T Toxoplasmosis O others Parvovirus B19 syphilis Varicella R Rubella C CMV H HSV Parvovirus B19 Parvo virus B19 is a small nonenveloped singlestranded DNA virus that causes ID: 933335
Download Presentation The PPT/PDF document "Torch infections Rina Karborani" is the property of its rightful owner. Permission is granted to download and print the materials on this web site for personal, non-commercial use only, and to display it on your personal computer provided you do not modify the materials and that you retain all copyright notices contained in the materials. By downloading content from our website, you accept the terms of this agreement.
Slide1
Torch infections
Rina Karborani
Slide2T= Toxoplasmosis
O= others (
Parvovirus B-19
,
syphilis
, Varicella)
R= Rubella
C=
CMV
H=
HSV
Slide3Slide4Parvovirus B-19
Parvo
virus B19 is a small, non-enveloped, single-stranded DNA virus that causes
1) erythema
infectiosum
fifth disease or slapped cheek disease) in children.2) papular-purpuric gloves and socks syndrome (PPGSS)3) Aplastic crisis
Slide5Transmission
Occurs Via :
Vertical transmission
Respiratory secretions
Transfusion of blood products
Slide6Rash & Joint symptoms occur
2-3 weeks after initial infection
Slide7Pathogenic
sequence is as follows: maternal
primary
infection (by respiratory droplets)
transplacental
transfer of virus infection of RBC precursor cells causing arrested RBC production leading to severe anemia ( HB less than 8 g/dl) congestive HF & edema.May cause severe fetal anemia causing fetal hydrops (edema and ascites)Fetuses that survive the infection have no fetal
Defects.
Slide8Slide9Treatment
Slide10C
ongenital Syphilis
chronic infectious disease caused
by Treponema pallidum (spirochete) Transmitted via sexual contact acquired by the fetus in the uterus before birth; Placental transmission as early as 6wks gestation.
Typically occurs during second half
of pregnancy
,
Mom
s
with primary or secondary syphilis
are
more
likely to transmit the infection than latent disease
.
Slide11 2/3 of affected live-born infants are asymptomatic at birth
3 major
classifications of clinical manifestations:
Fetal effects Early effects Late effects
Slide12Clinical Manifestations
Fetal:
Stillbirth
Neonatal death Hydrops fetalis Intrauterine death in 25% Perinatal mortality in 25-30% if untreated
Slide13
Early
congenital
(typically
in
1st 5 weeks): Cutaneous lesions (palms/soles) HSM Jaundice Anemia
Snuffles Periostitis and metaphysial dystrophy
Funisitis (umbilical cord vasculitis)
Slide14
Late congenital
:
Frontal
bossing Short maxilla High palatal arch Hutchinson teeth 8 th nerve deafness
Saddle nose Perioral fissures
(
rhagades
)
Can
be prevented with appropriate treatment
Slide15Slide16Diagnosing Syphilis
Available
serologic
testing
: 1) RPR/VDRL: nontreponemal test Sensitive but NOT specific Quantitative, so can follow to determine disease activity and treatment response 2)
MHA-TP/FTA-ABS: specific treponemal test
Used for confirmatory testing
Qualitative, once positive always
positive
Whenever a screening test (RPR, VDRL) is positive, a more specific test (FTA-ABS, TP-MHA) should be used to confirm the test and rule out a "biologic false positive."
Slide17Presumptive 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
Slide18Treatment
Penicillin G is THE drug of choice for ALL syphilis infections
Maternal treatment during pregnancy
is very
effective (overall 98% success) Treat newborn if: 1)Mom treated with non-PCN medication 2) Maternal titers do not show adequate response (less than 4-fold decline)
Slide19CMV
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 90% are asymptomatic at birth! Up to 15% develop symptoms later, notably sensorineural hearing
loss * Symptomatic
infection
10% :
SGA, HSM, petechiae, jaundice, chorioretinitis, periventricular calcifications, neurological
deficits
>80%
develop long term
complications Hearing loss, vision impairment, developmental delay
Slide20Slide21Diagnosis
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
Slide22Slide23Treatment
Ganciclovir
x6wks in symptomatic infants
Studies show improvement or no progression of hearing loss at 6mos Neutropenia often leads to cessation of therapy Treatment not recommended in asymptomatic infants due to side effects
Slide24Herpes Simplex (HSV)
HSV1 or HSV2
Primarily transmitted through infected maternal genital
tract
Rationale for C-section delivery prior to membrane rupture
Slide25Clinical manifestations
Most are asymptomatic at
birth
3 patterns of
symptoms between birth and 4wks: Skin, eyes, mouth (SEM) CNS disease Disseminated disease (present earliest)
Initial manifestations of
skin lesions
are
NOT necessarily present
Slide26Clinical manifestations
Skin and mouth vesicles and
ulcers
Kerato conjunctivitis
Encephalitis Disseminated form: (multi organ) =septic shock like
Slide27Diagnosis
Culture
and PCR
of maternal lesions if present at delivery Cultures in infant: Skin lesions, oro/nasopharynx, eyes, urine, blood, rectum/stool, CSF
Slide28Treatment
Infants with disseminated and/or CNS disease are given 20 mg/kg IV every 8 hours for
21 days
. After this regimen, infants with CNS disease are given oral acyclovir 300 mg/m
2
3 times a day for 6 months; this long-term regimen improves neurodevelopmental outcomes at 1 year of age but may cause neutropenia.Prevention:C-section for mothers with genital lesionsAcyclovir for pregnant mothers with primary HSV.
Slide29Thank you