Infectious/Communicable Disease Flashcards

1
Q

Cytomegalovirus (CMV)

Risk factors

A
  • Double stranded DNA herpes virus
  • Most common cause of congenital infection in developed country
  • Transmitted via all body fluids, sex, vertical
    • Usually urine or saliva
  • Remains latent in host cells after initial infection → latent virus can reactivate → recurrent infection
  • Risk factors:
    • Low- to-middle incomes
    • Black and Hispanic women - both higher seroprevalence of CMV and birth prevalence of congenital CMV
    • Day care workers and small children
    • Vertical transmission
      • 30 - 40 % after primary infection
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2
Q

Cytomegalovirus (CMV)

Clinical manifestations

A

Adult signs/sx:

  • Usually asymptomatic
  • Occasionally can mimick mononucleosis or flu
    • Fever
    • Sore throat
    • Aching muscles
    • Fatigue
    • Cervical lymphadenopathy

Fetal signs:

  • —Presence in fetal blood or amniotic fluid (not indicator of severity)
  • Ultrasound findings:
    • Intracranial calcifications
    • —Microcephaly
    • —Hydrocephaly
    • —IUGR
    • —Hydrops
    • —Poly or oligohydramnios
    • —Echogenic bowel or liver
    • —Ascites
    • —Ventriculomegaly
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3
Q

Cytomegalovirus (CMV)

Treatment plan

A
  • No vaccines or safe treatments
  • Depending on gestational age, pregnancy termination may be an option in the presence of congenital CMV or fetal anomalies.
  • Consultation/collaboration if primary infection or fetal anomalies for amniocentesis, serial ultrasounds, or available treatments
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4
Q

Cytomegalovirus (CMV)

Testing and Diagnosis

A

Laboratory testing recommended only when:

  • Pt presents with a mononucleosis-type illness
  • Fetal anomaly is detected
  • Maternal request

Diagnosis:

  • Presence of CMV-specific IgM and a four-fold increase in IgG titers in maternal serology.
  • PCR and viral cx are expensive
  • Amniocentesis for fetal testing
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5
Q

Cytomegalovirus (CMV)

Impact on fetal development

A
  • Leading cause of congential hearing loss
  • Transmission risk highest in 3rd tri, but infection in 1st tri associated with worse outcomes
  • Infection <20 weeks GA, infants may exhibit serious sequelae such as:
    • —low platelets
    • —enlarged liver and spleen
    • —jaundice
    • —petechiae
    • —sensorineural hearing loss
    • —developmental delays
    • —seizures
  • ~30% of severely infected infants die
  • 95% infants with congenital CMV infection exhibit no obvious clinical findings at birth
  • Neonatal infection usually asymptomatic/not associated with sequelae
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6
Q

Cytomegalovirus (CMV)

Prevention

A
  • Wear gloves and wash hands after changing diapers.
  • Wash hands after feeding a young child, wiping a young child’s nose or drool, or handling a child’s toys.
  • Avoid sharing cups/utensils with a young child,
  • contact with tears or saliva when kissing a child, putting a pacifier in her own mouth, or sharing a toothbrush with a young child.
  • Clean toys, countertops, and other surfaces that come in contact with a child’s urine or saliva.
  • Practice safe sex, including limiting the number of partners and correct use of condoms
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7
Q

Group B Strepococcus (GBS)

Risk factors and clinical manifestations

A
  • 10-30% of pregnant patients colonized with GBS in vagina or rectum
  • May be colonized without any signs or symptoms
  • Neonates can acquire the organism by vertical transmission in utero or during the birth process
    • Transmission rate 50% with vaginal delivery, but only 1–2% of the infected neonates develop GBS disease
  • Risk factors for early-onset GBS disease:
    • Intrapartum GBS colonization
    • Gestational age <37 completed weeks
    • PROM
    • Intra-amniotic infection
    • Young maternal age
    • Black race
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8
Q

Group B Strepococcus (GBS)

Testing and diagnosis

A
  • Universal screening for GBS colonization at 35–37 weeks’ gestation with the use of a single swab
    • Swab the lower vagina (vaginal introitus), then the rectum, inserting the swab through the anal sphincter.
    • Patient can self-collect following appropriate instruction
    • Cervical, perianal, perirectal, or perineal specimens are not acceptable and a speculum should not be used for culture collection
  • Exception: GBS UTI in pregnancy or previous baby with GBS disease
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9
Q

Group B Strepococcus (GBS)

Treatment plan

A
  • Intrapartum Penicillin G q 4 hours until delivery is prophylaxis of choice.
  • Prophylaxis indications:
    • Previous infant with GBS dz
    • GBS UTI with current pregnancy
      • GBS cx during current pregnancy
        • Unless planned C/S and no labor or ROM
    • Unknown GBS & any of following:
      • Delivery <37wks
      • ROM >18 hrs
      • Intrapartum temp > 100.4F
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10
Q

