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TOXOPLASMOSIS Acute toxoplasmosis during pregnancy is rare Acquired through ingestion of encysted organisms in raw or undercooked meat or through contact with infected cat feces or contaminated soil Overall risk of having affected child o 2% - 1 st trimester o 10% - 28 weeks o 4% - at term Diagnosis Maternal signs and symptoms o Non-tender posterior cervical adenopathy and flu-like
TOXOPLASMOSIS Acute toxoplasmosis during pregnancy is rare Acquired through ingestion of encysted organisms in raw or undercooked meat or through contact with infected cat feces or contaminated soil Overall risk of having affected child o 2% - 1 st trimester o 10% - 28 weeks o 4% - at term Diagnosis Maternal signs and symptoms o Non-tender posterior cervical adenopathy and flu-like
TOXOPLASMOSIS Acute toxoplasmosis during pregnancy is rare Acquired through ingestion of encysted organisms in raw or undercooked meat or through contact with infected cat feces or contaminated soil Overall risk of having affected child o 2% - 1 st trimester o 10% - 28 weeks o 4% - at term Diagnosis Maternal signs and symptoms o Non-tender posterior cervical adenopathy and flu-like
Goals in Pregnancy: Reduce risk of congenital structural abnormalities/deformities Optimize health care to minimize effects of vertical transmission Avoidance of horizontal transmission to health care providers Prevention
TORCH SYNDROME T oxoplasma O thers (Varicella zoster virus, Hepatitis, Parvovirus, HIV, Group B Streptococcus) R ubella C ytomegalovirus H epatitis virus
TOXOPLASMOSIS Acute toxoplasmosis during pregnancy is rare Acquired through ingestion of encysted organisms in raw or undercooked meat or through contact with infected cat feces or contaminated soil Overall risk of having affected child o 2% - 1 st trimester o 10% - 28 weeks o 4% - at term
Diagnosis Maternal signs and symptoms o Non-tender posterior cervical adenopathy and flu-like symptoms Serologic Test for Immunoglobulin G and M antibodies o IgG appears 1-2 weeks of infection and peaks between 6- 8 weeks o IgM - appears within 1 st week of infection then declines over several months and may persist for years PCR testing of amniotic fluid o Most accurate method to test for fetal infection o Done on 2 nd trimester or 4 weeks after an acute maternal infection
CONGENITAL TOXOPLASMOSIS Sonographic abnormalities o Ventricular dilatation (75%) o Intracranial calcifications (18%) o Increased placental thickness (32%) o Hepatosplenomegaly (14%) o Fetal ascites (15%) o Pericardial or pleural effusions o Microcephaly (5%) At birth maculopapular rash, hepatosplenomegaly, seizures, convulsions Blindness, deafness, mental retardation
Treatment Spiramycin (3-4 g/day) o Concentrates in the placenta o Given once maternal infection is confirmed until delivery Pyrimethamine (25-100mg PO QID) and Sulfadiazine (1-1.5g PO QID) and Solinic acid 10-25mcg o Given once fetal infection is confirmed o Both are folic acid antagonists and cross the placenta and penetrate the fetal brain and cerebrospinal fluid
RUBELLA A mild viral illness with 30% of mothers being asymptomatic or with a mild 3-day rash with potential auricular adenopathy Transmission: Airborne Diagnosis: Serologic testing of IgM or IgG antibody titer which becomes positive 4 weeks after exposure
CONGENITAL RUBELLA Risk of major fetal damage varies with the time of maternal infection: o 80-90% - first 3 months o 10% - >4 months o 6% - >5 months o No risk thereafter Congenital heart (patent ductus arteriosus), cataract, deafness Microcephaly Mental retardation
Prevention MMR children 12-15 months of age and at school age; non-pregnant women and ALL women at reproductive age group NO TREATMENT
CYTOMEGALOVIRUS Most common cause of viral intrauterine infection affecting 0.5- 2.5% of all neonates Infection can occur in-utero, intrapartum and through breast milk Transmission: Contact with body fluids or sexual contact 40% of pregnant women with primary infection CONGENITAL CMV 1-2% of newborn are CMV infected from primary maternal CMV or reactivation of prior infection
CONGENITAL CMV 85-90% of infected are asymptomatic at birth 5-10% unilateral/bilateral hearing impairment Blueberry muffin baby Other symptoms/signs: o Jaundice, thrombocytopenia, hepatosplenomegaly, chorioretinitis, deafness, microcephaly, mental retardation, or death due to DIC and sepsis
CMV INFECTION 4-8 weeks incubation period Viremia between 3-12 months Infected fetus shed virus up to 6 years Viral transmission via primary or recurrent maternal infection Rate of transmission increases with gestational age; highest at 3 rd
