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HIV and SYPHILIS IN PREGNANCY
PRESENTER: DR. MARIA ANSARI
MODERATOR: DR. PRADYUMNA BHANDARY
Syphilis and Pregnancy
Introduction
Usually the end of secondary syphilis is the end of the infectious
phase, except in pregnant women where the infectiousness to the
unborn child may last for 5 to 6 years or occasionally longer.
Effect of Pregnancy on Syphilis
• It appears that generally the course of syphilis is mild during
pregnancy.
• Most cases of congenital syphilis result from transmission of T.
pallidum to the fetus during early syphilis, while most adverse
pregnancy outcomes occur in women treated for syphilis in the
third trimester.
• It is believed that chancres are seen less frequently and
manifestations of secondary syphilis may be much milder than in
nonpregnant females.
• Women who become pregnant in the early stage of the disease
are evidently less likely to suffer from neurosyphilis.
Effect of Syphilis on Pregnancy
Syphilis is highly deleterious to the offspring, causing abortion,
stillbirth, or birth of a syphilitic child in a high percentage of
untreated pregnant patients.
Mode of Infection
• Transplacental
• Because of the inability of the fetus to mount an immune response
before the fourth month and deficiency of some biochemical
treponemal requirements in the young fetus, little inflammation is
produced in the first-trimester.
• The pathogenic changes occur only after the fetus becomes
immunocompetent, that is, after 18 to 20 weeks of gestation,
due to the presence of T. pallidum, which has crossed the
placenta in the first trimester
The outcome of pregnancy in untreated syphilis depends upon
the stage of infection.
A woman in the early contagious stage will certainly infect her
unborn child by hematogenous spread of organisms through the
placenta, producing a severe effect on the fetus because a large
number of treponemes cross the placenta.
The chance of a fetus being infected in the latent or late stages
depends largely on the duration of infection in the pregnant mother.
Usually, the effect on the fetus is less severe because of the
diminished number of circulating treponemes
Infection during pregnancy may result in abortion, premature
stillbirth, full_x0002_term stillbirth, birth of a live child with signs of
prenatal syphilis, birth of an apparently healthy infant developing
signs of early prenatal syphilis in the first few weeks or months of
life, birth of an apparently healthy child developing evidence of late
prenatal syphilis in later life, birth of a healthy child with positive
serological tests without any clinical signs, and finally birth of a
healthy normal child (Kassowitz’s law).
A healthy child may be born in between prenatal syphilitic ones or
the series of abortions and stillbirths may occur continuously
because of the chances of infection due to the intermittent release
of treponemes from a deep focus of infection, which may have an
immunological basis.
The infant may contract the infection and develop a primary chancre
via contact with infectious lesions in the birth canal of the mother
who has contracted the disease late in pregnancy
PRENATAL SYPHILIS
Prenatal syphilis is defined as the one transmitted by an infected
mother to the fetus in utero.
Clinical Manifestations
In two-third of cases, the clinical signs of early prenatal syphilis
begin to appear in the third to eighth week of life, and within 3
months in nearly all cases.
The earlier the onset, the poorer the prognosis.
The clinical spectrum of early prenatal syphilis ranges from
asymptomatic infection to fulminant sepsis to death.
• Cutaneous lesions
Skin lesions that develop soon after birth are frequently vesicular or
bullous (syphilitic pemphigus).
Lesions developing later are often macular or maculopapular with a
generalized symmetrical distribution similar to acquired syphilis,
though they have a predilection for certain sites (viz. face, around
the mouth, napkin area (back, extremities, palms, and soles).
Prenatal syphilis: Bullous lesions and erosions
simulating epidermolysis bullosa in a neonate.
Prenatal syphilis: Annular lesions in an infant.
Moist eroded areas on the buttocks Desquamation of the soles.
• Mucous Membrane Lesions
• Syphilitic rhinitis produces a nasal discharge (snuffles), which is
initially watery and later becomes thicker, purulent, and bloody,
and is highly infectious.
• Mucous patches on the buccal mucosa.
• Ulceration and perforation of the nasal septum, with flattening of
the nasal bridge producing the characteristic saddle nose.
• The nasal obstruction due to the discharge may cause breathing
and suckling difficulties, the latter resulting in weight loss.
• Throat lesions may cause pharyngitis and laryngitis resulting in a
hoarse cry and cough.
• Both skin and mucosal lesions are extremely infectious as they
are teeming with spirochetes.
• Bone Lesions
• Almost all cases show evidence of osteochondritis (epiphysitis) of
the long bones with the characteristic saw-tooth metaphysis seen
on X-ray after the first month of life.
• Sites- distal ends of the radius and ulna, the upper end of the
tibia, femur, humerus, and fibula.
• The cardinal symptoms and signs are pain, swelling, and
tenderness.
• The affected limb is invariably held immobilized (pseudoparalysis
of Parrot).
• Hematologic Manifestations
anemia,
leukocytosis or leukopenia,
monocytosis,
thrombocytopenia, and
raised ESR.
