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
TORCH Infections
Meredith Scannell, RN, CNM, MSN, MPH
Background
 Infections acquired in utero or during the birth process are
a significant cause of fetal and neonatal mortality.
 Most fetus if infected during the first trimester will suffer
congenital malformation
 Perinatal infections account for 2% - 3% of birth defects
which arise form a spectrum of organisms & have varying
modes of transmission
 Not all birth defects are routinely screened for during
prenatal care
TORCH Infections
 T=toxoplasmosis
 O=other (syphilis, Hepatitis, HIV)
 R=rubella
 C=cytomegalovirus (CMV)
 H=herpes simplex (HSV)
 Origin was based on 5
infections that presented
similarly, with rash and ocular
findings.
 First 4 are acquired antenately
 Herpes and hepatitis acquired
prenately or via delivery
 Term TORCH somewhat
obsolete as other disease are
important such as HIV
Toxoplasmosis
Toxoplasmosis - Transmission
 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
Toxoplasmosis
 Acute infection usually asymptomatic
 1/3 risk of fetal infection with primary maternal
infection in pregnancy
 Infection transmission rate higher with in 3rd
trimester
 Fetal death higher with in 1st
trimester
 Abnormal growth
Clinical Manifestations - Maternal
 Most are asymptomatic at birth
 Mononucleosis type symptoms:
 Fatigue
 Headache
 Malaise
 Lymphadenopathy (7% of infected individual)
 Blood test reveals seroconversion
Clinical Manifestations - Infant
 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
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 andTreatment
 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%)
 Symptomatic infants
 Pyrimethamine (with
leucovorin rescue) and
sulfadiazine
 Treatment for 12 months
total
 Prevetion
 Wash hands before eating,
after handleing raw mean
 Wash hands after contact
with cat feces
 Wash hands if in contact
with soil
 Cook meat adequately
Syphilis
Syphilis
 Syphilis is a systemic infection caused by the
spirochete Treponema pallidum
 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 –From MMWR –
Aug 2004Aug 2004
From MMWR – Aug
2004
Clinical Manifestations
 Fetal:
 Stillbirth
 Neonatal death
 Low birth weight
 Hydrops fetalis
 Congential Malformations
 Active congenital syphilis in
the neonate
 Long-term sequelae, such as
deafness and neurologic
impairment
 SAB after 4th
months when
the spirochetes cross the
placenta
 Repeated late abortion
 Intrauterine death in 25%
 Perinatal mortality in 25-
30% if untreated
Clinical Manifestations
Congenital syphilis Hutchinson Teeth Lores
•2/3 of affected live-born infants are
asymptomatic at birth
•Clinical symptoms split into early or late
Diagnosing Syphilis
Maternal
 Available serologic testing
 RPR/VDRL: nontreponemal test
 Sensitive but NOT specific
 RPR/VDRL screen in ALL pregnant women
early in pregnancy and at time of birth
 This is easily treated
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
Rubella
 Single-stranded RNA virus, spread via respiration
 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 within the first 16 weeks
 Risk of fetal infection 50-60% 1st
month
 Risk of fetal infection 22% in 2nd
month
 Risk of fetal infection 6-10% in 4th
month
Copyright ©2006 American Academy of PediatricsMeissner, H. C. et al. Pediatrics 2006;117:933-935
Reported rubella and CRS: United States, 1966-2004
Clinical Manifestations
 Microcephaly
 Cerebral palsy
 Sensorineural hearing loss (50-75%)
 Cataracts and glaucoma (20-50%)
 blindness
 Cardiac malformations (20-50%)
 Neurologic (10-20%)
 Others to include growth retardation, bone
disease, HSM, thrombocytopenia, “blueberry
muffin” lesions
Diagnosis
 Maternal IgG may represent immunization or
past infection
 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
Treatment
 Acute infection – droplet precautions
 Prevention…immunize, immunize, immunize! (before or after
pregnancy)
 20% of women of child bearing age do not possess rubella
anitbody
 Avoid pregnancy for 3 months after vaccination
 Supportive care only with parent education
Cytomegalovirus (CMV)
Clinical Manifestations
 1:100 babies are born with this congenital infection
 90% of newborns are asymptomatic at birth
 Symptomatic infection
 Small for Gestational dates
 Hepatospleenomegaly
 Petechiae
 Jaundice
 >80% develop long term complications
 Hearing loss, vision impairment, developmental delay
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
Herpes Simplex (HSV)
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
Varicella Zoster
Varicella Zoster
 Herpes Virus in a DNA virus
 Highly contagious & transmitted by respiratory droplets & by direct
personal contact with vesicle fluid.
