 1 (TH1), TH2, and TH3-like T-cell responses. Probiotic bacteria are organisms that live in the additional benefits on the which include with between cells, production of increased production, increased production of specific fatty and development of the mucosal immune usually are oligosaccharides after lower the of the local and the amount of available enhance the growth of probiotic bacteria in the Oligosaccharides are the third component in human milk in of quantity. Cow milk and formula contain less than of the oligosaccharides in human milk by The microflora of breastfed infants include and Bifidobacterium, which comprise up to of the The small portion of bacteria include and as well as and other organisms in even smaller The microflora of formula-fed infants are primarily of organisms and in much larger numbers than in breastfed infants and include very small amounts of and Bifidobacterium. and oligosaccharides, acids, including which lower the in the and limit the growth of as and molecular that by of are the of GI microflora and factors influencing intestinal and immunologic development at the level of the studies have suggested a protective of specific intestinal microflora against the risk of developing in preterm and very all the evidence for the immunologic benefits of human milk and the protection infants against specific organisms and separate clinical data also the of specific infections through human milk or direct contact with an maternal Although only a few infections are through human milk human viruses 1 and 2 and and these viruses are important because of their for or in the infant. In addition, other infections that are by human milk or breast contact should be in specific of infection through human milk is compared with the more of for and infants. infection is occurring the infection is due to through the birth and postnatal infection occurs via or contact other than with the The predominant of and the of infection are important in different clinical of the for via human milk for organisms can be and 4 and in the online edition of this article for of the for bacteria and infection of the mother with or is a to breastfeeding. on have documented approximately a rate in breastfed infants, rate in infants, and rate in exclusively formula-fed infants. that 1 of human milk can contain 1,000 T cells with studies from of that have high of have reported significant reductions in of the from mother to infant with of breastfeeding or limiting breastfeeding to less than 6 months' infection in the mother is infection that can be via human milk to the infant. In the and other of the where is successful and to breastfeeding are and mothers who have infection have been not to their infants. In of the where there is an increased risk of infectious nutritional and significant and for infants who are not breastfed and feeding is not breastfeeding by an mother can the infant the best of is in human milk and can be as and Factors associated with an increased risk of via breastfeeding include feeding breastfeeding, duration of breastfeeding, maternal and high lower in the and or in the mother. studies have documented that of the mother with breastfeeding can lead to lower for infants and lower for both mothers and infants. of the infant with breastfeeding also has been associated with decreased to the infant. Additional research on breastfeeding, and the infant's and growth are needed before an can be infection or even recent infection in a breastfeeding mother is not a to breastfeeding. infection via human milk occurs but is if significant in the term infant. In breastfeeding has been described as immunization" in the term infant. and very infants are at risk for significant postnatal infection via breastfeeding. This postnatal infection is more to between 3 and 12 weeks when occurs and milk can the load in human milk. A has been for infants human milk in that include preterm and very infants. The mothers for before providing human milk to their infants, or human milk from mothers before its and infants in the for evidence of acute the protective effects of a is the only other for which there has been evidence for via human milk with any studies the of as well as IgM and IgG antibodies against in human milk, but no clear evidence significant in infants through breastfeeding by mothers who have infection. The viruses as or is through contact with skin that contain the on the mother's or not through in the milk. of breastfeeding and milk from the mother's breast that has an identified due to of these viruses may be for the infant with maternal usually is to allow breastfeeding to via the respiratory respiratory acute respiratory are not through human milk. Most by the time a specific respiratory is in the the infant has been via respiratory is no to breastfeeding or the use of human milk, except when disease in the mother the ability to human milk. The numerous bioactive factors Igs if it is early in the maternal in human milk can provide the infant some ongoing bacterial infections in the mother is infection of the or breast or breast that the bacteria the milk or directly the infant's (See Table 4 for bacterial infections in the The risk of in the mother is related to via respiratory which is the same for breastfeeding or formula-fed infants in contact with their mothers. or of the breast are Breastfeeding or use of human milk from the mother who has can the mother is receiving and the infant is receiving or A infection of the breast can with breastfeeding. Breastfeeding or use of human milk can when the mother is with the after a during the mother's 24 hours of for the infant in with the maternal additional the same used to a specific infection in the mother are used and are in the infant and in the mother's milk. do human milk, but usually in very low

Cytomegalovirus Infection

Preventing Postnatal Cytomegalovirus Infection in the Preterm Infant: Should It Be Done, Can It Be Done, and at What Cost?