• Hepatosplenomegaly
• CNS Involvement -
• The neurologic involvement ranges from asymptomatic CNS
invasion by T. pallidum to acute syphilitic leptomeningitis.
• Convulsions, bulging fontanelles, stiffness of the neck, and
hydrocephalus.
• Generalized Lymphadenopathy -
The nodes are firm, discrete, rubbery, and nontender.
Epitrochlear lymphadenopathy.
• Ocular Involvement
Choroidoretinitis, glaucoma, and uveitis
• Nephrotic syndrome
• Syphilitic pneumonitis or pneumonia alba
• Diarrhea ,
• Myocarditis,
• Onychia, and
• Paronychia
Late Prenatal Syphilis
The late-stage of prenatal syphilis persists beyond 2 years of age.
• Interstitial Keratitis
• Most common late manifestation. It may begin at any time
between 5 and 16 years of age or even later.
• It is more common in females than in males.
• The symptoms are photophobia, pain, excess watering of the
eyes, and blurred vision.
Interstitial keratitis in a patient with late congenital syphilis.
• “Hutchinson’s triad”
1. Interstitial keratitis,
2. eighth nerve deafness, and
3. typical Hutchinson’s teeth
• Neurosyphilis - tabes dorsalis, general paresis and local
gummata
• Skin and Mucous Membrane Lesions
• Gummata- more common in the palate and nasopharynx.
• The latter may lead to nasal septal perforation, and the former to
palatal perforation and destruction resulting in nasal voice and
regurgitation of food.
• Leucomelanoderma of the palms and soles.
• Bone Involvement
• Localized osteoperiostitis of the skull, periostitis of the long bones,
and, dactylitis.
• Osteoperiostitis of the tibia may produce an appearance of
bowingof the legs .
• This hydrarthrosis is believed to be due to perisynovitis affecting
both the knees (occasionally the elbows).
• Paroxysmal Cold Hemoglobinuria
The urine becomes dark brown but clears within 24 hours.
The patient may experience rigor followed by fever, headache,
malaise, and transient jaundice.
Urticaria, acrocyanosis, and transient splenomegaly may occur.
• Stigmata of congenital syphilis
1. Rhagades
2. Saddle nose
3. Frontal and parietal bossing
4. Short maxillae
5. Bull dog jaw
6. High arched palate
7. Higouménakis’ sign
8. Sabre tibia thickening and anterior bowing of lower limb
9. Scaphoid scapulae
10. Hutchinson’s teeth
11. Mulberry or moon’s molars
12. Corneal opacities
13. Salt and pepper fundus
14. Optic atrophy
15. Eighth nerve deafness
DIAGNOSIS OF SYPHILIS
Serological tests for syphilis (STS):
a) Nontreponemal tests:
Antigen: Cardiolipin, cholesterol, and lecithin
Antibody: Reagin (Nonspecific)
Types:
i) Complement fixation tests, e.g., Wassermann reaction, Kolmer test
ii) Flocculation tests, e.g., VDRL slide test, rapid plasma reagin (RPR)
card test, automated reagin test (ART), reagin screen test (RST)
b) Treponemal tests
Antigen: The entire organism (T. pallidum living/dead) or its components
Antibody: Specific antibodies
Types:
i) T. pallidum immobilization test (TPI)
ii) Fluorescent treponemal antibody absorption test (FTA-Abs), and FTA-Abs
double staining test (FTA-Abs DS)
iii) T. pallidum hemagglutination assay (TPHA), microhemagglutination for T.
pallidum (MHA-TP), and hemagglutination treponemal test for syphilis (HATTS)
Enzyme-linked immunosorbent assay (ELISA)
Postnatal screening for prenatal syphilis in infants born to high-risk
mothers at 4 to 8 weeks of age may be appropriate in addition to
prenatal and at-delivery screenings.
Treatment
1. Procaine penicillin G.1.2 million units IM daily × 20 days
If the individual is allergic to penicillin, desensitization and treatment with the
appropriate regimen of penicillin is the preferred choice.
2. Erythromycin 500 mg orally q.i.d. × 2 weeks.
3. Ceftriaxone 1 g daily for 8–10 days
4. Early prenatal syphilis:
a. Aqueous crystalline penicillin G 50,000 units per kg 8–12 hours IV
× 10 days.
b. Procaine penicillin G 50,000 units per kg IM × 10 days.
5. Late prenatal syphilis:
a. Benzathine penicillin G 50,000 units per kg IM up to 2.4 million
units Neurosyphilis or no CSF examination.
b. Aqueous penicillin G 50,000 units per kg 4–6 hours. IV × 10–14
days.
HIV in Pregnancy
Introduction
• There are 2 main types of HIV infection with Type 1 infection
being the commonest one.
• HIV transmission among humans occur in 3 ways:
unprotected sexual intercourse,
blood and blood products,
donated semen or organs,
infected mother to her child.
