15. Congenital infections of the newborn. Flashcards by Janet Jincy

what are the three group of infections for newborn ?

INTRAUTERINE/ congenital infections - the signs and symptoms are present at birth

PERINATAL - infection can be acquired during birth and signs and symptoms present after birth and first 48hrs

POSTNATAL - signs and symptoms start 48 hrs after birth

How well did you know this?

Not at all

Perfectly

what are the most common causative agents for intrauterine/ congenital infection

TORCH

t - toxoplasmosis 
O- other syphillus (trepanoma palladium , varicella zoster , parvovirus )
R - rubella 
C - cytomegalovirus 
H- herpes simplex virus

and congenital listeriosis

How well did you know this?

Not at all

Perfectly

in which trimester is it most dangerous to acquire intrauterine infections ?

1st trimester - greater risk for fetus

especially because the infection with the mother can be asymptomatic

How well did you know this?

Not at all

Perfectly

how can TORCH infections be avoided ?

immunisation of rubella and VZV before pregnancy or in childhood

and some infections such as syphilus treated with benzylpenicillin

How well did you know this?

Not at all

Perfectly

what are the most common routes of intrauterine infections ?

hematologically - esp viruses

ascending infection from the vagina - bacteria and Herpes simplex virus type 2

How well did you know this?

Not at all

Perfectly

what is the source of transmission in toxoplasma gondii ?

cat feces , raw or insufficiency cooked meat , unpasteurised milk

How well did you know this?

Not at all

Perfectly

what are the clinical features in toxoplasmosis gondii ?

when the mother gets the infection in first trim
triad symptoms very severe
TRIAD:
chorioretinitis
DIFFUSE INTRACRANIAL calcifications
hydrocephalus / cerebral ventricular dilation

affected may die in utero or a few days after birth

===
Term newborns usually present with a milder form of the disease with symptoms such as hepatosplenomegaly and lymphadenopathy.

no apparent clinical manifestations at birth OR

intellectual disability

Recurring chorioretinitis resulting in vision loss

Motor delays

Learning disorders
Intellectual disability

SENORINEURAL HEARING LOSS

============

In comparison, preterm newborns exhibit severe symptoms

micro or macrocephaly

hydrocephalus

meningoencephalitis

nystagmus

petechia and purpura - blueberry muffin rash

lymphadenopathy

epilepsy / seizures

retinal scars
microphthalmia
retinochoroiditis

How well did you know this?

Not at all

Perfectly

what is the diagnosis of toxoplasmosis ?

suggestive sonographic findings

fetus - amniocenteisis and do PCR

===========
for NEWBORN

CT or MRI - intracranial periventricular calcifications , hydrocephalus , ring enhancing lesions

IgM Toxoplasma specific antibodies (concern for false positives due to maternal contamination of fetal blood during labor, repeat serological testing should be done 10 days after birth ; half-life of Toxoplasma IgM and IgA antibodies is 5 and 10 days)

Negative IgM and IgA antibodies do not exclude the infection. If the mother is affected later in her pregnancy, there is a delay in the production of antibodies in the newborn. When an infection is suspected, the antibodies should be repeated every 2 to 4 weeks until at least 3 months of age

Positive IgG is indicative of prior or current maternal infection. In the presence of other suggestive features but negative IgM and IgA antibodies, toxoplasma IgG testing requires repetition every 4 to 6 weeks until complete disappearance

PCR for T gondii DNA
positive Toxoplasma IgM or Ig A antibodies in the CSF

ophthalmological evaluation

How well did you know this?

Not at all

Perfectly

what is the treatmnet of congenital toxoplasmosis ?

mother 1st trimester - immediate spiramycin to prevent fetal toxoplasmosis

3grams a day

===========
after 18th week up to birth

pyrimethamine 100mg/day first two days and maintenance dose of 50mg/day

sulfadiazine - 75mg/kg/day

folinic acid - 15mg every 3 day

========
newborn - pyrimethamine , sulfadiazine and folinic acid
12 months

pyrimethamine
For Neonate
1 mg/kg twice daily for 2 days, then 1 mg/kg once daily for 6 months,
then 1 mg/kg 3 times a week for 6 months

sulfadiazine
50 mg/kg twice daily for 12 months

Folinic acid (leucovorin): 10 mg, 3 times per week

higher doses and longer duration (2 years) are the recommended approach when the presentation is severe, with over three intracerebral calcifications and/or more than one ocular sign or severe abnormalities at birth.

