1. CONGENITAL INFECTIONS

2. Sources of Infections Hematogenous spread
During delivery from birth canal
After birth from environmental sources
Postnatal infections
Viral infections
Fungal infections

3. CONGENITAL INFECTIONS
Rubella
CMV
Parvovirus
Varicella
Toxoplasmosis

4. RUBELLA
RNA virus
Spread by droplet infection
High rate of transmission in case infections occur within 12 weeks of gestation,
Can induce abortion and surviving babies may suffer of cataract, congenital heart defects, microcephaly etc

5. RUBELLA PATHOPHYSIOLOGY
Respiratory tract -->cervical lymph nodes-->hematogenous dissemination
Incubation period is 2 to 3 weeks

6. RUBELLA CLINICAL MANIFESTATIONS
Intrauterine and postnatal growth retardation
Retinopathy
Hepatosplenomegaly
Delayed manifestations include diabetes mellitus, thyroid dysfunction, growth hormone deficiency,
Malaise
Headache
Conjunctivitis, cataract
NON-PRURITIC, ERYTHEMATOUS, MACULOPAPULAR RASH
Central and peripheral hearing defects
Patent ductus arteriosus

7. Diagnosis
Ultrasound
Serology
Urine culture for organism

8. PREVENTION OF CONGENITAL RUBELLA
No effective treatment
Vaccination
Avoidance of exposure if susceptible

9. Cytomegalovirus
DNA virus
Humans are only host
Asymtomatic in 90% newborns

10. CMV CLINICAL MANIFESTATIONS
Malaise
Fever
Lymphadenopathy
Hepatosplenomegaly
Microcephaly
Intracranial calcifications
Jaundice
Growth restriction
Chorioretinitis
Hearing loss

11. CMV DIAGNOSIS
Amniocentesis - viral culture and polymerase chain reaction (PCR)
Ultrasound

12. SEVERE CONGENITAL CMV INFECTION

13. SEVERE CONGENITAL CMV INFECTION

14. PREVENTION OF CONGENITAL CMV INFECTION
Vaccine is not available
Anti-viral drugs do not prevent fetal injury
Anti-CMV antibody may be effective
Key to prevention is “universal precautions”

15. PARVOVIRUS EPIDEMIOLOGY
DNA virus
Humans are only known host
Transmission is by respiratory droplets and by blood
Incubation period is 4 to 20 days

16. PARVOVIRUS CLINICAL MANIFESTATIONS
Erythema infectiosum
Transient aplastic crisis

17. PARVOVIRUS ERYTHEMA INFECTIOSUM

18. PARVOVIRUS ERYTHEMA INFECTIOSUM

19. CONGENITAL PARVOVIRUS PATHOPHYSIOLOGY
Virus crosses the placenta and destroys red cell precursors
Fetal anemia --> high output congestive heart failure --> hydrops fetalis
Virus also directly injures myocardial cells

20. DIAGNOSIS OF CONGENITAL PARVOVIRUS INFECTION
Ultrasound
Assessment of Middle Cerebral Artery blood flow

21. TREATMENT OF CONGENITAL PARVOVIRUS INFECTION
Intrauterine transfusion

22. CONGENITAL PARVOVIRUS PROGNOSIS
If infant survives the hydropic state, the long-term prognosis is usually favorable

23. VARICELLA IN PREGNANCY
DNA virus
Member of Herpes family
Spread by respiratory droplets and direct contact
Highly contagious
Congenital infection is rare
Risk of fetal injury is < 2 % before 20 weeks and almost non-existent thereafter

24. VARICELLA CLINICAL MANIFESTATIONS
Macule  papule  vesicle  pustule
Lesions appear in crops
Intensely pruritic
Spread from central to peripheral

25. VARICELLA NEONATAL INFECTION
Newborn is vulnerable when delivery occurs within a few days of the time the mother shows signs of infection
Manifestations of infection
Disseminated skin lesions
Visceral infection
Pneumonia

26. VARICELLA MATERNAL RISK
Adults are more likely than children to develop two life-threatening complications:
Pneumonia ( 20 %)
Encephalitis (1 %)

27. VARICELLA PREVENTION
Vaccination of susceptible children and adults (live virus vaccine)
Avoidance of exposure in pregnancy if susceptible
Varicella-zoster immune globulin or antiviral chemotherapy if exposed

28. TOXOPLASMOSIS EPIDEMIOLOGY
Toxoplasma gondii is a protozoan
Organism exists in three forms
Trophozoite
Cyst
Oocyst

29. TOXOPLASMOSIS EPIDEMIOLOGY

30. TOXOPLASMOSIS DIAGNOSIS
Histology
Serology

31. CONGENITAL TOXOPLASMOSIS
The key danger is primary toxoplasmosis infection
Greatest risk to the fetus results from maternal infection in first half of pregnancy
Approximately 40 % of fetuses will be infected when primary maternal infection develops at < 20 weeks gestation

32. MANIFESTATIONS OF CONGENITAL TOXOPLASMOSIS
Hepatosplenomegaly
Chorioretinitis
CNS injury
Seizures
Mental retardation

33. DIAGNOSIS OF CONGENITAL TOXOPLASMOSIS
Amniocentesis
Cordocentesis
Ultrasound

34. TREATMENT OF CONGENITAL TOXOPLASMOSIS
Treatment of mother while fetus is still in utero (Spiramycin)
Early treatment of the infant
Pyrimethamine and a sulfonamide (sulfadiazine or sulfadoxine). These drugs should be continued throughout the first year of life and, in some cases, even longer.

35. PREVENTION OF CONGENITAL TOXOPLASMOSIS
Use precautions when handling cat litter box
Do not eat inadequately cooked meat

36. CONGENITAL INFECTIONS CONCLUSIONS
Congenital rubella – key is prevention by universal vaccination
Congenital CMV – key is prevention of exposure in pregnancy
Congenital parvovirus – avoidance of exposure is difficult, but intrauterine transfusion is life-saving
Varicella – risk to fetus is minimal, but risk to mother is great
Congenital toxoplasmosis – key is avoidance of exposure during pregnancy

37. Prevention of Infection in the Newborn
Tetanus toxoid administration
Five cleans at delivery
Clean surface
Clean hands
Clean blade
Clean cord tie
Clean clothes
Care of cord and skin
Exclusive breastfeeing
Early detection and treatment of minor infections
Immunization
Avoid overcrowding
Warm water baths (hospital policy)