Group B Strepococcus (GBS)

Impact on maternal health and fetal development

A
  • Usually no impact on pregnancy, danger is generally intra/postpartum
  • Parent
    • Rare: sepsis, UTI, chorioamnionitis, post-partum endometritis
  • Neonate
    • Early onset sepsis (within 7 days of birth)
      • Vertical transmission
      • Severe pneumonia and septecemia
    • Late onset sepsis (7 days - 3 months)
      • Vertical and horizonal transmission
      • Bacteremia, meningitis, and pneumonia
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11
Q

Hepatitis A

Risk factors

A
  • small RNA virus
  • transmitted by the fecal–oral route,
  • person-to-person contact or
  • consumption of contaminated food or water
  • Typically self-limited and does not result in chronic infection.
  • Risk factors:
    • Exposure to contaminated food or water
    • Substandard hygiene or sanitation
    • Illegal drug use
    • Having children in day care.
    • Recently emigrated from or recently traveled to high-risk countries
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12
Q

Hepatitis A

Testing and diagnosis, treatment plan, and the impact on maternal health and fetal development

A
  • Minimal risk associated with HAV in pregnancy
    • Vertical transmission negligible because parental anti-HAV IgG antibodies cross the placenta and protect the infant after birth
  • Dx by serological testing
    • IgM anti-HAV antibodies - appear early in the disease process and persist for several months.
    • IgG antibodies - predominate during the convalescent period, persist and provide immunity for life against reinfection. IgG antibodies will also be present after vaccination.
  • Treatment:
    • Post-exposure vaccine if known contact
    • Supportive therapy
    • limit physical activity (avoid liver trauma)
    • healthy diet
    • avoid alcohol and hepatotoxic meds
    • Give baby HAV immune globulin within 48 hrs
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13
Q

Symtoms of acute viral hepatitis

A

May include:

  • Jaundice
  • Malaise
  • Fatigue
  • Anorexia
  • N/V
  • RUQ pain
  • Hepatic transaminases and bilirubin moderately to markedly elevated
  • Liver biopsy shows extensive hepatocellular injury with prominent inflammatory infiltration
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14
Q

Hepatitis B

Risk factors and transmission

A
  • small DNA virus
  • 40-45% of ALL cases of hepatitis
  • 85-90% cases have complete resolution: asymptomatic and immune
  • 10-15% cases develop a chronic HBV (usually no sx)
    • 15-30% continued viral replication → hepato-cellular damage/carcinoma
  • Transmission: HIGHLY CONTAGIOUS
    • Direct blood-to-blood contact
    • Unprotected sex
    • Unsterile needles
    • Perinatal – vertical and intrapartum (mostly intrapartum or when aquired during 3rd tri)
  • Risk factors:
    • Injectable drug use
    • Sexual contact with at-risk and/or multiple partners
    • Asian women have highest infection rates
    • Health-care workers
    • Hemodialysis patients
    • Travelers to high-risk areas
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15
Q

Hepatitis B

Testing and diagnosis

A

Antigens

  • HBsAg
    • —surface marker on HBV.
    • Indicates INFECTIOUS (acute or chronic if present > 6 months)
    • May be negative if previously infected/cleared the virus
  • HBcAg
    • —only released within infected hepatocytes.
  • HBeAg
  • —indicates viral replication during acute and chronic infection

Antibodies

  • anti-HBs
    • recovery from B virus or immunity
    • —Also develops in response to immunization
  • anti-HBc
    • —response to Hep B infection
    • positive for life
  • anti-HBe
    • —response to replicating HBeANTIGEN.
    • indicates clearance of virus or response to antiviral therapy
  • IgM anti-HBc
    • —acute infection with Hep B. Usually within past 6 months
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16
Q

Hepatitis B

Treatment plan

A

HBV vaccine series and HBV immune globulin (HBIG) within 12 hours of birth if parent** **HBsAg-positive

Supportive care

  • —Test viral load between weeks 30-34 and provide counseling regarding risk of infection
  • —Determine acute vs chronic

GI consult may perform following based on disease state

  • —Co-mgmt with OB and GI to follow disease process and liver involvement
  • —Liver Biopsy; will grade stage of disease if chronic
  • —Hepatic US
  • —Evaluation of liver enzymes
  • —Offer immunization to susceptible patients

Comprehensive care

  • Offer HIV and other STI testing
  • Offer Hepatitis A vaccine to prevent further liver injury
  • Education on safe sexual practices
  • Education on abstinence of alcohol and substances that may lead to liver damage
  • Caution when prescribing medication excreted by the liver
  • Offer testing for household members and sexual contacts
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17
Q

