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MFM Written Boards (Andrews) > Perinatal infections > Flashcards

Perinatal infections Flashcards

1
Q

What is the leading cause of neonatal chorioretinitis?

A

a. CMV
b. Rubella
c. Syphilis

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2
Q

What percentage of pregnant women are IgG+ for HSV-2?

A

20-30%

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3
Q

What percentage of women HSV seroconvert during pregnancy?

A

2-4%

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4
Q

What percentage of HSV-2 infected people are not aware of having the infection?

A

75-90%

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5
Q

Symptoms of newly acquired HSV infection

A

Asymptomatic in 70% of pregnant women
30% - range from minimal lesions to widespread genital lesions, tender regional lymph node enlargement, fever, malaise, headache

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6
Q

HSV-1 causes what percentage of oral infections? genital?

A

90% oral

10% genital

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7
Q

HSV-2 causes what percentage of oral infections? genital?

A

10% oral
90% genital
(but among college-age populations, majority of new cases of genital HSV are HSV-1)

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8
Q

What percentage of neonatal HSV results from women who acquire HSV-1 or -2 near term?

A

50-80%

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9
Q

What is a “nonprimary first-episode HSV infection”?

A

HSV-2 confirmed in a person with prior HSV-1, or vice-versa. Symptoms are usually milder than a first-episode primary infection.

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10
Q

What is reactivation (recurrent) genital herpes?

A
  • Caused by reactivation of latent HSV, usually HSV-2.
  • Over 90% of HSV episodes in pregnancy are recurrent or non primary 1st
  • Symptoms last 7-10 days, with low viral load shedding for 3-5 days.
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11
Q

What is the incidence of neonatal HSV after a vaginal delivery during a first episode primary infection?

A

25-50%

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12
Q

What is the incidence of neonatal HSV after a vaginal delivery during a recurrent infection?

A

<1%

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13
Q

Why is the incidence of neonatal HSV after a primary maternal infection higher?

A

The infant of the mother with primary HSV lacks the protection of transplacental type-specific antibodies. The major sites of intrapartum viral entry are the neonatal eys, nasopharynx, or a break in the skin. Transplacental infection is rare.

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14
Q

What is GBS?

A

Streptococcus agalactiaeAn encapsulated gram-positive coccus that colonizes the vaginal & GI tract

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15
Q

Manifestations of GBS in the mother

A

Urinary tract infectionChorioamnionitisEndometritisBacteremiaStillbirth

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16
Q

What are the 2 types of newborn GBS infection?

A

Early-onset - usually within first 24 hrs of life, up to 6 days after birthLate-onset - Usually at 3-4 weeks of age, can occur any time from 7 days - 3 months

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17
Q

Symptoms of neonatal GBS

A

Early-onset:Respiratory distressShockPneumoniaMeningitis (occasionally)Late-onset:Bacteremia (common)Meningitis (common)Poor feedingIrritabilityExtreme drowsinessListlessnessLocalized infection: middle ear, sinuses, bones, joints, skin

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18
Q

Prevalence of asymptomatic GBS anovaginal colonization in pregnant women

A

20%, can be transient or persistentA substantial portion of women colonized in one pregnancy will not have colonization during a subsequent pregnancy

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19
Q

Percentage of neonates born to mothers colonized with GBS that are colonized themselves

A

40-75%

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20
Q

Risk factors for early-onset GBS disease

A

Prolonged ROM (>/= 18 hrs)Preterm birth (but >80% GBS are term)Termp >/= 38 deg CMaternal GBS colonization btw 35-37wPrevious infant with invasive GBS diseaseMaternal choioBlack or HispanicGBS bacteriuria during pregnancyDM or GBS colonization in a previous pregnancy are not risk factors

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21
Q

Neonatal mortality due to GBS disease

A

5%25% if < 33w GA

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22
Q

Is there a vaccine for GBS?

