Transmission of Infectious Diseases Through Breast Milk and Breastfeeding

A large body of evidence clearly demonstrates the protective effects of breastfeeding and documents the transmission of specific infections to infants through breast milk. The fear and anxiety that arise with the occurrence of any infectious disease are even greater for the breastfeeding mother-infant dyad. Uncertainty and lack of knowledge often lead to proscribing breastfeeding out of fear, which then deprives the infant of the potential protective, nutritional, and emotional benefits of breastfeeding exactly at the time when they are most needed (see the discussion of immunologic benefits of human milk in Chapter 5 ). Decisions concerning breastfeeding in a mother with an infectious illness should balance the potential benefits of breastfeeding against the known or estimated risk for the infant acquiring a clinically significant infection via breastfeeding and the potential severity of the infection.

Documenting transmission of infection from mother to infant by breastfeeding requires not only the exclusion of other possible mechanisms of transmission but also the demonstration of the infectious agent in the breast milk and a subsequent clinically significant infection in an infant that was caused by a plausible infectious process. The first step is to establish the occurrence of a specific infection (clinically or immunologically evident) in a mother and to demonstrate the persistence of the infectious agent, such that it could be transmitted to the infant. Isolation or identification of the infectious agent from the colostrum, the breast milk, or an infectious lesion of the breast is important, but it is not necessarily proof of transmission to an infant. Epidemiologic evidence of transmission must be considered, including identifying characteristics of the organism that relate an isolate from an infant to the maternal isolate. Infectious organisms can reach the breast milk either by secretion in the fluid or cellular components of breast milk or by contamination of the milk at the time of or after expression. A reasonable mechanism of infection via breast milk should be evident and proved through either animal or human studies. Demonstration of a subclinical or clinically evident infection in an infant should follow these outlined steps.

Exclusion of other possible mechanisms of transmission (exposure to mother or other persons/animals via airborne, droplet, arthropod, or vector modes of transmission or through direct contact with other infectious fluids) would complete the confirmation of transmission of infection via breastfeeding. It is essential to exclude prenatal or perinatal transmission of infection to a fetus or infant, but doing this can often be difficult.

Clinical case reports or studies confirming the isolation of an infectious agent from the milk are important. To determine a reasonable estimate of the risk for infection via breast milk, larger epidemiologic studies are needed that compare infection rates in breastfed infants versus formula-fed infants, addressing the issues just identified. The timing of breastfeeding is important relative to the timing of maternal infection and to the presence of a pathogen in the colostrum or breast milk. The duration of breastfeeding is another important variable to consider in the estimate of risk, because the shedding of a pathogen in breast milk may be intermittent.

These considerations are only some of the variables to be taken into account, in general, to assess the risk for transmission of an infectious agent from mother to infant via breast milk or breastfeeding. Efforts to prove transmission of infection in a particular maternal-infant dyad can be just as difficult and must consider many of the same factors.

This chapter focuses on a discussion of specific, clinically relevant, infectious agents and diseases, with reasonable estimates of the risk for infection to infants from breastfeeding. The basic tenet concerning breastfeeding and infection is that breastfeeding is rarely contraindicated in maternal infection. The few exceptions relate to specific infectious agents with strong evidence of transmission and to the association of an infant’s illness with significant morbidity and mortality.

The risk or benefit of breastfeeding relative to the immunization of a mother or infant is discussed for certain microorganisms. Appendix F addresses precautions and breastfeeding recommendations for maternal infections. Chapter 5 reviews how breastfeeding may protect against infection. Chapter 21 addresses specific concerns relating to banked breast milk and includes standards developed by the human Milk Banking Association of North America to guide the appropriate handling of banked human milk relative to possible infectious agents.

Infection-Control Considerations

Isolation precautions have undergone some revisions in terminology and conceptualization. Understanding that the transmission of microorganisms can occur with a known infection and with unrecognized sources of infection, recommendations have been made for standard precautions to be applied to all patients to protect health care workers from potentially infectious body fluids. Additionally, precautions based on the predominant modes of transmission have been recommended to protect against infection through the airborne route, direct contact, or contact with droplets. Although these precautions are intended to be used in clinical situations to protect health care workers, they may be applied in certain situations to the mother-infant dyad to prevent the transmission of infectious agents from one to the other or to other hospitalized mothers and infants. These precautions are useful most often when a mother and infant are still hospitalized. The use of such precautions within the home is not meant to limit breastfeeding. These precautions are intended to allow breastfeeding in the majority of cases and to facilitate the continuation of breastfeeding with some additional safeguards in certain situations, after short temporary periods of stopping breastfeeding. The guidelines also indicate when to safely use expressed breast milk (see Appendix F ).

Standard Precautions

Standard precautions include preventing contact with blood, all body fluids, secretions and excretions, nonintact skin, and mucous membranes by (1) careful handwashing before and after every patient contact; (2) use of gloves when touching body fluids, nonintact skin, mucous membranes, or any items contaminated with body fluids (linens, equipment, devices, etc.); (3) use of nonsterile gowns to prevent contact of clothing with body fluids; (4) use of masks, eye protection, or face shields when splashing with body fluids is possible; and (5) appropriate disposal of these materials. Standard precautions should be applied to all patients regardless of actual or perceived risks. The Centers for Disease Control and Prevention (CDC) does not consider breast milk to be a body fluid with infectious risks, and thus these policies do not apply to breast milk. (See section on misadministration of breast milk later in this chapter as a possible exception to this concept.)

In considering breastfeeding infant-mother dyads and standard precautions, body fluids other than breast milk should be avoided, and only in specified situations should breast milk also be avoided. In general, clothing or a gown for the mother, and bandages if necessary, should prevent direct contact with nonintact skin or secretions. Avoiding infant contact with maternal mucous membranes requires mothers to be aware of and understand the risks and to make a conscious effort to avoid this type of contact. The use of gloves, gowns, and masks on infants for protection is neither practical nor appropriate. The recommendations concerning the appropriateness of breastfeeding and breast milk are addressed for specific infectious agents throughout this chapter. Human immunodeficiency virus (HIV) infection is an example of one infection that can be prevented by the use of standard precautions, including avoiding breast milk and breastfeeding. The recommendations concerning breastfeeding and HIV and the various variables and considerations involved are discussed later.

Airborne Precautions

Airborne precautions are intended to prevent transmission via droplet nuclei (dried respiratory particles smaller than 5 mcm that contain microorganisms and can remain suspended in the air for long periods) or dust particles containing microorganisms. Airborne precautions include the use of a private room with negative-air-pressure ventilation and masks at all times. In the case of pulmonary tuberculosis (TB), respiratory protective devices (requiring personal fitting and seal testing before use) should be worn. Airborne precautions are recommended with measles, varicella or disseminated zoster, and TB. Breastfeeding in the presence of these maternal infections is prohibited during the infectious period. This is to protect against airborne transmission of the infection from the mother and to allow the infant to be fed the mother’s expressed breast milk by another individual. The exception to allowing breast milk would be local involvement of the breast by varicella-zoster lesions or Mycobacterium tuberculosis, such that the milk becomes contaminated by the infectious agent.

Droplet Precautions

Transmission via droplets occurs when an individual produces droplets that travel only a short distance in the air and then contact a new host’s eyes, nose, mouth, or skin. The common mechanisms for producing droplets include coughing, sneezing, talking (singing or yelling), suctioning, intubation, nasogastric tube placement, and bronchoscopy. In addition to standard precautions applied to all patients, droplet precautions include the use of a private room (preferred) and a mask if within 3 feet (0.9 m) of the patient. Droplet precautions are recommended for adenovirus, diphtheria, respiratory infections, Haemophilus influenzae, Neisseria meningitidis or invasive infection, influenza, mumps, mycoplasma, parvovirus, pertussis, plague (pneumonic), and rubella, as well as streptococcal pharyngitis, pneumonia, or scarlet fever. The institution of droplet precautions with a breastfeeding mother who has these infections should be specified for each particular infection. This may require some period of separation for the infant and mother (for the duration of the illness, for the short term, or complete treatment of the mother, for the infectious period) with use of expressed breast milk for nutrition in the interim. Prophylactic treatment of the infant, maternal use of a mask during breastfeeding or close contact, combined with meticulous hand washing and the mother’s avoidance of touching her mucous membranes, may be adequate and reasonable for certain infections.

Contact Precautions

Contact precautions are meant to prevent the transmission of an infectious agent via direct contact (contact between the body surfaces of one individual and another) and indirect contact (contact of a susceptible host with an object contaminated with microorganisms from another individual). Contact precautions include cohorting or a private room, gloves and gowns at all times, and handwashing after removal of gown and gloves. Contact precautions are recommended for a long list of infections, such as diarrhea in diapered or incontinent patients with Clostridium difficile infection, Escherichia coli O157:H7, Shigella , rotavirus, hepatitis A, respiratory illness with parainfluenza virus or respiratory syncytial virus (RSV), multidrug-resistant (MDR) bacteria (e.g., enterococci, staphylococci, gram-negative organisms), enteroviral infections, cutaneous diphtheria, impetigo, herpes simplex virus (HSV) infection, herpes zoster (disseminated or in immunocompromised individuals), pediculosis, scabies, Staphylococcus aureus skin infection, viral hemorrhagic fevers (e.g., Ebola, Lassa), conjunctivitis and abscesses, cellulitis, and decubitus that cannot be contained by dressings. For a breastfeeding mother-infant dyad, the implementation of precautions for each of these infections in a mother requires meticulous attention to gowning and handwashing by the mother and a specialized plan for each situation. This is particularly true for uncommon, but potentially serious or fatal, infections such as viral hemorrhagic fevers, including Ebola virus disease (EVD), or exposure. (Bausch DG et al.: JID, 2007, (accessed 17.01.15.) (accessed 9/6/15).

Each of these transmission-based precautions can be used in combination for organisms or illnesses that can be transmitted by more than one route. They should always be used in conjunction with standard precautions, which are recommended for all patients. The Red Book: Report of the Committee on Infectious Diseases by the American Academy of Pediatrics (AAP) remains an excellent resource for infection control guidelines and recommendations to prevent transmission in specific situations and infections.

Culturing Breast Milk

The routine culturing of breast milk or the culturing of breast milk to screen for infectious agents is not recommended, except when the milk is intended as donor milk for another mother’s child directly or through human milk banks. See Chapter 21 for specific bacterial count standards for raw donor milk and for pasteurization of donor milk. Breastfeeding and the expression of or pumping of breast milk (referred to as expressed breast milk) for later use are not sterile activities. An emerging practice related to an increase in the use of donor human milk is milk-sharing. (This is addressed in the next section and Chapter 21 .)

In general, expressed breast milk should not contain large numbers of microorganisms (less than 10 4 for raw milk and less than 10 6 for milk to be pasteurized), nor should it contain potential pathogens such as S. aureus , β-hemolytic streptococci, Pseudomonas species, Proteus species, or Streptococcus faecalis or faecium. Few studies have examined the “routine” culturing of milk and the significance of specific bacterial colony counts relative to illness in infants. Other studies have been primarily concerned with premature or low-birth-weight (LBW) infants who remain hospitalized and are commonly fed via enteral tubes. A study from Canada tested 7610 samples of milk for use in 98 preterm infants. The study did not identify any adverse events in the infants attributed to organisms growing in the milk samples, and the routine bacteriological testing of expressed breast milk was not recommended. A study from Chicago examined gram-negative bacilli in the milk used for premature infants. Samples were tested before feeding and from the nasogastric tubes during feeding. Milk samples from before feeding were less likely to contain gram-negative bacilli (36%) than milk samples from the nasogastric tubing (60%). Feeding intolerance was observed when there were more than 10 3 colony-forming units per milliliter (CFU/mL), and episodes of sepsis were identified when the bacterial counts in the milk were greater than or equal to 10 6 CFU/mL. This study recommended the routine bacteriologic testing of expressed breast milk. Another study from Arkansas focused on the contamination of feeding tubes during the administration of expressed breast milk or formula. Ten infants in the neonatal intensive care unit (NICU) were exposed to greater than 10 5 gram-negative bacteria in their feeding tubes. The three infants who were fed expressed breast milk with contamination at greater than 10 5 organisms remained well, but the seven formula-fed infants with high levels of bacterial contamination in the feeding tubes developed necrotizing enterocolitis. The gram-negative bacteria with high-level contamination in the feeding tubes were either Enterobacter or Klebsiella in all cases. Many NICUs consider 10 5 to 10 6 CFU/mL as the significant bacterial count for gram-negative bacilli in breast milk that places premature and LBW infants at greater risk for infection.

Even fewer data are available concerning specific bacterial colony counts for gram-positive organisms and the risk to the infant. Generally less than 10 3 gram-positive organisms per mL of milk is considered acceptable, with only case reports and no controlled trials to support this cutoff.

When the presence of an infectious illness in an infant and/or the breastfeeding mother’s breast and breast milk is seriously considered as a possible mechanism of transmission to the infant, culturing breast milk to identify the organism may be warranted and useful. More important than hurrying to culture breast milk is the careful instruction of mothers on the proper technique for collecting expressed breast milk, storing it, and cleaning the collection unit. The reinforcement of proper technique from time to time, especially when a question of contamination arises, is equally important. Many small reports comment on the contamination of breast milk with different collection methods. Relative comparisons suggest decreasing contamination of expressed breast milk when collected by the following methods: drip milk, hand-pumped milk, manual expression, modern electric-pumped milk. One group from Malaysia published results showing no difference in contamination between milk collected by electric pump versus manual expression when collected in the hospital. Expressed breast milk collected at home by breast pump had higher rates of contamination with staphylococci and gram-negative bacteria. Discussion continues about the need to discard the first few milliliters of milk to lower bacteria numbers in expressed breast milk without any evidence to suggest if this is truly necessary. No evidence shows that cleansing the breast with anything other than tap water decreases the bacterial counts in cultured expressed breast milk. If an infant is directly breastfeeding, collecting milk for culture by manual expression and trying to obtain a “midstream” sample (as is done with “midstream” urine collection for culture) is appropriate. If an infant is being fed expressed breast milk, collecting and culturing the milk at different points during collection (utilizing the same technique the mother uses [manual expression, hand pump, or electric pump]) and administration are appropriate. This might include a sample from immediately after collection, another of stored expressed breast milk, and a sample of milk from the most recent infant feeding at the time the decision to culture is made. See Box 13-1 for the basic steps in culturing expressed breast milk.

Box 13-1

Culturing Breast Milk

  • 1.

    Wash hands as per routine.

  • 2.

    Wash breast with warm tap water and a clean washcloth.

  • 3.

    Manually express breast milk (“midstream” collection is not required) or attach breast pump flange (previously cleaned as per routine) for collection and collect milk.

  • 4.

    Place a 3- to 5-mL sample of expressed breast milk in a sterile container with a nonleakable top.

  • 5.

    Deliver to the laboratory in less than 1 hour or refrigerate at 4° C until delivery. Before sending samples to the viral lab or for nucleic acid/polymerase chain reaction (PCR) testing, confirm that the laboratory will accept and process the sample as requested and that the appropriate collection container and prelaboratory management of the specimen are utilized.

  • 6.

    Processing of specimens:

    • a.

      Direct examination by Gram stain is not required.

    • b.

      Culture on blood agar (BA) and MacConkey agar (MAC) media as per lab standards.

    • c.

      Quantitate all isolates.

    • d.

      Send separate samples for fungal culture, acid-fast bacilli, and viral culture, as indicated, based on the clinical situation.

Perform routine sensitivity testing on all potential pathogens. (This will require some discussion with the clinician and perhaps a pediatric infectious disease specialist.)

The interpretation of such culture results can be difficult and should involve a pediatric infectious disease expert, a microbiologist, and a hospital epidemiologist. Additional organism identification is often required, utilizing antibiogram patterns or molecular fingerprinting by various techniques to correlate a bacterial isolate from breast milk with an isolate causing disease in infant or mother.

Donor Human Milk

The WHO, the United Nations Children’s Fund (UNICEF), and the AAP recommend the use of donor human milk when the infant’s own mother’s milk is unavailable. The AAP recommends pasteurized donor milk. The possible sources of donor human milk include wet nursing, cross nursing, milk sharing, and human milk banks. Milk sharing is a more informal process, as compared to human milk banks with guidelines and procedures to maintain safety and quality of the donated milk. Milk sharing occurs more directly among family and friends or now at greater distances between unknown donors and recipients via the Internet. Human milk banks are either not-for-profit banks (e.g., Human Milk Banking Association of North America [HMBANA] or established milk banks in numerous other countries) or commercial entities (e.g., Prolacta).

