Mohan P. Venkatesh, Karen M. Adams and Leonard E. Weisman
A newborn infant is uniquely susceptible to infectious diseases. This chapter presents causes of infectious diseases with particular emphasis on prevention, history, presenting signs and symptoms, laboratory data, treatment, and parent teaching methods of prevention applicable to the care of the neonate. Abbreviations for this chapter are listed in Box 22-1.
BOX 22-1
| AIDS | Acquired immunodeficiency syndrome |
| CF | Complement fixation (test) |
| CIE | Counterimmunoelectrophoresis |
| CRP | C-reactive protein |
| CRS | Congenital rubella syndrome |
| CSF | Cerebrospinal fluid |
| DFA | Direct fluorescent antibody |
| DNA | Deoxyribonucleic acid |
| ELISA | Enzyme-linked immunosorbent assay |
| FA | Fluorescent antibody (test) |
| FAMA | Fluorescent antibody to membrane antigen |
| FTA-ABS | Fluorescent treponemal antibody absorption (test) |
| GBS | Group B Streptococcus |
| HbsAg | Hepatitis B surface antigen |
| HIV | Human immunodeficiency virus |
| IAHA | Immune adherence hemagglutination |
| IFA | Indirect fluorescent antibody (test) |
| IHA | Indirect hemagglutination inhibition (test) |
| IPV | Inactivated poliovirus vaccine |
| IUGR | Intrauterine growth restriction |
| LA | Latex agglutination (test) |
| MHA-TP | Microhemagglutination test for Treponema pallidum infection |
| NAAT | Nucleic acid amplification test |
| OPV | Oral poliovirus vaccine |
| PCP | Pneumocystis jiroveci pneumonia* |
| PCR | Polymerase chain reaction |
| RNA | Ribonucleic acid |
| RPR | Rapid plasma reagin (test) |
| RT-PCR | Reverse transcriptase PCR |
| VDRL | Venereal Disease Research Laboratory (test) |
| *Formerly Pneumocystis carinii. |
|
PATHOPHYSIOLOGY AND PATHOGENESIS
An infection occurs when a susceptible host comes in contact with a potentially pathogenic organism. When the encountered organism proliferates and overcomes the host defenses, infection results. Sources of infection in a newborn can be divided into three categories: (1) transplacental acquisition (intrauterine infection), (2) perinatal acquisition during labor and delivery (intrapartum infection), and (3) hospital acquisition in the neonatal period (postnatal infection) from the mother, hospital environment, or hospital personnel.
In general, most infecting organisms can, under the proper circumstances, cross the placenta or ascend from the birth canal and invade the at-risk neonate. These infections may result in abortion, stillbirth, and disease present at birth or in the neonatal period.
The main goal is to prevent infections in the fetus and newborn. Unfortunately, few proven measures exist for the prevention of transplacentally or perinatally acquired infections. These measures are important, because most nonbacterial infections (except syphilis and possibly toxoplasmosis, cytomegalovirus [CMV] infection, and herpes simplex) do not respond to current therapy.
ETIOLOGY
Thorough data collection for diagnosis of infectious diseases includes a review of the perinatal history, signs and symptoms, and laboratory data. Intrauterine, intrapartum, or neonatal disease may be caused by a wide variety of organisms, many of which are discussed in this chapter.
SPECIFIC INFECTIOUS DISEASES
The following specific infectious diseases are grouped according to their source of infection.
Transplacental (Intrauterine) Acquisition
HUMAN IMMUNODEFICIENCY VIRUS INFECTION AND ACQUIRED IMMUNODEFICIENCY DISORDER
Prevention
The primary risk to infants for infection with human immunodeficiency virus (HIV), the causative agent of acquired immunodeficiency syndrome (AIDS), is intrauterine, intrapartum, and postpartum exposure to a mother with HIV infection. HIV has been isolated from blood and many body fluids. Epidemiologic evidence has implicated only blood, semen, vaginal secretions, and breast milk in transmission. In countries such as the United States, where safe alternatives exist, mothers with HIV infection should be discouraged from breast feeding. 93 HIV testing should be recommended and encouraged to all pregnant women. 5,6,114
Because the medical history and examination cannot reliably identify all patients infected with HIV (or other bloodborne pathogens) and because during delivery and initial care of the infant, perinatal care providers are exposed to large amounts of maternal blood, Standard Precautions (e.g., gloves) should be consistently used for all patients when handling the placenta or infant until all maternal blood has been washed away. 5,50
Data Collection
History
HIV infection in the mother is acquired primarily sexually or by intravenous (IV) drug abuse. Infection may be asymptomatic. Transmission from an untreated infected mother to the fetus or infant occurs in 13% to 39% of births. Approximately 40% of transmissions are before birth and the rest around the time of delivery. Two thirds of infections occurring before delivery are caused by transmission within the 14 days before delivery. 5 A high maternal plasma viral load, high cervico-vaginal viral load, low CD4 + lymphocyte count, advanced maternal illness, an increase in exposure of the fetus to maternal blood, premature delivery, prolonged labor, longer duration of rupture of membranes before delivery, and mode of delivery all increase perinatal transmission of HIV infection. 4,6,113
