Curs 6.

Infecţiile neonatale
Infecțiile neonatale pot fi clasificate, după mecanismul fiziopatogen,
debut și agentul infecțios, în:
1. sepsis neonatal
2. infecții perinatale/congenitale – sumarizate ca TORCH

1. Sepsisul neonatal este un sindrom clinic la un nou-născut (cu vârsta

până la 28 de zile de viață), manifestat prin semne sistemice de
infecție și izolare a unui agent patogen bacterian din sânge.
O situație subclinică - bacteriemia - se caracterizează prin absenţa
semnelor clinice, cu prezenţa pasageră germenilor în torentul
circulator.
Clasificarea sepsisului în funcţie de debut:
A. Infecţii precoce:
- 85% în primele 24 de ore de viaţă
- 5% la 24-48 de ore de viaţă
- un procent mai mic dupa 48 de ore de viaţă
B. Infecţii tardive:
- apar după 5 zile de viaţă
- în mod obişnuit la 1 săptămână de viaţă
C. Infecţii nozocomiale – de regulă cu debut tardiv

Agenţi etiologici implicaţi:

În infecţiile precoce: streptococ de grup B, E Coli, Haemophilus
influenzae, Listeria monocytogenes, Stafilococcus, enterococi,
anaerobi.
În infecţiile tardive: stafilococi, mai ales stafilococcus epidermidis,
Pseudomonas, Klebsiella, Serratia, Proteus, fungi.

Factori predispozanţi:
– colonizare bacteriană în momentul naşterii şi în cursul primelor
zile de viaţă
– imaturitatea mijloacelor de apărare în organismul fătului şi a
nou-născutului:
– deficienţa funcţiilor granulocitare
– producerea insuficientă de imunoglobuline locale şi circulante
– diminuarea reacţiei inflamatorii, ceea ce determină
răspândirea rapidă a infecţiei.
Moduri de transmitere la nou-născuţi:
Infecţia precoce:
– pe cale hematogenă transplacentară (treponema, virusuri,
Listeria, candida)
– pe cale ascendentă din căile genitale materne, caz în care nou-
născutul este colonizat cu agenţi patogeni în perioada
perinatală
– contaminarea directă în timpul naşterii prin contactul cu
secreţiile vaginale, ruperea membranelor, corioamniotită,
aspiraţie de lichid amniotic infectat (bacilul Coli, Streptococul
de grup B
Infecţii tardive:
– sunt implicaţi agenţii patogeni dobândiţi din tractul genital
matern, dar un rol important îl are şi transmiterea orizontală:
contactul uman şi echipamentele contaminate.
Infecţii nozocomiale:
– în majoritatea cazurilor, la copiii spitalizaţi în unităţile de
terapie intensivă neonatală, în special la prematuri.
– este implicată flora mediului ambiant din unităţile de terapie
intensivă neonatală, precum şi monitorizarea şi tehnicile
invazive

Criterii de diagnostic:
Diagnosticul trebuie stabilit cât mai rapid după naștere, utilizând atât
criterii anamnestice cât și semne clinice, pentru a se putea începe
tratamentul înainte de deteriorarea marcată a stării nou-născutului.