Prevention of mother to child transmission
• The Prevention of Parent to Child Transmission of HIV/AIDS
(PPCTC) was started in the country in 2002.
• AIM: prevent the perinatal transmission of HIV from an HIV
infected pregnant mother to her newborn baby.
• The susceptibility to HIV infection is influenced by various biological
and socio-cultural factors. In general, women in developing
countries are more prone to infection due to :
vulval and vaginal inflammation, pelvic
inflammatory disease, partially treated/silent Clamydia infections
which act as cofactors in HIV and other STDs like syphilis and
herpes.
poverty, gender bias, unemployment, low education forcing women
into prostitution, high risk behaviour of male partners, poor condom
usage, and desire and pressure for pregnancy precluding the use of
barrier methods.
Effects of Pregnancy on HIV
• Pregnancy does not alter disease progression in asymptomatic
women and those with early disease, athough there may be a
more rapid progression in women with late stage HIV infection.
Effects of HIV on Pregnancy
• Increased rates of spontaneous abortion
• Ectopic pregnancy
• Preterm labour
• Stillbirths
• Low birth weight babies
• Post partum infectious complications are high in HIV-positive
women, especially those with low CD4 counts.
MOTHER-TO-CHILD TRANSMISSION (MTCT)
• Transmission of HIV from mother to child may occur in-utero,
during labor and delivery, and/or through breastfeeding.
• The maximum transmission occurs late in pregnancy and during
labour.
• The factors which affect MTCT are briefly described as under:
viral load, clinical immuno-logical and nutritional
status drug use and sex practices, and availability of antiretroviral
therapy. Of these, maternal viral load is the strongest predictor of
vertical transmission. While there is no known level of viremia below
which transmission does not occur, it is reported to be very low if
HIV RNA <1000 copies/ml (<1%). With a viral load of >100,000
copies/ml, the transmission rate is 41%. Low levels of vitamin A in
serum are associated with a risk of increased transmission.
duration of ruptured membranes, mode
of delivery, intrapartum haemorrhage, obstetrical
procedures and inva-sive fetal monitoring. With rupture
beyond 4 hours, the risk rises from 14 to 25% and
continues to rise by 2% every hour upto 24 hoursElective
caesarean reduces transmission rates, while obstetric
procedures like external cephalic version, amniocentesis,
operative vaginal delivery, fetal scalp electrode and invasive
fetal testing increase the risk.
prematurity, multiple pregnancy,
breastfeeding, genetic susceptibility and immature
gastrointestinal and immune system. Premature infants
have a 3.7 times higher risk of intrapartum transmission due
to increased fetal cell susceptibility to HIV infection, reduced
functional immune res- ponse, incompetent mucosal barrier
and reduced level of acquired maternal antibody. First-born
twins have a twofold higher risk of transmission.
The total risk of transmission is 25-40% in the absence of any
intervention. The distribution of risk is as follows:
• Antepartum: 10-15% mainly transplacental spread in-utero.
• Intrapartum: 65-75% secondary to direct contact with infected
blood/cervicovaginal secretions and passage through an infected
birth canal. Transmission during labour may also be due to
transplacental microtransfusion as placental integrity is disrupted.
• Postpartum: 10-15% through breast milk
The WHO strategy to prevent new infections among mothers and
children involves a four-pronged approach:
• Primary prevention among women and children.
• Prevention of unwanted pregnancies.
• Prevention of HIV transmission from infected women to their
children (PTCT).
• Provision of treatment, care and support for women with HIV, their
children and family (PPTCT Plus)
The antenatal care of HIV infected mothers require a
multidisciplinary approach and should include:
• Regular antenatal checkup and assessment of fetal growth,
detailed anomaly scan, especially after first trimester exposure to
HAART
• Nutritional support- provide iron/folic acid/ calcium/multivitamins
• Screen for STI/Hepatitis B/C, tuberculosis
• Avoid procedures like external cephalic version/invasive fetal tests
• Prophylaxis for opportunistic infections like Pneumocystis Carinii
pneumonia, toxopla- smosis, tuberculosis - Mycobacterium avium
complex, varicella zoster, hepatitis A and B
• Plasma viral load and CD4 T-lymphocyte count three-monthly to
advise regarding choice and timing of antiretroviral therapy.
• Monitor for drug toxicity in women on antiretroviral therapy
PREVENTION OF MTCT
The interventions to prevent MTCT are:
1. Universal screening of antenatal women, offer therapeutic
termination if positive.
2. Behavioural interventions
3. ART in pregnancy
4. Elective caesarean section
5. Avoid breastfeeding
6. Neonatal ART
7. Contraception
1. Universal screening of antenatal women
The discovery of HIV infection in early pregnancy is traumatic for a
patient and leading her to emotional dilemma. However, the benefits
of early detection far outweigh the cosequences.
Universal screening in high seroprevalence areas and selective
screening of high-risk cases in low prevalence areas has been
suggested, although there are concerns that such a strategy would
leave out a large number of infected women.
