Early onset sepsis can occur in the first week of life. It usually is apparent on the first day after birth. This type of infection is usually acquired before the birth of the infant. Premature rupture of membranes and other obstetrical complications can add to the risk of early-onset sepsis. If the amniotic membrane has been ruptured greater than 18 hours before delivery the infant may be at more risk for this complication. Prematurity, low birth weight, chorioamnionitis, maternal urinary tract infection and/or maternal fever are complications that increase the risk for early-onset sepsis. Early onset sepsis is indicated by serious respiratory symptoms. The infant usually suffers from pneumonia, hypothermia, or shock. The mortality rate is 30 to 50%.

Sixty percent of mothers of preterm infants are infected with cytomegalovirus (CMV). Infection is asymptomatic in most instances but 9% to 12% of postnatally infected low birth weight, preterm infants have severe, sepsis-like infection. CMV infection duration can be long and result in pneumonitis in association with fibrosis. CMV infection in infants has an unexpected effect on the white blood cells of the immune system causing them to prematurely age. This leads to a reduced immune response similar to that found in the elderly.

Most healthy people working with infants and children face no special risk from CMV infection. However, for women of child-bearing age who previously have not been infected with CMV, there is a potential risk to the developing unborn child (the risk is described above in the Pregnancy section). Contact with children who are in day care, where CMV infection is commonly transmitted among young children (particularly toddlers), may be a source of exposure to CMV. Since CMV is transmitted through contact with infected body fluids, including urine and saliva, child care providers (meaning day care workers, special education teachers, as well as mothers) should be educated about the risks of CMV infection and the precautions they can take. Day care workers appear to be at a greater risk than hospital and other health care providers, and this may be due in part to the increased emphasis on personal hygiene in the health care setting.

Recommendations for individuals providing care for infants and children:

- Employees should be educated concerning CMV, its transmission, and hygienic practices, such as handwashing, which minimize the risk of infection.

- Susceptible nonpregnant women working with infants and children should not routinely be transferred to other work situations.

- Pregnant women working with infants and children should be informed of the risk of acquiring CMV infection and the possible effects on the unborn child.

- Routine laboratory testing for CMV antibody in female workers is not specifically recommended due to its high occurrence, but can be performed to determine their immune status.

Recommendations for pregnant women with regard to CMV infection:

- Throughout the pregnancy, practice good personal hygiene, especially handwashing with soap and water, after contact with diapers or oral secretions (particularly with a child who is in day care). Sharing of food, eating and drinking utensils, and contact with toddlers' saliva should be avoided.

- Women who develop a mononucleosis-like illness during pregnancy should be evaluated for CMV infection and counseled about the possible risks to the unborn child.

- Laboratory testing for antibody to CMV can be performed to determine if a woman has already had CMV infection.

- Recovery of CMV from the cervix or urine of women at or before the time of delivery does not warrant a cesarean section.

- The demonstrated benefits of breast-feeding outweigh the minimal risk of acquiring CMV from the breast-feeding mother.

- There is no need to either screen for CMV or exclude CMV-excreting children from schools or institutions because the virus is frequently found in many healthy children and adults.

Treatment with hyperimmune globulin in mothers with primary CMV infection has been shown to be effective in preventing congenital disease in several studies. One study did not show significant decrease in the risk of congenital cytomegalovirus infection.

In the western world, GBS (in the absence of effective prevention measures) is the main cause of bacterial infections in newborns, such as septicemia, pneumonia, and meningitis, which can lead to death or long-term after effects.

GBS infections in newborns are separated into two clinical types, early-onset disease (GBS-EOD) and late-onset disease (GBS-LOD). GBS-EOD manifests from 0 to 7 living days in the newborn, most of the cases of EOD being apparent within 24 h from birth. GBS-LOD starts between 7 and 90 days after birth.

The most common clinical syndromes of GBS-EOD are septicemia without apparent location, pneumonia, and less frequently meningitis. Bacteremia without a focus occurs in 80-85%, pneumonia in 10-15%, and meningitis in 5-10% of cases. The initial clinical findings are respiratory signs in more than 80% of cases. Neonates with meningitis often have an initial clinical presentation identical to presentation in those without meningeal affectation. An exam of the cerebrospinal fluid is often necessary to rule out meningitis.

