Perinatal Infections Flashcards

0
Q

Infection routes

A

Ø1. Transcervically (ascending)
Ø2. Transplacentally (Hematologic)
Ø3. Combination 1+2

ØThe most common means of infection of the fetus is via the blood stream (transplacentally)
ØLess common means of infections is
via cervix (Transcervically)

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1
Q
Vertically transmitted ( mother to child ) infections
of the fetus and newborn can generally be divided 2 major categories:
A
  1. Congenital infections : which are transmitted to the fetus in utero.
  2. Perinatal infections : which are acquired intrapartum or in the postpartum period
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2
Q

Facts about congenital infections

A
  1. The time to provide information to mothers about these infections is before pregnancy begins, because this is the best time for preventive measures.
  2. The first trimester is usually the most dangerous time to acquire these infections.
  3. Infection in the mother can often be accompanied by trivial or even no symptoms, and the condition may not be remembered or diagnosed.
  4. Infection in the mother does not always mean that the baby will be affected.
  5. Some infections can be avoided by the mother through simple measures, e.g. immunization (Rubella, VZV ) during childhood and before pregnancy.
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3
Q

The most common organisms causing Congenital Infections

A

Etiologic Agents (TORCH):

  1. Toxoplasmosis
  2. Others [syphilis, tuberculosis, listeriosis ]
  3. Rubella
  4. Cytomegalovirus
  5. Herpes simplex
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4
Q

Other common congenital infections not caused by TORCH

A
  1. Hepatitis B
  2. Parvovirus B19
  3. HIV
  4. Campylobacter fetus.
  5. Fungi: Candida albicans.
  6. Parasites: Plasmodium spp., Trypanosoma cruzi
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5
Q

TORCH

A

ØTORCH group of infections are grouped together because they evoke similar clinical and pathologic manifestations:

  1. Fever
  2. Encephalitis
  3. Chorioretinitis
  4. Hepatosplenomegaly
  5. Pneumonitis
  6. Myocarditis
  7. Hemolytic anemia
  8. Vesicular or hemorrhagic skin lesions
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6
Q

Hematologic infections

A
Usually through chorionic villi
ØToxoplasma
ØMalaria
ØMost of  Viral Infections
ØBacterial: Listeria, Treponema
ØHIV usually through
maternal-to-fetal transfusion
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7
Q

Transcervical Infections

A

Acquired in Utero or around the time of birth (Premature Rupture of Membranes)
1. Inflammation of placental membranes→
2. Increased level of prostaglandins →
3. Contractions and labor →
4. Inhalation of infected amniotic fluid by fetus/newborn→
5. Pneumonia →Sepsis →Meningitis →
6. Death
MC transcervically entered pathogens are:
Bacterial (Streptococcus Group B!!!!)
Viral (Herpes Simplex II) Infections

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8
Q

Syndromes in neonates caused by congenital infections

A

Toxoplasma gondii
Hydrocephalus, diffuse intracranial calcification, chorioretinitis

Rubella virus
Cardiac defects, sensorineural hearing loss, cataracts

Cytomegalovirus
Microcephalus, periventricular calcification

Varicella - zoster virus
Limb abnormalities, cicatricial (scar) lesions

Erythrovirus B19 (Parvovirus B19)
Diffuse edema (in utero hydrops fetalis)

Herpes simplex virus
Vesicular lesions, keratoconjunctivitis

Treponema pallidum
Bullous, macular, and eczematous skin lesions involving the palms and the soles; rhinorrhea, dactylitis osteochondritis and periostitis

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9
Q

CMV- cytomegalovirus

A

ØCMV is a congenital and opportunistic pathogen that usually produces asymptomatic infection
ØFetus and immunocompromized patients are particularly vulnerable to CMV destructive effects
Ø CMV infects 0.5% to 2.0% of all fetuses and injures 10% to 20% of those infected, making it the most common congenital pathogen
ØThe most common cause of in-utero infection.
Ø Fetal infection is greatest ( 40% ) during primary maternal infection & rarely during recurrent infection.
Ø Only 10% of infants born with congenital infections are symptomatic at birth.
Ø Infection during 1st trimester usually causes severe affection.