HIV screening in pregnancy can be done in one of the two ways:
• Opt-in strategy: The patient requests for HIV testing after
informed consent and proper pre-test counselling followed by
post-test counselling.
• Opt-out strategy: The screening is universal with informed
consent, but the patient has the right to decline testing.
The opt-out strategy encourages higher screening rates. Screening
is ideally carried. out at the first prenatal visit, in the first trimester
itself. Pre and post-test counselling should be the norm. The
diagnosis of HIV is made by either 3 rapid tests or 2 ELISA-based
tests.
2. Behavioural interventions
Behavioural interventions include reduction in the frequency of
unprotected intercourse during pregnancy, reduction in the number of
sexual partners, and avoidance of drug use and smoking during
pregnancy.
3. ART in pregnancy
The goals of ART in pregnancy are twofold:
• To reduce MTCT (i.e., for the baby's health)
• To prevent disease progression in the mother (i.e., for the
mother's own health)
All HIV-positive women should receive ART during pregnancy and
delivery.
ART to prevent disease progression
HAART
Zidovudine (AZT) 300 mg BD + Lamivudine (3TC) 150 mg BD +
Nevirapine (NVP) 200 mg BD (if CD4 <250) is given in antepartum,
intrapartum and postpartum periods.
Alternatively, AZT + 3TC + Efavirenz (EFV) can be given if CD4 is
between 250 and 350 but initiation should be delayed to 2nd
trimester as EFV is embryotoxic.
• The infant should receive AZT 2 mg/kg x 7 days.
• If the mother had received <4 weeks of AZT or HAART, then infant
AZT should be continued for at least 4 weeksIf the mother had
received at least 4 weeks of AZT before delivery, omission of
maternal NVP may be considered.
In general, the side effects of ART are:
• Preterm labour
• Anaemia
• Hyperglycemia
• Hepatotoxicity
• Rarely a woman becomes pregnant while on ART; in such cases,
if she is on Efavirenz (EFV)-containing regimen in first trimester, it
should be substituted with NVP, although exposure to EFV is not
an indication for abortion.
• Women who are receiving EFV in the second or third trimester of
pregnancy can continue the current regimen
• Elective caesarean at 38 weeks should be discussed and offered
to all HIV infected women who are not on HAART and with HIV-
RNA load >1000 copies/ml, as it has been shown to reduce
MTCT.
• Doubtful benefit is observed with elective caesarean in women
who are already on HAART and who have a viral load <1000
copies/ml. In such cases, decision regarding mode of delivery
should be individualized.
Universal precautions should be followed in labour and
delivery.
• Avoid prolonged membrane rupture
• Invasive fetal monitoring like fetal blood sampling, scalp
electrodes and operative vaginal delivery to minimize fetal contact
with maternal blood and cervicovaginal secretions.
• Prophylactic antibiotics are given as routine policy.
• Early cord clamping
• Immediate baby bath
• Waste disposal after delivery should be appropriately done.
• Placenta should be soaked in 1% sodium hypochlorite for 30 min
before discarding in a disposable plastic bag for incineration.
• Contaminated linen and delivery items should also be treated with
1% sodium hypochlorite before mixing with other items.
5. Breastfeeding practices
• Since HIV DNA is present in breast milk, HIV transmission can
occur through breastfeeding, with maximum chances in the first
few months.
• This exposure increases in the event of cracked nipples, mastitis,
mixed feeding and oral candidiasis in the infant.
Mechanism of transmission through breast milk may involve:
• Infection via cell-free HIV in breast milk or via HIV infected cells
• Susceptibility of immature neonatal GI tract to virus
• GI tract mucosal damage
The transmission rate increases with increasing duration of breast
feeding.
• The ideal substitute is sterile artificial feeds which fulfil the
(Acceptable, Feasible, Affordable, Sustainable and Safe).
• In women of low socio-economic status, after counselling and
discussing the risks, the patient should be advised exclusive
breast milk (EBM) for 4 months followed by abrupt weaning.
• Mixed feeding is strongly condemned as it significantly increases
MTCT due to immune factors and growth factors in breast milk
and mucosal damage associated with mixed feeding.
6. Neonatal ART
• Blood sample of the neonate should be taken for assessment of
ART requirement.
• If the virus is detectable by PCR within 48 hours of birth, the fetus
is assumed to be infected in utero, while intrapartum infection is
suspected when viral studies are negative within the first week but
become positive between 7 and 90 days.
• HIV status of the infant should be determined by a DNA- PCR at
6-8 weeks and ELISA at 18 months Neonatal ART is given as
outlined earlier
Contraception
In , one barrier method which is moderately
effective against pregnancy, but highly efficacious in preventing HIV
transmission should be combined with another regular contraceptive
like oral pills, intrauterine devices, implants or even voluntary
sterilization which is highly effective but does not prevent HIV
transmission to the partner.
References
• V K Sharma’s Textbook of Sexually Transmitted Diseases.
• IADVL Textvook of Dermatology.