Congenital Cytomegalovirus

Congenital infection with human cytomegalovirus (HCMV) is most common intrauterine acquired virus infection in infants in the developed world. Rates of congenital HCMV infection range from 0.2%-2.0% in live births. Although maternal infection with this virus rarely results in clinical symptoms, approximately 10% infants born with congenital HCMV infection can exhibit symptomatology ranging from mild hepatitis to severe multiorgan dysfunction, including damaging central nervous system infection. CNS infection can result in microcephaly, retinitis, and abnormalities in psychomotor function. More commonly, infants are clinically asymptomatic at birth but between 10-20% of infected infants will exhibit long term deficits in neurological function, with hearing loss being the most common long-term sequelae. Congenital HCMV infection is thought to be the most common non-familial cause of hearing loss. Although these characteristics of congenital HCMV infection are well described in studies from the developed world, little is known about the natural history of this infection in resource constrained countries. However, several studies have demonstrated that the incidence of congenital HCMV infection increases with increasing maternal infection. Recent findings from Brazil and India are consistent with these earlier studies and indicate that congenital HCMV infection occurs in 1-2% of newborn infants in most of the world's populations. Because HCMV infection is universal in these maternal populations and infection is acquired early in life, these findings indicate that maternal immunity to this virus is insufficient to prevent infection and perhaps can only modulate the incidence of disease in infected infants. Studies from the US have demonstrated that infected infants born to women with preconceptional immunity exhibit rates of developmental abnormalities similar to those infants born to women with primary infection acquired during pregnancy. The mechanisms that account for the inability of maternal immunity to prevent infection and limit disease in the developing fetus infected with HCMV have not been defined, but reinfection with new strains of virus has been shown to occur in normal host following community exposure. Reinfection of previously infected hosts with new strains of virus is common in animal models and recent studies in normal women suggest that rates of reinfection could exceed 20% per annum. HCMV has been shown to encode a number of viral functions that can evade both innate and adaptive immunity in-vitro and in experimental animal models. Although antiviral antibodies have been shown to neutralize virus in-vitro, strain dependent virus neutralizing antibody responses have been well described and appear to arise from minor sequence variation (1-3%) in some envelop glycoproteins such as gB whereas significant variations of > 25% have been reported in other envelop glycoproteins (gN). Whether these differences account for reinfection with different strains of HCMV and contribute to disease in congenitally infected infants remains to be determined. However, the apparent contribution of reinfection to the natural history of this congenital infection in the developing world suggests that HCMV could be a significant cause of morbidity in infants in resource-constrained countries as well as in the developed world. from Fourth Dominique Dormont International Conference. Host-Pathogen Interactions in Chronic Infections Paris, France. 13-15 December 2007

Screening for congenital cytomegalovirus infection: A tapestry of controversies

Microbial antigen in human milk: a natural vaccine?

Comparative major oligosaccharides and lactose between Chinese human and animal milk

Mother-to-child transmission (MTCT) of cytomegalovirus (CMV) occurs transplacentally (congenital infection), during birth and through breast milk, although the latter 2 modes of transmission are not associated with the central nervous system sequelae that occur with congenital infection. CMV persists indefinitely in its human host, and MTCT can occur if the mother was infected in the past or during the current pregnancy. The goal of efforts to prevent MTCT of CMV is to prevent congenital infection, an important cause of disability due to hearing loss, impaired vision, cognitive impairment, and neuromotor deficits. Vaccines for prevention of maternal and congenital CMV infection are being developed but will not likely be available for at least a decade. Rather than waiting for an effective vaccine to solve the problem, more effort must be devoted to defining the potential for public health measures to prevent congenital CMV infection by reducing rates of maternal infection during pregnancy.

