The microorganisms most often responsible for congenital infections have been grouped as TORCH infections. These include toxoplasmosis, others, rubella, cytomegalovirus, and herpes. The "others" category includes various microorganisms that have been responsible for congenital infections. However, the list of microorganisms implicated in congenital infections has grown, so the acronym is no longer inclusive. It still means all infections acquired by the fetus in utero (Ford-Jones, 1999).
Acute toxoplasmosis in a pregnant woman often goes undetected and undiagnosed. Maternal transmission occurs from the consumption of poorly cooked meat or ingesting infected cat feces. The risk of transmission is highest in the third trimester. First-trimester transmission usually ends in spontaneous abortion. Clinical questioning after identifying an infected infant often leads to reflection and memories of a period of enlarged lymph nodes and fatigue but no fever. Women often report a mononucleosis-like syndrome that may have a febrile course, with malaise, headache, fatigue, sore throat, and sore muscles (Congenital toxoplasmosis, 2019).
In an infant, toxoplasmosis can present with hydrocephalus, chorioretinitis, and intracranial calcification. There is an incredible variety of clinical signs in the scope of the disease. Severe erythroblastosis, hydrops fetalis, and other clinical signs can occur from a normal picture at birth. Neurological signs similar to encephalitis may be the only significant presentation of this clinical problem, including seizures, bulging fontanels, nystagmus, and abnormal increase in circumference of the head. If the infant is treated, signs and symptoms may disappear, allowing normal cerebral growth and development (Congenital toxoplasmosis, 2019).
The delayed disease may occur in the first two months of life in term infants and is usually milder. Clinical signs may include generalized sepsis, enlarged liver, spleen, late-onset jaundice, enlarged lymph nodes, or late-onset central nervous system problems, including hydrocephalus and eye lesions. Infants with congenital toxoplasmosis may have new lesions appearing until age five years.
The typical presentation of the rubella virus is mild, with malaise, low-grade fever, headache, and conjunctivitis. In 1 to 5 days, a macular rash appears on the face and usually disappears after 3 to 4 days. Natural viremia is necessary for placental and fetal primary disease. Most cases occur following primary disease. Skin rashes that resemble rubella may occur due to adenovirus, enterovirus, or other respiratory virus infections. Laboratory titers are recommended to confirm the diagnosis of rubella infection since there is a strong possibility of subclinical infection. It takes about 4 to 6 weeks to obtain clinical confirmation of rubella isolation. The detection of rubella antibodies confirms the presence of the infection (Congenital rubella, 2020).
A fetus infected with rubella often has cardiac defects and deafness. The central nervous system seems particularly vulnerable to the rubella virus, especially if the virus is acquired prior to the first 16 weeks of gestation. The CDC describes congenital rubella syndrome as hearing loss, mental retardation, cardiac malformations, and eye defects. The rubella virus can slow cell replication. This slowed replication causes intrauterine growth retardation and cell differentiation failure during fetal organ formation. Tissue damage seems to occur from the inflammatory response to the infection. Myocarditis, pneumonitis, hepatosplenomegaly, and vascular stenosis can also be present. As seen with other severe congenital infections, signs and symptoms may continue to develop until 10 or 20 years of age. This disease's late clinical signs include insulin-dependent diabetes, thyroid abnormalities, hypoadrenalism, hearing loss, and eye damage (Congenital rubella, 2020).