THANK YOU

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HIV and Syphilis in Pregnancy: Diagnosis and Treatment

  • 1. HIV and SYPHILIS IN PREGNANCY PRESENTER: DR. MARIA ANSARI MODERATOR: DR. PRADYUMNA BHANDARY
  • 3. Introduction Usually the end of secondary syphilis is the end of the infectious phase, except in pregnant women where the infectiousness to the unborn child may last for 5 to 6 years or occasionally longer.
  • 4. Effect of Pregnancy on Syphilis • It appears that generally the course of syphilis is mild during pregnancy. • Most cases of congenital syphilis result from transmission of T. pallidum to the fetus during early syphilis, while most adverse pregnancy outcomes occur in women treated for syphilis in the third trimester.
  • 5. • It is believed that chancres are seen less frequently and manifestations of secondary syphilis may be much milder than in nonpregnant females. • Women who become pregnant in the early stage of the disease are evidently less likely to suffer from neurosyphilis.
  • 6. Effect of Syphilis on Pregnancy Syphilis is highly deleterious to the offspring, causing abortion, stillbirth, or birth of a syphilitic child in a high percentage of untreated pregnant patients.
  • 7. Mode of Infection • Transplacental
  • 8. • Because of the inability of the fetus to mount an immune response before the fourth month and deficiency of some biochemical treponemal requirements in the young fetus, little inflammation is produced in the first-trimester. • The pathogenic changes occur only after the fetus becomes immunocompetent, that is, after 18 to 20 weeks of gestation, due to the presence of T. pallidum, which has crossed the placenta in the first trimester
  • 9. The outcome of pregnancy in untreated syphilis depends upon the stage of infection. A woman in the early contagious stage will certainly infect her unborn child by hematogenous spread of organisms through the placenta, producing a severe effect on the fetus because a large number of treponemes cross the placenta. The chance of a fetus being infected in the latent or late stages depends largely on the duration of infection in the pregnant mother. Usually, the effect on the fetus is less severe because of the diminished number of circulating treponemes
  • 10. Infection during pregnancy may result in abortion, premature stillbirth, full_x0002_term stillbirth, birth of a live child with signs of prenatal syphilis, birth of an apparently healthy infant developing signs of early prenatal syphilis in the first few weeks or months of life, birth of an apparently healthy child developing evidence of late prenatal syphilis in later life, birth of a healthy child with positive serological tests without any clinical signs, and finally birth of a healthy normal child (Kassowitz’s law).
  • 11. A healthy child may be born in between prenatal syphilitic ones or the series of abortions and stillbirths may occur continuously because of the chances of infection due to the intermittent release of treponemes from a deep focus of infection, which may have an immunological basis.
  • 12. The infant may contract the infection and develop a primary chancre via contact with infectious lesions in the birth canal of the mother who has contracted the disease late in pregnancy
  • 13. PRENATAL SYPHILIS Prenatal syphilis is defined as the one transmitted by an infected mother to the fetus in utero.
  • 14. Clinical Manifestations In two-third of cases, the clinical signs of early prenatal syphilis begin to appear in the third to eighth week of life, and within 3 months in nearly all cases. The earlier the onset, the poorer the prognosis. The clinical spectrum of early prenatal syphilis ranges from asymptomatic infection to fulminant sepsis to death.
  • 15. • Cutaneous lesions Skin lesions that develop soon after birth are frequently vesicular or bullous (syphilitic pemphigus). Lesions developing later are often macular or maculopapular with a generalized symmetrical distribution similar to acquired syphilis, though they have a predilection for certain sites (viz. face, around the mouth, napkin area (back, extremities, palms, and soles).
  • 16. Prenatal syphilis: Bullous lesions and erosions simulating epidermolysis bullosa in a neonate. Prenatal syphilis: Annular lesions in an infant.
  • 17. Moist eroded areas on the buttocks Desquamation of the soles.
  • 18. • Mucous Membrane Lesions • Syphilitic rhinitis produces a nasal discharge (snuffles), which is initially watery and later becomes thicker, purulent, and bloody, and is highly infectious. • Mucous patches on the buccal mucosa. • Ulceration and perforation of the nasal septum, with flattening of the nasal bridge producing the characteristic saddle nose.
  • 19. • The nasal obstruction due to the discharge may cause breathing and suckling difficulties, the latter resulting in weight loss. • Throat lesions may cause pharyngitis and laryngitis resulting in a hoarse cry and cough. • Both skin and mucosal lesions are extremely infectious as they are teeming with spirochetes.
  • 20. • Bone Lesions • Almost all cases show evidence of osteochondritis (epiphysitis) of the long bones with the characteristic saw-tooth metaphysis seen on X-ray after the first month of life. • Sites- distal ends of the radius and ulna, the upper end of the tibia, femur, humerus, and fibula.
  • 21. • The cardinal symptoms and signs are pain, swelling, and tenderness. • The affected limb is invariably held immobilized (pseudoparalysis of Parrot).
