INFECTIONS IN THE NEWBORN INFANT

The fetus and the newborn infant are very susceptible to infections. There are three major routes of perinatal infection: (1) blood-borne transplacental infection of the fetus (eg, cytomegalovirus, rubella, syphilis); (2) ascending infection with disruption of the barrier provided by the amniotic membranes (eg, bacterial infections after 12–18 hours of ruptured membranes); and (3) infection upon passage through an infected birth canal or exposure to infected blood at delivery (eg, herpes simplex, hepatitis B, bacterial infections).
Susceptibility of the newborn infant to infection is related to immaturity of both the cellular and humoral immune systems at birth. This feature is particularly evident in the preterm neonate. Passive protection against some organisms is provided by transfer of IgG across the placenta during the third trimester of pregnancy. Preterm infants, especially those born at less than 30 weeks’ gestation, do not have the benefit of the full amount of this passively acquired antibody.


BACTERIAL INFECTIONS

1. BACTERIAL SEPSIS

• Essentials of Diagnosis & Typical Features
• Most infants with early-onset sepsis present at <>
• Respiratory distress is the most common presenting symptom.
• Hypotension, acidemia, and neutropenia are associated clinical findings.
• The presentation of late-onset sepsis is more subtle.

General Considerations
The incidence of early-onset (< 5 days) neonatal bacterial infection is 4–5 per 1000 live births. If rupture of the membranes occurs more than 24 hours prior to delivery, the infection rate increases to 1 per 100 live births. If there is early rupture of membranes with chorioamnionitis, the infection rate increases further to 1 per 10 live births. Irrespective of membrane rupture, infection rates are five times higher in preterm than in term infants.

Clinical Findings
Early-onset bacterial infections appear most commonly on day 1 of life, and the majority of cases appear at less than 12 hours. Respiratory distress due to pneumonia is the most common presenting sign. Other features include unexplained low Apgar scores without fetal distress, poor perfusion, and hypotension. Late-onset bacterial infection (at more than 5 days of age) presents in a more subtle manner, with poor feeding, lethargy, hypotonia, temperature instability, altered perfusion, new or increased oxygen requirement, and apnea. Late-onset bacterial sepsis is more often associated with meningitis or other localized infections.
Low total white counts, absolute neutropenia (< 1000/µL), and elevated ratios of immature to mature neutrophils are suggestive of neonatal bacterial infection. Thrombocytopenia is also a common feature. Other laboratory signs are hypoglycemia or hyperglycemia with no change in glucose administration and unexplained metabolic acidosis. In early-onset bacterial infection, pneumonia is invariably present; chest x-ray films show infiltrates, but these infiltrates cannot be distinguished from those resulting from other causes of neonatal lung disease. Definitive diagnosis is made by positive cultures from blood, CSF, and the like.
Early-onset infection is most often caused by group B b-hemolytic streptococci (GBS) and gram-negative enteric pathogens (most commonly E coli). Another organism to consider is Haemophilus influenzae. Late-onset sepsis is caused by coagulase-negative staphylococci (most common in infants with indwelling central venous lines), Staphylococcus aureus, GBS, Enterococcus, Pseudomonas, and other gram-negative organisms.

Treatment
A high index of suspicion is important in the diagnosis and treatment of neonatal infection. Table 1–22 presents guidelines for the evaluation and management of term infants with risk factors or clinical signs of infection. Because the risk of infection is greater in the preterm infant and because respiratory disease is a common sign of infection, any preterm infant with respiratory disease requires blood cultures and broad-spectrum antibiotic therapy for 48–72 hours pending the results of cultures. An examination of CSF should be performed when infection is highly suspected on a clinical basis (eg, associated hypotension, persistent metabolic acidosis, neutropenia). Antibiotic coverage should be directed initially toward suspected organisms. Early-onset sepsis is usually caused by GBS or gram-negative enteric organisms; broad-spectrum coverage, therefore, should include ampicillin plus an aminoglycoside or third-generation cephalosporin—eg, ampicillin, 100 mg/kg/d divided every 12 hours, and gentamicin, 2.5 mg/kg/dose every 12–24 hours (depending on gestational age), or cefotaxime, 100 mg/kg/d divided every 12 hours. Late-onset infections can also be caused by the same organisms, but coverage may need to be expanded to include staphylococci. In particular, the preterm infant with an indwelling line is at risk for infection with coagulase-negative staphylococci, for which vancomycin is the drug of choice in a dosage of 10 mg/kg every 8–24 hours depending on gestational and postnatal ages. Other supportive therapy includes the administration of intravenous immune globulin (500–750 mg/kg) to infants with known overwhelming infection. The duration of treatment for proved sepsis is 10–14 days of intravenous antibiotics. In addition, recombinant human granulocyte colony-stimulating factor (rhG-CSF) is under investigation for treatment of neutropenia in the septic infant. In sick infants, the essentials of good supportive therapy should be provided: intravenous glucose, volume expansion, use of pressors as needed, and oxygen and ventilator support.
Prevention of neonatal GBS infection has been achieved with intrapartum administration of penicillin to selected maternal GBS carriers identified antepartum or intrapartum who have associated risk factors (preterm labor, premature rupture of the membranes before 37 weeks, rupture of the membranes beyond 18 hours at any gestational age, multiple births, maternal fever). If maternal GBS status is unknown, chemoprophylaxis may be indicated for one or more of the risk factors listed above (Figure 1–9). Figure 1–10 presents a suggested strategy for the infant born to a mother who received intrapartum prophylaxis. Some authors also recommend selective neonatal prophylaxis with 50,000 U/kg of penicillin G given intramuscularly if adequate intrapartum treatment has not been given.