Hepatitis B

Impact on maternal health and fetal development

A
  • Report positive HBsAg screen to state and local hepatitis prevention programs
  • Refer to a liver disease specialist
  • Chronic HBV can have flare during pregnancy - monitor liver panel and viral load periodically
  • Perinatal transmission with amniocentesis low/minimal, but avoid if possible
  • Breastfeeding is safe as long as not on antiviral meds, and the infant has received HBIG and vaccine.
    • abstain from breastfeeding with bleeding nipples until healed
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18
Q

Hepatitis C

Risk factors

A
  • RNA virus
  • Most common blood borne infection in US + leading cause of chronic liver disease
  • Risk factors:
    • Hx of IV drug use
    • Hx of blood transfusion received before 1992
    • Hx of body tattoos or body piercings
    • Health-care workers, especially those experiencing
    • needlestick injury
    • Multiple sexual partners
    • Hx prior STI
    • HIV infection
  • Mostly asymptomatic (clinical sx in ~25% of exposed)
    • Onset is 2–24 weeks after exposure and may include:
      • Fatigue
      • Joint pain
      • Jaundice
      • Myalgia
      • Generalized pruritis.
      • llness is generally mild/often be ignored or mistaken for transient viral illness.
  • Chronic HCV infection develops in the majority of individuals who are positive for HCV
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19
Q

Hepatitis C

Impact on maternal health and fetal development

A
  • Parental:
    • higher risk for cholestasis
    • Premature rupture of membranes
    • Preterm birth
    • Congenital malformations
    • Placental abruption,
    • GDM
    • overall perinatal mortality
  • Fetus:
    • more likely to be LBW or admitted to a NICU
  • Risk of perinatal transmission depends on HCV viral load, HIV status, and ALT levels
    • undetectable HCV RNA → unlikely to transmit HCV to their infants
    • increased risk with higher viral titers (>100,000 copies/mL)
    • HIV infection (2-3x higher transmission risk)
    • Highter if ALT levels were elevated in the year preceding the pregnancy
  • Transmission may be increased with invasive fetal monitoring, amniocentesis, and ROM > 6 hours
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20
Q

Hepatitis C

Testing and diagnosis

A
  • Only test at-risk women: ie IV drug use
  • Screen (ELISA) for antibody to HCV.→ positive → hepatitis C viral RNA testing to check for current infection and their viral load.
  • Antibodies appear 6–10 weeks after the onset of illness and are present in more than 97% of infected persons within 6 months after exposure
  • hepatitis C viral RNA positive within 1–3 weeks after exposure.
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21
Q

Hepatitis C

Treatment plan

A
  • No tx for HCV in pregnancy other than expectant management
  • Rever to liver specialist
  • Counsel to abstain from alcohol and potentially hepatotoxic meds
  • Give vaccinations for hepatitis A and B
  • Vaginal birth and breastfeeding are not contraindicated.
    • HCV in breast milk at very low levels but is inactivated in the infant’s GI tract
    • Abstain from breastfeeding with cracked or bleeding nipples until healed
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22
Q

Parvovirus B19

Risk factors, clinical manifestations, pathophysiology

A
  • Aka fifths disease or slapped cheek disease
  • Single stranded DNA, preferentially infects rapidly dividing cells
  • Mostly found in children
  • Transmission mostly respiratory, also oral and blood
    • crosses placenta
  • 50% adults immune from prior exposure
  • *Animal parvoviruses can’t infect humans
  • Mostly asymptomatic.
    • If present, likely to be mild/nonspecific
      • fever, arthralagia, stuffy nose, headache, and nausea, occurring approximately 1–2 weeks after exposure.
      • Bright facial exanthema, or rash on cheeks, giving “slapped cheek” appearance in 3rd week. Also may have lacy red rash on trunk and extremities
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23
Q

Parvovirus B19

Testing and diagnosis

A
  • Test if pt exposed, develops sx, or when abnormal ultrasound findings suggest congenital infection.
  • serum ELISA testing for IgG and IgM antibodies.
    • IgG + but IgM - → immunity
    • If both negative, and the test was performed after the incubation period → patient not immune and has not been infected.
    • If both antibodies are positive → patient has been infected in the previous 7–120 days
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24
Q

Parvovirus B19

treatment plan, and the impact on maternal health and fetal development

A
  • No treatment or vaccine
  • Good handwashing
  • Majority of patients who become infected with parvovirus B19 have no adverse pregnancy outcome,
  • Replicates rapidly in RBCs and is a potent inhibitor of erythropoiesis → anemia and hydrops
  • ~ 3-5% of infected women experience miscarriage, severe fetal anemia, or nonimmune hydrops fetalis
    • especially if infected in first 20 wks
    • if fetal hydrops and ascites seen on US think parvo
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25
Q

