Fetopathies Flashcards
Route of infection in Toxoplasmosis
- fecal-oral (from cat feces)
- contaminated water or soil, inadequatly cooked meat
- transmission to embryo via placenta or during birth
- mother can have acute infection or chronic if she is immunocompromised
- The older the fetus, the higher the risk of fetal transmission
Clinical manifestations of congenital toxoplasmosis
FIRST TRIMESTER
- death, ophthalmologic and central nervous system consequences
SECOND TRIMESTER
- Classic triad (hydrocephalus, intracranial calcifications, chorioretinitis)
- rash (blueberry muffin)
- hepatosplenomegaly
- anemia
- lymphadenopathy
- microcephaly
- developmental delay
- visual problems and hearing loss
- seizures
THIRD TRIMESTER
- common, but often asymtpomatic at birth
Diagnosis of toxoplasmosis
IN FETUS
- Amniocentesis –> PCR
- maternal ELISA
IN BORN CHILD
- ophthalmologic examination
- CT
- Examine CSF for elevated protein and pleocytosis
Treatment of Toxoplasmosis
IN FETUS
- if mother is infected, but not fetus –> spiramycin to prevent infection
- when fetus is infected: give mother a combination of pyrimethamine, sulfadiazine, and folinic acid
BORN CHILD
- Pyrimethamine, sulfadiazine and folinic acid for at least 1 year
- if there is elevated protein concentration in CSF or severe chorioretinitis –> we can add corticosteroid like prednisolone
Congenital syphilis
- general information
- caused by T. pallidum
- transmitted via placenta
- can lead to spontaneous abortion, stillborth or to congenital syphilis
- can be infected at any developmental age
Classification of congenital syphilis
early congenital syphilis
–> develops in perinatal period, up to two years of age
Late congenital syphilis
–> develops after 2 years
Early congenital syphilis presentation
- vesiculobulbous eruptions
- maculopapular rash on palms, soles, nose, mouth and in diaper area
- lymphadenopathy, hepatosplenomegaly
- failure to thrive, fever, pneumonia
- blood-stained nasal discharge
- meningitis, choroiditis, hydrocephalus, seizures
- ascites
- within first 8 months: osteochondritis of the long bones and ribs can occur
Late congenital syphilis presentation
- gummatous ulcers (nose and septum)
- Hutchungton’s triad
1- Syphilitic keratosis
2- syphilitic conjunctivitis
3- Hutchington’s teeth - clutton’s joints, saddle nose, saber shins, high palate, palate perforation, frontal bone protusion, short maxilla, mandible protrusion
Diagnosis of early congenital syphilis
- clinical examination
- dark-field microscope
- lumbar puncture for CSF analysis
- Long bone and cest X-ray –> wimberger sign (symmetric erosions of upper tibtia and long bones)
- serologic testing
- -> treponemal test
- -> non-treponemal test
If NTT antibody titer >4 times the maternal titer, it indicates in most cases syphilis
Diagnosis of late congenital syphilis
- clinical history and examination
- positive serologic tests (same as in early CS)
- Hutchington’s triad is indicative
- poritive fluoroscent treponemal antibody absorption test
Treatment in early CS
- benzathiene benzylpenicillin G (BPG)
- alternatives: doxycycline, ceftriaxone, azithromycin
Treatment in late CS
- BPG
- if allergig: penicillin desensitization or doxycycline
Neurosyphilis treatment
- Benzylpenicillin
- second choice: ceftriaxone, probenecid
Treatment of CS in pregnancy
for early syphilis
- erythromycin
- azitromycin
- ceftriaxone
For late:
- erythromycin
DO NOT GIVE DOXYCYCLINE
Herpes simplex virus
- route of infection
- direct contact with infected lesions or mucosa
- neonates most oft4en thorugh an infected vaginal canal during birth
- c-section reduces risk of infection if there is active maternal sheddign of HSV
Herpes simplex virus
- clinical manifestations
- will present in firt 6 weeks of life
- presents in one of three ways:
- Neurological symptoms: meningoencephalitis (mostly after 10-14 days)
- Systemic symptoms: major overwhelming illnes including shock, respiratory failure and severe haptitis and coagulation disorders, sometimes meningoencephalitis
- Cutaneous symptoms: rash, blisters and keratoconjunctivitis in second week of life
