CONGENITAL INFECTIONS

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

CONGENITAL INFECTIONS Rubella CMV Parvovirus Varicella Toxoplasmosis

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

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

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

Diagnosis Ultrasound Serology Urine culture for organism

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

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

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

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

SEVERE CONGENITAL CMV INFECTION

SEVERE CONGENITAL CMV INFECTION

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”

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

PARVOVIRUS CLINICAL MANIFESTATIONS Erythema infectiosum Transient aplastic crisis

PARVOVIRUS ERYTHEMA INFECTIOSUM

PARVOVIRUS ERYTHEMA INFECTIOSUM

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

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

TREATMENT OF CONGENITAL PARVOVIRUS INFECTION Intrauterine transfusion

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

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

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

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

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

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

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

TOXOPLASMOSIS EPIDEMIOLOGY

TOXOPLASMOSIS DIAGNOSIS Histology Serology

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

MANIFESTATIONS OF CONGENITAL TOXOPLASMOSIS Hepatosplenomegaly Chorioretinitis CNS injury Seizures Mental retardation

DIAGNOSIS OF CONGENITAL TOXOPLASMOSIS Amniocentesis Cordocentesis Ultrasound

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.

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

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

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)