Congenital Infections Flashcards
How are congenital infections contracted
4
in utero,
transplacental
Via ruptured membranes
from the birth canal during delivery (intrapartum)
What is a TORCH and why is it important in paediatrics
group of diseases that cause congenital abnormalities if the fetus undergoes intrauterine exposure from maternal infection
T: Toxoplasma gondii. O: Others= Syphilis, Parvovirus, Varicella zoster. R: Rubella. C: Cytomegalovirus (CMV). H: Herpes zoster.
name a few General characteristics of congenital infections
New active maternal infection is obligatory
No risk for subsequent pregnancies.
Most often affected organs: Brain and liver.
Morphologic changes: necrosis and inflammation.
Diagnostic criteria:
°IgM in umbilical blood > 0.2 g/l (first 24 hrs).
°Elevated specific IgM in the newborn.
° Elevated specific IgG in the newborn that exceeds maternal blood level
General clinical presentation of a newborn w/ a congenital infection ( when in doubt & syphillis )
Intrauterine growth retardation.
Enlargement of the liver and spleen.
Jaundice especially w/ hepatomegaly and hepatitis
Rashes of different types( syphillis & aids)
Necrotizing encephalitis, intracerebral calcifications → microcephaly, hydrocephalus.
Chorioretinitis.
Hematologic manifestations: Anemia, thrombocytopenia
Why is the Risk of contracting intrapartum and postpartum infection is inversely proportional to gestational age.
Although antibodies are actively transported across the placenta,
effective levels of Maternal IgG are not achieved until near term so infecti me are more likely at an early gestational age than a later one
Consequences of congenital infections
depend on the agent and timing of infection in gestation
spontaneous abortion,
intrauterine growth restriction,
premature birth, stillbirth,
congenital malformation (eg, rubella),
symptomatic (eg, CMV, toxoplasmosis, syphilis) asymptomatic (eg, CMV) neonatal infection.
How does Congenital toxoplasmosis occur
transplacental acquisition !!of Toxoplasma gondii parasite after the mother is infected by
1) consumption of raw or undercooked meat
2) from contact with the faeces of recently infected cats.
Although the rate of fetal transmission is higher when women are infected later during pregnancy fetuses infected earlier in gestation have more severe disease.
Manifestation of congenital toxoplasmosis
Sx vs asx
Newborns can be
Symptomatic General sx of congenital infections
Asymptotic: remain at risk of developing chorioretinitis into adulthood.
Dg of Congenital toxoplasmosis
serologic testing of maternal IgG
PCR of the amniotic fluid.
Neuro: Brain imaging, CSF analysis, ophthalmologic evaluation (for neonatal infection)
Rx of Congenital toxoplasmosis
pyrimethamine, sulfadiazine, and leucovorin for a year.
Sometimes spiramycin is used for pregnant women yet to give birth
How does Congenital rubella infection occu
primary maternal infection w/ Rubella virus which invades the upper respiratory tract, and causes subsequent viremia. Once I’m the blood Virus then disseminates to the placenta.
highest risk of developmental abnormalities when infected during the first 16 wk of gestation! particularly the first 8 to 10 wk!! As early infection increases chances of chronic uterine infection
Sx of rubella In the pregnant women and the Fetus
Maternal URT symptoms, mild fever, conjunctivitis, Sub occipital/ post auricular lymphadenopathy a maculopapular rash.
Infant 👶
No effect
Congenital rubella syndrome
Death In utero
What is congenital rubella syndrome
Head heart hearing 👀
Mx abnormalities cause by congenital rubella infection consisting Of
Intrauterine growth restriction Microcephaly!! Meningoencephalitis!!! Cataracts Retinopathy Hearing loss Cardiac defects (PDA and pulmonary artery stenosis) Hepatosplenomegaly
Dg of Congenital rubella infection
maternal serum rubella titers,
viral detection in the mother via culture
reverse transcriptase–PCR (RT-PCR)
of amniotic fluid, nose, throat (preferred), urine, CSF, or blood specimens
infant antibody titers.
Can congenital rubella be rx
No specific therapy is available for maternal or congenital rubella infection.
most pregnancies end in termination.
Prevention with the MMR (measles, mumps and rubella) vaccine is only therapeutic option
How is Congenital CMV infection acquired
Prenatal(transplancental) perinatal acquisition ( during delivery)
Most common congenital infection
Sx of Congenital CMV infection
90% are normal at birth and develop normally a
5% have general clinical features of TORCH at birth
Can be acquired in late infancy and present w/ pneumonia,
hepatosplenomegaly,
hepatitis,
thrombocytopenia,
sepsis-like syndrome,
atypical lymphocytosis.
Typical dg work up of Congenital CMV infection
Virus= PCR
viral detection using
1) culture using urine, saliva, or tissue
2) PCR using urine, saliva, blood, or tissue.
Rx for Congenital CMV infection
Supportive rx for deteriorated hearing
Parenteral ganciclovir or oral valganciclovir given to infants with symptomatic disease identified in the neonatal period.
What are the clinical sx of CONGENITAL SYPHILIS:
Same as general TORCH manifestation
Specific sx are
A characteristic rash on the soles of the feet and hands.
Bone lesions.
Dg of congenial syphillis
Why are there two types of dg Tests
nontreponemal tests: detect cardiolipin. B antibody.
-Venereal Disease Research Laboratory (VDRL)
-Rapid Plasma Reagin (RPR) tests
Often false positive So require confirmation
treponemal tests: confirmation of +ve non trep test
- Fluorescent Treponemal Antibody-Absorption (FTA-ABS) test
- Microhemagglutination Assay-Treponema pallidum(MHA-TP) test.
Principles for syphillis tests
Gestational syphilis is diagnosed most commonly by routine serological screening of all women during early pregnancy.
Women who are considered to be at high risk for acquiring syphilis during pregnancy should undergo repeat testing in the third trimester and at delivery.
Describe the key clinical features of CONGENITAL HEPATITIS:
symptoms usually appear at 1-2 months of age.
Jaundice: Yellow eyes and skin. Pain in the abdomen. Dark urine. Loss of appetite and no normal weight gain. Nausea and vomiting.
Dg of giant cell CONGENITAL HEPATITIS:
liver biopsy -
shows combo of 4-5 liver cells into a large cell that still functions, but not as well as a normal liver cell.
This type of neonatal hepatitis is called “giant cell hepatitis.”
What are the four types of complications of congenital hepatitis depending on the type
Neonatal hepatitis caused by rubella or cytomegalovirus
- Increase risk of brain infection leading to mental retardation or cerebral palsy.
- increased risk of permanent liver disease from scarring (cirrhosis).
Infants with giant cell hepatitis
- usually recover (80 percent of cases) with little or no scarring to the liver.
- 20 % have jaundice lasting six months of age & require a liver transplant d/2 develop chronic liver disease/ cirrhosis
Vitamin deficiency
-Because of the blockage of the bile ducts and the damage caused to liver cells, infants with chronic neonatal hepatitis will not be able to digest fats and will not be able to absorb vitamins.
-Vitamin D def: rickets
-Vitamin A def: is also needed for normal growth and good vision.
Vitamin K def: coagulopathy = easy bruising and a tendency to bleed
-Vitamin E def: results in poor coordination.
Chronic neonatal hepatitis will lead to the inability of the liver to eliminate toxins in the bile. This causes itching, skin eruptions and irritability.
Major and minor criteria for dg of congenital HIV Infection
Major
1) weight loss / failure to thrive
2) chronic diarrhoea ( over a month)
3) chronic fever (over a month)
Minor
General lymphadenopathy
Oropharyngeal candidiasis
Recurrent common infections
General dermatitis
Confirmed maternal HIV
What are is he classifications of HIV sx
CNS
Respiratory System:
CVS
GI
SKIN
opportunistic infections
Malignancy
CNS sx of aids
Microcephaly.
Progressive neurological deterioration.
Developmental delay/regression.
Predisposition to CNS infections.
Resp sx of HIV
Recurrent infections (pneumonia, sinusitis, otitis media). Tuberculosis. Pneumocystis jiroveci pneumonia or lymphoid interstitial pneumonitis.
Cvs sx of HIV
Cardiomyopathy with congestive cardiac failure.
GI sx of HIV
AIDS enteropathy (malabsorption, infections with various pathogens) → chronic diarrhea resulting in failure to thrive. Abdominal pain, dysphagia, chronic hepatitis or pancreatitis. Renal.
Renal sx of HIV
AIDS nephropathy: the most common presentation nephrotic syndrome.
Skin sx of HIV
Eczema. Seborrheic dermatitis. Candida infections. Molluscum contagiosum. Anogenital warts.
Opportunistic infec HIV
Pneumocystis jiroveci pneumonia. Cyptosporidium. Epstein Barr Virus. Measles. Cryptococcus meningitis. Toxoplasmosis.
Malignancies in HIV
Non Hodgkin’s Lymphoma.
Primary CNS lymphoma.
Kaposi sarcoma