Colonization with GBS during labour is the primary risk factor for the development of GBS-EOD. GBS-EOD is acquired vertically (vertical transmission), through exposure of the fetus or the baby to GBS from the vagina of a colonized woman, either "in utero" (because of ascending infection) or during birth, after rupture of membranes. Infants can also be infected during passage through the birth canal, nevertheless, newborns who acquire GBS through this route can only become colonized, and these colonized infants usually do not develop GBS-EOD.

Roughly 50% of newborns of GBS colonized mothers are also GBS colonized and (without prevention measures) 1-2% of these newborns will develop GBS-EOD.

In the past, the incidence of GBS-EOD ranged from 0.7 to 3.7 per thousand live births in the US, and from 0.2 to 3.25 per thousand in Europe.

In 2008, after widespread use of antenatal screening and intrapartum antibiotic prophylaxis, the Centers for Disease Control and Prevention of United States reported an incidence of 0.28 cases of GBS-EOD per thousand live births in the US.

Though maternal GBS colonization is the key determinant for GBS-EOD, other factors also increase the risk. These factors are:

- Onset of labour before 37 weeks of gestation (premature birth)

- Prolonged rupture of membranes (longer duration of membrane rupture) (≥18 h before delivery)

- Intrapartum (during childbirth) fever (>38 °C, >100.4 °F)

- Amniotic infections (chorioamnionitis)

- Young maternal age

Nevertheless, most babies who develop GBS-EOD are born to colonized mothers without any of these risk factors. Heavy GBS vaginal colonization is also associated with a higher risk for GBS-EOD. Women who had one of these risk factors but who are not GBS colonized at labour are at low risk for GBS-EOD compared to women who were colonized prenatally, but had none of the aforementioned risk factors.

Presence of low levels of anticapsular antibodies against GBS in the mother are also of great importance for the development of GBS-EOD.

Because of that, a previous sibling with GBS-EOD is also an important risk factor for the development of the infection in subsequent deliveries, probably reflecting the lack of protective antibodies in the mother.

Overall, the case fatality rates from GBS-EOD have declined, from 50% observed in studies from the 1970s to between 2 and 10% in recent years, mainly as a consequence of improvements in therapy and management. Fatal neonatal infections by GBS are more frequent among premature infants.

GBS-LOD affects infants from 7 days to 3 months of age and has a lower case fatality rate (1%-6%) than GBS-EOD. Clinical syndromes of GBS-EOD are bacteremia without a focus (65%), meningitis (25%), cellulitis, osteoarthritis, and pneumonia.

Prematurity has been reported to be the main risk factor. Each week of decreasing gestation increases the risk by a factor of 1.34 for developing GBS-LOD.

GBS-LOD is not acquired through vertical transmission during delivery; it can be acquired later from the mother from breast milk or from environmental and community sources.

GBS-LOD commonly shows nonspecific signs, and diagnosis should be made obtaining blood cultures in febrile newborns. Hearing loss and mental impairment can be a long-term consequence of GBS meningitis.

Babies can also become infected by their mothers during birth. Some infectious agents may be transmitted to the embryo or fetus in the uterus, while passing through the birth canal, or even shortly after birth. The distinction is important because when transmission is primarily during or after birth, medical intervention can help prevent infections in the infant.

During birth, babies are exposed to maternal blood, body fluids, and to the maternal genital tract without the placental barrier intervening. Because of this, blood-borne microorganisms (hepatitis B, HIV), organisms associated with sexually transmitted disease (e.g., "Neisseria gonorrhoeae" and "Chlamydia trachomatis"), and normal fauna of the genitourinary tract (e.g., "Candida albicans") are among those commonly seen in infection of newborns.

The embryo and fetus have little or no immune function. They depend on the immune function of their mother. Several pathogens can cross the placenta and cause (perinatal) infection. Often, microorganisms that produce minor illness in the mother are very dangerous for the developing embryo or fetus. This can result in spontaneous abortion or major developmental disorders. For many infections, the baby is more at risk at particular stages of pregnancy. Problems related to perinatal infection are not always directly noticeable.