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10
Q

Epidemiology: CMV

A

ØCMV spreads:

  1. from person to person by contact with infected secretions and bodily fluids -children spread it in saliva or urine, while transmission among adolescents and adults is primarily through sexual contact
  2. to fetus across the placenta
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11
Q

CMV pathogenesis

A

ØWhen an infected pregnant woman passes CMV to her fetus, the fetus is not protected by maternally derived antibodies and the virus invades fetal cells
ØDue to the little initial immunologic response, there is a widespread necrotic and inflammatory changes in various tissues

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12
Q

CMV PATHOLOGY of FETUS

A
Most commonly involves:
1.Brain
2.Inner ears
3.Eyes
4.Liver
5.Bone marrow
Signs:
6.Microcephaly
7.Hydrocephalus
8.Cerebral calcifications
9.Hepatosplenomegaly and jaundice.
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13
Q

CLINICAL FEATURES of Congenital CMV

A

ØCongenitally acquired CMV has diverse clinical presentations:

  1. Severe disease causes fetal death in utero, conspicuous CNS lesions, liver disease and bleeding problems
  2. Moderate form causes fetal growth restriction (FGR), microcephaly with periventricular calcifications
  3. Most congenital CMV infections do not produce gross abnormalities, but manifest as subtle neurologic or hearing defects, which may not be detected until later in life.
  4. If the infection is acquired during labour the symptoms may appear after an incubation period of 4-12 wk or pass unnoticed only to be discovered with hearing abnormalities later.
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14
Q

Diagnosis and treatment of CMV

A
Ø Culture.
Ø PCR.
Ø CMV IgM & IgG.
Ø CT scan, abnormal CT predicts high
    probability of CNS sequalae.
 Treatment:
    Gancyclovir – valgancyclovir
Prevention:
Ø Attenuated virus vaccine.
Ø Hyper immune CMV immunoglobulin.
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15
Q

Rubella

A

ØSingle-stranded RNA virus
ØVaccine-preventable disease
•No longer considered endemic in the U.S.
ØMild, self-limiting illness usually associated with a rash (also known as “German measles”).
ØInfection earlier in pregnancy has a higher probability of affected infant

16
Q

Epidemiology of rubella

A

ØRubella virus spreads from person to person, primarily by the respiratory route.
Ø Infection occurs worldwide.
ØRubella is not highly contagious, and in unvaccinated populations, 10% to 15% of young women remain susceptible to infection into their reproductive years.
ØThe currently available live attenuated viral vaccine prevents rubella and has largely eliminated the disease from developed countries

17
Q

Pathogenesis of Rubella

A

ØRubella infects respiratory epithelium, then disseminates through the bloodstream and lymphatics
ØThe rubella rash is result from an immunologic response to the disseminated virus
ØFetal infection occurs through the placenta
ØCongenitally infected fetus remains persistently infected and sheds large amounts of virus in body fluids, even after birth.
ØMaternal infection after 20 weeks’ gestation usually does not cause significant fetal disease

18
Q

Clinical manifestation of Rubella

A
ØSensorineural hearing loss (50-75%)
ØCataracts and glaucoma (20-50%)
ØCardiac malformations (20-50%)
ØNeurologic (10-20%)
ØOthers: growth retardation, bone disease, HepatoSplenoMegaly, thrombocytopenia, “blueberry muffin” lesions
19
Q

CONGENITAL RUBELLA SYNDROME (CRS)

A

ØThe risk of infection is greatest in 1st trimester, cardiac and hearing abnormalities invariably occur
Ø The classic CRS is characterized by:
* Eye anomalies: cataracts, retinopathy,
microphthalmia.
* Congenital heart: PDA, Pulmonary Stenosis, VSD – ventricular Septal Defect
* Neurological: meningoencephalitis, EEG abnormalities, psychomotor retardation.
* Sensorineural hearing loss.
* Hematological: HepatoSplenoMegaly, purpura.
* Radiological: bone lucencies.

Ø Some of these anomalies may not show until
months or years later.

20
Q

Diagnosis for Rubella

A

ØMaternal IgG may represent immunization or past infection - Useless!
ØCan isolate virus from nasal secretions
•Less frequently from throat, blood, urine, CSF
ØSerologic testing
•IgM = recent postnatal or congenital infection
•Rising monthly IgG titers suggest congenital infection
ØDiagnosis after 1 year of age difficult to establish
Treatment:
ØPrevention…immunize, immunize, immunize!
ØSupportive care only with parent education

21
Q

Erythrovirus ( Parvovirus B19 ) Erythema Infectiosum

A

Ø A common viral infection causing the slapped
cheek syndrome; fifth disease.
Ø Has been implicated in 10% of cases of fetal
non-immune hydrops fetalis.
ØA small percentage of susceptible women exposed to the virus are infected.

