Congenital infections of the CNS

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• Tropical and parasitic infections of the CNS
• Congenital infections of the CNS
• Retroviral infections and AIDS
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• Brett's Paediatric Neurology 3rd edition

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Introduction

The placenta and fetal membranes are remarkably efficient barriers to infection, and most infections occurring during pregnancy are of little consequence to the fetus. However, a number of specific microorganisms may cross the placenta and infect the fetus during pregnancy, and others may gain access to the fetus by ascending infection from the cervix and amniotic fluid (Table 22.20)

Table 22.20

. Although fortunately rare, fetal infections commonly damage the CNS, and are important causes of long-term disability and neurological abnormality. Some infections, such as rubella virus, are teratogenic and predominantly damage developing organs. Most others, including CMV and toxoplasmosis, destroy tissues which have already been formed and may cause progressive organ damage for months or years after birth (Hanshaw et al 1985a[1]). The clinical manifestations of most congenital infections are overlapping (Table 22.21)

Table 22.21

. Although characteristic patterns of abnormalities may suggest a particular infectious agent, the diagnosis must usually be confirmed by sero-logical studies or culture. Congenital infections are often characterized by a state of persistent infection, resulting in prolonged excretion of the virus, as occurs in congenital CMV or rubella. The persistent infection occurs despite specific antibody production by the fetus, and indicates an incomplete fetal immune response. Specific antibody synthesis by the fetus is, however, the basis for serodiagnosis of congenital infections.

Rubella

Fetal infection results from primary infection in pregnancy, and although reinfection may occur as a subclinical phenomenon there is no convincing evidence that the fetus is at risk in these circumstances. The types and risks of damage caused by rubella are related to fetal age at the time of infection. It is estimated that the risk is of the order of 40-60% for infection up to 8 weeks, 30-35% for the third month and approximately 10% for the fourth month of gestation (Dudgeon 1967[2]). A small risk extends up to 20-24 weeks. The earlier the infection, the more likely there is to be multiple organ involvement. Infection after the tenth week is more likely to result in involvement of only a single organ, which is usually the organ of Corti, leading to perceptive deafness. Fetal infection may occur at any stage of gestation without evidence of damage at birth.

Virus can be detected in urine and throat washings for up to 12 months after birth and transmission of infection to susceptible contacts is well documented. IgM rubella antibody is present in cord blood and can be detected for several months after birth. Persistence of antibody beyond 6 months of age is another method of serodiagnosis.

The "rubella syndrome', the combination of congenital heart defects, cataracts, deafness and mental retardation, is only part of the spectrum of disorders caused by the virus. Additional multisystem involvement can occur with hepatitis, splenomegaly, thrombocytopenic purpura and glaucoma.

The effects of congenital rubella on the CNS are complex, and most children show a combination of abnormalities reflecting damage to the brain, as well as visual and auditory defects. Microcephaly is common and up to 30% of children have intellectual impairment (Cooper 1985[3]).

Meningoencephalitis is often present at birth and in early infancy. There may be irritability and increased tension of the anterior fontanelle, which is usually enlarged. Convulsions are rare. The CSF frequently shows some increase in protein and a mild pleocytosis and it is often possible to isolate the virus from CSF (Desmond et al 1976[4]). These CSF abnormalities may be present in infants who appear neurologically normal, and Desmond and his colleagues (1978) believe that some degree of damage can be detected in such children when assessed towards the end of the first decade of life.

In later infancy the defects are remarkably diverse and include disorders of intelligence, behaviour, tactile perception, gait and posture. Hearing loss may become more severe or develop with the passage of time. On the other hand, the incidence of abnormal tone and reflexes decreases. Infants who have been considered to have cerebral palsy in infancy may no longer exhibit signs of such a disorder (Desmond et al 1978[5]).

Visual defects result mainly from cataracts which are usually present at birth but may occasionally appear at several weeks of age. These are unilateral in about 50% of affected children. The eye containing the cataract is often small, but mild degrees of microphthalmia are difficult to assess if bilateral cataracts are present. Microcornea may also be present. The virus is very often isolated from cata-ractous material even at several years of age. A few children also have raised intraocular pressure (buphthalmos) which may be associated with cloudiness of the cornea (Wolf 1973[6]). Strabismus is common in children with these various eye disorders.