1) Argumente anamnestice:
a. Factori care favorizează apariţia unei infecţii:
– col uterin dehiscent
 – infecţia urinară maternă
– infecţia cervicovaginală (vaginoza bacteriană)
– ruperea precoce a membranelor amniotice (peste 12 ore)
– travaliu prelungit
b. Factori care pot determina infecţia fătului:
– febra maternă (mai mare de 38 oC în timpul naşterii, în special
la începutul primelor contracţii);
– ruperea prematură a sacului amniotic înainte de începerea
travaliului;
– traume fetale inexplicabile din punct de vedere obstetrical;
lichid verde, uneori fetid;
– naştere prematură inexplicabilă (în special dacă este un eşec
de tocoliză)
2) Semne clinice de sepsis:
!! Nu există semne specifice ale infecţiei. Aceasta poate să se
manifeste prin diverse simptome şi poate fi asociată cu orice altă
afecțiune a nou-născutului.
Semne nespecifice:
– refuzul alimentaţiei
– hiporeactivitate
– tentă teroasă sau cianotică
– instabilitate termică
– meteorism abdominal.
Semne de gravitate:
– disfuncţie respiratorie
– tulburări hemodinamice
– anorexie/vărsături şi meteorism abdominal
– icter precoce.
Semne clinice tardive (în cursul evoluției bolii):
– incapacitatea dureroasă a unui membru: osteoartrita (în
special a şoldurilor)
– tulburări ale comportamentului şi a conştienţei, însoţite uneori
de convulsii
– febră, refuzul alimentaţiei, stagnare ponderală, deshidratare
3) Examinări paraclinice:
– !! examenul bacteriologic este esenţial - trebuie realizat
înainte de începerea tratamentului antibiotic – este important
prelevarea culturilor centrale (hemocultura, în principal,
urocultura, cultura LCR);
– culturile periferice: aspiratul gastric, aspiratul traheal,
coprocultura – se obține un rezultat mai rapid, care poate
ghida antibioterapia;
 – alte examinări complementare: analiza gazelor sangvine (AGS),
bilirubinemia, glicemia, radiografia toracică, examinări ale
placentei pentru corioamniotită.
Semnele biologice ale infecţiei bacteriene:
– formula leucocitară: iniţial leucopenie < 5.000/mm3, apoi
hiperleucocitoză >25.000/mm3 cu polinucleare neutrofile
crescute şi uneori trombocitopenie < 150.000 plachete/ mm3;
– creşterea proteinei C reactive > 20 mg/l după 12 ore de viaţă
este un semn important; normalizarea sa demonstrează
eficacitatea tratamentului;
– fibrinogen > 4 g/l;
– citokinele IL-6, IL-8, mediatori majori ai răspunsului la infecţie,
produşi de monocitele activate şi de către macrofage; sunt
necesare laboratoare specializate şi sunt mai costisitoare.
Infecţii nozocomiale (recent denumite infecții asociate actului
medical IAAM)
Definiţie: orice infecţie dobândită în timpul internării intraspitaliceşti.
Pentru nou născuţi: infecţii care survin după primele 72 de ore de viaţă
– discuție legată de diagnosticul diferențial cu infecția matero-fetală
cu debut tardive.
Incidenţa - la pacienţii pediatrici incidenţa este mai mică decât la adulţi
şi are valori crescute în special la copiii cu vârsta sub 1 an.
În secţiile de nou - născuţi la termen: 0,40 infecţii la 100 externări.
În secţiile de Terapie Intensivă Neonatală:14 infecţii la 100 externări.
Epidemiologie - sursele germenilor patogeni sunt din:
– flora genitală maternă
– sursele de alimentaţie
– personal
– mediul înconjurător din maternitate
Mod de transmitere
– contact (direct, indirect, picături)
– obiect contaminat
– aerian
– prin vectori
Factori de risc
– Greutate mică la naştere - copil imatur imunologic
– Colonizare bacteriană
– Spitalizare prelungită
– Aglomerare, personal insuficient
– Proceduri invazive – catetere, corpi străini
– Folosirea neraţională a antibioticelor
– Antibioterapie prelungită
– Corticoterapie
– Hiperalimentaţie
Agenţi etiologici
– Bacterii de pe tegumente, enterice (adesea rezistente la
antibiotice)
– Micobacterii
– Virusuri – respiratorii, din sângele transfuzat, din laptele uman
– Fungi - de pe tegumente, din emulsiile de lipide (în secţia TIN),
proliferaţi în timpul terapiei antibacteriene
Semnele clinice şi evaluarea sepsisului sunt cele descrise anterior, la
infecţiile precoce. Localizarea infecţiei poate fi în:
– Torentul sangvin
– Plămâni
– Sfera ORL
– Tegument, ţesuturi moi
– Tract gastro-intestinal
– Altele
Tratamentul sepsisului neonatal
Se foloseşte cel mai puţin scump şi cel mai sigur antibiotic eficient
împotriva bacteriilor întâlnite în mod obişnuit în secţia de terapie
intensivă. Antibioticele mai noi şi cu spectru mai larg sunt mai scumpe
şi ar trebui păstrate pentru infecţiile cu germeni rezistenţi.
!! Combinaţia standard în prezent: Ampicilina cu Gentamicina
Deoarece sepsisul rămâne o cauză importantă de mortalitate (10-15%
din decesele neonatale), orice suspiciune de sepsis trebuie să fie
tratată prompt!
Raţiunile tratamentului cu antibiotice precoce, empiric:
– Capacitatea limitată de apărare a nou-născutului împotriva
infecţiilor
– Semnele clinice de sepsis sunt nespecifice
– Tratamentul este salvator
!! Deşi infecţiile suspectate clinic trebuie să fie adesea tratate,
profilaxia cu antibiotice poate fi ineficientă şi poate promova
instalarea rezistenţei la antibiotic.
Trebuie evitată rezistenţa la antibiotic prin:
– Izolarea în culturi a germenilor infectanţi şi testarea
sensibilităţii la antibiotice
– Folosirea celui mai îngust spectru, a acoperirii cu cel mai sigur
antibiotic care va fi eficient
2. Infecţii congenitale/perinatale