In a recent article on mother-to-child transmission (MCT) of human immunodeficiency virus type 1 (HIV-1) in the Congo Lallemant and colleagues reported a 40.4% MCT rate in the Congo and attributed the seroconversion of 3 additional children who were seronegative at 12-15 months to breastfeeding; however these infants were excluded from the calculation of MCT rate. These cases were discovered only because seroconversion occurred after maternal antibody had been lost. Since current technology does not distinguish between children who were infected in the early postnatal period (when maternal antibody was still present) and those who were infected at birth the 3 infants represent a minimal estimate of the number of children in their cohort who were postnatally infected. The accompanying editorial by Ryder and Behets discussed reasons for the wide variation in reported rates of MCT without mentioning breastfeeding as a potential transmission route and restricted their definition of postpartum MCT to the period occurring immediately after birth. Although the observed variation in reported MCT rates may be accounted for by the clinical and nutritional status of pregnant women methodologic variations in MCT studies selection biases or differential transmission of different HIV variants transmission through breast milk has been well documented. Growing numbers of children have seroconverted after losing passively transferred maternal antibody according to these studies. A meta-analysis examining MCT through breast milk estimated the risk of transmission to be 14%. This is of particular importance in formulating policy in the developing world. Future investigations should monitor any breast fed child with antibody testing for at least 24 months or until at least 3 months after cessation of breastfeeding. All children infected by any route of MCT should be included in MCT transmission rate calculations. Polymerase chain reaction genetic sequencing and other molecular techniques should be used in ascertaining the time at which MCT occurs.

The purpose of this work was to study the relation between maternal trimester of primary infection with cytomegalovirus and the occurrence of sensorineural hearing loss in the congenitally infected offspring. Thirty-four consecutive live-born children diagnosed with a congenital cytomegalovirus infection after maternal primary cytomegalovirus infections were included in the study. Five were lost for follow-up, and 1 died. Of the remaining 28 congenitally infected children, an estimation of the maternal trimester in which cytomegalovirus primary infection occurred was performed. All of the children were investigated for potential sensorineural hearing loss. Five of the maternal infections occurred in the first trimester, 12 in the second trimester, and 11 in the third trimester of pregnancy. Sensorineural hearing loss was detected in 4 (80%) of the 5 congenitally infected children who were infected after a primary maternal infection in the first trimester of pregnancy and in 1 (8%) of the 12 children when the maternal infection occurred in the second trimester of pregnancy. No sensorineural hearing loss was detected after primary maternal infection occurring in the third trimester. Fluctuation and improvement of sensorineural hearing loss were seen regardless the trimester of pregnancy during which maternal primary infection occurred. Progression of sensorineural hearing loss occurred in 2 children born after a maternal primary infection of the first trimester. Hearing loss seemed more common in infants with congenital cytomegalovirus infection who were born to women who experienced a primary cytomegalovirus infection in the first trimester of pregnancy than when infection took place later in pregnancy.

In a recent article on mother-to-child transmission (MCT) of human immunodeficiency virus type 1 (HIV-1) in the Congo Lallemant and colleagues reported a 40.4% MCT rate in the Congo and attributed the seroconversion of 3 additional children who were seronegative at 12-15 months to breastfeeding; however these infants were excluded from the calculation of MCT rate. These cases were discovered only because seroconversion occurred after maternal antibody had been lost. Since current technology does not distinguish between children who were infected in the early postnatal period (when maternal antibody was still present) and those who were infected at birth the 3 infants represent a minimal estimate of the number of children in their cohort who were postnatally infected. The accompanying editorial by Ryder and Behets discussed reasons for the wide variation in reported rates of MCT without mentioning breastfeeding as a potential transmission route and restricted their definition of postpartum MCT to the period occurring immediately after birth. Although the observed variation in reported MCT rates may be accounted for by the clinical and nutritional status of pregnant women methodologic variations in MCT studies selection biases or differential transmission of different HIV variants transmission through breast milk has been well documented. Growing numbers of children have seroconverted after losing passively transferred maternal antibody according to these studies. A meta-analysis examining MCT through breast milk estimated the risk of transmission to be 14%. This is of particular importance in formulating policy in the developing world. Future investigations should monitor any breast fed child with antibody testing for at least 24 months or until at least 3 months after cessation of breastfeeding. All children infected by any route of MCT should be included in MCT transmission rate calculations. Polymerase chain reaction genetic sequencing and other molecular techniques should be used in ascertaining the time at which MCT occurs.