2. MENINGITIS
Any newborn with bacterial sepsis is also at risk for meningitis. The incidence is low in infants with early-onset sepsis but much higher in infants with late-onset infection. The workup for any newborn with signs of infection should include a spinal tap. Diagnosis is suggested by a CSF protein greater than 150 mg/dL, glucose less than 30 mg/dL, more than 25 leukocytes/µL, and a positive Gram stain. The diagnosis is confirmed by culture. The most common organisms are GBS and gram-negative enteric bacteria. Although sepsis can be treated with antibiotics for 10–14 days, meningitis should be treated for 21 days. The mortality rate of neonatal meningitis is approximately 25%, with significant neurologic morbidity present in one third of the survivors. Use of dexamethasone has not been studied in neonates.

3. PNEUMONIA
The respiratory system can be infected in utero or upon passage through the birth canal. Early-onset neonatal infection is usually associated with pneumonia. Pneumonia should also be suspected in older neonates with a recent onset of tachypnea, retractions, and cyanosis. In infants already receiving respiratory support, an increase in the requirement for oxygen or ventilator support may indicate pneumonia. Not only common bacteria but also viruses (cytomegalovirus, respiratory syncytial virus, adenovirus, influenza, herpes simplex, parainfluenza) and Chlamydia can cause the disease. In infants with preexisting respiratory disease, intercurrent pulmonary infections may contribute to the ultimate severity of chronic lung disease.

4. URINARY TRACT INFECTION
Infection of the urine is uncommon in the first days of life. Urinary tract infection in the newborn occurs most commonly in association with genitourinary anomalies and is caused by gram-negative enteric pathogens. Urine should be evaluated as part of the workup for late-onset infection. Culture should be obtained either by suprapubic aspiration or bladder catheterization. Antibiotic therapy is continued intravenously for 10–14 days. Evaluation for genitourinary anomalies, starting with an ultrasound examination and a voiding cystourethrogram, should be done subsequently.

5. OTITIS MEDIA
Otitis media occurs in a significant number of long-term nursery occupants. It is particularly common in infants who have had prolonged endotracheal intubation or an indwelling nasogastric feeding tube. Evaluation for infection in such an infant is not complete without an ear examination. Gram-negative enteric pathogens are more commonly found infecting agents in nursery occupants than in outpatients.

6. OMPHALITIS
A normal umbilical cord stump will atrophy and separate at the skin level. A small amount of purulent material at the base of the cord is common but can be minimized by keeping the cord open to air and cleaning the base with alcohol several times a day. The cord can become colonized with streptococci, staphylococci, or gram-negative organisms that can cause local infection. Infections are more common in cords manipulated for venous or arterial lines. Omphalitis is diagnosed when redness and edema develop in the soft tissues around the stump. Local and systemic cultures should be obtained. Treatment is with broad-spectrum intravenous antibiotics. Complications are determined by the degree of infection of the cord vessels and include septic thrombophlebitis, hepatic abscess, necrotizing fasciitis, and portal vein thrombosis. Surgical consultation should be obtained because of the potential for necrotizing fasciitis.


