Antenatal Fetal Infections 2022 PDF
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Duhok College of Medicine
2022
Dr. Khalida Hassan Muho
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Summary
This presentation discusses antenatal fetal infections, covering various infectious agents that can affect the fetus during pregnancy. It details sources of infection, risk factors, diagnosis, and management approaches for conditions like HIV, hepatitis B, and TORCH infections.
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Antenatal fetal infections Dr.Khalida Hassan Muho Specialist OB\GYN Most perinatal infections are asymptomatic in the mother, but may have serious consequences for the fetus. Source of maternal infection: Community & from contact with infected children. Most infections in pregnancy resolve spo...
Antenatal fetal infections Dr.Khalida Hassan Muho Specialist OB\GYN Most perinatal infections are asymptomatic in the mother, but may have serious consequences for the fetus. Source of maternal infection: Community & from contact with infected children. Most infections in pregnancy resolve spontaneously without therapy or are readily treated with antimicrobial agents. Sources of fetal infection: 1. Transplacental spread (usual route). 2. Extension of infection into adjacent maternal tissues and organs, during delivery, or as a result of invasive procedures, such as the use of monitors, CVS, sampling of fetal blood and intrauterine transfusion. 3. Before rupture of fetal membranes, organisms in the genital tract may invade the amniotic fluid and infect the fetus. Microorganisms of concern include those identified in the acronym TORCH: toxoplasmosis, rubella, cytomegalovirus, and herpes virus; the ‘O’ in TORCH originally stood for ‘other infections’. A new acronym should include other well described causes of in utero infection: syphilis, hepatitis B, HIV and parvovirus. the National Screening Committee and published in the National Institute for Health and Care Excellence (NICE) antenatal care guidelines: 1. All pregnant women are offered screening at the booking visit for rubella antibody, syphilis, HIV and hepatitis B (regardless of immunization history). 2. If screening has been declined at booking, it should be re-offered at 28 weeks of gestation. 3. If there is a screen positive result, a second sample should be taken for syphilis, hepatitis B and HIV to confirm the screening result. Following this result the women should be referred for specialist counseling and appropriate follow up and management. 4. Pregnant women arriving in labour who have not received antenatal care elsewhere are offered screening for infectious diseases. HIV infection remains one of the greatest public health challenges in the 21st century. Two types: 1 (more) and 2 Mother – child transmission is rare in developed countries due to: 1. Routine antenatal screening for HIV 2. use of ART in pregnancy 3. elective C/S 4. Avoidance of breastfeeding Pathogenesis: it is a retrovirus causing destruction of T – lymphocytes resulting in immunosuppression and eventually leading to AIDS. Transmission: sexual contact, contaminated blood, mother to child transmission (occur in utero 20-25%, during labour and delivery, or postnatally through breastfeeding 15%). Predictors of perinatal infection are: 1. Maternal plasma HIV RNA level (strongest predictor) 2. Women with advanced clinical disease, 3. Acute HIV infection during pregnancy, 4. Low CD4+ counts. 5. Obstetric risk factors associated with increased risk of transmission include vaginal delivery, prolonged rupture of membranes, chorioamnionitis and invasive obstetric procedures. Diagnosis and treatment If primary laboratory screen‐positive result (positive ELISA), confirmation of dx is by specific test for HIV (at least 2 assays) CD4 count and a viral load provides the clinician with a useful snapshot of the patient’s status and medication needs when she is first encountered. Specialist counseling and support Advice (by MDT) about management of their infection and interventions to reduce the risk of vertical and sexual transmission, including discussions on the use of antiretrovirals and caesarean section, early treatment and care for the child, and decisions about breastfeeding. Paediatric care plan is determined prior to the birth. ART has significantly reduce the rate of vertical transmission. Zidovudine (monotherapy) chemoprophylaxis given in the prenatal and intrapartum period and to the newborn reduces vertical transmission from 27.7 to 7.9%. It is inappropriate in mothers with high viral load or low CD4 counts because it fails to suppress viral replication and increases the risk of development of viral resistance. Combination ART in order to achieve prolonged viral suppression when treatment is indicated, with the aim of reducing the viral load to below detectable levels All pregnant women should have commenced ART by week 24 of pregnancy. For women with a plasma viral load of less than 50 HIV RNA copies/mL at 36 weeks, and in the absence of obstetric contraindications, a planned vaginal delivery is recommended. Where the viral load is 400 HIV RNA at 36 weeks, elective caesarean delivery is recommended. Where the indication for caesarean section is the prevention of vertical transmission, delivery should be