Asymptomatic infants with positive serology or newborn screening receive treatment for 3 months. Some experts recommend adding steroids to this regimen when the CSF protein is high or severe chorioretinitis affecting vision. Steroid therapy continues until the disappearance of protein in CSF or resolution of chorioretinitis

How well did you know this?

Not at all

Perfectly

prevention of toxoplasmosis gondii is very important to be to taught to mother what are the preventive methods ?

avoid raw undercooked meat

avoid contact with CAT LITTER

How well did you know this?

Not at all

Perfectly

how is trepanoma palladium transmitted ?

sexual transmission

or perinatal transmission during birth

How well did you know this?

Not at all

Perfectly

what are the clinical features of syphillus ?

inutero
miscarriage , stillbirth , hydrocephalic fetus

====
neonates born with CS are asymptomatic at birth

early congenital syphilus usually appear by three months, <2years old onset

hepatomegaly and jaundice
rhinorrhea - Copious, persistent white discharge is noted, which contains spirochetes that can be visualized under darkfield microscopy.

maculopapular rash on palms and soles ,back, buttocks, posterior thigh

skeletal abnormalities

and generalised lymphadenopathy

=======

late congenital syphilus (onset >2 years of age)

saddle nose
frontal bossing
short maxilla

hutchinson teeth - hypoplastic notched and widely spaced teeth upper central incisors

SABER SHINS

sensorineural hearing loss

perioral fissures

Skin and mucous membrane gummas

cranial nerve palsy - nerve 8 causing deafness

Eye- interstitial keratitis

Intellectual disability

Sensorineural hearing loss

Hutchinson triad (Hutchinson teeth, interstitial keratitis, and sensorineural hearing loss)

How well did you know this?

Not at all

Perfectly

what is the diagnosis for congenital syphillus ?

newborn and mother

Maternal screening for syphilis in early pregnancy important

All neonates born to mothers who have reactive nontreponemal and treponemal test results should be evaluated with a quantitative nontreponemal serologic test (RPR or VDRL) performed on the neonate’s serum!
because umbilical cord blood can become contaminated with maternal blood and yield a false-positive result,
and Wharton’s jelly within the umbilical cord can yield a false-negative result

===========
Non-treponemal tests

RPR -Rapid Plasma Reagin test
detects nonspecific anti-cardiolipin antibodies
is sensitive but not specific

VDRL Detects nonspecific anti-cardiolipin antibodies - is sensitive, but not specific

=========

Specific treponemal tests:

Conducting a treponemal test on neonatal serum is not recommended because it is difficult to interpret

Fluorescent treponemal antibody absorption (FTA-ABS) and/or micro hemagglutination test for antibodies to T.Pallidum (MHA-TP) testing

=======

CSF abnormalities including reactive CSF VDRL, CSF pleocytosis, elevated CSF protein
CSF PCR for detection of treponemal DNA

======

Long bone radiographs that may show findings of pathologic fractures, metaphyseal serration, localized demineralization, and osseous destruction.

=====

always confirmatory test - dark field microscopy or PCR of suspicious lesion or bodily fluid (bullous rash and nasal discharge)

==========
in FETUS - repeated US examinations for plaentomegaly , hepatomegaly ascitis or hydrocephalus

How well did you know this?

Not at all

Perfectly

what is the treatment for congenital syphilus ?

Infants up to 4 weeks of age: Aqueous crystalline penicillin G, 50,000 -75,000 units/kg intravenously every 12 hours in the first seven days of life. After 7 days of life, 50,000 units/kg per dose intravenously (IV) every 8 hours for 10 to 14 days. Alternatively, procaine penicillin G, 50,000 units/kg/day intramuscularly for 10 to 14 days.

