Intrauterine Infections - PDF

INTRAUTERINE INFECTIONS Associate Professor Ziya Kalem M.D İSTİNYE UNIVERSITY LIV BAHÇEŞEHİR HOSPITAL Infectious disease is the single most common problem encountered by the obstetrician. Urinary tract infections, endometritis, and mastitis, pose a risk primarily to the mo...

INTRAUTERINE INFECTIONS Associate Professor Ziya Kalem M.D İSTİNYE UNIVERSITY LIV BAHÇEŞEHİR HOSPITAL Infectious disease is the single most common problem encountered by the obstetrician. Urinary tract infections, endometritis, and mastitis, pose a risk primarily to the mother. Other disorders, such as group B streptococcal (GBS) infection, herpes simplex virus (HSV) infection, rubella, cytomegalovirus (CMV) infection, and toxoplasmosis are of principal concern because of the risk of fetal or neonatal complications. Candidiasis (Monilial Vaginitis) Vulvovaginal candidiasis (VVC) is primarily caused by Candida albicans Seventyfive percent of women will have at least one episode of VVC during their lifetime Predisposing factors associated with vaginal colonization with C. albicans include diabetes mellitus, pregnancy, obesity, recent use of antibiotics or steroids, and immunosuppression Symptomatic VVC affects 15% of pregnant women. Congenital candidiasis characteristically manifests at birth or within the first 24 hours after birth. It usually results from an intrauterine infection or heavy maternal vaginal coloniza- tion at the time of labor and delivery VVC has not been associated with preterm birth, preterm labor, low birth weight, or premature rupture of the membranes (PROM). The clinical manifestations of VVC in pregnancy include pruritus and burning, dysuria, dyspareunia, fissures. The vaginal pH in women with VVC is normal (1 year), patients are not contagious by sexual transmission, but the spirochete may still be transplacentally transmitted to a fetus. Without treatment, one third of patients progress to tertiary syphilis CONGENITAL SYPHILIS The clinical spectrum in congenital syphilis includes stillbirth, neonatal death, nonimmune hydrops, clinically apparent syphilis during the early months of life (early congenital syphilis), and the classic stigmata of late congenital syphilis Untreated or incompletely treated early congenital syphilis will progress to the classic manifestations of late congenital syphilis. T. pallidum can cross the placenta and infect the fetus as early as the sixth gestational week The risk to the fetus is present throughout pregnancy, and the degree of risk is related to the quantity of spirochetes in the maternal bloodstream. Maternal primary syphilis and secondary syphilis are associated with a 50% probability of congenital syphilis and a 50% rate of perinatal death Late latent maternal syphilis is associated with a 10% risk of congenital syphilis. DIAGNOSIS The most definitive methods for diagnosing early syphilis are dark-field microscope examination or direct fluorescent anti- body tests of lesion exudates or tissue. Nonspecific antibody tests include the Venereal Disease Research Laboratory (VDRL) test and the rapid plasma reagin (RPR) test. These assays are used for screening. Congenital syphilis is unusual if the mother received adequate treatment with penicillin during pregnancy Toxoplasmosis Toxoplasma gondii is a protozoan that has three distinct life forms: trophozoite, cyst, and oocyst. The life cycle of this organism is dependent on wild and domestic cats, which are the only known host for the oocyst. Human infection occurs when infected meat is ingested or oocysts are ingested via contamination by cat feces. Clinically significant infection occurs in only 1 in 8000 pregnancies. Immunity to this infection is mediated primarily through T lymphocytes Routine screening for toxoplasmosis in pregnancy is not indicated Serologic tests suggestive of an acute infection include identification of IgM- specific antibody, demonstration of an extremely high IgG antibody titer, and documentation of IgG seroconversion from negative to positive. Approximately 40% of neonates born to mothers with acute toxoplasmosis have evidence of infection Congenital infection is most likely to occur when maternal infection develops during the third trimester. The risk of injury to the fetus is greatest when maternal infection occurs in the first trimester. Clinical manifestations of