Signs and Symptoms
Infants with perinatally acquired HIV infection uncommonly have symptoms in the neonatal period, but the majority of these infants present with clinical illness by 24 months of life (median age at onset of symptoms is 11 to 12 months). One fifth of infants infected with HIV perinatally develop serious disease or die in the first year of life. 114 Symptoms include failure to thrive, developmental disabilities, neurologic dysfunction, hepatosplenomegaly, generalized lymphadenopathy, parotitis, persistent oral candidiasis (thrush), and chronic or recurrent diarrhea. Lymphoid interstitial pneumonia is frequently seen in these infants. HIV-infected infants commonly have osteomyelitis, septic joints, pneumonia, sepsis, meningitis, and otitis media with common organisms (e.g., Streptococcus pneumoniae, Haemophilus influenzae type b), and these infections may be recurrent. 4,114
Laboratory Data
HIV nucleic acid detection by polymerase chain reaction (PCR) of DNA extracted from peripheral blood mononuclear cells is the gold standard for early diagnosis of infected infants, and results are available within 24 hours. 114 About 30% of HIV-infected infants have a positive DNA PCR assay from samples obtained within 48 hours of age; 93% have detectable HIV DNA by 2 weeks; and almost all by 1 month of age. The primary serologic laboratory test for HIV antibody is the enzyme-linked immunosorbent assay (ELISA). The Western blot test is used for confirmation of positive ELISA results. Differentiation of the child with passively acquired antibody from the infant with active infection is critical but difficult. Acquired antibody is undetectable in 75% of infants by 12 months of age and in most infants by 15 to 18 months of age. Infants have also been described with negative serology but active infection. 79 Virus isolation by culture is difficult and expensive, and p24 antigen detection is less sensitive. 4,72 The plasma HIV RNA PCR assay is currently used for quantifying the viral load but not routinely used for diagnosis. Although hypogammaglobulinemia has been reported (<10% of patients), hypergammaglobulinemia usually is present.
Treatment
Antiretroviral therapy with zidovudine (ZDV) alone or in combination with other antiretroviral agents reduces HIV transmission from infected mothers to their newborns. 69,78,79ZDV should be given to infants of infected women beginning at 8 to 12 hours of life and should be continued for 6 weeks.6,69 ZDV is administered orally at 2 mg/kg body weight/dose every 6 hours. 6 If the infant is confirmed to be HIV positive, ZDV is changed to a multidrug antiretroviral regimen. Infants who are perinatally infected with HIV are at high risk for developing Pneumocystis jiroveci pneumonia (PCP, formerly known as Pneumocystis carinii pneumonia) early in the first year of life. Guidelines recommend initiating prophylaxis for the prevention of PCP for all HIV-exposed infants at 4 to 6 weeks of age, regardless of their CD4 + cell count. For infants receiving ZDV, PCP prophylaxis should begin after completion of the 6-week course of ZDV. The recommended PCP prophylaxis may be provided by 150 mg/m 2/day (5 mg/kg/day) of trimethoprim (TMP) and 750 mg/m 2/day (25 mg/kg/day) of sulfamethoxazole (SMX) administered in two divided doses for three consecutive days in a week. 4,6,69 TMP/SMX prophylaxis should be continued through the first year of life or until HIV infection is reasonably excluded. 6,69
Parent Teaching
Care of an infant at risk for HIV requires close and long-term follow-up. Involvement of the parents is essential to this process. Education of the parents will maximize the success of such a care plan, and utilization of all available community resources should provide additional support. In addition to the rationale for and importance of the medical management just outlined, the parents should be counseled concerning the need for the following:
• Immunizations following the American Academy of Pediatrics schedule
• Rapid consultation with the infant’s physician if he or she is exposed to varicella (may need treatment with varicella-zoster immune globulin [VZIG] within 96 hours of exposure) or measles (needs immune globulin intramuscularly regardless of immunization status)
• Rapid consultation with the physician for tetanus-prone wounds (requires tetanus immune globulin irrespective of immunization status)
• Rapid consultation with the physician for thrush, a diaper rash, or any other signs or symptoms of illness
Prevention of infections is important, and this requires good handwashing, regular bathing, appropriate food preparation skills (wash bottles, nipples, and pacifiers), and good skin care (changing diapers and moisturizing skin in other areas to prevent drying and cracking). 4
CYTOMEGALOVIRUS INFECTION
Prevention