Infants older than 4 weeks and older children: Aqueous penicillin G, 50,000 units/kg every 6 hours intravenously for 10 to 14 days.

How well did you know this?

Not at all

Perfectly

how is listeria transmitted?

RAW milk products such as soft cheese -feta, brie, and camembert cheeses
or fish ,
meat

Do not eat refrigerated pâtés or meat spreads

direct contact with infected vaginal secretion or blood during delivery

How well did you know this?

Not at all

Perfectly

what are the clinical features of listeria ?

Listeriosis of pregnancy :

premature birth and spontaneous abortion
Early-onset syndrome: granulomatosis infantiseptica - evere disseminated form of disease characterized by widespread microabscesses and granulomas

respiratory distress

Pustular erythematous lesion

fever

meningitis

=====

premature delivery with amnionitis

======
Neonatal listeriosis

may be apparent within hours or days of birth (early onset) - frequentlylow birth weight, associated obstetric complications, show evidence of neonatal sepsis soon after birth with circulatory or respiratory insufficiency or both

Infants with late-onset listeriosis are generally full term, healthy at birth
source of listerial infection in this group is not known, but is possibly the mother’s alimentary tract or the environment, as the organism is rarely isolated from the mother’s genital tract

Late-onset syndrome (5 days to 3 weeks after birth): Listeria meningitis/encephalitis

How well did you know this?

Not at all

Perfectly

diagnosis of listeriosis ?

can only be made by culturing,
from a sterile site such as blood, amniotic fluid, or spinal fluid or CSF sample for pleocytosis.

Vaginal or stool cultures not helpful because some women carriers but no clinical disease

Laboratory confirmation of the organism involves biochemical testing and observation of motility using a slide test or showing motility in semisolid media

what is the treatmnet of listeriosis ?

for mother

IV ampicillin and penicillin , amoxicillin

(Some in vitro studies suggest a synergistic effect when gentamicin is added to treatment regimens; however, animal models do not reliably show a synergistic effect. Given the toxicities of gentamicin some clinicians have questioned the value of adding it to the treatment regimen)

antibiotic must bind to the penicillin-binding protein 3 (PBP3) of Listeria, which causes cell death, these drugs block several PBP

Whichever antibiotic is chosen, dosage is critical

6 g or more per day of ampicillin during pregnancy (2 g every 6 to 8 hours) in IV duration of one to two weeks - if fetus survives continue

second line is erythromycin 4g/d iv - same time frame as ampicillin

=========
neonate

infants less than 7 days and less than 2kg
= ampicillin 100mg/kg/day IV (divided bid)
gentamicin - 2.5mg/kg/ every 12hr IV

two weeks course usually satisfactory (21 days for meningitis)
but the optimal duration is unknown

infants 8 days to 1 month and more than 2kg:
200mg/kg/day IV divided qid
2.5mg/kg/day IV very 8 hours

what is the transmission of varicella zoster virus (chicken pox) ?

seronegative patients risk of acquiring VZV during pregnancy

airborne droplets
vesicle fluid contact from shingles

or reactivation in immunocompromised individuals

{ responsible for chickenpox (primary VZV infection) and herpes zoster (or shingles) reactivation of latent infection in the dorsal root ganglia}

what are the clinical features of VZV?

first and second trim :

congenital varicella syndrome

hypertrophic cictrical skin lesions

limb defects - hypoplasia / atrophy / malformation

cataracts / chorioretintis / nystagmus

CNS : microcephaly,
cortical atrophy,
seizures,
mental retardation.

Autonomic nervous system : neurogenic bladder, hydronephrosis,
esophageal dilation, gastrointestinal reflux

what is the diagnosis of VZV ?