Protocol privind limitarea transmiterii verticale a infectiei HIV

Infectarea cu virusul HIV a nou-născutului din mamă HIV, se face:
- antenatal- pe cale transplacentară, prin înghiţirea de lichid amniotic
infectat sau pe cale sangvină
- în timpul naşterii- prin contactul nou-născutului cu sângele şi
secreţiile infectate din tractul genital matern
- postnatal- prin laptele de mamă
Riscuri pentru nou-născutul din mamă cu HIV: restricţie de creştere
intrauterină, hipoxie la naştere, hipoglicemie, asociere cu alte maladii
infecţioase.
Scopul protocolului- limitarea transmiterii verticale a infecţiei HIV-SIDA
Măsuri de prevenire
-antenatal- profilaxia antiretrovirală la mamă
-perinatal- profilaxie antiretrovirală în travaliu + naştere prin operaţie
cezariană
-postnatal- nu se aspiră cu presiune mare secreţiile (risc de
microhemoragii)- creşte riscul de
infecţie
- profilaxie postnatală cu antiretroviale:
· Zidovudina (ZDV)- sirop 10 mg/ml, 8 mg/kg corp la 6 ore
(2mg/kg/doza)
· Lamivudina- sirop 10 mg/ml, 2 mg/kg corp la 12 ore
· Nevirapina (NVP) asociat în condiţii de risc maxim (mama nu a
urmat tratamentul), 2 mg/kg/zi, 14 zile, apoi 4 mg/kg/zi
Durata tratamentului- 6 săptămâni
Tratamentul începe la maxim 6 ore după naştere
La prematur- Zidovudina- VG >30 s, 2 mg/kg la 12 ore, 2 săptămâni,
apoi 2 mg/kg la 8 ore, 4 săptămâni.
- VG<30 s, 2x2 mg/kg/zi – 4 săptămâni, apoi 3x2 mg/kg/zi, 2
săptămâni.
Rolul neonatologului
-anunţă medicul coordonator compartiment HIV- absenţă anunţă
medicul coordonator de program- dr. -izolează nou-născutul -
administrare profilactică a terapiei antiretrovirale: Zidovudina şi
Lamivudina.
-!! alimentaţia artificială a nou-născutului cu formulă de lapte
-asigură împreună cu echipa îngrijirile uzuale: asigurarea confortului
termic, toaleta tegumentelor, evaluarea icterului
-efectuarea de explorări pentru confirmarea diagnosticului (2 teste de
identificare a virusului pozitive) şi efectele terapiei (hemograma
completă pentru a evalua efectele tratamentului asupra măduvei, în
evoluţie- anemie secundară —> determinarea Hb).
-vaccinarea în spital: anti Hbs şi BCG
-externarea nou-născutului: - se face de comun acord cu părinţii
- alimentaţie artificială
- se anunţă Spitalul de Boli Infecţioase despre externarea copilului -
dispensarizare prin Sp.Boli Infecţioase
- biletul de externare va cuprinde obligatoriu diagnosticul: copil expus
perinatal la infecţie HIV, tratamentul primit în spital, recomandări de
tratament la domiciliu
Protocol atitudine faţă de nou-născutul din mamă cu antigen HBs
pozitiv
1. În timpul sarcinii-Procurarea imunoglobulinei specifice
antihepatita B, din resurse propii, cu administrare i.v. Recomandarea
obstetricianului care dispensarizează sarcina.
2. După naştere, precoce, după evaluarea clinică a nou-născutului
de câtre neonatolog- administrare iv de IG specifică anti Hbs,
împreună cu vaccinul AHB.
3. Nu se contraindică alimentaţia naturală la aceste cazuri.
4. La nou-născutii la care nu s-a administrat IG specifică din lipsă,
nu se contraindică alimentaţia naturală; se efectuează vaccinarea
antihepatita B precoce pe secţie, după care se recomandă schema de
imunizare după protocol.
5. Atenţie la ragade. Când apar, laptele de mamă se mulge. Se
întrerupe alăptatul până la vindecarea sânului.
Protocol atitudine faţă de nou-născutul din mamă purtătoare de
virus hepatic C
Mama trebuie informată despre riscul posibil de trecere a virusului
prin laptele matern. În mod obişnuit, nu se contraindică alimentaţia
naturală.