trimester Severity of disease is inversely proportional to gestational age Neonatal CMV through breast milk does not lead to visceral or neurological sequelae
Primary Maternal Infection (CMV IgM + or PCR +)
30-40% fetal infection (CMV PCR + in AF) 90% asymptomatic at birth 10- 15% develop abnormalities 10% symptomatic at birth 85-90% develop abnormalities
RECURRENT INFECTION Occur with immunosuppressive and during pregnancy Recurrent infection during pregnancy are often asymptomatic and primarily caused by reactivation of the endogenous virus or low grade chronic infection or reinfection by a different strain of CMV Risk of vertical transmission is 0.5-2% Risk of CMV congenital infection is only 0.5% Neonates infected from recurrent infection has <8% risk of hearing loss and chorioretinitis
Diagnosis Usually asymptomatic or with mononucleosis-like or flu-like symptoms Presence of symptoms or abnormal laboratories highly suggestive of primary infection CMV screening not routinely recommended IgM and IgG screening at 8-12 weeks AFP PCR for CMV to detect in-utero infection
NEONATAL CMV INFECTION CMV virus in AF by PCR at 21 weeks at 6 weeks interval Ultrasound findings o Ventriculomegaly o Oligohydramnios o Echogenic bowel o Choroid plexus cyst o Pleural effusion o Brain/liver calcifications
Role of CMV specific Hyperimmune Globulin For mothers with primary CMV to reduce maternal systemic or placental viral loads Reduce placental and fecal inflammation in infected fetuses increase fetal blood flow with enhanced fetal nutrition and oxygenation
Prevention Hygiene avoid direct contact with children, frequent hand washing, glove use Live-attenuated CMV vaccine Glycoprotein B construct vaccine
HERPES SIMPLEX VIRUS Recurrent STD caused by o HSV-1: 90% oral, 10% genital o HSV-2: 10% oral, 90% genital Ulceration in genitalia with severe local pain, dysuria, sacral paresthesia, tender inguinal lymph nodes, fever, malaise
PRIMARY FIRST EPISODE HSV confirmed in a person without prior HSV-1 or HSV-2 antibodies 2-4% of IgG negative women seroconvert (acquire) to HSV-1 or HSV-2 during pregnancy No fetal consequences unless convert shortly before labor and delivery
NON-PRIMARY FIRST EPISODE HSV-2 confirmed with prior findings of HSV-1 antibodies or vice-versa 1.5-2% of HSV-1 IgG + women seroconvert to HSV-2 Risk of conversion from HSV-2 IgG + to HSV-1 + <1% Symptoms milder
RECURRENT GENITAL HERPES Caused by reactivation of latent HSV usually HSV-2 20-30% of pregnant women are IgG+ for HSV-2 with intermittent shedding from vaginal mucosa Virions travel from the skin or mucosa to the sensory dorsal root ganglion where latency established Viral replication recurrent clinical outbreaks Trauma, UV radiation, extreme temperature, stress, hormonal fluctuations, immunosuppression
Risk of Fetal Transmission Maternal-fetal transmission of HSV via contact with infected genital secretions 40-50% neonatal HSV infection if delivery occurs during primary infection 0-3% neonatal HSV infection occurs during recurrent infection Sites of intrapartum viral entry are the fetal eye, nasopharynx, or break in the skin
NEONATAL HSV INFECTION First episode primary infection microcephaly, ventriculomegaly, spasticity, echogenic bowel, hepatosplenomegaly, flexed extremities 30% of infants die 40% neurogenic sequelae
Diagnosis History Maternal signs/symptoms HSV culture 48-72 hours at appearance of lesions Serologic testing PCR assay of genital lesions Tzanck smear multinucleated giant cells and viral inclusions
Prevention Avoid sexual contact with infected individuals Condoms Suppression decreases recurrent genital lesions at term, and viral shedding
Anti-viral Drugs Acyclovir (Zovirax) inhibits viral thymidine kinase, crosses placenta but safe Valacyclovir (Valtrex) prodrug of acyclovir, better absorption, longer half-life, decrease shedding Fanciclovir prodrug of Penciclovir, no specific studies in pregnancy
Management 1. Primary HSV Analgesia Hygiene Antiviral Acyclovir 400mg PO TID 7-14 days or Valacyclovir 1g PO 7-14 days Suppression Acyclovir 400mg PO BID or Valacyclovir 500mg PO OD at 36 weeks to delivery
2. First episode within 6-12 weeks of delivery IV Acyclovir intrapartum to both mother and neonate Daily Acyclovir or Valacyclovir from 36 weeks until delivery
3. Complicated CMV infection IV Acyclovir 5-10mg/kg BW q 8 hours until improved followed by oral antiviral drug for 10 days
Mode of Delivery With active lesions at term CS PPROM remote from term Expectant Cesarean delivery should not be offered solely for a history of HSV