  • 22. • Hematologic Manifestations anemia, leukocytosis or leukopenia, monocytosis, thrombocytopenia, and raised ESR.
  • 23. • Hepatosplenomegaly • CNS Involvement - • The neurologic involvement ranges from asymptomatic CNS invasion by T. pallidum to acute syphilitic leptomeningitis. • Convulsions, bulging fontanelles, stiffness of the neck, and hydrocephalus.
  • 24. • Generalized Lymphadenopathy - The nodes are firm, discrete, rubbery, and nontender. Epitrochlear lymphadenopathy. • Ocular Involvement Choroidoretinitis, glaucoma, and uveitis • Nephrotic syndrome
  • 25. • Syphilitic pneumonitis or pneumonia alba • Diarrhea , • Myocarditis, • Onychia, and • Paronychia
  • 26. Late Prenatal Syphilis The late-stage of prenatal syphilis persists beyond 2 years of age.
  • 27. • Interstitial Keratitis • Most common late manifestation. It may begin at any time between 5 and 16 years of age or even later. • It is more common in females than in males. • The symptoms are photophobia, pain, excess watering of the eyes, and blurred vision.
  • 28. Interstitial keratitis in a patient with late congenital syphilis.
  • 29. • “Hutchinson’s triad” 1. Interstitial keratitis, 2. eighth nerve deafness, and 3. typical Hutchinson’s teeth
  • 30. • Neurosyphilis - tabes dorsalis, general paresis and local gummata • Skin and Mucous Membrane Lesions • Gummata- more common in the palate and nasopharynx. • The latter may lead to nasal septal perforation, and the former to palatal perforation and destruction resulting in nasal voice and regurgitation of food. • Leucomelanoderma of the palms and soles.
  • 31. • Bone Involvement • Localized osteoperiostitis of the skull, periostitis of the long bones, and, dactylitis. • Osteoperiostitis of the tibia may produce an appearance of bowingof the legs . • This hydrarthrosis is believed to be due to perisynovitis affecting both the knees (occasionally the elbows).
  • 32. • Paroxysmal Cold Hemoglobinuria The urine becomes dark brown but clears within 24 hours. The patient may experience rigor followed by fever, headache, malaise, and transient jaundice. Urticaria, acrocyanosis, and transient splenomegaly may occur.
  • 33. • Stigmata of congenital syphilis 1. Rhagades 2. Saddle nose 3. Frontal and parietal bossing 4. Short maxillae 5. Bull dog jaw 6. High arched palate 7. HigoumĂŠnakis’ sign 8. Sabre tibia thickening and anterior bowing of lower limb 9. Scaphoid scapulae 10. Hutchinson’s teeth 11. Mulberry or moon’s molars 12. Corneal opacities 13. Salt and pepper fundus 14. Optic atrophy 15. Eighth nerve deafness
  • 34. DIAGNOSIS OF SYPHILIS Serological tests for syphilis (STS): a) Nontreponemal tests: Antigen: Cardiolipin, cholesterol, and lecithin Antibody: Reagin (Nonspecific) Types: i) Complement fixation tests, e.g., Wassermann reaction, Kolmer test ii) Flocculation tests, e.g., VDRL slide test, rapid plasma reagin (RPR) card test, automated reagin test (ART), reagin screen test (RST)
  • 35. b) Treponemal tests Antigen: The entire organism (T. pallidum living/dead) or its components Antibody: Specific antibodies Types: i) T. pallidum immobilization test (TPI) ii) Fluorescent treponemal antibody absorption test (FTA-Abs), and FTA-Abs double staining test (FTA-Abs DS) iii) T. pallidum hemagglutination assay (TPHA), microhemagglutination for T. pallidum (MHA-TP), and hemagglutination treponemal test for syphilis (HATTS) Enzyme-linked immunosorbent assay (ELISA)
  • 36. Postnatal screening for prenatal syphilis in infants born to high-risk mothers at 4 to 8 weeks of age may be appropriate in addition to prenatal and at-delivery screenings.
  • 37. Treatment 1. Procaine penicillin G.1.2 million units IM daily × 20 days If the individual is allergic to penicillin, desensitization and treatment with the appropriate regimen of penicillin is the preferred choice. 2. Erythromycin 500 mg orally q.i.d. × 2 weeks. 3. Ceftriaxone 1 g daily for 8–10 days
  • 38. 4. Early prenatal syphilis: a. Aqueous crystalline penicillin G 50,000 units per kg 8–12 hours IV × 10 days. b. Procaine penicillin G 50,000 units per kg IM × 10 days. 5. Late prenatal syphilis: a. Benzathine penicillin G 50,000 units per kg IM up to 2.4 million units Neurosyphilis or no CSF examination. b. Aqueous penicillin G 50,000 units per kg 4–6 hours. IV × 10–14 days.
  • 40. Introduction • There are 2 main types of HIV infection with Type 1 infection being the commonest one. • HIV transmission among humans occur in 3 ways: unprotected sexual intercourse, blood and blood products, donated semen or organs, infected mother to her child.