Prenatal ultrasounds may be used to identify severe manifestations of intrauterine VZV infection

newborn and mother
skin lesions
DFA (Direct immunofluorescent antibody technique) or PCR of blisters or CSF

Viral cultures can also be obtained but often take up to 1 week to yield results

====
fetus - amniocentsis PCR

what is the treatment of VZV ?

antiviral therapy in the newborn not expected to have much impact

However, if the infant develops clinical signs of active infection, acyclovir should be administered intravenously - 10mg/kg
therapy duration is determined based on active VZV replication with either cessation of new skin lesion formation or with negative VZV PCR testing.

If mother develops chickenpox infection during the high-risk time period for neonatal varicella infection (5 days before through 2 days after delivery), infants should receive Varicella-zoster immune globulin (VZIG) immediately after birth or as soon after the maternal symptoms appear in the two days after delivery

Cesarean delivery if lesions are present at the delivery

prevention of VZV?

Immunization of seronegative women before pregnancy

VZIG in pregnant women without immunity within 10 days of exposure

what is the transmission of rubella ?

airborne droplets

is after 20 weeks of gestation the mother is contracted with rubella there is no documented cases

what are the clinical features of rubella ?

intrauterine - miscarriage , preterm and fetal growth restrictions ==== congenital infection is high in first and last weeks of pregnancy (birth defects high in late esp first 12 weeks) ====== congenital rubella syndrome - triad : - cardiac defect -patent ductus arteriosus or pulmonary artery stenosis , ventricular and atrial septal defect - cataracts (leading to salt and pepper retinopathy) - cochlear defect - bilateral senorinueral hearing loss ============= ``` early features : -hepatospelanomegaly , jaundice - blueberry muffin rash - hemolytic anemia -thrombocytopenia micropthalmia cerebral calcifications meningoencephalitis radiolucent bones - celery stalk of long bone metaphases ``` ``` late features : microcephaly intellectual diabsility skeletal abnormalities chorioretinits delayed onset of insulin dependent diabetes and thyroid diseases ```

diagnosis of rubella ?

maternal screening PCR for RNA serology - RV-IgG and IgM Viral culture (nasopharynx, blood) prenatal fetal igM antibody serology PCR for rubella RNA through amniocentesis postnatal RV-IgG antibodies in neonatal serum using ELISA Confirmation of infection virus in nasopharyngeal swabs, urine and oral fluid using PCR

what is the treatmnet for rubella ?

<16 weeks = counsel to terminate pregnancy >16 weeks - reassurance

how can we prevent rubella ?

immunisation before pregnancy Children with congenital rubella syndrome should be considered contagious until at least one year of age

how does the transmission of cytomegalovirus occur?

humans are the main reservoir Important risk factor for primary infection during pregnancy is prolonged exposure to young children.CMV infected children under 2 years of age secrete the virus in their urine and saliva for about 24 months. mother contaminated via CMV-contaminated blood, urine, saliva, and genital secretions Sexual transmission Transplant-transmitted infection postnatal via breastmilk from infected mother

clinical features of cytomegalovirus ?

Primary infection cannot clinically be distinguished from Epstein Barr virus (EBV) : fever, malaise, headache, pharyngitis, lymphadenopathy, hepatosplenomegaly, arthralgia ======= Fetal infection IUGR Microcephaly Sensorineural hearing loss - hallmark Chorioretinitis, optic atrophy and cataracts Petechiae, purpura -(blueberry muffin rash) Hepatosplenomegaly, jaundice Small for gestational age (SGA) Seizures hydrocephalus, ventriculomegaly periventricular calcifications, or intraventricular hemorrhage ======= most infected newborns are asymptomatic

diagnosis of cmv ?

mother CMV IgM antibodies IgM antibodies can persist for several months. More sophisticated testing such as IgG antibody avidity testing is necessary for sorting out the timing of infection. With recent infections, the avidity is low (antibodies bind less tightly with their protein); thus the presence of IgM levels along with a low IgG avidity index is highly suggestive of a recent primary infection Viral culture or PCR for CMV DNA (urine, saliva) ======== Fetus via amniocentesis for amniotic fluid PCR with or without viral culture Replication of the virus in the fetal kidney, leading to shedding in the urine, occurs at least 5 to 7 weeks after infection. Thus, the optimal time for performing this test is after 21 weeks gestation and 7 weeks after maternal infection

treatment for cmv ?

