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PATRICK DUFF, M.D. UNIVERSITY OF FLORIDA PREVENTION OF

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PATRICK DUFF, M.D. UNIVERSITY OF FLORIDA PREVENTION OF CONGENITAL CMV INFECTION Vaccine is not commercially available Anti-viral drugs do not prevent fetal injury ... – PowerPoint PPT presentation

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Title: PATRICK DUFF, M.D. UNIVERSITY OF FLORIDA PREVENTION OF


1
CONGENITAL INFECTIONS
  • PATRICK DUFF, M.D.
  • UNIVERSITY OF FLORIDA

2
CONGENITAL INFECTIONSOVERVIEW
  • Rubella
  • CMV
  • Parvovirus
  • Toxoplasmosis

3
CONGENITAL INFECTIONSOVERVIEW
  • Epidemiology and pathophysiology
  • Manifestations of congenital infection
  • Diagnosis of congenital infection
  • Prevention and treatment

4
CONGENITAL INFECTIONSKEY QUESTIONS
  • Manifestations of congenital infection
  • Most valuable diagnostic tests
  • Prevention and treatment

5
CONGENITAL INFECTIONSBIG PICTURE
  • Maternal infection in the first half of
    pregnancy, particularly the first trimester,
    poses the greatest risk to the fetus
  • Organisms reach fetus by hematogenous
    dissemination across the placenta

6
RUBELLAEPIDEMIOLOGY
  • RNA virus
  • Only a single serotype
  • Occurs primarily in children and adolescents
  • Most highly teratogenic of essentially all
    organisms

7
RUBELLAEPIDEMIOLOGY
  • With licensure of an effective vaccine in 1969,
    the frequency of infection has declined by 99
  • Accordingly, congenital infection is extremely
    rare

8
RUBELLAPATHOPHYSIOLOGY
  • Transmission is by respiratory droplets
  • Respiratory tract --gtcervical lymph
    nodes--gthematogenous dissemination
  • Incubation period is 2 to 3 weeks

9
RUBELLACLINICAL MANIFESTATIONS
  • Malaise
  • Headache
  • Myalgias and arthralgias

10
RUBELLACLINICAL MANIFESTATIONS
  • Post-auricular adenopathy
  • Conjunctivitis
  • NON-PRURITIC, ERYTHEMATOUS, MACULOPAPULAR RASH

11
RUBELLACLINICAL MANIFESTATIONS
12
RUBELLACLINICAL MANIFESTATIONS
13
RISK OF CONGENITAL RUBELLA

Time of Maternal Infection
14
MANIFESTATIONS OF CONGENITAL RUBELLA

15
CONSEQUENCES OF CONGENITAL RUBELLA
  • Only 25 attend mainstream schools
  • Estimated lifetime cost of caring for an affected
    child - 300,000

16
OBSTETRIC MANAGEMENT OF CONGENITAL RUBELLA
  • Diagnosis is by ultrasound
  • Management options
  • Pregnancy termination
  • Expectant management

17
PREVENTION OF CONGENITAL RUBELLA
  • Vaccination
  • Avoidance of exposure if susceptible

18
CMVEPIDEMIOLOGY
  • DNA virus
  • Humans are only host
  • May remain latent in host cells

19
CMVEPIDEMIOLOGY
  • Horizontal transmission
  • Vertical transmission
  • In utero greatest danger
  • During delivery minimal risk
  • Breast feeding minimal risk

20
CMVCLINICAL MANIFESTATIONS
  • Malaise
  • Fever
  • Lymphadenopathy
  • Hepatosplenomegaly
  • More severe manifestations if patient is
    immunosuppressed

21
CMV DIAGNOSIS
  • Cytology
  • Serology
  • IgM and IgG
  • IgG avidity
  • Culture
  • PCR
  • Urine and blood

22
CONGENITAL CMVDETERMINANTS OF FETAL RISK
  • Primary vs recurrent maternal infection
  • Trimester of exposure

23
CONGENITAL CMV DETERMINANTS OF FETAL RISK
  • THE GREATEST RISK IS ASSOCIATED WITH PRIMARY
    MATERNAL INFECTION IN THE FIRST HALF OF PREGNANCY

24
CONGENITAL CMVDETERMINANTS OF FETAL RISK
  • Recurrent maternal infection poses much less risk
    to fetus
  • Infection acquired during delivery or via breast
    feeding poses negligible risk

25
RISK OF CONGENITAL CMV WITH PRIMARY MATERNAL
INFECTION
  • 1 to 4 of pregnant women seroconvert?
  • 40 - 50 of fetuses are infected?
  • 5 - 15 of these fetuses will be symptomatic at
    birth

26
OUTCOME OF PRIMARY CMV INFECTION

27
MANIFESTATIONS OF SEVERE CONGENITAL CMV INFECTION
  • Hepatosplenomegaly
  • Intracranial calcifications
  • Jaundice
  • Growth restriction
  • Chorioretinitis
  • Hearing loss

