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TORCH_maranich - TORCH Infections TORCH Ashley M Maranich...

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Unformatted text preview: TORCH Infections TORCH Ashley M. Maranich, MD CPT/USA/MC Pediatric Infectious Disease Fellow TORCH Infections TORCH • • • • • T=toxoplasmosis O=other (syphilis) R=rubella C=cytomegalovirus (CMV) H=herpes simplex (HSV) • • • You are taking care of a term newborn You male with birth weight/length <10th %ile. male 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 Index • When do you think of TORCH When infections? infections? • • • • • • IUGR infants HSM Thrombocytopenia Unusual rash Concerning maternal history “Classic” findings of any specific infection Diagnosing TORCH Infection Diagnosing !!!!!!DO NOT USE TORCH TITERS!!!!!! Diagnosing TORCH Infection Diagnosing • Good maternal/prenatal history • Remember most infections of concern are Remember mild illnesses often unrecognized mild • • Thorough exam of infant Directed labs/studies based on most Directed likely diagnosis… likely • Again, DO NOT USE TORCH TITERS! Screening TORCH Infections Screening • • • Retrospective study of 75/182 infants with IUGR who Retrospective were screened for TORCH infections were 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 Shotgun” particularly useful particularly Diagnostic work-up should be logical and directed by Diagnostic history/exam findings history/exam Khan, NA, Kazzi, SN. Yield and costs of screening growth-retarded infants for torch Toxoplasmosis Toxoplasmosis • • Caused by protozoan – Toxoplasma gondii Domestic cat is the definitive host with Domestic infections via: infections • Ingestion of cysts (meats, garden products) • Contact with oocysts in feces • • • Much higher prevalence of infection in Much European countries (ie France, Greece) European Acute infection usually asymptomatic 1/3 risk of fetal infection with primary maternal 1/3 infection in pregnancy infection • Infection rate higher with infxn in 3rd trimester • Fetal death higher with infxn in 1st trimester Clinical Manifestations Clinical • • Most (70-90%) are asymptomatic at birth Classic triad of symptoms: • Chorioretinitis • Hydrocephalus • Intracranial calcifications • • Other symptoms include fever, rash, HSM, Other microcephaly, seizures, jaundice, thrombocytopenia, lymphadenopathy thrombocytopenia, Initially asymptomatic infants are still at high risk Initially of developing abnormalities, especially chorioretinitis chorioretinitis Chorioretinitis of congenital toxo Chorioretinitis Diagnosis Diagnosis • • • Maternal IgG testing indicates past Maternal infection (but when…?) infection Can be isolated in culture from Can placenta, umbilical cord, infant serum placenta, PCR testing on WBC, CSF, placenta • Not standardized • Newborn serologies with IgM/IgA Newborn Toxo Screening Toxo • • Prenatal testing with varied sensitivity Prenatal not useful for screening not Neonatal screening with IgM testing Neonatal implemented in some areas implemented • Identifies infected asymptomatic infants Identifies who may benefit from therapy who Prevention and Treatment Prevention • Treatment for pregnant mothers diagnosed with acute toxo • Spiramycin daily • Macrolide antibiotic • Small studies have shown this reduces likelihood of congenital Small transmission (up to 50%) transmission • If infant diagnosed prenatally, treat mom • Spiramycin, pyrimethamine (anti-malarial, dihydrofolate reductase Spiramycin, inhib), and sulfadiazine (sulfa antibiotic) inhib), • 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 Improved (compared to untreated pts or those treated for only one month) (compared Syphilis Syphilis • • • Treponema pallidum (spirochete) Transmitted via sexual contact Placental transmission as early as 6wks Placental gestation gestation • Typically occurs during second half • Mom with primary or secondary syphilis more Mom likely to transmit than latent disease likely • Large decrease in congenital syphilis since Large late 1990s late • In 2002, only 11.2 cases/100,000 live births In reported reported From MMWR – Aug 2004 Aug From MMWR – Aug 2004 Aug Congenital Syphilis Congenital • • • 2/3 of affected live-born infants are 2/3 asymptomatic at birth asymptomatic Clinical symptoms split into early or late Clinical (2 years is cutoff) (2 3 major classifications: • • • Fetal effects Early effects Late effects Clinical Manifestations Clinical • Fetal: • Stillbirth • Neonatal death • Hydrops fetalis • • Intrauterine death in 25% Perinatal mortality in 25-30% if Perinatal untreated untreated Clinical Manifestations Clinical • 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 seen Clinical Manifestations Clinical • Late congenital: • • • • • • • • Frontal bossing Short maxilla High palatal arch Hutchinson teeth 8th nerve deafness Saddle nose Saddle Perioral fissures Can be prevented with appropriate treatment Hutchinson teeth – late result of congenital syphilis congenital Diagnosing Syphilis Diagnosing (Not in Newborns) • Available serologic testing • RPR/VDRL: nontreponemal test • • Sensitive but NOT specific Quantitative, so can follow to determine disease activity Quantitative, and treatment response and • MHA-TP/FTA-ABS: specific treponemal test • Used for confirmatory testing • Qualitative, once positive always positive • RPR/VDRL screen in ALL pregnant