Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Microbiology - Path > Viral infections in pregnancy > Flashcards

Viral infections in pregnancy Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

What are the different presentations and potential organisms that cause the following;

  1. Congenital infections
A
  1. Congenital infection:

Manifestations:

  • Growth retardation - low birth weight
  • Congenital malformations
  • Fetal loss - still births

Organisms:

  • CMV
  • HIV
  • Toxoplasma gondii
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the different presentations and potential organisms that cause the following;

  • Perinatal infections:
A

Manifestations;

  • Meningitis
  • Septicemia
  • Pneumonia
  • Preterm labour

Organisms:

  • Neisseria gonorrohoea
  • Chlanydia trachomatis
  • HSV
  • Group B strep
  • E.coli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the different presentations and potential organisms that cause the following;

  • Post natal infection
A

Manifestation:

  • Meningitis
  • Septicemia
  • Conjuctivitus
  • Pnuemonitis

Organisms;

  • breast milk –> HIV, CMV, HBV
  • Umbilicus –> staph aureus, tetanus
  • Person to person –> Group B strep, listeria monocytogenes, e.coli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What type of virus is Rubella?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the pathogenesis of the rubella virus causing tetraogenicity?

A
  • Decrease in the rate of cell division (structural malformations)
  • Decrease in overall number of cells (small babies)
  • Interference with development of key organs
  • Tissue necrosis due to virus replication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the signs and symptoms of congenital rubella syndrome

A
  • Sensorineural hearing loss – commonest sequelae
  • Other neurologic problems
    • psychomotor /mental retardation
    • Meningoencephalitis
    • Microcephaly, intracranial calcifications
  • Ophthalmic problems
    • cataract, glaucoma
    • retinopathy, microphthalmia
  • Intrauterine growth retardation
    • Congenital heart defects such as patent ductus arteriosus and others
  • Hepatosplenomegaly
  • Thrombocytopaenic purpura
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the timing of the maternal infection with rubella, and the risks to the fetus to developing congenital abnormalities - and what will be affected

  • 0-12 weeks
  • 13-20 weeks
  • >20 weeks
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  1. How is an acute infection with rubella diagnosed?
  2. How is an immune status screen for rubella done?
A
  1. Diagnosis of acute infection
  • Rubella IgG
    • Seroconversion
    • Avidity
  • Rubella IgM
  • Detection of virus
    • Molecular diagnosis (PCR)
    • Respiratory secretions, blood, urine, tissues
  1. Immune status screen:
    * Rubella IgG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What should be done if there is a pre-natal diagnosis of Rubella in the mother?

A

All cases of symptomatic rubella infection in the first gestational trimester should be considered for termination of pregnancy without prenatal diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How can Rubella be prevented?

A

Vaccine:

  • Highly effective live attenuated vaccine with 95% efficacy
  • Universal vaccination of all infants as part of the MMR regimen
  • Both universal and selective vaccination policies will work provided that the coverage is high enough
  1. Antenatal screening
  • All pregnant women attending antenatal clinics are tested for immune status against rubella
  • Non-immune women are offered rubella vaccination in the immediate post partum period
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
  1. What type of infection is CMV?
  2. How is it transmitted?
A
  • Beta herpes virus that causes latent infection
  • Horizontal transmission
  • Vertical transmission
  • —In utero (transplacental)
  • —During delivery
  • —Breast feeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  1. Define congenital CMV infection
  2. What can it cause?
A
  • Defined as the detection of CMV from body fluids or tissues within 3 weeks of birth
  • Commonest congenital viral infection
  • Leading nongenetic cause of neurosensory hearing loss
  • Transmission to the foetus may occur following primary or recurrent maternal CMV infection
  • May be transmitted to the foetus during all stages of pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Defined the signs and symptoms of Cytomegalic inclusion disease

A
  • CNS abnormalities - microcephaly, mental retardation, spasticity, epilepsy, periventricular calcification
  • Eye - choroidoretinitis and optic atrophy
  • Ear - sensorineural deafness
  • Liver - hepatosplenomegaly and jaundice which is due to hepatitis.
  • Lung - pneumonitis
  • Heart - myocarditis
  • Thrombocytopenic purpura, Haemolytic anaemia
  • Late sequelae in individuals asymptomatic at birth - hearing defects and reduced intelligence.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the pathogenesis of congenital CMV?

A
  • Little is known about the molecular mechanisms responsible for the pathogenesis of tissue damage
  • No evidence of teratogenecity, damage to the fetus may result from destruction of target cells once they are formed
  • CNS is the major target organ for tissue damage in the developing fetus
  • Infection of endothelial cells (viral angiitis) may be responsible for perfusion failure in the developing brain with resultant maldevelopment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the possible outcomes of maternal CMV infection?

A
  • May cause congenital infection on 40% –> only 5-10% will have abnormalities at birth. The rest may be asymptomatic at birth but 10% will go on to have abnormalities on follow-up
  • CMV can reactivate/re-infect and transmission from person to person. - Low risk of foetal abnormalities, although severe disease may occur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What organ does congential CMV target the most?