Protocol atitudine faţă de nou-născutul din mamă cu citomegalvirus

Alimentaţia naturală se contraindică. Se indică ablactarea mamei.

Protocol atitudine fata de nou-nascutul din mama cu varicela

Forma clinice: -varicela fetala
-varicela congenitala
Varicela congenitala poate apare la 25% din mamele care au prezentat
varicela in perioada peripartum. Debutul bolii apare, de obicei , la 13-
15 zile de la aparitia rasului matern. Cand aparitia rash-ului la nou-
nascut s-a realizat in primele 10 zile, transmisia s-a realizat intrauterin.
Fiziopatologic-varicela la < 5 zile inainte de nastere= boala severa la
nou-nascut- pasaj de anticorpi insuficient—>deces in 30% din cazuri.
-varicela la > 5 zile inainte de nastere- forma usoara de boala la nou-
nascut- pasaj transplacentar de anticorpi materni
Diagnostic- PCR, culturi din vezicule, Ig M serice.
Atitudine in infectia cu VZV in sarcina:
toate gravidele care au contact cu VZV, care nu au contact cu
varicela, si sunt seronegative, vor primi ZIG imunoglobulina specifica in
primele 72 de ore de la contact.
terminarea nasterii nu are nici un beneficiu
consiliere pentru riscul de varicela congenitala
este incurajata alaptarea nou-nascutilor infectati sau expusi
este necesara izolarea fata de alte mame si nou-nascuti, in faza de
boala acuta.
Ingrijirile nou-nascutului in maternitate:
izolarea nou-nascutului
limitarea vizitatorilor
utilizarea Ig si la alti nou-nascuti expusi
folosirea unui bilet de avertizare la usa de la intrare in salon
sterilizarea materialelor si a lenjeriei folosite
ceilalti nou-nascuti vor fi externati din maternitate inainte de a
contacta infectia nu este necesara izolarea mama-nou-nascut propiu
Tratament: acyclovir-60mg/kg divizat la 8 ore; profilaxie cu
imunoglobulina specifica in primele 72 ore de la expunere, 125 unitati
im.
 Lecture no. 6