A

accination against GBS is potentially the most effective method of preventing the morbidity and mortality caused by infection. GBS vaccines have been investigated as a tool to reduce maternal colonization and prevent transmission to the neonate; however, a licensed vaccine is not yet available.

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23
Q

What percentage of neonates with early-onset GBS sepsis are born to women without risk factors?

A

20.00%

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24
Q

How effective is a screening-based strategy compared to a risk factor-based strategy for GBS?

A

> 50% more effective for early-onset GBS, but does not affect the incidence of late-onset GBS sepsis

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25
Q

For whom is intrapartum GBS prophylaxis indicated?

A

Previous infant with invasive GBS diseaseGBS bacteriuria during current pregnancy+GBS screening culture during current pregnancy (unless C/S prior to ROM)Unknown GBS status and: /= 18 hrs Intrapartum temp >38 deg C Intrapartum NAAT GBS+

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26
Q

For whom is intrapartum GBS prophylaxis NOT indicated?

A

Previous pregnancy with a positive GBS screening culture (unless indication present during current pregnancy)C/S in absence of labor or ROM (regardless of culture status)Negative vaginal & rectal GBS screening culture 35-37w, regardless of intrapartum risk factors

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27
Q

What is the NPV of GBS cultures at 35-37w

A

95-98%, if prevalence 20%

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28
Q

Recommended regimen for GBS prophylaxis

A

Penicillin G, 5 million units IV x 1, then 2.5-3 million units IV q 4 hrs until delivery

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29
Q

Alternative GBS regimen

A

Amp 2 g IV x 1, then 1 g IV q 4 hrs until delivery

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30
Q

GBS prophylaxis - PCN allergic, but not at high risk for anaphylaxis

A

Cefazolin 2 g IV x 1, then 1 g IV q 8 hrs until delivery

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31
Q

GBS prophylaxis - PCN allergic, at high risk for anaphylaxis, susceptible to clinda & erythro

A

Clinda 900 mg IV q 8 hrs until delivery

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32
Q

GBS prophylaxis - PCN allergic, but not at high risk for anaphylaxis - resistant to clinda or erythro or susceptibility unknown

A

Vancomycin 1 g IV q 12 hrs until delivery

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33
Q

How is susceptibility testing for GBS performed?

A

Resistance to erythromycin is often, but not always, associated with clindamycin resistance. If a strain is resistant to erythromycin, but appears susceptible to clindamycin, it may still have inducible resistance to clindamycin. Treatment with erythromycin is not recommended.

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34
Q

Have current prevention strategies decreased the incidence of late-onset GBS disease.

A

Nope.

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35
Q

How long is a GBS screening culture valid for?

A

5 weeks

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36
Q

Parvovirus B19 structure

A

Single-stranded DNA virus

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37
Q

What percent of women of reproductive age are Parvovirus immune?

A

50-75% of women are IgG+ (immune)

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38
Q

When is Parvovirus infection more common?

A

Winter and spring

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39
Q

Among which group does Parvovirus infection occur the most?

A

Schoolteachers, day care workers, and women with nursery or school-aged children in the home. Around 50% to 80% of susceptible household members and 20% to 30% of individuals exposed in a classroom acquire acute infection from an infected child.

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40
Q

Parvovirus - adverse prognostic factors

A

Older maternal age
Maternal immunity and seroconversion
Raised maternal serum alpha-fetoprotein
Ultrasound findings

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41
Q

How common are symptoms in adults with Parvovirus? What are the symptoms?

A

In adults at least half of the infections are asymptomatic.

About 30% may have flulike symptoms, arthralgias, and adenopathy.

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42
Q

What are symptoms of Parvovirus in children?

A

Parvovirus B19 causes a common exanthematous disease in children 5 to 14 years old, called fifth disease or erythema infectiosum. Children have symptoms such as low- grade fever and ’¢ŠäŒ–slapped-cheeks’¢ŠäŒÎ rash, and are usually diagnosed just based on these symptoms.

