TORCH Flashcards

1
Q

What does TORCH stand for?

A
Toxoplasmosis
Other= syphilis, parvovirus B19, VZV, Zika
Rubella
CMV
HSV
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2
Q
  1. What’s causing Toxoplasmosis?
  2. What’s the several forms of Toxoplasmosis? which form is invasive?
  3. How do human get infected with Toxoplasmosis?
  4. Maternal manifestations of toxoplasmoisis?
  5. What’s the chances of vertical transmission in each pregnancy?
  6. What increased the risk of vertical transmission? what increase the risk of the severity of fetal infection?
  7. Should we do routine serologic screening of pregnant women for toxoplasmosis? What’s the seroprevalence rate?
A
  1. intracellular parasite Toxoplasma gondii
  2. a trophozoite, which is the invasive form, and a cyst or an oocyst, which are latent forms
    • by consumption of cysts in undercooked meat from infected animals, insect-contaminated food (dairy, produce, or water)
    • contact with oocysts from the feces of infected cats (the only definitive hosts), or contact with infected materials or insects in soil
  3. Asymptomatic –> after incubation period of 5–18 days –> nonspecific self-limited symptoms may occur: - Immunocompetent patients: asymptomatic cervical lymphadenopathy, fever, malaise, night sweats, myalgias, and hepatosplenomegaly.
  4. The later in gestation that the infection occurs, the more likely transmission is to occur. The rate of vertical transmission increases from 10% to 15% in the first trimester, to 25% in the second trimester, and to more than 60% in the third trimester
  5. The later in gestation that the infection occurs, the more likely transmission is to occur. The severity of fetal infection depends on gestational age at the time of transmission. The earlier the fetus is infected, the more severe the disease
  6. No. Seroprevalence (approximately 38% of pregnant women have evidence of prior toxoplasmosis infection)
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3
Q

Do infants of Toxoplasmosis have clinical signs of infection at birth? What kind of sequelae?

A

Most infected infants do not have clinical signs of infection at birth, but as many as 90% will develop sequelae, including chorioretinitis and subsequent severe visual impairment, hearing loss, or severe neurodevelopmental delay.

Other clinical manifestations of congenital toxoplasmosis include rash, hepatosplenomegaly, ascites, fever, periventricular calcifications, ventriculomegaly, and seizures

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4
Q

For toxoplasmosis, what does each of the follow represent?

  1. A negative IgM test result and a positive IgG test result ?
  2. Negative IgM and IgG test results
  3. IgM and IgG test results are positive?
  4. How soon should you repeat serological testing if your suspicion for Toxoplasmosis is high?
  5. If maternal toxoplasmosis infection has been serologically confirmed, what should you do? What does low avidity mean?
A
  1. A negative IgM test result and a positive IgG test result are indicative of remote infection and pose no concern for fetal transmission in an immunocompetent woman.
  2. Negative IgM and IgG test results indicate either the absence of infection or a recent acute infection without enough time for seroconversion.
  3. If IgM and IgG test results are positive, the patient has had either a recent infection or a false-positive result.
  4. If acute infection is a possibility, serologic testing should be repeated in 2–3 weeks to look for an increase in IgG antibodies consistent with recent infection
  5. Reference laboratories can perform IgG avidity testing to determine when the infection may have occurred.
  6. Low avidity is indicative of primary infection within the past 5 months, which may be helpful information in prenatal diagnosis and counseling
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5
Q
  1. What’s the ultrasonographic findings of severe congenital toxoplasmosis?
  2. What do you do if you see these ultrasound findings?
  3. Can you perform amniocentesis at 15 weeks like usual?
A
  1. ventriculomegaly, intracranial calcifications, microcephaly, ascites, hepatosplenomegaly, and intrauterine growth restriction
  2. Suspicious for fetal toxoplasmosis –> Amniocentesis, PRC of fluid for diagnostic test
  3. Amniocentesis should be performed after 18 weeks of gestation to lessen the chance of a false-negative test result
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6
Q