Rubella

Risk factors, clinical manifestations

A
  • Single stranded RNA
  • Typically affects children/young adults
  • Transmitted person-to-person, respiratory droplets, or via placenta
  • Usually mild illness in adults (fetus can get sick)
  • 50% have no sx
  • Parent sx:
    • Non-pruritic rash.
    • Starts on face then trunk then extremities
    • Malaise
    • Fever
    • Conjunctivitis
    • Lymphadenopathy
26
Q

Rubella

Testing and diagnosis, treatment plan

A
  • Parent Diagnosis:
    • Positive for IgM specific for rubella indicates exposure or infection
    • (IgG indicates immunity)
  • Fetal Diagnosis:
    • Viral PCR on CVS or amnio
    • IgM on cordocentesis (must be after 22 wks))
    • Via ultrasonography
    • Common ultrasound findings:
      • —Cardia defects
      • —Microcephaly
      • —Early growth retardation
  • Maternal Treatment:
  • Typically self-limited, no current tx
  • Encourage patients who are non-immune to avoid possible exposure to the virus
27
Q

Rubella

Impact on maternal health and fetal development

A
  • Maternal course mild, self limiting
  • Congenital Rubella Infection
  • Associated with growth restriction, miscarriage, stillbirth and can have significant deleterious effects on the fetus
  • 1st tri infection
    • 80% transmission to fetus (risk lessens w/increaseing GA)
    • Risk for miscarriage
    • Highest risk for congenital rubella syndrome (CRS)
      • Sensorineural hearing loss
      • Cataracts
      • Glaucoma
      • Retinitis
      • Patent ductus arteriosus
      • Cardiac lesions
  • Rubella vaccine is live - give 4 weeks prior to conception or post partum (safe to breastfeed)
28
Q

Toxoplasmosis

risk factors/transmission

A

Transmission:

  • Zoonotic (animal-to-human)
    • Cat eats infected small animal → T. gondii lives in the cat’s intestines → oocyst excreted in feces for up to 3 weeks → feces contaminates the litterbox and soil or water if outdoor → people or other mammal eat something contaminated, clean literbox, drink infected water → trophozite released → forms cysts in brain and muscle
  • Foodborne (uncooked meat, unwashed veg)
  • Congenital (mother-to-child) - only if primary infection during or right before pregnancy
    • 30% transmission
  • Rare instances: organ transplant and blood transfusion
29
Q

Toxoplasmosis

Clinical manifestations, testing and diagnosis

A
  • Parent Signs and Symptoms :
    • May be asymptomatic
    • May have similar sx as mononucelosis:
      • Fatigue
      • Malaise
      • Sore throat
      • Fever
      • Swollen lymph nodes in your neck and armpits
      • Swollen tonsils
      • Headache
      • Skin rash
    • Rarely vision changes
  • Patient Diagnosis:
    • Presence of IgM-specific antibody
    • Very high IgG antibody titer
  • Fetal Indicators for maternal serum testing:
    • Abnormal ultrasound
      • Hydrocephaly
      • CNS abnormalities (intracranial calcifications, ventriculomegaly)
      • Hepatosplenomegaly/ascites
      • Plural effusion
      • Symmetric FGR
      • Nonimmune hydrops
  • Fetal testing: amnio and PCR to confirm congenital infection after 18 wks.
30
Q

Toxoplasmosis

Treatment plan

A

Spiramycin

Only available through the FDA

Used in 1st and early 2nd trimester

Pyrimethamine, Sulfadiazine and Leucovorin

Used in 2nd and 3rd trimester

Acutely-infected mothers need to be referred to MFM for co-management.

Infected infants aggressively treated with combo abx X 1 year

31
Q

Toxoplasmosis

Impact on maternal health and fetal development

A
  • Mother usually unaffected unless severely immunocomprimised (ie AIDS)
  • Congenital infection more likely when contracted in 3rd tri BUT sx are worse if contracted in 1st tri
  • Congenital toxoplasmosis sx:
    • Rash
    • Hepatosplenomegaly Ascites
    • Fever
    • Chorioretinitis Periventricular calcifications Ventriculomegaly
    • Seizures
    • Intellectual disability
    • Uveitis
32
Q

What does TORCHS stand for?

A

T – Toxoplasmosis

O – Other infections

R – Rubella

C – Cytomegalovirus

He – Herpes

S – Syphilis

33
Q

What is hydrops fetalis?

A

Condition in the fetus characterized by an abnormal collection of fluid in at least two compartments:

  • Edema
    • Fluid beneath the skin, more than 5 mm
  • Ascites
    • Fluid in abdomen
  • Pleural effusion
    • Fluid in the pleural cavity, the fluid-filled space that surrounds the lungs
  • Pericardial effusion
    • Fluid in the pericardial sac, covering that surrounds the heart

In addition, hydrops fetalis is frequently associated with polyhydramnios and a thickened placenta (>6 cm).