There are no practical methods for preventing CMV infection. Avoiding exposure is virtually impossible because of the ubiquitous and asymptomatic nature of the infections. Avoiding unnecessary blood transfusions or using CMV-seronegative blood donors, white blood cell–depleted blood products, or frozen deglycerolized blood cells has proved to be important in minimizing the occurrence of postnatally acquired CMV, particularly in premature infants. 4,5
The question frequently arises about assignment of staff to infants with a possible diagnosis of CMV infection. Staff members who may be pregnant have heightened concern about this issue. Staff members should be aware that many infants with CMV infection are often asymptomatic and therefore not identified while in the hospital. To avoid any problems, staff members should employ good handwashing technique with all infants. Wearing gloves when handling urine and other secretions is a strategy that can also be employed by staff members who are working in the neonatal intensive care unit (NICU) and are pregnant or of childbearing age. The actual risk for an infected infant’s transmitting disease to a susceptible health care worker is unknown but probably small. 4
Data Collection
History
Signs and Symptoms
An infant with CMV infection is usually asymptomatic. Congenital manifestations include intrauterine growth restriction (IUGR), neonatal jaundice (increased direct fraction), purpura, hepatosplenomegaly, microcephaly, seizures, intracerebral calcification, chorioretinitis, and progressive sensorineural hearing loss. 12
Laboratory Data
CMV may be cultured from urine, pharyngeal secretions, and peripheral leukocytes. Isolation of the virus within 3 weeks of birth indicates transplacental acquisition. A paired sera demonstration of a fourfold titer rise or histopathology demonstration of characteristic nuclear inclusions in certain tissues can confirm infection. Examining the urine for intranuclear inclusions is not helpful. PCR detection of viral DNA in tissues and cerebrospinal fluid is also available. 4
Treatment
Ganciclovir, foscarnet, valganciclovir, and cidofovir are the only licensed antiviral agents effective against CMV. These drugs are approved only for treatment of life- and sight-saving disease. In a randomized controlled trial that evaluated 42 neonates with congenital CMV infection involving the central nervous system (CNS), 6 weeks of IV ganciclovir therapy prevented hearing deterioration at 6 months. However, two thirds of neonates treated with ganciclovir had significant neutropenia. 67 More studies are necessary before ganciclovir can be routinely recommended in congenital CMV infection involving the CNS. 4,33
Parent Teaching
The need for good handwashing technique by parents and caregivers of infants with suspected CMV should be included in discharge instructions.
RUBELLA
Prevention
Medical personnel should ensure that all mothers have a protective hemagglutination titer before conception. If the woman is susceptible, vaccinate her with rubella vaccine before conception and advise her that she should avoid conception for 28 days after receiving the vaccine. 4,74 If a woman is found to lack immunity to rubella during pregnancy, she should receive rubella immunization in the postpartum period even if she is breast feeding. 43,74
Data Collection
History
Signs and Symptoms
Congenital manifestations of rubella include IUGR, sensorineural deafness, cataracts, neonatal jaundice (increased direct fraction), purpura, hepatosplenomegaly, microcephaly, chronic encephalitis, chorioretinitis, and cardiac defects (especially patent ductus arteriosus and peripheral pulmonic stenosis). Less frequent manifestations include bone lesions and pneumonitis. 4
Laboratory Data
The virus may be isolated from the throat, blood, urine, and cerebrospinal fluid (CSF). A paired sera demonstration of a fourfold titer rise, such as an indirect hemagglutination (IHA) inhibition test or an indirect fluorescent antibody (IFA) test, is diagnostic. The IHA test generally has been replaced by one of several more sensitive methods including enzyme linked immunoassay, or latex agglutination, and reverse transcriptase polymerase chain reaction (RT-PCR) assays. 4,18
Parent Teaching
Infants with congenital rubella syndrome (CRS) may secrete the virus for many years. This requires that discharge instructions include preventive strategies that should be employed to decrease the chance of contact of susceptible pregnant women with the infant. Parents should be informed of their responsibility to ensure that potentially seronegative women of childbearing age avoid direct contact with the infant.4 The challenge arises to impress this on the family and at the same time avoid ostracizing the infant or negatively affecting the parent-infant attachment process. In discharge planning with these families, a collaborative approach should be employed, using community health, medical, nursing, and social work input and support. Another challenge is to impress on parents that an infant exposed to rubella during pregnancy may appear normal at birth, but the first appearance of some CNS symptoms may extend into childhood. Thus families and clinicians should keep a watchful eye on these children during the early childhood years. 74