A useful clinical marker of congenital rubella is the retinal disorder; a diffuse disturbance of pigment is very common and consists of patchy dark pigmentation interspersed with patchy depigmentation. It may be extensive but does not affect vision (Kresky & Nauheim 1967[7]). Very rarely severe visual disturbance may result from a so-called disciform degeneration of the macula which occurs in childhood in patients with rubella retinopathy (Deutman & Grizzard 1978[8]).

X-rays of the skull often show poor mineralization of the vault in early infancy. Intracranial calcification is extremely rare in congenital rubella and it is probably the result of small haemorrhages caused by severe neonatal thrombocytopenia.

Deafness is one of the most frequent consequences and the most common defect, sensorineural deafness being caused by damage to the organ of Corti. It may be unilateral and may not be detected for some years. The frequency of unilateral deafness is not known. It is important to realize that sensorineural deafness may develop several months or even years after birth (Peckham 1972[9]). A less common defect of hearing is central auditory imperception (Ames et al 1970[10]).

Hearing defects, unless recognized and treated, lead to impaired speech, but disturbance of speech with normal hearing has also been observed in children with congenital rubella. In the second decade of life, a few children known to have congenital rubella have developed a fatal progressive pan encephalitis. Very high titres of rubella antibody are present in serum and CSF and rubella virus has been isolated from the brain by co-cultivation technique (Weil et al 1975[11], Townsend et al 1975[12]).

The assessment of the child with congenital rubella can be extremely difficult as much of the handicap may be due to defects of hearing and vision, but direct damage to the brain can be an important contributory factor. The hyperactivity and easy distractibility of these children may be striking and a serious handicap to learning. Autistic features are not infrequently present (Chess 1971[13]). The defects in other systems necessitate a multidisciplinary approach to the care of these children.

Although some of the attenuated strains of the virus used in the rubella vaccines have been isolated from the products of conception and fetal tissues in a number of instances (Modlin et al 1975), there is as yet no evidence that this virus causes fetal damage. The diagnosis of congenital rubella is confirmed by isolation of rubella virus from the affected infant in the first few months of life, detection of rubella-specific IgM in cord blood or serum samples obtained in infancy, or detection of persistent rubella antibody response beyond the time of disappearance of maternally acquired antibody (Enders 1985[14]).

Cytomegalovirus (CMV)

CMV is a member of the herpes group, and is an ubiquitous virus which causes asymptomatic infection in normal infants, children or adults. However, patients with immature or impaired host defences such as the fetus and newborn, or immunosuppressed patients, may develop severe disease which often affects the central nervous system. Unlike rubella and toxoplasmosis, which can only be transmitted to the fetus if a primary maternal infection occurs during pregnancy, fetal or perinatal CMV infection may occur after either primary infection or after secondary reactivation of the virus during pregnancy (Stagno et al 1982[15]).

Congenital infection occurs as a result of transplacental transmission during maternal viraemia. Perinatal infection may also occur during passage down the birth canal, via breast milk or by blood transfusion. From 90-95% of neonates with congenital CMV infection are asymptomatic in the neonatal period, but a proportion of these may later develop abnormalities. Babies born to mothers with primary CMV infection during pregnancy are much more likely to be symptomatic as neonates than are newborn of mothers with recurrent infection. The severity of the illness is greatest when fetal infection occurred early in gestation.

Three major patterns of congenital CMV infection are recognized (Hanshaw et al 1985b[16]):

1. Approximately 1 % of infected neonates have severe multisystem disease present at birth, with intrauterine growth retardation, jaundice, hepatosplenomgaly, thrombocytopenia, microcephaly, intracranial calcification, pneumonitis and encephalitis. These infants have a high mortality and the survivors are usually microcephalic and have severe mental retardation.

2. Five per cent of infected neonates have milder symptoms with hepatosplenomegaly and thrombocytopenia as well as jaundice. Nearly half of these infants who have no neurological abnormalities at birth will later be found to have central nervous system abnormalities including mental retardation, deafness, microcephaly, spasticity or seizures.

3. Ninety-four per cent of CMV infected neonates are asymptomatic at birth. However, 15-30% of these infants will have hearing defects or impaired intellectual performance when reassessed at school age (Hanshaw et al 1976[17], Pass et al 1980[18]).

