Neonatal Infections

Janet Wong, M.D.

Typical Syndrome of Congenital Infection

SGA (Small gestational age) or intrauterine growth retardation is characterized by jaundice, chorioretinitis, hepatosplenomegaly microcephaly, and hydrocephaly which are the direct result of the congenital infection and microbial invasion. By contrast, eye defects and cardiac defects are caused by cell death or chromosomal damage.

Feature SGA

Comment Causal relationship exist for rubella, CMV, toxoplasmosis


Reflects microbial invasion and proliferation (not a defect in

Jaundice Chorioretinitis Eye defects Cardiac defects


Cause by cell death or chromosomal damage

Microcephaly Hydrocephaly

Consequence of lesions from congenital infection rather than teratogenesis

Signs Common to Congenital Infections
• Purpura, jaundice, hepatosplenomegaly, pneumonitis, meningoencephalitis • Common to rubella, CMV, HSV, Coxsackie B, T. gondii, T. pallidum
Signs common to congenital infections include purpura, jaundice, hepatosplenomegaly, pneumonitis, meningoencephalitis. They are not all present in every patient within congenital infection, but any of these features can be associated with various etiologies. They are common to rubella, cytomegalovirus, herpes simplex virus, Coxsackie B infections, Toxoplasma, and syphilis.

syphilis, whereas many of the others do not have an exanthem. None of them commonly have an exanthem, although some might have one.

Hepatosplenomegaly Jaundice Exanthem Purpura/petechiae Hydrocephalus Microcephaly

+ + + + -

+ + + + ++ ++ + + -

+ + + + ++ + ++ ++ +

+ + ++ + + + + -

Another feature of diagnostic significance is the presence of intracranial calcifications which would suggest CMV. Keep in mind also toxoplasmosis, although a less common congenital infection, also can give you intracranial infections, whereas if you had that finding of intracranial calcification, your patient and you were thinking about syphilis or rubella, you would not think that would be etiologically compatible.

Intracranial calcifications Heart defects Bone lesions Glaucoma Chorioretinitis Cataracts ++ ++ ++ ++ ++

• •

About 50% of childbearing-aged women are immune After household exposure, ~50% of susceptibles become infected

Risk of presumed parvovirus-related fetal death from household exposure in first 20 weeks of pregnancy is 3-9%

nonimmune and therefore susceptible. If a woman has a household exposure, we know that about 50% of the susceptibles in a household will become infected. There is a parvovirus B19 infection. So if a woman is pregnant and her two-year-old comes home with classic erythema infectiosum, she has about a 50% chance if she is susceptible of becoming infected. The risk of presumed of parvovirus-related fetal death from household exposure in the first 20 weeks (early in pregnancy) is estimated at 3% to 9%. By contrast, after 20 weeks of gestation, the risk is absolutely unknown. It is estimated at less than one-percent. Third trimester infection may cause some newborn anemia, but usually this is not the hydrops fetalis type of scenario.

Risk alter 20 weeks of pregnancy is unknown; 3rd trimester infection may cause newborn anemia

Virus causes fetal anemia, heart failure and death (hydrops fetalis)

• •

Risk of fetal death after occupational exposure is low (<1%) No association with fetal anomaly

secondary heart failure, and in utero death with the fetus that shows all the histopathologic features of hydrops fetalis. The risk of fetal death after occupational exposure is low. Most of the times the hospital’s employee has been shown to be seropositive and, therefore, not at risk.

Rubella • Virus Culture: Nasopharynx is the most reliable site; conjunctivae, CSF or urine also are potential sites • Cord serum for rubella-specific IgM • CSF for rubella-specific • Persistence of rubella-specific IgG for 6-12 months CMV • Viral isolation: urine, saliva, tissues • Rapid viral diagnostic techniques

somebody being susceptible, you are going to have to do a serologic test. If the person has an immunity to parvovirus, then they are not susceptible then you do not have to deal with these pregnancy-related issues. If they are pregnant, depending on the time of gestation, you can at least counsel the patient, based on the gestation, about potential risk. The one thing to remember about parvovirus B19 is that you are not going to see fetal anomalies. So this virus is red cell specific. It causes anemia depending on the time of gestation and the anemia can cause spontaneous abortion or intrauterine death due to hydrops or presentation of a quite currently ill baby with hydrops fetalis.