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43
Q

Transmission of Parvovirus

A

Respiratory droplets

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44
Q

Parvovirus incubation period? When is infectivity greatest?

A

Incubation period 13-18 days

Infectivity greatest 7-10 days before the onset of symptoms

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45
Q

What are the target cells for Parvovirus infection?

A

Erythroid progenitors bearing the main cellular parvovirus B19 receptor P blood group antigen globoside on their surface

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46
Q

Fetal complications of Parvovirus infection

A

Of the infected fetuses, about 5% to 20% can develop anemia, of which 30% to 50% develop hydrops fetalis (about 2–6% of all infected fetuses), with some series showing hydrops rates as high as 66% of anemic fetuses.

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47
Q

What percentage of fetuses of mothers with primary Parvovirus infection will become infected themselves?

A

25-30% of fetuses of mothers with primary parvovirus B19 infection become infected themselves by vertical transmission.

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48
Q

What percentage of Parvovirus-infected fetuses will develop complications?

A

10%

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49
Q

What percentage of Parvovirus-infected fetuses will develop complications?

A

10%

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50
Q

Of fetuses infected with Parvovirus, what percentage will develop anemia?

A

5-20%

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51
Q

Of fetuses that develop anemia from Parvovirus, what percentage will develop hydrops fetalis?

A

30-50 (2-6% of all infected fetuses)

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52
Q

What is the risk of fetal death from Parvovirus?

A

1-6%. Fetal death occurs almost exclusively in hydropic cases diagnosed at 20 weeks are treated with timely transfusion (90% survival).

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53
Q

US findings in fetal parvovirus infection

A 
Pericardial or pleural effusion
Ascites
Abdominal wall/skin edema
Bilateral hydroceles
Oligohydramnios or hydramnios
Increased (>95th percentile) cardiac biventricular outer diameter
Rare:
Hydrocephalus
Microcephaly
Intracranial and hepatic calcifications
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54
Q

Treatment of Parvovirus exposure

A

Intravenous immunoglobulin (IVIG) prophylaxis is reasonable to consider for documented exposures in immunocompromised patients, although it is not currently recommended for prophylaxis in pregnancy.

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55
Q

Diagnosis of maternal Parvovirus infection

A

Maternal infection is usually diagnosed by IgM+ or by IgG seroconversion. IgM appears by 3 days of an acute infection, peaks at 25 to 30 days, and disappears by 4 months. Serum IgG appears a few days after IgM, and coincides with resolution of maternal symptoms. The detection of viral DNA by PCR is another means of diagnosis.

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56
Q

After maternal Parvovirus infection has been diagnosed, how do you screen for fetal anemia?

A
  • Anemia can be detected by increased PSV of the MCA prior to the appearance hydrous
  • With fetal anemia there is an increase of fetal cardiac output to maintain adequate oxygen delivery to tissues, leading to increased blood flow velocities
  • MCA PSV using a threshold of >/=1.50 MoM has a high sensitivity (100%) and specificity (100%) for detecting fetal anemia
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57
Q

Surveillance of fetuses after maternal Parvovirus infection

A
  • If MCA PSV values are <1.50 MoM, it is suggested to continue weekly ultrasound scans for 10 to 12 weeks after the exposure
  • The peak incidence of hydrops is at about four to six weeks after maternal infection
  • Fetal surveillance should be initiated no later than four weeks after the onset of illness or estimate of seroconversion
  • In cases of elevated MCA PSV but no hydrops, surveillance should be increased with US two to three per week to detect any sign of hydrops, or umbilical cord sampling performed.
58
Q

How is fetal Parvovirus infection confirmed

A

Amniotic fluid PCR

59
Q

Is there antiviral therapy available for Parvovirus?

A

There are no trials evaluating therapeutic interventions. No antiviral therapy is available.

60
Q

Can fetal anemia caused by Parvovirus resolve spontaneously?