What’s the treatment for

  1. Pregnant women who are acutely infected with toxoplasmosis?
  2. Fetal infection with toxoplasmosis
  3. infants with symptomatic congenital toxoplasmosis
A
  1. spiramycin to reduce transplacental parasitic transfer.
    Spiramycin is a macrolide antibiotic that concentrates in, but does not readily cross, the placenta
  2. a combination of pyrimethamine, sulfadiazine, and folinic acid because this regimen more effectively eradicates parasites in the placenta and fetus than spiramycin alone and can lessen the severity of disease in the affected fetus
  3. pyrimethamine, sulfadiazine, and folinic acid for 1 year
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7
Q
  1. What causes the childhood exanthema erythema infectiosum? What is exanthema erythema infectiosum also known as?
  2. What does the child look like with exanthema erythema infectiosum? Symptoms for adults?
A
  1. Parvovirus B19 is a single-stranded DNA virus that causes the childhood exanthema erythema infectiosum, also known as fifth disease.
  2. a facial rash, slapped cheek, in addition to possible fever, body rash, and joint pain
    - immunocompetent adults: a reticular rash on the trunk and peripheral arthropathy, 20% asymptomatic, transient aplastic crisis, which is more common in those with an underlying hemoglobinopathy
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8
Q
  1. How is Parvovirus B19 transmitted?
  2. When is the infected person generally infectious ?
  3. What’s the seropositivity of Parvo of reproductive-aged women?
  4. What does positive IgM mean? Positive IgG without IgM? positive IgM and IgG?
  5. What’s the rates of maternal-to-fetal transmission after acute parvovirus B19 infection during pregnancy?
  6. When are severe effects seen most frequently among fetuses?
A
  1. through respiratory secretions and hand-to-mouth contact
  2. 5–10 days after exposure, before the onset of the rash or other symptoms, and is no longer infectious by the time of onset of the rash
  3. Prevalence of seropositivity to parvovirus B19 increases with age, and 50–65% of reproductive-aged women are seropositive
  4. The IgM response, which persists for 1 month to several months, is indicative of a recent infection. IgG antibodies persist indefinitely and, in the absence of IgM, indicate prior infection and lifelong immunity.
    Women who are IgM and IgG negative are susceptible to parvovirus B19 infection and serologic testing should be repeated in 4 weeks.
    Women who are IgM negative and IgG positive have evidence of previous exposure and immunity and, thus, are not at risk of transplacental transmission. Women who are IgM positive, regardless of IgG status, should be monitored for potential fetal infection
  5. 17-33%
  6. Severe effects are seen most frequently among fetuses when maternal parvovirus B19 infection occurs before 20 weeks of gestation
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9
Q

Fetal parvovirus B19 is associated with what negative pregnancy outcomes?

A

spontaneous abortion, hydrops fetalis, and stillbirth.

Cytotoxic parvovirus –> aplastic anemia, myocarditis or chronic fetal hepatitis –> hydrops fetalis

The rate of fetal loss among women with serologically proven parvovirus B19 infection ranges from 8–17% before 20 weeks of gestation to 2–6% after 20 weeks of gestation.

An estimated 8–10% (potentially up to 18–27%) of cases of nonimmune hydrops fetalis are associated with parvovirus B19 infection.

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10
Q

After maternal parvovirus B 19 infection, when will you see stillbirth and hydrops?

A

Stillbirth that results from maternal infection has occurred from 1 week up to 11 weeks after maternal infection. However, hydrops is unlikely to develop if it has not occurred by 8 weeks after maternal infection

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11
Q

Which methods are used to diagnose fetal parvovirus B19 infection and what are the diagnostic criteria?

A

qualitative PCR to detect parvovirus B19 DNA in amniotic fluid

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12
Q

Management of pregnant women with acute parvovirus B19 infection based on serologies

A
  • serial ultrasonography to monitor for the development of fetal anemia, ascites, placentomegaly, cardiomegaly, hydrops fetalis, and impaired fetal growth. Every 1–2 weeks for 8–12 weeks after exposure.
  • Doppler assessment of the peak systolic velocity of the fetal middle cerebral artery

Fetal death can occur without evidence of hydrops fetalis.

If hydrops fetalis is present or severe fetal anemia is suspected in the setting of parvovirus B19, fetal blood sampling should be performed to determine the fetal hematocrit in preparation for fetal transfusion.

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13
Q

Can we prevent parvovirus B19?

A

Don’t exclude pregnant women from the workplace during endemic periods.

If pregnant women are exposed to individuals who are suspected or known to be infected with parvovirus B19, they should report this exposure to their obstetrician–gynecologists or other obstetric providers.

No routine serologic screening of pregnant women for parvovirus B19

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14
Q

What’s the period of infectivity of VZV?

A

The period of infectivity begins 48 hours before the rash appears and lasts until the vesicles crust over

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15
Q
  1. Symptoms of nonpregnant VZV?

2. Symptoms of VZV in pregnancy?

A

The primary infection causes chickenpox, which is characterized by fever, malaise, and a maculopapular pruritic rash that becomes vesicular.

After the primary infection, VZV remains dormant in sensory ganglia and can be reactivated to cause a vesicular erythematous skin rash known as herpes zoster, or shingles

  1. Benign and self-limited in children, but adults suffering more serious morbidity, such as encephalitis and pneumonia. Approximately 10–20% of pregnant women with varicella infection will develop pneumonia, which is a significant risk factor for maternal mortality, estimated to be as high as 40%
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16
Q

Why do we give VZV vaccine?

A

The antibody to VZV develops within a few days after the onset of infection, and prior infection with VZV confers lifelong immunity to primary infection, but not secondary!

