Obstetric and perinatal infections – Clinical manifestation and diagnosis of infections by body system

Obstetric and perinatal infections - Clinical manifestation and diagnosis of infections by body system

3 OPHTHALMIA NEONATORUM The clinical presentation of conjunctivitis in the first 4 weeks of life is reported with widely varying frequencies in different parts of the world. Another name for conjunctivitis is pink eye. Common viral agents include herpes simplex viruses, HIV, CMV, and hepatitis B. At 35 days of age, the baby presented with symptoms of an upper respiratory tract infection and was discharged with no specific treatment. Other systemic features of this first branchial arch syndrome include preauricular skin tags, blind-ended preauricular fistulas, hypoplasia of the facial bones, and other vertebral anomalies. How would you treat this child? Viral conjunctivitis occurring in twenty percent of cases is caused by an array of viral forms and mostly accompanying symptoms of cold.

Therefore, simple Gram stain and routine bacterial culture are often the only investigations that are required in most cases.6 Although simple investigation suffices, treatment has to be adequate because systemic complication and severe visual loss can occur in infection particularly with Chlamydia trachomatis and Neisseria gonorrhoea.7 Apart from bacteria, herpes viruses can also cause neonatal conjunctivitis. The patient’s symptoms settled, and she was discharged from the hospital 3 days after admission. No case showed a positive result for HSV by the FA method using conjunctival swabs; however, the FA test was positive in all strains isolated by cell culture. If trauma, foreign body, or significant eye disease is a possibility, fluorescein and slit-lamp examinations, and a funduscopic examination should also be performed. blennorrhoea neonatorum; gonococcal ophthalmia; neonatal conjunctivitis. Dr Matejcek is a member and Dr Goldman is Director of the PRETx program. The picture is further complicated when there is malnutrition, which in itself impairs host defences by weakening immune responses, decreasing metabolic reserves and interfering with the integrity of epithelial surfaces.

Ottawa: Health Canada 1994; 168-75. Here, our interests focus on the few microorganisms that are capable of more subtle, non-lethal effects. They overcome the placental barrier by infecting it so that the infection then spreads to the fetus. They can then interfere with fetal development or cause lesions so that a live but damaged baby is born. After primary infection during pregnancy, certain microorganisms enter the blood, establish infection in the placenta, and then invade the fetus. The incidence of chlamydial infection seems to be directly related to the level of sexual activity and to geography. Sometimes the eyelids are stuck together, as if by glue.

The infant is generally small and fails to thrive. The one eye swab taken for virus culture (patient 1) was isolation negative even after 4 weeks of incubation. When the membrane is peeled, the epithelium tears to leave a raw, bleeding surface. July 1991 26-48. Contact lens wearers, particularly those who use it for extended periods of time might be more susceptible to suffering from bacterial conjunctivitis. N. In addition, an antigen detection method (immune dot blot test) was used for detection of C.

The isolates were identified by standard neutralisation test (NT). Performing visual field testing is quick and easy. Most of these infections, HSV, rubella, CMV and syphilis, can also, at times, kill the fetus. They generally follow primary infection of the mother during pregnancy, so their incidence depends upon the proportion of non-immune females of childbearing age. Congenitally infected babies may be symptomless, especially in cytomegalovirus infection. They are often small, fail to thrive or show detectable abnormalities later in childhood. In all cases, the baby remains infected, often for long periods, and may infect others.

Routine antenatal screening for rubella antibody, treponemal antibody (which includes syphilis, yaws, pinta or bejel, which cannot be identified individually by serology), hepatitis B surface antigen and HIV antibody is being carried out to differing degrees worldwide. These tests help identify women who are infected with hepatitis B or HIV, infected or have been exposed in the past to treponemal infections, the most important of which is syphilis in this setting, or are susceptible to rubella. Routine screening programmes lead to clinical management issues for both the mother and child. Lid edema, chemosis, and conjunctival injection and discharge are variable and often indistinguishable from the same signs seen with other causes of neonatal conjunctivitis. In addition, the child will then be followed up for at least 12    months using sensitive tests to determine whether HIV has been transmitted vertically. Diagnosis of chronic hepatitis B infection will result in determination of the maternal level of infectivity, and subsequently offering an accelerated course of hepatitis B vaccine alone or, if the mother is highly infectious, vaccine and HBV-specific immunoglobulin to the baby. Vertical transmission may be suggested by the presence of symptoms in mothers preceding or shortly after delivery and the occurrence of symptoms in the neonate evident within the first 3 days of life.

