1. Neonatal Varicella:
1.1. العنقز
1.2. slide 15
1.3. Treated by Acyclovir
2. Herpes Simplex Virus (HSV):
2.1. slide 29
2.2. Treated by high dose of Acyclovir
3. Mnemonic:
3.1. TORCH
3.1.1. Toxoplasmosis
3.1.2. Other (syphilis ,parvovirus &VZV)
3.1.2.1. New Node
3.1.3. Rubella
3.1.4. CMV
3.1.5. Herpes( Hepatitis &HIV)
4. CytoMegaloVirus (CMV):
4.1. Most common congenital viral infection~40,000 infants per year.
4.2. Mild, self limiting illness
4.3. # one of the most common cause of deafness in children is congenital CMV - the problem it's Asympyomatic so if pt, does not present at birth with infection does not mean the pt. is not infected with CMV that's why we do screening !
4.4. Epedemiology:
4.4.1. Transmission can occur with primary infection or reactivation of virus but 40% risk of transmission in primary infection
4.4.2. Increased risk of transmission later in pregnancy but more severe sequalae associated with earlier acquisition
4.5. Clinical presentation:
4.5.1. 90% are asymptomatic at birth
4.5.2. Up to 15% develop symptoms later
4.5.3. periventricular calcifications
4.5.4. Microcephaly, neurological deficits, HSM, petechiae, jaundice, chorioretinitis
4.5.5. >80% develop long term complications:
4.5.5.1. Hearing loss
4.5.5.2. vision impairment
4.5.5.3. developmental delay
4.6. Diagnosis
4.6.1. � Maternal IgG shows only past infection
4.6.2. � Viral isolation from urine or saliva in 1st 3 weeks of life
4.6.3. � Viral load and DNA copies can be assessed by PCR
4.6.4. � Detection of Cytomegalic Inclusion bodies in affected tissue
4.6.5. � Serologies not helpful given high antibody in population
4.7. Treatment & Prevention
4.7.1. Ganciclovir x6wks in symptomatic infants
5. Rubella
5.1. German measles
5.1.1. الحصبة الألمانية
5.2. R=rubella , RNA enveloped virus, member of the togaviridae family.
5.3. Spread by respiratory droplets and transplacentally.
5.4. - what's Rubella party? when a girl get Rubella she invite her relatives so that they all get rueblla bcoz it's mild disease and give immunity, but if she get it when she become married and pregnant she may transmit it to the baby which is harmful to the baby.
5.5. Epidemiology:
5.5.1. Vaccine-preventable disease
5.5.2. No longer considered endemic.
5.5.3. Mild, self-limiting illness
5.5.4. Infection earlier in pregnancy has a higher probability of affected infant (first 12 wks 70% and 13-16 wks 20% and rare >16 wks of pregnancy)
5.6. Clinical Features:
5.6.1. Cataracts, glaucoma
5.6.2. Cardiac malformations
5.6.3. Neurologic (less common)
5.6.4. Others to include growth retardation, bone disease, HSM, thrombocytopenia,
5.6.5. "blueberry muffin” lesions
5.6.6. Sensorineural hearing loss (most common)
5.7. Diagnosis:
5.7.1. � Maternal IgG is useless! � Viral isolation virus from nasal secretions, throat, blood, urine, CSF. � Serologic testing. IgM = recent postnatal or congenital infection. � Rising monthly IgG titers suggest congenital infection.
5.8. Rx & Prevention:
5.8.1. Supportive care only with parent education
5.8.2. Prevention by immunization
5.8.3. Maternal screening
5.8.4. Vaccinate if not immune (avoid pregnancy for three months)
6. Parvovirus B 19
6.1. Causative agent of Fifth disease (also called erythema infectiosum = redness in the face)
6.1.1. fifth disease is so named because it was the fifth childhood disease characterized by a rash to be identified. Measles was first, followed by scarlet fever, rubella, and chicken pox. Fifth is the only one still identified by its number, though the official viral name is human parvovirus B19.