The federal government in the United States does not regulate or oversee milk banking, but HMBANA maintains milk-banking guidelines and procedures for banks within their association. Prolacta Bioscience, Inc. follows FDA guidelines for both food and pharmaceuticals in the production of their human milk products. Donor selection, screening, exclusion, and education, Holder pasteurization (HP) or high-temperature short-time (HTST) pasteurization, and postpasteurization bacterial culture testing are the main components utilized to maintain the safety and quality of donor milk from human milk banks (see Chapter 21 ).

The proper pasteurization of donor human milk virtually eliminates any infectious risks from donor human milk. Risk from drug exposure in donor milk is primarily addressed through donor selection and exclusion, although Prolacta includes donor milk drug testing as part of the screening process.

The notable increase in donor human milk sharing via Internet sites has raised concerns about the safety and quality of milk obtained in this manner. Although several of the larger Internet organizations (e.g., Human Milk for Human Babies [HM4HB, ], Eats on Feets [ ], and MilkShare [ ]) promote the concepts of safe and ethical milk sharing, informed consent, “informal donor screening,” safe collection, storage, shipment and handling, and home pasteurization, there are many other avenues on the Internet for milk sharing, and the safety of milk sharing via the Internet has not been extensively studied.

Two publications by the same group have looked at the process of purchasing human milk on the Internet in terms of the ease and reliability of the process, shipping, costs, delays, the condition of packaging and milk containers, the temperature of the milk samples on arrival, and microbial contamination. Geraghty et al. and Keim et al. reported receiving 50% of the packages on the day after shipment and 37% on the second day after shipment. Nine percent of these shipping boxes were rated as severely damaged, 15% of the milk containers had evidence of leaking milk, and 45% of the milk samples arrived with a surface temperature of the milk > 4° C, the recommended refrigerator temperature for the storage of human milk. The surface milk temperature was noted to correlate with the cost of shipping, time in transit, and milk-container condition rating. The authors also compared the bacteriologic culture results of milk obtained via the Internet and milk obtained from a human milk bank. The Internet samples were colonized with gram-negative bacteria 74% of the time or had colony counts of > 10 4 CFU/mL. Compared with samples from a human milk bank, Internet samples had higher mean total aerobic counts, total gram-negative counts, coliform counts, and Staphylococcus sp. counts. Milk bank samples were CMV DNA positive 5% of the time, with 21% of Internet samples being CMV DNA positive. None of the samples tested positive for HIV-RNA.

Despite the fact that the larger milk-sharing websites recommend guidelines for hygienic collection, appropriate storage, and shipping, the quality and safety of human milk obtained via milk sharing on the Internet fall short of expected standards for donor human milk. This highlights the relative importance of proper, effective home pasteurization of donor human milk by the receiving mother prior to giving it to an infant.

Clearly, more study of the safety and quality of donor human milk obtained via the Internet is needed, with a particular focus on obtaining outcome data on the infants receiving this milk. Additionally, increasing the availability and decreasing the cost of donor human milk from not-for-profit and commercial milk banks, while maintaining quality and safety, is essential to providing for the needs of an increasing number of infants who have an inadequate supply of their own mother’s milk.

Misadministration of Breast Milk

The misadministration of breast milk, also known as misappropriation, breast milk exposure, and accidental ingestion of breast milk, among other terms, is a medical-legal issue when it occurs in a hospital. This scenario occurs when one infant receives breast milk from another mother by mistake. This occurrence can be very distressing to the families (recipient patient, recipient parent, and donor mother) and medical staff involved. The actual risk for transmission of an infectious agent to an infant via a single ingestion of expressed breast milk (the most common occurrence) from another mother is exceedingly low. In this scenario, the CDC recommends treating this as an accidental exposure to a body fluid that could be infectious. Bacterial, fungal, or parasitic infection from the one exposure is highly unlikely. The concern is about viral pathogens, known to be blood-borne pathogens that have been identified in breast milk and include but are not limited to hepatitis B virus (HBV), hepatitis C virus (HCV), cytomegalovirus (CMV), West Nile virus, human T-cell lymphotropic virus (HTLV), and HIV.

Most hospitals have protocols for managing the situation from both the infection control/prevention and the medical-legal perspectives. These protocols advise informing both families about what occurred, discussing the theoretical risks of harm from the exposure, and reviewing test results and/or recommending testing to determine the infectious status of each mother relative to the mentioned viruses. HCV is not a contraindication to breastfeeding, and West Nile virus infection in lactating women is rare. Neither infection has a documented effective form of prevention or acute treatment. Testing either the donor mother or the mother of the recipient infant for these agents is not warranted. Prenatal testing for HIV is more commonplace throughout the world. The incidence of HIV among women of childbearing age is low, although it varies significantly by geographic location, and the hospital or locale-specific incidence would be important to know in order to estimate risk. Most women and medical staff are aware that HIV can be transmitted by breastfeeding; therefore, breast milk from HIV-positive women is rarely if ever stored in hospitals. The risk for transmission of HIV via breastfeeding is due to the volume of feedings over months (estimated at 400 to 500 feedings in the first 2 months of life) compared to the small “dose of exposure” from one or two “accidental feedings.” Transmission of HIV from a single breast milk exposure has never been documented. Immunologic components in breast milk, along with time and cold storage temperatures, inactivate the HIV in expressed breast milk. For these reasons, the risk for transmission of HIV via expressed breast milk consumed by another child is thought to be extremely low. HTLV-I/II infection in childbearing women is uncommon, except in certain geographic regions (Japan, Africa, the Caribbean, and South America). Transmission of HTLV via breast milk does occur and, like HIV, appears to be related to the volume and duration of breastfeeding. Limiting the duration of breastfeeding is effective in decreasing transmission. Freezing and thawing expressed breast milk decreases the infectivity of HTLV-I. In areas of low prevalence, a positive test in a mother should be suspected to be a false positive test, and retesting with both antibody and polymerase chain reaction (PCR) testing should be performed. For these reasons the transmission of HTLV-I/II via accidental expressed breast milk exposure is thought to be extremely low. Although the majority of women are CMV-positive by childbearing age and CMV transmission occurs via breastfeeding, the risk for CMV in a full-term infant is low. Premature or LBW infants are at greater risk for developing disease with CMV infection. Freezing expressed breast milk (at − 20° C) for 3 to 5 days significantly decreases the infectivity of CMV. Here again, the risk for CMV transmission from a single accidental exposure to CMV-positive expressed breast milk is extremely low.

Any discussion of theoretical risk should be accompanied by a discussion of possible preventive interventions, such as vaccination or antimicrobial postexposure prophylaxis. If donor mothers are positive for HBV, it is appropriate to give recipient infants hepatitis B virus immunoglobulin (HBIG) and HBV vaccines if they have not already received them. If a donor mother is HIV- or HTLV-I/II-positive, the potential utility of postexposure prophylaxis with antiretroviral medications should be considered on a case-by-case basis. Clinicians participating in these decisions can refer to the AAP Red Book or the updated United States Public Health Service Guidelines for the Management of Occupational Exposures to HIV and Recommendations for Postexposure Prophylaxis (available at (Accessed 9/6/15). It may also be appropriate to consult a pediatric infectious disease specialist.

Additional important components of the hospital-based protocols for managing accidental expressed breast milk exposure include ongoing psychosocial support for the families and staff, documentation of medical discussions with the families, investigative steps, consents and interventions, and the demonstration of ongoing infection control efforts to prevent additional events of misadministration of breast milk.

Clinical Syndromes and Conditions

Microorganisms produce a whole spectrum of clinical illnesses affecting mothers and infants. Many situations carry the risk for transmission of the involved organism from a mother to the infant, or vice versa; in general, however, infants are at greater risk because of such factors as inoculum size and immature immune response. As always, an infection must be accurately diagnosed in a timely manner. Empiric therapy and initial infection-control precautions should begin promptly based on the clinical symptoms and the most likely etiologic agents. When dealing with a maternal infection, clarifying the possible modes of transmission and estimating the relative risk for transmission to the infant are essential first steps to decision making about isolating a mother from her infant and the appropriateness of continuing breastfeeding or providing expressed breast milk. Breastfeeding is infrequently contraindicated for specific maternal infections. Often, the question of isolation and interruption of breastfeeding arises when symptoms of fever, pain, inflammation, or other manifestations of illness first develop in a mother and the diagnosis is still in doubt. A clinical judgment must be made based on the site of infection, probable organisms involved, possible or actual mechanisms of transmission of these organisms to the infant, estimated virulence of the organism, and likely susceptibility of the infant. Additionally, by the time the illness is clearly recognized or diagnosed in a mother, the infant has already been exposed. Given the dynamic nature of the immunologic benefits of breast milk, the continuation of breastfeeding at the time of diagnosis or illness in a mother can provide the infant protection rather than continued exposure in most illnesses. Stopping breastfeeding is rarely necessary. Many situations associated with maternal fever do not require separation of mother and infant, such as engorgement of the breasts, atelectasis, localized nonsuppurative phlebitis, or urinary tract infections.

Appendix F lists a number of clinical syndromes, conditions, and organisms that require infection-control precautions in hospitals. This appendix also includes short lists of possible etiologic agents for these conditions and appropriate precautions and recommendations concerning breastfeeding for different scenarios or organisms. This chapter considers specific infectious agents that are common, clinically significant, or of particular interest.

Bacterial Infections


Bacillus anthracis , a gram-positive, spore-forming rod, causes zoonotic disease worldwide. Human infection typically occurs due to contact with animals or their products. Three forms of human disease occur: cutaneous anthrax (the most common), inhalation anthrax, and gastrointestinal (GI) anthrax (rare). Person-to-person transmission can occur as a result of discharge from cutaneous lesions, but no evidence of human-to-human transmission of inhalational anthrax is available. No evidence of transmission of anthrax via breast milk exists. Standard contact isolation is appropriate for hospitalized patients or patients with draining skin lesions.

The issue of anthrax as a biologic weapon has exaggerated its importance as a cause of human disease. The primary concerns regarding anthrax and breastfeeding are antimicrobial therapy or prophylaxis in breastfeeding mothers and the possibility that infant and mother were exposed by intentional aerosolization of anthrax spores. The CDC published recommendations for treatment and prophylaxis in infants, children, and breastfeeding mothers. The recommendations include the use of ciprofloxacin, doxycycline, amoxicillin, and several other agents without discontinuing breastfeeding. Little information is available on ciprofloxacin and doxycycline in breast milk for prolonged periods of therapy or prophylaxis (60 days) and possible effects on infants’ teeth and bone or cartilage growth during that time period. Depending on the clinical situation and sensitivity testing of the identified anthrax strain, other agents can be substituted to complete the 60-day course. The CDC has approved the use of ciprofloxacin and doxycycline for breastfeeding women for short courses of therapy (less than several weeks).

The simultaneous exposure of infant and mother could occur from primary aerosolization or from spores “contaminating” the local environment. In either case, decontamination of the mother-infant dyad’s environment should be considered.

Breastfeeding can continue during a mother’s therapy for anthrax as long as she is physically well. Open cutaneous lesions should be carefully covered, and, depending on the situation, simultaneous prophylaxis for the infant may be appropriate.


Considerable justifiable concern has been expressed because of the reports of sudden infant death from botulism. Infant botulism is distinguished from foodborne botulism from improperly preserved food containing the toxin and from wound botulism caused by spores entering a wound. Infant botulism occurs when the spores of Clostridium botulinum germinate and multiply in the gut and produce the botulinal toxin in the GI tract. The toxin binds presynaptically at the neuromuscular junction, preventing acetylcholine release. The clinical picture is a descending, symmetric flaccid paralysis. Not every individual who has C. botulinum identified in the stool experiences a clinical illness. The age of infants seems to relate to their susceptibility to illness. The illness is mainly in children younger than 12 months of age; the youngest patient described in the literature was 6 days old. Most children become ill between 6 weeks and 6 months of age. The onset of illness seems to occur earlier in formula-fed infants compared with breastfed infants. When a previously healthy infant younger than 6 months of age develops constipation, followed by weakness and difficulty sucking, swallowing, crying, or breathing, botulism is a likely diagnosis. The organisms should be looked for in the stools, and electromyography may or may not be helpful.

In a group reviewed by Arnon et al., 33 of 50 patients hospitalized in California were still being nursed at onset of the illness. A beneficial effect of human milk was observed in the difference in the mean age at onset, with breastfed infants being twice as old as formula-fed infants with the disease. The breastfed infants’ symptoms were milder. Breastfed infants receiving iron supplements developed the disease earlier than those who were breastfed but unsupplemented. Of the cases of sudden infant death from botulism, no infants were breastfed within 10 weeks of death. All were receiving iron-fortified formulas. In most cases, no specific food source of C. botulinum can be identified, but honey is the food most often implicated, and corn syrup has been implicated in infants older than 2 months of age. Honey may contain botulism spores, which can germinate in the infant gut. However, botulin toxin has not been identified in honey. It has been recommended that honey not be given to infants younger than 12 months of age. This includes putting honey on a mother’s nipples to initiate an infant’s interest in suckling.

Arnon reviewed the first 10 years of infant-botulism monitoring worldwide. The disease has been reported in 41 of the 50 states in the United States and in eight countries on four continents. The relationship to breastfeeding and human milk is unclear. In general, the acid stools (pHs 5.1 to 5.4) of human milk-fed infants encourage Bifidobacterium species. Few facultative anaerobic bacteria, or clostridia, existing as spores, are present in breastfed infants. In contrast, formula-fed infants have stool pHs ranging from 5.9 to 8.0, with few bifidobacteria, primarily gram-negative bacteria, especially coliforms and Bacteroides species. C. botulinum growth and toxin production decrease with declining pH and usually stop below pH 4.6. Breast milk also contains additional protective immunologic components, which purportedly have activity against botulinum toxin.

The relationship between the introduction of solid foods or weaning in both formula-fed and breastfed infants and the onset of botulism remains unclear. For a breastfed infant, the introduction of solid food may cause a major change in the gut, with a rapid rise in the growth of enterobacteria and enterococci, followed by progressive colonization by Bacteroides species, clostridia, and anaerobic streptococci. Feeding solids to formula-fed infants minimally changes the gut flora because these organisms already predominate. Although more hospitalized infants have been breastfed, sudden-death victims are younger and have been formula fed, which supports the concept of immunologic protection in the gut of a breastfed infant.

Much work remains to understand this disease. Clinically, constipation, weakness, and hypotonicity in a previously healthy child constitute botulism until ruled out, especially with recent dietary changes. At this time, no reason exists to suspect breastfeeding as a risk for infant botulism, and some evidence suggests a possible protective effect from breastfeeding. Breastfeeding should continue if botulism is suspected in the mother or infant.


Brucella melitensis has been isolated in the milk of animals. Foods and animals represent the primary sources of infection in humans. Brucellosis demonstrates a broad spectrum of illness in humans, from subclinical to subacute to chronic illness with nonspecific signs of weakness, fever, malaise, body aches, fatigue, sweats, arthralgia, and lymphadenitis. In areas where the disease is enzootic, childhood illness has been described more frequently. The clinical manifestations in children are similar to those in adults. Infection can occur during pregnancy, leading to abortion (infrequently), and can produce transplacental spread, causing neonatal infection (rarely).

The transmission of B. melitensis through breast milk has been implicated in neonatal infection. There have been eight cases of brucellosis in infants that were possibly associated with breastfeeding, but Brucella was not isolated from the breast milk in any of those cases. One case of brucellosis in an infant caused by breast milk transmission involved B. melitensis being isolated from the breast milk before antibiotic treatment was given to the mother. Additionally, B. melitensis has been cultured from women with breast lumps and abscesses. Only one of six women described in this report was lactating at the time of diagnosis, and no information about the infant was given. Brucellosis mastitis or abscess should be considered in women presenting with appropriate symptoms and occupational exposure to animals, contact with domestic animals in their environment, or exposure to animal milk or milk products (especially unpasteurized products). The breast inflammation tends to be granulomatous in nature (without caseation) and is often associated with axillary adenopathy; occasionally, systemic illness in the woman is evident. Brucellosis mastitis or abscess should be treated with surgery or fine-needle aspiration, as indicated, accompanied by 4 to 6 weeks of combination antibiotic therapy with two or three medications. The temporary interruption of breastfeeding with breast pumping and discarding the milk to continue the stimulation of milk production is appropriate. Breastfeeding should then continue after an initial period of 48 to 96 hours of therapy in the mother. Acceptable medications for treating the mother, while continuing breastfeeding, include gentamicin, streptomycin, tetracycline, doxycycline, trimethoprim-sulfamethoxazole, and rifampin.