SYPHILIS
Prevention
Pregnant women should avoid exposure to syphilis. Monitor the serum early and late in pregnancy, and treat the mother for the appropriate stage of disease. Erythromycin, previously used in penicillin-sensitive women, is not considered adequate treatment during gestation because of 30% treatment failure rates in adults and failure to establish a cure in newborns as a result of poor transplacental passage of erythromycin. Infants born to women treated with erythromycin should be considered high risk for infection and appropriately evaluated and treated. If penicillin allergy is confirmed in the pregnant woman, acute desensitization is necessary. Desensitization can be accomplished using increasing doses of oral penicillin over 4 to 6 hours. 106
Data Collection
History
A congenital infection may be manifested by a multisystem disease. A primary syphilitic chancre on the cervix or rectal mucosa in a mother may be unnoticed. 106
Signs and Symptoms
An infant exposed to syphilis may be asymptomatic at birth, or virtually all organ systems may be involved. Clinical findings may include hepatitis, pneumonitis, bone marrow failure, myocarditis, meningitis, nephrotic syndrome, rhinitis (snuffles), a rash involving the palms and soles, and pseudoparalysis of an extremity. 4,26,106
Laboratory Data
The microscopic darkfield examination identifies spirochetes from nonoral lesions. Nonspecific, nontreponemal reaginic tests, such as Venereal Disease Research Laboratory (VDRL) tests and rapid plasma reagin (RPR) tests, followed serially with a rise or absence of fall after birth, are useful for screening. 26,106 Specific treponemal antibody serologic tests, such as a fluorescent treponemal antibody absorption (FTA-ABS) test or a microhemagglutination test for Treponema pallidum (MHA-TP), provide diagnostic confirmation of a reactive nontreponemal test, but an FTA-ABS IgM test is unreliable. 26,106 False-positive results may occur with nontreponemal tests secondary to other medical conditions or other spirochetal diseases. Therefore confirmation of diagnosis is necessary. 4 A long-bone x-ray examination showing metaphysitis or periostitis may help in diagnosing syphilis. VDRL tests on CSF are mandatory in all infants suspected of having congenital syphilis. When the diagnosis of active congenital syphilis is equivocal, often it is best to treat and ascertain the diagnosis by serial serologic determinations. 4,26,106
Treatment
Table 22-1 outlines the treatment for syphilis. 4
| Condition | Treatment |
|---|---|
| SEPSIS AND/OR MENINGITIS | |
| Initial Therapy | |
| Early onset | Intravenous (IV) ampicillin and gentamicin or IV amikacin (if gentamicin-resistant organisms are present in nursery, ampicillin plus cefotaxime is a suitable alternative, particularly if meningitis is present). |
| Late onset | IV vancomycin plus cefotaxime or IV aminoglycoside (see “Early onset”). |
| ONCE SPECIFIC ORGANISMS ARE IDENTIFIED | |
| Group B Streptococcus | IV ampicillin and gentamicin for 10 to 14 days (gentamicin may be discontinued if strain is not tolerant). |
| Coliform species | IV ampicillin and gentamicin for 10 to 14 days (cefotaxime may replace gentamicin). |
| Listeria monocytogenes | IV ampicillin and IV gentamicin for 14 to 21 days. |
| Enterococci | Same as for Listeria monocytogenes. For ampicillin resistance, use vancomycin. |
| Group A Streptococcus | IV penicillin G for 10 to 14 days. |
| Group D Streptococcus (non-enterococcus) | Same as for Group A Streptococci. |
| Staphylococcus aureus | IV nafcillin for 10 to 14 days; IV vancomycin for methicillin-resistant strains. |
| Staphylococcus epidermidis | IV vancomycin for 10 to 14 days. |
| Pseudomonas aeruginosa | IV ceftazidime and aminoglycoside for 10 to 14 days. |
| Anaerobes | IV metronidazole, clindamycin, or meropenem. |
| PNEUMONIA | |
| Group B Streptococcus | Same as for sepsis (respiratory distress syndrome may mimic pneumonitis and vice versa). |
| Staphylococcus aureus | Same as for sepsis. |
| Chlamydia trachomatis | Oral (PO) erythromycin for 14 days. |
| Pneumocystis jiroveci | PO or IV trimethoprim and sulfamethoxazole, or IV pentamidine isethionate. |
| Pertussis | PO or IV azithromycin for 5 days (clinical course is unchanged, but shedding of organism is diminished significantly). |
| Other organisms | Same as for sepsis. |
| SKIN AND SOFT TISSUE INFECTIONS | |
| Impetigo | IV or intramuscular (IM) nafcillin; PO cephalexin for 7 days (depending on clinical severity). For methicillin-resistance, use vancomycin. Also consider topical mupirocin. |
| Group A Streptococcus infections | IV penicillin G for 7 days. |
| Breast abscess | IV nafcillin and gentamicin for 7 days pending identification of etiologic agent (change to IV penicillin if Streptococcus is etiologic agent; IV ampicillin or gentamicin should be used for coliform species pending sensitivities); value of surgical drainage is individualized; vancomycin for methicillin-resistant strains. |
| Omphalitis and/or funisitis | IV nafcillin for 7 days (penicillin may be used if infection is caused by group A or B streptococci); if gram-negative rods, consider gentamicin or cefotaxime also. |