VARICELLA-ZOSTER VIRUS A double-stranded DNA. Herpes virus acquired in childhood Primary infection manifests as Varicella (chickenpox) Herpes Zoster (shingles) is an eruption from reactivation of latent HSV infection of dorsal root ganglia Transmission: Direct contact and respiratory droplet
Diagnosis Varicella Maculopapular vesicular pruritic lesions Herpes Zoster Painful lesions over sensory nerve root distribution Laboratory diagnosis: o ELISA VZV IgI titer o Tissue culture o Tzanck smear o Direct fluorescent antibody test o Nucleic acid amplification test
CONGENITAL VARICELLA SYNDROME Occurs in 2% when mothers have the infection <20 weeks Varicella Embryopathy (cutaneous scar, denuded skin, limb hypoplasia, muscle atrophy, rudimentary digits, microcalcephaly, intracranial calcification, cortical atrophy, cataracts, chorioretinitis, mocrophthalmia, psychomotor retardation)
NEONATAL VZV INFECTION Fetal exposure just before or during delivery result in 25-50% of cases Varicella Zoster Immune Globulin to neonates whose mother developed Varicella 5 days before to up to 2 days post delivery
Treatment Supportive care Acyclovir 500mg q8 hours for complicated varicella or immunocompromised Varicella Zoster Immune globulin up to 96 hours post exposure
Prevention Varivax not recommended to pregnant women
HEPATITIS A Caused by RNA virus transmitted by fecal-oral route Average incubation period is 28 days with symptoms lasting 2 to 6 months Children are usually asymptomatic in contrast to adults who are always symptomatic Prevalent in areas with poor sanitation and closed-living conditions Occurs in <1:1000 pregnancies
Risks of acquiring HAV Travel to prevalent countries Homosexuals IV drug users Working with non-human primates Chronic liver disease
Management in Pregnancy Supportive No perinatal transmission
HEPATITIS B Most common form of viral hepatitis in pregnancy Caused by DNA virus transmitted parenterally and sexual contact Acute hepatitis occurs in 1-2:1000 pregnancies in the US Chronic carrier state occurs in 6- 10:1000 pregnancies Incubation period is 60 to 90 days
Risk Factors Perinatal transmission highest risk of chronic HBV infection Sexual contact IV drug users STDs Multiple sexual partners House contacts Mental institutions/prisons Acupuncture HBV infected at high risk of HIV and HCV infections
Pathophysiology Incubation period depends on viral exposure than laboratory changes Antigens o S Surface infected if present >6 months; Chronic HBV infection o c Core o e Infectious Antibodies o S Immune o C covers window period, usually precedes HbsAb conversion
Pregnancy Considerations Vertical transmission is high when laboratory is as follows: o HbsAg + 10-20% o HbsAg + HbeAg + 80-90% Vertical transmission is trimester related o 10% first trimester o 80-90% third trimester Only 10% is transmitted transplacental, hematogenous or thru breastfeeding
ACUTE HEPATITIS B IN PREGNANCY Document conversion of HBsAg to + Outpatient supportive therapy If with co-morbidities like bilirubin 15mg/dL Vit K 10mg/IM q8 hrs for 3 doses Consider interferon
Exposure to HBV during Pregnancy If HBsAg (-) and HBsAb (-) HBIg and HB vaccine (prevents .5% of transmission) HBIg must be given within 14 days of exposure
Vertical Transmission Prevention All newborns of mothers HBsAg+ should receive HBIg and HB vaccine within 12 hours of birth 95% prevention of neonatal HBV
HEPATITIS C Caused by RNA virus acquired via infected blood, sexual contact or mother-to-infant (vertical transmission) Incubation period: 30 to 60 days Complications: Cirrhosis and Hepatocellular Carcinoma
Definition of types of HCV infection HCV: HCVAb (+) Chronic HCV: HCVAb (+) and HCV RNA (+) Chronic Active HCV: HCVAb (+) and HCV RNA (+) and increased LFTs
Risk factors for HCV infection BT or exposure to blood products IV drug users Multiple sexually transmitted disease HIV infection Multiple sexual partners History of body piercing or tattooing Organ transplant: Berone 1992 Unexplained elevated transaminases Patient or staff involved in chronic dialysis programs Participant in in-vitro fertilization program from anonymous donors
Prevention Avoid risk factors Prevent complications by avoiding alcohol and hepatotoxic medicine and foods
Effects of Pregnancy on Hepatitis C Pregnancy DOES NOT affect the clinical course of acute or chronic Hepatitis C Linear increase in HCV viremia throughout pregnancy Chronic Hepatitis C associated with increased preterm delivery and IUGR Long term effects cirrhosis, cancer, death
Therapy No approved treatment of HCV infection during pregnancy No HCV vaccine or Ig Pegylated interferon and ribavirin eradicated virus >50% in non- pregnant women