planned at 38–39 weeks Intrapartum use of IV zidovudine. Neonatal post-exposure prophylaxis (usually oral zidovudine) should be commenced very soon after birth, certainly within 4 hours and should be given for 4 weeks. Avoid breastfeeding Hepatitis B Infection of the liver caused by the hepatitis B virus (HBV). The incubation period ranges from 40 to 160 days (average 60–90 days). Overall, the prevalence in antenatal women in the UK is around 0.14%. It is DNA virus. The risk of chronic infection is greater than 90% in neonates Transmitted by: parenteral exposure to infected blood or body fluids. mostly occurs through vaginal or anal intercourse, as a result of blood‐to‐ blood contact (e.g. sharing of needles and ‘needlestick’ injuries) or through perinatal transmission from mother to child. Diagnosis by the presence of HBsAg in the serum. Perinatal transmission occurs at or near the time of birth or by transplacental transmission might be responsible for perinatal infections or by amniocentesis in HBsAg positive mothers. 70–90% of mothers who are HBeAg positive will transmit the infection to the baby. Management If a woman is screen‐positive for HBV, she should be referred to an appropriate specialist (hepatologist, gastroenterologist or infectious disease specialist) within 6 weeks of a positive result for full evaluation. All babies born to these mothers should receive a complete course of vaccine on time. Babies born to highly infectious mothers, should receive hepatitis B immunoglobulin (HBIG) as well as active immunization. HBIG should preferably be given within 24 hours of delivery Rubella Is one of the most teratogenic infections known. Incidence of rubella and congenital rubella syndrome decrease.due to vaccination. Rubella is caused by a togavirus and spread by droplet transmission. Following exposure, almost 80% of susceptible individuals become infected. Replication occurs and viraemia develops 5–7 days after exposure. Viraemia usually results in placental and fetal infection. The incubation period is 14–21 days, and in most cases a rash develops 14–17 days after exposure. Individuals with rubella are infectious from 1 week before symptoms appear to 4 days after the onset of the rash. Rubella immune status should be assessed at first Maternal rubella infection in pregnancy may result in fetal loss or in congenital rubella syndrome (CRS). Infection from 8 to 10 weeks of pregnancy results in damage in up to 90% of surviving infants. The risk of damage declines to about 10–20% when infection develops between 11 and 16 weeks’ gestation. The risk of fetal damage is small when infection happens after 16 weeks of pregnancy CRS presents with one or more of the following: cataracts and other eye defects; deafness; most common cardiac abnormalities; microcephaly; retardation of intrauterine growth; inflammatory lesions of brain, liver, lungs and bone marrow. Diabetes mellitus occurs frequently in later childhood in those with CRS. Diagnosis and Mx Serology by Detection of rubella IgM indicates recent infection, Following a primary rubella infection, IgM can be detected within 5–7 days and may persist up to 2 months. Specific IgG develops by 2 weeks and persists for life. A history of exposure to, or possible recent infection with, rubella in early pregnancy is actively sought. Mx depends on when during gestation she was exposed and on her state of immunity. Confirming the diagnosis, counseling about the risks of infection of and damage to the fetus, and discussing all the available options, including the use of immunoglobulin and consideration of termination of pregnancy, Isolation may also be important to reduce spread of infection. There is no treatment for rubella and supportive care should be offered. Droplet precautions are recommended for 7 days after the onset of the rash. Human immunoglobulin is not recommended for the protection of pregnant women exposed to rubella. MMR vaccine should not be given to pregnant women. If MMR vaccine is given to adult women, they should be advised to guard against pregnancy for 1 month. Breastfeeding is not a contraindication to MMR immunization Syphilis Treponema pallidum, the causative agent of syphilis, is a Gram-negative bacterium Can be acquired either horizontally ( by direct contact) or vertically ( mother to child transmission causing congenital syphilis). The incubation period averages 3 weeks (3–90 days). The likelihood of vertical transmission increases with advancing gestation. A newborn occasionally may be infected perinatally, by contact at delivery with an infectious lesion present in the birth canal or perineum. Postnatal transmission from mother to child is rare. The extent of damage to a fetus affected by congenital syphilis depends on the stage of development when infection occurs and the elapsed time before treatment. congenital syphilis is characterized by the presence of hepatosplenomegaly, lymphadenopathy, rash, mucocutaneous lesions, haemolytic anaemia or thrombocytopenia, osteochondritis and pseudoparalysis, periostitis, rhinitis and central nervous system (CNS) involvement, all of which usually appear within the first 2–8 weeks of life. Late congenital syphilis usually present after 2 years of life and often in early adolescence, Congenital syphilis can be prevented or treated in