women RPR/VDRL early in pregnancy and at time of birth early • This is easily treated!! CDC Definition of Congenital Syphilis Syphilis • • Confirmed if T. pallidum identified in skin Confirmed lesions, placenta, umbilical cord, or at autopsy 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 Diagnosing • • IgG can represent maternal antibody, IgG not infant infection not This is VERY intricate and often This confusing confusing • Consult your RedBook (or peds ID folks) Consult when faced with this situation when Treatment Treatment • • • Penicillin G is THE drug of choice for ALL Penicillin syphilis infections syphilis Maternal treatment during pregnancy very Maternal effective (overall 98% success) effective 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 Maternal (less than 4-fold decline) (less Rubella 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 Infection higher probability of affected infant higher Reported rubella and CRS: United States, 1966-2004 Meissner,©2006 American Academy of 2006;117:933-935 Copyright H. C. et al. Pediatrics Pediatrics Clinical Manifestations Clinical • • • • • Sensorineural hearing loss (50-75%) Cataracts and glaucoma (20-50%) Cardiac malformations (20-50%) Neurologic (10-20%) Others to include growth retardation, Others bone disease, HSM, thrombocytopenia, “blueberry muffin” lesions “blueberry “Blueberry muffin” spots representing extramedullary hematopoesis Diagnosis Diagnosis • • Maternal IgG may represent immunization or Maternal past infection - Useless! past 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 Rising infection infection • Diagnosis after 1 year of age difficult to Diagnosis establish establish Treatment Treatment • • Prevention…immunize, immunize, Prevention…immunize, immunize! immunize! Supportive care only with parent Supportive education education Cytomegalovirus (CMV) Cytomegalovirus • Most common congenital viral infection • ~40,000 infants per year in the U.S. • • Mild, self limiting illness Transmission can occur with primary infection Transmission or reactivation of virus or • 40% risk of transmission in primary infxn • Studies suggest increased risk of Studies transmission later in pregnancy transmission • However, more severe sequalae associated with However, earlier acquisition earlier Clinical Manifestations Clinical • 90% are asymptomatic at birth! • Up to 15% develop symptoms later, Up notably sensorineural hearing loss notably • Symptomatic infection • SGA, HSM, petechiae, jaundice, SGA, chorioretinitis, periventricular calcifications, periventricular neurological deficits neurological • >80% develop long term complications • Hearing loss, vision impairment, developmental Hearing delay delay Ventriculomegaly and calcifications of congenital CMV congenital Diagnosis Diagnosis • Maternal IgG shows only past infection • Infection common – this is useless • Viral isolation from urine or saliva in 1st 3weeks of life 3weeks • Afterwards may represent post-natal infection • Viral load and DNA copies can be assessed Viral by PCR by • Less useful for diagnosis, but helps in following Less viral activity in patient viral • Serologies not helpful given high antibody in Serologies population population Treatment Treatment • Ganciclovir x6wks in symptomatic infants • Studies show improvement or no progression of Studies hearing loss at 6mos hearing • No other outcomes evaluated (development, etc.) • Neutropenia often leads to cessation of therapy • • Treatment currently not recommended in Treatment asymptomatic infants due to side effects asymptomatic Area of active research to include use of Area valgancyclovir, treating asx patients, etc. valgancyclovir, Herpes Simplex (HSV) Herpes • • HSV1 or HSV2 Primarily transmitted through infected Primarily maternal genital tract maternal • Rationale for C-section delivery prior to Rationale membrane rupture membrane • Primary infection with greater Primary transmission risk than reactivation transmission Clinical Manifestations Clinical • • Most are asymptomatic at birth 3 patterns of ~ equal frequency with patterns symptoms between birth and 4wks: symptoms • • • • Skin, eyes, mouth (SEM) CNS disease Disseminated disease (present earliest) Initial manifestations very nonspecific with Initial skin lesions NOT necessarily present skin Presentations of congenital HSV Presentations Diagnosis Diagnosis • • Culture of maternal lesions if present at Culture delivery delivery Cultures in infant: • Skin lesions, oro/nasopharynx, eyes, urine, blood, Skin rectum/stool, CSF rectum/stool, • • CSF PCR Serologies again not helpful given high Serologies prevalence of HSV antibodies in population prevalence Treatment Treatment • High dose acyclovir 60mg/kg/day High divided q8hrs divided • • • X21days for disseminated, CNS disease X14days for SEM Ocular involvement requires topical Ocular therapy as well therapy Which TORCH Infection Presents With… With… • Snuffles? • syphilis • Chorioretinitis, hydrocephalus, and Chorioretinitis, intracranial calcifications? • toxo • Blueberry muffin lesions? • rubella • Periventricular calcifications? • CMV • No symptoms? • All of them Which TORCH Infections Can Absolutely Be Prevented? Absolutely • Rubella • Syphilis When Are TORCH Titers Helpful in Diagnosing Congenital Infection? Infection? • NEVER! Questions? Questions? ...
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