Fetus termination of the pregnancy Severe anemia: intrauterine blood transfusions Thrombocytopenia: platelet transfusions ======== Newborn first line with symptomatic CCMV should receive oral valganciclovir for 6 months 16 mg/kg/dose twice daily. This therapy has been shown to preserve normal hearing or prevent the progression of hearing loss Alternative: • Ganciclovir IV 6 mg/kg/dose twice daily ======= Mother: valacyclovir - only therapy approved during pregnancy

what type of causative agent is HERPES simplex virus ?

``` genital herpes HSV 2 (type 1 - oral rare) ```

what is the transmission of HSV2?

ontact with contaminated oral secretions via small skin lesions Reactivation: usually in immunocompromised individuals transmission through vaginal delivery

what is the clinical features of HSV2

Intrauterine HSV infection (∼ 5% of cases) ``` Fetal demise, preterm birth, very low birth weight Microphthalmia and chorioretinitis Vesicular skin lesions ``` ====== Perinatal and postnatal transmission persistent fever and negative bacterial cultures SKIN EYE AND MOUTH DISEASE : 1) Vesicular skin lesions 2) Keratoconjunctivitis leading to cataracts, chorioretinitis CNS DISEASE 1) Meningoencephalitis - Seizures 2) vesicular skin lesions DISSEMINTAED DISEASE prominently liver and lungs (fever or hypothermia, irritability, lethargy, respiratory distress, apnea, abdominal distension, hepatomegaly, ascites) Thrombocytopenia 2) Vesicular skin lesions When skin lesions are not present, it can be challenging to diagnose neonatal HSV infection

what is the diagnosis of HSV2?

neonates Swab specimens from the mouth, nasopharynx, conjunctivae, and anus (“surface cultures”) for HSV culture and, if desired, for HSV PCR assay; Specimens of skin vesicles for HSV culture and, if desired, for PCR assay; CSF sample for HSV PCR assay; Whole blood sample for HSV PCR assay; and Whole blood sample for measuring alanine aminotransferase (ALT). Positive cultures obtained from any of the surface sites more than 12 to 24 hours after birth indicate viral replication and are, therefore, suggestive of infant infection rather than merely contamination

treatmnet of HSV2

IV acyclovir 60 mg/kg per day in 3 divided doses or 14 days in SEM disease Given intravenously for a minimum of 21 days in CNS disease or disseminated disease repeat lumbar puncture performed near the end of therapy to document that the CSF is negative for HSV DNA on PCR assay

prevention of HSV2?

Antiviral therapy (acyclovir) beginning at 36 weeks of gestation for individuals with a known history of HSV lesions Cesarean delivery in women with active genital lesions or prodromal symptoms (e.g., burning pain)

if the mother is infected with HIV what's the chance the baby having it ?

there is a 25 percent chance the fetus being affected depending on : high viremia , AIDS or low CD4+ CELL COUNT

HOW is HIV passed from mother to fetus ?

late in pregnancy through haematological route , and highest during delivery

what are the clinical manifestations of HIV in fetes ?

``` fever hepatomegaly splenomegaly lyphadenectomy freq opportunistic infection - such as oral thrush ``` usually do not have symptoms until opportunistic infections occur

diagnosis of hiv in children and adults

Diagnosis in infants: if < 18 months, diagnosis is confirmed via PCR, not ELISA ==== detect both HIV antigen (p24 capsid protein) and anti-HIV antibodies (IgG antibodies against HIV-1/HIV-2) through ELISA → a negative result essentially rules out HIV infection (almost 100% sensitivity) Not recommended for suspected neonatal HIV infection (results may be false-positive due to maternally transferred anti-HIV antibodies) Confirmatory tests HIV-1/HIV-2 antibody differentiation immunoassay