Chlamydial Infections

Chlamydial infection is the most frequent sexually transmitted disease (STD) in the United States and is a frequent cause of conjunctivitis and pneumonitis in an infant from perinatal infection. The major determinant of whether chlamydial infection occurs in a newborn is the prevalence rate of chlamydial infection of the cervix. Specific chlamydial immunoglobulin A (IgA) has been found in colostrum and breast milk in a small number of postpartum women who were seropositive for Chlamydia. No information is available on the role of milk antibodies in protecting against infection in infants. It is not believed that Chlamydia is transmitted via breast milk. The use of erythromycin or tetracycline to treat mothers and oral erythromycin and ophthalmic preparations of tetracyclines, erythromycin, or sulfonamides to treat suspected infection in infants is appropriate during continued breastfeeding. Separating infants from mothers with chlamydial infections or stopping breastfeeding is not indicated. The simultaneous treatment of mothers and infants may be appropriate in some situations.


Corynebacterium diphtheriae causes several forms of clinical disease, including membranous nasopharyngitis, obstructive laryngotracheitis, and cutaneous infection. Complications can include airway obstruction from membrane formation and toxin-mediated central nervous system (CNS) disease or myocarditis. The overall incidence of diphtheria has declined, even though immunization does not prevent infection but does prevent severe disease from toxin production. Fewer than five cases are reported annually in the United States.

Transmission occurs via droplets or direct contact with contaminated secretions from the nose, throat, eye, or skin. Infection occurs in individuals whether they have been immunized or not, but infection in the nonimmunized is more severe and prolonged. As long as the skin of the breast is not involved, no risk for transmission exists via breast milk. No toxin-mediated disease from a toxin transmitted through breast milk has been reported in an infant.

Breastfeeding, along with chemoprophylaxis and the immunization of affected infants, is appropriate in the absence of cutaneous breast involvement (see Appendix F ).

Gonococcal Infections

Maternal infection with Neisseria gonorrhoeae can produce a large spectrum of illness ranging from uncomplicated vulvovaginitis, proctitis, pharyngitis, and conjunctivitis, as well as more severe and invasive disease, including pelvic inflammatory disease, meningitis, endocarditis, and disseminated gonococcal infection. The risk for transmission from mother to infant occurs mainly during delivery in the passage through the infected birth canal and occasionally from postpartum contact with the mother (or her partner). The risk for transmission from breast milk is negligible, and N. gonorrhoeae does not seem to cause local infection of the breasts. Infection in neonates is most often ophthalmia neonatorum and less often a scalp abscess or disseminated infection. Mothers with presumed or documented gonorrhea should be reevaluated for other STDs, especially Chlamydia trachomatis and syphilis, because some therapies for gonorrhea are not adequate for either of these infections.

With the definitive identification of gonorrhea in a mother, empiric therapy should begin immediately, and the mother should be separated from the infant until the completion of 24 hours of adequate therapy. Treatment of the mother with ceftriaxone, cefixime, penicillin, or erythromycin is without significant risk for the infant. Single-dose treatment with spectinomycin, ciprofloxacin, ofloxacin, or azithromycin has not been adequately studied, but it would presumably be safe for the infant, given the 24-hour separation and a delay in breastfeeding without giving the infant the expressed breast milk (pump and discard). Doxycycline use in a nursing mother is not routinely recommended.

Careful preventive therapy for ophthalmia neonatorum should be provided, and close observation of the infant should continue for 2 to 7 days, the usual incubation period. Empiric or definitive therapy against N. gonorrhoeae may be necessary, depending on an infant’s clinical status, and it should be chosen on the basis of the maternal isolate’s sensitivity pattern. The mother should not handle other infants until after 24 hours of adequate therapy, and the infant should be separated from the rest of the nursery population, with or without breastfeeding.

Haemophilus influenzae

H. influenzae type B can cause severe invasive disease such as meningitis, sinusitis, pneumonia, epiglottitis, septic arthritis, pericarditis, and bacteremia. Shock can also occur. Because of the increased utilization of the H. influenzae type B conjugate vaccines, invasive disease caused by Haemophilus has decreased dramatically, with a greater than 95% reduction in the United States. Most invasive disease occurs in children 3 months to 3 years of age. Older children and adults rarely experience severe disease but do serve as sources of infection for young children. Children younger than 3 months of age seem to be protected because of passively acquired antibodies from the mothers, and some additional benefits may be received from breast milk.

Transmission occurs through contact with respiratory secretions, and droplet precautions are protective. No evidence suggests transmission through breast milk or breastfeeding. Evidence supports that breast milk limits the colonization of H. influenzae in the throat.

In the rare case of maternal infection, an inadequately immunized infant in a household is an indication to provide rifampin prophylaxis and close observation for all household contacts, including the breastfeeding infant. Expressed breast milk can be given to an infant during the 24-hour separation after the mother’s initiation of antimicrobial therapy, or if the mother’s illness prevents breastfeeding, it can be reinitiated when the mother is able (see Appendix F ).


Although uncommon in the United States, leprosy occurs throughout the world. This chronic disease presents with a spectrum of symptoms depending on the tissues involved (typically the skin, peripheral nerves, and mucous membranes of the upper respiratory tract) and the cellular immune response to the causative organism, Mycobacterium leprae. Transmission occurs through long-term contact with individuals with untreated or multibacillary (large numbers of organisms in the tissues) disease.

Leprosy is not a contraindication to breastfeeding, according to Jeliffe and Jeliffe. The importance of breastfeeding and the urgency of treatment are recognized by experts who treat infants and mothers early and simultaneously. No mother-infant contact is permitted except to breastfeed. Dapsone, rifampin, and clofazimine are typically and safely used for infant and mother, regardless of the method of feeding (see Appendix D ).


Listeriosis is a relatively uncommon infection that can have a broad range of manifestations. In immunocompetent individuals, including pregnant women, the infection can vary from being asymptomatic to presenting as an influenza-like illness, occasionally with GI symptoms or back pain. Severe disease occurs more frequently in immunodeficient individuals or infants infected in the perinatal period (pneumonia, sepsis, meningitis, and granulomatosis infantisepticum).

Although listeriosis during pregnancy may manifest as mild disease in a mother and is often difficult to recognize and diagnose, it is typically associated with stillbirth, abortion, and premature delivery. Transmission seems to occur through the transplacental hematogenous route, infecting the amniotic fluid, although ascending infection from the genital tract may occur. Early and effective treatment of a woman can prevent fetal infection and sequelae. Neonatal infection occurs as either early- or late-onset infection from transplacental spread late in pregnancy, ascending infection during labor and delivery, infection during passage through the birth canal, or, rarely, during postnatal exposure.

No evidence in the literature suggests that Listeria is transmitted through breast milk. Treatment of the mother with ampicillin, penicillin, or trimethoprim-sulfamethoxazole is not a contraindication to breastfeeding as long as the mother is well enough. Expressed colostrum or breast milk can also be given if the infant is able to feed orally. The management of lactation and feeding in neonatal listeriosis is conducted supportively, as it is in any situation in which an infant is extremely ill, beginning feeding with expressed breast milk or directly breastfeeding as soon as reasonable.

Meningococcal Infections

N. meningitidis most often causes severe invasive infections, including meningococcemia or meningitis, often associated with fever and a rash and progressing to purpura, disseminated intravascular coagulation, shock, coma, and death.

Transmission occurs via respiratory droplets. Spread can occur from an infected, ill individual or from an asymptomatic carrier. Droplet precautions are recommended until 24 hours after initiation of effective therapy. Despite the frequent occurrence of bacteremia, no evidence indicates breast involvement or transmission through breast milk.

The risk for maternal infection to an infant after birth is from droplet exposure and exists whether the infant is breastfeeding or bottle feeding. In either case, the exposed infant should receive chemoprophylaxis with rifampin, 10 mg/kg/dose every 12 hours for 2 days (5 mg/kg/dose for infants younger than 1 month of age), or ceftriaxone, 125 mg intramuscularly (IM) once, for children younger than 15 years of age. Close observation of the infant should continue for 7 days, and breastfeeding during and after prophylaxis is appropriate. The severity of maternal illness may prevent breastfeeding, but it can continue if the mother is able, after the mother and infant have been receiving antibiotics for 24 hours. A period of separation from the index case for the first 24 hours of effective therapy is recommended; expressed breast milk can be given during this period.


Respiratory illness caused by Bordetella pertussis evolves in three stages: catarrhal (nasal discharge, congestion, increasing cough), paroxysmal (severe paroxysms of cough sometimes ending in an inspiratory whoop, i.e., whooping cough), and convalescent (gradual improvement in symptoms).

Transmission is via respiratory droplets. The greatest risk for transmission occurs in the catarrhal phase, often before the diagnosis of pertussis. The nasopharyngeal culture usually becomes negative after 5 days of antibiotic therapy. Chemoprophylaxis for all household contacts is routinely recommended. No evidence indicates transmission through breast milk, with similar risk to breastfed and bottle-fed infants.

In the case of maternal infection with pertussis, chemoprophylaxis for all household contacts, regardless of age or immunization status, is indicated. In addition to chemoprophylaxis of the infant, close observation and subsequent immunization (in infants older than 6 weeks of age) are appropriate. Prophylaxis for the infant should be azithromycin or erythromycin, although trimethoprim-sulfamethoxazole can be used when the infant is 6 weeks or older. Despite chemoprophylaxis, droplet precautions and the separation of mother and infant during the first 5 days of effective maternal antibiotic therapy are recommended. Expressed breast milk can be provided to the infant during this period.

Staphylococcal Infections

Staphylococcal infection in neonates can be caused by either S. aureus or coagulase-negative staphylococci (most often Staphylococcus epidermidis ) and can manifest in a wide range of illnesses. Localized infection can be impetigo, pustulosis in neonates, cellulitis, or wound infection, and invasive or suppurative disease includes sepsis, pneumonia, osteomyelitis, arthritis, and endocarditis. S. aureus requires only a small inoculum (10 to 250 organisms) to produce colonization in newborns, most often of the nasal mucosa and umbilicus. By the fifth day of life, 40% to 90% of the infants in the nursery will be colonized with S. aureus. The organism is easily transmitted to others from mother, infant, family, or health care personnel through direct contact.

Outbreaks in nurseries were common in the past. Mothers, infants, health care workers, and even contaminated, unpasteurized, banked breast milk were sources of infection. Careful use of antibiotics, changes in nursery layout and procedures, standard precautions, and cohorting as needed decreased the spread of S. aureus in nurseries. Now the occurrence of methicillin-resistant S. aureus (MRSA) is again a common problem, requiring cohorting, occasional epidemiologic investigation, and careful infection-control intervention. There are numerous reports of MRSA outbreaks in NICUs. The significance of colonization with Staphylococcus and the factors leading to development of disease in individual patients are not clear. The morbidity and mortality related to S. aureus infection in neonates is well described, and the management of such outbreaks has been reviewed. Little has been written about the role of breastfeeding in colonization with S. aureus in NICUs, well-baby nurseries, or at home.

MRSA is an important pathogen worldwide. Community-acquired MRSA is different from hospital-acquired MRSA. Community-acquired MRSA is usually defined as occurring in an individual without the common predisposing variables associated with hospital-acquired MRSA. Community-acquired MRSA also lacks an MDR phenotype (common with hospital-acquired MRSA); frequently carries multiple exotoxin virulence factors (such as Panton-Valentine leukocidin toxin), as well as the smaller type IV staphylococcal cassette cartridge for the MecA gene on a chromosome (hospital-acquired MRSA carries the types I-III staphylococcal cassette cartridge); and is molecularly distinct from the common nosocomial strains of hospital-acquired MRSA. Community-acquired MRSA is most commonly associated with skin and soft tissue infections and necrotizing pneumonia and less frequently associated with endocarditis, bacteremia, necrotizing fasciitis, myositis, osteomyelitis, or parapneumonic effusions. Community-acquired MRSA is so common that it is now being observed in hospital outbreaks. Community-acquired MRSA transmission to infants via breast milk has been reported. Premature or small-for-gestational-age infants are more susceptible to and at increased risk for significant morbidity and mortality due to MRSA, in part because of prolonged hospitalization, multiple courses of antibiotics, invasive procedures and intravenous (IV) lines, their relative immune deficiency related to prematurity and illness, and altered GI tract due to different flora and decreased gastric acidity. Therefore, colonization with MRSA may pose a greater risk to infants in NICUs in the long run. Full-term infants develop pustulosis, cellulitis, and soft tissue infections, but invasive disease has rarely been reported. Fortunov et al. from Texas reported 126 infections in term or late-preterm previously well infants, including 43 with pustulosis, 68 with celluliltis or abscesses, and 15 invasive infections. A family history of soft tissue skin infections and male sex were the only variables associated with risk for infection; cesarean delivery, breastfeeding, and circumcision were not. Nguyen et al. reported MRSA infections in a well-infant nursery from California. The eleven cases were all in full-term boys with pustular-vesicular lesions in the groin. The infections were associated with longer length of stay, lidocaine injection use in infants, maternal age older than 30 years, and circumcision. Breastfeeding was not an associated risk factor for MRSA infection. The question of the role of circumcision in MRSA outbreaks was addressed by Van Howe and Robson. They reported that circumcised boys are at greater risk for staphylococcal colonization and infection.

Others report that S. aureus carriage in infants (and subsequent infection) is most likely affected by multiple variables, including infant factors (antibiotics, surgical procedures [circumcision being the most common], duration of hospital stay as a newborn), maternal factors (previous colonization, previous antibiotic usage, mode of delivery, length of stay), and environmental factors (MRSA in the family or hospital, nursery stay versus rooming-in, hand hygiene). Gerber et al. from the Chicago area published a consensus statement for the management of MRSA outbreaks in the NICU. The recommendations, which were strongly supported by experimental, clinical, and epidemiologic data, included using a waterless, alcohol-based hand hygiene product, monitoring and enforcing hand hygiene, placing MRSA-positive infants in contact precautions with cohorting if possible, using gloves and gowns for direct contact and masks for aerosol-generating procedures, cohorting nurses for care of MRSA-positive infants when possible, periodic screening of infants for MRSA using nares or nasopharyngeal cultures, clarifying the MRSA status of infants being transferred into the NICU, limiting overcrowding, and maintaining ongoing instruction and monitoring of health care workers in their compliance with infection-control and hand-hygiene procedures. The evaluation of the outbreak could include screening of health care workers and environmental surfaces to corroborate epidemiologic data and laboratory molecular analysis of the MRSA strains if indicated epidemiologically. The use of mupirocin or other decolonizing procedures should be determined on an individual basis for each NICU.

S. aureus is the most common cause of mastitis in lactating women. Recurrence or persistence of symptoms of mastitis is a well-described occurrence and an important issue in the management of mastitis. Community-acquired MRSA has been associated with mastitis as well (see Chapter 16 for a complete discussion of mastitis).

Two studies, one from France and one from Brazil, investigated the occurrence of MRSA in expressed breast milk. Barbe et al. cultured 9171 expressed breast milk samples from 378 women and tested 2351 samples before pasteurization and 6820 samples after pasteurization. MRSA and methicillin-susceptible S. aureus were identified, respectively, in 8 samples (0.8%) from 3 mothers and 281 samples (19.3%) from 73 mothers, using the tested expressed breast milk before pasteurization. After pasteurization, S. aureus was not detected in any of the 6820 samples of expressed breast milk. Colonization of one infant with MRSA was identified, but no MRSA infections were identified in any of the hospitalized infants in the NICU during the 18 months of the study. Novak et al. identified MRSA in 57 of 500 samples (11%) of expressed fresh-frozen milk from 500 different donors from five Brazilian milk banks. Only 3 of the 57 samples were positive with high-level bacterial counts of MRSA (greater than 10,000 CFU/mL). These were the only samples that would not have been acceptable by bacteriological criteria according to Brazilian or American criteria for raw milk use. They did not investigate other epidemiological data to identify possible variables associated with low- or high-level contamination of expressed breast milk with MRSA.

The management of an infant and/or mother with MRSA infection, relative to breastfeeding or use of breast milk, should be based on the severity of disease and whether the infant is premature, LBW, very low birth weight (VLBW), previously ill, or full term.

When full-term infants or their mothers develop mild to moderate infections (impetigo, pustulosis, cellulitis/abscess, mastitis/breast abscess, or soft tissue infection), those infants can continue breastfeeding after a short period of interruption (24 to 48 hours). During this time, pumping to maintain the milk supply should be supported, an initial evaluation for other evidence of infection should be done in the maternal-infant dyad, the infected child and/or mother should be placed on “commonly” effective therapy for the MRSA infection, and ongoing observation for clinical disease should continue. The mother and infant can “room-in” together in the hospital, if necessary, with standard and contact precautions. Culturing the breast milk is not necessary. Empiric therapy for the infant may be chosen based on medical concerns for the infant and the known sensitivity testing of the MRSA isolate. Appropriate antibiotic choices include short-term use of azithromycin (erythromycin use during infancy [less than 6 weeks of age], or breastfeeding associated with an increased risk for hypertrophic pyloric stenosis), sulfamethoxazole-trimethoprim (in the absence of G6PD deficiency and older than 30 days of age), clindamycin, and perhaps linezolid for mild to moderate infections.