Cytomegalovirus (CMV), a member of the herpes family, is a very common infection. More damage occurs to the fetus when the exposure to and acquisition of CMV occur from a primary lesion. Congenital CMV occurs in about 0.2 to 2.2 percent of all newborn infants. Primary lesions cause intrauterine growth retardation, microcephaly, periventricular calcifications, deafness, blindness, congenital cataracts, profound mental retardation, hepatosplenomegaly, and jaundice. A characteristic pattern of Petechiae, called "blueberry muffin" syndrome, is associated with congenital CMV. Severe complications at birth are seen in approximately 5 percent of congenital infections. Urine culture for CMV is the most rapid and sensitive indicator of infection. IgG and IgM antibody titers are also indicated. Elevated IgM levels alone denote exposure to CMV but are not diagnostic because there is no method to determine the timing of the exposure. Elevate IgG titers indicate perinatally acquired CMV infection. The transmission of CMV via infected blood products has been significantly decreased through CMV-negative donors or irradiation of blood products. Premature and low birth weight infants are especially vulnerable to the infusion of this virus in blood products. The best prevention method is the institution of standard precautions, including good hand washing (Congenital cytomegalovirus, 2019).
When newborns acquire syphilis from hematogenous spread across the placenta, the effects are on the major organ systems of the fetus, especially the central nervous system. Common presentations of the infected infant are hepatosplenomegaly, jaundice, low birth weight, intrauterine growth retardation, anemia, and osteochondritis. There is often a bilaterally superficial peeling of the skin on the neonatal palms and soles. Nonimmune hydrops is a very common presentation in congenital syphilis. The symptomatology of perinatal syphilis is similar to that of any other viral infection that spreads hematogenously from the mother to the placenta and onto the developing fetus. A lumbar puncture for CSF analysis and radiographs of the long bones facilitate the definitive diagnosis. Congenital neurosyphilis is always a consideration, and the CSF should be examined for the presence of spirochetes. X-ray changes such as blurring the epiphyseal borders demonstrate recent fetal infection, and periostitis represents prolonged involvement (Congenital syphilis, 2017).
Acquisition of the herpes simplex virus in utero can result in spontaneous abortion, preterm birth, or a normal baby. Manifestations of the disease are very broad. The clinical presentation of the congenital acquisition of the infection includes skin vesicles or scarring, hypopigmentation, chorioretinitis, microcephaly, and hydranencephaly. Greater than 20 percent of newborns with the disseminated disease do not develop skin vesicles, making identifying positive infants more difficult. Laboratory tests are the most common way to differentiate HSV from other bacterial and viral infections. The most rapid method includes a cytologic exam. Routine cultures should include any vesicles on the skin, oropharyngeal or eye secretions, or stool. Viral typing is only done for epidemiologic purposes. Intrapartal transmission is more likely to occur in the presence of ruptured membranes. Other risk factors include intrauterine fetal monitoring (scalp electrodes and intrauterine pressure catheters) and fetal scalp sampling. It is not recommended that women infected with HSV be monitored by these methods. Transmission from mother to infant from an infected breast lesion and oral lesions has been reported (UpToDate, 2018).
Varicella is a member of the herpes virus family that commonly causes chickenpox and varicella-zoster. Most women of childbearing age have been exposed to or have contracted this virus; those that have not should receive the varicella vaccine prior to pregnancy. Symptoms of varicella are usually present 10 to 20 days after exposure and include fever, malaise, and an itchy rash. The maculopapular rash eventually forms vesicles and crusts over. Potential complications include pneumonia, encephalitis, arthritis, and bacterial cellulitis. If the virus is contracted early in pregnancy, the damage is likely to be cutaneous musculoskeletal, neurological, and ocular. Infants have intrauterine growth retardation, microcephaly, cerebellar and cortical atrophy, cataracts, and chorioretinitis. Viral infection in the last three weeks of pregnancy will infect one in four newborns. The timing of the exposure determines the severity of the newborn disease. Infections are generally severe if contracted within four days before delivery and two days after delivery. Severe viral respiratory distress with significantly depleted maternal passive antibody transmission puts the infant at greater risk for other complications (Blumental and Lepage, 2018).
Gonorrhea appears most frequently in young adults, ages 15 to 24 years. Symptoms are mild, but in the pregnant woman can cause inflammation and weakening of the fetal membranes and early rupture. Gonococcal conjunctivitis in the newborn has historically been a risk from transmission via the birth canal. Prophylaxis has been mandated by law, with the use of silver nitrate 1 percent solution or erythromycin in both eyes at birth. Fetal scalp electrodes have been identified as a potential method of organism transmission to the fetus.