Infants with congenital CMV may show CSF abnormalities with mild elevation of protein or increase in cells. These changes may be present in the absence of any signs of congenital infection (Hanshaw et al 1976[17]). Eye defects are infrequent in congenital CMV: severe microcephaly may be associated with optic atrophy, and chorioretinitis of a type similar to that seen in congenital toxoplasmosis is described; a squint may draw attention to the retinal lesions. Intracranal calcification is not infrequent and is characteristically periventricular in distribution; it may be progressive.

In infancy the CT scan may show areas of low attenuation in the periventricular areas and can be very useful to detect calcification which is not visible on plain X-rays (Anders et al 1980[19]). Virus persistence is a feature of the infection and viruria may be detected for several years after birth. Similar virological findings occur in infants who acquire infection at the time of delivery or soon after but these infections are not believed to cause damage in later life (Alford et al 1980[20]). In those infants with perinatal infection virus shedding does not commence until after 7-10 days of age.

Treatment of congenital CMV infection with antiviral agents such as DHPG (gancyclovir) has not yet been shown to be beneficial. Cessation of virus excretion has been observed during treatment but recurrence has taken place on discontinuation of the drug.

Herpesvirus hominis (HVH) (Herpes simplex)

Primary HVH infection in early pregnancy is rare and the few reported cases have involved the birth of a micro-cephalic infant with intracranial calcification and skin lesions or scars. Atrophy of the cerebral hemispheres and retinal dysplasia have also been present (Hutto et al 1987).

The major clinical impact of this virus is the result of genital tract infection at or near the time of delivery. Clinical disease need not be present in the mother. In most instances type 2 or "genital' strain of the virus is involved. The illness in the infant may take the form of a generalized 'septicaemic' illness, usually with vesicles on the skin, and sometimes involving the conjunctivae and cornea. An ence-phalilic illness may be present. In both forms there is a very high mortality rate, particularly in premature infants, and a very high incidence of sequelae is observed in survivors (Whitley et al 1980[21]). Treatment with acyclovir is effective in preventing dissemination of herpes infection when it is confined to the skin (Whitley et al 1983[22]). Infants with disseminated disease and CNS involvement have responded less well to treatment, and a significant proportion are left with neurological defects. The outcome of infants affected by herpesvirus 1 has been reported to be better than those affected by herpesvirus 2 (Corey et al 1988[23]).

The risk of neonatal infection can be reduced if Cae-sarean section is performed in mothers who have a primary genital herpes lesion at the time of delivery. Screening programmes to detect herpes infection during pregnancy have, however, been found to be of little value (Prober et al 1988[24]).

Varicella zoster (VZ) virus

Primary infection with VZ virus causes chickenpox or reactivation of latent infection manifests as shingles. Shingles in pregnancy is not recognized as being hazardous to the fetus, but when a pregnant woman develops chickenpox the effect on the fetus depends on the time of maternal infection. Early gestational chickenpox usually has no observable effect, but fetal loss may be increased or the congenital varicella syndrome occurs (Paryani & Arvin 1986[25], Alkalay et al 1987[26]) (Table 22.22)

Table 22.22

. The two most characteristic features of this syndrome are the cicatricial skin lesions and hypoplasia of bone; the latter may cause shortening of part of a limb. Neurological involvement with mental retardation, limb paresis and microcephaly also occur. Infection in mid-or late pregnancy may result in intra-uterine chickenpox with the birth of a healthy infant who may then develop shingles within a few months of birth (Brunell & Kotchmar 1981[27]). Infection near to term may result in congenital chickenpox (within 10 days of birth) or neonatal chickenpox. Congenital chickenpox can range from a mild illness to severe multisystem disease with involvement of the brain and death. The mortality is confined to infants born to mothers who develop chickenpox within the period of 4 days prior to and 2 days after delivery (De Nicola & Hanshaw 1979[28]). These infants develop the disease 5-10 days after birth (Table 22.23)

Table 22.23

. This group should be given immunoprophylaxis in the form of zoster immune globulin (ZIG) at birth, but disseminated varicella may still occur despite the administration of ZIG. Treatment with intravenous acyclovir should be commenced at the first sign of congenital chickenpox (King et al 1986[29]). Neonatal chickenpox occurs if the infant is infected after delivery and usually follows a benign course.

Poliovirus

Poliovirus infection in adults is now extremely rare because of the development of highly effective vaccines. Nevertheless, maternal infection and the birth of an infant with congenital poliomyelitis is well documented.