Toxoplasmosis • Demonstration of IgM antibodies to toxoplasmosis in cord serum or infant serum is diagnostic; IgM antibodies in CSF supports the diagnosis in CNS infection • Double sandwich IgM-ELISA method is more sensitive than IgM-IFA • IgA antibodies to toxoplasmosis in infant • Demonstration of Toxoplasma antigens in CSF

Parvovirus • Detection of IgM antibodies to parvovirus in infant serum • Parvovirus-specific PCR

Mother with positive nontreponemal tests confirmed by a positive treponemal test and:

• • •

Untreated or inadequately treated syphilis Treatment in pregnancy with non-penicillin regimen Lack of expected decrease in nontreponemal antibody titer after penicillin treatment

then the best way to make the clinical diagnosis is to get cord serum for specific IgG antibody. In patients who have meningoencephalitis, the spinal fluid actually may have IgM detectable antibodies too, so there are two specimens that can be serologically tested for IgM rubella specific antibody. You can culture this virus if you do have serology laboratory access, the nasopharyngeal secretions are the most reliable.

• • •

Treatment <1 month before delivery Treatment not documented Insufficient follow-up to assess response and current status

IgG comes from the mother and is another serologic piece of information that is useful in congenitally infected babies. IgG persists for six to twelve months, and after that time you know that IgG is being made by the baby because passive antibody from the mother has gone away by that time. CMV. The cardinal way to make the diagnosis is isolation of this virus from a urine specimen. You also may isolate CMV from saliva or from tissues. There are a number of rapid viral diagnostic techniques for CMV. Urine cultures are fairly standard. The virus is not fastidious and the least expensive and easiest way to make a specific diagnosis is to grow CMV from the urine. In order to make the diagnosis of congenital CMV, you have to have access to your patient in the first two weeks of life because after that, acquiring CMV becomes a complicated interpretation problem.

• • • • • •

Physical examination Quantitative nontreponemal serologic test CSF analysis for cells, protein, VDRL Antitreponemal IgM test Long bone x-rays Other clinically indicated tests (e.g., CBC, CXR)

because the mother is going to have high levels of IgG that are transferred to the baby. We are looking for detection of toxoplasmosis, specific IgM antibodies in cord serum are tested. If the CNS is involved there is a serologic assay for cerebral spinal fluid that would support the diagnosis of CNS infection due to toxoplasmosis. The ELISA is much more sensitive than the indirect fluorescent antibody test as opposed to the IFA. It is a more desirable method because it is more sensitive.

The IgA antibody test is not a passively acquired antibody, so the baby has to be making it, and is very helpful as an adjunctive serologic piece of information in establishing the diagnosis of toxoplasmosis. Parvovirus is a virus that cannot be cultured. Serologic detection of IgM in the infant serum or cord serum is diagnostic. More and more places are now getting parvovirus specific PCR.