Hepatitis B Virus (HBV) infection early in pregnancy causes a 50 percent risk of neonatal HBV and a 90 percent risk of developing HBV by their first birthday. Untreated infants are likely to become carriers, eventually leading to primary hepatocellular carcinoma. Treatment for these infants should be HBV vaccine with hepatitis B immunoglobulin. Prematurity, low birth weight, and hyperbilirubinemia are clinical signs of HBV infection. Hepatosplenomegaly is also a common presenting symptom of an infant that is infected. An infected infant may be asymptomatic or present with a picture of fulminant sepsis (Tesini, 2018b).
Human Papilloma Virus (HPV) – genital warts can cause laryngeal papillomatosis in the newborn, demonstrated by a weak cry or hoarseness if the mother is not treated. The newborn may have stridor or other respiratory symptoms. The presence of these warts during vaginal delivery can be extremely uncomfortable. Intrapartal transmission is possible if the warts are visible. Prenatal treatment is associated with low complications and recurrence rates. The treatment alleviates the need for cesarean delivery. Examination, treatment, and follow-up of sexual partners are important aspects of treatment because 50 percent of partners are infected (LaCour and Trimble, 2012).
Chlamydia is a bacterium that grows between cells. It is one of the most common sexually transmitted diseases. Chlamydia conjunctivitis can present in the newborn with a very watery discharge that may progress to purulent exudates. Application of erythromycin ointment at birth for ocular prophylaxis will successfully treat both Chlamydia and gonococcal conjunctivitis. Pneumonia can occur in newborns that have contracted Chlamydia from their mother's genital tract. The typical presentation is tachypnea, barrel chest, and an increased oxygen requirement. The infant may have interstitial infiltrations, hepatosplenomegaly, and increased eosinophils. Diagnosis is based on physical examination and conjunctivitis (Chlamydial Infections, 2015).
Adenovirus and Rotavirus can be enteric and can cause significant viral gastroenteritis. Breastfeeding can protect against these organisms. Early signs of illness include lethargy, irritability, and poor feeding, followed by passage of watery yellow or green stools free of blood but containing mucus. Vomiting and a slight fever may accompany diarrhea. Rotavirus has been shown to cause necrotizing enterocolitis (Censoplano, 2018).
Candida albicans is a fungus that may result from prolonged broad-spectrum antibiotic use in small premature infants. Yeast infections can localize in any organ system. Administration of hyperalimentation, frequent use of indwelling venous lines, and invasive procedures may also predispose the infant to Candida. The infants may present with thrush or cutaneous (perianal area) or acute disseminated candidiasis (systemic infection). The infant presents with signs and symptoms of sepsis, often worsening with no presence of positive cultures. The infant may have respiratory distress, abdominal distention, guaiac-positive stools, carbohydrate intolerance, candiduria, temperature instability, and hypotension. Cutaneous infection may be treated with Nystatin, but systemic infection requires treatment with Amphotericin (Greenberg and Benjamin, 2014).
HIV/AIDS offers the infant three modes of transmission: a) transplacental, b) intrapartal, where there is exposure to maternal blood and vaginal secretions, and c) postnatal through maternal secretions like breast milk. HIV causes immunosuppression in the neonate. An HIV mom is more susceptible to other opportunistic organisms, such as CMV and HSV, which put the infant at risk. Neonates born to HIV-positive mothers are usually asymptomatic. Infant symptoms usually do not appear until 4-6 months of age. These later symptoms include failure to thrive, persistent thrush, hepatosplenomegaly, recurrent diarrhea, recurrent bacterial infections, and hepatitis. These infants should be treated immediately after birth with AZT if the mother's HIV status is known. If the mother was treated during pregnancy with AZT, the baby has a better chance of not getting the virus. Immunizations for HIV-exposed infants should NOT be a live virus (Initial Postnatal Management, 2019).