| GASTROINTESTINAL INFECTIONS | |
| Salmonella species | IV ampicillin for 7 to 10 days; or IV cefotaxime or ceftriaxone for 7 to 10 days depending on sensitivities (focal complications of meningitis and arthritis should be monitored closely). |
| Shigella species | PO trimethoprim/sulfamethoxazole or PO or IV ampicillin, depending on sensitivities. |
| Necrotizing enterocolitis | IV ampicillin and IV gentamicin for 2 to 3 weeks (if Pseudomonas is isolated, IV ceftazidime or piperacillin/tazobactam combination may be substituted for ampicillin); supportive measures (gastrointestinal suction) are appropriate. |
| OSTEOMYELITIS OR SEPTIC ARTHRITIS | |
| Group B Streptococcus | IV penicillin G for 21 days minimum. |
| Staphylococcus aureus | IV oxacillin for 21 days minimum. |
| Coliform species | IV gentamicin for 21 days (IV ampicillin for 21 days minimum if organism is sensitive). |
| Gonococcus species | IV penicillin G for 10 days. |
| Unknown | IV oxacillin and gentamicin for 21 days minimum. |
| URINARY TRACT INFECTIONS | Suspect predisposing anatomic defect if urinary tract infection; individualize workup and follow-up. |
| Coliform species | Gentamicin, 3 mg/kg/day divided q 8 hr for 10 days. |
| Enterococcus species | Ampicillin, 30 mg/kg/day divided q 8 hr for 10 days. |
| MISCELLANEOUS CONDITIONS | |
| Congenital syphilis | If more than 1 day of treatment is missed in either of the following regimens, the entire course should be restarted. |
| Without central nervous system (CNS) involvement | IM procaine penicillin G (50,000 units/kg) daily for 10 to 14 days (follow-up Venereal Disease Research Laboratory [VDRL] test results should revert to negative if treatment is adequate by 1 year). |
| With CNS involvement | IV aqueous crystalline penicillin G 100,000-150,000 units/kg/day, administered as 50,000 for a total units/kg/dose q 12 hr for the first 7 days of life and q 8 hr thereafter for 10 days. Repeat lumbar puncture about every 6 months until results are normal. |
| Toxoplasmosis |
PO sulfadiazine, 100-120 mg/kg/day divided q 12 hr and PO pyrimethamine, 1 mg/kg/day divided q 12 hr (duration of treatment is debatable but should be long [i.e., months]; supplemental folic acid, 1 mg/day, should be added).
Ocular, CNS, or human immunodeficiency virus (HIV) involvement may require additional therapy.
|
| Herpes simplex infections | IV acyclovir, 20 mg/kg/dose q 8 hr, for 14 days if skin or mucous membrane involvement; 21 days if CNS involvement. |
| Conjunctivitis | |
| Chlamydia species | PO erythromycin for 10 days (topical may be ineffective). |
| Gonococcus species | IV penicillin G for 10 days; cefoxitin for penicillin-resistant strains. |
| Otitis media | |
| In otherwise normal neonate | PO amoxicillin/clavulanic acid (Augmentin), 40 mg/kg. |
| In neonate with nosocomial infection | PO or IV ampicillin and IV gentamicin (if there is no response to treatment, consider diagnostic tympanocentesis; Staphylococcus aureus and coliform species may be present). |
Parent Teaching
Adequate follow-up of both symptomatic and asymptomatic neonates is very important. A physical evaluation should be conducted at 1, 2, 3, 6, and 12 months. Serologic testing should be performed at 3, 6, and 12 months after completion of therapy regimen, or until titer decreases fourfold. Noninfected or adequately treated infants’ titers should be decreased by 3 months and nonreactive by 6 months. If titers fail to decline or if they increase or are still present after 6 to 12 months of age, the infant should be reevaluated and retreated. Infants with neurosyphilis should have a repeat CSF examination every 6 months until it is normal and VDRL nonreactive. If CSF VDRL is still reactive at 6 months or CSF white cell count is not decreasing at each reexamination or is abnormal at 24 months, retreatment is indicated. 4
TOXOPLASMOSIS
Prevention
Women should avoid unnecessary exposure to raw meat, cat feces, and eating fruits or vegetables not peeled or washed thoroughly. Using a pair of gloves when emptying the litter box may provide protection if the pregnant woman (or a woman attempting to become pregnant) must empty the litter box. 4 A pregnant woman (or woman attempting to become pregnant) should use hot soapy water to wash her hands immediately after exposure to any infectious source, even after wearing gloves. 17
Data Collection
History
Congenital infections are represented by a wide range of disease, from asymptomatic disease to profound symptomatic disease, and all require treatment. 4,111 Mothers may have noted an influenza-like illness, posterior cervical adenitis, or chorioretinitis but usually lack accompanying signs or symptoms. A history of exposure to cat feces or ingestion of raw meat occasionally may be obtained. 5,60,111
Signs and Symptoms
Laboratory Data
Isolating Toxoplasma gondii from blood or body fluids is difficult and tedious. Cysts may be found in the placenta or tissues of a fetus or newborn. 81 Most congenitally infected infants have a Sabin-Feldman dye test titer greater than 1:1000 at birth.