  • 41. Prevention of mother to child transmission • The Prevention of Parent to Child Transmission of HIV/AIDS (PPCTC) was started in the country in 2002. • AIM: prevent the perinatal transmission of HIV from an HIV infected pregnant mother to her newborn baby.
  • 42. • The susceptibility to HIV infection is influenced by various biological and socio-cultural factors. In general, women in developing countries are more prone to infection due to : vulval and vaginal inflammation, pelvic inflammatory disease, partially treated/silent Clamydia infections which act as cofactors in HIV and other STDs like syphilis and herpes. poverty, gender bias, unemployment, low education forcing women into prostitution, high risk behaviour of male partners, poor condom usage, and desire and pressure for pregnancy precluding the use of barrier methods.
  • 43. Effects of Pregnancy on HIV • Pregnancy does not alter disease progression in asymptomatic women and those with early disease, athough there may be a more rapid progression in women with late stage HIV infection.
  • 44. Effects of HIV on Pregnancy • Increased rates of spontaneous abortion • Ectopic pregnancy • Preterm labour • Stillbirths • Low birth weight babies • Post partum infectious complications are high in HIV-positive women, especially those with low CD4 counts.
  • 45. MOTHER-TO-CHILD TRANSMISSION (MTCT) • Transmission of HIV from mother to child may occur in-utero, during labor and delivery, and/or through breastfeeding. • The maximum transmission occurs late in pregnancy and during labour.
  • 46. • The factors which affect MTCT are briefly described as under: viral load, clinical immuno-logical and nutritional status drug use and sex practices, and availability of antiretroviral therapy. Of these, maternal viral load is the strongest predictor of vertical transmission. While there is no known level of viremia below which transmission does not occur, it is reported to be very low if HIV RNA <1000 copies/ml (<1%). With a viral load of >100,000 copies/ml, the transmission rate is 41%. Low levels of vitamin A in serum are associated with a risk of increased transmission.
  • 47. duration of ruptured membranes, mode of delivery, intrapartum haemorrhage, obstetrical procedures and inva-sive fetal monitoring. With rupture beyond 4 hours, the risk rises from 14 to 25% and continues to rise by 2% every hour upto 24 hoursElective caesarean reduces transmission rates, while obstetric procedures like external cephalic version, amniocentesis, operative vaginal delivery, fetal scalp electrode and invasive fetal testing increase the risk.
  • 48. prematurity, multiple pregnancy, breastfeeding, genetic susceptibility and immature gastrointestinal and immune system. Premature infants have a 3.7 times higher risk of intrapartum transmission due to increased fetal cell susceptibility to HIV infection, reduced functional immune res- ponse, incompetent mucosal barrier and reduced level of acquired maternal antibody. First-born twins have a twofold higher risk of transmission.
  • 49. The total risk of transmission is 25-40% in the absence of any intervention. The distribution of risk is as follows: • Antepartum: 10-15% mainly transplacental spread in-utero. • Intrapartum: 65-75% secondary to direct contact with infected blood/cervicovaginal secretions and passage through an infected birth canal. Transmission during labour may also be due to transplacental microtransfusion as placental integrity is disrupted. • Postpartum: 10-15% through breast milk
  • 50. The WHO strategy to prevent new infections among mothers and children involves a four-pronged approach: • Primary prevention among women and children. • Prevention of unwanted pregnancies. • Prevention of HIV transmission from infected women to their children (PTCT). • Provision of treatment, care and support for women with HIV, their children and family (PPTCT Plus)
  • 51. The antenatal care of HIV infected mothers require a multidisciplinary approach and should include: • Regular antenatal checkup and assessment of fetal growth, detailed anomaly scan, especially after first trimester exposure to HAART • Nutritional support- provide iron/folic acid/ calcium/multivitamins • Screen for STI/Hepatitis B/C, tuberculosis
  • 52. • Avoid procedures like external cephalic version/invasive fetal tests • Prophylaxis for opportunistic infections like Pneumocystis Carinii pneumonia, toxopla- smosis, tuberculosis - Mycobacterium avium complex, varicella zoster, hepatitis A and B • Plasma viral load and CD4 T-lymphocyte count three-monthly to advise regarding choice and timing of antiretroviral therapy. • Monitor for drug toxicity in women on antiretroviral therapy
  • 53. PREVENTION OF MTCT The interventions to prevent MTCT are: 1. Universal screening of antenatal women, offer therapeutic termination if positive. 2. Behavioural interventions 3. ART in pregnancy 4. Elective caesarean section 5. Avoid breastfeeding 6. Neonatal ART 7. Contraception
  • 54. 1. Universal screening of antenatal women The discovery of HIV infection in early pregnancy is traumatic for a patient and leading her to emotional dilemma. However, the benefits of early detection far outweigh the cosequences. Universal screening in high seroprevalence areas and selective screening of high-risk cases in low prevalence areas has been suggested, although there are concerns that such a strategy would leave out a large number of infected women.