17
Q
  1. The risk of congenital varicella syndrome in each trimester?
  2. What symptoms congenital varicella syndrome?
A
  1. first trimester 0.4%, second trimester 2%, third trimester 0%
  2. skin scarring, limb hypoplasia, chorioretinitis, and microcephaly
18
Q
  1. How do you diagnose Varicella in pregnancy?
  2. Ultrasound findings consistent with congenital varicella
  3. How to treat VZV?
  4. When is Varicella-zoster immune globulin (VZIG) indicated?
  5. What should treat Infants who develop varicella within the first 2 weeks of life with?
A
  1. diagnosed based on the clinical findings of a classic pruritic, vesicular rash. If you have use laboratory diagnosis, a sample taken from an unroofed skin lesion or vesicular fluid can be tested using a qualitative varicella PCR assay
  2. hydrops, hyperechogenic foci in the liver and bowel, cardiac malformations, limb deformities, microcephaly, and fetal growth restriction
  3. Oral acyclovir
    - reduce the duration of new lesion formation and the total number of new lesions and to improve constitutional symptoms
    - reduce maternal morbidity and mortality associated with varicella pneumonia
    - Does not ameliorate or prevent the fetal effects of congenital varicella syndrome
  4. Varicella-zoster immune globulin (VZIG) should be given to infants born to women who develop varicella between 5 days before and 2 days after delivery, although this treatment does not universally prevent neonatal varicella
  5. Intravenous acyclovir
19
Q

What’s the varicella vaccine regimen for

  • baby
  • non immune pregnant women
A
  1. 12 months of age or older as a two-dose regimen.
  2. receive the first dose of varicella vaccine upon completion or termination of the pregnancy. The second dose should be administered 4–8 weeks after the first dose
20
Q

How long should conception be delayed for?

A

Conception should be delayed for 3 months after the last dose because there is a small chance of mild varicella infection after vaccination with the live, attenuated vaccine.

varicella vaccine exposure during early pregnancy does not warrant pregnancy termination

21
Q

Treatment for Pregnant women who are not immune to VZV and are exposed to someone with active primary infection with chickenpox

A

VZIG as soon as possible, ideally within 96 hours of exposure, to prevent or attenuate the disease manifestations of VZV infection.
Still may be given up to 10 days after exposure

22
Q

A history of chickenpox infection is ___% predictive of the presence of serology consistent with past infection and life-long immunity

23
Q

How is CMV transmitted?

A

Cytomegalovirus is a ubiquitous double-stranded DNA herpesvirus that is transmitted by sexual contact or direct contact with infected blood, urine, or saliva.

24
Q

Symptoms of primary CMV?

Can CMV have recurrent or secondary infection?

A

mostly asymptomatic, mononucleosis-like syndrome, with fever, chills, myalgias, malaise, leukocytosis, lymphocytosis, abnormal liver function, and lymphadenopathy

Yes.

25
Q

What causes secondary infection of CMV?

A

Secondary infection (intermittent viral excretion in the presence of host immunity) can occur after reactivation of the latent endogenous CMV strain or by reinfection with a different exogenous viral strain

26
Q

How does vertical transmission of CMV happen?

A

Vertical transmission of CMV may occur as a result of transplacental infection after primary or secondary infection, exposure to contaminated genital tract secretions at delivery, or breastfeeding

27
Q

Ultrasound findings of CMV and Toxo

A

CMV:
These findings include abdominal and liver calcifications, hepatosplenomegaly, echogenic bowel or kidneys, ascites, cerebral ventriculomegaly, intracranial paraventricular calcifications, microcephaly, hydrops fetalis, and growth restriction

Toxo:
ventriculomegaly, intracranial calcifications (individual clumps), microcephaly, ascites, hepatosplenomegaly, and intrauterine growth restriction

28
Q

Congenital CMV diagnosis?

A

Amniotic fluid PCR or culture

29
Q
  1. What’s the overall vertical transmission risk of CMV?
  2. When is the risk of transmission the greatest?
  3. What is the risk for primary CMV vertical transmission in each trimester?
  4. Which trimester primary CMV vertical transmission will you see more serious fetal sequelae?
A
  1. With primary maternal CMV infection, the overall risk of transmission to the fetus is approximately 30–40%
  2. Third trimester
  3. Transmission rates for primary infection are 30% in the first trimester, 34–38% in the second trimester, and 40–72% in the third trimester.
  4. More serious fetal sequelae occur after maternal CMV infection during the first trimester.
30
Q

Symptoms for CMV in the fetus

A

Most infants with congenital CMV are asymptomatic at birth. Clinical findings of symptomatic congenital CMV infection include jaundice, petechiae, thrombocytopenia, hepatosplenomegaly, growth restriction, myocarditis, and nonimmune hydrops.

Congenital hearing loss is typically the most severe sequela of secondary infection, and congenital infection after recurrent infection is unlikely to produce multiple sequela