FUNGAL SEPSIS

With the survival of smaller, sicker infants, infection with Candida species has become more common. Infants of low birth weight with central lines who have had repeated exposures to broad-spectrum antibiotics are at highest risk. For infants of birth weight less than 1500 g, colonization rates of 27% have been demonstrated, with many of these infants developing cutaneous lesions. A much smaller percentage (2–5%) develop systemic disease.
Clinical features of fungal sepsis can be indistinguishable from those of late-onset bacterial sepsis but may be more subtle. Thrombocytopenia may be the earliest and only sign. Deep organ involvement (renal, eye, endocarditis) is commonly associated with systemic candidiasis. Treatment is with amphotericin B. In severe infections, flucytosine can be added for synergistic coverage. (See Chapter 38.)
Malassezia furfur is also seen in infants with central lines receiving intravenous fat emulsion. To eradicate this organism, as well as Candida species, it is necessary to remove the indwelling line.


CONGENITAL VIRAL & PARASITIC INFECTIONS

1. CYTOMEGALOVIRUS INFECTION
Cytomegalovirus (CMV) is the most common virus transmitted in utero. The incidence of congenital infection ranges from 0.2% to 2.2% of live births. Transmission of CMV can occur during either primary or reactivated infection in the mother. An important source of infection is children (especially those in a day care setting), who transmit the virus to parents and workers. The incidence of primary infection in pregnancy is 1–4%, with a 40% transplacental transmission rate to the fetus. Of these infants, 85–90% are asymptomatic at birth, whereas 10–15% have clinically apparent disease—hepatosplenomegaly, petechiae, small size for gestational age, microcephaly, direct hyperbilirubinemia, thrombocytopenia, intracranial calcifications, and chorioretinitis. The risk of neonatal disease is higher when the mother acquires the infection in the first half of pregnancy. The incidence of reactivated infection in pregnancy is less than 1%, with an incidence of clinically apparent disease of 0–1%. Diagnosis in the neonate should be confirmed by culture of the virus from urine. Rapid diagnosis is possible with antigen detection techniques and identification of viral DNA by polymerase chain reaction (PCR) testing. Diagnosis can also be confirmed in utero from an amniocentesis specimen. Although experimental and not routinely recommended, ganciclovir therapy has been used in some severely ill neonates.
The mortality rate in patients with symptomatic congenital CMV may be as high as 20%. Sequelae such as hearing loss, mental retardation, delayed motor development, chorioretinitis and optic atrophy, seizures, language delays, and learning disability occur in 90% of symptomatic survivors. The incidence of complications is 5–15% in asymptomatic infants; the most frequent complication is hearing loss, which can be progressive.
Perinatal infection can also occur with acquisition of virus around the time of delivery. These infections are generally asymptomatic and without sequelae. Postnatal infection is usually asymptomatic but can cause hepatitis, pneumonitis, and neurologic illness in compromised seronegative premature infants. The virus can be acquired postnatally through transfusions or ingestion of CMV-infected breast milk. Transfusion risk can be minimized by using frozen, washed red blood cells or CMV antibody-negative donors.

2. RUBELLA
Congenital rubella infection occurs as a result of rubella infection in the mother during pregnancy. The frequency of infection and damage in the fetus is as high as 80% in mothers infected during the first trimester. Fetal infection rates decline in the second trimester before increasing again in the third trimester. Fetal damage generally does not occur in infections acquired after 18 weeks’ gestation. Clinical features of congenital rubella include adenopathy, bone radiolucencies, encephalitis, cardiac defects (pulmonary arterial hypoplasia and patent ductus arteriosus), cataracts, retinopathy, growth retardation, hepatosplenomegaly, thrombocytopenia, and purpura. Affected infants can be asymptomatic at birth but develop clinical sequelae during the first year of life. The diagnosis should be suspected in cases of a characteristic clinical illness in the mother (rash, adenopathy, arthritis) confirmed by serologic testing. Diagnosis can be confirmed by culture of pharyngeal secretions in the baby. Congenital rubella is now rare because prevention is possible with immunization.

3. VARICELLA
Congenital varicella is rare (< 5% after infection acquired during the first or second trimester) but may cause a constellation of findings including limb hypoplasia, cutaneous scars, microcephaly, cortical atrophy, chorioretinitis, and cataracts. Perinatal exposure (5 days before to 2 days after delivery) can cause severe to fatal disseminated varicella in the infant. If maternal varicella develops within this perinatal risk period, 1.25 mL of varicella immune globulin should be given to the newborn. If this has not been done, the illness can be treated with intravenous acyclovir (30 mg/kg/d divided every 8 hours).
Hospitalized premature infants of at least 28 weeks’ gestation whose mothers have no history of chickenpox—and all infants of less than 28 weeks’ gestational age—should receive varicella immune globulin following any postnatal exposure.Susceptible women of childbearing age should be immunized with varicella vaccine.

4. TOXOPLASMOSIS
Toxoplasmosis is caused by the protozoan Toxoplasma gondii. Maternal infection occurs in 0.1– 0.5% of pregnancies and is usually asymptomatic. When primary infection occurs during pregnancy, up to 40% of the fetuses become infected, of whom 15% have severe damage. The sources of transmission include exposure to cat feces and ingestion of raw or undercooked meat. Although the risk of transmission increases to 90% near term, fetal damage is most likely to occur when maternal infection occurs in the second to sixth months of gestation.
Clinical findings include growth retardation, chorioretinitis, seizures, jaundice, hydrocephalus, microcephaly, cerebral calcifications, hepatosplenomegaly, adenopathy, cataracts, maculopapular rash, thrombocytopenia, and pneumonia. The majority of affected infants are asymptomatic at birth but show evidence of damage (chorioretinitis, blindness, low IQ, hearing loss) at a later time. Serologic tests, first for IgG and then for the specific IgM antibody, make the diagnosis. Infants with suspected infection should have an eye examination and CT scan. Organism isolation and PCR tests are also available for diagnosis in the neonate and from amniocentesis specimens.
Treatment of the acutely infected pregnant woman does not prevent transmission to the fetus but reduces the rate of sequelae. Neonatal treatment using pyrimethamine and sulfadiazine with folinic acid can improve long-term outcome. (See Chapter 38.)


PERINATALLY ACQUIRED VIRAL INFECTIONS

1. HERPES SIMPLEX
Herpes simplex virus (HSV) infection is most commonly acquired at the time of birth during transit through an infected birth canal. The mother may have either primary or reactivated secondary infection. Primary maternal infection, because of the high titer of organism and the absence of maternal antibodies, poses the greatest risk to the infant. The risk of neonatal infection with vaginal delivery in this setting is 33–50%. Seventy percent of mothers with primary herpes at the time of delivery are asymptomatic. The risk to an infant born to a mother with recurrent herpes simplex is much lower (< 3–5%). Time of presentation of localized (skin, eye, mouth) or disseminated disease (pneumonia, shock, hepatitis) in the infant is usually 5–14 days of age. CNS disease usually presents at 14–28 days with lethargy and seizures. In about one third of patients, localized skin, eye, and mouth disease is the first indication of infection. In another third, disseminated or CNS disease precedes skin, eye, and mouth findings, whereas the remaining third have disseminated or CNS disease in the absence of skin, eye, and mouth disease. Preliminary diagnosis can be made by scraping the base of a vesicle and finding multinucleated giant cells. Viral culture from vesicles, usually positive in 24–72 hours, makes the definitive diagnosis. In some cases, PCR DNA technology may assist in diagnosis.
Acyclovir (30–60 mg/kg/d given every 8 hours) is the drug of choice for neonatal herpes infection. Treatment improves survival of neonates with CNS and disseminated disease and prevents the spread of localized disease. Prevention is possible by not allowing delivery through an infected birth canal (eg, by cesarean section within 6 hours after rupture of the membranes). However, antepartum cervical cultures are poor predictors of the presence of virus at the time of delivery. Furthermore, given the low incidence of infection in the newborn in secondary maternal infection, cesarean section is not indicated for asymptomatic mothers with a history of herpes. In most settings, cesarean sections are still performed in mothers with active lesions (either primary or secondary) at the time of delivery. Infants born to mothers with a history of HSV infection but no active lesions can be observed closely after birth. Cultures should be obtained and acyclovir treatment initiated only for clinical signs consistent with herpes virus infection. Infants born to mothers with active lesions—irrespective of the route of delivery—should be cultured (eye, oropharynx, umbilicus, rectum) 24 hours after delivery. If the infant is colonized (positive cultures) or if symptoms consistent with herpes infection develop, treatment with acyclovir should be started. In cases of maternal primary infection at the time of vaginal delivery, the infant should be cultured and started on acyclovir pending the results of cultures. The major problem facing perinatologists is the high percentage of asymptomatic primary maternal infection. In these cases, infection in the neonate is currently not preventable. Therefore, any infant who presents at the right age with symptoms consistent with neonatal herpes should be cultured and started on acyclovir pending the results of those cultures.
The prognosis is good for localized skin and mucosal disease that does not progress. The mortality rate for both disseminated and CNS herpes is high, with significant rates of morbidity among survivors despite treatment.

