Perinatal Infections Flashcards
(32 cards)
Infection routes
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)
Vertically transmitted ( mother to child ) infections of the fetus and newborn can generally be divided 2 major categories:
- Congenital infections : which are transmitted to the fetus in utero.
- Perinatal infections : which are acquired intrapartum or in the postpartum period
Facts about congenital infections
- The time to provide information to mothers about these infections is before pregnancy begins, because this is the best time for preventive measures.
- The first trimester is usually the most dangerous time to acquire these infections.
- Infection in the mother can often be accompanied by trivial or even no symptoms, and the condition may not be remembered or diagnosed.
- Infection in the mother does not always mean that the baby will be affected.
- Some infections can be avoided by the mother through simple measures, e.g. immunization (Rubella, VZV ) during childhood and before pregnancy.
The most common organisms causing Congenital Infections
Etiologic Agents (TORCH):
- Toxoplasmosis
- Others [syphilis, tuberculosis, listeriosis ]
- Rubella
- Cytomegalovirus
- Herpes simplex
Other common congenital infections not caused by TORCH
- Hepatitis B
- Parvovirus B19
- HIV
- Campylobacter fetus.
- Fungi: Candida albicans.
- Parasites: Plasmodium spp., Trypanosoma cruzi
TORCH
ØTORCH group of infections are grouped together because they evoke similar clinical and pathologic manifestations:
- Fever
- Encephalitis
- Chorioretinitis
- Hepatosplenomegaly
- Pneumonitis
- Myocarditis
- Hemolytic anemia
- Vesicular or hemorrhagic skin lesions
Hematologic infections
Usually through chorionic villi ØToxoplasma ØMalaria ØMost of Viral Infections ØBacterial: Listeria, Treponema ØHIV usually through maternal-to-fetal transfusion
Transcervical Infections
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
Syndromes in neonates caused by congenital infections
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
CMV- cytomegalovirus
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.
Epidemiology: CMV
ØCMV spreads:
- 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
- to fetus across the placenta
CMV pathogenesis
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
CMV PATHOLOGY of FETUS
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.
CLINICAL FEATURES of Congenital CMV
ØCongenitally acquired CMV has diverse clinical presentations:
- Severe disease causes fetal death in utero, conspicuous CNS lesions, liver disease and bleeding problems
- Moderate form causes fetal growth restriction (FGR), microcephaly with periventricular calcifications
- 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.
- 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.
Diagnosis and treatment of CMV
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.Rubella
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
Epidemiology of rubella
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
Pathogenesis of Rubella
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
Clinical manifestation of Rubella
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
CONGENITAL RUBELLA SYNDROME (CRS)
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.
Diagnosis for Rubella
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
Erythrovirus ( Parvovirus B19 ) Erythema Infectiosum
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.
Pathology of b19
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)
5th disease
- Measles
- Rubella
- Chicken pox
- Roseola
- 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,