A

Yes. Anemia and even hydrops can resolve spontaneously over four to six weeks (about 30% spontaneous resolution for hydrops)
Resolution is more common in older (>20 weeks) fetuses because of a more mature immune system.

61
Q

Treatment of anemia in the fetus affected by Parvovirus between 24 and 33 6/7w

A
  • Between 24 and 33 6/7 weeks, steroids for fetal lung maturity should be given
  • Fetal cordocentesis to document anemia and transfusion as necessary improve outcome in anemic and/or hydropic fetuses.
  • Frequently, one transfusion is sufficient.
62
Q

Treatment of anemia in the fetus affected by Parvovirus before 24w

A

-Before 24 weeks, with severe hydrops, termination may be offered, but transfusion can be beneficial, with apparently minimal to no significant sequelae if successful

63
Q

Treatment of anemia in the fetus affected by Parvovirus after 34w

A

After 34 weeks, delivery should be considered.

64
Q

In addition to fetal RBC transfusion for Parvovirus, what else should be considered?

A

Platelets should also be ready at the time of PUBS, as multiple series have demonstrated a concomitantly high incidence of fetal thrombocytopenia at the time of transfusion.

65
Q

Long-term prognosis for infants born to mothers infected by Parvovirus

A
  • Infants born to IgM+ mothers are born IgG+ (mostly maternal), and 25% stay IgG+ at one year, as they were infected and have become immune.
  • General health status of survivors is no different compared with the general population-Some trials illustrate an incidence of developmental delay similar to the general population even in cases of fetuses transfused in utero for hydrous
  • More recent data of survivors aged six months to eight years demonstrated a 32% incidence of psychomotor developmental delay, independent of pretransfusion hemoglobin, platelet, or blood pH values.
  • Patients need to be counseled regarding the overall uncertainty regarding long-term neurodevelopmental outcome among survivors
66
Q

What is Toxoplasma gondii (TG)?

A

An obligate intracellular protozoan (parasite)

67
Q

Symptoms of TG

A

Almost always, no maternal symptoms. Occasionally flu/mononucleosis-like fever, fatigue, rash, head/neck lymphadenopathy.
Rarely, pregnant women will present with visual changes due to chorioretinitis from recently acquired infection or reactivation of chronic infection.

68
Q

What is the definitive host of TG?

A

The definitive host is the cat (only one that can support both sexual and asexual reproduction).

69
Q

What forms does TG exist in?

A
  1. Trophozoite (invasive form)
  2. Cyst (latent form)
  3. Oocyst (only in cats: result of sexual reproduction, which occurs in the small intestine of a cat who has eaten outside tissue cysts containing TG)
70
Q

When are cats infectious with TG?

A

Only during first exposure is the cat infectious, as these oocysts are produced for two weeks and contain infectious sporozoites; the oocysts require one to five days to become infected; after two weeks the cat becomes immune and not infectious. In soil, oocysts can remain infectious for years.

71
Q

How does human infection with TG occur?

A

Human infection starts with ingestion (from food, water, hands, or insects) of cysts from uncooked/undercooked meat of infected animals (e.g., lamb and mutton) or contact with oocysts from infected cats (who get it from infected mice, etc.) or contaminated soil.

72
Q

What happens when a pregnant woman ingests TG oocysts?

A

The infected oocysts become infective inside the pregnant woman in 4 to 10 (average 7) days, leading to parasitemia. Eventually, TG can infect and live forever in striated muscle or brain.

73
Q

Does congenital TG occur in women infected prior to conception?

A

Only a very few cases of congenital toxoplasmosis transmitted by mothers who were infected prior to conception have been reported; they can be attributed to either reinfection with a different strain or to reactivation of chronic disease. This reactivation is very rare, but can occur especially in an immunocompromised woman. Immunocompetent women with prior toxoplasmosis can be reassured that the risks to the subsequent fetus/neonate are miniscule, especially >9 months after infection.