Treatment
Table 22-1 outlines the treatment of toxoplasmosis. 4
Perinatal Acquisition During Labor and Delivery
CHLAMYDIA TRACHMOMATIS INFECTION
Prevention
Data Collection
History
Signs and Symptoms
Conjunctivitis may be manifested as congestion and edema of the conjunctiva, with minimal discharge developing 1 to 2 weeks after birth and lasting several weeks with recurrences, particularly after topical therapy. Infants with pneumonitis usually do not have a fever but have a prolonged staccato cough, tachypnea, mild hypoxemia, and eosinophilia. Otitis media and bronchiolitis also may occur. 4,118
Laboratory Data
Definitive diagnosis is made by isolating the organism in tissue culture and by nucleic acid amplification tests (NAATs) (e.g., PCR). Demonstrating chlamydial antigen in clinical specimens by the direct fluorescent antibody method or enzyme immunoassay is very reliable. To enhance the likelihood of obtaining an adequate sample, scrape the lower conjunctiva (for conjunctivitis) or obtain deep tracheal secretions or a nasopharyngeal aspirate (for pneumonia). NAATs are not recommended for nasopharyngeal aspirates. Scraping conjunctival epithelial cells and demonstrating characteristic intracytoplasmic inclusion bodies by a Giemsa stain is diagnostic. Although serologic tests for conjunctivitis are unreliable, a significant titer rise in IgM specific antibody may be reliable in cases of pneumonia. Eosinophilia (>300 eosinophils/mm 3) may suggest Chlamydial pneumonia. 4,118
ENTEROVIRUS (COXSACKIEVIRUS A, COXSACKIEVIRUS B, ECHOVIRUS, AND POLIOMYELITIS) INFECTIONS
Enterovirus infections are the most commonly diagnosed viral infections in the neonatal intensive care unit, and coxsackievirus B1 was the most common in 2007 by the National Enterovirus Surveillance System. 23,65,119
Prevention
To prevent poliomyelitis, it is essential to maintain poliomyelitis immunity with active immunization before conception. Passive protection with pooled human serum globulin may help in selected exposures (0.2 mL/kg body weight, given intramuscularly). Routine nursery infection control procedures must be observed. It is recommended that only inactivated poliovirus vaccine (IPV) be used in the nursery. The IPV is administered intramuscularly and contains no live virus, whereas oral poliovirus vaccine (OPV) (OPV is no longer available in the United States) is administered orally and contains live but attenuated virus, which has been reported to cause infection in immunocompromised patients. 4
Data Collection
History
Infection may occur year-round but is more prevalent from June to December in temperate climates. Most enterovirus infections are asymptomatic. Poliomyelitis is rare because of a high level of vaccine-induced immunity in most of the world. 4
Signs and Symptoms
Mothers with enteroviral infections are usually mildly ill, with fever or diarrhea. Infants may be asymptomatic or have fever or diarrhea. Infants who acquire the infection without maternal antibody have severe disease and high mortality. Fever, irritability, lethargy, and rash are common. Severe disease with sepsis, meningoencephalitis, myocarditis, pneumonia, hepatitis, or coagulopathy may occur. 1 Prematurity, early onset of illness (<7 days), maternal history of illness, high white blood cell count (≥15,000/mm 3), and low hemoglobin (<10.7 g/dL) have been shown to be risk factors of severe infection. 73
Laboratory Data
The virus may be isolated from the throat, rectum, or CSF. Isolating coxsackievirus A may require suckling mouse inoculation. Serologic screening is impractical because of the large number of serotypes. PCR assay for enterovirus RNA in CSF and other specimens is available and is more sensitive than viral isolation. 4
Treatment
The antiviral agent pleconaril is undergoing clinical evaluation in neonates to treat enteroviral infections.98 Pleconaril has a novel mechanism of action by preventing the viral attachment and entry into the host cells and seems to be well tolerated in neonates. 2,99 Hand hygiene is paramount to control spread of enteroviral infections. 4
GROUP B STREPTOCOCCUS INFECTION
Prevention
Intrapartum (during labor) treatment of the mother with penicillin significantly decreases disease caused by group B Streptococcus (GBS) in the neonate and maternal postpartum endometritis.4,15,76,83 Neonatal sepsis has been reported with less than 4 hours of maternal antibiotics at term and with up to 48 hours in preterm infants. 121 Five to fifteen percent of clinical GBS isolates are resistant to clindamycin and 16% to 22% to erythromycin, and antibiotic prophylaxis with clindamycin in penicillin-allergic women may not prevent neonatal GBS disease. 32,34,58,77
Data Collection
Treatment
Table 22-1 outlines the treatment of group B Streptococcus infection.
Parent Teaching
See the section on bacterial infections and bacterial sepsis on pp. 571-572 and 575.
