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.
From Williams Obstetrics, 19th Edition, p. 1281
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
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.
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
Nurse-Midwifery, Helen Varney, Second Edition, p. 419
Maternity and Gynecologic Care, Bobak, Jensen, Zalar, Fourth Edition, p. 470
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].
These web pages were originally composed by Ronnie
Falcao, LM MS, in Sept., 1997.
They have been updated as new information has become available.
Permission to link to these pages is hereby granted.
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