28
SEVERE CONGENITAL CMV INFECTION
29
SEVERE CONGENITAL CMV INFECTION
Blueberry Muffin Baby
30
RISK OF CONGENITAL CMV WITH RECURRENT MATERNAL
INFECTION
  • Only 5 - 10 of infants become infected
  • None are symptomatic at birth
  • Late sequelae include hearing and visual defects
    and developmental delays

31
DIAGNOSIS OF CONGENITAL CMV INFECTION
  • Amniocentesis
  • Viral culture
  • PCR
  • Ultrasound

32
ULTRASOUND DIAGNOSIS OF CMV INFECTION
33
ULTRASOUND DIAGNOSIS OF CMV INFECTION
34
PREVENTION OF CONGENITAL CMV INFECTION
  • Vaccine is not commercially available
  • Anti-viral drugs do not prevent fetal injury
  • Anti-CMV antibody may be effective
  • Key to prevention is universal precautions

35
PARVOVIRUSEPIDEMIOLOGY
  • DNA virus
  • Only a single serotype exists
  • Humans are only known host

36
PARVOVIRUSEPIDEMIOLOGY
  • Transmission is by respiratory droplets and by
    blood
  • Incubation period is 4 to 20 days

37
PARVOVIRUSCLINICAL MANIFESTATIONS
  • Erythema infectiosum (fifth disease)
  • Transient aplastic crisis

38
PARVOVIRUSERYTHEMA INFECTIOSUM
39
PARVOVIRUSERYTHEMA INFECTIOSUM
40
CONGENITAL PARVOVIRUSPATHOPHYSIOLOGY
  • Virus crosses the placenta and destroys red cell
    precursors
  • Fetal anemia --gt high output congestive heart
    failure --gt hydrops fetalis
  • Virus also directly injures myocardial cells

41
RISK OF CONGENITAL PARVOVIRUS INFECTION

Time of Maternal Infection
42
PARVOVIRUS INFECTIONDIAGNOSIS IN THE MOTHER
43
DIAGNOSIS OF CONGENITAL PARVOVIRUS INFECTION
  • Ultrasound
  • Identification of hydrops
  • MCA doppler velocimetry

44
TREATMENT OF CONGENITAL PARVOVIRUS INFECTION
  • Intrauterine transfusion ? fetal umbilical vein

45
CONGENITAL PARVOVIRUSPROGNOSIS
  • If infant survives the hydropic state, the
    long-term prognosis is usually favorable

46
TOXOPLASMOSISEPIDEMIOLOGY
  • Toxoplasma gondii is a protozoan
  • Organism exists in three forms
  • Trophozoite
  • Cyst
  • Oocyst

47
TOXOPLASMOSISEPIDEMIOLOGY
48
TOXOPLASMOSISCLINICAL MANIFESTATIONS
  • Most infections are asymptomatic
  • When symptoms are present, they mimic
    mononucleosis

49
TOXOPLASMOSISCLINICAL MANIFESTATIONS
  • Toxoplasmosis may cause devastating infection in
    patients who are immune deficient
  • Chorioretinitis
  • CNS infection ? brain abscess

50
TOXOPLASMOSISDIAGNOSIS
  • Histology
  • PCR
  • Serology
  • IgM antibody
  • IgG antibody

51
CONGENITAL TOXOPLASMOSIS
  • The key danger is primary toxoplasmosis infection
  • Greatest risk to the fetus results from maternal
    infection in first half of pregnancy
  • Approximately 40 of fetuses will be infected
    when primary maternal infection develops at lt 20
    weeks gestation

52
MANIFESTATIONS OF CONGENITAL TOXOPLASMOSIS
  • Hepatosplenomegaly
  • Chorioretinitis
  • CNS injury
  • Seizures
  • Mental retardation

53
DIAGNOSIS OF CONGENITAL TOXOPLASMOSIS
  • Amniocentesis - PCR
  • Ultrasound

54
TREATMENT OF CONGENITAL TOXOPLASMOSIS
  • Treatment of mother while fetus is still in utero
  • Early treatment of the infant

55
PREVENTION OF CONGENITAL TOXOPLASMOSIS
  • Use precautions when handling cat litter box
  • Do not eat inadequately cooked meat

56
CONGENITAL INFECTIONSCONCLUSIONS
  • Congenital rubella key is prevention by
    universal vaccination
  • Congenital CMV key is prevention of exposure in
    pregnancy and treatment with hyperimmune globulin
    if fetus is infected

57
CONGENITAL INFECTIONSCONCLUSIONS
  • Congenital parvovirus avoidance of exposure is
    difficult, but intrauterine transfusion is
    life-saving

58
CONGENITAL INFECTIONSCONCLUSIONS
  • Congenital toxoplasmosis
  • Avoid exposure during pregnancy
  • Treat infected mother during pregnancy
  • Treat neonate after delivery
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