74
Q

Of congenitally infected fetuses (PCR+ amnio for TG), what percent have subclinical infection? What percent have fetal/childhood illness?

A
  • 74% to 81% manifest only subclinical infection (only serologically positive)
  • 19% to 26% have fetal/childhood illness even if they received treatment
75
Q

What percentage of fetuses of primary TG-infected mothers are affected?

A

7.00%

76
Q

Fetal/neonatal TG disease is more common if maternal infection occurs in what trimester?

A

3rd trimester

77
Q

Fetal or neonatal TG disease is more severe if maternal infection occurs in what trimester?

A

1st trimester. But there is less than a 1/1000 chance of fetal infection if GA is less than 4w at time of maternal infection.

78
Q

Probability of congenital TG if maternal infection occurs preconception

A

1%

79
Q

Probability of congenital TG if maternal infection occurs in 1st trimester

A

10-25%

80
Q

Probability of congenital TG if maternal infection occurs in 2nd trimester

A

30-55%

81
Q

Probability of congenital TG if maternal infection occurs in 3rd trimester

A

60-80%

82
Q

Signs of fetal TG infection

A 
Ventriculomegaly (75%)
Placentomegaly (32%)
Hepatomegaly (12%)
Ascites (15%)
Intracranial calcifications (18%)
Hydrocephalus (4%)
Microcephaly (5%)
HSM (4%)
83
Q

Neonatal signs of TG infection

A

Chorioretinitis (26%)
Deafness
Decreased IQ
Subsequent blindness, seizures, neuropsychomotor delay

84
Q

Complications of congenital TG infection

A

PTB
Not IUGR, when seroconversion occurs before 20w
Stillbirth/neonatal death is rare

85
Q

Prevention of congenital TG

A

-Avoid raw or undercooked meat (or eggs) of any origin-Avoid contact with raw meat or soil-Wash fruits and vegetables before eating-Cats: Avoid changing cat litter. Hand-wash after handling cat. Do not let cats outside the house (could eat infected mice). No stray cats in the house. No feeding raw meat to cats. Avoid raw milk.

86
Q

When do IgG TG antibodies appear?

A

Usually within 2w of infection, persist indefinitely

87
Q

IgM in the diagnosis of recent TG infection

A

IgM antibodies are considered to be a sign of recent infection and can be detected by enzyme immunoassays (EIAs) or an immunosorbent agglutination assay test (IAAT) within two weeks of infection. They often remain positive for up to one to two years.

88
Q

What is the gold-standard test for TG infection?

A

The Sabin—Feldman dye test (SFDT) is still considered the gold standard. It detects the presence of anti-TG- specific antibodies (total Ig). The absolute antibody titer is also important: values over 250 IU/mL are considered highly suggestive of recent infection.

89
Q

How does IgG avidity aid in the diagnosis of TG infection?

A

IgG avidity testing is based on the increase in functional affinity (avidity) between TG-specific IgG and antigen over time, as the host immune response evolves. Pregnant women with high avidity antibodies are those who have been infected at least three to five months earlier.

90
Q

Diagnosis of maternal TG infection

A

Maternal infection is diagnosed by sending maternal serology to a reference laboratory (http://www.pamf.org/serology/clinicianguide.html). It is best to make the diagnosis based on two different serum specimens collected at least four weeks apart. Usually, the reference laboratory reports many serologic results, with a high possibility of infection if there is:

  1. Seroconversion during pregnancy;
  2. Increase in both specific IgG titer (>3-fold) and dye test (>3-fold)
  3. Presence of specific IgM and dye test >/= 300 IU/mL.
91
Q

How is fetal congenital TG infection diagnosed?

A

Fetal congenital infection is diagnosed by -AF PCR: Spec and PPV are close to 100%; sens is around 70% to 80%, but is best when maternal infxn occurs btw 17w and 21w.