Pregnant women are more severely affected by influenza, hepatitis E, herpes simplex and malaria. The evidence is more limited for coccidioidomycosis, measles, smallpox, and varicella. Pregnancy may also increase susceptibility for toxoplasmosis.

During the 2009 H1N1 pandemic, as well as during interpandemic periods, women in the third trimester of pregnancy were at increased risk for severe

disease, such as disease requiring admission to an intensive care unit or resulting in death, as compared with women in an earlier stage of pregnancy.

For hepatitis E, the case fatality rate among pregnant women has been estimated to be between 15% and 25%, as compared with a range of 0.5 to 4% in the population overall, with the highest susceptibility in the third trimester.

Primary herpes simplex infection, when occurring in pregnant women, has an increased risk of dissemination and hepatitis, an otherwise rare complication in immunocompetent adults, particularly during the third trimester. Also, recurrences of herpes genitalis increase in

frequency during pregnancy.

The risk of severe malaria by "Plasmodium falciparum" is three times as high in pregnant women, with a median maternal mortality of 40% reported in studies in the Asia–Pacific region. In women where the pregnancy is not the first, malaria infection is more often asymptomatic, even at high parasite loads, compared to women having their first pregnancy. There is a decreasing susceptibility to malaria with increasing parity, probably due to immunity to pregnancy-specific antigens. Young maternal age and increases the risk. Studies differ whether the risk is different in different . Limited data suggest that malaria caused by "Plasmodium vivax" is also more severe during pregnancy.

Severe and disseminated coccidioidomycosis has been reported the occur in increased frequency in pregnant women in several reports and case series, but subsequent large surveys, with the overall risk being rather low.

Varicella occurs at an increased rate during pregnancy, but mortality is not higher than that among men and non-pregnant women.

Listeriosis mostly occurs during the third trimester, with Hispanic women appearing to be at particular risk. Listeriosis is a vertically transmitted infection that may cause miscarriage, stillbirth, preterm birth, or serious neonatal disease.

Some infections are vertically transmissible, meaning that they can affect the child as well.

Though GBS colonization is asymptomatic and, in general, does not cause problems, it can sometimes cause serious illness for the mother and the baby during gestation and after delivery. GBS infections in the mother can cause chorioamnionitis (intra-amniotic infection or severe infection of the placental tissues) infrequently, and postpartum infections (after birth). GBS urinary tract infections may induce labour and cause premature delivery (preterm birth) and miscarriage.

The current incidence in the United States is somewhere around 0.5% per year; overall, the incidence rate for developed world falls between 0.2–0.7%. In developing countries, the incidence of omphalitis varies from 2 to 7 for 100 live births. There does not appear to be any racial or ethnic predilection.

Like many bacterial infections, omphalitis is more common in those patients who have a weakened or deficient immune system or who are hospitalized and subject to invasive procedures. Therefore, infants who are premature, sick with other infections such as blood infection (sepsis) or pneumonia, or who have immune deficiencies are at greater risk. Infants with normal immune systems are at risk if they have had a prolonged birth, birth complicated by infection of the placenta (chorioamnionitis), or have had umbilical catheters.

In early-onset neonatal meningitis, acquisition of the bacteria is from the mother before the baby is born or during birth. The most common bacteria found in early-onset are group B "Streptococcus" (GBS), "Escherichia coli", and "Listeria monocytogenes". In developing countries, Gram-negative enteric (gut) bacteria are responsible for the majority of early onset meningitis.

