It is estimated that HIV infection and AIDS occur in 15 to 30 percent of infants born to HIV-seropositive mothers (see Prober and Gerson). Infected infants present special difficulties in diagnosis, and the infection runs a more accelerated course in them than in adults. In the perinatal period, infected and noninfected infants can only rarely be distinguished clinically, and laboratory diagnosis is hampered by the presence of maternally derived antibody to HIV. The initial clinical signs usually appear within a few months after birth; practically all infected infants become ill before their first birthday, and very few are asymptomatic beyond 3 years of age. Early signs consist of lymphadenopathy, splenomegaly, hepatomegaly, failure to thrive, oral candidiasis, and parotitis. In the European Collaborative Study, comprising 600 children born to HIV-infected mothers, 83 percent of infected children showed laboratory or clinical features of HIV infection by 6 months of age. By 12 months, 26 percent had clinical symptoms of AIDS and 17 percent had died of HIV-related diseases. Once AIDS is established in children, it does not differ materially from the syndrome in adults as described in Chap. 32.
There is often a delay in the attainment of psychomotor milestones. Or after a period of normal development, a psychomotor decline begins, with corticospinal or peripheral nerve signs, often with pleocytosis in the CSF. The typical giant cell AIDS encephalitis, neuritis, and myelitis are easily distinguished from CMV encephalitis and toxoplasmosis.
Infected children are also subject to a variety of opportunistic infections, including bacterial meningitis, toxoplasmosis, CMV encephalitis, fungal infections (cryptococcosis, aspergillosis, candidiasis), herpes simplex, syphilis, zoster, and mycobacterial meningitis. There may also be vascular lesions, with infarction or hemorrhage and lymphoid neoplasia. These are discussed in Chaps. 31 and 32. Treatment of newborns exposed to HIV or who test positive for HIV is with antiretroviral drug therapy.
Infection with this flavivirus during the first trimester of pregnancy infection has been strongly linked to microcephaly and developmental delay, usually severe in degree. The frequency in various outbreaks and models has been from less than 1 percent to over 10 percent but the best estimates are in the lowest part of the range. Clinical infection, usually a mild febrile flu-like illness transmitted by mosquito, had been considered rare but serologic surveys have shown exposure rates of about 6 percent in some parts of the world.
It came as somewhat of a surprise that an outbreak occurred in Micronesia and French Polynesia and subsequently in parts of South America, particularly Brazil, and in parts of Africa several years ago and that offspring of infected mothers had severe microcephaly. There is viral transmission from infected mother to child and an estimated one-third of infants are affected by microcephaly. Viral genome is found in infant brains and the brain is extremely small with reduced gyration in the few autopsy studies available (Mlakar and colleagues). An association with Guillain-Barré syndrome has been established in adults.
This tiny protozoan Toxoplasma gondii, occurring freely or in pseudocyst form, is a frequent cause of meningoencephalitis in utero or in the perinatal period of life. The disease exists in all parts of the world but is more frequent in countries with hot, humid climates than it is in the United States. The mother is most often infected by exposure to cat feces, handling uncooked infected meat, or eating partially cooked meat, but she is nearly always asymptomatic or has only a mild fever and cervical lymphadenopathy.