Herpes simplex virus
- complications
- unctreated –> high morbidity and mortality
- recurrent skin outbreaks despite treatment
- neurologic outome for infants with CNS disease, even with treatment
Herpes simplex virus
- diagnosis
- serum HSV IgM
- HSV PCR
- HSV culture of a lesion
Herpes simplex virus
- treatment
- IV acyclovir
Rubella
- route of infection
- contact wiht respiratory secretions and transplacentally
Rubella
- clinical manifestations
- blueberry muffin rash
- lymphadenopathy
- hepatosplenomegaly
- thrombocytopenia
- interstitial pneumonitis
- intrauterine growth restriction
- infection after 12 weeks may have no clinical manifestations but is more likely to resilt in futre hearing loss and visual problems
- eye problems: microphthalmos, pigmentary retinopathy, cataracts and congenital glaucoma
- cardiac: pulmonic stenosis, patent ductus arteriosus
- Endocrine: DM
- Neurologic: developmental delay, encephalitis, hearing loss
Rubella
- diagnosis
- virus can be isolated from blood, urine, CSF, oral and nasal secretions –> culture
- serologic tseting for rubella-specific IgM and IgG in pregnant woman
- rubella-specific IgG positive, considered immune
Rubella
- treatment
- prevented by maternal vaccination, 2 doses of MMR vaccine
- no treatment of rubella outside of supportive measures
Varizella-Zoster Virus (VZV)
- route of infection
- respiratory droplets
- direct contact with skin lesions
- congenital varicella: transplacentally
VZV clinical manifestations
- early symptoms: cold symptoms, fever, abdominal pain, headaches, general malaise
- infection transmitted under 20 weeks: risk of fetus developing congenital varicella syndrome –> skin scarring, eye abnormalities, limb hypoplasia, cortical atrophy and microcephaly
- infection a week beofre or up to 28 days: high risk of fatal varicella
- Zoster immunoglobulin should be given immediatly to infants at high risk of congenital varicella
VZV diagnosis
- should be suspected in mother who presents with typical signs
- in an infant who presnts with typical vesicular lesions –> PCR or direct fluoroscent antibody of the fluid
- serology-speficic IgM and IgG antibodies in blood
VZV treatment
- pregnant women –> acyclovir
- infants born with congenital varicella –> acyclovir and varizella-zoster immunoglobulin
- vaccine (but not in pregnant women)
- pregnant women who are exposed to VZV_ varizella-zoster immunoglobulin
Cytomegalovirus (CMV)
- route of infection
- saliva
- genital secretions
- breast milk
- blood products
- transplacentally
CMV
- clinical presentation
- most infants are asymptomatic at birth
- petechiae
- jaundice
- hepatosplenomegaly
- thrombocytopenia
- small size
- microcephaly
- intracranial calcifications
- sensironeural hearing loss
- chorioretinitis
- seizures
CMV
- diagnosis
PRENATAL
- Ultrasound
- Amniocentesis
- Fetal blood sampling for IgM
POSTNATAL
- PCR or viral isolation in newborns under 3 weeks of age
- clinical signs
- liver panel: increased liver transaminases and bilirubin
- Blood count: thrombocytopneia and decreased platelets
- neuroimaging: calcifications, enlarged ventricles, polymicrogyria, lenticulostriate vasculopathy, white matter disease
Long term consequences of CMV
- hearing loss
- neurodevelopmental disablities
- cerebral palsy
- intellectual disability
- seizures
- ocular damage
CMV
- prevention and treatment
- hygiene measures for mothers
- pregnancy titers to identify at risk mothers
- ganciclovir, valganciclovir (oral)
- IV ganciclovir
- no vaccine available
Diabetic embryopathy
up to 9th week of gestation
- heart defects, skeletal defects, neuronal tube defects
- can be improved with pre-conception glycemic control
Diabetic fetopathy
from 9th week of gestation
- macrosomia in the 3rd semester
- birth weight over 4000g
- increased risk for labor complications: shoulder dystocia, asphyxia, birth injury
- transient hypoglycemia, congestive heart failure
late onset neonatal sepsis
- diagnosis
- blood culture
- PCR
- serum inflammatory biomarkers
- monitoring of physiological data, heart rate
Hematologic scoring system (HSS)
Based on follwing severn criteria:
- high values of total leukocyte count
- high PMN level
- elevated immature PMN count
- Elevated immature to total PMN ratio
- Immature to mature PMN ratio > 0.3
- platelet count > 150.000/mm3
- pronounced degenerative changes in PMNs
score > 2 –> likelyhood of sepsis
IL6 and IL8 in late neonatal sepsis
- they can be detected in blood early
- short half life
CRP in late neonatal sepsis
- best diagnostic marker
Pro-calcitonin and presepson in late neonatal sepsis
- more specific than CRP in bacterial infections
Additional investigations in late neonatal sepsis
- chest x-ray
- blood gas
- renal function test
- liver function test
- coagulation profile
late neonatal sepsis
- clinical presentation
- depends on virulence of pathogens
- body temperature may be elevated or depressed
- mtoro functions are reduced
- delayed weight gain
- pale skin
- reduction of activity
- cyanosis, apnea, tachycardia, bradycardia, hypotension
- jaundice sometimes only symptom
- CNS: drowsiness, irritability, lethargy, conculsions, increased tension at fontanelles
- GI: vomiting, diarrhea, anorexia, abdominal distension
- Cardiac: bradycardia, tachycardia, poor perfusion
- oliguria and anuria
late neonatal sepsis
- treatment
- empiric therapy until identification of the casative therapy
- usually vancomycin and an Aminoglycoside
- duration from 7 to 21 days
- supoortive therapy
late neonatal sepsis
- prevention
- universal GBS screening of all pregnant wimen at 35-37 weeks of gestation
- penicillin, ampicillin, cezazolin or clindamycin at least 4 hours before delivery
- breastfeeding
- administration of lactoferrin
- probiotics
late neonatal sepsis
- definition
- onset of manifestation after 72 hours of life
- during first 3 months: innate immune system provides defence against pahtogens
- Decreased function of neutrophils and lower concentration of immunoglobulins increase
susceptibility of infections.
late neonatal sepsis
- transmission
- horizontla: postnatally from hospital environment or from community
- hand contamination is most common
- parturition
late neonatal sepsis
- risk factors
- poor hygiene
- low birth weight
- prematurity
- invaisve ventilation
- prolonged use of antibiotics
- breakage of natural barriers
- H2 receptor antagonists
late neonatal sepsis
- microorganisms
Group B streptococcus and coagulase negative staphylococcus (S.aureus, especially in neonates with vascular access catheters) • Gram negative organisms • Gram positive organisms • Acinetobacter spp • Klebsiella • E. coli • Candida spp. (Candida parapsilosis) • Herpes simplex virus • Enterovirus
Infrequent • Streptococcus pyogenes • Neisseria gonorrhoeae • Enterococcus faecalis • Streptococcus pneumoniae
Early onset neonatal sepsis
- definition
- day 0-3
- most present in first 24 hours
- most rapid onset is in premature neonates
Early onset neonatal sepsis
- route of infection
- blood, placenta, ascending cervical infection
- neonate bay be exposed to mother’s Genitourinary tract during birth (Group B streptococci, E. coli, coagulase negative staphylococci, H. influenza, L. monocytogenes)
Early onset neonatal sepsis
- prophylaxis
- intrapartum prophylactic antibiotic treatment in mothers
- GBS screening in weeks 35 and 37
- culture obtained with vaginal and anal swabs
- delivering baby wihtin 12 to 24 hours of then membrane breaks
Early onset neonatal sepsis
- treatment
- combination of IV glycosides with expanded spectrum penicillin
- specific antibiotics are chosen based on mothers history and trends of organism colonization and susceptibility
Early onset neonatal sepsis
- diagnosis
- blood tests: CBC, CPR, blood culture
- skin and stool cultures
- lumbar puncture (CSF)
Early onset neonatal sepsis
- clinical presentatio
- general: lethary, hypothermia, poor feeding
- non-specific signs: anuria and acidosis
- Respiratory symptoms: apnea, tachypnea, nasal flaring
- Cardiac symtpoms: cyanosis, desaturation, bradycardia
preterm infants: apnea, bradycradia, cyanosis as first signs
