Sie sind auf Seite 1von 47

TORCH Infections

Medical Faculty University of Jember

TORCH Infections
T=toxoplasmosis O=other (syphilis) R=rubella C=cytomegalovirus (CMV) H=herpes simplex (HSV)

Introduction
You are taking care of a term newborn male with birth weight/length <10th %ile. Physical exam is normal except for a slightly enlarged liver span. A CBC is significant for low platelets. What, if anything, do you worry about? How do you proceed with a work-up?

Index of Suspicion
When do you think of TORCH infections?
IUGR infants Thrombocytopenia Unusual rash Concerning maternal history Classic findings of any specific infection

Diagnosing TORCH Infection

!!!!!!DO NOT USE TORCH TITERS!!!!!!

Diagnosing TORCH Infection


Good maternal/prenatal history
Remember most infections of concern are mild illnesses often unrecognized

Thorough exam of infant Directed labs/studies based on most likely diagnosis


Again, DO NOT USE TORCH TITERS!

Screening TORCH Infections


Retrospective study of 75/182 infants with IUGR who were screened for TORCH infections 1/75 with clinical findings, 11/75 with abnl lab findings All patients screened:
TORCH titers, urine CMV culture, head US Only 3 diagnosed with infection
NONE by TORCH titer!!

Overall cost of all tests = $51,715

Shotgun screening approach NOT cost effective nor particularly useful Diagnostic work-up should be logical and directed by history/exam findings
Khan, NA, Kazzi, SN. Yield and costs of screening growth-retarded infants for torch

Toxoplasmosis
Caused by protozoan Toxoplasma gondii Domestic cat is the definitive host with infections via:
Ingestion of cysts (meats, garden products) Contact with oocysts in feces

Much higher prevalence of infection in European countries (ie France, Greece) Acute infection usually asymptomatic 1/3 risk of fetal infection with primary maternal infection in pregnancy
Infection rate higher with infxn in 3rd trimester Fetal death higher with infxn in 1st trimester

Clinical Manifestations
Most (70-90%) are asymptomatic at birth Classic triad of symptoms:
Chorioretinitis Hydrocephalus Intracranial calcifications

Other symptoms include fever, rash, HSM, microcephaly, seizures, jaundice, thrombocytopenia, lymphadenopathy Initially asymptomatic infants are still at high risk of developing abnormalities, especially chorioretinitis

Chorioretinitis of congenital toxo

Diagnosis
Maternal IgG testing indicates past infection (but when?) Can be isolated in culture from placenta, umbilical cord, infant serum PCR testing on WBC, CSF, placenta
Not standardized

Newborn serologies with IgM/IgA

Toxo Screening
Prenatal testing with varied sensitivity not useful for screening Neonatal screening with IgM testing implemented in some areas
Identifies infected asymptomatic infants who may benefit from therapy

Prevention and Treatment


Treatment for pregnant mothers diagnosed with acute toxo
Spiramycin daily
Macrolide antibiotic

Small studies have shown this reduces likelihood of congenital transmission (up to 50%)

If infant diagnosed prenatally, treat mom


Spiramycin, pyrimethamine (anti-malarial, dihydrofolate reductase inhib), and sulfadiazine (sulfa antibiotic) Leucovorin rescue with pyrimethamine

Symptomatic infants
Pyrimethamine (with leucovorin rescue) and sulfadiazine Treatment for 12 months total

Asymptomatic infants
Course of same medications Improved neurologic and developmental outcomes demonstrated (compared to untreated pts or those treated for only one month)

Syphilis
Treponema pallidum (spirochete) Transmitted via sexual contact Placental transmission as early as 6wks gestation
Typically occurs during second half Mom with primary or secondary syphilis more likely to transmit than latent disease

Large decrease in congenital syphilis since late 1990s


In 2002, only 11.2 cases/100,000 live births reported

From MMWR Aug 2004

From MMWR Aug 2004

Congenital Syphilis
2/3 of affected live-born infants are asymptomatic at birth Clinical symptoms split into early or late (2 years is cutoff) 3 major classifications:
Fetal effects Early effects Late effects

Clinical Manifestations
Fetal:
Stillbirth Neonatal death Hydrops fetalis

Intrauterine death in 25% Perinatal mortality in 25-30% if untreated

Clinical Manifestations
Early congenital (typically 1st 5 weeks):
Cutaneous lesions (palms/soles) HSM Jaundice Anemia Snuffles Periostitis and metaphysial dystrophy Funisitis (umbilical cord vasculitis)

Periostitis of long bones seen in neonatal syphilis

Clinical Manifestations
Late congenital:
Frontal bossing Short maxilla High palatal arch Hutchinson teeth 8th nerve deafness Saddle nose Perioral fissures

Can be prevented with appropriate treatment

Hutchinson teeth late result of congenital syphilis

Diagnosing Syphilis
(Not in Newborns)
Available serologic testing
RPR/VDRL: nontreponemal test
Sensitive but NOT specific Quantitative, so can follow to determine disease activity and treatment response

MHA-TP/FTA-ABS: specific treponemal test


Used for confirmatory testing Qualitative, once positive always positive

RPR/VDRL screen in ALL pregnant women early in pregnancy and at time of birth
This is easily treated!!