 Complicates 3 in 1,000 pregnancies
 Incubation period-10-21 days. Infectious 48 hrs before the rash - vesicle
crust over.
 If primary infection occurs in the first trimester 4.9% risk of congenital
vaircella
 Infection acquired in the last 10 days of pregnancy result in variable
congential infection with neonatal mortality as high as 34%
Varicella
Maternal
 Greater morbidity
 Pneumonia
 Up 10% of pregnant
women
 Severity increases later in
gestion
 Encephalatis
 Hepatitis
 Under 20 weeks gestation
 No increase in SAB
Fetal
 1-2% of maternal infections
 Characterised by skin
scarring
 eye defects,
 hypoplasia of limbs
 neurological
abnormalities
 microcephaly
FetalVaricella
Varicella
 Serology (IgG and IgM).
 Screening: Routine screening generally not recommended
 Prevention: If pregnant woman (with no history of previous
chickenpox) is exposed, perform STAT Varicella IgG. Exposed
neonate should receive VZIG prophylaxis.
Treatment and Prevention
 In non-immune adult who plans to become pregnant - Live
attenuated varicella vaccine is safe & effective in preventing
chickenpox
 If nonimmune - Give VZIG within 10 days of exposure
 Avoid contact with susceptible individual.
 Symptomatic treatment
 Oral acyclovir reduces the duration of symptoms if started
within 24 hours of development of rash.
Herpes Zoster (Shingles)
 Caused by reactivation of a latent varicella zoster virus
infection
 Can occur years or decades after illness with chickenpox
 Generally associated with normal aging and with anything that
causes reduced immunocompetence
 Lifetime risk of 32% in the United States
 Estimated 1 million cases zoster diagnosed annually in the U.S.
 ***Vaccine Contraindicated in Pregnancy***
Questions?
References
 Gilbert, R., Gras, L., & European Multicentre Study on
Congenital Toxoplasmosis. (2003). Effect of timing and type of
treatment on the risk of mother to child transmission of
Toxoplasma gondii. BJOG: an international journal of obstetrics
and gynaecology, 110(2), 112.

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Infections in pregnancy 1 3 15

  • 2. Background  Infections acquired in utero or during the birth process are a significant cause of fetal and neonatal mortality.  Most fetus if infected during the first trimester will suffer congenital malformation  Perinatal infections account for 2% - 3% of birth defects which arise form a spectrum of organisms & have varying modes of transmission  Not all birth defects are routinely screened for during prenatal care
  • 3. TORCH Infections  T=toxoplasmosis  O=other (syphilis, Hepatitis, HIV)  R=rubella  C=cytomegalovirus (CMV)  H=herpes simplex (HSV)  Origin was based on 5 infections that presented similarly, with rash and ocular findings.  First 4 are acquired antenately  Herpes and hepatitis acquired prenately or via delivery  Term TORCH somewhat obsolete as other disease are important such as HIV
  • 5. Toxoplasmosis - Transmission  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
  • 6. Toxoplasmosis  Acute infection usually asymptomatic  1/3 risk of fetal infection with primary maternal infection in pregnancy  Infection transmission rate higher with in 3rd trimester  Fetal death higher with in 1st trimester  Abnormal growth
  • 7. Clinical Manifestations - Maternal  Most are asymptomatic at birth  Mononucleosis type symptoms:  Fatigue  Headache  Malaise  Lymphadenopathy (7% of infected individual)  Blood test reveals seroconversion
  • 8. Clinical Manifestations - Infant  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
  • 9. 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
  • 10. Prevention andTreatment  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%)  Symptomatic infants  Pyrimethamine (with leucovorin rescue) and sulfadiazine  Treatment for 12 months total  Prevetion  Wash hands before eating, after handleing raw mean  Wash hands after contact with cat feces  Wash hands if in contact with soil  Cook meat adequately
  • 12. Syphilis  Syphilis is a systemic infection caused by the spirochete Treponema pallidum  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
  • 13. From MMWR –From MMWR – Aug 2004Aug 2004
  • 14. From MMWR – Aug 2004
  • 15. Clinical Manifestations  Fetal:  Stillbirth  Neonatal death  Low birth weight  Hydrops fetalis  Congential Malformations  Active congenital syphilis in the neonate  Long-term sequelae, such as deafness and neurologic impairment  SAB after 4th months when the spirochetes cross the placenta  Repeated late abortion  Intrauterine death in 25%  Perinatal mortality in 25- 30% if untreated