  • Real-time PCR - sens of 92%, NPV of 98%, and may not be as GA dependent as conventional PCR.
  • Negative AF PCR does not always completely rule out congenital infection.
  • AF PCR should obviously be done after 15 weeks.
  • Ultrasound can also aid in diagnosis of fetal infection, but it has very poor sensitivity and specificity.
92
Q

Treatment of TG if maternal infxn diagnosed

A
  • If maternal infection is detected, counsel regarding the risks, along with possibility of termination (esp 1st trimester), and management.
  • If maternal infection is confirmed by a reference lab, start spiramycin 3 to 4 g/day (1 g q 8 hrs). This is available in the United States only by the FDA when Palo Alto serology is positive.
  • Spiramycin concentrates in the placenta, and therefore may not be reliable for treatment of infection in the fetus.
93
Q

Treatment of congenital TG in the fetus

A
  • If + AF PCR, start sulfadiazine (initial dose of 75 mg/kg, followed by 50 mg/kg q12h w/ max of 4 g/d), pyrimethamine (50 mg po q 12h for two days followed by 50 mg/d), and folinic acid (leucovorin) 10 to 20 mg with each dose of pyrimethamine (decreases bone marrow toxicity) and one week after completion of pyrimethamine.
  • Length of therapy is controversial, has varied from a minimum of 28 days (with 1/2 dose until term), versus continuing tx as is until term.
  • Treatment with pyrimethamine and sulfadiazine to prevent fetal infection is contraindicated during the first trimester (pyrimethamine is teratogenic), but at this time sulfadiazine can be used alone.
  • This treatment should be stopped in the last few weeks of pregnancy.
  • Other drugs such as spiramycin (3-4 g/day x 3-4 weeks) are recommended in certain circumstances. Spiramycin is used to prevent placental infection; it is used in European countries, but in the United States it is not approved by the FDA. Treatment decreases complications of TG, but possibly not fetal infection.
94
Q

How successful is treatment of congenital TG in the fetus?

A
  • It is estimated that for every three congenitally infected fetuses that are treated, one case of serious neurological sequela is prevented.
  • In one study, fetuses/neonates treated and subsequently followed for 12 to 250 months had a 17% rate of congenital TG, with 74% of the children asymptomatic, 26% developing chorioretinitis (72% peripheral and unilateral), and all except one child having age-appropriate neurological and intellectual development.
95
Q

TG infection in the immunocompromised patient

A

Dysfunction of the CNS is the most common manifestation of infection. Findings typically include encephalitis, meningoencephalitis, and intracerebral abscess. Pneumonitis, myocarditis, and generalized lymphadenopathy also occur commonly.

96
Q

What is the structure of CMV?

A

Double-stranded virus of herpes family

97
Q

What is the most common cause of viral intrauterine infection?

A

CMV. Affects 0.5 - 2.5% of all neonates in different parts of the world.

98
Q

How is CMV transmitted?

A

Contamination from urine, saliva, blood, semen, cervical excretions.

99
Q

Risk factors for CMV infection?

A 
Low SES
Exposure to infected individuals
Multiple partners
Extremes of age
Multiparity
Blood transfusion
0.1-0.4% per unit of cellular blood products containing leukocytesIn most cases, pregnant women acquire CMV by exposure to children in their home or occupational exposure to children
100
Q

Symptoms of CMV infection

A

Usually asymptomatic, or symptoms so mild that it goes undiagnosed.
May include a mononucleosis-like or flu-like syndrome, malaise, fatigue, lymphadenopathy, persistent fever, lymphocytosis, incr transaminases
Rarely - HSM, cough, headache, rash, GI sx

101
Q

CMV incubation period

A

4-8w

102
Q

CMV viremia period

A

3-12 months (infants can shed virus for up to 6 yrs)

103
Q

In whom does serious CMV disease occur?

A

Fetuses

Immunocompromised adults

104
Q

Does CMV transmission occur with primary or recurrent infection?

A

Both, but 99.5% of fetal infections occur following primary maternal infection.