However, if the treatment is based upon clinical characteristics alone, a broad-spectrum antibiotic with good gram-positive coverage such as a third- or fourth-generation fluoroquinolone, 10% sodium sulfacetamide, or trimethoprim-polymyxin may be used for 7–10 days. Women found to have been exposed to treponemal infection in pregnancy are offered antibiotic treatment and the baby is followed up for the first year using serology to identify active infection, as congenital syphilis can result from earlier untreated infection of the mother. Puffiness, redness and soreness in the eyelids is apparent. The likelihood of fetal infection is increased when the mother develops a poor immune response, when the concentration of infectious agents in her blood is high (primary or secondary syphilis, e antigen positive hepatitis B carrier, HIV), or in a primary infection. In 11 of the 13 neonates (85%), infection was fatal, with death occurring 4 to 19 days after onset of symptoms. The highest incidence from June to August was similar to that observed for adenoviral conjunctivitis in Japan. Ideally, funduscopic examination is best performed after dilation.

Intrauterine exchange blood transfusion is used to manage hydrops fetalis. At this time, the heart, brain, eyes and ears are being formed and the infecting virus interferes with their development. If the fetus survives, it may show certain abnormalities (Fig. 23.1). Not all fetuses are affected; in one study, detectable congenital defects were seen in 15% of cases when maternal rubella occurred in the first month of pregnancy, 25% in the second month, 18% in the third month and 7% in the fourth month. The figure for the first month is relatively low because fetal death is a common sequel at this stage. Clinical manifestations of congenital rubella include low birth weight and eye (Fig.

23.2) and heart lesions. Effects on the brain and ears may not become detectable until later in childhood, in the form of mental retardation and deafness. Up to 80% of infected infants eventually suffer from deafness. About 25% of congenitally infected children develop insulin-dependent diabetes mellitus later in life (the virus replicates in the pancreas), but rubella is a very uncommon cause of this disease. There is 15% mortality in infants showing signs of infection at birth, often associated with hypogammaglobulinaemia. Maceration and crusting of the lateral canthal angle are seen in chronic angular blepharitis caused by Moraxella species. Maternal IgG antibodies are also present and together with interferons help control the spread of infection in the fetus.

Obstetric and perinatal infections - Clinical manifestation and diagnosis of infections by body system
Proparacaine anesthetic eye drops are also administered in conjunct to lessen pains. The infant sheds virus into the throat and urine for several months and can infect susceptible individuals. Mailing address: Virology, 3rd Floor, Clinical Sciences Building 1, Manchester Royal Infirmary, Oxford Road, Manchester M13 9WL, United Kingdom. Conjunctival hyperaemia was present in 23 eyes (88.5%). For children who are admitted, early consultation with an ophthalmologist is important. Pregnancy is a contraindication to vaccination, as it is a live vaccine, and the only safe time during reproductive life is the immediate postpartum period. This is an interesting example of a vaccine that is given to protect an as yet non-existent individual (the future fetus), the infection being only subclinical or mild in the mother.

Until effective vaccines became available in the late 1960s (Box 23.1), rubella was an important cause of congenital heart disease, deafness, blindness and mental retardation. The virus continues to circulate in the community and damage fetuses in countries with less extensive rubella vaccination programmes. Dr Norman McAllister Gregg (1892–1966) was ophthalmic surgeon to the Royal Alexandra Hospital for Children in Sydney, and during the Second World War, he noticed what he called an ‘epidemic’ of congenital cataract in infants. He went further and made the astute observation that all the mothers had suffered from rubella during early pregnancy. There were 78 infants with cataract, and 68 of the mothers had a history of rubella in early pregnancy. Many of the infants had heart defects, were small, and two-thirds of them had microphthalmia. He published his findings in 1941, providing the first clear demonstration that an environmental factor could cause congenital malformations.

It is a striking feature of the infection that, whereas the fetus suffers cruel malformations, the mother shows little or no signs of illness. We now know that several other viruses, notably CMV, can do this, as well as factors such as thalidomide and folate deficiency. Later studies on rubella revealed that congenitally infected infants also developed deafness and brain defects. 55-9 and 55-10 ). It was not until 1962 that the causative virus was isolated and grown in cell culture. A rubella epidemic in the USA in 1964–1965 left in its wake 20 000 infants with the congenital rubella syndrome. By the late 1960s, an effective live virus vaccine was available, and congenital rubella is now seen only when vaccination cover is poor.

The fetus is exquisitely vulnerable to rubella during the first trimester of pregnancy. Although 34.6% of cases were treated with topical steroids, no case developed herpetic keratitis, such as dendritic ulcer or keratouveitis. Topical antibiotic treatment is indicated, as distinction between viral and bacterial etiologies may not be possible in the ED. The fetus is good at repairing damage but it cannot at a later stage compensate for the failure in basic organ development. The antimitotic action of the virus also means that the total number of cells in the body is reduced, and this is why the rubella-infected infants are smaller. The rubella virus remains in infected organs such as the lens and brain for more than 1    year, but eventually there is an adequate cell-mediated immune response and the virus is eliminated. After primary maternal infection during pregnancy, about 40% of fetuses are infected, and 5% of these show signs at birth.