Congenital and Perinatal Infections

Infections in the newborn infant can be classified as congenital

or perinatal. It is important to make this distinction as the clinical
presentations, causative organisms, diagnostic approaches,
treatments and long-term considerations differ for these two groups.
A congenital infection is an infection seen in the newborn
infant that was acquired transplacentally during the first, second, or
early third trimester.
In contrast, a perinatal infection is acquired either around the
time of delivery or during the first week of extrauterine life.
 A. Congenital infections
The incidence of congenital infection in the fetus and newborn
infant is relatively high at 0.5-2.5%. The most common causative
agents are:
– rubella virus,
– cytomegalovirus (CMV),
– Toxoplasma gondii,
– Treponema pallidum,
– human immunodeficiency virus (HIV).
Despite the diversity of these organisms, many produce similar
syndromes in the newborn infant grouped under the acronym TORCH.
Common manifestations of congenital infections include
growth retardation, hepatomegaly, splenomegaly, jaundice (secondary
to direct hyperbilirubinemia), hemolytic anemia, petechiae and
ecchymoses, microcephaly, hydrocephaly, and pneumonitis. However,
the majority of affected infants are entirely asymptomatic.
 Rubella syndrome. The incidence of congenital rubella
syndrome is 0.5 per 1000 live births. Infants are usually born small for
gestational age.
Common clinical findings include:
– purpura, thrombocytopenia,
– hepatosplenomegaly,
– cardiac defects,
– eye defects (glaucoma and cataracts),
– pneumonia and
– meningoencephalitis.
Diffuse purpuric lesions on the skin resembling a "blueberry
muffin", represent cutaneous extramedullary hematopoietic tissue
that may be seen in this and other congenital infections.
Congenital rubella infection can be diagnosed with an elevated
anti-rubella IgM titer in the perinatal period or high anti-rubella IgG
titers throughout the first year of life. Virus can also be isolated from
a throat swab, CSF or urine.
 Common long term problems seen in infants with congenital
rubella include communication disorders, hearing defects, mental
and/or motor retardation, microcephaly, learning deficits, balance and
gait disturbances, and behavioral problems.
Although live attenuated rubella virus vaccine is available to
prevent the disease, there is no specific therapy for congenital rubella.

Congenital cytomegalovirus infection. CMV infection occurs in

roughly 1% of all neonates with those who are not congenitally
infected contracting the infection possibly through breast milk. Twelve
percent of these infants will die and more than 90% of survivors will
suffer late complications, most commonly sensorineural hearing loss.
Congenital CMV infection may be the result of a newly acquired
maternal infection or a reactivated old maternal infection. Although
less common, newly acquired maternal infection poses a much higher
risk of severe disease and a worse prognosis. Ninety percent of
infected newborns are surprisingly asymptomatic at birth. However,
those that are symptomatic are small for gestational age and often
present with petechiae, ecchymoses, thrombocytopenia, jaundice,
direct hyperbilirubinemia, anemia, hepatosplenomegaly, elevated
SGOT, microcephaly, seizures and chorioretinitis. The diagnosis of
congenital CMV infection is best made by isolating the virus in urine
culture. Periventricular calcifications can be seen on cranial
ultrasound. Of the affected infants that survive the neonatal period,
1/3 will have hearing loss, one third will have neuromuscular disorders
(seizures or spasticity) and a few will have vision problems secondary
to chorioretinitis. Although there is no specific therapy for congenital
CMV infection, trials examining the effectiveness of ganciclovir, alpha
interferon and CMV immune globulin are underway.

