Documents

Infections in Pregnancy

Description
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
Categories
Published
of 5
All materials on our website are shared by users. If you have any questions about copyright issues, please report us to resolve them. We are always happy to assist you.
Related Documents
Share
Transcript
  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
We Need Your Support
Thank you for visiting our website and your interest in our free products and services. We are nonprofit website to share and download documents. To the running of this website, we need your help to support us.

Thanks to everyone for your continued support.

No, Thanks
SAVE OUR EARTH

We need your sign to support Project to invent "SMART AND CONTROLLABLE REFLECTIVE BALLOONS" to cover the Sun and Save Our Earth.

More details...

Sign Now!

We are very appreciated for your Prompt Action!

x