utero. Other effects of untreated syphilis: fetal demise or late‐term stillbirth occurs, but premature delivery or neonatal death may also occur Diagnosis and management All pregnant women should have serological screening for syphilis at their first antenatal assessment. Diagnosis is usually performed by a non-treponemal ((plasma reagin (RPR) and Venereal Disease Research Laboratory (VDRL) assay)) serological screening test, with a treponemal ((treponemal enzyme immunoassay (EIA), treponemal chemiluminescent assay (CLIA), T. pallidum haemagglutination assay (TPHA) and fluorescent treponemal antibody absorption test (FTA‐abs)) serological test for confirmation. The diagnosis of congenital syphilis can be suggested by US findings of hydrops, hepatomegaly, polyhydromnios. Polymerase chain reaction (PCR) can be performed on amniotic fluid. Once a screen positive result is confirmed, the woman and her family should be referred to a specialist in genitourinary medicine for assessment, counseling and possible treatment. A single dose of benzathine penicillin G 2.4 million units is effective in most cases. When treatment of early syphilis is initiated in the third trimester, a second dose of benzathine penicillin 1 week after the first is recommended Toxoplasmosis Toxoplasma gondii is an intracellular parasite that can infect humans and almost all warm‐blooded animals. The incubation period is 5–18 days following exposure. The infection is transmitted through infected cat faeces, undercooked raw meat, and transplacentally. It is common but rarely reported ( no symptoms in more than 90%). Routine antenatal serological screening for toxoplasmosis is not indicated. The risk of developing congenital toxoplasmosis increases with advancing gestational age. The incidence of transmission is 3–9% if infection occurs in the first trimester and highest (60–81%) if it occurs in the third trimester. The severity of disease is worse if infection occurs in the first trimester, with a risk of development of clinical signs in the infected fetus of 60%. Infection prior to pregnancy confers immunity with minimal risk of vertical transmission. Congenital toxoplasmosis is characterized by the tetrad of chorioretinitis, hydrocephalus, intracranial calcification and convulsion. Diagnosis and manegment Serological tests for the detection of specific antiToxoplasma IgG and IgM antibodies are the most widely used. A positive IgG test before pregnancy means that the fetus is not at risk. IgM antibodies are the first to appear after an acute infection. Absence of IgM when IgG antibodies are detected helps to exclude a recent infection. IgG avidity is often useful in pregnant women who present with antibodies in their first sample. IgG avidity measures the strength of antigen–antibody binding, which increases with the time elapsed since infection. High avidity allows the exclusion of an infection acquired in the last 12–20 weeks. The prenatal diagnosis of fetal infection is based on ultrasound scanning (suspicious feature of congenital infection) and PCR testing of amniotic fluid or blood. Prevention of toxoplasmosis in pregnant women is paramount: such as washing hands before handling food, thoroughly washing all fruit and vegetables, thoroughly cooking raw meats and readymade meals, wearing gloves and washing hands after handling soil/gardening, and avoiding cat faeces in cat litter or in soil Treatment depends on: maternal immune status, gestational age and presence of fetal infection. Drug regimens most commonly used rely primarily on spiramycin and a pyrimethamine/sulfadiazine combination. Women should be counseled on the option of termination of pregnancy in the case of severe morphological lesions. CMV Cytomegalovirus (CMV) is the most common congenital infection in the UK, affecting around 3 per 1000 births, double-stranded DNA herpesvirus that is transmitted by sexual contact or direct contact with infected blood, urine, nasopharyngeal secretions or saliva. The incubation period is 28.60 days and viraemia can be detected for 2.3 weeks after primary infection. After the primary infection, CMV remains latent in host cells and recurrent, or secondary, infection can occur. Vertical transmission of CMV mostly occurs by transplacental infection after primary or secondary infection, but can also follow exposure to contaminated genital tract secretions at delivery, or breastfeeding. With primary maternal CMV infection, the overall risk of transmission to the fetus is approximately 30–40%. 12–18% will have signs and symptoms of CMV at birth and up to 25% will develop sequelae. Only 0.15–1% of women with recurrent infection will transmit the virus to the fetus. The risk of transmission is greatest in the third trimester (40–72%), compared with a lower risk in the first trimester (30%). However, fetal damage is more serious the earlier in gestation transmission occurs. congenital CMV infection Other developmental abnormalities, including sensorineural hearing loss, microcephaly, motor defects, mental retardation, chorioretinitis, dental defects diagnosis and management Primary maternal CMV infection diagnosed by appearance of specific IgG in the serum of a woman who was previously seronegative, or on identification of specific IgM associated with low IgG avidity. A secondary infection should