  • 16. Clinical Manifestations Congenital syphilis Hutchinson Teeth Lores •2/3 of affected live-born infants are asymptomatic at birth •Clinical symptoms split into early or late
  • 17. Diagnosing Syphilis Maternal  Available serologic testing  RPR/VDRL: nontreponemal test  Sensitive but NOT specific  RPR/VDRL screen in ALL pregnant women early in pregnancy and at time of birth  This is easily treated
  • 18. 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)
  • 20. Rubella  Single-stranded RNA virus, spread via respiration  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 within the first 16 weeks  Risk of fetal infection 50-60% 1st month  Risk of fetal infection 22% in 2nd month  Risk of fetal infection 6-10% in 4th month
  • 21. Copyright ©2006 American Academy of PediatricsMeissner, H. C. et al. Pediatrics 2006;117:933-935 Reported rubella and CRS: United States, 1966-2004
  • 22. Clinical Manifestations  Microcephaly  Cerebral palsy  Sensorineural hearing loss (50-75%)  Cataracts and glaucoma (20-50%)  blindness  Cardiac malformations (20-50%)  Neurologic (10-20%)  Others to include growth retardation, bone disease, HSM, thrombocytopenia, “blueberry muffin” lesions
  • 23. Diagnosis  Maternal IgG may represent immunization or past infection  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
  • 24. Treatment  Acute infection – droplet precautions  Prevention…immunize, immunize, immunize! (before or after pregnancy)  20% of women of child bearing age do not possess rubella anitbody  Avoid pregnancy for 3 months after vaccination  Supportive care only with parent education
  • 26. Clinical Manifestations  1:100 babies are born with this congenital infection  90% of newborns are asymptomatic at birth  Symptomatic infection  Small for Gestational dates  Hepatospleenomegaly  Petechiae  Jaundice  >80% develop long term complications  Hearing loss, vision impairment, developmental delay
  • 27. 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
  • 28. 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
  • 30. 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
  • 31. 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
  • 33. 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
  • 34. Treatment  High dose acyclovir 60mg/kg/day divided q8hrs  X21days for disseminated, CNS disease  X14days for SEM  Ocular involvement requires topical therapy as well
  • 36. Varicella Zoster  Herpes Virus in a DNA virus  Highly contagious & transmitted by respiratory droplets & by direct personal contact with vesicle fluid.  Complicates 3 in 1,000 pregnancies  Incubation period-10-21 days. Infectious 48 hrs before the rash - vesicle crust over.  If primary infection occurs in the first trimester 4.9% risk of congenital vaircella  Infection acquired in the last 10 days of pregnancy result in variable congential infection with neonatal mortality as high as 34%
  • 37. Varicella Maternal  Greater morbidity  Pneumonia  Up 10% of pregnant women  Severity increases later in gestion  Encephalatis  Hepatitis  Under 20 weeks gestation  No increase in SAB Fetal  1-2% of maternal infections  Characterised by skin scarring  eye defects,  hypoplasia of limbs  neurological abnormalities  microcephaly
  • 39. Varicella  Serology (IgG and IgM).  Screening: Routine screening generally not recommended  Prevention: If pregnant woman (with no history of previous chickenpox) is exposed, perform STAT Varicella IgG. Exposed neonate should receive VZIG prophylaxis.
  • 40. Treatment and Prevention  In non-immune adult who plans to become pregnant - Live attenuated varicella vaccine is safe & effective in preventing chickenpox  If nonimmune - Give VZIG within 10 days of exposure  Avoid contact with susceptible individual.  Symptomatic treatment  Oral acyclovir reduces the duration of symptoms if started within 24 hours of development of rash.
  • 41. Herpes Zoster (Shingles)  Caused by reactivation of a latent varicella zoster virus infection  Can occur years or decades after illness with chickenpox  Generally associated with normal aging and with anything that causes reduced immunocompetence  Lifetime risk of 32% in the United States  Estimated 1 million cases zoster diagnosed annually in the U.S.  ***Vaccine Contraindicated in Pregnancy***
  • 43. References  Gilbert, R., Gras, L., & European Multicentre Study on Congenital Toxoplasmosis. (2003). Effect of timing and type of treatment on the risk of mother to child transmission of Toxoplasma gondii. BJOG: an international journal of obstetrics and gynaecology, 110(2), 112.

Editor's Notes

  1. Fale positives
  2. Lores are cracks and fissures around the mouth and hard palette