HEPATITIS B
Prevention
Prenatal screening of women for hepatitis B surface antigen (HBsAg) is indicated and is cost effective. Use of active and passive immunization in infants born to HBsAg-positive mothers is indicated (Tables 22-2and22-3).4Use of active immunization for infants born to HBsAg-negative women is recommended at birth by the Advisory Committee on Immunization Practices. However, the Centers for Disease Control and Prevention (CDC) analyzed data from the 2006 National Immunization Survey (for the years 2003 to 2005) showed only 50.1% of newborns had hepatitis B vaccine by day 3 of life with a considerable geographical variation. 24
| HBIG, Hepatitis B immune globulin; HSIG, human serum immune globulin; TIG, tetanus immune globulin (human); ZIG, zoster immune globulin. | ||||
| *Should be used in conjunction with active immunization with hepatitis B virus (HBV) vaccine (see Table 22-3). | ||||
| Modified from Remington JS, Klein JO, editors: Infectious diseases of the fetus and newborn infant, ed 5, Philadelphia, 2001, Saunders. | ||||
| Disease | Indications | When to Use | Product | Dose |
|---|---|---|---|---|
| Hepatitis A | Active infection in mother or close family contacts | As soon as possible | HSIG | 0.02-0.04 mL/kg body weight, give intramuscularly (IM) |
| Hepatitis B | Mothers with acute type B infection or who are antigen (+) | As soon as possible (within 12 hr) | HBIG* | 0.5 mL/kg body weight IM |
| Tetanus | Inadequately immunized mothers with contaminated infant (e.g., dirty cord) | As soon as possible | TIG | 250 units given IM (optimal dose not established) |
| Varicella | Infant born to a mother who develops lesions <5 days before delivery or within 2 days after delivery | Within 72 hours of birth | ZIG | 2 mL given IM |
| HBsAg, Hepatitis B surface antigen. | ||||
| *As soon as possible. |
||||
| Disease | Indication | When to Use | Product | Dose |
|---|---|---|---|---|
| Hepatitis B | HBsAg-positive or HBsAg-negative | 3 separate doses: at birth*; at 1 month; and at 6 months | Recombivax HB® | 0.5 mL intramuscularly (IM) |
| Engerix-B® | 0.5 mL IM | |||
| Pertussis | To control outbreak in nursery | As soon as possible | Pertussis vaccine | 0.25-0.5 mL administered subcutaneously |
| Tuberculosis | Selected infants at risk for contracting tuberculosis | As soon as possible | Calmette-Guérin bacillus (CGB) | 0.1 mL given intradermally and divided into 2 sites over deltoid muscle |
Data Collection
History
Mothers who are HBsAg positive because of the chronic carrier state or acute disease before delivery may pass the infection to their infants at delivery. 5 Women at high risk include those of Asian, Pacific Island, or Alaskan Eskimo descent; women born in Haiti or sub-Saharan Africa; and those with a history of liver disease, IV drug abuse, or frequent exposure to blood in a medical-dental setting.
Signs and Symptoms
A neonate with hepatitis B is usually asymptomatic. Occasionally, infected infants demonstrate elevated liver enzymes or acute fulminating hepatitis. 4 Neonatal infection with subsequent chronic carriage has been implicated in the development of primary hepatocellular carcinoma later in life.
Laboratory Data
Most infants at risk for acquiring hepatitis from their mother are HBsAg negative at birth. Many untreated infants become HBsAg positive 4 to 12 weeks after birth and become lifelong asymptomatic carriers or develop hepatitis B. 4
HEPATITIS C
Prevention
Neonates acquire hepatitis C virus (HCV) infection mostly through vertical transmission from the mother and rarely through transfusion of hepatitis C–contaminated blood products. Vertical transmission rates from the mother to the infant vary (≈5%), and risk factors associated with increased transmission are HCV viral load, co-infection with HIV, rupture of membranes more than 6 hours, and internal fetal monitoring. 31,75,87,88 Reducing viral load by maternal antiviral therapy, especially in HIV co-infected women, and avoiding internal fetal monitoring are interventions that can reduce transmission but have not been evaluated. Breast feeding is not associated with increased rates of transmission and is not contraindicated. 4 Screening of blood products for HCV is mandatory for prevention of transfusion-related HCV infection.
Data Collection
History
One to two percent of pregnant women in the United States are seropositive for HCV, but vertical transmission occurs only if the mother is HCV RNA positive at the time of delivery. 4 HCV RNA titers rise many weeks after birth in infants, indicating a perinatal acquisition rather than an intrauterine transmission. 31
Signs and Symptoms
Neonates with perinatal acquisition of HCV infection are usually asymptomatic without jaundice and with normal or only mildly elevated liver transaminase levels. 88,95,115 Progression to chronic hepatitis is common and occurs in approximately 80% of infected infants. Liver biopsies in infants with perinatally acquired HCV during follow-up show evidence of chronic inflammation. A small percentage (20%) of infants may spontaneously resolve their infection. 40
Laboratory Data
The essential diagnostic feature is HCV RNA positivity on at least two occasions by PCR. Sensitivity of the PCR is 22% in infants younger than 1 month and 97% after 1 month of age. 37 Maternal antibodies may persist in the infant for 13 to 18 months and are not useful for diagnosis. Following liver transaminase levels may help monitor the course of hepatic inflammation.