Treponema pallidum

Antenatal screening and treatment in pregnancy have made a major contribution to the reduction in the incidence of congenital syphilis.

Fetal infection is extremely rare before the fourth month of gestation. Intrauterine death is common. The infection in the neonate lacks pathognomonic symptoms and signs. Lymphadenopathy, hepatosplenomegaly, anaemia, fever, vomiting and failure to thrive may be prominent. The skin and mucous membrane manifestations, if present, frequently provide the clue to the infection; mucopurulent or haemorrhagic nasal discharge and vesicular and papulo-squamous rashes, especially affecting the palms and soles, occur. Osteochondritis and periostitis are important features of congenital syphilis (Mascola et al 1985[30]).

The CSF is often abnormal, with raised levels of protein and a pleocytosis, and these changes may be present in the absence of any clinical manifestations of the infection in the infant.

In later infancy and childhood the well-known classical manifestations of congenital syphilis evolve. The early features of the disease are primarily meningitic, while in later infancy vomiting, seizures and progressive hydrocephalus may occur. Juvenile paresis does not appear until later in childhood or early adolescence. Tabes dorsalis is rarer, but involvement of the cerebral cortex and the spinal cord become evident. There may be optic atrophy, multiple cranial nerve lesions and deafness. The non-CNS manifestations consist of interstitial kera-titis, abnormalities of the secondary dentition, deafness and skull bone and cartilage disease.

Treatment in pregnancy with benzathine penicillin is effective, but in congenital infection intramuscular or intravenous penicillin G (50 000 units/kg/d) should be given for 14 days (McCracken & Kaplan 1974[31]).

Toxoplasmosis

The protozoon Toxoplasmagondiimay cause an easily recognizable syndrome of congenital infection consisting of chorioretinitis, hydrocephalus and irregular calcification scattered throughout the cerebral hemispheres. As with many of the intrauterine infections, this is but one part of a spectrum of severity ranging from subclinical infection to severe disease (McCabe & Remington 1988[32]). Hepatosplenomegaly, jaundice, anaemia and lymphadenopathy may also occur. Increase in cells and protein in the CSF may be seen in all the clinical forms as well as in subclinical infection.

The major features of the disease in the survivors are chorioretinitis (Fig. 22.14)

Fig 22.14

, cerebral palsy, mental retardation and seizures. Significant defects can occur later in infants who do not show disease in the newborn period or early infancy (Wilson et al 1980). Calcification is often visible on CT scan (Fig. 22.15)

Fig 22.15

. There is a wide variation in the incidence of congenital infection (Table 22.24)

Table 22.24

. Unlike rubella, the risk of infection and fetal damage extends throughout pregnancy. Early gestational infection is less likely to result in fetal infection, but the infected infants are more likely to show signs of the disease. Infections later in pregnancy result in a higher rate of congenital infection but there are more mildly affected infants and infants with subclinical infection (Fig. 22.16)

Fig 22.16

.

There is no evidence to show that there is a risk to a fetus during a subsequent pregnancy (Carter & Frank 1986)[33, 34].

The diagnosis of congenital toxoplasmosis may be established by serological means using the IgM toxoplasma fluorescent antibody test or the persistence of IgG antibody beyond 12-18 months. Culture of the parasite may be achieved from cord blood or placenta. PCR is another useful means of identifying the infection. Careful examination of the CSF may show the presence of the organism. Treatment of maternal infection with spiramycin from the time of diagnosis, and with pyramethamine, sulphadiazine and folinic acid after 26 weeks of gestation may lessen the severity of fetal disease (Daffos et al 1988). All infected infants should be treated aggressively as the disease may progress and cause worsening CNS damage or blindness during the first years of life. Pyrimethamine and sulphadiazine, together with folinic acid to reduce the bone marrow toxicity of the former drug, are the most effective treatment and should be administered for 6-12 months. Some authorities recommend alternating 6-week courses of pyrimethamine and sulphadiazine with spiramycin to reduce the risk of toxicity.

Susceptible women can reduce the risk of infection by avoiding uncooked or partially cooked meat and by reducing exposure to the faeces of infected cats during pregnancy.

Other congenital infections

A variety of other organisms have been suggested as causes of damage to the fetal CNS. However, the evidence that influenza A virus, mumps or the enteroviruses Coxsackie or echo cause fetal damage is inconclusive (Table 22.20)

Table 22.20

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