A newborn does not yet have a mature immune system and is often unable to mount an effective immune response. Newborns are generally protected by the antibodies they receive through the placenta before birth and through their mother's breastmilk after birth. These antibodies will be the same ones that are circulating in the mother's system, which will include antibodies to the microorganisms in the mother's home environment and other places she frequents. Therefore, babies generally have antibodies to the germs in their own homes.

However, many of the germs in a hospital environment are foreign to both the mother and the baby, so the baby will not have antibodies to protect against these germs, and the baby cannot create its own antibodies against these new germs. This problem can be mitigated by making sure that the baby is touched minimally by people other than the mother and the immediate family, who share a common germ pool.

The greatest infectious danger to a newborn in the hospital is the prevalence of bacteria that have developed resistance or complete protection against antibiotics. Antibiotics are no longer effective against these "superbugs", so there is no effective antibiotic treatment for a "superbug" infection.

If a baby in the hospital develops an infection from one of these "superbugs", nothing other than prayer can help them.

A major mechanism for inducing infection subsequent to birth is from those caring for the infant who may be colonized with the organism or may passively transfer it from another infected infant.

Myles Textbook for Midwives, Bennett/Brown, Twelfth Edition

Immunological adaptations, p. 508

Neonates demonstrate a marked susceptibility to infections, particularly those gaining entry through the mucosa of the respiratory and gastro-intestinal systems. Localisation of infection is poor, "minor" infections having the potential to become generalised very easily.

The baby has some immunoglobulins at birth, but the sheltered intra-uterine existence limits the need for learned immune responses to specific antigens. There are three main immunoglobulins, IgG, IgA and IgM, and of these only IgG is small enough to cross the placental barrier. It affords immunity to specific viral infections. At birth the baby's levels of IgG are equal to or slightly higher than those of the mother. This provides passive immunity during the first few months of life.

IgM and IgA do not cross the placental barrier but can be manufactured by the fetus. Levels of IgM at term are 20% those of the adult, taking 2 years to attain adult levels (elevation of IgM levels at birth are suggestive of intra-uterine infection). This relatively low level of IgM is thought to render the infant more susceptible to enteric infections. IgA levels are very low and produced slowly although secretory salivary levels attain adult values within 2 months. IgA protects against infection of the respiratory tract, gastro-intestinal tract and eyes.

Breast milk, and especially colostrum, provides the infant with passive immunity in the form of lactobacillus bifidus, lactoferrin, lysozymes and secretory IgA among others.

Properties and Components of Breast Milk, p. 523

Anti-infective factors - During the first 10 days there are more white cells per ml than there are in blood.

Macrophages and neutrophils are amongst the most common leucocytes in human milk and they surround and destroy harmful bacteria by their phagocytic activity.

Secretory IgA and interferon are important anti-infective agents produced in abundance by lymphocytes in human milk.

Immunoglobulins IgA, IgG, IgM and IgD are all found in human milk. Of these the most important is IgA, which appears to be both synthesised and stored in the breast. It 'paints' the intestinal epithelium and protects the mucosal surfaces against entry of pathogenic bacteria and enteroviruses. It affords protections against E. coli, salmonellae, shigellae, streptococci, staphylococci, pneumococci, poliovirus and the rotaviruses.

Lysozyme is present in breast milk in concentrations 5000 times greater than in cow's milk. It is a well known general anti-infective agent and its activity appears to increase during lactation.

Lactoferrin is abundant in human milk but is not present in cow's milk. It effects the absorption of enteric iron, thus preventing pathogenic E. coli from obtaining the iron they need for survival.

The bifidus factor in human milk promotes the growth of Gram-positive bacilli in the gut flora, particularly Lactobacillus bifidus, which discourages the multiplication of pathogens. Babies who are fed on cow's milk formula have Gram-negative (potentially pathogenic) bacilli in their gut flora.

Nurse-Midwifery, Helen Varney, Second Edition, p. 419

Immune System Changes

The neonate has an impaired ability to react to invading organisms. On a cellular level there is a decreased ability of leukocytes to concentrate where necessary. These leukocytes are less bactericidal and phagocytic. At the humoral level the newborn has low or nonexistent levels of the immunoglobulin antibodies IgM, IgE, and IgA. The neonate is born, however, with IgG antibodies acquired from the mother, which confer protection from some specific diseases. There is a slow rise of immunoglobulin levels after 3 months of age to levels of older children.

Maternity and Gynecologic Care, Bobak, Jensen, Zalar, Fourth Edition, p. 470

Immune System

All newborns and especially preterm newborns are at high risk for infection during the first several months of life. During this period, infection represents one of the leading causes of morbidity and mortality. The newborn is unable to limit the invading pathogen to the portal of entry because of a generalized hypofunction of the inflammatory and immune mechanisms (Medici, 1983).

Resistance to infection (immunity) includes both non-specific and specific protective mechanisms. Medici (1983) summarizes the newborn's defense mechanisms as follows:

The term and preterm neonate has an increased incidence of infection for the first 4 to 6 weeks of life. This reflects the immaturity of a number of protective systems which significantly increases the risk of infection in this patient population. Natural barriers such as the acidity of the stomach or the production of pepsin and trypsin which maintain sterility of the small intestine are not fully developed until 3 to 4 weeks. The membrane protective IgA is missing from the respiratory and urinary tracts, and unless the newborn is breast-fed, it is absent from the gastrointestinal tract as well. The immune system is in great part suppressed; possibly this is a mechanism for preventing maternal recognition of paternal antigens with subsequent reject of the fetus. Finally, the qualitative and quantitative response of the inflammatory factors and sluggish responses of the phagocytic cells [leave the baby vulnerable to infection].