22
Q

Pathology of b19

A

ØHuman parvovirus B19 gains entry to erythroid precursor cells via the P erythrocyte antigen and produces characteristic cytopathic effects in those cells.
ØNuclei of affected cells are enlarged, with the chromatin displaced peripherally by central glassy eosinophilic material nuclear inclusion bodies (giant pronormoblasts)

23
Q

5th disease

A
  1. Measles
  2. Rubella
  3. Chicken pox
  4. Roseola
  5. Erythema infectiosum

ØPerinatal and intrapartum infections are very rare.
ØInutero infections can result in fetal death, nonimmune fetal hydrops, birth defects ( eyes, CNS ) and prematurity,

24
Q

Diagnosis of 5th disease

A

Serum IgM & IgG:
Ø Absent IgG antibodies in mother rules out
infection.

Ø IgM appears by day 3 after infection and
persists for 3 months at least.

25
Q

Prevention

A

Pregnant women SHOULD AVOID :

1- Contact with ill people.

2- Eating raw or undercooked meat.

3- Contact with cat feces.

4- Sexual contact with partner infected with genital
herpes or HIV.

Ø Immunization for Rubella, Hepatitis and VZV before pregnancy if they are seronegative.

Ø Live viral vaccines should be given 3-6 months before conception.

Ø No Live Viral Vaccine should be given to pregnant women for fear of causing congenital infection.

26
Q

Clinical signs of neonatal infections acquired in utero or at delivery (TRCH)

A

Hepatosplenomegaly:
Rubella+ CMV+ HSV+ Toxoplasma+
Jaundice:
Rubella+ CMV+ HSV+ Toxoplasma+
Adenopathy:
Rubella+ CMV- HSV- Toxoplasma+
Pneumonitis:
Rubella+ CMV+ HSV+ Toxoplasma+
Microcephaly:
Rubella- CMV++ HSV+ Toxoplasma+
Hydrocephalus:
Rubella+ CMV+ HSV+ Toxoplasma++
Intracranial calcifications:
Rubella- CMV++ HSV- Toxoplasma++
(periventricular)
Hearing deficits:
Rubella+ CMV+ HSV- Toxoplasma-
Skin lesions purpura:
Rubella+ CMV+ HSV+ Toxoplasma+
Vesicles:
Rubella- CMV+ HSV++ Toxoplasma+
Maculopapular rash:
Rubella- CMV- HSV+ Toxoplasma+
CNS:Meningo-encephalitis
Rubella+ CMV+ HSV+ Toxoplasma+

27
Q

Hydrops Fetalis

A

ØFetal Hydrops – accumulation of edema fluid during intrauterine growth
ØExist in 2 forms: non-immune and immune

ØMost common Hydrops Fetalis for is non-immune
Hydrops fetalis - generalized accumulation of fluid in the fetus. When there’s fluid accumulation is particularly prominent in the soft tissues of the neck, and this condition has been termed cystic hygroma. Cystic hygromas are characteristically seen, but not limited to, constitutional chromosomal anomalies such as 45,X0 karyotypes

28
Q

Pathogenesis of HF

A

ØIncreased Central Venous Pressure
Øimbalance of interstitial fluid production and the lymphatic return
ØImpaired cardiac output (tachyarrhithmias)
ØLow hepatic synthesis of albumin (hypoalbuminemia)

All Leading to edema

29
Q

Immune hydrops

A

ØFetus inherits red cell antigens from the father that are foreign to the mother
ØMother forms IgG antibodies which cross the placenta and destroy fetal RBCs
ØFetus develops severe anemia with CHF and compensatory ↑ hematopoiesis (frequently extramedullary)
ØMost cases involve Rh D antigen
•mother is Rh Neg and fetus is Rh Pos
ØABO and other antigens involved less often

30
Q

Treatment for Hydrops

A
ØIn utero
•identification of at risk infants via blood typing by amniocentesis, (Chorionic Villi Sampling) CVS, or fetal blood sampling
•fetal transfusions via umbilical cord
•early delivery
ØLive born infant
•monitoring of hemoglobin and bilirubin
•exchange transfusions
31
Q

Pathogenesis of sensitization

A

ØFetal RBCs gain access to maternal circulation largely at delivery or upon abortion
ØSince IgM antibodies are involved in primary response and prior sensitization is necessary, the first pregnancy is not usually affected
ØMaternal sensitization can be prevented in most cases with Rh immune globulin (Rhogam) given at time of delivery or abortion (spontaneous or induced)