We evaluated a screening program for the detection of congenital cytomegalovirus in 3075 unselected pregnant women. From each live-born child urine for CMV culture was collected within 7 days after birth. Each fetus expelled after a spontaneous second trimester abortion and each stillborn infant were also evaluated for a possible congenital CMV infection. For each congenital infection stored maternal sera were analysed to determine whether maternal infection was primary or recurrent. Fifteen out of the 3075 pregnancies studied resulted in a congenitally infected infant (0.49%). Nine maternal CMV infections were primary infections; five were recurrent infections, and in one case the type of infection could not be determined. Three congenital infections resulted in severe sequelae, leading to the termination of pregnancy in two instances and to neonatal death in one case. One of these severe fetal infections was due to a recurrent maternal infection. Follow-up of the other 12 neonates demonstrated hearing disorders in two children. One was born after a primary maternal infection and one after a recurrent maternal infection. We conclude that congenital CMV infections occurs in 0.49% of all pregnancies in the population studied. Twenty percent of the congenitally infected infants present severe sequelae at birth or during pregnancy, and an additional 17% have audiological deficits at 1 year of age. Severe sequelae may occur after both primary and recurrent maternal CMV infection.

Breast milk is the best food for infants. However, worrying about the transmission of pathogens to their offspring, mothers who have ongoing infections are usually hesitated on breastfeeding, or even unwillingly give up breastfeeding. This article summarized some basic knowledge and evidence on breastfeeding when maternal infections occur and emphasized that there is no risk of hepatitis virus transmission during breastfeeding. After taking appropriate measures, mothers with transmittable diseases through breastfeeding can still breastfeed their babies. This review provides reasonable medical advice on whether to breastfeed when maternal infection occurs in order to increase breastfeeding rate. Key words: Mothers; Communicable diseases; Breast feeding

Introduction:Most infants at risk for cytomegalovirus (CMV)-associated sensorineural hearing loss (SNHL) are unrecognized because of the absence of a universal neonatal CMV screening. The search of CMV-DNA by molecular methods in salivary swabs was demonstrated to be a reliable approach. This study describes the results obtained by carrying out a universal screening for congenital CMV (cCMV) infection including all live-born newborns in three Italian sites, as well as the therapeutic interventions and clinical outcome of the CMV-infected neonates. Moreover, CMV maternal infection's characteristics were evaluated.MethodsTo confirm or exclude cCMV infection, a CMV-DNA-positive result on a first salivary swab was followed by repeated saliva and urine samples collected within 21 days of age. Breast milk samples were also collected. The search of CMV-DNA was performed with a single automated quantitative commercial real-time PCR assay, regardless of the type of samples used.ResultsA total of 3,151 newborns were enrolled; 21 (0.66%) of them were congenitally infected (median saliva viral load at screening, 6.65 [range, 5.03–7.17] log10 IU/ml). Very low/low viral load in screening saliva samples (median value, 1.87 [range, 1.14–2.59] log10 IU/ml) was associated with false-positive results (n = 54; 1.7%). CMV-DNA was detected in almost half of the breast milk samples of mother–infant pairs with a false-positive result, suggesting that contamination from breast milk may not be the only explanation in the study population. cCMV infection confirmation with the search of CMV-DNA in a urine sample proved to be the gold standard strategy, since false-positive results were observed in 4/54 (7.5%) of the repeated saliva samples. Symptomatic cCMV infection was observed in 3/21 (14.3%) infants; notably, one (4.7%) developed moderate unilateral SNHL at 5 months after birth. Finally, two symptomatic cCMV infections were associated with primary maternal infection acquired in the first trimester of gestation; one newborn with severe cCMV symptoms was born to a mother with no CMV checkups in pregnancy.ConclusionWithout universal neonatal CMV screening, some infected infants who develop late neurological sequelae may not be recognized and, consequently, they are not able to benefit early from instrumental and therapeutic interventions to limit and/or treat CMV disease.