A study performed at Strong Memorial Hospital in Rochester, New York, showed that infants ≤ 60 days old meeting the following criteria were at low-risk for having a serious bacterial illness:

- generally well-appearing

- previously healthy

- full term (at ≥37 weeks gestation)

- no antibiotics perinatally

- no unexplained hyperbilirubinemia that required treatment

- no antibiotics since discharge

- no hospitalizations

- no chronic illness

- discharged at the same time or before the mother

- no evidence of skin, soft tissue, bone, joint, or ear infection

- White blood cells (WBCs) count 5,000-15,000/mm

- absolute band count ≤ 1,500/mm

- urine WBC count ≤ 10 per high power field (hpf)

- stool WBC count ≤ 5 per high power field (hpf) "only in infants with diarrhea"

Those meeting these criteria likely do not require a lumbar puncture, and are felt to be safe for discharge home without antibiotic treatment, or with a single dose of intramuscular antibiotics, but will still require close outpatient follow-up.

One risk for Group B streptococcal infection (GBS) is Preterm rupture of membranes. Screening women for GBS (via vaginal and rectal swabbing) and treating culture positive women with intrapartum chemoprophylaxis is reducing the number of neonatal sepsis caused by GBS.

Late-onset meningitis is most likely infection from the community. Late onset meningitis may be caused by other Gram-negative bacteria and "staphylococcal" species. In developing countries "Streptococcus pneumoniae" accounts for most cases of late onset.

There are several potential risk factors or causes to this increased risk:

- An increased immune tolerance in pregnancy to prevent an immune reaction against the fetus

- Maternal physiological changes including a decrease in respiratory volumes and urinary stasis due to an enlarging uterus.

- The presence of a placenta for pathogens to use as a habitat, such as by "L. monocytogenes" and "P. falciparum".

This depends on the age of the animal affected and the efficiency of its immune system.

Colostral protection lasts up to 5 months of age, after which it decreases to an all-time low to increase yet again at about 12 months of age.

- Prenatal infection: virus travels from infected mother to fetus via the placenta. In this case, the time of gestation determines the result of the infection.

- If the fetus is infected in the first 30 days of fetal life, death and absorption of all, or some of the fetuses may occur. In this case, some immunotolerant healthy piglets may be born.

- If the infection happens at 40 days, death and mummification may occur. Also in this case, some or all the fetuses are involved, i.e. some of the fetuses can be born healthy and immunotolerant, or else carriers of the disease.

- If the viruses crosses the placenta in the last trimester, neonatal death may occur, or the birth of healthy piglets with a protective pre-colostral immunity.

- Postnatal infection (pigs up to 1 year of age): Infection occurs oro-nasally, followed by a viremic period associated with transitory leucopenia.

- Infection in adults (over 1 year of age): These subject would have an active, protective immune system which protects them from future exposures (e.g. mating with an infected male).

Therefore, it is important to note that the virus is particularly dangerous for the sow in her first gestation, which would be at 7–8 months of age, as she would have a particularly low antibody count at this age and could easily contract the virus via copulation.

Developing countries are more severely affected by TORCH syndrome.

TORCH syndrome can be prevented by treating an infected pregnant person, thereby preventing the infection from affecting the fetus.

"Listeria monocytogenes" is ubiquitous in the environment. The main route of acquisition of "Listeria" is through the ingestion of contaminated food products. "Listeria" has been isolated from raw meat, dairy products, vegetables, fruit and seafood. Soft cheeses, unpasteurized milk and unpasteurised pâté are potential dangers; however, some outbreaks involving post-pasteurized milk have been reported.

Rarely listeriosis may present as cutaneous listeriosis. This infection occurs after direct exposure to "L. monocytogenes" by intact skin and is largely confined to veterinarians who are handling diseased animals, most often after a listerial abortion.

Infection in the newborn is accompanied by a strong immune response and is correlated with the need for prolonged mechanical ventilation.

Infection with "U. urealyticum" in pregnancy and birth can be complicated by chorioamnionitis, stillbirth, premature birth, and, in the perinatal period, pneumonia, bronchopulmonary dysplasia and meningitis. "U. urealyticum" has been found to be present in amniotic fluid in women who have had a premature birth with intact fetal membranes.

"U. urealyticum" has been noted as one of the infectious causes of sterile pyuria. It increases the morbidity as a cause of neonatal infections. It is associated with premature birth, preterm rupture of membranes, preterm labor, cesarean section, placental inflammation, congenital pneumonia, bacteremia, meningitis, fetal lung injury and death of infant. "Ureaplasma urealyticum" is associated with miscarriage.