When infants in NICUs (premature, LBW, VLBW, and/or previously ill) or their mothers have a MRSA infection, those infants should have the breast milk cultured and suspend breastfeeding or receiving breast milk from their mothers until the breast milk is shown to be culture-negative for MRSA. The infant should be treated as indicated for infection or empirically treated if symptomatic (with pending culture results) and closely observed for the development of new signs or symptoms of infection. Pumping to maintain the milk supply and the use of banked breast milk are appropriate. The infant should be placed on contact precautions, in addition to the routine standard precautions. The infant can be cohorted with other MRSA-positive infants, with nursing care cohorted as well. The mother with MRSA infection should be instructed concerning hand hygiene; the careful collection, handling, and storage of breast milk; contact precautions to be used with her infant; and the avoidance of contact with any other infants. The mother can receive several possible antibiotics for MRSA that are compatible with breastfeeding when used for a short period. If the mother remains clinically well, including without evidence of mastitis, but her breast milk is positive for MRSA greater than 10 4 CFU/mL, empiric therapy to diminish or eradicate colonization would be appropriate. Various regimens have been proposed to “eradicate” MRSA colonization, but none has been proven to be highly efficacious. These regimens usually include systemic antibiotics with one or two medications (rifampin added as the second medication), as well as nasal mupirocin to the nares twice daily for 1 to 2 weeks with routine hygiene, with or without the usage of hexachlorophene (or similar topical agent or cleanser) for bathing during the 1- to 2-week treatment period. There is no clear information concerning the efficacy of using similar colonization-eradication regimens for other household members or pets in preventing recolonization of the mother or infant. Before reintroducing the use of the mother’s breast milk to the infant, at least one negative breast milk culture should be obtained after the completion of therapy.

The routine screening of breast milk provided by mothers for their infants in NICUs for the presence of MRSA is not indicated in the absence of MRSA illness in the maternal-infant dyad, a MRSA outbreak in NICUs, or a high frequency of MRSA infection in a specific NICU.

Toxin-Mediated Staphylococcus Disease

One case of staphylococcal scalded skin syndrome was reported by Katzman and Wald in an infant breastfed by a mother with a lesion on her areola that did not respond to ampicillin therapy for 14 days. Subsequently, the infant developed conjunctivitis with S. aureus , which produced an exfoliative toxin, and a confluent erythematous rash without mucous membrane involvement or Nikolsky sign. No attempt to identify the exfoliative toxin in the breast milk was made, and the breast milk was not cultured for S. aureus. The child responded to IV therapy with nafcillin. This emphasizes the importance of evaluating mother and infant at the time of a suspected infection and the need for continued observation of the infant for evidence of a pyogenic infection or toxin-mediated disease, especially with maternal mastitis or breast lesions.

This case also raises the issue of when and how infants and their mothers become colonized with S. aureus and what factors lead to infection and illness in each. The concern is that Staphylococcus can be easily transmitted through skin-to-skin contact, colonization readily occurs, and potentially serious illness can occur later, long after colonization. In the case of staphylococcal scalded skin syndrome or toxic shock syndrome (TSS), the primary site of infection can be insignificant (e.g., conjunctivitis, infection of a circumcision, or simple pustulosis), but a clinically significant amount of toxin can be produced and lead to serious disease.

TSS can result from S. aureus or Streptococcus pyogenes infection and probably from a variety of antigens produced by other organisms. TSS-1 has been identified as a “superantigen” that affects the T lymphocytes and other components of the immune response, producing an unregulated and excessive immune response and resulting in an overwhelming systemic clinical response. TSS has been reported in association with vaginal delivery, cesarean delivery, mastitis, and other local infections in mothers. Mortality rates in mothers may be as high as 5%.

The case definition of staphylococcal TSS includes meeting all four major criteria: fever greater than 38.9° C, rash (diffuse macular erythroderma), hypotension, and desquamation (associated with subepidermal separation seen on skin biopsy). The definition also includes involvement of three or more organ systems (GI, muscular, mucous membrane, renal, hepatic, hematologic, or CNS); negative titers for Rocky Mountain spotted fever, leptospirosis, and rubeola; and lack of isolation of S. pyogenes from any source or S. aureus from the cerebrospinal fluid (CSF). A similar case definition has been proposed for streptococcal TSS. Aggressive empiric antibiotic therapy against staphylococci and streptococci and careful supportive therapy are essential for decreasing illness and death. Oxacillin, nafcillin, first-generation cephalosporins, clindamycin, erythromycin, and vancomycin are acceptable antibiotics, even for a breastfeeding mother. The severity of illness in the mother may preclude breastfeeding, but it can be reinitiated when the mother is improving and wants to restart. Standard precautions, with breastfeeding, are recommended.

Staphylococcal enterotoxin F has been identified in breast milk specimens collected on days 5, 8, and 11 from a mother who developed TSS at 22 hours postpartum. S. aureus that produced staphylococcal enterotoxin F was isolated from the mother’s vagina but not from breast milk. Infant and mother lacked significant levels of antibodies against staphylococcal enterotoxin F in their sera. The infant remained healthy after 60 days of follow-up. Staphylococcal enterotoxin F is pepsin inactivated at pH 4.5 and therefore is probably destroyed in the stomach environment, presenting little or no risk to the breastfeeding infant. Breastfeeding can continue if the mother is able.

Coagulase-Negative Staphylococcus

Coagulase-negative staphylococcal infection ( S. epidermidis is the predominant isolate) produces minimal disease in healthy, full-term infants but is a significant problem in hospitalized or premature infants. Factors associated with increased risk for this infection include prematurity, high colonization rates in specific nurseries, invasive therapies (e.g., IV lines, chest tubes, intubation), and antibiotic use. Illness produced by coagulase-negative staphylococci can be invasive and severe in high-risk neonates but rarely in mothers. There are reports of necrotizing enterocolitis associated with coagulase-negative Staphylococcus . At 2 weeks of age, for infants still in the nursery, S. epidermidis is a frequent colonizing organism at multiple sites, with colonization rates as high as 75% to 100%. Serious infections with coagulase-negative staphylococci (e.g., abscesses, IV line infection, bacteremia/sepsis, endocarditis, osteomyelitis) require effective IV therapy. Many strains are resistant to penicillin and the semisynthetic penicillins, so that sensitivity testing is essential. Empiric or definitive therapy may require treatment with vancomycin, gentamicin, rifampin, teicoplanin, linezolid, or combinations of these for synergistic activity. Transmission of infection in association with breastfeeding appears to be no more common than with bottle feeding. As with S. aureus , infection control includes contact and standard precautions. Occasionally, during presumed outbreaks, careful epidemiologic surveillance may be required, including cohorting, limiting overcrowding and understaffing, surveillance cultures of infants and nursery personnel, reemphasis of meticulous infection-control techniques for all individuals entering the nursery, and, rarely, removal of colonized personnel from direct infant contact.

S. epidermidis has been identified as part of the fecal microbiota of breastfed infants. S. epidermidis has also been identified in the breast milk of women with clinical evidence of mastitis. Nevertheless, S. epidermidis is rarely associated with infection in full-term infants. Conceivably, breast milk for premature infants could be a source of S. epidermidis colonization in the NICUs. The other factors associated with hospitalization in an NICU noted previously presumably play a significant role in both colonization and infection in premature infants. The benefits of early full human milk feeding potentially outweigh the risk for colonization with S. epidermidis via breast milk. Ongoing education and assistance should be provided to mothers about the careful collection, storage, and delivery of human breast milk for their premature infants.

Streptococcal Infections

Group A

S. pyogenes (β-hemolytic group A Streptococcus [GAS]) is a common cause of skin and throat infections in children, producing pharyngitis, cellulitis, and impetigo. Illnesses produced by GAS can be classified into three categories: (1) impetigo, cellulitis, or pharyngitis without invasion or complication; (2) severe invasive infection with bacteremia, necrotizing fasciitis, myositis, or systemic illness (e.g., streptococcal TSS); and (3) autoimmune-mediated phenomena, including acute rheumatic fever and acute glomerulonephritis. GAS can also cause puerperal sepsis, endometritis, and neonatal omphalitis. Significant morbidity and mortality rates are associated with invasive GAS infection; the mortality rate is 20% to 50%, with almost half the survivors requiring extensive tissue débridement or amputation. Infants are not at risk for the autoimmune sequelae of GAS (rheumatic fever or poststreptococcal glomerulonephritis). Transmission is through direct contact (rarely indirect contact) and droplet spread. Outbreaks of GAS in the nursery are rare, unlike with staphylococcal infections. Either mother or infant can be initially colonized with GAS and transmit it to the other.

In the situation of maternal illness (extensive cellulitis, necrotizing fasciitis, myositis, pneumonia, TSS, and mastitis), it is appropriate to separate mother and infant until effective therapy (penicillin, ampicillin, cephalosporins, and erythromycin) has been given for at least 24 hours. Breastfeeding should also be suspended and may resume after 24 hours of therapy for the mother.

Group B

Group B Streptococcus (GBS, Streptococcus agalactiae ) is a significant cause of perinatal bacterial infection. In parturient women, infection can lead to asymptomatic bacteriuria, urinary tract infection (often associated with premature birth), endometritis, or amnionitis. In infants, infection usually occurs between birth and 3 months of age (1 to 4 cases per 1000 live births). It is routinely classified by the time of onset of illness in the infant: early onset (0 to 7 days, majority less than 24 hours) and late onset (7 to 90 days, generally less than 4 weeks). Infants may develop sepsis, pneumonia, meningitis, osteomyelitis, arthritis, or cellulitis. Early-onset GBS disease is often fulminant, presenting as sepsis or pneumonia with respiratory failure; three-quarters of neonatal disease is early onset. Type III is the most common serotype causing disease.

Transmission is believed to occur in utero and during delivery. Colonization rates of mothers and infants vary between 5% and 35%. Postpartum transmission is thought to be uncommon, although it has been documented. Risk factors for early-onset GBS disease include delivery before 37 weeks of gestation, rupture of membranes for longer than 18 hours before delivery, intrapartum fever, heavy maternal colonization with GBS, or low concentrations of anti-GBS capsular antibody in maternal sera. The common occurrence of severe GBS disease before 24 hours of age in neonates has led to prevention strategies. Revised guidelines developed by the AAP Committees on Infectious Diseases and on the Fetus and Newborn have tried to combine various variables for increased risk for GBS infection (prenatal colonization with GBS, obstetric and neonatal risk factors for early-onset disease) and to provide intrapartum prophylaxis to those at high risk (CDCP Prev of Perinatal GBS Disease MMWR 2010 and Comm on Inf Dis and Comm on the Fetus and Newborn Pediatrics 2011) ( Figure 13-1 ). The utilization of these guidelines, universal culture-based screening, and intrapartum prophylaxis across the United States have decreased the incidence of early-onset disease by approximately 80% from an estimated 1.4 cases of early-onset GBS disease (EOD) per 1000 live births in 1990 to 0.28 cases per 1000 live births in 2012 (Van Dyke et al.)

Figure 13-1

Empiric management of a neonate born to a mother who received intrapartum antimicrobial prophylaxis (IAP) for the prevention of early-onset group B streptococcal (GBS) disease. CSF, Cerebrospinal fluid; CBC, complete blood count. This algorithm is not an exclusive course of management. Variations that incorporate individual circumstances or institutional preferences may be appropriate.

(From Committee on Infectious Diseases, American Academy of Pediatrics: Red book report of the committee on infectious disease , ed 26, Elk Grove, Ill., 2003, American Academy of Pediatrics, p 590.)

The incidence of late-onset GBS disease (LOD) remains unchanged since 1990 (~ 0.3 to 0.4 cases per 1000 live births) despite the implementation of screening and guidelines for preventing EOD (CDCP 2013 Active Bacterial Core Surveillance Report). LOD is thought to be the result of transmission during delivery or in the postnatal period from maternal, hospital, or community sources. Dillon et al. demonstrated that 10 of 21 infants with late-onset disease were colonized at birth, but the source of colonization was unidentified in the others. Gardner et al. showed that only 4.3% of 46 children who were culture-negative for GBS at discharge from the hospital had acquired GBS by 2 months of age. Anthony et al. noted that many infants are colonized with GBS, but the actual attack rate for GBS disease is low and difficult to predict.

Acquisition of GBS through breast milk or breastfeeding is uncommon and remains a controversial topic. Cases of LOD associated with GBS in the maternal milk have been reported. Some of the mothers had bilateral mastitis, at least one had delayed evidence of unilateral mastitis, and the others were asymptomatic. It was not clear when colonization of the infants occurred or when infection or disease began in the infants. The authors discussed the possibility that the infants were originally colonized during delivery, subsequently colonized the mothers’ breasts during breastfeeding, and then became re-infected at a later time. Butter and DeMoor showed that infants initially colonized on their heads at birth had GBS cultured from their throat, nose, or umbilicus 8 days later. Whenever they cultured GBS from the nipples of mothers, the authors also found it in the nose or throat of the infants.

Berardi et al. studied GBS colonization prospectively in 160 mother-infant dyads. They noted that few culture-positive women had GBS cultured from their milk through 60 days post hospital discharge. Neonates who were colonized at more than one site (throat, ear, or rectum) were most commonly born to culture-positive carrier mothers who were GBS positive at delivery. One of the three cases of neonatal GBS infection presented as LOD at 35 days of age, and one presented with EOD at birth. The third infant presented with EOD at 20 hours of age and was adequately treated. That same infant was retreated at 18 days of age for a GBS urinary tract infection. They concluded that there was no evidence that mother’s milk was the cause of the neonatal infections and that the occurrence of GBS in human milk could have been contamination or colonization from infants who were already heavily colonized with GBS. Filleron et al. reviewed 48 cases in the literature of late-onset neonatal infection (LONI) associated with GBS and breast milk. They noted four cases of LONI that occurred in the absence of maternal GBS detection, in infants born by cesarean section and with GBS-positive mother’s milk as the probable source of infection. Their analysis also demonstrated a high rate of recurrence of LONI (35% of the 48 neonates) had more than one LONI. They concluded, as others have recommended (Berardi et al., Byrne et al., Lombard et al., and Davanzo et al. ), that additional attention should be given to the handling and use of raw human milk in “vulnerable” neonates and instances of GBS culture-positive human milk with or without maternal mastitis. Byrne et al. presented a review of GBS disease associated with breastfeeding and made recommendations to decrease the risk for transmission of GBS to infants via breastfeeding or breast milk. Some of their recommendations included confirming appropriate collection and processing procedures for GBS cultures in medical facilities to decrease false-negative cultures; reviewing proper hygiene for pumping, collection, and storage of expressed breast milk with mothers; reviewing the signs and symptoms of mastitis with mothers; and utilizing banked human milk as needed instead of mother’s milk. Davanzo et al. describe proposed “best practice guidance” for managing human milk feeding and group B Streptococcus in developed countries. This guidance includes the following: (1) Do not routinely perform microbial cultures of breast milk from the mother of the term or preterm infant. (2) Interruption of breastfeeding in most situations of maternal mastitis and healthy full term infants is unnecessary, but conservative management, including milk removal, supportive measures, and antibiotics for the mother, are appropriate if her symptoms persist or worsen. (3) In the case of mastitis in mothers of preterm infants, drain the affected breast, culture the milk, and treat the mother empirically. If the milk is GBS-positive, then the milk should either be pasteurized prior to giving it to the premature infant or discarded until there is a subsequent negative culture of the milk. (4) Prevention and management strategies for EOD GBS infection should follow the revised CDC guidelines from 2010 and the more recent recommendations for the prevention of perinatal GBS disease from the AAP’s Committee on Infectious Diseases and Committee on Fetus and Newborn, 2011 [CDCP Prev Perinatal GBS Dis Rev Guidelines 2010, Comm on ID and Comm on Fetus Newborn Policy Statement re GBS prevention 2011]. These documents do not recommend routine discontinuation of breastfeeding, discarding breast milk, or pasteurization of breast milk after EOD GBS, because there is no evidence that this is protective against LOD GBS. (5) In the situation of LOD GBS disease and a positive breast milk culture for GBS, treat the mother to eradicate colonization (ampicillin or amoxicillin plus rifampin), pasteurize or discard breast milk until adequate therapy has been given to the mother or there is a negative breast milk culture, track breast milk cultures through hospitalization, and consider adding rifampin to the infant’s antibiotic treatment to eradicate colonization in the infant, even though the “eradication” of colonization is difficult and inconsistent.