Congenital toxoplasmosis. The incidence of congenital

toxoplasmosis infection varies with geographic location and local
dietary habits. Maternal toxoplasma infection is usually due to
ingestion of tissue cysts found in raw or undercooked meats or
consumption of water or other foods containing oocysts from infected
cats. Congenital infection with Toxoplasmosis gondii occurs during
maternal parasitemia. In the neonate, the primary focus of
toxoplasma infection is in the central nervous system, leaving necrotic,
calcified cystic lesions dispersed within the brain. Less commonly,
similar lesions can be found in liver, lungs, myocardium, skeletal
muscle, spleen and other tissue. Approximately 85% of infants with
congenital infection have normal examinations and are asymptomatic.
Those infants that exhibit illness at birth frequently present with fever,
hepatosplenomegaly, jaundice, rash and pneumonitis. The classic
triad of toxoplasmosis, chorioretinitis, hydrocephalus and intracranial
calcification occurs in only a small proportion of symptomatic patients.
Abnormal laboratory findings include anemia, thrombocytopenia,
eosinophilia, and abnormal CSF studies. Seizures, mental retardation,
spasticity, and relapsing chorioretinitis are common long-term
complications of congenital toxoplasmosis, even if not present at
birth. Antenatal ultrasound can suggest the diagnosis of congenital
toxoplasma infection when bilateral, symmetric ventricular dilatation,
intracranial calcifications, increased placental thickness, hepatomegaly
and ascites are noted. Postnatal diagnosis is also made by detection
of anti-Toxoplasma IgM antibodies in the infant's serum. Treatment,
antenatally and postnatally, consists of pyrimethamine and
sulfadiazine. Spiramycin may also be used, if available. Historically,
prognosis in untreated infants is poor. However, with recent advances
in antenatal diagnostic capabilities and available medical therapies,
the frequency of major neurologic sequelae has decreased.

Congenital syphilis is caused by the spirochete Treponema

pallidum. Transplacental transmission usually occurs during the
second half of pregnancy. Most infants born to mothers with primary
or secondary syphilis have congenital infection; though only half of
those who are infected are symptomatic. Because congenital syphilis
is associated with significant neurodevelopmental morbidity, it is
imperative that both maternal status and infant risk for syphilis be
checked in all pregnancies. Early features of congenital syphilis
include hepatosplenomegaly, skin rash, anemia, jaundice,
metaphyseal dystrophy, periostitis and CSF abnormalities including
elevated protein and mononuclear pleocytosis. However, in some
cases, the infant is asymptomatic and may not develop any signs or
symptoms of congenital infection for weeks or months. "Snuffles" is
obstruction of the nose with initial clear discharge progressing to
purulent or sanguineous discharge. It is seen in infants with
congenital syphilis usually after the newborn period. Detection of IgM-
FTA-ABS (fluorescent treponemal antibody absorption) in the
newborn's blood is the most reliable method of diagnosing congenital
syphilis. However, this test is not always positive early on in life, thus
repeat testing at 3 to 4 week intervals is frequently indicated.
Treatment for both the pregnant mother and baby is penicillin G.
Despite antibiotic therapy, it is recommended that infants undergo
repeat blood and CSF testing during the first 12-15 months of life until
negative or stable low titer levels are achieved. Vision, hearing and
developmental evaluations are also indicated before three years of
age in infants with congenital syphilis.

B. Perinatal infections
Perinatally acquired infections are those that are acquired
either around the time of delivery or during the first week of
extrauterine life. Common pathogens include bacteria, such as group
B streptococci, E. Coli, and Listeria, herpes simplex virus, hepatitis
viruses and human immunodeficiency virus. Infants with perinatally
acquired viral infections are often normal at birth, developing illness
later in life.
A few pathogens like cytomegalovirus (CMV) can cause both
congenital and perinatally acquired infection in the newborn with
striking contrasts in presentation. The infants with congenital
infections can present with growth restriction, anemia,
thrombocytopenia, extramedullary hematopoiesis, and intracranial
calcifications, all indicative of a chronic process; namely, congenital
CMV infection that was transmitted transplacentally during the first or
second trimester of pregnancy. Perinatally, CMV can be transmitted
through breast milk or vaginal secretions. Premature infants however,
are particularly susceptible to transmission through transfusion of
blood products. The resulting syndrome is characterized by shock,
pneumonitis and lymphocytosis. The role of ganciclovir in perinatally
acquired CMV infection is unclear.
The majority of neonatal herpes simplex virus (HSV) infection
is acquired from the maternal genital tract with an incidence of
approximately 1 case per 3500 live births. However, infection may
also be acquired after birth from mother or other persons with non-
genital tract lesions (e.g., oral herpes, herpetic whitlow) following
close contact with the infant or handling. Primary maternal infection
is associated with a 50% risk of perinatal/neonatal infection, while a
risk of <5% is seen with recurrent maternal infection. Of note, active
HSV lesions are present at the time of delivery in only 1/3 of mothers
of affected infants. Several defects in cellular immune function
contribute to neonatal susceptibility to HSV. Perinatally acquired HSV
infection results in massive coagulation necrosis of the liver, lungs,
adrenal glands and brain. Most infants are asymptomatic at birth,
developing illness during first 1 to 2 weeks of life. Clinical illness can be
characterized as being localized or disseminated. Disseminated illness
can be further described as those with and those without central
nervous system involvement. Systemic symptoms of disseminated
HSV infection usually present towards the end of the first week of life,
including poor feeding, lethargy, fever, irritability, and seizures with
rapid progression to hypotension, disseminated intravascular
coagulation, apnea and shock. Skin vesicles are present in less than
half of patients. With antiviral therapy, 15-20% of patients die and 40-
55% of survivors suffer long-term neurologic impairment. Localized
disease may involve the central nervous system alone, the central
nervous system and skin, eyes, and oral mucosa or only the skin, eyes
and oral mucosa. Except in cases of isolated viral encephalitis, HSV is
readily recovered in culture from scrapings of skin vesicles, blood,
cerebrospinal fluid, conjunctivae, respiratory secretions, and urine.
Once neonatal HSV infection is suspected, antiviral therapy should be
started immediately. Parenteral acyclovir is the treatment of choice
for herpes neonatorum. Treatment duration varies depending on
whether the infection involves the CNS and/or is disseminated.
Despite antiviral therapy, overall outcome for survivors is poor. More
than half of infants who survive disseminated disease will develop
microcephaly, spasticity, paralysis, seizures, deafness, or blindness.
Those with skin involvement may be subject to recurrent vesicular
outbreaks for several years. Of note, HSV can also be transmitted in
utero during the first or second trimesters of pregnancy (congenital
infection). Those fetuses that are not stillborn or spontaneously
aborted demonstrate a syndrome similar to other congenital viral
infections like CMV. Treatment is supportive as acyclovir has no
proven benefit for these infants.
Hepatitis. The most important of the hepatitis viruses for the
general pediatrician is Hepatitis B. The virus is found primarily in the
liver parenchyma, but can be found in circulating blood from a few
days to many years. Regardless of maternal acute or chronic infection,
the virus rarely crosses the placenta, thus perinatal/neonatal infection
is most likely acquired from infected maternal blood encountered
during the delivery process. Overall, there is 60-70% chance of
transmission during delivery if mother has an acute infection at that
time. Mothers may also be carriers which still has a risk of
transmission to the newborn. By 2 to 6 months of age, liver enzymes
are often elevated and infants are antigen seropositive. Occasionally,
infection may present with jaundice, fever, hepatomegaly and
anorexia, followed by complete recovery or chronic active disease.
Approximately 95% of perinatally acquired HBV infection can be
prevented by early active and passive immunoprophylaxis of infants
born to HBsAg positive mothers. Infants born to HBsAg positive
mothers should receive the initial dose of hepatitis B vaccine and
hepatitis B immune globulin (HBIG) within 12 hours of birth (given at
separate injection sites). Infants born to unscreened mothers should
receive their first hepatitis B vaccine within 12 hours of birth while
awaiting maternal blood test results. If the mother should be found to
be HBsAg positive, HBIG should be given within the first week of life.
All infants should complete the hepatitis B immunization series by 6
months of age. Infants born to HBsAg positive mothers should be
tested for anti-HBsAg antibodies and HBsAg 1 to 3 months after the
third dose of vaccine is given to determine those who may be
chronically infected and those who may require additional doses of
the vaccine. Breastfeeding by an HBsAg positive mother has not been
shown to cause hepatitis B infection in infants.
Once seen exclusively in children who had received blood
products, pediatric human immunodeficiency virus (HIV) infection is
now overwhelmingly the result of perinatal transmission. There are
three distinct modes of transmission of human immunodeficiency
virus (HIV) from mother to fetus. Congenital HIV infection results from
the transplacental transmission of virus during early pregnancy.
Intrapartum transmission may occur following exposure of the infant
to mother's blood or as a result of maternal-fetal transfusion during
the delivery. Perinatal infection with HIV can occur either during the
birthing process or shortly after birth through breastfeeding. Risk
factors associated with perinatal HIV transmission include maternal
viral load (plasma and genital tract), primary infection of late stage
HIV, low CD4 count, STDs/other co-infections, pre-term delivery,
increasing duration of rupture of membranes, placental disruption,
invasive fetal monitoring (eg. scalp probes), vaginal delivery and lack
of AZT prophylaxis. The transmission rate from mother to infant is
approximately 20-30%. However, recent studies have shown that for
select HIV-infected women, zidovudine (AZT) may decrease
transmission to 8% of their infants. Maternal treatment with AZT in
combination with elective cesarean section delivery prior to rupture of
membranes and the onset of labor has shown further reduction of the
transmission rate to 2%. Infants with congenital infection present in a
similar fashion to other congenital infections and may also exhibit
craniofacial abnormalities. Infants with perinatally acquired infection
are usually asymptomatic at birth. To maximize the opportunity to
prevent perinatal transmission of HIV infection, maternal HIV status
should be determined during the first trimester of pregnancy. Anti-
retroviral therapy should be started in those found to be HIV positive.
During labor and delivery, AZT, 2mg/kg should be administered IV
during the first hour, then 1mg/kg per hour until delivery. The infant
should then be started on AZT syrup, 8-12 hours after birth, 2mg/kg
QID until 6 weeks of age when the infant's HIV status can be
determined. Detection of HIV antibody by ELISA or Western blot in
the newborn is complicated by transplacental passage of maternal IgG
and should not be performed before 18 months of age. Detection of
HIV DNA by PCR is the preferred test for diagnosis of HIV infection in
infants. Testing should be performed at birth, then at 1-2 months of
age, and a third time between 3 and 6 months of age. Any time an
infant tests positive, a second repeat specimen should be obtained
immediately to confirm the diagnosis of HIV infection. Viral culture for
HIV can also be done; however, issues of cost, regional availability and
delay in reporting results make it less useful than HIV DNA by PCR.
Umbilical cord blood should not be used for testing. An infant with at
least 2 negative HIV virology tests from separate specimens, 1 of
which was performed at 1 month of age and 1 of which was
performed after 4 months of age can be considered "not infected with
HIV". Finally, because transmission of HIV through breastmilk has
been reported, counseling to discourage breastfeeding should be
provided to all mothers who are HIV positive.

Questions
1. What physical findings suggest that an infant has a
congenital infection (TORCH)?
2. How does a congenital infection differ from an infection that
is acquired perinatally?
3. What are the most common causes for congenital infection?
4. True/False: A term infant with a normal physical exam and
no risk factors for infection may have congenital infection.
 5. Periventricular calcifications in the brain are seen with
which congenital infection? Diffuse calcifications?
6. True/False: An infant born to a woman with recurrent
herpes infection is at higher risk for developing herpes neonatorum
than one born to a woman with primary herpes infection at the time
of delivery?
7. Administration of what agents can prevent 95% of
perinatally acquired hepatitis B infections?
8. True/False: Breastfeeding should be encouraged in all
mothers who are HIV positive, but do not have AIDS.
Answers to questions
1. Small for gestational age, microcephaly, jaundice, pale skin,
petechiae, blueberry muffin spots, hepatomegaly, and splenomegaly
2. A congenital infection is an infection seen in the newborn
infant that was acquired transplacentally during the first, second, or
early third trimester. A perinatal infection is acquired either around
the time of delivery or during the 1st week of extrauterine life.
3. Rubella virus, cytomegalovirus (CMV) Toxoplasma gondii,
Treponema pallidum, human immunodeficiency virus (HIV)
4. True
5. Periventricular calcifications are seen in congenital CMV
while diffuse calcifications in the brain are seen in congenital
toxoplasmosis.
6. False
7. Hepatitis B vaccine and hepatitis B immune globulin.
8. False