be diagnosed when a significant rise of IgG antibody titre is documented independently of the presence of IgM and high IgG avidity Congenital CMV may be suspected prenatally on the basis of ultrasound findings suggestive of infection. The prenatal diagnosis of CMV is possible by testing amniotic fluid obtained by amniocentesis, where sensitivity of PCR can reach 100% if the test is performed after 21 weeks of gestation and at least 7 weeks after presumed time of maternal infection. Currently, no therapies are available for the treatment of maternal or fetal CMV infection. Use of antiviral Medications in routine clinical care of pregnant women is not recommended. passive immunization with CMV‐specific-hyperimmune globulin is not recommended outside of a research protocols. Education of susceptible pregnant women has been shown to significantly reduce the incidence of infection. Preventive measures, like hand washing and minimizing exposure from high‐risk areas such as nurseries, must be recommended. When a recent primary infection is diagnosed, invasive testing can be offered to identify infected fetuses When a primary maternal infection is documented, parents should be informed of a 30–40% risk for fetal infection, and a 20–25% risk for development of sequelae postnatally in infected fetuses. The only options following a prenatal diagnosis of CMV infection are termination of pregnancy or observation. Fetal MRI may improve the prognostic evaluation, especially when brain abnormalities are seen on ultrasound. Herpesvirus Neonatal herpes is rare in the UK. Herpes simplex virus (HSV) types 1 and 2 are members of the large family of herpesviruses (all have latency). Transmission of HSV most often occurs by person-to person contact. Transplacental intrauterine infection (rarely) The incubation period is 3–6 days. The risk of neonatal HSV depends on multiple factors: the type of maternal infection (primary or recurrent), the presence of maternal antibodies, the duration of rupture of membranes before delivery, the use of fetal scalp electrodes and the mode of delivery. The risks are greatest for a primary infection occurring in the third trimester, particularly within 6 weeks of delivery. Diagnosis and management Patient history and clinical examination can help in the diagnosis of HSV infection. All the lesions identified should be unroofed and the fluid cultured For women presenting with first episode of genital herpes in the third trimester, particularly within 6 weeks of expected delivery, specific HSV antibody testing (IgG to HSV‐1 and HSV‐2 ) is advisable. Women with suspected genital herpes should be referred to a genitourinary medicine physician, Aciclovir is not licensed for use in pregnancy. Following primary HSV infection, providing that delivery does not ensue within the following 6 weeks, the pregnancy should be managed expectantly and vaginal delivery anticipated. Daily suppressive aciclovir 400 mg three times daily from 36 weeks of gestation should be given. In the third trimester (high risk of neonatal transmission), treatment will usually continue with daily suppressive aciclovir 400 mg three times daily until delivery. Caesarean section should be the recommended mode of delivery for all women developing first‐episode genital herpes in the third trimester. In the case of a recurrent infection, women should be informed that the risk of neonatal herpes is low. Parvovirus B19 Is a single‐stranded DNA virus with a predilection for infecting rapidly dividing cell lines, such as bone marrow erythroid progenitor cells, leading to severe anaemia in the fetus. 50–70% of women of reproductive age have immunity to parvovirus B19. About 1–3% of susceptible pregnant women will develop serological evidence of infection in pregnancy. Women at increased risk of infection include mothers of preschool and school‐age children and school teachers. Transmission is probably by droplets from oral or nasal secretions also be transmitted parenterally through blood or blood product transfusion, or vertically from mother to fetus. Risk of intrauterine infection rise with increasing gestational age, ranging from 15% when infection occurs before 16 weeks of gestation, to 25–70% thereafter. Parvovirus has been associated with hydrops fetalis (non-immune), with an overall incidence of 2.9%. Spontaneous miscarriage and stillbirth. In patients with a rash, recent parvovirus infection should be confirmed or excluded by testing for parvovirus B19-specific IgG and IgM on the first serum obtained. Fetal parvovirus infection should be considered if non-immune hydrops is detected on ultrasound. Fetal infection can be diagnosed using PCR to detect parvovirus B19 DNA in amniotic fluid or fetal blood samples Treatment Women with acute parvovirus B19 infection should be monitored for the development of fetal anaemia using serial ultrasonography every 1–2 weeks, up to 12 weeks after infection. Doppler assessment of peak systolic velocity of the fetal middle cerebral artery should be performed as an accurate predictor of fetal anaemia. If hydrops fetalis is present or severe fetal anaemia is suspected, fetal blood sampling should be performed to determine the need for a fetal transfusion. If a transfusion is performed and the fetus survives, 94% will recover within 6–12 weeks. Thank you