Note that, in neonates, sepsis is difficult to diagnose clinically. They may be relatively asymptomatic until hemodynamic and respiratory collapse is imminent, so, if there is even a remote suspicion of sepsis, they are frequently treated with antibiotics empirically until cultures are sufficiently proven to be negative. In addition to fluid resuscitation and supportive care, a common antibiotic regimen in infants with suspected sepsis is a beta-lactam antibiotic (usually ampicillin) in combination with an aminoglycoside (usually gentamicin) or a third-generation cephalosporin (usually cefotaxime—ceftriaxone is generally avoided in neonates due to the theoretical risk of kernicterus.) The organisms which are targeted are species that predominate in the female genitourinary tract and to which neonates are especially vulnerable to, specifically Group B Streptococcus, "Escherichia coli", and "Listeria monocytogenes" (This is the main rationale for using ampicillin versus other beta-lactams.) Of course, neonates are also vulnerable to other common pathogens that can cause meningitis and bacteremia such as "Streptococcus pneumoniae" and "Neisseria meningitidis". Although uncommon, if anaerobic species are suspected (such as in cases where necrotizing enterocolitis or intestinal perforation is a concern, clindamycin is often added.

Granulocyte-macrophage colony stimulating factor (GM-CSF) is sometimes used in neonatal sepsis. However, a 2009 study found that GM-CSF corrects neutropenia if present but it has no effect on reducing sepsis or improving survival.

Trials of probiotics for prevention of neonatal sepsis have generally been too small and statistically underpowered to detect any benefit, but a randomized controlled trial that enrolled 4,556 neonates in India reported that probiotics significantly reduced the risk of developing sepsis. The probiotic used in the trial was "Lactobacillus plantarum".

A very large meta-analysis investigated the effect of probiotics on preventing late-onset sepsis (LOS) in neonates. Probiotics were found to reduce the risk of LOS, but only in babies who were fed human milk exclusively. It is difficult to distinguish if the prevention was a result of the probiotic supplementation or if it was a result of the properties of human milk. It is also still unclear if probiotic administration reduces LOS risk in extremely low birth weight infants due to the limited number of studies that investigated it. Out of the 37 studies included in this systematic review, none indicated any safety problems related to the probiotics. It would be beneficial to clarify the relationship between probiotic supplementation and human milk for future studies in order to prevent late onset sepsis in neonates.

Doxycycline is the drug of choice, but azithromycin is also used as a five-day course rather than a single dose that would be used to treat "Chlamydia" infection; streptomycin is an alternative, but is less popular because it must be injected. Penicillins are ineffective — "U. urealyticum" does not have a cell wall, which is the drug's main target.

During the 1950s there were outbreaks of omphalitis that then led to anti-bacterial treatment of the umbilical cord stump as the new standard of care. It was later determined that in developed countries keeping the cord dry is sufficient, (known as "dry cord care") as recommended by the American Academy of Pediatrics. The umbilical cord dries more quickly and separates more readily when exposed to air However, each hospital/birthing center has its own recommendations for care of the umbilical cord after delivery. Some recommend not using any medicinal washes on the cord. Other popular recommendations include triple dye, betadine, bacitracin, or silver sulfadiazine. With regards to the medicinal treatments, there is little data to support any one treatment (or lack thereof) over another. However one recent review of many studies supported the use of chlorhexidine treatment as a way to reduce risk of death by 23% and risk of omphalitis by anywhere between 27-56% in community settings in underdeveloped countries. This study also found that this treatment increased the time that it would take for the umbilical stump to separate or fall off by 1.7 days. Lastly this large review also supported the notion that in hospital settings no medicinal type of cord care treatment was better at reducing infections compared to dry cord care.

Incidence in 2004–2005 was 2.5–3 cases per million population a year in the United States, where pregnant women accounted for 30% of all cases. Of all nonperinatal infections, 70% occur in immunocompromised patients. Incidence in the U.S. has been falling since the 1990s, in contrast to Europe where changes in eating habits have led to an increase during the same time. In the EU, it has stabilized at around 5 cases per annum per million population, although the rate in each country contributing data to EFSA/ECDC varies greatly.