When a breastfed infant develops LOD, it is appropriate to culture the milk. (See discussion of culturing breast milk earlier in this chapter.) Consider treatment of the mother to prevent reinfection if the milk is culture positive for GBS (greater than 10 4 CFU/mL), with or without clinical evidence of mastitis in the mother. Withholding the mother’s milk until it is confirmed to be culture negative for a pathogen is appropriate and should be accompanied by providing ongoing support and instruction to the mother concerning pumping and maintaining her milk supply. Serial culturing of expressed breast milk after treatment of the mother for GBS disease or colonization would be appropriate to insure the ongoing absence of a pathogen in the expressed breast milk. There are reports of reinfection of the infant from breast milk. Eradication of GBS mucosal colonization in the infant or the mother may be difficult. Some authors have recommended using rifampin prophylactically in both the mother and infant at the end of treatment to eradicate mucosal colonization. (See Chapter 16 for management of mastitis in the mother.) A mother or infant colonized or infected with GBS should be managed with standard precautions while in the hospital. Ongoing close evaluation of the infant for infection or illness and empiric therapy for GBS in the infant are appropriate until the child has remained well and cultures are subsequently negative at 72 hours. Occasionally, epidemiologic investigation in the hospital will utilize the culturing of medical staff and family members to detect a source of LOD in the nursery. This can be useful when more than one case of LOD is detected with the same serotype. Cohorting in such a situation may be appropriate. Selective prophylactic therapy for colonized infants to eradicate colonization may be considered, but unlike GAS or Staphylococcus infection, GBS infection in nurseries has not been reported to cause outbreaks. No data support conducting GBS screening on all breastfeeding mothers and their expressed breast milk as a reasonable method for protecting against spread of GBS infection via expressed breast milk or LOD GBS infection. Selective culturing of expressed breast milk may be appropriate in certain situations.


The face of TB is changing throughout the world. In the United States the incidence of TB rose from 1986 through 1993 and has been declining since then. In 2013, the incidence rate was 3.0 cases per 100,000 population, which represents a decrease of 4.2% from 2012 (Alami et al. ).

TB during pregnancy has always been a significant concern for patients and physicians alike. It is now clear that the course and prognosis of TB in pregnancy are less affected by the pregnancy and more determined by the location and extent of disease, as defined primarily by chest radiograph, and by the susceptibility of the individual patient. Untreated TB in pregnancy is associated with maternal and infant mortality rates of 30% to 40%. Effective therapy is crucial to the clinical outcome in both pregnant and nonpregnant women. TB during pregnancy rarely results in congenital TB, although congenital TB has a mortality rate as high as 50%.

Any individual in a high-risk group for TB should be screened with a tuberculin skin test (TST). No contraindication or altered responsiveness to the TST exists during pregnancy or breastfeeding. Interpretation of the TST should follow the most recent guidelines, using different sizes of induration in different-risk populations as cutoffs for a positive test, as proposed by the CDC. Figure 13-2 outlines the evaluation and treatment of a pregnant woman with a positive TST.

Figure 13-2

Evaluation and treatment of a pregnant woman with a positive tuberculin skin test.

(From Starke JR: Tuberculosis, an old disease but a new threat to mother, fetus, and neonate, Clin Perinatol 24:107, 1997.)

Treatment of active TB should begin as soon as the diagnosis is made, regardless of the fetus’s gestational age, because the risk for disease to mother and fetus clearly outweighs the risks of treatment. Isoniazid, rifampin, and ethambutol have been used safely in all three trimesters. Isoniazid and pyridoxine therapy during breastfeeding is safe, although the risk for hepatotoxicity in the mother may be a concern during the first 2 months postpartum.

Congenital TB is extremely rare, if one considers that 7 to 8 million cases of TB occur each year worldwide and that less than 300 cases of congenital TB have been reported in the literature. As with other infectious diseases presenting in the perinatal period, distinguishing congenital infection from perinatal or postnatal TB in infants can be difficult.

Postnatal TB infection in infancy typically presents with severe disease and extrapulmonary extension (meningitis; lymphadenopathy; and bone, liver, spleen involvement). Airborne transmission of TB to infants is the major mode of postnatal infection because of close and prolonged exposure in enclosed spaces, especially in their own household, to any adult with infectious pulmonary TB. Potential infectious sources could be the mother or any adult caregiver, such as babysitters, day care workers, relatives, friends, neighbors, and even health care workers. Mittal et al. recently reviewed the management of the newborn infant exposed to their mother with TB.

The suspicion of TB infection or disease in a household with possible exposure of an infant is a highly anxiety-provoking situation ( Figure 13-3 ). Although protecting an infant from infection is foremost in everyone’s mind, separation of the infant from the mother should be avoided when reasonable. Every situation is unique, and the best approach will vary according to the specifics of the case and accepted principles of TB management. The first step in caring for the potentially exposed infant is to determine accurately the true TB status of the suspected case (mother or household contact). This prompt evaluation should include a complete history (previous TB infection or disease, previous or ongoing TB treatment, TST status, symptoms suggestive of active TB, results of most recent chest radiograph, sputum smears, or cultures), physical examination, a TST if indicated, a new chest radiograph, and mycobacterial cultures and smears of any suspected sites of infection. All household contacts should be evaluated promptly, including history and TST with further evaluation as indicated. Continued risk to the infant can occur from infectious household contacts who have not been effectively evaluated and treated.

Figure 13-3

Management of a newborn infant exposed to tuberculin-positive household contact. CXR, Chest X-ray film; INH, isoniazid; MDR, multidrug-resistant; TB, tuberculosis.

An infant should be temporarily separated from the suspected source if symptoms suggest active disease or a recent TST documents conversion, and separation should continue until the results of the chest radiograph are seen. Because of considerable variability in the course of illness and the concomitant infectious period, debate continues without adequate data about the appropriate period of separation. This should be individualized given the specific situation. HIV testing and assessment of the risk for MDR TB should be done in every case of active TB. Sensitivity testing should be done on every M. tuberculosis isolate. Table 13-1 summarizes the management of the newborn infant whose mother (or other household contact) has TB.

Table 13-1

Management of a Newborn Whose Mother (or Other Household Contact) Has Tuberculosis (TB)

Mother/Infant Status Additional Workup Recommended 1 Therapy for Mother/Contact Therapy for Infant Separation 2 Breast Milk 3 Breastfeeding 3
1. TB infection, no disease 4 None for mother/contact Prophylactic 5 None No Yes Yes
2. TB infection: Abnormal CXR not suggestive of active disease Decide active vs. inactive disease
a. Symptoms or physical findings suggestive of active TB Aerosolized sputum (culture, smears) 6 Active disease: empiric 5 Isoniazid 7 Yes Yes No 8
Inactive disease: prophylactic 5 None No Yes Yes
b. No symptoms or physical findings suggestive of active TB Aerosolized sputum in select cases Prophylactic 5 None No Yes Yes
3. TB infection: Abnormal CXR suggestive of active disease Aerosolized sputum (culture, smears) 6 Empiric therapy 5 Isoniazid 7 Yes Yes No 8
4. Active pulmonary TB: Suspected MDR TB Aerosolized sputum (culture, smears) 6 Consult TB specialist for best regimen 9 Consult pediatric TB specialist 9 Yes Yes No
Consider bacille Calmette-Guérin vaccine
5. TB disease: Suspected mastitis 10 Aerosolized sputum (culture, smears) 6 Empiric 5 Isoniazid 7 Yes No 11 No
6. TB infection: Status undertermined 12 Perform/interpret CXR within 24 hours Yes, until CXR interpreted (see a and b) Yes No
a. Abnormal CXR not suggestive of active disease Proceed as in 2 As in 2 As in 2 As in 2
b. Abnormal CXR suggestive of active disease Proceed as in 3 As in 3 As in 3 As in 3

Data from the Committee on Infectious Diseases, American Academy of Pediatrics: Red book: report of the committee on infectious diseases , ed 26, Elk Grove Village, Ill., 2003, American Academy of Pediatrics.

1 Further workup should always include the evaluation of the TB status of all other household (or close) contacts by tuberculin skin testing (TST), review of symptoms, physical examination, and chest X-ray (CXR). Sputum smears and cultures should be done as indicated.

2 Separation should occur until interpretation of CXR confirms the absence of active disease, or, with active disease, separation should continue until the individual is no longer considered infectious: three negative consecutive sputum smears, adequate ongoing empiric therapy, and decreased fever, cough, and sputum production. Separation means movement to a different house or location, not simply separate rooms in a household. The duration of separation should be individualized for each case, in consultation with the TB specialist.

3 This assumes no evidence of breast involvement, suspected TB mastitis, or lesions (except in status 5, when breast involvement is considered). The risk to the infant is via aerosolized bacteria in the sputum from the lung. Expressed breast milk can be given even if separation of mother and infant is advised.

4 TST positive, no symptoms or physical findings suggestive of TB, negative CXR.

5 Prophylactic therapy: isoniazid 10 mg/kg/day, maximum 300 mg for 6 months; pyridoxine 25 to 50 mg/day for 6 months. Empiric therapy: standard three- or four-drug regimens for 2 months, and treatment should continue for total of 6 months with isoniazid and rifampin when the organism is shown to be sensitive. Suspected MDR TB requires consultation with a TB specialist to select the optimum empiric regimen and for ongoing monitoring of therapy and clinical response.

6 Sensitivity testing should be done on any positive culture.

7 Isoniazid 10 mg/kg/day for 3 to 9 months, depending on the mother’s or contact’s status; repeat TST at 3 months and obtain a normal CXR in the infant before stopping isoniazid. Before beginning therapy, a workup of the infant for congenital or active TB may be appropriate. This workup should be determined based on the clinical status of the infant and the suspected potential risk, and it may include TST after 4 weeks of age, with CXR, complete blood count, and erythrocyte sedimentation rate, liver function tests, cerebrospinal fluid analysis, gastric aspirates, and sonography or computed tomography of liver, spleen, and chest, if congenital TB is suspected.

8 Breastfeeding is proscribed when the separation of the mother and infant is indicated because of risk for aerosolized transmission of bacteria. Expressed breast milk given to the infant via bottle is acceptable in the absence of mastitis or breast lesions.

9 Consult with a TB specialist about MDR TB. Empiric therapy will be chosen based on the most recent culture sensitivities of the index patient or perhaps the suspected source case, if known, as well as medication toxicities and other factors.

10 TB mastitis usually involves a single breast with associated axillary lymph node swelling and, infrequently, a draining sinus tract. It can also present as a painless mass or edema of breast.

11 With suspected mastitis or breast lesions caused by TB, even breast milk is contraindicated until the lesion or mastitis heals, usually after 2 weeks or more.

12 Patient has a documented, recent TST conversion, but has not been completely evaluated. Evaluation should begin and CXR should be done and evaluated in less than 24 hours to minimize separation of this person from the infant. Further workup should proceed as indicated by symptoms, physical findings, and CXR results.

Initiation of prophylactic isoniazid therapy in the infant has been demonstrated to be effective in preventing TB infection and disease in the infant. Therefore, continued separation of the infant and mother is unnecessary after therapy in both mother and child has begun. The AAP recommends isoniazid (INH) prophylaxis for all infants whose mothers have been diagnosed with active pulmonary TB in the postpartum period. The real risk requiring infant separation is airborne transmission. Separation of the infant from a mother with active pulmonary TB is appropriate, regardless of the method of feeding. However, in many parts of the world, after therapy in the mother and prophylaxis with isoniazid in the infant has begun, the infant and mother are not separated. With or without separation, the mother and infant should continue to be closely observed throughout the course of maternal therapy to ensure good compliance with medication by both mother and infant and to identify, early on, any symptoms in the infant suggestive of TB. The mother should be followed to confirm that she is no longer considered infectious, with negative smears and cultures within 2 to 4 weeks of beginning TB therapy.

Tuberculous mastitis occurs rarely in the United States, but it does occur in other parts of the world and can lead to infection in infants, frequently involving the tonsils. A mother usually has a single breast mass and associated axillary lymph node swelling and infrequently develops a draining sinus. TB of the breast can also present as a painless mass or edema. Involvement of the breast can occur with or without evidence of disease at other sites. Evaluation of the extent of the disease is appropriate, including lesion cultures by needle aspiration, biopsy, or wedge resection and milk cultures. Therapy should be with multiple anti-TB medications, but surgery should supplement this, as needed, to remove extensive necrotic tissue or a persistently draining sinus. Neither breastfeeding nor breast milk feeding should be done until the lesion is healed, usually after 2 weeks or more. Continued anti-TB therapy for 6 months in the mother and prophylactic isoniazid for the infant for 3 to 6 months is indicated.

In the absence of tuberculous breast infection in the mother, the transmission of TB through breast milk has not been documented. Thus even though temporary separation of infant and mother may occur pending complete evaluation and initiation of adequate therapy in the mother and prophylactic isoniazid therapy (10 mg/kg/day as a single daily dose) in the infant, breast milk can be expressed and given to the infant during the short separation. Breastfeeding can safely continue when the mother, infant, or both are receiving anti-TB therapy. Anti-TB medications (isoniazid, rifampin, pyrazinamide, aminoglycosides, ethambutol, ethionamide, p -aminosalicylic acid) have been safely used in infancy, and therefore, the presence of these medications in smaller amounts in breast milk is not a contraindication to breastfeeding.

Although conflicting, reports indicate that breastfeeding by TST-positive mothers does influence infants’ responses to bacille Calmette-Guérin vaccine, the TST, and perhaps the M. tuberculosis bacillus. Despite efforts to identify either a soluble substance or specific cell fractions (gamma/delta T cells) in colostrum and breast milk that affect infants’ immune responsiveness, no unified theory explains the various reported changes, and no evidence has identified a consistent, clinically significant effect.

Viral Infections


Arboviruses were originally a large collection of viruses grouped together because of the common mode of transmission through arthropods. They have now been reclassified into several different families: Bunyaviridae, Togaviridae, Flaviviridae, Reoviridae, and others. They include more than 30 human pathogens.

These organisms primarily produce either CNS infections (encephalitis, meningoencephalitis) or undifferentiated illnesses associated with fever and rash, severe hemorrhagic manifestations, and involvement of other organs (hepatitis, myalgia, polyarthritis). Infection with this array of viruses may also be asymptomatic and subclinical, although how often this occurs is uncertain. Some of the notable human pathogens include Bunyaviridae (California serogroup viruses), Hantavirus , Hantaan virus, Phlebovirus (Rift Valley fever), Nairovirus (Crimean-Congo hemorrhagic fever), Alphavirus (western, eastern, and Venezuelan equine encephalomyelitis viruses, chikungunya virus), Flavivirus (St. Louis encephalitis virus, Japanese encephalitis virus, dengue viruses, yellow fever virus, tick-borne encephalitis viruses, West Nile virus), and Orbivirus (Colorado tick fever). Other than for Crimean-Congo hemorrhagic fever and for reported cases of Colorado tick fever associated with transfusion, direct person-to-person spread has rarely been described. Outbreaks in 2005 and 2007 of chikungunya virus infection in Reunion Island and in India appear to have involved infection in young infants probably secondary to vertical spread from mother to infant transplacentally. A few cases of early fetal deaths were associated with infection in pregnant women. The cases of vertical transmission occurred with near-term infection in the mothers, and the infants developed illness within 3 to 7 days of delivery. No evidence for transmission via breast milk or breastfeeding is available.

Overall, little evidence indicates that these organisms can be transmitted through breast milk. The exceptions to this include evidence of transmission of three flaviviruses via breast milk: dengue virus, West Nile virus, and yellow fever vaccine virus. Standard precautions are generally sufficient. With any of these infections in a breastfeeding mother, the severity of the illness may determine the mother’s ability to continue breastfeeding. Providing the infant with expressed breast milk is acceptable. (See the discussion of dengue virus, West Nile virus, and yellow fever vaccine virus later in this chapter.)

In general, treatment for these illnesses is supportive. However, ribavirin appears to decrease the severity of and mortality from Hantavirus pulmonary syndrome, hemorrhagic fever with renal failure, and Crimean-Congo hemorrhagic fever. Ribavirin has been described as teratogenic in various animal species and is contraindicated in pregnant women. No information is available concerning ribavirin in breast milk, with limited information available on the use of intravenous or oral ribavirin in infants.


Arenaviruses are single-stranded ribonucleic acid (RNA) viruses that infect rodents and are acquired by humans through the rodents. The six major human pathogens in this group are (1) lymphocytic choriomeningitis virus, (2) Lassa fever virus, (3) Junin virus (Argentine hemorrhagic fever), (4) Machupo virus (Bolivian hemorrhagic fever), (5) Guanarito virus (Venezuelan hemorrhagic fever), and (6) Sabia virus. The geographic distribution of these viruses and the illness they cause are determined by the living range of the host rodent (reservoir). The exact mechanism of transmission to humans is unknown and hotly debated. Direct contact and aerosolization of rodent excretions and secretions are probable mechanisms.