congenital toxoplasmosis include; disseminated purpuric rash enlargement of the spleen and liver ascites chorioretinitis uveitis periventricular calcification ventriculomegaly seizures mental retardation. Once amniocentesis has confirmed toxoplasmic infection, targeted ultrasound examination is indicated to look for specific findings suggestive of severe fetal injury. TREATMENT In the immunocompetent adult, toxoplasmosis usually is an asymptomatic or self-limited illness that does not require treatment. Immunocompromised patients should be treated with a combination of oral sulfadiazine (4-g loading dose followed by 1 g four times daily) plus pyrimethamine (50 to 100 mg ini- tially, then 25 mg daily). When acute toxoplasmosis occurs during pregnancy, treatment is indicated, because maternal therapy reduces the risk of congenital infection and decreases the late sequelae of infection. Aggressive early treatment of infants with congenital toxoplasmosis is indicated and consists of combination therapy with pyrimethamine, sulfadiazine, and leucovorin for 1 year. Early treatment reduces, but does not eliminate, the late sequelae of toxoplasmosis (e.g., chorioretinitis) Pregnant women should be advised to avoid contact with cat litter if at all possible. Varicella-Zoster Virus Infection The varicella-zoster virus (VZV) is a DNA organism that is a member of the herpesvirus family. Varicella is of great importance in pregnancy because it poses risks to the mother, fetus, and neonate Varicella occurs in approximately 1 to 5 cases per 10,000 pregnancies The lesions typically occur in crops and evolve in sequential fashion from papule to vesicle to pustule, eventually crusting over to form a dry scab All pregnant women should be questioned about prior varicella at the time of their first prenatal appointment Women who are not certain of prior exposure should have an anti-VZV IgG assay. If a susceptible pregnant patient is exposed to someone with varicella, she should be treated within 72 to 96 hours with one of two agents to prevent active infection. The most extensively tested regimen is intramuscular varicella-zoster immune globulin (VZIG). An alternative method of prophylaxis is to administer oral acyclovir (800 mg, five times daily for 7 days) or oral valacyclovir (1000 mg, three times daily for 7 days). Pregnant women who develop varicella despite immunoprophylaxis should be treated with oral acyclovir or valacyclovir in the same dose as outlined for prophylaxis. Acute varicella infection during pregnancy has been associated with spontaneous abortion, intrauterine fetal death, and congenital anomalies. These complications are rare. Investigations have shown that the frequency of fetal anomalies is less than 1% when maternal infection occurs in weeks 1 through 12 of pregnancy and 2% or less when infection occurs in weeks 13 through 20. The most valuable test to identify fetal injury due to congenital varicella is ultrasound examination. Ultrasonic findings include ; intrauterine growth restriction, microcephaly, ventriculomegaly, echogenic foci in the fetal liver, and limb anomalies. Viral Influenza Influenza is caused by an RNA virus of the myxovirus family. Pregnant women have suffered dis- proportionate morbidity and mortality during influenza pandemics, including the H1N1 epidemic. In pregnancy, the major concern is the increased risk for development of life- threatening pneumonia Influenza virus has not been associated with an increased risk of spontaneous abortion, stillbirth, or congenital anomalies. Viral Hepatitis HEPATITIS A The infection is caused by an RNA virus that is transmitted by fecal-oral contact. The diagnosis is best confirmed by detection of IgM antibody specific for the hepatitis A virus. Perinatal transmission rarely occurs, and, therefore, the infection does not pose a major risk to either the mother or the baby HEPATITIS B Hepatitis B is caused by a DNA virus that is transmitted parenterally and via sexual contact In the absence of intervention, approximately 20% of mothers who are seropositive for hepatitis B surface antigen will transmit infection to their neonates. Infants delivered to seropositive mothers should receive hepatitis B immune globulin (HBIG) within 12 hours after birth. Before their discharge from the hospital, these infants also should begin the hepatitis B vaccination series.