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Torch infections  Rina Karborani Torch infections  Rina Karborani

Torch infections Rina Karborani - PowerPoint Presentation

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Torch infections Rina Karborani - PPT Presentation

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

infection disease test treatment disease infection treatment test infants maternal positive manifestations birth syphilis fetal vdrl asymptomatic clinical primary

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Presentation Transcript

Slide1

Torch infections

Rina Karborani

Slide2

T= Toxoplasmosis

O= others (

Parvovirus B-19

,

syphilis

, Varicella)

R= Rubella

C=

CMV

H=

HSV

Slide3

Slide4

Parvovirus 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

Slide5

Transmission

Occurs Via :

Vertical transmission

Respiratory secretions

Transfusion of blood products

Slide6

Rash & Joint symptoms occur

2-3 weeks after initial infection

Slide7

Pathogenic

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.

Slide8

Slide9

Treatment

Slide10

C

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

Slide12

Clinical 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

Slide15

Slide16

Diagnosing 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."

Slide17

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

Slide18

Treatment

 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)

Slide19

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 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

Slide20

Slide21

Diagnosis

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

Slide22

Slide23

Treatment

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

Slide24

Herpes Simplex (HSV)

 HSV1 or HSV2

Primarily transmitted through infected maternal genital

tract

 Rationale for C-section delivery prior to membrane rupture

Slide25

Clinical 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

Slide26

Clinical manifestations

Skin and mouth vesicles and

ulcers

Kerato conjunctivitis

Encephalitis Disseminated form: (multi organ) =septic shock like

Slide27

Diagnosis

Culture

and PCR

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

Slide28

Treatment

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.

Slide29

Thank you