A

CNS involvement

only 0.2-2% have congenital CMV, and of those that are symptomatic (10%) - 75% will have CNS involvement e.g. hearing loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is CMV in the mother diagnosed?

A

Virus Detection (blood, urine, respiratory secretions)

  • Cell culture
  • Detection of Early Antigen Fluorescent Foci

DEAFF – accelerated cell culture system

  • CMV DNA (Polymerase Chain Reaction)

Serology

  • CMV IgG seroconversion
  • CMV IgG avidity
  • CMV IgM
18
Q

How is diagnosis made of suspected intrauterine infection with CMV:

  1. Pre-natal
  2. Post-natal?
A
  1. PRE-NATAL
    * Detection of CMV DNA in amniotic fluid at 21 weeks gestation
  2. POST-NATAL
  • CMV detection within 3 weeks of life
  • Positive result beyond that time will NOT make a diagnosis of congenital infection
  • Urine/Salivary swab/blood
  • Serology
    • CMV IgM (low sensitivity)
19
Q

How is congenital CMV

  1. Prevented
  2. Treated?
A
  1. Key to prevention is “universal precautions”
  2. CMV with significant organ disease:
  • valganciclovir or ganciclovir for 6/12
  • audiology f/u until 6 years of age
  • ophthalmology review
20
Q

What factors influence neonatal trasnmission of an infection?

A
  • Type of maternal infection
  • Maternal antibody status (neutralizing Ab)
  • Duration of rupture of membranes
  • Integrity of mucocutaneous barriers (e.g., use of foetal scalp electrodes)
  • Mode of delivery (cesarean section versus vaginal)
21
Q

What is the risk of neonatal infections based on maternal HSV status?

A

Nature of maternal infection

  • First episode 1 yr –> risk of neonatal infection = 57%
  • First episode non 1yr –> risk of neonatal infection = 25%
  • Recurrent –> risk of neonatal infection = 2%
22
Q

When is there the highest risk of neonatal infection with HSV?

A

Maternal primary HSV infection in the third trimester

  • particularly within 6 weeks of delivery
    • continuing viral shedding
    • birth before development of protective maternal antibodies
    • C-section recommended (RCOG)
23
Q

When are most infections transmitted to the neonate?

  1. Intrauterine
  2. Peripartum
  3. Postpartum
A
  1. Peripartum/perinatal - 85% of infections
24
Q

What is the clinical presentation of an intrauterine infection with HSV?

  • Neurological
  • Cutaneous
  • Opthalmologic
A

Neurologic involvement

  • microcephaly,encephalomalacia, hydranencephaly, and/or intracranial calcification

Cutaneous manifestations

  • scarring, active lesions, hypo- and hyperpigmentation

Ophthalmologic findings

  • microopthalmia, retinal dysplasia, optic atrophy, and/or chorioretinitis),
25
Q

What are the signs and symptoms of an infection with HSV in peripartum and postpartum?

A

Disseminated disease ~ 25%

  • DIC
  • Pneumonia
  • Hepatitis
  • CNS involvement (60% to 75%)

Encephalitis (CNS disease) ~ 30%

  • Seizures
  • Lethargy
  • Irritability
  • Poor feeding
  • Temperature instability

Skin, eyes, and/or mouth (SEM disease) ~ 45%

26
Q

Describe disseminated disease with HSV in a new born

A

Poor prognosis even with antiviral treatment

  • mortality around 30%
  • long-term neurological sequelae in 17%
  • Encephalitis in 60-70% of cases

Severe coagulopathy, liver dysfunction, pneumonitis

> 20% will NOT have skin lesions

27
Q

What are the signs and symptoms of CNS disease with HSV in a new born?

A
  • Local CNS disease often presents late
    • between 10 days and 4 weeks postnatally
    • with treatment, mortality is around 6% and neurological morbidity 70%
  • Seizures (both focal and generalized)
  • Lethargy, irritability
  • Tremors, poor feeding, temperature instability
  • Bulging fontanelle
28
Q

How can infection with HSV be prevented/outcomes improved?

A
  • Raise awareness of this infection
  • Decrease the time to diagnostic consideration
    • In the mother
    • In the newborn baby
  • Early initiation of antiviral therapy
    • Prompt collection of specimens for diagnosis
    • HSV cultures/PCR of skin vesicles (if present), oropharynx, conjunctivae,urine, blood and cerebrospinal fluid
    • Liver transaminase levels (suggest disseminated HSV infection)
29
Q

What is the antiviral therapy for HSV for a new born?