Lymphocytic choriomeningitis virus is well recognized in Europe, the Americas, and other areas. Perinatal maternal infection can lead to severe disease in the newborn, but no evidence suggests transmission through breast milk. Standard precautions with breastfeeding are appropriate.

Lassa fever (West Africa) and Argentine hemorrhagic fever (Argentine pampas) are usually more severe illnesses, with dramatic bleeding and involvement of other organs, including the brain. These fevers more frequently lead to shock and death than do the forms of hemorrhagic fever caused by the other viruses in this group. Person-to-person spread of Lassa fever is believed to be common, and transmission within households does occur. This may relate to prolonged viremia and excretion of the virus in the urine of humans for up to 30 days. The possibility of persistent virus in human urine, semen, and blood after infection exists for each of the arenaviruses. The possibility of airborne transmission is undecided. Current recommendations by the CDC are to use contact precautions for the duration of the illness in situations of suspected viral hemorrhagic fever. No substantial information describes the infectivity of various body fluids, including breast milk, for these different viral hemorrhagic fevers. Considering the severity of the illness in mothers and the risk to the infants, it is reasonable to avoid breastfeeding in these situations if alternative forms of infant nutrition can be provided for the short term.

As more information becomes available, reassessment of these recommendations is advisable. A vaccine is in trials in endemic areas for Junin virus and Argentine hemorrhagic fever. Preliminary studies suggest it will be effective, but data are still being accumulated concerning the vaccine’s use in children and pregnant or breastfeeding women.


CMV is one of the human herpesviruses. Congenital infection of infants, postnatal infection of premature infants, and infection of immune-deficient individuals represent the most serious forms of this infection in children. The time at which the virus infects the fetus or infant and the presence or absence of antibodies against CMV from the mother are important determinants of the severity of infection and the likelihood of significant sequelae (congenital infection syndrome, deafness, chorioretinitis, abnormal neurodevelopment, learning disabilities). About 1% of all infants are born excreting CMV at birth, and approximately 5% of these congenitally infected infants will demonstrate evidence of infection at birth (approximately 5 symptomatic cases per 10,000 live births). Approximately 15% of infants born after primary infection in a pregnant woman will manifest at least one sequela of prenatal infection.

Various studies have detected that 3% to 28% of pregnant women have CMV in cervical cultures and that 4% to 5% of pregnant women have CMV in their urine. Perinatal infection certainly occurs through contact with virus in these fluids, but it is not usually associated with clinical illness in full-term infants. The lack of illness is thought to result from the transplacental passive transfer of protective antibodies from the mother.

Postnatal infection later in infancy occurs via breastfeeding or contact with infected fluids (e.g., saliva, urine), but, again, it rarely causes clinical illness in full-term infants. Seroepidemiologic studies have documented the transmission of infection in infancy, with higher rates of transmission occurring in day care centers, especially when the prevalence of CMV in the urine and saliva is high. CMV has been identified in the milk of CMV-seropositive women at varying rates (10% to 85%), using viral cultures or CMV deoxyribonucleic acid (DNA) PCR. CMV is more often identified in the breast milk of seropositive mothers than in vaginal fluids, urine, and saliva. The CMV isolation rate from colostrum is lower than that from mature milk. The reason for the large degree of variability in the identification of CMV in breast milk in these studies probably relates to the intermittent nature of the reactivation and excretion of the virus, in addition to the variability, frequency, and duration of sampling of breast milk in the different studies. Some authors have hypothesized that the difference in isolation rates between breast milk and other fluids is caused by viral reactivation in cells (leukocytes or monocytes) in the breast leading to “selective” excretion in breast milk. Vochem et al. reported that the rate of virolactia was greatest at 3 to 4 weeks postpartum, and Yeager et al. reported significant virolactia between 2 and 12 weeks postpartum. Antibodies (e.g., secretory IgA) to CMV are present in breast milk, along with various cytokines and other proteins (e.g., lactoferrin). These may influence virus binding to cells, but they do not prevent transmission of infection.

Several studies have documented increased rates of postnatal CMV infection in breastfed infants (50% to 69%), compared with bottle-fed infants (12% to 27%), observed through the first year of life. In these same studies, full-term infants who acquired CMV infection postnatally were only rarely mildly symptomatic at the time of seroconversion or documented viral excretion. Also, no evidence of late sequelae from CMV was found in these infants.

Postnatal exposure of susceptible infants to CMV, including premature infants without passively acquired maternal antibodies against CMV, infants born to CMV-seronegative mothers, and immunodeficient infants, can cause significant clinical illness (pneumonitis, hepatitis, thrombocytopenia). In one study of premature infants followed up to 12 months, Vochem et al. found CMV transmission in 17 of 29 infants (59%) exposed to CMV virolactia and breastfed, as compared with no infants among the 27 exposed to breast milk without CMV. No infant was given CMV-seropositive donor milk or blood. Five of the 12 infants who developed CMV infection after 2 months of age had mild signs of illness, including transient neutropenia, and only one infant had a short increase in episodes of apnea and a period of thrombocytopenia. Five other premature infants with CMV infection before 2 months of age had acute illness, including sepsis-like symptoms, apnea with bradycardia, hepatitis, leukopenia, and prolonged thrombocytopenia. In a prospective study done in the United States, Josephson et al. examined the role of transfusions and breastmilk causing CMV infection in VLBW infants. In the mothers, the seroprevalence of CMV was 76.2% (352/462). In 301 infants receiving 2061 transfusions of CMV-seronegative and leukoreduced blood, there were no CMV infections linked to transfusion. Postnatal CMV infection had a cumulative incidence at 12 weeks post birth of 6.9% (95% CI, 4.2% to 9.2%), and 5 of 29 CMV-infected infants developed symptomatic disease or died. Twenty-seven of the 29 infants received CMV-positive breast milk. Factors associated with a higher risk of postnatal CMV infection were a higher CMV viral load in the breast milk and a higher number of breast milk-fed days. This study also demonstrated that the use of CMV-seronegative and leukoreduced blood products is effective at preventing transfusion-related CMV infection. In a systematic review and meta-analysis, Lanzieri et al. utilized data from17 studies published between 2001 and 2011. They reported on 299 infants who received untreated breast milk. Of these infants, 19% acquired CMV infection and 4% developed a sepsis-like syndrome related to CVM infection. Among the 212 infants included who received frozen breast milk (at various temperatures and durations in different studies—18° C to 20° C for over 24 hours or 72 hours), 13% developed CMV infection and 5% had an associated sepsis-like syndrome. Although the overall rate of CMV infection related to breast milk was slightly lower in the untreated breast milk group there was no difference in the occurrence of sepsis-like syndrome in the two groups.

Relative to long-term sequelae related to postnatal CMV infection in VLBW infants, Vollmer et al. followed premature infants with early postnatal CMV infection acquired through breast milk for 2 to 4.5 years to assess neurodevelopment and hearing function. None of the children had sensorineural hearing loss. There was no difference between the 22 CMV-infected children and 22 matched premature control CMV-negative infants in terms of neurologic, speech and language or motor development. Neuberger et al. examined the symptoms and neonatal outcome of CMV infection transmitted via human milk in premature infants in a case-control fashion; 40 CMV-infected premature infants were compared with 40 CMV-negative matched premature infants. Neutropenia, thrombocytopenia, and cholestasis were associated with CMV infection in these infants. No other serious effects or illnesses were found directly associated with the infection, including intraventricular hemorrhage, periventricular leukomalacia, retinopathy of prematurity, necrotizing enterocolitis, bronchopulmonary dysplasia, duration of mechanical ventilation or oxygen therapy, duration of hospital stay or weight, gestational age, or head circumference at the time of discharge. More recent studies do not clarify the long-term effects on the neurodevelopmental status of premature or LBW infants with symptomatic postnatal CMV infection. They present contradictory evidence concerning the occurrence of adverse neurologic outcomes or sensorineural hearing loss in these children.

Exposure of CMV-seronegative, premature, or VLBW infants to CMV-positive milk (donor or natural mother’s) should be avoided. Various methods of inactivating CMV in breast milk have been reported, including HP, freezing (− 20° C for 3 days), and brief high temperature (72° C for 10 seconds). One small prospective study suggests that freezing breast milk at − 20 °C for 72 hours protects premature infants from CMV infection via breast milk. Sharland et al. reported on 18 premature infants (less than 32 weeks) who were uninfected at birth and exposed to breast milk from their CMV-seropositive mothers. Only 1 of 18 (5%) infants became positive for CMV at 62 days of life, and this infant was clinically asymptomatic. This transmission rate is considerably lower than others reported in the literature. CM-seronegative and leukocyte-depleted blood products were used routinely. Banked breast milk was pasteurized and stored at − 20° C for various time periods, and maternal expressed breast milk was frozen at − 20° C before use whenever possible. The infants received breast milk for a median of 34 days (range: 11 to 74 days), and they were observed for a median of 67 days (range: 30 to 192 days). Breast milk samples pre- or postfreezing were not analyzed by PCR or culture for the presence of CMV. Buxmann et al. demonstrated no transmission of CMV in 23 premature infants receiving thawed frozen breast milk until 33 weeks (gestational age + postnatal age) (less than or equal to 31 weeks’ gestational age) born to 19 mothers who were CMV-IgG negative. CMV infection was found in 5 premature infants of 35 infants born to 29 mothers who were CMV-IgG positive and who provided breast milk for their infants. Three of the five children remained asymptomatic. One child developed a respirator-dependent pneumonia, and the second developed an upper respiratory tract infection and thrombocytopenia in association with their CMV infections. Yasuda et al. reported on 43 preterm infants (median gestational age 31 weeks), demonstrating a peak in CMV DNA copies, detected by a real-time PCR assay, in breast milk at 4 to 6 weeks postpartum. Thirty of the 43 infants received CMV DNA-positive breast milk. Three of the 30 had CMV DNA detected in their sera, but none of the three had symptoms suggestive of CMV infection. Much of the breast milk had been stored at − 20° C before feeding, which the authors propose is the probable reason for less transmission in this cohort. Lee et al. reported on the use of maternal milk frozen at − 20 °C for a minimum of 24 hours before feeding to premature infants in a NICU; 23 infants had CMV-seropositive mothers and 39 infants had CMV-seronegative mothers. Two infants developed CMV infection, which was symptomatic. They were both fed frozen and then thawed milk from CMV-seropositive mothers. Others have reported individual cases of CMV infection in premature infants despite freezing and thawing breast milk. More recent studies, including a prospective cohort study of breast milk transmission of CMV by Josephson et al. and a systematic review and meta-analysis of breast milk-acquired CMV infection in VLBW and premature infants by Lanzieri et al., demonstrate that frozen-thawed breast milk provides minimal protection, at best, against breast milk-acquired CMV infection. It is clear that the simple freezing and thawing of breast milk does not completely prevent transmission of CMV to premature and VLBW infants. The efficacy of freezing and thawing breast milk for varying lengths of time to prevent CMV infection in premature infants has not been studied prospectively in a randomized controlled trial. Eleven of 36 neonatal units in Sweden (27 of which have their own milk banks) freeze maternal milk to reduce the risk for CMV transmission to premature infants.

A prominent group of neonatologists and pediatric infectious disease experts in California, who recognize the significant benefits of providing human milk to premature and LBW infants, recommend screening mothers of premature infants for CMV IgG at delivery and, when an infant’s mother is CMV IgG positive at delivery, using either pasteurized banked human milk or frozen and then thawed maternal breast milk for premature infants until they reach the age of 32 weeks. In consideration of the low rates of CMV virolactia in colostrum and the predominant occurrence of virolactia between 2 and 12 weeks (peak at 3 to 4 weeks) postpartum, they reasonably propose beginning colostrum and breast milk feedings for all infants until the maternal CMV-serologic screening is complete. They recommend close observation and follow-up of premature infants older than 3 weeks of age for signs, symptoms, and laboratory changes of CMV infection until discharge from the hospital or out to 32 weeks postconceptual age. Additional research and discussion will be necessary to devise a protocol for the use of human milk in premature and VLBW infants to optimize their growth, development, and immune protection at the same time as preventing the risk of acquiring postnatal CMV infection.

There has been much discussion of the use of CMV immunoglobulin and/or antiviral medications (acyclovir, ganciclovir, valganciclovir) to treat women during pregnancy in order to protect against congenital CMV infection. Although these agents have also been used to treat infants with symptomatic congenital CMV and symptomatic acute postnatal CMV infection, they have not been studied as prophylaxis against postnatal CMV infection.

Full-term infants can be safely fed human milk from CMV-seropositive mothers because, despite a higher rate of CMV infection than in formula-fed infants observed through the first year of life, infection in this situation is not associated with significant clinical illness or acute or long-term sequelae.

Dengue Disease

Dengue viruses (serotypes dengue 1 to 4) are flaviviruses associated primarily with febrile illnesses and rash; dengue fever, dengue hemorrhagic fever, and dengue shock syndrome. The mosquito Aedes aegypti is the main vector of transmission of dengue virus in countries lying between latitudes 35 degrees north and 35 degrees south. More than 2.5 billion people live in areas where transmission occurs; dengue virus infects over 100 million individuals a year and causes approximately 24,000 deaths per year. Although dengue hemorrhagic fever and dengue shock syndrome occur frequently in children younger than 1 year of age, they are infrequently described in infants younger than 3 months of age. There are also differences in the clinical and laboratory findings of dengue virus infection in children, as compared to adults. Boussemart et al. reported on two cases of perinatal/prenatal transmission of dengue and discussed eight additional cases in neonates from the literature. Prenatal or intrapartum transmission of the same type of dengue as the mother was confirmed by serology, culture, or PCR. Phongsamart et al. described three additional cases of dengue virus infection late in pregnancy, with apparent transmission to two of the three infants and passive acquisition of antibody in the third infant. Sirinavin et al. reported on 17 cases in the literature of vertical dengue infection, all presenting at less than 2 weeks of age, but no observations or discussion of breast milk or breastfeeding as a potential source of infection were published. Watanaveeradej et al. presented an additional three cases of dengue infection in infants, documenting normal growth and development at follow-up at 12 months of age.

It has been postulated that more severe disease associated with dengue disease occurs when an individual has specific IgG against the same serotype as the infecting strain in a set concentration, leading to antibody-dependent enhancement of infection. The presence of preexisting dengue serotype-specific IgG in an infant implies either previous primary infection with the same serotype, passive acquisition of IgG from the mother (who had a previous primary infection with the same serotype), or perhaps acquisition of specific IgG from breast milk. Watanaveeradej et al. documented transplacentally transferred antibodies against all four serotypes of dengue virus in 97% of 2000 cord sera at delivery. Follow-up of 100 infants documented the loss of antibodies to dengue virus over time, with losses of 3%, 19%, 72%, 99%, and 100% at 2, 4, 6, 9, and 12 months of age, respectively.

No evidence is available in the literature about more severe disease in breastfed infants compared with formula-fed infants. There is no evidence of the interperson transmission of dengue virus in the absence of a mosquito vector. There is one case report of apparent transmission of dengue virus via breast milk to a 4-day-old infant, however. The mother had clinical illness consistent with dengue virus disease at delivery, and the infant developed disease on day 4 of life. The mother’s blood was positive for dengue virus by RT-PCR on days 0 to 6 after delivery, and her breast milk was positive on days 2 and 4 after delivery. The infant’s blood from days 0 and 2 and the cord blood were repeatedly negative by RT-PCR, but subsequently, the infant’s blood was PCR positive for dengue virus on days 4 to 13 of life. There is one report of a factor in the lipid portion of breast milk, which inhibits the dengue virus, but no evidence for antibody activity against the dengue virus in human breast milk is known. Given the apparent rarity of the transmission of dengue virus via breast milk, breastfeeding during maternal or infant dengue disease should continue, as determined by the mother’s or infant’s severity of illness.

Epstein-Barr Virus

Epstein-Barr virus (EBV) is a common infection in children, adolescents, and young adults. It is usually asymptomatic, but it most notably causes infectious mononucleosis and has been associated with chronic fatigue syndrome, Burkitt lymphoma, and nasopharyngeal carcinoma. Because EBV is one of the human herpesviruses, concern has been raised about lifelong latent infection and the potential risk for infection to a fetus and neonate from the mother. Primary EBV infection during pregnancy is unusual because few pregnant women are susceptible. Although abortion, premature birth, and congenital infection from EBV are suspected, no distinct group of anomalies is linked to EBV infection in the fetus or neonate. Also, no virologic evidence of EBV as the cause of abnormalities was found in association with suspected EBV infection.

Culturing of EBV from various fluids or sites is difficult. The virus is detected by its capacity to transform B lymphocytes into persistent lymphoblastoid cell lines. PCR and DNA hybridization studies have detected EBV in the cervix and in breast milk. One study, which identified EBV DNA in breast milk cells in more than 40% of women donating milk to a breast milk bank, demonstrated that only 17% had antibodies to EBV (only IgG, no IgM). EBV DNA was identified in 33% of 40 human milk samples from normal lactating women in a separate study. However, a study by Kusuhara et al. examining serologic specimens from breastfed and bottle-fed infants showed similar seroprevalence of EBV at 12 to 23 months of age (36/66 [54.5%] and 24/43 [55.8%]) in the breastfed and bottle-fed children, respectively. This suggests that early acquisition of EBV infection in infants is not significantly affected by the consumption of breast milk.

The question of the timing of EBV infection and the subsequent immune response and clinical disease produced requires continued study. Differences exist among the clinical syndromes that manifest at different ages. Infants and young children are asymptomatic, have illness not recognized as related to EBV, or have mild episodes of illness, including fever, lymphadenopathy, rhinitis, cough, hepatosplenomegaly, and rash. Adolescents or young adults who experience primary EBV infection more often demonstrate infectious mononucleosis syndrome or are asymptomatic. Chronic fatigue syndrome is more common in adolescents and young adults. Burkitt lymphoma, observed primarily in Africa, and nasopharyngeal carcinoma, seen in southeast Asia, where primary EBV infection usually occurs in young children, are tumors associated with early EBV infection. These tumors are related to “chronic” EBV infection and tend to occur in individuals with persistently high antibody titers to EBV viral capsid antigen and early antigen. The questions of why these tumors occur with much greater frequency in these geographic areas and what cofactors (including altered immune response to infection associated with coinfections, immune escape by EBV leading to malignancy, or increased resistance to apoptosis secondary to EBV gene mutations) may contribute to their development remain unanswered.

It also remains unknown to what degree breast milk could be a source of early EBV infection, as compared to other sources of EBV infection in an infant’s environment. Similar to the situation of postnatal transmission of CMV in immunocompetent infants, clinically significant illness rarely is associated with primary EBV infection in infants. More data concerning the pathogenesis of EBV-associated tumors should be obtained before proscribing against breastfeeding is warranted, especially in areas where these tumors are common but the protective benefits of breastfeeding are high. In areas where Burkitt lymphoma and nasopharyngeal carcinoma are uncommon, EBV infection in mother or infant is certainly not a contraindication to breastfeeding.


Marburg and Ebola viruses cause severe and highly fatal hemorrhagic fevers. The illness often presents with nonspecific symptoms (conjunctivitis, frontal headache, malaise, myalgia, bradycardia) and progresses with worsening hemorrhage to shock and subsequent death in 50% to 90% of patients. Person-to-person transmission through direct contact, droplet spread, or airborne spread is the common mode of transmission. However, the animal reservoir or source of these viruses in nature for human infection has not been identified. Attack rates in families are 5% to 16%. No postexposure interventions have proved useful in preventing spread, and no treatment other than supportive is currently available.

One report documented the presence of Ebola virus in numerous body fluids, including breast milk. One acute breast milk sample on day 7 after the onset of illness in the mother and a “convalescent” breast milk sample on day 15 from the same woman were positive for Ebola virus by both culture and PCR testing. In the same study, testing other body fluids in different persons, saliva remained virus positive for a mean of 16 days after disease onset, urine was positive for a mean of 28 days, and semen for a mean of 43 days after the onset of disease in survivors of Ebola infection.

No information is available concerning the risk for transmission of these viruses in breast milk or additional risks or benefits from breastfeeding in an area involved in an Ebola outbreak or with household members who are infected.

Contact precautions have been recommended for Marburg and Ebola virus infections and contact and airborne precautions for Ebola virus infection. The largest epidemic of EVD in West Africa (predominantly Guinea, Liberia, Sierra Leone), involving over 21,000 cases and over 8400 deaths, occurred through 2014 to 2015. This outbreak has dramatically raised concerns about the transmission of Ebola to family members, close contacts, travelers, and health care personnel. To date, there are no newer publications for this epidemic on transmissibility from different body fluids and particularly from breast milk. The WHO and CDC have developed updated guidance for the use of personal protective equipment for health care workers (CDCP ). This guidance continues to be updated (CDCP ). Both of these guidelines reinforce the high risk of Ebola virus infection without careful protection against contact with body fluids from a person with EVD. Given the high attack and mortality rates associated with EVD, these precautions should be carefully instituted within health care facilities, and breastfeeding should not be allowed if the mother has suspected EVD. If any other suitable source of nutrition can be found for an infant, expressed breast milk should also be proscribed for the infant of a mother with either of these infections for at least 3 weeks postrecovery.

Hepatitis in the Mother

The diagnosis of hepatitis in a pregnant woman or nursing mother causes significant anxiety. The first issue is determining the etiology of the hepatitis, which then allows for an informed discussion of risk to the fetus or infant. The differential diagnosis of acute hepatitis includes (1) common causes of hepatitis, such as hepatitis A, B, C, and D; (2) uncommon causes of hepatitis, such as hepatitis E and G, CMV, echoviruses, enteroviruses, EBV, HSV, rubella, varicella-zoster virus, yellow fever virus; (3) rare causes of hepatitis, such as Ebola virus, Junin virus, and Machupo virus (cause hemorrhagic fever), Lassa virus, and Marburg virus; and (4) nonviral causes, such as hepatotoxic drugs, alcoholic hepatitis, toxoplasmosis, autoimmune hepatitis, bile duct obstruction, ischemic liver damage, Wilson disease, α 1 -antitrypsin deficiency, and metastatic liver disease. The following sections focus on hepatitis viruses A to G. Other infectious agents that can cause hepatitis are considered individually in other sections. Box 13-2 provides hepatitis terminology.

Box 13-2

Terminology for Hepatitis

Hepatitis A Virus (HAV)
IgM anti-HAV Immunoglobulin M (IgM) antibody against HAV
HAV RNA HAV ribonucleic acid
Hepatitis B Virus (HBV)
HBsAg Hepatitis B surface antigen
HBeAg Hepatitis Be antigen
HBcAg Hepatitis B core antigen
Anti-HBe Antibody against hepatitis Be antigen
IgM anti-HBcAg IgM antibody against hepatitis B core antigen
HBV DNA HBV deoxyribonucleic acid
HBIG Hepatitis B immunoglobulin
Hepatitis C Virus (HCV)
Anti-HCV Antibody against HCV
HCV RNA HCV ribonucleic acid
Hepatitis D Virus (HDV)
Anti-HDV Antibody against HDV
Hepatitis E Virus (HEV)
HEV RNA HEV ribonucleic acid
Hepatitis G Virus (HGV)
HGV RNA HGV ribonucleic acid
TT Virus (TTV)
TTV DNA TT virus deoxyribonucleic acid
NANBH Non-A, non-B hepatitis
ISG Immune serum globulin

Martin et al. outline a succinct diagnostic approach to a patient with acute viral hepatitis and chronic viral hepatitis ( Figures 13-4 and 13-5 ). The approach involves using the four serologic markers (IgM anti-hepatitis A virus, hepatitis B surface antigen [HBsAg], IgM anti-HBcAg, anti-HCV) as the initial diagnostic tests. Simultaneous consideration of other etiologies of acute liver dysfunction is appropriate depending on a patient’s history. If the initial diagnostic tests are all negative, subsequent additional testing for anti-hepatitis D virus (HDV), HCV RNA, hepatis G virus (HGV) RNA, anti-hepatitis E virus (HEV), or HEV RNA may be necessary. If initial testing reveals positive HBsAg, testing for anti-HDV, HBeAg, and HBV DNA is appropriate. These additional tests are useful in defining the prognosis for a mother and the risk for infection to an infant. During the diagnostic evaluation, it is appropriate to discuss with the mother or parents the theoretic risk for transmitting infectious agents that cause hepatitis via breastfeeding. The discussion should include an evaluation of the positive and negative effects of suspending or continuing breastfeeding until the exact etiologic diagnosis is determined. The relative risk for transmission of infection to an infant can be estimated and specific preventive measures provided for the infant ( Table 13-2 ).

Figure 13-4

Diagnostic approach to a patient with acute viral hepatitis. See Box 13-2 for definitions of abbreviations.

(From Martin P, Friedman L, Dienstag J: Diagnostic approach. In Zuckerman A, Thomas H, editors: Viral hepatitis: scientific basis and clinical management , Edinburgh, 1993, Churchill Livingstone.)

Figure 13-5

Diagnostic approach to a patient with chronic viral hepatitis. See Box 13-2 for definitions of abbreviations.

(From Martin P, Friedman L, Dienstag J: Diagnostic approach. In Zuckerman A, Thomas H, editors: Viral hepatitis: scientific basis and clinical management , Edinburgh, 1993, Churchill Livingstone.)

Table 13-2

Viral Hepatitis in Association With Breastfeeding *

Hepatitis Virus Identified in Breast Milk Factors for Perinatal/Postnatal Transmission Prevention Breastfeeding
A Picornaviridae (RNA) ? Vertical transmission uncertain or rare ISG Limited evidence of transmission via breastfeeding or of serious disease in infants
HAV in pregnancy associated with premature birth HAV vaccine Breastfeeding OK after ISG and vaccine
B Hepadnaviridae (DNA) HBsAg Increased risk for vertical transmission with HBeAg +, in countries where HBV is endemic, or early in maternal infection, before Ab production HBIG Low theoretic risk
HBV DNA HBV vaccine Virtually no risk after HBIG and HBV vaccine, breastfeeding OK after HBIG and vaccine
C Flavivirus (RNA) HCV RNA detected Increased risk when mother HIV + and HCV + or with increased HCV RNA titers None Positive theoretic risk, inadequate data on relative risk, breastfeeding OK after informed discussion with parents
Vertical transmission uncommon
D Delavirdine (RNA−strand, circular) ? Requires coinfection/superinfection with HBV None (except to prevent HBV infection, give HBIG/HBV vaccine) Prevent HBV infection with HBIG and vaccine
Vertical transmission rare Breastfeeding OK after HBIG and vaccine
E Caliciviridae (RNA) + Severe disease in pregnant women (20% mortality) ISG and subunit vaccine being tested Usually subclinical infection in children, breastfeeding OK
G Related to calicivirus and flavivirus (RNA) ? Vertical transmission occurs None Inadequate data
TT TT virus (DNA, circular, single stranded) TTV DNA detected Vertical transmission occurs None Inadequate data

Data from Committee on Infectious Diseases, American Academy of Pediatrics: Red book: report of the committee on infectious diseases , ed 26, Elk Grove, Ill., 2003, American Academy of Pediatrics.

* See Box 13-2 for abbreviations. Ab, Antibody; HIV, human immunodeficiency virus.

With any type of infectious hepatitis, discussion of what is known and not known concerning transmission should be related to the mother/parents, and an informed decision can then be made by the involved adults concerning breastfeeding.

Hepatitis A

Hepatitis A virus (HAV) is usually an acute self-limited infection. The illness is typically mild, and it is generally subclinical in infants. Occasionally, HAV infection is prolonged or relapsing, extending 3 to 6 months, and rarely, it is fulminant, but HAV infection does not lead to chronic infection. The incidence of prematurity after maternal HAV infection is increased, but no evidence to date indicates obvious birth defects or a congenital syndrome. HAV infection in premature infants may lead to prolonged viral shedding. Transmission is most often person to person (fecal-oral), and transmission in foodborne or waterborne epidemics has been described. Transmission via blood products and vertical transmission (mother to infant) are rare. Transmission in day care settings has been clearly described.

Infection with HAV in newborns is uncommon and does not seem to be a significant problem. The usual period of viral shedding and presumed contagiousness lasts 1 to 3 weeks. Acute maternal HAV infection in the last trimester or in the postpartum period could lead to infection in an infant. Symptomatic infection can be prevented by immunoglobulin (Ig) administration, and 80% to 90% of disease can be prevented by Ig administration within 2 weeks of exposure. HAV vaccine can be administered simultaneously with Ig without affecting the seroconversion rate to produce rapid and prolonged HAV serum antibody levels.

The transmission of HAV via breast milk has been implicated in one case report, but no data exist on the frequency of isolating HAV from breast milk. Because HAV infection in infancy is rare and usually subclinical without chronic disease and because exposure has already occurred by the time the etiologic diagnosis of hepatitis in a mother is made, no reason exists to interrupt breastfeeding with maternal HAV infection. The infant should receive Ig and HAV vaccine, administered simultaneously.

Hepatitis B

HBV infection leads to a broad spectrum of illness, including asymptomatic seroconversion, nonspecific symptoms (fever, malaise, fatigue), clinical hepatitis with or without jaundice, extrahepatic manifestations (arthritis, rash, renal involvement), fulminant hepatitis, and chronic HBV infection. Chronic HBV infection occurs in up to 90% of infants infected via perinatal and vertical transmission and in 30% of children infected between 1 and 5 years of age. Given the increased risk for significant sequelae from chronic infection (chronic active hepatitis, chronic persistent hepatitis, cirrhosis, primary hepatocellular carcinoma), the prevention of HBV infection in infancy is crucial. Transmission of HBV is usually through blood or body fluids (stool, semen, saliva, urine, cervical secretions).

Vertical transmission, either transplacentally or perinatally during delivery, has been well described throughout the world. Vertical transmission rates in areas where HBV is endemic (Taiwan and Japan) are high, whereas transmission to infants from HBV-carrier mothers in other areas where HBV carrier rates are low is uncommon. The transmission of HBV to infants occurs in up to 50% of infants when the mothers are acutely infected immediately before, during, or soon after pregnancy.

HBsAg is found in breast milk, but transmission by this route is not well documented. Beasley and Beasley et al. demonstrated that, although breast milk transmission is possible, seroconversion rates were no different between breastfed and nonbreastfed infants in a long-term follow-up study of 147 HBsAg-positive mothers. Hill et al. followed 101 breastfed infants and 268 formula-fed infants born to women who were chronically HBsAg positive. All infants received HBIg at birth and a full series of hepatitis B vaccine. None of the breastfed infants and nine of the formula-fed infants were positive for HBsAg after completion of the HBV vaccine series. Breastfeeding had occurred for a mean of 4.9 months (range: 2 weeks to 1 year). Transmission, when it does happen, probably occurs during labor and delivery. Another report from China followed 230 infants born to HBsAg-positive women. The infants received the appropriate dosing and timing of HBIG and HBV vaccine. At 1 year of age, anti-HBs antibodies were present in 90.9% of the breastfed infants and 90.3% of the bottle-fed infants. Risk factors associated with immunoprophylaxis failure against vertical transmission of HBV include HBeAg-seropositive mothers and elevated HBV DNA “viral loads” in the mothers. Zhang et al. also demonstrated in over 67,000 pregnant women and 1150 HBsAg-positive mothers that breastfeeding did not increase the risk of HBV mother-to-child transmission, as compared to formula-fed infants. A systematic review and meta-analysis by Shi et al. including 10 controlled clinical trials reported an odds ratio for the development of hepatitis B surface antibodies in breastfeeding infants, compared with non-breastfeeding infants, of 0.98 (CI 0.69 to 1.40). In 2009, the AAP Committee on Infectious Diseases stated “that breastfeeding of the infant by a HBsAg-positive mother poses no additional risk for acquisition of HBV infection by the infant with appropriate administration of hepatitis B vaccine and HBIG.”

Screening of all pregnant women for HBV infection is an essential first step to preventing vertical transmission. Universal HBV vaccination at birth and during infancy, with the administration of HBIg immediately after birth to infants of HBsAg-positive mothers, prevents HBV transmission in more than 95% of cases. Breastfeeding by HBsAg-positive women is not contraindicated, but the immediate administration of HBIG and HBV vaccine should occur. Two subsequent doses of vaccine should be given at appropriate intervals and dosages for the specific HBV vaccine product. This decreases the small theoretic risk for HBV transmission from breastfeeding to almost zero.

When acute peripartum or postpartum hepatitis occurs in a mother and HBV infection is a possibility, with its associated increased risk for transmission to the infant, a discussion with the mother or parents should identify the potential risks and benefits of continuing breastfeeding until the etiology of the hepatitis can be determined. If an appropriate alternative source of nutrition is available for the infant, breast milk should be withheld until the etiology of the hepatitis is identified. HBIG and HBV vaccine can be administered to the infant who has not already been immunized or has no documented immunity against HBV. If acute HBV infection is documented in a mother, breastfeeding can continue after immunization has begun.