HERPES SIMPLEX (TYPES 1 AND 2) INFECTION
Prevention
The key to preventing herpes simplex is avoiding exposure. Mothers with active lesions or prodrome should have a cesarean section preferably within 4 to 6 hours of membrane rupture. Treatment with acyclovir should begin at the first sign of neonatal disease or when infants have been exposed to an active lesion.4,5
Communication is necessary between obstetric and neonatal staff to determine the status of a family with a history of herpes. Unnecessary restrictions should not be placed on postpartum mothers who are not actively infected. 5 Health professionals should employ all family-centered strategies used in their institutions with families unless such strategies are precluded by the need for the infant’s treatment.
Data Collection
History
Disease caused by type 1 herpes simplex usually is spread by the oral route, whereas disease caused by type 2 herpes simplex is usually spread by the genital route. 4Many mothers who transmit herpes simplex to their newborn infants are asymptomatic.68 The risk to the infant from recurrent lesions is minimal. 4,46
Signs and Symptoms
Laboratory Data
A cytologic examination of the base of skin vesicles with a Giemsa stain (Tzanck test) may reveal characteristic but nonspecific giant cells and eosinophilic intranuclear inclusions. The virus may be readily identified on a tissue culture within 48 hours from the respiratory and genital tracts, blood, urine, and CSF. 82 Rapid viral diagnosis by direct fluorescent antibody tests is widely available. 4 Detection of virus in CSF by PCR assay is preferred, if available. 19 Although tests of paired serology such as complement fixation (CF) test, ELISA, and neutralization are available, they are of little value in an acute clinical situation. 4 Elevated liver transaminases and thrombocytopenia may indicate herpes infection. 16
Treatment
Table 22-1 outlines the treatment of herpes simplex infection.
Parent Teaching
Families with herpes simplex require consistent and detailed teaching about prevention of transmission of herpes to the infant. Breast-feeding mothers can be reassured that they may continue to breast feed as long as no lesions are on their breasts. Emphasis should be placed on the need for breast-feeding mothers to check their breasts for lesions.5
Parents with active herpes simplex should employ good handwashing technique while caring for their infants. Parents with oral herpes should avoid kissing their infants while lesions are open and draining. 4
LISTERIA MONOCYTOGENES INFECTION
Prevention
Data Collection
Treatment
Table 22-1 outlines the treatment of Listeria monocytogenes infection.
Parent Teaching
See the section on bacterial infections and bacterial sepsis on pp. 571-572 and 575.
MYCOBACTERIUM TUBERCULOSIS INFECTION
Prevention
Mothers at risk for Mycobacterium tuberculosis infection may be identified with a tuberculin test during pregnancy. If the mother is a tuberculin converter (has had a positive skin test result within the past 2 years), a radiographic examination of the chest and lungs should be performed. If the mother has active tuberculosis, she should be treated with isoniazid plus rifampin and ethambutol for at least 9 months. Safety of pyrazinamide in pregnancy is not well established, and this drug is not used routinely in pregnant women. Pyridoxine (vitamin B 6) always should be given with isoniazid during pregnancy and breast feeding because of the increased requirements for this vitamin. If the mother does not have active tuberculosis, household contacts should be screened. If the disease is identified in the mother or household contacts, the infant is at high risk for developing tuberculosis. 4
Separate infants of mothers with active disease from the mother until the mother is not contagious (usually negative sputum). Treat high-risk infants with isoniazid (10 mg/kg/day) or a tuberculosis vaccine (Calmette-Guérin bacillus) (see Table 22-3). 4,5
Data Collection
History
A strong history of maternal contact with tuberculosis favors the diagnosis. This is especially true in high-risk populations (Southeast Asians, American Indians, and families with a known cavitary disease). Mothers with HIV infection are at an increased risk for developing active tuberculosis. 4,112
Signs and Symptoms
Mothers may be relatively asymptomatic or have signs and symptoms that are generalized (fever and weight loss) or localized to the respiratory tract. 4 A congenital infection is extremely rare. 5Nonspecific signs and symptoms such as failure to thrive and unexplained hypothermia or hyperthermia are the most common manifestations in the neonatal period.
Laboratory Data
Acid-fast organisms found on smears of gastric aspirates, sputum, CSF, or infected tissues strongly suggest tuberculosis in the neonate. Isolating Mycobacterium tuberculosis by culture is diagnostic and should be sought aggressively. The tuberculin test result usually is positive (>10-mm induration) in active tuberculosis. However, a positive skin test result requires 3 to 12 weeks after infection to manifest itself, and the test result usually is negative in a neonate. A chest radiograph examination also usually yields a negative result in a neonate. 4
Treatment
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