Long term prognosis depends on underlying cause and severity of the heart failure.

If the cause of NIH cannot be determined, the perinatal mortality is approximately 50%

Prognosis is much poorer if diagnosed at less than 24 weeks , pleural effusion is present, or structural abnormalities are present .

Pulmonary hypoplasia is a common cause of death in neonates with plerual effusions.

Fetal hydrops associated with a structural heart defect is associated with an almost 100% mortality rate.

34
Q

Varicella (VZV)

Risk factors, clinical manifestations

A
  • 95% of adults are immune
  • Transmission: respiratory droplets, close contact, placenta or ascending lesions from vagina
    • Highly contageous
  • Symptoms:
    • Primary infection manifests as chickenpox
      • Maculopapular pruritic rash
        • —face, scalp, trunk
        • —rash → vesicles → pustules → crusts
      • Adults typically have prodromal symptoms:
        • —1-2 days before rash
        • Fever, HA, Malaise, Abdominal pain
    • Varicella pneumonia - dangerous, unpredictable medical emergency
      • More severe but not more likely in pregnant patients
    • Zoster (Shingles)
      • Dormant VZV in sensory ganglion after primary infection reactivated
      • Prodrome: HA, photophobia, malaise, fever, abnormal skin sensations, and excruciating pain
      • Unilateral erythematous vesicular skin rash on trunk or face
      • Pain (rather than itching)
      • Contagious until lesions have dried
      • Most common in elderly and immunocompromised pts
35
Q

Varicella

Testing and diagnosis

A
  • Characteristic lesions
  • PCR lesions (if not healed) or sometimes oral secretions
  • Single IgM or IgG results cannot be used to confirm infection.
    • Rash + positive IgM → diagnistic varicella.
    • A positive IgM suggests primary infection but doesnt exclude reinfection/reactivation of latent
    • IgM is considerably less sensitive then PCR testing of skin lesions.
    • IgM may not be reliable; and false negative IgM common
  • Congenital varicella syndrome ultrasound markers:
    • Combo of limb hypoplasia, skin lesions, microphthalmos, and abnormal positioning of limbs.
    • Nonimmune hydrops findings include: hepatosplenomegaly, ascites, pleural effusion, pericardial effusion, and liver calcification
    • VZV DNA testing in placental villi, fetal blood or amniotic fluid and for VZV IgM in fetal blood may be done
    • Presence of VZV DNA does not necessarily correlate with fetal disease
36
Q

Varicella

Treatment plan

A
  • Administer varicella immunoglobulin (VZIG) ASAP post exposure
    • May be effective as late as 96 hours after exposure
    • 125 units per 10 kg, with a max of 625 units.
  • Supportive care: calamine lotion, antipyretics, and if necessary, systemic antipruritics.
  • Acyclovir (800 mg PO 5x/day) or valacyclovir (1 g PO 3x/day)
    • Give to everyone - if instituted within 24 hours of rash emergence → decreased duration
  • Maternal varicella pneumonia - 5% maternal mortality and presents 3 to 5 days following the rash
    • IV acyclovir q 8 hours.
  • If varicella occurs within 5 days before and 2 days after delivery, give VZIG to newborn and isolate from the patient until all vesicles have crusted over to prevent VZV transmission.
  • If possible, delay delivery 5 to 7 days following the onset of maternal illness to potentially prevent neonatal VZV (20% to 30% mortality)
37
Q

Varicella

Impact on maternal health and fetal development

A

Maternal complications:

  • Secondary skin bacterial infections, CNS manifestations, such as meningoencephalitis or cerebellar ataxia, and pneumonia or pneumonitis, either viral or bacterial.
  • Less common: hepatitis, hemorrhagic complications, thrombocytopenia, and nephritis
  • HZ ophthalmicus when ophthalmic division of trigeminal nerve is involved can → chronic ocular complications, reduced vision, and blindness

Risks of Fetal/Neonatal Infection

  • Congenital Varicella Syndrome (CVS)
    • VZV during 5th - 20th wk. Only 2% risk, but 30% mortality
    • Severe forms can be fatal
    • Signs:
      1. Skin lesions
      2. Microcephaly
      3. Skin scarring
      4. Chorioretinitis
      5. Limb hypoplasia
      6. Developmental delay
  • Neonatal Varicella
    • VZV near term (ie 5 days before birth - 2 days after)
    • If placental transfer, sx by 10 days old
    • May cause severe or fatal illness in newborn
    • Death from VZV much more likely if parent develops rash btw 4 - 5 days before and 2 days after delivery (no time for antibodies)
    • Try to delay delivery if possible
    • VZIG either IM or IV after delivery
  • Zoster in infancy or early childhood
    • Extremely rare
    • Increased in frequency in neonates whose mothers had gestational varicella
    • Mild and not painful
38
Q