A
  • High dose acyclovir at 60 mg/kg/day IV in three divided daily doses
  • Duration of therapy
    • 21 days (minimum) in disseminated or CNS disease
    • Repeat LP and CSF PCR testing
    • Continue with ACV until PCR negative
  • 14 days (minimum) in SEM disease
  • Monitor Neutrophil count
30
Q
  1. How is VZV spread?
  2. What are the complications of a VZV infection while pregnant (mother and fetus)
A
  • DNA virus, Herpes family, Spread by respiratory droplets and direct contactcand highly contagious
  • Varicella in pregnant women is associated with a risk of VZV transmission to the foetus or newborn
  • Risk to mother: pneumonia/encephalitis
  • Intrauterine VZV infection might result in
    • Congenital varicella syndrome
    • Neonatal varicella
    • Herpes Zoster during infancy or early childhood
31
Q

How can congenital varicella syndrome manifest itself in the newborn?

A

Can be manifested by

  • Low birth weight
  • Cutaneous scarring
  • Limb hypoplasia
  • Microcephaly
  • Cortical atrophy
  • Chorioretinitis
  • Cataracts
32
Q

Describe the risk of causing congenital varicella zoster syndrome

A
  • Maternal infection during 0-12 weeks’ gestation 0.4% risk
  • Maternal infection during 13-20 weeks’ gestation Highest risk (2%)
  • Rare cases involving birth defects consistent with congenital varicella syndrome have been reported after maternal varicella beyond 20 weeks’ gestation (with the latest occurring at 28 weeks)
  • Zoster during pregnancy does not pose risk to the foetus
33
Q
  1. Describe varicella neonatal infection
  2. How does the infection manifest itself?
A

Newborn is vulnerable when maternal infection occurs within 7 days prior to delivery or 7 days post-partum

  • —No time for passive transfer of VZV antibodies

Manifestations of infection may include

  • —Mild course of infection
  • —Disseminated skin lesions
  • —Visceral infection
  • —Pneumonia
34
Q

How can infection with varicella be prevented?

A
  • Live virus vaccine available (give preconception)
  • Avoidance of exposure in pregnancy if susceptible
  • Varicella-zoster immune globulin (given with 10 days of exposure)
  • Antiviral chemotherapy if exposed (aciclovir from day 7 to 14 post exposure)
35
Q

Measles paramyxovirus RNA:

  • Transmission
  • Incubation
  • Symptoms
  • Complications
A
  • Transmission: respiratory, conjuctiva
  • Incubation: 7-18 days (typically 10 days)
  • Symptoms:
    • prodrome 2-4 days- fever, malaise, congestion, conjuctivitis, koplik’s spots
    • Rash classically starts behind ears & on forehead then spreads
  • Complications
    • Opportunistic bacterial infections
      • Otitis media
      • Pneumonia, bronchitis
  • Encephalitis
  • SSPE
36
Q

Human parvovirus

  • Type of virus
  • Incubation
  • Clinical presentation
A
  • DNA virus, Family Parvoviridae, genus Erythrovirus
  • Transmission is by respiratory droplets and by blood
  • Incubation period is 4 to 20 days
  • Clinical presentation
    • —Erythema infectiosum (fifth disease)
    • —Transient aplastic crisis
    • —Arthralgia
    • —Non-immune hydrops foetalis
37
Q

What is the pathophysiology of Parvovirus?

A
  • Unique tropism for rapidly dividing erythrocyte precursors
  • Virus requires the P blood antigen receptor (globoside) to enter the cell
  • Suppression of erythrogenesis
  • No reticulocytes are available to replace aging or damaged erythrocytes as they are cleared by the reticuloendothelial system

Virus crosses the placenta and destroys red cell precursors

Foetal anaemia –> high output congestive heart failure –> hydrops fetalis
Virus also directly infects and injures myocardial cells

38
Q

Parvovirus B19 in pregnancy

  • What can happen if there is a maternal infection before 20/40?
  • After 20/40 weeks?
A

Maternal infection before 20/40

  • —Transplacental transmission estimated at 33%
  • —9% risk of infection overall
  • —3% risk of hydrops fetalis if infection from 9-20/40
  • —Risk of foetal anomalies less than 1%

Maternal infection after 20/40

  • —No documented risk
39
Q
  • How is maternal diagnosis of Parvovirus made?
  • How is fetal infection diagnosis made?
A

Maternal Infection

  • Parvovirus DNA amplification from blood, respiratory samples
  • Serology
  • Parvovirus IgG seroconversion
  • Parvovirus IgM

Foetal Infection

  • Foetal blood and amniotic fluid for serology and PCR
40
Q

How is congenital parvovirus infection treated?

A

Intrauterine transfusion

Some cases resolve spontaneously

If infant survives the hydropic state, long-term prognosis is usually favorable

41
Q

Zika virus is usually asymptomatic. What are the consequences of Zika virus in pregnancy?

A
  • Miscarriage/stillbirth/microcephaly
  • Congenital Zika syndrome is described by 5 features:
  • Severe microcephaly + skull deformity
  • Decreased brain tissue, seizures
  • Retinopathy, deafness
  • Talipes
  • Hypertonia

Associated with travel to Caribbean/Central/South America

Microbiology - Path (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions