current info on torch syndrome in pregnancy

1. TORCH-S IN PREGNANCY
Presenter Dr B.Msumi
Facilitator Sr Dr Happy(MD,MMED)

2. Overview
• TORCH COMPLEX is a medical acronym which
stands for toxoplasmosis,other,rubella
virus,cytomegalovirus infection and herpes
simplex virus infection
• The TORCH infections can lead to severe fetal
anomalies or even fetal loss
• They are a group of viral,bacterial and protozoan
infections that gain access to the fetal
bloodstream transplacentally via the chorionic
villi

3. • Hematogenous transmission may occur at any
time during gestation or occasionally at the time
of delivery via maternal to fetal transfusion
• The gestational age of fetus influenced the
degree of severity
• Treatment of maternal infection frequently has
no impact on fetal outcome
• They have mild maternal morbidity but serious
fetal consequences

4. Toxoplasmosis
• Is the disease caused by intracellular parasite
toxoplasma gondii
• a ubiquitous protozoan parasite that infects
humans in various settings
• mainly acquired during childhood and
adolescence
• Much higher rates of infection (up to 80 percent)
are found in the tropics in communities exposed
to contaminated soil, undercooked meat, or
unfiltered water

5. Prevalence
• Seroprevalence rates of toxoplasmosis vary
substantially among different countries
• Approximately 15 percent in the United States to more
than 50 percent in certain European countries
• In Tanzania only three studies have reported
seroprevalence of T.gondii infection among pregnant
women
• Two of them are recently conducted in mwanza and
KCMC with reported seroprevalence of 30.9% and
41.7% respectively
• An older study in Dar es salaam reported
seroprevalence of 35%

6. Vertical transmission
• Congenital infection occurs via tachyzoites
placental transmission after primary maternal
infection during pregnancy
• The risk of fetal transmission varies depending
upon the GA during which maternal infection
occurs
• Transmission of toxoplasma to the foetus typically
occurs after the placenta has become infected
• Determinant of transmission is the development
of placental blood flow which explains the
increased rate of transmission later in pregnancy

9. Clinical features
• Acute infection in adult humans goes
unrecognized in as many as 90% of cases
• The most common manifestations are
nontender lymphadenopathy, fatigue,
headache, malaise and myalgia
• First trimester fetal infection on the other
hand, often results in miscarriage, stillbirth, or
severe sequelae in the newborn

10. Diagnosis
Maternal infection
• Serologic tests represent the most commonly
used method to establish the diagnosis
• Documentation of recent seroconversion is
the best evidence of recent infection
• IgG antibodies appear within one to two
weeks of infection, peak in six to eight weeks
and then decline over the next two years; they
remain detectable for life

11. • IgM antibodies may appear within the first
week of infection and generally decline within
a few months
• Sometimes persist for years after the initial
infection
• Thus, the presence of IgM antibodies should
not be used to confirm a recent or acute
infection.

12. Interpretation of results of serological tests for toxoplasmosis performed at
clinical (nonreference) laboratories
IgG
test
resu
lt
IgM test
result
Clinical relevance
Neg Neg Interpreted to indicate that the women has not been infected
with T.gondii,serial testing during pregnancy is advised.if such
woman acquire primary infection during gestation ,they are at
risk of transmitting infection to fetus
Pos Neg During 1st or 2nd trimester most often reflects an infection
acquired before the present pregnancy
Neg Pos or
equivocal
IgM antibodies are detected early in the acute infection,because
they may persist for prolonged period.IgM antibodies may be
detected in pregnant women who were infected in the distant
past and before gestation,hence +ve IgM result should be
followed by confirmatory test at toxo reference lab
Pos Pos or
equivocal
Same as above

13. Fetal infection
• Prenatal diagnosis of congenital toxoplasmosis
is made by detection of the Toxoplasma gondii
parasite in fetal blood or amniotic fluid or
presence of Toxoplasma gondii IgM or IgA
antibodies in fetal blood
• (PCR) testing is the preferred diagnostic
modality

14. • Certain abnormalities on antenatal
sonography are suggestive, but not diagnostic,
of fetal infection.
• They include intracranial densities, increased
placental thickness and/or hyperdensity,
ventricular dilatation, intrahepatic densities,
hepatomegaly, ascites, pericardial and/or
pleural effusion.

15. Newborn infection diagnosis
• history and physical examination
• Ophthalmologic, auditory, and neurologic
examinations
• lumbar puncture and (CT) of the head
• Serum from the newborn can also be tested
for IgM and IgA antibodies

16. • IgM measurement appears to be more
sensitive when conducted with ELISA and
ISAGA than IFA
• IgA antibody measurment may be more
sensitive than IgM, but specificity is not
assured
• Most experts recommend a combination of
serologic tests.

17. Treatment
• Spiramycin(1g 8hrly ) should be given until
term
• Once fetal infection is
established,pyrimethamine 25mg bd orally
and sulphadiazine 1g 8hrly orally for 3/52
alternating with 3/52 course of spiramycin 1g
8hrly until delivery

18. • Pyrimethamine 25mg od orally and
sulphadiazine 4g/day administered
continously until term
• Leucovorin calcium 10-25mg/day orally is
added during pyrimethane and sulphadiazine
• Weekly monitoring of CBC and platelets
counts
• Treatment discontinued if significant
abnormal results reported

19. Prevention
• Women should avoid drinking unfiltered water
in any setting
• Avoid ingesting soil by observing strict hand
hygiene after touching soil
• Fruits and vegetables should be washed
before eating
• Women should avoid tasting meat while
cooking

20. Syphilis
• Definition
• Syphilis is a systemic human disease caused by Treponema
pallidum
Classification
Acquired (usually by sexual contact or through blood
transfusion).
 Early (includes: primary, secondary and early latent syphilis).
 Late (includes: latent and tertiary gummatous,
cardiovascular and neurosyphilis).
Congenital (transmitted from mother to child in utero).
 Early (first 2 years).
 Late, including stigmata of congenital syphilis

21. Syphilis has three clinical stages
• The primary stage:the infected person develops
painless ulcer called chancre(starts 21 days(range
10-90days)following infection,last 2-6 weeks)
WHO 2007
• The secondary stage:characterized by skin rash
over the whole body,often with fever and muscle
pain(starts 2-3 month after onset of chancre, last
2-6 weeks)followed by latent phase of many
years with no sign or symptoms(WHO 2007)

22. • Latent syphilis-is the period after infection
during which patients are seropositive but
have no clinical manifestation of the disease
• Early latent is when infection was acquired
within preceding year
• Late latent syphilis include all other
cases(PAHO 2008)

23. Syphilis in pregnancy
• Manifestation of syphilis in pregnancy are the
same as for non-pregnant women
• Syphilis may be acquired at any stage of
pregnancy whenever pregnant woman is
exposed
• If the pregnant woman is infected,T.pallidum
organisms that enter her blood can be
transmitted to the fetus

24. • Transmission to the fetus usually occur
between 16-18 weeks of pregnancy(but can
happen as early as 9 weeks)
• The likehood of transmission is directly related
to the stage of syphilis in the infected
pregnant woman
• The concentration of spirochaettes in blood is
highest in the primary and secondary stages of
disease and decrease slowly thereafter

25. Risks associated with syphilis in
pregnancy
1. Early fetal death
2. Low birth weight
3. Preterm delivery
4. Neonatal death
5. Infection or disease in newborn

26. Mother-to-child transmission of syphilis: a
continuing public health burden
• Nearly 1.5 million pregnant women are infected
with syphilis each year
• Approximately half of infected pregnant women
who are untreated,will experience adverse
outcomes due to syphilis
• MTCT of syphilis is relatively simple to
eliminate,but despite treatments that have been
available for over 60 years,MTCT of syphilis
persist as major public health problem

27. • Screening all pregnant women using simple
and low cost technologies,and effective
treatment with penicillin is feasible even in
low resource setting
• The exact proportion of pregnant women
globally who receive adequate testing and
treatment is unknown due to inadequate
surveillance

28. 1. Many of these visits are too late to avert an
adverse outcome
2. Clinics may not have offered testing
3. Testing may not have been affordable
4. Women may not have followed up or received
their test results
5. Treatment may not have been available
6. Treated women may have been re-infected by
untreated sexual partner

29. Diagnosis and screening
• Non-treponemal screening test ,VDRL and RPR
test detect antibody to reaginic antigen which
found in T.pallidum and some other condition
• False positive non-treponemal test result can be
associated with various medical conditions
unrelated to syphilis,including autoimmune
condition,older age and inj drug use
• Treponemal test to confirm diagnosis of syphilis
should be done

30. • If a screening test is positive,the serum is then
tested by confirmatory treponemal test,using an
antigen of T.pallidum,TPHA and TPPA
• Treponemal test are more specific than non-
treponemal,but they cant differentiate between
active untreated syphilis and succcessfuly treated
previous infection
• Non-treponemal test can distinguish current or
recent infection from old or treated infection

31. Treatment
• In early latent stage:single dose of 2.4 million
units benzathine penicillin G im
• In late latent stage:3 doses of 2.4 million units
of benzathine penicillin G im is given once in a
week
• Erythromycin stearate can be given if there is
penicillin hypersensitivity but it crosses
placenta poorly

32. • The newborn baby must therefore be treated
with a course of penicillin and consideration
given to re-treating the mother
• Ceftriaxone 250mg IM for 10 days in many
cases

33. Congenital syphilis
Classification
• Early congenital syphilis
• Late congenital syphilis

34. Early congenital infection
• Defined by clinical manifestations with onset
before two years of age
• Clinical manifestations in untreated infants
usually appear by three month of age,60-90%
are asymptomatic at birth
• The presence of signs at birth depends upon
the timing of intrauterine infection and
treatment

35. Clinical manifestation
• Gestational/perinatal:placenta large,thick and
pale. Umblical cord inflammed with abscess
like foci of necrosis within wharton’s jelly
• Systemic :fever,hepatomegaly,generalized
lymphadenopathy,failure to thrive ,edema
• Mucocutaneous :syphilitic
rhinitis,maculopapular rash,vesicular
rash,condylomata lata,jaundice

36. Late congenital syphilis
• Defined by clinical manifestations with onset after 2yrs
of age
• Manifestations are related to scarring or persistent
inflammation from early infection and characterized by
gumma formation in various tissues
• Developed in 40% of untreated syphilis during
pregnancy
• Some can be prevented by treatment of mother during
pregnancy or treatment of infant within 3 month
• Some cannot be prevented despite of appropriate
treatment

37. Clinical manifestation
Haematologic Musculoskeletal Neurologic Miscellaneous
Anaemia
(haemolytic in
newborn,non
haemolytic or chr
after 1 month
Pseudoparalysis of
parrot
CSF
abnormalities:reacti
ve csf vdrl,elevated
csf wbc
count,elevated csf
protein
Pneumonia,pneum
onitis,respiratory
distress
Thrombocytopenia(
bleeding or
petechiae)
Radiographic
abnormalities:perio
statis,wegner
sign,wimberger sign
Acute syphilitic
leptomeningitis
Nephrotic
syndrome
Leukopenia Chronic
meningovascular
syphilis
Leukocytosis

39. Investigation
• RPR/VDRL, TPPA/TPHA (quantitative)
• anti-treponemal IgM-EIA, treponemal IgM
• Full blood count, liver function, electrolytes.
• Cerebrospinal fluid (CSF): cells, protein,
RPR/VDRL, TPHA/TPPA
• X-rays long bones
• Ophthalmic assessment as indicated

40. Treatment(WHO and CDC recommendations )
Infants with signs of congenital syphilis
• Aqueous cristalline benzypenicillin 100000-
150000 units/kg daily for 10 days
Infants without signs of congenital syphilis
• Benzathine benzylpenicillin G 50000 units/kg
im up to adult dose of 2.4 million units in a
single dose

41. Rubella (german measles)
• Is the disease caused by the rubella virus,a
togavirus
• Enveloped ,has a single stranded RNA genome
• This virus causes self limited infection in most
host
• During pregnancy the virus can have
potentially devastating effects on developing
fetus

42. • The child may be born with CRS if the mother
is infected within the 1st16 weeks of
pregnancy
• The virus has teratogenic properties
• After infecting the placenta ,virus spreads
through vascular system of the developing
fetus,causing cytopathic damage to blood
vessels and ischaemia in the developing
organs

43. • Acquired rubella is transmitted via airborne
droplet emission from the upper respiratory
tract of active cases and replicates in the
nasopharynx and lymph nodes
• The virus may also be present in the
urine,faeces and on the skin
• The disease has an incubation period of 2 to 3
weeks

44. Clinical features
• Rash (erythmatous maculopapular eruption)
on the face which spread to the trunk and
limbs ,usually fades after 3 days
• The facial rash usually clears as it spreads to
other part of the body
• Low grade fever,joint pains,headache
conjuctivitis,sore throat,cough and coryza
• Swollen glands(sub occipital and posterior
cervical lymphadenopathy)

45. Congenital rubella syndrome
CRS characterized by;
Intrauterine growth restriction
Intracranial calcifications
Microcephaly
Cataracts
Cardiac defects
Neurologic disease
Osteitis and hepatosplenomegaly

46. Vertical transmission and risk of CRS
GESTATIONAL AGE RISK OF INFECTION RISK OF CONGENITAL MALFORMATION
<11 weeks 80-90% 90%
11-12 weeks 80-90% 33%
13-14 weeks 80-90% 11%
15-16 weeks 60% 25-50%
17-20 weeks 25% negligible
27-30 weeks 35% negligible
>36 weeks 100% negligible

47. Diagnosis
Maternal infection
• A four fold rise in Rubella IgG antibody titre
between acute and convalescent serum
specimen
• A positive serologic test for rubella specific
IgM antibody
• A positive rubella culture

48. Fetal infection
• PCR on CVS(chorionic villus sampling) for
prenatal diagnosis of intrauterine infection at
10-12 week GA
• USS(biometric data)

49. Management of rubella infection
GESTATION
AGE
STATE OF
IMMUNITY
MANAGEMENT
> 12weeks Known immune No further testing is necessary,CRS has not been
reported after maternal infection beyond 12wks
<12 weeks Known immune Appropriate counselling should be provided
<16weeks Non –immune or
immunity unkown
Acute and convalescent IgG and IgM should be
obtained
16-20 weeks Non –immune or
immunity unkown
Appropriate counselling,CRS is rare may be
manifested by sensorineural deafness
>20 weeks Non –immune or
immunity unknown
Reassured,no studies document CRS after 20wks

50. Prevention
• Active immunisation programs using
live,disabled virus vaccines
• All girls should be vaccinated against rubella
before entering the child bearing years
• Women wishing to conceive should be
counselled and encouraged to have their
antibody status determined and vaccinated if
needed

51. Cytomegalovirus
• CMV is a double stranded DNA herpes virus
• The CMV seropositivity rate increases with
age,geographical location,socioeconomic class
and work exposure
• CMV infection requires intimate contact through
saliva,urine and other body fluids
• Possible routes of transmission include sexual
contact,organ transplantation,transplacental
transmission,transmission via breast milk and
blood transfusion

52. • Primary ,reactivation or recurrent CMV infection can
occur in pregnacy and can lead to congenital CMV
infection
• Transplacental infection can result in
IUGR,sensorineural hearing
loss,intracalcifications,microcephaly,hydrocephalus,hep
atosplenomegaly,delayed psychomotor
development,thrombocytopenia and /or optic atrophy
• Vertical transmission can occur at any stage of
pregnancy,however severe sequelae are more common
with infection in the 1st trimester,while the overall risk
of infection is greater in the 3rd trimester

53. • The transmission rate to the fetus is between 30-50%
according to the organization of teratology information
service
• Of those babies who become infected,only 10-15% show
signs of congenital CMV after primary maternal infection
• Congenital CMV affects about 0.2-2.5% of babies
worldwide
• Of these only 1-10% of the babies born with the CMV
infection will have symptoms at birth and another 10-15%
may not show any symptoms at birth,but still may have
longterm affects such as hearing loss and learning disability

54. Diagnosis and management
• Serological testing in women with suspected
CMV
• Amniocentesis
• Ultrasonography
• Quantitative polymerase chain reaction for
viral DNA in amniotic fluid
• Iv treatment with CMV hyperimmune globulin
• Ganciclovir treatment

55. Serological test interpretation
CMV IgG CMV IgM CMV IgG avidity interpretation
Non-reactive Non-rective Not applicable Infection unlikely
Reactive Non-reactive High avidity Past infection
Reactive Reactive Low avidity Primary infection
Reactive Reactive High avidity Non primary
infection,low risk
for in utero
transmission

56. Herpes Simplex Virus infection
• HSV is an ubiquitous enveloped and double
stranded DNA virus(family Herpesviridae)
• During pregnancy the major concern of
maternal HSV infection is transmission to the
fetus
• HSV-1 predominate orofacial lesion(trigeminal
ganglia)
• HSV-2 found in the lumbosacral ganglia

57. Clinical manifestation
• Vary depend on the stage of infection and
prior immune status
• First episode primary infection,describes cases
in which HSV is isolated from genital
secretions in the absence of HSV antibodies
• Present with severe painful genital
ulcers,pruritus,dysuria,fever,tender inguinal
lymphadenopathy and headache

58. • First episode non-primary infection,diagnosed
when HSV is isolated in woman who have only
the other serum HSV-type antibody present
• Eg HSV2 isolated from genital secretions in
women already expressing serum HSV-1
antibody
• Normally genital infection is milder than the
primary infection

59. • Recurrent episodes of HSV infection are
characterized by the presence of antibody against
the same HSV type and the herpes outbreaks are
usually mild (7-10days) with less severe
symptoms than the first episode
• Preceded by prodromal symptoms such as
pruritus,burning or pain before lesion are visible
• Mild symptoms and few lesions or no symptoms
at all

60. Vertical transmission
• occurs during labor and delivery as a results of
direct contact with virus shed from infected
sites(cervix,vaginal,perianal area)
• Viral shedding can occur in the absence of
maternal symptoms and lesions
• The frequency of shedding is higher in HSV-2
versus HSV-1 infection

61. Diagnosis
• Presence of vesicular or ulcerated lesion
• PCR
• Viral culture
• Direct fluoroscent antibody test

62. Management
• ACOG recommends that women with active
recurrent genital herpes should be offered
• Suppressive viral therapy from 36 weeks until
delivery
valacyclovir 500mg orally bd or
Acyclovir 400mg orally tds
• C/S is recommended for all women in
labour/rupture of membrane with active genital
lesions or prodromal symptoms such vulvar
pain,burning

63. • Sitz bath to relieve vulvar pain,fever,dysuria
and other local symptoms
• Analgesia eg acetaminophen
• Avoid transcervical
procedure(cerclage,chorionic villus sampling)
in women with genital lesions

64. Prevention
• Avoidance of sexual activity during disease
• Use of barrier protection
• Chronic suppressive therapy to reduce risk of
transmission to an uninfected partner
• Patient education

65. References
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Mwanza,Tz,Berno Mwambe et al
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to be considered in Tanzania antenatal package ,Mirambo et al
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