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pediatria > Congenital TORCH infections > Flashcards

Congenital TORCH infections Flashcards

1
Q

TORCH infections

A

TORCH infections: vertically transmitted infections that are capable of significantly influencing fetal and neonatal morbidity and mortality
Toxoplasmosis
Others (e.g., syphilis, varicella, parvovirus B19 infection, listeriosis)
Rubella
Cytomegaly (CMV)
Herpes simplex virus (HSV) infection

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2
Q

Congenital toxoplasmosis: pathogen and life cycle

A

Pathogen: Toxoplasma gondii
Life cycle of Toxoplasma gondii: Transmission - Mother; Cat feces; Raw or insufficiently cooked meat; Transplacental transmission

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3
Q

congenital toxoplasmosis: clinical features

A 
Clinical features
First trimester
Classic triad of toxoplasmosis
Chorioretinitis (a form of posterior uveitis)
Diffuse intracranial calcifications
Hydrocephalus
Possible other nonspecific clinical features
Petechiae and purpura (blueberry muffin rash)
Lymphadenopathy
Sequelae of congenital toxoplasmosis
Epilepsy
Blueberry muffin syndrome
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4
Q

congenital toxoplasmosis: Diagnostics

A

Fetus: PCR for T. gondii DNA
Newborn
CT/MRI: intracranial calcifications, hydrocephalus, ring-enhancing lesions
T. gondii-specific IgM antibodies
PCR for T. gondii DNA
Ophthalmological evaluation: chorioretinitis
Congenital toxoplasmosisCerebral toxoplasmosisMacular scar in congenital toxoplasmosis

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5
Q

congenital toxoplasmosis: treatment and prevention

A

Treatment
Mother: spiramycin
Fetus: pyrimethamine, sulfadiazine, and folinic acid
Newborn: pyrimethamine, sulfadiazine, and folinic acid
Prevention
Avoid raw, undercooked, and cured meats.
Avoid contact with cat litter.

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6
Q

Congenital syphilis: Pathogen

A

Pathogen: Treponema pallidum
Transmission: Mother: Sexual contact; Fetus: transplacental transmission from infected mother
Neonate: perinatal transmission during birth

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7
Q

Congenital syphilis: Clinical features

A

Clinical features
Early congenital syphilis (onset < 2 years of age)
Hepatomegaly and jaundice
Rhinorrhea
Maculopapular rash on palms and soles
Skeletal abnormalities
Generalized lymphadenopathy (nontender)
Late congenital syphilis (onset > 2 years of age)
saddle nose, frontal bossing
Hutchinson’s teeth (notched, widely spaced teeth); mulberry molars (poorly developed first molars)
interstitial keratitis, sensorineural hearing loss
saber shins
cranial nerve palsies (e.g., CN VIII defect causing deafness)
Skin alterations in congenital syphilisHutchinson’s Teeth resulting from congenital syphilis

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8
Q

Congenital syphilis: Diagnosis; Treatment; Prevention

A

Diagnosis
Newborn and mother
Initial test: RPR or VDRL (serum)
Confirmatory test: dark-field microscopy or PCR of lesions or bodily fluids
Fetus: repeated ultrasound examinations (placentomegaly, hepatomegaly, ascites, and/or hydrops fetalis)
Spirochetes on dark-field microscopy

Treatment: IV penicillin G for both pregnant women and newborns
Prevention: Maternal screening

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9
Q

Congenital listeriosis: Pathogen and Transmission

A

Pathogen: Listeria monocytogenes
Transmission: Mother; Contaminated food: especially raw milk products; Other possible sources: meat
Fetus
Transplacental transmission from an infected mother
Direct contact with infected vaginal secretions and/or blood during delivery

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10
Q

Congenital listeriosis: Clinical features

A

Intrauterine transmission
Increased risk of premature birth and spontaneous abortion
Early-onset syndrome: granulomatosis infantiseptica
Severe systemic infection characterized by disseminated abscesses
Most common findings: respiratory distress and skin lesions
Signs of meningitis may already develop.
Transmission during birth or postnatally (via contact with the mother or contaminated environment)
Late-onset syndrome (5 days to 3 weeks after birth): Listeria meningitis/encephalitis

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11
Q

Congenital listeriosis: Diagnosis; Treatment; Prevention

A

Diagnosis
Culture from blood or CSF samples (pleocytosis)
Treatment
IV ampicillin and gentamicin
Prevention
Avoidance of soft cheeses
Avoidance of potentially contaminated water and food

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12
Q

Congenital varicella infection: pathogen; transmission

A

Pathogen: Varicella-zoster virus (VZV)
Transmission: Mother
Primary infection: Airborne droplets; Direct skin contact with vesicle fluid
Reactivation: usually in immunocompromised individuals
Fetus: transplacental transmission from an infected mother

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13
Q

Congenital varicella infection: Clinical features

A

Congenital varicella syndrome (infection during first and second trimester)
Hypertrophic scars (cicatricial skin lesions)
Limb defects (e.g., hypoplasia)
cataracts
cortical atrophy

Neonatal varicella
Mild infection (maternal exanthem > 5 days before birth)
Severe infection (maternal exanthem < 5 days before birth): hemorrhagic exanthem; congenital varicella syndrome
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14
Q

Congenital varicella infection: Diagnosis

A

Newborn and mother
Usually clinical diagnosis is confirmed by appearance of skin lesions
DFA or PCR of fluid collected from blisters or cerebrospinal fluid (CSF)
Serology
Fetus: PCR for VZV DNA

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15
Q

Congenital varicella infection: Treatment and prevention

A

Treatment: acyclovir
Administer postexposure prophylaxis in newborns if mother displays symptoms of varicella < 5 days before delivery: IgG antibodies (varicella-zoster immune globulin, VZIG)
Cesarean section if lesions are present at delivery

Prevention: Immunization of seronegative women before pregnancy
VZIG in pregnant women without immunity within 10 days of exposure

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16
Q

Congenital parvovirus B19 infection: pathogen and transmission

A

Pathogen: Parvovirus B19
Transmission: transplacental transmission from infected mother

17
Q

Congenital parvovirus B19 infection: Clinical features

A

Severe anemia and possibly fetal hydrops
Fetal demise and miscarriage/stillbirth
Most intrauterine infections do not result in fetal developmental defects.

18
Q

Congenital parvovirus B19 infection: Diagnosis and treatment

A

Diagnosis
Mother: serologic assays for IgG and IgM against parvovirus B19
Positive IgM and negative IgG: very recent infection
Positive IgM and IgG: acute infection
Positive IgG and negative IgM: maternal immunity
Negative IgG and negative IgM: no maternal immunity
Fetus
PCR for parvovirus B19 DNA (amniotic fluid or blood)

Treatment
Intrauterine fetal blood transfusion

19
Q

Congenital rubella infection: pathogen and transmission

A

Pathogen: Rubella virus
Transmission: Mother - airborne droplets; Fetus - Transplacental from infected mother
Risk of congenital rubella syndrome
In the first trimester (period of organogenesis): 90%
> 20 weeks gestation: no documented cases

20
Q

Congenital rubella infection: Clinical features

A

Miscarriage, preterm birth, fetal growth restriction
Congenital rubella syndrome
Triad of congenital rubella syndrome
Cataracts: Other eye manifestations may also occur later in life (e.g., salt and pepper retinopathy, glaucoma).
Cochlear defect: bilateral sensorineural hearing loss
Cardiac defect: most common defect (e.g., patent ductus arteriosus, pulmonary artery stenosis)

Additional nonspecific clinical features
Early
Hepatosplenomegaly, jaundice
Hemolytic anemia, thrombocytopenia
Petechiae and purpura, i.e., blueberry muffin rash (in the case of congenital rubella infection the rash is caused by extramedullary hematopoiesis in the skin)
Late
CNS defects: microcephaly, intellectual disability
Skeletal abnormalities
21
Q

Congenital rubella infection: Diagnosis

A 
Newborn and mother
PCR for rubella RNA
Serology
Fetus
IgM antibody serology
PCR for rubella RNA
22
Q

Congenital rubella infection: treatment and prevention

A

Treatment
Intrauterine rubella infection
< 16 weeks: Counsel to terminate pregnancy.
> 16 weeks: reassurance
Prevention
Immunization of seronegative women before pregnancy

23
Q

Congenital CMV infection: pathogen and transmission

A

Pathogen: Cytomegalovirus
Transmission: Mother: via CMV-contaminated blood, urine, saliva, and genital secretions; Sexual transmission; Transplant-transmitted infection; Fetus: transplacental transmission from an infected mother
Newborn: postnatal via breastmilk from infected mother

24
Q

Congenital CMV infection: Clinical features

A 
Symptomatic infection at birth (∼ 10%)
Fetal infection
Intrauterine growth restriction
hyperechogenic foci
Sequelae of fetal and newborn infection
CNS findings
Abnormalities on brain imaging in 70% of symptomatic infants (e.g., periventricular calcifications)
Microcephaly
Sensorineural hearing loss
Chorioretinitis
Nonspecific findings (similar to other TORCH infections)
Petechiae, purpura (blueberry muffin rash)
Hepatosplenomegaly, jaundice
Small for gestational age (SGA)

Late complications
Hearing loss, vision impairment

25
Q

Congenital CMV infection: Diagnosis

A

Fetus and newborn: periventricular calcifications
Newborn and mother
CMV IgM antibodies
Viral culture or PCR for CMV DNA (urine; )
Fetus
Viral culture or PCR for CMV DNA (amniotic fluid)
Congenital CMV infectionCongenital CMV infection

26
Q

Congenital CMV infection: treatment

A

Treatment
Fetus
Severe anemia: intrauterine blood transfusions
Thrombocytopenia: platelet transfusions
Newborn
Ganciclovir, valganciclovir, or foscarnet

27
Q

Congenital herpes simplex virus infection: pathogen and transmission

A

Pathogen: herpes simplex virus 2 (HSV-2); HSV-1
Transmission: Mother
Primary infection: contact with contaminated oral secretions via small skin lesions
Reactivation: usually in immunocompromised individuals
Fetus: Transplacental transmission from an infected mother (rare)
Newborn: perinatal transmission during birth

28
Q

Congenital herpes simplex virus infection: Clinical features

A 
Intrauterine HSV infection (congenital herpes simplex virus infection) (∼ 5% of cases)
Vesicular skin lesions
Perinatal and postnatal transmission
Skin, eye, and mouth disease
Vesicular skin lesions
Keratoconjunctivitis → cataracts, chorioretinitis
CNS disease
Meningoencephalitis
vesicular skin lesions
Disseminated disease
sepsis
Vesicular skin lesions
29
Q

Congenital herpes simplex virus infection: Diagnosis

A

Newborn (and mother)
viral culture of HSV from skin lesions
PCR for HSV DNA

30
Q

Congenital herpes simplex virus infection: Treatment and Prevention

A

Treatment
IV acyclovir or valaciclovir
Prevention
Antiviral therapy (acyclovir) beginning at 36 weeks of gestation for individuals with a known history of HSV lesions
Cesarean section in women with active genital lesions or prodromal symptoms

pediatria (13 decks)

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