2. HEPATITIS B & C
Infants can be infected with hepatitis B at the time of birth. Clinical illness is rare in the neonatal period, but infants exposed in utero are at high risk of becoming chronic HBsAg carriers, developing chronic active hepatitis and, later, hepatocellular carcinoma. The presence of HBsAg should be determined in all pregnant women. If the result is positive, the infant should receive HBIG and hepatitis B vaccine as soon as possible after birth, followed by two subsequent vaccine doses at 1 and 6 months of age. If HBsAg has not been tested prior to birth in a mother at risk, the test should be run after delivery and hepatitis B vaccine given within 12 hours after birth. If the mother is subsequently found to be positive, HBIG should be given as soon as possible (preferably within 48 hours, but not later than 1 week after birth). Subsequent vaccine doses should be given at 1 and 6 months of age. In premature infants born to HBsAg-positive mothers, vaccine and HBIG should be given at birth, but a three-vaccine hepatitis B series should be given after a weight of 2000 g is attained.
Hepatitis C perinatal transmissions occur in about 5% of infants born to mothers who carry the virus. At the present time, no prevention strategies exist.

3. ENTEROVIRAL INFECTION
Enteroviral infections occur with greatest frequency in the late summer and early fall. Infection is usually acquired in the perinatal period. There is often a history of maternal illness (fever, diarrhea, rash) in the week prior to delivery. The illness appears in the infant in the first 2 weeks of life and is most commonly characterized by fevers, lethargy, irritability, diarrhea, and rash but is not severe. More severe forms occasionally occur, including meningoencephalitis and myocarditis, as well as a disseminated illness with hepatitis, pneumonia, shock, and disseminated intravascular coagulation. Diagnosis can be confirmed by culture (rectum, CSF, blood) or by the more rapid PCR techniques.
There is no therapy of proved efficacy. The prognosis is good for all symptom complexes except severe disseminated disease, which carries a high mortality rate.

4. HIV INFECTION
Human immunodeficiency virus (HIV) can pass transplacentally, can be acquired at the time of delivery, or can be transmitted postpartum via breast milk. The prevalence of HIV infection among women of childbearing age in the United States is 1.5:1000. Transmission of virus occurs in about 30% of births. Administration of zidovudine during pregnancy, intrapartum, and for 6 weeks in the newborn period at a dosage of 2 mg/kg orally four times a day decreases vertical transmission to 8%. Shorter courses of zidovudine are also associated with decreased disease transmission, as is cesarean delivery. The addition of protease inhibitor therapy may further reduce the risk of ante- and intrapartum viral transmission. The risk of transmission is increased in mothers with advanced disease, low CD4 counts, and p24 antigenemia. Prematurity, vaginal delivery, ruptured membranes over 4 hours, and chorioamnionitis also increase the transmission rate. With zidovudine treatment, transmission of virus to the newborn correlates with maternal level of HIV-1 RNA. Diagnosis is based on clinical, immunologic, and serologic findings. Newborns with congenitally acquired HIV are often free of symptoms. Jaundice, neonatal giant cell hepatitis, and thrombocytopenia have been reported at birth. Failure to thrive, lymphadenopathy, hepatosplenomegaly, oral thrush, chronic diarrhea, bacterial infections with common organisms, and an increased incidence of upper and lower respiratory diseases, including lymphoid interstitial pneumonitis, may appear early in life or may be delayed for months to years.
The presence of maternal antibody acquired transplacentally confuses diagnosis in the neonate. The presence of anti-HIV antibody is not diagnostic of infection until after 18 months of age. An infant who is not infected should remain healthy, and the titer of antibody should decline during the first year of life. Diagnosis can be made in infants in the first few months of life by culture or detection of HIV DNA sequences by PCR. These tests should be done at birth and repeated at 1–2 months and 4 months of age. An infant who is age 4 months with no positive culture, PCR, or p24 antigen has a greater than 95% chance of not being infected. Follow-up should document antibody disappearance. An HIV-exposed infant is considered uninfected when there are no physical findings of HIV, immunologic tests are normal, virologic studies are negative, and two HIV antibody tests are negative.
Protection of health care workers is an important issue. Testing should be performed in all pregnant women. Because such testing will fail to identify some infected patients, however, universal precautions should be used. Gloves should be worn during all procedures involving blood and blood-contaminated fluids, intubation, and any invasive procedures using needles. When a splash exposure is possible (eg, in the delivery room), a mask and eye covers should be used.