105
Q

What percentage of IgG negative women will acquire CMV infection during pregnancy?

A

2.00%

106
Q

What percentage of pregnant women with a primary CMV infection transmit it to their fetus?

A

EBMFM: 1/3 (range 30-75%)
Creasy: among women who acquire primary CMV infection during pregnancy, approximately half will infect their fetus.
Williams: primary maternal CMV infection is transmitted to the fetus in about 40 percent of cases and can cause severe morbidity

107
Q

When is the transmission rate of CMV highest in pregnancy?

A

3rd trimester

108
Q

The severity of CMV disease is highest in what trimester of pregnancy?

A

1st trimester

109
Q

What percentage of CMV-infected infants develop sequelae?

A

15-20% (about 5-8% of infants of infected mothers develop sequelae)

110
Q

How does recurrent CMV infection occur?

A

Occurs w/ immunosuppression and during pregnancy
Recurrent infxn in pregnancy is usu asx and primarily caused by reactivation of the endogenous virus, but can also be caused by a low-grade chronic infection or reinfection by a different CMV strain.

111
Q

What is the risk of vertical transmission with recurrent CMV infection?

A

1.4%

112
Q

What percentage of neonates infected from recurrent maternal infection will have sequelae?

A

<10% (usu have no sx at birth, and do not have CMV+ urine)

113
Q

What are the clinical neonatal findings of symptomatic congenital CMV infection?

A 
Jaundice
Petechiae ("blueberry muffin baby")
Thrombocytopenia
Hepatosplenomegaly
Growth restriction
Microcephaly
Intracranial calcifications
Nonimmune hydrops
Preterm birth
114
Q

What are the late complications of neonatal CMV disease?

A 
Hearing loss
Mental retardation
Delay in psychomotor development
Chorioretinitis
Optic atrophy
Seizures
Expressive language delays
Learning disabilities
115
Q

What is the most common cause of congenital sensorineural hearing loss?

A

CMV

116
Q

What is the long-term mortality rate in neonatal CMV disease?

A

10-30%

117
Q

Diagnosis of congenital CMV infection in amniotic fluid

A

Quantitative PCR count of >/= 10^3 genome equivalents/mL is a certain sign of infxn>/= genome equivalents/mL can predict symptomatic infection

118
Q

If no ultrasonographic abnl due to CMV are seen, what is the incidence of postnatal neurologic abnormalities?

A

15-20%

119
Q

How effective is hygiene in preventing CMV seroconversion in pregnancy?

A

Avoiding intimate contact w/ children, frequent handwashing, and glove use is associated with an 84% decrease in CMV seroconversion during pregnancy, esp in women who work in day care.

120
Q

Is there a vaccine available for CMV?

A

A live-attenuated CMV vaccine is available, but may be reactivated, and safety issues have not been resolved. In a trial including CMV-seronegative women of childbearing age, a glycoprotein B vaccine demonstrated a 50% efficacy in preventing CMV infection.

121
Q

What is chance of a CMV-affected neonate after maternal seroconversion, with a nl US?

A

5%

122
Q

What is chance of a CMV-affected neonate after maternal seroconversion, with an abnl US?

A

35%

123
Q

What is chance of a CMV-affected neonate after maternal seroconversion, with positive AF PCR and a nl US?

A

15%

124
Q

What is chance of a CMV-affected neonate after maternal seroconversion, with a positive AF PCR and an abnl US?

A

80%

125
Q

How long does CMV IgM persist after seroconversion?

A

4-8 months

126
Q

How sensitive is CMV IgM testing?

A

75%. If first test is negative, consider a second test at 18-20w, and a third, if needed, at 30-32w.

127
Q

How can CMV IgM/IgG testing be used to assure no risk of primary infection?

A

IgM negative, IgG positive, with a high IgG avidity index (>65%).