Sign HSV Enterovirus HBV HIV

the RPR or VDRL. The first thing that happens is that we cannot say that she does not have a biologic false-positive, so we need to make sure, that if she has a treponemal test, that it is confirmed with a nontreponemal test. The MHATP is a common one and you need both of these to make a firm serologic diagnosis in the mother and the baby. For the definitive diagnosis of syphilis you have to have microscopic evidence of spirochetes, a dark field or direct fluorescent antibody specimen from some sort of mucopurulent secretions. The congenitally-infected patient, unless they have the typical exanthem, the pustule, where you can open them and they are teeming with spirochetes, before you treat the patient and do a dark field on that, all of our diagnoses of congenital syphilis is presumptive at best, and to make the presumptive diagnosis, you have to have a nontreponemal test that is confirmed with a treponemal antigen test. After the mother has confirmed both tests positive, she is untreated during her pregnancy. Inadequate treatment is a non-penicillin regimen. Obstetricians are told to desensitize the patient and treat with penicillin, but that does not always happen. Inadequate treatment would mean a non-penicillin drug or inappropriate dose, or inappropriate duration. Lack of expected decrease in VDRL or RPR after the patient has been treated, and usually what we are looking for is a four-fold or greater decrease. Treatment less than one month before delivery is considered inadequate. Treatment is considered inadequate if it can not be documented. Documented means that you have documented evidence. The patient saying that she was treated with penicillin is insufficient to document treatment. Insufficient follow-up to assess response is considered inadequate. For example, you may not have access to a previous serology and you cannot assess her response to therapy unless you have previous results. So, once you have decided that the patient needs a diagnostic evaluation based on the mother’s situation, you do a physical examination, you do a quantitative nontreponemal serologic test. You do a spinal fluid through a lumbar puncture. You look at the cell count, protein and VDRL. Here we are in a situation where you really need spinal fluid that does not have contaminating blood, because if you had contaminating blood it is difficult to interpret the protein and the cell count, it is virtually impossible to do a reliable VDRL when you have blood in the spinal fluid, you can send a VDRL, and if it is negative it is informative , but if it is positive you do not know whether that is from the blood or whether the patient has neurosyphilis. There are a lot of babies with completely normal cell counts and proteins who has positive VDRLs. Then there are some babies who have abnormal cell counts and abnormal proteins and negative VDRLs. They should all be treated for neurosyphilis. The IgM is a test that is not commercially available, but the CDC will do an IgM test for you. It is reliable for the diagnosis. Long bone x-rays are necessary because patients with congenital syphilis can have a completely normal physical examination and normal CSF analysis and have the osteolytic and periosteal elevation changes caused by congenital syphilis. This is clinically silent early, but still needs to be treated. For hepatitis B virus , babies who are more than a month of

Hepatosplenomegaly Adenopathy Pneumonitis Petechiae or purpura Vesicles Meningoencephalitis Paralysis Myocarditis Conjunctivitis or Keratoconjunctivitis

+ + + ++ + + ++

++ + + + + ++ ++ +

++ -

++ ++ ++ + + -

look to these, and so the timings areas at four to six months of age or somewhat older.


• Specimens for culture from vesicle, mouth or throat, conjunctiva, blood and CSF yield virus in 1-3 days; DFA of vesicle scrapings or EIA of HSV antigens are specific but less sensitive
• Enterovirus

Usually the viral agent is transmitted intrapartum. Typical findings at presentation, four to six months of age or slightly older, hepatomegaly, prominent adenopathy; the patient may have pneumonitis, and this is not an opportunistic infection, but usually the lymphoid intrastitial pneumonitis syndrome that we see typically with HIV. One comment about enteroviruses, is where as we see a disseminated fulminant presentation with hepatosplenomegaly, adenopathy, coagulopathy and often death. They may have very helpful clues to this presentation, with paralysis or myocarditis. That may help the clinician, but those are very ominous presentations because we do not have specific therapies for enteroviral disease and those patients typically do quite poorly. Diagnosis for HSV. For the patient that presents with the vesicle this is the most accessible way to have rapid viral diagnosis by culture virus. Without skin vesicles present, the mouth or throat, the conjunctiva are very good places to grow HSV virus. You also can also grow it from the blood, CSF. As I said, if you have a vesicle there is high titer of virus in those vesicles and virus grows rapidly, but you can also take direct scraping specimens and get the answer in minutes. There are quite specific - remember if your rapid test is negative, still wait for your culture because depending on the titer of virus these rapid tests may be negative. Enteroviruses. Throat and rectum are the sites that you usually grow the virus, but if you have a patient who has neonatal enteroviral infection and has meningoencephalitis, this CSF can yield the virus, or the amount of tissue, viral isolation is appropriate. Hepatitis B virus. You look for the presence of appropriate antigens to confirm the diagnosis in the infant’s serum.

• Specimens for viral isolation from throat and rectum and sites of clinical involvement (CSF, blood, biopsy material)

• Detection of HBsAg in infant's serum

• Intrinsic/host Immaturity

• Decreased IgG levels in direct proportion to gestation • Decreased opsonic capacity in proportion to decreased C3 and B levels • Decreased PMN chemotaxis; early depletion of marrow storage reserves • Decreases lymphocyte motility or adherence

Extrinsic/iatrogenic/Factors: • Cutaneous barriers violated • Indwelling intravascular devices • Suppression of normal flora by antimicrobials • Tracheal intubation • Consequences of oxygen therapy • Multiple exposures to pathogens

seem to have an outbreak you could even decide to close your nursery to preadmissions while the outbreak is brought under control.

Surveillance for nosocomial infection: prompt recognition of outbreaks; initiation of control measures

Appropriate handwashing procedures are the single most important aspect.

Appropriate handwashing procedures are the single-most important aspect of preventing infections, not only in low birth rate preterm babies, but in immunocompromised patients. Gloves are not a substitute for handwashing. Isolation procedures. Among preemies who are less than 32 weeks gestation, almost one-half have BPD, and about onequarter are without BPD. Preemies less than 32 weeks frequently require rehospitalization within a short period of time.

Isolation procedures: based on mode of transmission

Among premature infants <32 wk gestation 45% with bronchopulmonary dysplasia (BPD), require re-hospitalization, and 25% without bronchopulmonary dysplasia (BPD), require re-hospitalization

than 37 weeks gestation is getting neonatal sepsis, incidence is 10-fold higher than the risk of a term baby getting neonatal sepsis, and If this risk persists, the immunologic problems persist and, therefore, the attack rate persists. If you have babies with BPD, they are much more likely to require hospital readmissions, and they are much more likely to require a full month stay than those without lung disease. From July to December preemies are more likely to be exposed to RSV during the RSV and other respiratory virus season, and if you are exposed, you are more likely to be readmitted. So the respiratory virus is responsible for this seasonal distribution of readmissions. Increased airway resistance and bronchial hyperactivity add to the predisposition of bronchopulmonary dysplasia infants to viral illnesses. Abnormal lung mechanics, abnormal immunity makes you more susceptible both to viral and bacterial infections. Presumptive therapy is indicated for infections in infants with BPD.

Premature infants without BPD require re-hospitalization at a rate 10-fold higher than term infants

BPD infants are more likely to require multiple re-admissions and prolonged stays than those without lung disease

Infants discharged before RSV and influenza season (JulyDec.) are significantly more likely to be readmitted than infants discharged in other months

Increased airway resistance and bronchial hyperreactivity add to predisposition of BPD infants to viral (especially RSV) and bacterial pneumonias

Presumptive therapy is indicated for infections in infants with BPD

• • • • •


Definition: Infection of the umbilicus Predisposing Features: LBW infant; complicated delivery Incidence: 2% Onset: Mean age 3 days Agents: S. aureus, group A streptococci, Bacteroides
The mean age of onset is three days, and the pathogens that we are thinking about are staph aureus, group A streptococcus, bacteroids. Group A strep is on the list if the newborn goes home because a sibling with impetigo, touches that moist cord before it dry. Group A strep is very easily transmissible and very rapidly progressive, and so the infant will present quite quickly.

• Inflammation of the Umbilical Cord • Agents

chorioamnionitis, for example, without the isolation of an organism. Syphilis could be a diagnostic possibility if you have the placenta and the cord remaining. For the diagnosis of congenital syphilis, it can cause a necrotizing funisitis of the umbilical cord, and the cord is swollen, and it has a barber pole appearance (red, white, and blue). This involves matrix perivascular inflammation and then endarteritis, so you see this red, white, and blue thing. You see the red is the inflammation, the white and the blue are manifestations in the endoarteritis thrombosis, and lack blood flow to those particular areas.

Group A Streptococcus: wet, malodorous umbilical stump with minimal inflammation

Syphilis: "necrotizing funisitis," umbilical cord swollen, discolored red, white and blue--resembling a barber's pole. Involves matrix with perivascular inflammation and obliterative endarteritis

Candida: in association with congenital cutaneous disease

Diagnosis and Therapy • Culture from purulent exudate or subcutaneous aspirate (differentiate from colonization) (omphalitis/funisitis) • • Histopathologic evaluation of cord (funisitis) Parenteral antibiotics and, for streptococcal funisitis, topical treatment (triple dye or antibiotic)

funisitis, you cut the cord. Histologic examination will show the inflammation. Parenteral antibiotics are indicated in these particular situations most of the time.

• • •

Colonizes urogenital tract of ~50% of healthy adults Accounts for 20-30% of non-chlamydial NGU cases Associated with spontaneous abortion, chorioamnionitis and fetal demise; causation?

this organism requires urea for its metabolic pathway. It colonizes the urogenital tract in 50% of healthy adults, so it is a very common colonizer in sexually active adults. It accounts for 20% to 30% of nonchlamidial NGU cases. It is associated with spontaneous abortion, chorioamnionitis and fetal demise; but the organism may not necessarily be causing these events. Vertical transmission during vaginal delivery occurs about 50%, so if your pregnancy population is colonized 50%, you can know that about one in four babies might be colonized with this organism. The colonization sites in the newborn are the eyes, the throat, the umbilicus, and the perineum, and this persists for many months. It may last six to twelve months, then it goes away, and you do not see ureaplasma again until the age of sexual activity, and then you go up to 50%.

• •

Vertical transmission rate during vaginal delivery is ~50% Colonizes the eyes, throat, umbilicus and perineum of newborns; may persist for months


Associated causally with 'pneumonia' in some low birth weight infants, but incidence and impact is uncertain

gestation infants, but the exact incidence is unknown, and the impact of these lung abnormalities are unknown. If you have somebody with radiographic lung disease and you grow ureaplasma urealyticum from tracheal aspirate secretions, erythromycin is the drug of choice here, just like with Chlamydia, the optimal duration is ten days. It has been isolated from the CSF of preterm infants with or without cell inflammation signs in its spinal fluid, but its pathological role is not clear at this time.

Presence in tracheal aspirate cultures does not predict respiratory deterioration in low birth weight, intubated infants with lung disease

It has been isolated from CSF of preterm infants; pathologic role is unclear

Isolation requires special transport media and urea-containing broth

Erythromycin (25-40 mg/kg/day in 4 doses) for 10 days is treatment of choice

Source usually is maternal but nosocomial acquisition is possible

Predisposing factors include maternal chorioamnionitis, preterm delivery, and prolonged rupture of membranes

• •

50% of cases have onset <7 days of age (3-7 most common) K1 capsular polysaccharide-containing strains: ~40% of bacteremias, 75% of meningitis cases

born infection. With E. coli, nosocomial transmission is possible. Usually we are talking about late onset acquisition when we are talking about nosocomial acquisition. The predisposing factors include the same kinds of maternal factors that predispose patients to infection with other agents besides E. coli, such as maternal chorioamnionitis. Preterm delivery and prolonged rupture of membrane. Half of those started in the first seven days of life. It was interesting that there was a peak between age three and age seven, and then a later peak of late onset disease.

Initial Therapy: ampicillin and gentamicin or ampicillin and cefotaxime when gram-negative meningitis suspected

Modify antimicrobial therapy based on susceptibility testing; minimum duration 21 days

onset meningitis, and this is quite adequate initially, realizing that some strains are going to be ampicillin resistant. Ampicillin and cefotaxime, would be used, based on susceptibility; 21 days of therapy is required. Some complicated patients, especially those with ventricular illnesses are going to require longer term therapy for cure. Ventriculitis with obstruction must be determined early, and the easiest way to do that is with a head ultrasound. If you see ventricular dilatation then you can suspect there is a block and you may need to assess the ventricular fluid as part of your culture follow-up and efficacy of cure. If you have ventriculitis, if the CSF is sterilized, ventricular fluid is persistently positive, that is going to be a patient who is going to relapse if you treat only 21 days and you need to treat longer. The case fatality rates are still substantial. Case fatality is 15% to 20%.

• •

Assess ventricular status early (head ultrasound or CT) Case-fatality rates (15-40%); neurologic sequelae mandate careful audiologic and neurologic follow-up

Perinatal Period • • • Transplacental or ascending intrauterine infection Exposure during delivery Environmental sources (late-onset disease)

is something that can be transmitted transplacentally, or you can see ascending intrapartum transmission like the more typical neonatal pathogens. This may be going on for a very long time at the time you see the baby. Exposure during delivery may also occur with Listeria, and the clinical syndromes that you see with exposure during delivery are quite similar to the clinical syndrome with E. coli , sepsis and group B strep sepsis. The distinctive feature of Listeria is the ability to pass the placenta early on and cause quite a distinct transplacental syndrome. Pregnant women are also vulnerable. Listeria colonization of the genital tract is uncommon, but when it is there it may be associated with preterm delivery and other obstetric complications. The most common one is chorioamnionitis. These women are quite ill. They do fine with appropriate antimicrobial therapy, but they have high fever, leukocytosis, and flu-like syndrome. Food-borne Listeria has a variety of sources related to food. Contaminated dairy products is the big one because Mexican goat cheese is a favorite.

Maternal genital tract occurs in association with preterm delivery and other obstetric complications (e.g. amnionitis)

outbreaks of listeriosis. Remember that the mother may eat these things and transmit the organism to the fetus. When the baby develops listeriosis, the mother may say that she has not been that ill but she has had some sort of a viral illness. In more than half of the babies, an intrapartum history of amnionitis is present.

Food-borne • • • • Contaminated dairy products
Undercooked poultry

Prepared meats (pate, hot dogs) Cabbage contaminated with animal manure

mediated immunity are at risk for listerial infections. The one thing to remember is that healthy people with a contaminated food exposure may become ill with Listeria, and occasionally present with high fever, flu-like symptoms and documentation of bacteremia or occasionally meningitis.

• Maternal

• Fecal or genital carriage • Amnionitis • Flu-like illness (fever, malaise, headache, myalgia)
• Infant

• Mother with symptomatic prodrome (65%) or amnionitis
• Decreased Cell-mediated Immunity

• Cancer chemotherapy; steroid therapy; congenital immunodeficiency; HIV disease; hepatic or renal disease
• Healthy Host

• Ingestion of contaminated food

• Infection (<16 wks) may cause abortion or stillbirth • Maternal influenza-like illness occurs 2-14 days before

illness. If you have somebody in July who has a flu-like illness, you should be suspicious. If it’s a pregnant woman, ery, and it may be precipitated by recurrence of fever at the time of delivery.

delivery; delivery is often precipitated by recurrence of fever
• Chorioamnionitis is frequent, favoring the transplacental route

of transmission Maternal recovery is usually complete

• Meconium staining (green or brown amniotic fluid), cyanosis,

analogy in terms of age of onset, birth weight, obstetric usually a bacteremic illness early, and a meningeal focus late. Case fatality ratios are going to be significantly higher

apnea, respiratory distress at delivery
• Common signs of infection: pneumonia (with hypoxia), sepsis,

meningitis (less common)
• Granulomatous






(erythematous base) on skin and in pharynx

• Onset 1-8 weeks of age (male predominance) • Major form of infection is meningitis

help with a diagnosis in addition to cultures. There seems to be a male predominance. The age of onset goes into the month. The major form of late onset infection is meningitis and the symptoms are not distinct. These patients present a diagnosis by doing a lumbar puncture.

Symptoms are not distinctive (fever, irritability, lethargy, poor feeding)
• CSF pleocytosis (150-3,000 WBC/mm early monocytic then

later, lymphocytic predominance

• Clinical Settings

rhomboencephalitis, brain abscess, osteomyelitis, and endocranitis.