CDC Definition of Congenital Syphilis


Confirmed if T. pallidum identified in skin lesions, placenta, umbilical cord, or at autopsy Presumptive diagnosis if any of:
Physical exam findings CSF findings (positive VDRL) Osteitis on long bone x-rays Funisitis (barber shop pole umbilical cord) RPR/VDRL >4 times maternal test Positive IgM antibody

Diagnosing Congenital Syphilis


IgG can represent maternal antibody, not infant infection This is VERY intricate and often confusing
Consult your RedBook (or peds ID folks) when faced with this situation

Treatment
Penicillin G is THE drug of choice for ALL syphilis infections Maternal treatment during pregnancy very effective (overall 98% success) Treat newborn if:
They meet CDC diagnostic criteria Mom was treated <4wks before delivery Mom treated with non-PCN med Maternal titers do not show adequate response (less than 4-fold decline)

Rubella
Single-stranded RNA virus Vaccine-preventable disease
No longer considered endemic in the U.S.

Mild, self-limiting illness Infection earlier in pregnancy has a higher probability of affected infant

Reported rubella and CRS: United States, 1966-2004

Meissner, H. C.American et al. Pediatrics Copyright 2006 Academy of 2006;117:933-935 Pediatrics

Clinical Manifestations
Sensorineural hearing loss (50-75%) Cataracts and glaucoma (20-50%) Cardiac malformations (20-50%) Neurologic (10-20%) Others to include growth retardation, bone disease, HSM, thrombocytopenia, blueberry muffin lesions

Blueberry muffin spots representing extramedullary hematopoesis

Diagnosis
Maternal IgG may represent immunization or past infection - Useless! Can isolate virus from nasal secretions
Less frequently from throat, blood, urine, CSF

Serologic testing
IgM = recent postnatal or congenital infection Rising monthly IgG titers suggest congenital infection

Diagnosis after 1 year of age difficult to establish

Treatment
Preventionimmunize, immunize, immunize! Supportive care only with parent education

Cytomegalovirus (CMV)
Most common congenital viral infection
~40,000 infants per year in the U.S.

Mild, self limiting illness Transmission can occur with primary infection or reactivation of virus
40% risk of transmission in primary infxn

Studies suggest increased risk of transmission later in pregnancy


However, more severe sequalae associated with earlier acquisition

Clinical Manifestations
90% are asymptomatic at birth!
Up to 15% develop symptoms later, notably sensorineural hearing loss

Symptomatic infection
SGA, HSM, petechiae, jaundice, chorioretinitis, periventricular calcifications, neurological deficits >80% develop long term complications
Hearing loss, vision impairment, developmental delay

Ventriculomegaly and calcifications of congenital CMV

Diagnosis
Maternal IgG shows only past infection
Infection common this is useless

Viral isolation from urine or saliva in 1st 3weeks of life


Afterwards may represent post-natal infection

Viral load and DNA copies can be assessed by PCR


Less useful for diagnosis, but helps in following viral activity in patient

Serologies not helpful given high antibody in population

Treatment
Ganciclovir x6wks in symptomatic infants
Studies show improvement or no progression of hearing loss at 6mos No other outcomes evaluated (development, etc.) Neutropenia often leads to cessation of therapy

Treatment currently not recommended in asymptomatic infants due to side effects Area of active research to include use of valgancyclovir, treating asx patients, etc.

Herpes Simplex (HSV)


HSV1 or HSV2 Primarily transmitted through infected maternal genital tract
Rationale for C-section delivery prior to membrane rupture

Primary infection with greater transmission risk than reactivation

Clinical Manifestations
Most are asymptomatic at birth 3 patterns of ~ equal frequency with symptoms between birth and 4wks:
Skin, eyes, mouth (SEM) CNS disease Disseminated disease (present earliest)

Initial manifestations very nonspecific with skin lesions NOT necessarily present

Presentations of congenital HSV

Diagnosis
Culture of maternal lesions if present at delivery Cultures in infant:
Skin lesions, oro/nasopharynx, eyes, urine, blood, rectum/stool, CSF

CSF PCR Serologies again not helpful given high prevalence of HSV antibodies in population

Treatment
High dose acyclovir 60mg/kg/day divided q8hrs
X21days for disseminated, CNS disease X14days for SEM

Ocular involvement requires topical therapy as well

Which TORCH Infection Presents With


Snuffles?
syphilis

Chorioretinitis, hydrocephalus, and intracranial calcifications?


toxo

Blueberry muffin lesions?


rubella

Periventricular calcifications?
CMV

No symptoms?
All of them

Which TORCH Infections Can Absolutely Be Prevented?


Rubella Syphilis

When Are TORCH Titers Helpful in Diagnosing Congenital Infection?


NEVER!

Questions?

Das könnte Ihnen auch gefallen