Chlamydia

Risk factors, clinical manifestations

A
  • Highest rates: adolescents and young adults. Rate for African Americans 8x > Caucasians
  • Mostly asymptomatic
  • May have:
    • Vaginal discharge
    • Postcoital bleeding
    • Dysuria
    • Vague lower abdominal pain
    • Mucopurulent cervical discharge
    • Tenderness on bimanual exam
    • Numerous WBCs on wet mount, but not diagnostic
39
Q

Chlamydia

Testing and diagnosis, treatment plan

A
  • Testing:
    • Screen at 1st prenatal visit.
    • NAATs, rapid test, culture on urine or vaginal swab
    • Retest any high risk in 3rd tri
    • Age < 25 years
    • New sexual partners or multiple partners
    • Women who test positive at 1st prenatal visit should be retested 3–6 months later, preferably in the 3rd tri
  • Treatment:
    • Azithromycin 1 gram PO single dose OR
    • Amoxicillin 500mg PO TID x7days
    • 5-10% of pts do not respond to tx, TOC need to be done in 2-3wks s/p tx (or 3-4 wks per Gabbe)
    • Abstain from sexual contact until 7 days after completion of antibiotic therapy.
40
Q

Chlamydia

Impact on maternal health and fetal development

A
  • Impact on Pregnancy:
    • May cause localized infection of urethra, endocervix and rectum
    • May cause peri-hepatitis and pneumonia
  • Impact on Newborn:
    • May cause Opthalmia Neonatorum and pneumonia
      • May have perforation of the globes of the eye and blindness
41
Q

Gonorrhea

Risk factors, clinical manifestations, testing and dx

A
  • 2nd most common STD
  • Most common among age 15 - 19
  • Signs and Symptoms:
    • May be asymptomatic
    • Vaginal mucopurulent discharge
    • Lower abdominal pain/tenderness
    • Fever
    • Dysuria/urinary frequency
    • Tenderness in the area of Bartholin’s or Skene’s glands
  • Diagnosis:
    • NAAT
    • Culture of endocervix and vagina
    • Urine culture
    • Prenatal assessment- 1st and 3rd trimester for HR patients (<25 yrs highest risk)
42
Q

Gonorrhea

Impact on maternal health and fetal development

A

May cause PROM and/or PTD

May pass to newborn → Opthalmia Neonatorum & sepsis

43
Q

Syphilis

risk factors, clinical manifestations

A
  • More common in males than females (1.5:1)
  • 30x more common in blacks than in whites
  • 20-24 year olds at greatest risk
  • Primary
    • Raised painless chancre 10-90 days after infection, goes away in 3-6 wks
  • Secondary
    • Macropapular rash on palms of hands and soles of feet and mucous membranes, usually 2-6 months after. Spontaneously resolves in 2-6 wks.
    • Only 1/3 of un-tx primary cases progress to 2nd
    • Most contageous at this stage
  • Tertiary—neurosyphilis, cardiac lesions (ie aortic aneurysm)
44
Q

Syphilis

Impact on maternal health and fetal development

A

Ultrasonography findings

  • —Placentomegaly
  • —IUGR
  • —Microcephaly
  • —Hepatosplenomegaly
  • —Hydrops

Congenital syphilis

  • transplacental, can happen at any stage of infection (almost 100% in early stage) and any GA
  • Often associated with infections of the bone, brain, heart, lungs, and abdominal organs
  • Leading cause of stillbirth and neonatal death in the developing world
  • Early Clinical Manifestations:
    • Macupapular rash
    • Snuffles (Syphilis rhinitis)
    • Mucous patches
    • Hepatosplenomegaly
    • Jaundice
    • Pneumonia
    • Lymphadenopathy
    • Osteochondritis
    • Chorioretinitis
    • Iritis
  • Late Clinical Manifestations:
    • Hutchinson teeth
    • Mulberry molars
    • Intestational keratitis
    • Deafness
    • Saddle nose
    • Rhagades
    • Saber shins
    • Mental retardation
    • Hydrocephalus
    • Generalized paresis
    • Optic nerve atrophy
    • Clutton joints
45
Q

Syphilis

testing and diagnosis, treatment plan, and the impact on maternal health and fetal development

A
46
Q

HSV

(active 1º and 2º infections, past hx of infection)

Transmission to baby, impact on maternal health and fetal development

A

Neonatal herpes transmission:

  • Transmission to rarely through placenta, usually through birth
    • Recommend C/S for active genital lesions or prodromal symptoms such as vulvar pain or burning at delivery
    • Suppressive therapy for anyone who has had a vaginal outbreak during pregnancy starting at 36 weeks
  • 80% of infected infants are born to parents with no reported hx of HSV
  • Primary HSV @ delivery- 30-60%
  • Recurrent HSV lesion @ delivery- 1-3%
  • H/O recurrent HSV, but NO lesions @ delivery- 1-3%

Clinical manifestations:

  • Skin, eye, mouth disease
  • Localized CNS disease
  • Disseminated state involving multiple organs
  • Non-specific symptoms such as irritability, fever, poor feeding or lethargy

Neonatal Herpetic Infection Complications:

  • Seizures
  • Psychomotor retardation
  • Blindness
  • Learning disabilities
  • Death
47
Q

HSV

(active 1º and 2º infections, past hx of infection)

Treatment plan

A
  • Primary outbreak:
    • —Acyclovir: 400mg PO TID x 7-10 days
    • —Valacyclovir: 1g PO BID x7-10 days
    • Famcyclovir: 250 mg PO TID x 7-10 days
  • Symptomatic recurrent episode:
    • —Acyclovir: 800 mg PO BID x 5 days or TID x 2 days
    • —Valacylcovir 500mg PO BID x 3 days or 1g PO QD x 5 days
  • Daily suppression:
    • —Acyclovir 400mg PO BID from 36 wks until delivery
    • —Valacyclovir 500-1000 mg PO QD from 36wks until delivery
48
Q

HSV

(active 1º and 2º infections, past hx of infection)

clinical manifestations, testing and diagnosis

A
  • Culture (turn around time is 72-96 hrs)
  • PCR assays- faster and very/most sensitive
  • Serology to test for antibodies- may be able to differentiate between HSV-1 and HSV-2, depending on lab
    • IgG and IgM can help determine whether the episode is primary or recurrent as well as identify the infection subtype to better characterize the risk of vertical trans- mission.
    • Antibodies 2–12 weeks after infection, and cannot be used alone to diagnose acute infection.
49
Q

Trichomonas

Impact on maternal health/fetal development

A
  • Associated with adverse pregnancy outcomes including:
    • Premature ROM
    • PTB
    • LBW
  • Vertical transmission in about 5% of pregnancies.
    • Most cases of neonatal infection resolve within 1 month after birth without tx.
  • Treatment for T. vaginalis during pregnancy may be associated with an increase in the rate of PTB).
    • Current consensus- symptomatic patients and their partners should be treated to relieve suffering, though it remains unclear if this course of action prevents or promotes PTB
50
Q

Bacterial vaginosis

Impact on maternal health and fetal development

A
  • Maternal implications
    • —Chorioamnionitis
    • —Endometritis
    • —C-section wound infection
  • Neonatal implications
    • —Preterm labor/delivery
    • —PPROM
    • SAB
51
Q

Bacterial vaginosis

Trreatment

A
  • Treat all symptomatic pregnant women regardless of risk factors
  • —High risk asymptomatic pregnant women should be treated according to some experts.
  • —Treatment of asymptomatic low risk pregnant patients is inconclusive
  • BV and chorioamnionitis may increase the risk of perinatal transmission of HIV → extra important to tx HIV infected patients
  • Medications:
    • —Metronidazole 500 mg PO BID x7 days
    • —Clindamycin 300mg PO BID x7 days
    • —Vaginal administration has lower efficacy and is not recommended during pregnancy
52
Q

HIV

risk factors, testing and diagnosis, treatment plan

A
  • Risk factors:
    • Women usually aquire by heterosexual contact
    • Black Americans 65% of new cases
  • Testing:
    • HIV 1 and 2 antibody assay at 1st prenatal visit and in 3rd trimester for anyone at increased risk
      • if positive → confirmation of infection with an HIV-1/HIV-2 antibody differentiation immunoassay and HIV-1 nucleic acid test
  • Treatment:
    • Combination care with at least 3 drugs from at least 2 classes of ARVs
    • If CD4 < 200 → need prophylaxis against OI’s
    • Viral load check q trimester if on stable, effective regimen
53
Q

HIV

Impact on maternal health and fetal development

A
  • Most perinatal HIV transmission occurs within the intrapartum period
    • effective cART or scheduled C/S in patients without viral suppression (VL > 1,000) substantially reduces transmission
  • Early/sustained control associated with decreased HIV transmission → initiate cART as early in pregnancy as possible for all women not treated preconceptionally
  • Breast feeding not recommended in the US (benefits of BF do not outweigh risks of transmission)
  • Test infant:
    • 14 to 21 days of life
    • 1 to 2 months
    • 4 to 6 months
    • 2 positive tests on different specimens, (excluding cord blood), required to dx HIV infection; 1 positive test is a presumptive diagnosis.
    • Presumptively excluded: 2 negative tests at age 14 days or older and age 1 month or older.
    • Defnitive exclusion in a non-breastfed infant is based on 2 negative tests at age 1 month or older and at age 4 months or older
54
Q