• Renal transplantation, malignancy, HIV infection
• Usual Presentations

• Meningitis or sepsis
• Less Common Manifestations

• Rhomb encephalitis, brain abscess, arthritis, osteomyelitis, endocarditis, endophthalmitis, peritonitis
• Infection in Normal Host

• Occurs, but rarely

• Ampicillin,





bacteriostatic; TMP-SMX, ampicillin appear bactericidal
• Recommended initial regimen: ampicillin and gentamicin

nervous system infections, most people use combination therapy initially, and complete therapy with ampicillin. Ampicillin is usually preferred because it is more active and in vitro. Cephalosporins are not active.

(combination is bactericidal); then ampicillin alone
• Penicillin-allergic patient: vancomycin and gentamicin or (for

non-perinatal infections) TMP-SMX
• Cephalosporins are not active against Listeria

• Vertical transmission in 50% of infants born to GBS colonized

women (not given intrapartum penicillin)
• Neonatal colonization:

>24 hrs = rectum > throat > umbilicus >30 days = rectum >throat
• Onset of sexual activity

Sites = gastrointestinal tract > genital > throat

tal GBS Infection
Feature Mean age at onset Incidence 13-3.7/1000 live births Obstetric complications Manifestations Pneumonia (40%) Bacteremia (45%) Meningitis (15%) Serotypes All Bacteremia (50%)Meningitis (35%) Type III predominates Fatality rate 8-6% 2-10% Common
0.6-1.7/1000 live births

Early-Onset 8 hr

Late-Onset 27 days


GBS During Pregnancy
• Screening at 26-28 weeks gestation has PPV of 73% and

NPV at 92% for colonization status at delivery; at 35-37 weeks, these increase to 96% and 100%
• Swab of lower vagina and anorectum necessary to define

• Process culture in selective broth medium



Dose (per kg/d)

Duration (days) Until CSF sterile and susceptibility known; complete 14-21


Ampicillin + gentamicin then penicillin G

300-400 mg 7.5 mg then 400,000500,000 U

Bacteremia , soft tissue infection pneumonia Septic arthritis Osteomyelitis Endocarditis

Penicillin G

150,000200,000 U


Penicillin G

200,000 U


Penicillin G Penicillin G plus gentamicin for the initial 7-14 days

200,000 U 300,000400,00 U

21-28 >28

• Choice of obstetrical strategies: GBS culture-based or risk

• Penicillin G IV (5 MU initially; 2.5 MU Q4h) until delivery

(alternatives = clindamycin or erythromycin)
• Timing: 4 hours (>2 doses) before delivery assures greatest

efficacy (Pylipow, Pediatrics 1994;98:631-5)

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Bortolussi R, Schlech WF III. Listeriosis. In: Remington JS, Klein JO, editors. Infections diseases of the fetus and newborn infant. 4* ed. Philadelphia: W.B. Saunders Co., 1995; 1055-1073.

Committee on Infectious Diseases. American Academy of Pediatrics. Parvovirus, erythema infectiosum and pregnancy. Pediatrics 1990;85:131-133.

Committee on infectious diseases and committee on fetus and newborn, AAP. Revised guidelines for prevention of early-onset group B streptococcal (GBS) infection. Pediatrics 1997;99:489-496.

Cunningham CK, McMillan JA, Gross SJ. Rehospitalization for respiratory illness in infants of less than 32 weeks gestation. Pediatrics 1991;88:527-532. Da Silva O, Gredson D, Hammerberg O. Role of Ureaplasma urealyticum and Chlamydia trachomatis in development of bronchopulmonary dysplasia in very low birth weight infants. Pediatr Infect Dis J 1997;16:364-369.

Glaser JH. Ureaplasma urealyticum. In: Long SS, Pickering LK, Prober CG, editors. Principles and practice of pediatric infectious diseases. New York: Churchill Livingstone, Inc., 1997; 1111-1114.

Klein JO, Remington JS. Current concepts of infections of the fetus and newborn. In: Remington JS, Klein JO, editors. Infectious diseases of the fetus and newborn infant. 4* ed. Philadelphia: W.B. Saunders Co., 1995; 1-19.

Red Book of the American Academy of Pediatrics. Syphilis. 1997;504-514.

Risks associated with human parvovirus B-19 infection. MMWR 1989;38:81-97.