OTHER INFECTIONS

1. CONGENITAL SYPHILIS
The infant is usually infected in utero by transplacental passage of Treponema pallidum. Active primary and secondary maternal syphilis leads to fetal infection in nearly 100% of infants; latent disease in 40%; and late disease in 10%. Fetal infection is rare at under 18 weeks’ gestation. Fetal infection can result in stillbirth or prematurity. Findings consistent with early congenital syphilis (presentation at under 2 years) include mucocutaneous lesions, lymphadenopathy, hepatosplenomegaly, bony changes, and hydrops. However, in the newborn period, infants are often asymptomatic, so that diagnosis is based on maternal and infant serologic testing and is only presumptive. Later manifestations (at over age 2 years) include Hutchinson disease and mulberry molars, keratitis, chorioretinitis, glaucoma, hearing loss, saddle nose, saber shins, and mental retardation. An infant should be evaluated for congenital syphilis if it is born to a mother with positive nontreponemal tests confirmed by a positive treponemal test but without documented adequate treatment (parenteral penicillin G), including the expected fourfold decrease in nontreponemal antibody titer. Evaluation should include physical examination, a quantitative nontreponemal serologic test for syphilis, CSF examination, long bone x-rays, and antitreponemal IgM. A definitive diagnosis can be made on rare occasions when the organism is identified by dark-field microscopy or pathologic examination of the placenta. Guidelines for therapy are presented in Table 1–23. Infants should be treated for congenital syphilis if they have proved or probable disease, as evidenced by (1) physical or x-ray evidence, (2) quantitative nontreponemal antibody titers four times higher than the mother, (3) elevated CSF protein or cell count or positive VDRL, or (4) a positive antitreponemal IgM test. Asymptomatic infants should be treated if the mother did not receive adequate treatment for syphilis.

2. TUBERCULOSIS
Congenital tuberculosis is rare but may occur in the infant of a mother with hematogenously spread tuberculosis or by aspiration of infected amniotic fluid in cases of tuberculous endometritis. Women with pulmonary tuberculosis are not likely to infect the fetus until after delivery. Postnatal acquisition is the most common mechanism of neonatal infection. Management in these cases is based on the mother’s evaluation.

1. Mother with a positive skin test and negative chest x-ray, or mother with an abnormal chest x-ray but no evidence of acute disease: Investigate family contacts. Treat the mother with isoniazid (INH).
2. Mother has an abnormal chest x-ray: Mother and infant should be separated until the mother is evaluated. If active tuberculosis is found, maintain separation until the mother is receiving antituberculosis therapy. Investigate family contacts.
3. Mother with clinical or x-ray evidence of acute and possibly contagious tuberculosis: Evaluate the infant for congenital tuberculosis (skin test, chest x-ray, lumbar puncture, cultures) and HIV. Treat the mother and infant and separate them until the mother is felt to be noncontagious. If congenital tuberculosis is suspected, multidrug therapy should be initiated.

3. CONJUNCTIVITIS
Neisseria gonorrhoeae may colonize an infant during passage through an infected birth canal. Gonococcal ophthalmitis presents at 3–7 days with purulent conjunctivitis. The diagnosis can be suspected when gram-negative intracellular diplococci are seen on a Gram-stained smear and confirmed by culture. Treatment is with intravenous or intramuscular ceftriaxone, 25–50 mg/kg (not to exceed 125 mg) given once. Prophylaxis at birth is with 1% silver nitrate or 0.5% erythromycin ointment. Infants born to mothers with known gonococcal disease should also receive a single dose of ceftriaxone.
Chlamydia trachomatis is another important cause of conjunctivitis, appearing at 5 days to several weeks of age with congestion, edema, and minimal discharge. The organism is acquired at birth after passage through an infected birth canal. Acquisition occurs in 50% of infants born to infected women, with a 25–50% risk of conjunctivitis. Prevalence in pregnancy is over 10% in some populations. Diagnosis is by isolation of the organism or by rapid antigen detection tests. Treatment is with oral erythromycin (30 mg/kg/d in divided doses every 8–12 hours) for 14 days. Topical treatment alone will not eradicate nasopharyngeal carriage, leaving the infant at risk for the development of pneumonitis. Infants born to mothers with untreated chlamydial infection should also be treated with oral erythromycin.