There are four distinct clinical syndromes:

- Infection in pregnancy: "Listeria" can proliferate asymptomatically in the vagina and uterus. If the mother becomes symptomatic, it is usually in the third trimester. Symptoms include fever, myalgias, arthralgias and headache. Miscarriage, stillbirth and preterm labor are complications of this infection. Symptoms last 7–10 days.

- Neonatal infection (granulomatosis infantiseptica): There are two forms. One, an early-onset sepsis, with "Listeria" acquired in utero, results in premature birth. "Listeria" can be isolated in the placenta, blood, meconium, nose, ears, and throat. Another, late-onset meningitis is acquired through vaginal transmission, although it also has been reported with caesarean deliveries.

- Central nervous system (CNS) infection: "Listeria" has a predilection for the brain parenchyma, especially the brain stem, and the meninges. It can cause cranial nerve palsies, encephalitis, meningitis, meningoencephalitis and abscesses. Mental status changes are common. Seizures occur in at least 25% of patients.

- Gastroenteritis: "L. monocytogenes" can produce food-borne diarrheal disease, which typically is noninvasive. The median incubation period is 21 days, with diarrhea lasting anywhere from 1–3 days. Patients present with fever, muscle aches, gastrointestinal nausea or diarrhea, headache, stiff neck, confusion, loss of balance, or convulsions.

"Listeria" has also been reported to colonize the hearts of some patients. The overall incidence of cardiac infections caused by "Listeria" is relatively low, with 7-10% of case reports indicating some form of heart involvement. There is some evidence that small subpopulations of clinical isolates are more capable of colonizing the heart throughout the course of infection, but cardiac manifestations are usually sporadic and may rely on a combination of bacterial factors and host predispositions, as they do with other strains of cardiotropic bacteria.

Neonatal HSV rates in the U.S. are estimated to be between 1 in 3,000 and 1 in 20,000 live births. Approximately 22% of pregnant women in the U.S. have had previous exposure to HSV-2, and an additional 2% acquire the virus during pregnancy, mirroring the HSV-2 infection rate in the general population. The risk of transmission to the newborn is 30-57% in cases where the mother acquired a primary infection in the third trimester of pregnancy. Risk of transmission by a mother with existing antibodies for both HSV-1 and HSV-2 has a much lower (1-3%) transmission rate. This in part is due to the transfer of significant titer of protective maternal antibodies to the fetus from about the seventh month of pregnancy. However, shedding of HSV-1 from both primary genital infection and reactivations is associated with higher transmission from mother to infant.

HSV-1 neonatal herpes is extremely rare in developing countries because development of HSV-1 specific antibodies usually occurs in childhood or adolescence, precluding a later genital HSV-1 infection. HSV-2 infections are much more common in these countries. In industrialized nations, the adolescent HSV-1 seroprevalance has been dropping steadily for the last 5 decades. The resulting increase in the number of young women becoming sexually active while HSV-1 seronegative has contributed to increased HSV-1 genital herpes rates, and as a result, increased HSV-1 neonatal herpes in developed nations. A recent three-year study in Canada (2000–2003) revealed a neonatal HSV incidence of 5.9 per 100,000 live births and a case fatality rate of 15.5%. HSV-1 was the cause of 62.5% of cases of neonatal herpes of known type, and 98.3% of transmission was asymptomatic. Asymptomatic genital HSV-1 has been shown to be more infectious to the neonate, and is more likely to produce neonatal herpes, than HSV-2, However, with prompt application of antiviral therapy, the prognosis of neonatal HSV-1 infection is better than that for HSV-2.

The majority of cases (85%) occur during birth when the baby comes in contact with infected genital secretions in the birth canal, most common with mothers that have newly been exposed to the virus (mothers that had the virus before pregnancy have a lower risk of transmission), an estimated 5% are infected in utero, and approximately 10% of cases are acquired postnatally. Detection and prevention is difficult because transmission is asymptomatic in 60% - 98% of cases.