Infections in Pregnancy

INFECTIONS IN PREGNANCY Dr. Irma Lee March 2, 2012 Transcribed by: Paula Siongco 3D-2013 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 – ytomegalov
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  INFECTIONS IN PREGNANCY Dr. Irma Lee March 2, 2012 Transcribed by: Paula Siongco 3D-2013 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 4.   Recurrent HSV      Analgesia    Hygiene    Antiviral    Suppression therapy 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   MATERNAL PRIMARY VARICELLA    Pneumonitis    Bacterial superinfection (cellulitis, abscess formation) 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” Im mune
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