It is not known whether the fetus is especially vulnerable at certain stages of pregnancy. The fetus is also infected following CMV reactivation during pregnancy in women with previous CMV exposure, but fetal damage is then uncommon. As many as 1–2% of infants born in the USA are infected, and up to about 10% of these are symptomatic, with up to 1 million infectious doses of virus present per millilitre of urine. However, the incidence of congenital CMV infection is likely to be an underestimate worldwide. In large cohorts of pregnant women studied it has been shown that 2% develop a primary CMV infection, but over 95% were asymptomatic. Of those women with a primary infection in the first trimester, up to 30% of babies may develop central nervous system (CNS) sequelae including sensorineural hearing loss. Although the percentage is much reduced if the maternal infection is later in pregnancy, a degree of CNS damage still occurs.

However, the relationship between a first trimester infection and outcome is much clearer in rubella infections than with CMV. Pale, discrete, avascular spots, which resemble Koplik’s spots seen in the mouth, may appear on the conjunctiva. The frequency and outcome of congenital CMV infections in reactivation or reinfection in pregnancy is still not well understood. However, the incidence of symptomatic congenital CMV infections has been reported to be similar in pregnant women with primary infections and reactivations or reinfections. Clinical features of congenital CMV include mental retardation, choroidoretinitis and optic atrophy, hearing defects, hepatosplenomegaly, thrombocytopenic purpura and anaemia (Fig. 23.3). Deafness and mental retardation may not be detectable until later in childhood.

If a pseudomembrane is present, remove it with wet cotton-tipped forceps. Virus can also be isolated from throat swab or urine samples. Live attenuated vaccines have been investigated (AD169 and Towne strains), and in preliminary studies no-one who became pregnant after vaccination transmitted the virus to the infant. As a result of routine serologic screening for syphilis in antenatal clinics and treatment with penicillin (see Ch. 21), congenital syphilis is now rare, but is more common in resource-poor countries. Clinical features in the infant include rhinitis (snuffles), skin and mucosal lesions, hepatosplenomegaly, lymphadenopathy, and abnormalities of bones, teeth and cartilage (saddle-shaped nose). Pregnancy often masks the early signs of syphilis, but the mother will have serological evidence of treponemal infection, and treponemal IgM will be detected in the fetal blood.

Vertical transmission most commonly takes place after 4    months of gestation; therefore treatment of the mother before the fourth month of pregnancy should prevent fetal infection. Approximately 35% of healthy adults have serological evidence of previous Toxoplasma gondii infection. Clinical features of congenital toxoplasmosis in the infant include convulsions, microcephaly, chorioretinitis, hepatosplenomegaly and jaundice, with later hydrocephaly, mental retardation and defective vision (see Ch. 25). There are often no detectable abnormalities at birth, but signs (e.g. chorioretinitis; see Fig. Corneal involvement includes a superficial punctate keratitis, small marginal or central infiltrates, EKC-like subepithelial infiltrates, limbal swelling, and a superior limbal pannus.

The incidence of fetal infection and damage (leading to abortion, stillbirth or disease in the newborn) increases from 14% when maternal infection is in the first trimester to 59% when in the third trimester. Damage is more severe the earlier in pregnancy infection is contracted. Toxoplasma-specific IgM antibodies may be detected in cord blood. Treatment of a pregnant woman or an infected infant is with spiramycin or (with care to avoid toxicity) sulphadiazine plus pyrimethamine plus folinic acid. Clinically, congenital HIV infection manifests as poor weight gain, susceptibility to sepsis, developmental delays, lymphocytic pneumonitis, oral thrush, enlarged lymph nodes, hepatosplenomegaly, diarrhea and pneumonia, and some infants develop encephalopathy and AIDS by 1    year of age. The most frequent cause of ON is chemical conjunctivitis resulting from prophylactic silver nitrate drops, which occurs in 10% of neonates. IgG antibodies present in the neonatal blood sample may be maternal in origin and can persist for at least 1    year.

The mainstay of laboratory diagnosis therefore involves detection of HIV-1 proviral DNA or HIV-1 RNA by polymerase chain reaction (PCR), although these tests may not be positive until several months after birth, in conjunction with HIV antibody and antigen detection using the combination assay. L. monocytogenes in the pregnant woman causes a mild influenza-like illness or is asymptomatic, but there is a bacteraemia which leads to infection of the placenta and then the fetus. This may cause abortion, premature delivery, neonatal septicaemia or pneumonia with abscesses or granulomas. The infant can also be infected shortly after birth, for instance, from other babies or from hospital staff, and this may lead to a meningitic illness. Viral infections (e.g. rubella, CMV) are generally less damaging to the fetus when the maternal infection occurs late in pregnancy.

Primary infection with varicella-zoster virus (VZV) in the first 20    weeks of pregnancy can lead to limb deformities and other severe lesions in the newborn. HSV infection in this setting is underdiagnosed and can lead to neonatal morbidity and mortality.

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