Hepatitis C

Acute infection with HCV can be indistinguishable from hepatitis A or B infection; however, it is typically asymptomatic or mild. HCV infection is the major cause of blood-borne non-A, non-B hepatitis (NANBH). Chronic HCV infection is reported to occur 70% to 85% of the time regardless of age at time of infection. Sequelae of chronic HCV infection are similar to those associated with chronic HBV infection. Bortolotti et al. described two groups of children with HCV infection who they observed for 12 to 48 months. The first group of 14 children, who acquired HCV infection early in life, presumably from their mothers, demonstrated biochemical evidence of liver disease in the first 12 months of life. Two of these children subsequently cleared the viremia and had normal liver function, an additional three children developed normal liver function despite persistent HCV viremia, and the remaining children had persistent viremia and abnormal liver function. The second group of 16 children, with chronic HCV infection, remained free of clinical symptoms of hepatitis, but 10 (62%) of them had mild alanine aminotransferase elevations, and 7 of the 16 (44%) who had liver biopsies had histologic evidence of mild to moderate hepatitis.

The two commonly identified mechanisms of transmission of HCV are transfusions of blood or blood products and IV drug use. However, other routes of transmission exist because HCV infection occurs even in the absence of obvious direct contact with significant amounts of blood. Other body fluids contaminated with blood probably serve as sources of infection. Transmission through sexual contact occurs infrequently and probably requires additional contributing factors, such as coinfection with other sexually transmitted agents or high viral loads in serum and other body fluids. Studies of transmission in households without other risk factors have demonstrated either low rates of transmission or no transmission.

The reported rates of vertical transmission vary widely. In mothers with unknown HIV status or known HIV infection, the rates of vertical transmission were 4% to 100%, whereas the rates varied between 0% and 42% in known HIV-negative mothers. These same studies suggest that maternal coinfection with HIV, HCV genotype, active maternal liver disease, and the serum titer of maternal HCV RNA may be associated with increased rates of vertical transmission. The correlation between HCV viremia, the HCV viral load in a mother, and vertical transmission of HCV is well documented. The clinical significance and risk for liver disease after vertical transmission of HCV are still unknown. The timing of HCV infection in vertical transmission is also unknown. In utero transmission has been suggested by some studies, whereas intrapartum or postpartum transmission was proposed by Ohto et al. when they documented the absence of HCV RNA in the cord blood of neonates who later became HCV RNA positive at 1 to 2 months of age. More recently, Gibb et al. reported two pieces of data supporting the likelihood of intrapartum transmission as the predominant time of vertical transmission: (1) low sensitivity of PCR for HCV RNA testing in the first month of life with a marked increase in sensitivity after that for diagnosing HCV infection in infants and (2) a lower transmission risk for elective cesarean delivery (without prolonged rupture of membranes) compared with vaginal or emergency cesarean delivery. Another group, McMenamin et al., analyzed vertical transmission in 559 mother-infant dyads. The overall vertical transmission rate was 4.1% (18/441), with another 118 infants not tested or lost to follow-up. Comparison of the vertical transmission rate was no different for vaginal delivery or emergency cesarean in labor versus planned cesarean (4.2% vs. 3.0%). This held true even when mothers had hepatitis C RNA detected antenatally (7.2% vs. 5.3%). The authors did not support planned cesarean delivery to decrease vertical transmission of hepatitis C infection. No prospective, controlled trials of cesarean versus vaginal delivery and the occurrence of vertical hepatitis C transmission are available.

The risk for HCV transmission via breast milk is uncertain. Anti-HCV antibody and HCV RNA has been demonstrated in colostrum and breast milk, although the levels of HCV RNA in milk did not correlate with the titers of HCV RNA in serum. Nevertheless, transmission of HCV via breastfeeding (and not in utero, intrapartum, or from other postpartum sources) has not been proven in the small number infants studied. Transmission rates in breastfed and nonbreastfed infants appear to be similar, but various important factors have not been controlled, such as HCV RNA titers in mothers, examination of the milk for HCV RNA, exclusive breastfeeding versus exclusive formula feeding versus partial breastfeeding, and duration of breastfeeding. Zanetti et al. documented the absence of HCV transmission in 94 mother-infant dyads when the mother had only HCV (no HIV) infection and no transmission in 71 mother-infant dyads who breastfed, including 23 infants whose mothers were seropositive for HCV RNA. Eight infants in that study were infected with HCV and their mothers had both HIV and HCV, and 3 of these 8 infants were infected with both HIV and HCV. The HCV RNA levels were significantly higher in the mothers coinfected with HIV than they were in mothers with HCV alone.

Overall, the risk for HCV infection via breastfeeding is low, the risk for HCV infection appears to be more frequent in association with HIV infection and higher levels of HCV RNA in maternal serum, no effective preventive therapies (Ig or vaccine) exist, and the risk for chronic HCV infection and subsequent sequelae with any infection is high. It is therefore appropriate to discuss the theoretic risk for breastfeeding in HCV-positive mothers with the mother or parents and to consider proscribing breast milk when appropriate alternative sources of nutrition are available for the infants. HIV infection is a separate contraindication to breastfeeding. Additional study is necessary to determine the exact role of breastfeeding in the transmission of HCV, including the quantitative measurement of HCV RNA in colostrum and breast milk, the relative risk for HCV transmission in exclusively or partially breastfed infants versus the risk in formula-fed infants, and the effect of duration of breastfeeding on transmission.

The current position of the CDC is that no data indicate that HCV virus is transmitted through breast milk. Therefore, breastfeeding by an HCV-positive, HIV-negative mother is not contraindicated.

Infants born to HCV RNA-positive mothers require follow-up through 18 to 24 months of age to determine the infants’ HCV status, regardless of the mode of infant feeding. Infants should be tested for alanine aminotransferase and HCV RNA at 3 months and 12 to 15 months of age. Alanine aminotransferase and anti-HCV antibody should be tested at 18 to 24 months of age to confirm an infant’s status: uninfected, ongoing hepatitis C infection, or past HCV infection.

Hepatitis D

HDV is a defective RNA virus that causes hepatitis only in persons also infected with HBV. The infection occurs as either an acute coinfection of HBV and HDV or a superinfection of HBV carriers. This “double” infection results in more frequent fulminant hepatitis and chronic hepatitis, which can progress to cirrhosis. The virus uses its own HBV RNA (circular, negative-strand RNA) with an antigen, HDAg, surrounded by the surface antigen of HBV, HBsAg. HDV is transmitted in the same way as HBV, especially through the exchange of blood and body fluids. HDV infection is uncommon where the prevalence of HBV is low. In areas where HBV is endemic, the prevalence of HDV is highly variable. HDV is common in tropical Africa and South America, as well as in Greece and Italy, but it is uncommon in the Far East and in Alaskan Inuit despite the endemic occurrence of HBV in these areas.

The transmission of HDV has been reported to occur from household contacts and, rarely, through vertical transmission. No data are available on the transmission of HDV by breastfeeding. HDV infection can be prevented by blocking infection with HBV; therefore, HBIG and HBV vaccine are the best protection. In addition to HBIG and HBV vaccine administration to the infant of a mother infected with both HBV and HDV, discussion with the mother or parents should include the theoretic risk for HBV and HDV transmission through breastfeeding. As with HBV, once HBIg and HBV vaccine have been given to the infant, the risk for HBV or HDV infection from breastfeeding is negligible. Therefore, breastfeeding after an informed discussion with the parents is acceptable.

Hepatitis E

Hepatitis E virus (HEV) is a cause of sporadic and epidemic, enterically transmitted NANBH, which is typically self-limited and without chronic sequelae. HEV is notable for causing a high mortality rate in pregnant women. Transmission is primarily via the fecal-oral route, commonly via contaminated water or food. High infection rates have been reported in adolescents and young adults (ages 15 to 40 years). Tomar reported that 70% of cases of HEV infections in the pediatric population in India manifest as acute hepatitis. Maternal-neonatal transmission was documented when the mother developed hepatitis E infection in the third trimester. Although HEV was demonstrated in breast milk, no transmission via breast milk was confirmed in this report. Five cases of transfusion-associated hepatitis E were reported. In a review by Krain et al., vertical transmission was noted in reports from India and Ghana in the infants of pregnant women with acute viral hepatitis or fulminant hepatic failure. Chibber et al. reported on the presence of HEV RNA in the colostrum of HEV-infected mothers in significantly lower levels than in maternal serum. They also noted six infants who became infected within 2 weeks postpartum after being anti-HEV antibody and HEV RNA negative at birth. Four of these six infants were formula fed due to severe maternal illness. There was no transmission of HEV in 87 other infants who were exclusively breastfed and born to mothers positive for anti-HEV antibodies or HEV RNA in the third trimester. Epidemics are usually related to contamination of water. Person-to-person spread is minimal, even in households and day care settings. Although Ig may be protective, no controlled trials have been done. Animal studies suggest that a recombinant subunit vaccine may be feasible.

HEV infection in infancy is rare but does occur after maternal infection in the third trimester of pregnancy. Limited available data suggest that transmission of HEV by breastfeeding is rare. There is no evidence of clinically significant postnatal HEV infection or chronic sequelae in association with HEV infection in infants via breast milk. Currently no contraindication exists to breastfeeding with maternal HEV infection. Ig has not been shown to be effective in preventing infection, and no vaccine is available for HEV.

Hepatitis G

Hepatitis G virus (HGV) has recently been confirmed as a cause of NANBH distinct from hepatitis viruses A through E. Several closely related genomes of HGV, currently named GBV-A, -B, and -C, appear to be related to HCV; the pestiviruses and the flaviviruses. Epidemiologically, HGV is most often associated with the transfusion of blood, although studies have identified nontransfusion-related cases. HGV genomic RNA has been detected in some patients with acute and chronic hepatitis and a small number of patients with fulminant hepatitis. GBV-C/HGV has also been found in some patients with inflammatory bile duct lesions, but the pathogenicity of this virus is unconfirmed. HGV RNA has been detected in 1% to 3% of healthy blood donors in the United States. Feucht et al. described maternal-to-infant transmission of HGV in three of nine children. Two of the three mothers were coinfected with HIV and the third with HCV. None of these infants developed signs of liver disease. Neither the timing nor the mode of transmission was clarified. Lin et al. reported no HGV transmission in three mother-infant dyads after cesarean delivery and discussed transplacental spread via blood as the most likely mode of HGV infection in vertical transmission. Wejstal et al. reported on perinatal transmission of HGV to 12 of 16 infants born to HGV-viremic mothers, identified by PCR. HGV did not appear to cause clinical hepatitis in these children.

Fischler et al. followed eight children born to HGV-positive mothers and found only one to be infected with HGV. That child remained clinically well, while his twin, also born by cesarean delivery and breastfed, remained HGV negative for 3 years of observation. Five of the other six children were breastfed for variable periods without evidence of HGV infection. Ohto et al. examined HGV mother-to-infant transmission. Of 2979 pregnant Japanese women who were screened, 32 were identified as positive for GBV-C/HGV RNA by PCR; 26 of 34 infants born to the 32 HGV-positive women were shown to be HGV RNA positive. Reportedly, none of the infants demonstrated a clinical picture of hepatitis, although two infants had persistent mild elevations (less than two times normal) of alanine aminotransferase. The viral load in mothers, who transmitted HGV to their infants, was significantly higher than it was in nontransmitting mothers. Infants born by elective cesarean delivery had a lower rate of infection (3 in 7) compared with infants born by emergency cesarean delivery (2 of 2) or born vaginally (21 of 25). In this study, HGV infection in breastfed infants was four times more common than it was in formula-fed infants, but this difference was not statistically significant because only four infants were formula fed. The authors report no correlation between infection rate and duration of breastfeeding. Testing of the infants was not done frequently and early enough routinely through the first year of life to determine the timing of infection in these infants. Schröter et al. reported transmission of HGV to 3 of 15 infants born to HGV RNA-positive mothers at 1 week of age. None of 15 breast milk samples was positive for GBV-C/HGV RNA, and all of the children who were initially negative for HGV RNA in serum remained negative at follow-up between 1 and 28 months of age.

The foregoing data suggest that transmission is more likely to be vertical before or at delivery rather than via breastfeeding. The pathogenicity and the possibility of chronic disease due to HGV infection remain uncertain at this time. Insufficient data are available to make a recommendation concerning breastfeeding by HGV-infected mothers.

Herpes Simplex Virus

HSV types 1 and 2 (HSV-1 and HSV-2) can cause prenatal, perinatal, and postnatal infections in fetuses and infants. Prenatal infection can lead to abortion, prematurity, or a recognized congenital syndrome. Perinatal infection is the most common form of infection (1 in 2000 to 5000 live births, 700 to 1500 cases per year in the United States) and is often fatal or severely debilitating. The factors that facilitate intrapartum infection and predict the severity of disease have been extensively investigated. Postnatal infection is uncommon but can occur from a variety of sources, including oral or genital lesions and secretions in mothers or fathers, hospital workers and home caregivers, and breast lesions in breastfeeding mothers. A number of case reports have documented severe HSV-1 or HSV-2 infections in infants associated with HSV-positive breast lesions in the mothers. Cases of infants with HSV gingivostomatitis inoculating the mothers’ breasts have also been reported.

In the absence of breast lesions, breastfeeding in HSV-seropositive or culture-positive women is reasonable when accompanied by careful handwashing, covering the lesions, and avoiding fondling or kissing with oral lesions until all lesions are crusted. Breastfeeding during maternal therapy with oral or IV acyclovir or valacyclovir can continue safely as well. Inadequate information exists concerning famciclovir, ganciclovir, and foscarnet in breast milk to make a recommendation at this time. Breastfeeding by women with active herpetic lesions on their breasts should be proscribed until the lesions are dried. Treatment of the mothers’ breast lesions with topical, oral, and/or IV antiviral preparations may hasten recovery and decrease the length of viral shedding.

Human Herpesvirus 6 and Human Herpesvirus 7

Human herpesvirus 6 (HHV-6) is a cause of exanthema subitum (roseola, roseola infantum) and is associated with febrile seizures. HHV-6 appears to be most similar to CMV based on genetic analysis. No obvious congenital syndrome of HHV-6 infection has been identified, although prenatal infection has been reported. Seroepidemiologic studies show that most adults have already been infected by HHV-6. Therefore, primary infection during pregnancy is unlikely, but reactivation of latent HHV-6 infection may be more common. No case of symptomatic HHV-6 prenatal infection has been reported. The significance of reactivation of HHV-6 in a pregnant woman and the production of infection and disease in the fetus and infant remains to be determined. Primary infection in children occurs most often between 6 and 12 months of age, when maternally acquired passive antibodies against HHV-6 are waning. Febrile illnesses in infants younger than 3 months of age have been described with HHV-6 infection, but infection before 3 months or after 3 years is uncommon.

Various studies involving the serology and restriction enzyme analysis of HHV-6 isolates from mother-infant dyads support the idea that postnatal transmission and perhaps perinatal transmission from the mothers are common sources of infection. One study was unable to detect HHV-6 in breast milk by PCR analysis in 120 samples, although positive control samples seeded with HHV-6-infected cells did test positive.

Given the limited occurrence of clinically significant disease and the absence of sequelae of HHV-6 infection in infants and children, the almost universal acquisition of infection in early childhood (with or without breastfeeding), and the absence of evidence that breast milk is a source of HHV-6 infection, breastfeeding can continue in women known to be seropositive for HHV-6.

Human herpesvirus 7 (HHV-7) is closely related to HHV-6 biologically. Primary infection with HHV-7 occurs most often in childhood, usually later in life than HHV-6 infection. The median age of infection is 26 months, with 75% of children becoming HHV-7 positive by 5 years of age. The seroprevalence of HHV-7 antibodies has been reported to be 80% to 98% in adults, and passive antibodies are present in almost all newborns. Like HHV-6, HHV-7 infection can be associated with acute febrile illness, febrile seizures, and irritability, but in general, it is a milder illness than with HHV-6, with fewer hospitalizations. Virus excretion of HHV-7 occurs in saliva, and PCR testing of blood cells and saliva is frequently positive in individuals with past infection. Congenital infection of HHV-6 was detected via DNA PCR testing in 57 of 5638 of cord blood samples (1%), but HHV-7 was not detected in any of 2129 cord blood specimens.

HHV-7 DNA was detected by PCR in 3 of 29 breast milk mononuclear cell samples from 24 women who were serum positive for the HHV-7 antibody. In the same study, small differences were seen in the HHV-7 seropositive rates between breastfed infants and bottle-fed infants at 12 months of age (21.7% versus 20%), at 18 months of age (60% versus 48.1%), and at 24 months of age (77.3% versus 58.3%). None of these differences was statistically significant. Given that HHV-6 infection generally occurs earlier than HHV-7 infection in most infants and that HHV-6 is rarely found in breast milk, it seems unlikely that HHV-7 in breast milk is a common source of infection in infants and children. The infrequent occurrence of significant illness with HHV-7 infection, with the absence of sequelae, except in patients who had transplantation surgery at older ages, and the common occurrence of infection in childhood suggests that there is no reason to proscribe breastfeeding for HHV-7-positive women.

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Jul 13, 2019 | Posted by in PEDIATRICS | Comments Off on Transmission of Infectious Diseases Through Breast Milk and Breastfeeding
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