Coxsackie virus

Patho/transmission, impact on pregnancy

A
  • Causes hand, foot, and mouth disease
  • Enterovirus transmitted through the fecal-oral route
  • Several serotypes exist, and adult infection typically results in a self-limited febrile illness that requires no treatment
  • During pregnancy has been associated with liver failure (non-life threatening), miscarriage, and an increased rate of insulin-dependent diabetes in offspring, although a causative relationship has not been established
55
Q

Asymptomatic Bacteriuria vs Acute Cystitis

risk factors, clinical manifestations, testing and diagnosis

A
  • Asymptomatic bacteriuria 5-10% of pregnancies (often predates pregnancy)
  • Acute cystitis about 1 %
  • 1/3 will develop pyelonephritis if untreated
  • Common organisms: e. coli, klebsiella, proteus
  • Urine culture at 1st prenatal visit for everyone
    • Positive is > 100,000 colonies/mL
  • Acute cystitis sx:
    • frequency
    • dysuria,
    • urgency
    • suprapubic pain
    • hesitancy
    • dribbling
    • Gross hematuria may be present, leukocyte esterase and nitrate usually positive
    • High fever and systemic symptoms are uncommon
56
Q

Asymptomatic Bacteriuria vs Acute Cystitis

treatment plan

A
  • 3 day course of antibiotics seems as effective as a 7 - 10 day course (according to Gabbe)
    • use longer course for recurrent
  • If sensitivities are available use them to make antibiotic choice
  • Nitrofurantoin (Macrobid) - effective against most common pathogens except proteus. Has minimal effect on vaginal/bowel flora
  • Ampicillin, amoxicillin, cephalexin (keflex), amoxicillin-clavulanic acid (Augmentin) - more likely to cause diarrhea and monilial vulvovaginitis
  • Augmentin or Bactrim for empiric tx of suspected resistant infections
57
Q

Pyelonephritis

risk factors, clinical manifestations

A
  • Incidence is 1-2% in pregnancy
  • Usually undiagnosed UTI or inadequate tx
  • Normal pregnacy changes: progesterone inhibits ureter peristalsis + gravid uterus compresses uterers → urinary stasis → increased risk of infection
  • 75-80% of cases occur on right side
  • E. coli is prominent pathogen
  • klebsiella and proteus in recurrent infection
  • Symptoms:
    • Fever
    • Chills
    • Flank pain and tenderness
    • Urinary frequency or urgency
    • Hematuria
    • Dysuria
    • May have signs of preterm labor, septic shock, and acute respiratory distress syndrome (ARDS).
    • Urinalysis is usually positive for WBC casts, RBCs, and bacteria
58
Q

Pyelonephritis

Treatment plan

A
  • Outpatient if mild disease, hemodynamically stable, and no evidence of PTL
    • amoxicillin-clavulanic acid 875 mg BID or double-strength trimethoprim-sulfamethoxazole BID x 7 to 10 days.
  • Alternatively, a visiting home nurse may administer a parenteral agent such as intravenous (IV) or intramuscular (IM) ceftriaxone 2 g once daily.
  • Although an excellent drug for lower tract infections, nitrofurantoin monohydrate does not consistently achieve the serum and renal parenchymal concentrations necessary for successful treatment of more serious infections.
  • Patients who appear to be moderately to severely ill or who show any signs of preterm labor should be hospitalized for IV antibiotic therapy
  • Take macrobid suppression once better due to recurrence risk and screen for bacteriuria q visit
59
Q

Describe maternal alterations in immune response during pregnancy

  • Review cell-mediated and humoral response to infection
  • Describe the normal changes that occur in the WBC count during pregnancy
A
  • T helper and cytotoxic T cells are suppressed
    • thought to be why autoimmune diseases like MS, rheumatoid arthritis (etc) go into remission
  • Humoral (B-cells) dont really change
    • IgA - present in breastmilk
    • IgG - crosses placenta, present in breastmilk
      • can potentially harm fetus (ie parental Graves disease → neonatal hypothyroid in 1% of cases, another example: Rh issues)
  • WBCs can be 5,000 - 15,000 normally in pregnancy
    • Mostly neutrophils
    • Can get as high as 30,000 in labor without infection
60
Q

Infections that cross the placenta

A
  1. Toxoplasmosis
  2. Rubella
  3. Parvo
  4. CMV
  5. VZV
  6. Listeriosis
  7. Syphilis
61
Q

Infections that do not cross the placenta

A
  1. GBS
  2. Hepatitis A, B, C
  3. GC/CT
  4. HIV
  5. Flu