  • 55. HIV screening in pregnancy can be done in one of the two ways: • Opt-in strategy: The patient requests for HIV testing after informed consent and proper pre-test counselling followed by post-test counselling. • Opt-out strategy: The screening is universal with informed consent, but the patient has the right to decline testing.
  • 56. The opt-out strategy encourages higher screening rates. Screening is ideally carried. out at the first prenatal visit, in the first trimester itself. Pre and post-test counselling should be the norm. The diagnosis of HIV is made by either 3 rapid tests or 2 ELISA-based tests.
  • 57. 2. Behavioural interventions Behavioural interventions include reduction in the frequency of unprotected intercourse during pregnancy, reduction in the number of sexual partners, and avoidance of drug use and smoking during pregnancy.
  • 58. 3. ART in pregnancy The goals of ART in pregnancy are twofold: • To reduce MTCT (i.e., for the baby's health) • To prevent disease progression in the mother (i.e., for the mother's own health) All HIV-positive women should receive ART during pregnancy and delivery.
  • 59.
  • 60. ART to prevent disease progression HAART Zidovudine (AZT) 300 mg BD + Lamivudine (3TC) 150 mg BD + Nevirapine (NVP) 200 mg BD (if CD4 <250) is given in antepartum, intrapartum and postpartum periods. Alternatively, AZT + 3TC + Efavirenz (EFV) can be given if CD4 is between 250 and 350 but initiation should be delayed to 2nd trimester as EFV is embryotoxic.
  • 61. • The infant should receive AZT 2 mg/kg x 7 days. • If the mother had received <4 weeks of AZT or HAART, then infant AZT should be continued for at least 4 weeksIf the mother had received at least 4 weeks of AZT before delivery, omission of maternal NVP may be considered.
  • 62. In general, the side effects of ART are: • Preterm labour • Anaemia • Hyperglycemia • Hepatotoxicity
  • 63. • Rarely a woman becomes pregnant while on ART; in such cases, if she is on Efavirenz (EFV)-containing regimen in first trimester, it should be substituted with NVP, although exposure to EFV is not an indication for abortion. • Women who are receiving EFV in the second or third trimester of pregnancy can continue the current regimen
  • 64. • Elective caesarean at 38 weeks should be discussed and offered to all HIV infected women who are not on HAART and with HIV- RNA load >1000 copies/ml, as it has been shown to reduce MTCT. • Doubtful benefit is observed with elective caesarean in women who are already on HAART and who have a viral load <1000 copies/ml. In such cases, decision regarding mode of delivery should be individualized.
  • 65. Universal precautions should be followed in labour and delivery. • Avoid prolonged membrane rupture • Invasive fetal monitoring like fetal blood sampling, scalp electrodes and operative vaginal delivery to minimize fetal contact with maternal blood and cervicovaginal secretions. • Prophylactic antibiotics are given as routine policy.
  • 66. • Early cord clamping • Immediate baby bath • Waste disposal after delivery should be appropriately done. • Placenta should be soaked in 1% sodium hypochlorite for 30 min before discarding in a disposable plastic bag for incineration. • Contaminated linen and delivery items should also be treated with 1% sodium hypochlorite before mixing with other items.
  • 67. 5. Breastfeeding practices • Since HIV DNA is present in breast milk, HIV transmission can occur through breastfeeding, with maximum chances in the first few months. • This exposure increases in the event of cracked nipples, mastitis, mixed feeding and oral candidiasis in the infant.
  • 68. Mechanism of transmission through breast milk may involve: • Infection via cell-free HIV in breast milk or via HIV infected cells • Susceptibility of immature neonatal GI tract to virus • GI tract mucosal damage The transmission rate increases with increasing duration of breast feeding.
  • 69. • The ideal substitute is sterile artificial feeds which fulfil the (Acceptable, Feasible, Affordable, Sustainable and Safe). • In women of low socio-economic status, after counselling and discussing the risks, the patient should be advised exclusive breast milk (EBM) for 4 months followed by abrupt weaning. • Mixed feeding is strongly condemned as it significantly increases MTCT due to immune factors and growth factors in breast milk and mucosal damage associated with mixed feeding.
  • 70. 6. Neonatal ART • Blood sample of the neonate should be taken for assessment of ART requirement. • If the virus is detectable by PCR within 48 hours of birth, the fetus is assumed to be infected in utero, while intrapartum infection is suspected when viral studies are negative within the first week but become positive between 7 and 90 days. • HIV status of the infant should be determined by a DNA- PCR at 6-8 weeks and ELISA at 18 months Neonatal ART is given as outlined earlier
  • 71. Contraception In , one barrier method which is moderately effective against pregnancy, but highly efficacious in preventing HIV transmission should be combined with another regular contraceptive like oral pills, intrauterine devices, implants or even voluntary sterilization which is highly effective but does not prevent HIV transmission to the partner.
  • 72. References • V K Sharma’s Textbook of Sexually Transmitted Diseases. • IADVL Textvook of Dermatology.