128
Q

Fetal ultrasound findings in congenital CMV infection

A 
Growth restriction
Oligohydramnios
Ventriculomegaly
Choroid plexus cyst (unilateral)
Pleural effusion
Brain and liver calcifications
Fetal hydrops
129
Q

What are US findings that increase the risk for neonatal CMV infection?

A

Microcephaly
Hydrocephaly
Intracranial calcifications
Periventricular “halo” - assoc w/ white-matter lesions

130
Q

Ultrasound detects fetal abnormalities in what percent of congenitally CMV-infected fetuses?

A

Only 15%

131
Q

Is CMV-specific IgM+ only found in primary disease?

A

No, CMV IgM can be found in 10% of women with recurrent disease

132
Q

What is the sensitivity of CMV PCR in amniotic fluid?

A

80-100%. It increases after 21w, and after a minimum of 6w interval following maternal primary infxn, so if amnio performed before this interval, it should be repeated later.

133
Q

How is CMV infection diagnosed in the neonate?

A

Based on CMV PCR in body fluids, esp urine.

134
Q

Is there therapy to prevent fetal CMV infxn in pregnancy?

A
  • No randomized trials exist (yet). In a nonrandomized study, CMV hyperimmune globulin IV 100 U/kg q mo until delivery to the mother w/ primary CMV infection was associated with a decrease in infected neonates from 40% to 16%.
  • Maternal CMV hyperimmune globulin 200 U/kg IV to the mother (with additional AF or umbilical cord infusions for persistent US findings) for CMV DNA + fetuses was associated with a decrease in symptomatic CMV disease at birth from 50% in controls to 3%.
  • A trial demonstrated reduction of hearing loss in neonates with proven congenital CMV infection with CNS involvement when tx was begun within one month of birth.
  • Valacyclovir (8g/day orally for 7 weeks) given to women with congenitally CMV-infected fetuses at about 30w was associated with about a 50% normal child outcome at 1 to 5 years of age in one study.
135
Q

How is CMV transmitted perinatally?

A

Transplacentally, in the birth canal, through breast milk

136
Q

What are the fetal manifestations of first-episode primary HSV infection in pregnancy?

A 
Microcephaly
Ventriculomegaly
Intracranial calcifications
Spasticity
Echogenic bowel
Hepatosplenomegaly
Flexed extremities
Placental calcifications
137
Q

What are the manifestations of neonatal HSV?

A
  • Classic triad = skin lesions, chorioretinitis, CNS abnl
  • Disseminated or CNS disease (seizures, lethargy, irritability, tremors, poor feeding, temperature instability, and bulging fontanelles) in approximately 55% of cases.
  • Up to 30% of infants will die and more than 50% can have neurologic damage despite antiviral therapy
138
Q

A quantitative CMV PCR count of > ___ genome equivalents/mL of amniotic fluid is a certain sign of congenital infection

A

10^3

139
Q

A quantitative CMV PCR count of > ___ genome equivalents/mL of amniotic fluid can predict congenital infection

A

10^5

140
Q

Is there prevention or treatment for fetal CMV infection?

A

-CMV hyperimmune globulin or ganciclovir (Both experimental)
-There is insufficient evidence to recommend CMV-specific hyperimmune globulin for prevention or treatment of CMV congenital infection.
In a nonrandomized study, CMV hyperimmune globulin IV 100 U/kg every month until delivery to the mother for prevention of vertical transmission in primary maternal CMV infection was associated with a decrease in the incidence of infected neonates from 40% in controls to 16% (27).
Maternal CMV hyperimmune globulin 200 U/kg IV to the mother (with additional AF or umbilical cord infusions for persistent ultrasound findings) for therapy of known CMV DNA + fetuses was associated with a decrease in the incidence of symptomatic CMV disease at birth from 50% in controls to 3%.
-A trial of ganciclovir demonstrated reduction of hearing loss in neonates with proven congenital CMV infection with CNS involvement when treatment was begun within one month of birth.

MFM Written Boards (Andrews) (33 decks)

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