6.1.1.1. Source: http://mamasoncall.com/2010/01/why-is-it-called-fifth-disease/
6.2. Spread by the respiratory route, blood and transplacental
6.3. Epidemiology:
6.3.1. Most of the population is eventually infected.
6.3.2. Half of women of childbearing age are susceptible to infection.
6.3.2.1. New Node
6.3.3. Risk of fetal death highest when infection occurs during the second trimester of pregnancy (1st 20 wks of pregnancy (12%).
6.3.4. Minimal risk to the fetus if infection occurred during the third trimesters of pregnancy
6.4. Clinical Faeture:
6.4.1. Known to cause fetal loss through hydrops fetalis; severe anaemia, congestive heart failure, generalized oedema and fetal death.
6.4.1.1. New Node
6.4.2. No evidence of teratogenecity
6.5. Diagnosis
6.5.1. Serology IgM, persistant IgG , PCR , US
6.6. Treatment:
6.6.1. intrauterine transfusions
6.6.2. administration of digoxin to the fetus.
6.6.3. no specefic Rx for the infection
7. Syphilis
7.1. Etiology:
7.1.1. Treponema pallidum (spirochete)
7.2. Transmission:
7.2.1. Transmitted via sexual contact
7.2.2. Mother with primary or secondary syphilis
7.2.2.1. Typically occurs during second half of pregnancy
7.3. Clinical Presentation:
7.3.1. IntraUterine death in 25%
7.3.2. 3 major classifications
7.3.2.1. see slide 9
7.3.2.2. interstitial Keratitis
7.3.2.2.1. Corneal scarring
7.3.2.3. Hutchinson teeth
7.3.2.4. 8th Nerve deafness
7.4. Treatment
7.4.1. Penecillin G
7.5. Diagnosis:
7.5.1. 1. RPR/VDRL: non-treponemal test
7.5.1.1. (RPR) Rapid plasma reagin
7.5.1.2. New Node
7.5.2. 2. MHA-TP/FTA-ABS: specific treponemal test
7.5.2.1. (FTA-ABS) The fluorescent treponemal antibody absorption
7.5.2.2. (MHA-TP) microhemagglutination assay - Treponema pallidum
7.5.2.3. New Node
7.5.3. 3. Confirmed if T. pallidum identified in skin lesions, placenta, umbilical cord, or at autopsy.
7.6. Prevention:
7.6.1. RPR/VDRL screen in ALL pregnant women early in pregnancy and at time of birth
8. Toxoplasmosis
8.1. Parasite
8.2. Toxoplasma gondii
8.3. Transmission
8.3.1. Definitive host is the domestic cat
8.3.1.1. dry stool of the cats contains oocysts whcih may become areuloised (fly in the air) the pregnant may smell it !! so pregnants shouldn't clean the cats stool , especially if it's dry!
8.3.2. Ingestion of cysts (meats, garden products)
8.3.3. Can be transmitted from the mother to the baby
8.4. Clinical presentation
8.4.1. Mostly asymptomatic
8.4.2. Classic Triad
8.4.2.1. Chorioretinitis
8.4.2.2. Hydrocephalus
8.4.2.3. Intracranial calcifications
8.4.3. Other symptoms include fever, rash, HSM, microcephaly, seizures, jaundice, thrombocytopenia, lymphadenopathy
8.5. Infection (Transmission) rate higher with infection in 3rd trimester
8.5.1. This is mercy from Allah bcoz the transmisson is higher when the risk is low in the baby (3rd trimester where the baby already has organogenesis)
8.6. Fetal death higher with infection in 1st trimester
8.7. more in European countries (ie France, Greece)
8.8. Diagnosis
8.8.1. 1. Maternal serology IgM/IgA , IgG.
8.8.2. 2. Fetal tissue culture, PCR. and Ultrasound
8.8.3. 3. Newborn - Serology - Culture - PCR
8.9. Treatment:
8.9.1. 1. Spiramycin
8.9.1.1. it's Macrolide antibiotic
8.9.2. 2. Pyrimethamine and sulfadiazine
8.10. Question:
8.10.1. Q: mother exposed to cat durging pregnancy and her infant has Intracranial calcifications what's the most likey organism? - Toxoplasmosis - Rubella A: Toxoplasmosis bcoz of cat exposure !
8.11. Prevention
8.11.1. Avoid exposure to contaminated food or water and undercooked meat
8.11.2. Hand washing