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X. Killian, M.B. B.CH. B.A.O., Ph.D.

Clinical Director, Sidney Kimmel Medical College at Thomas Jefferson University

The assembly of new virions consists of the formation of the critical viral enzymes, including reverse transcriptase, integrase, ribonuclease, and a protease, and the aggregation into a ribonucleoprotein core [150,151]. The core subsequently moves to the cell surface and buds as mature virions through the plasma membrane. In addition, the vif and vpr sequences of transmitting mothers were more heterogeneous and more functional than sequences of nontransmitting mothers [153,160]. These data indicate that high viral load is a critical determinant of pediatric disease progression and provides a strong argument for early and aggressive intervention with antiretroviral therapy. In the European Collaborative Study, hypergammaglobulinemia (IgG, IgM, and IgA) identified 77% of infected infants at age 6 months with 97% specificity [188]. There was no clear correlation of the incidence of bacterial infections with specific subclass deficiencies. Although the exact mechanism of vertical transmission is unknown, intrapartum transmission probably results from infant mucosal exposure to maternal blood or cervicovaginal tract secretions during delivery [58]. In the absence of antiretroviral therapy, the levels decrease only gradually over the first 24 to 36 months of life [172]. A positive enzyme immunoassay must be confirmed by a secondary test, typically a Western blot. Chorionic villus sampling and percutaneous umbilical blood sampling are associated with a higher risk for the fetus. Noninvasive techniques such as fetal ultrasonography or the clinical assessment of the mother give unspecific and not very predictive information. A cord blood specimen should not be used because of possible contamination with maternal blood. Of uninfected infants, 75% lose these passively transferred antibodies between 6 and 12 months of age, but persistence of maternal antibodies has been documented in 2% up to 18 months of age [239]. Adapted from 1994 Revised classification system for human immunodeficiency virus infection in children less than 13 years of age. Zidovudine is discontinued at 6 wk of age; however, other antiretroviral therapy should be started in a child who is proved to be infected according to pediatric treatment guidelines with close laboratory monitoring. When classified in a more severe category, a child is not reclassified in a less severe category even if the clinical or immunologic status improves. A value should be confirmed before the child is reclassified into a less severe category. Children are more likely than adults to have serious bacterial infections, and lymphocytic interstitial pneumonitis is almost entirely restricted to the pediatric age group. Common clinical features seen during the first year of life include lymphadenopathy and hepatosplenomegaly. The difficulty in treating these infectious episodes, their chronicity, and their tendency to recur distinguish them from the normal infections of early infancy. It is helpful to document each episode and to evaluate the course and frequency of their recurrences. This increased incidence of pneumococcal infections has been confirmed by other studies [263,264]. Congenital syphilis may be missed if serologic tests are not performed on the mother and child at the time of delivery and repeated later if indicated. Premature birth has been reported in 19%, with no difference between children born to drug-using mothers and children of mothers who were infected through other routes [188,258]. Children of drug-addicted mothers had significantly lower birth weights and smaller head circumferences, however. An important issue for the neonatologist is whether the mother is infected with M. In children older than 6 years, the adult threshold of 50 cells/mm3 can be used [278]. The distinction between a self-limited, benign hyperproliferation and the development of a monoclonal lymphoid malignancy is crucial for determining treatment and prognosis.

Given the frequency of international travel, all countries will remain at risk of imported disease during the foreseeable future. Maintaining high levels of immunization, ongoing surveillance (recognizing that the sporadic nature of new cases likely will add to delay in diagnosis), and prompt outbreak control measures remain critical for achieving and maintaining elimination of rubella. Neva, Propagation in tissue culture of cytopathic agents from patients with rubella-like illness, Proc. Vynnycky, Modelling the incidence of congenital rubella syndrome in developing countries, Int. Wolinsky, Immunochemical identification of rubella virus hemagglutinin, Virology 126 (1983) 194. Wolinsky, Detailed immunologic analysis of the structural polypeptides of rubella virus using monoclonal antibodies, Virology 143 (1985) 153. Dorsett, Rubella virus antigens: localization of epitopes involved in hemagglutination and neutralization by using monoclonal antibodies, J. Marr, Sequence of the region coding for virion proteins C and E2 and the carboxy terminus of the nonstructural proteins of rubella virus: comparison with alphaviruses, Gene 62 (1988) 85. Sugiura, Antibody response to the individual rubella virus proteins in congenital and other rubella virus infections, J. Myers, Latex-agglutination test for rubella antibody: validity of positive results assessed by response to immunization and comparison with other tests, J. Diemier, Evaluation of a rapid passive hemagglutination assay for anti-rubella antibody: comparison to hemagglutination inhibition and a vaccine challenge study, J. Edson, Latex agglutination test for rubella antibodies: report based on data from the College of American Pathologists surveys, 1983 to 1985, J. Dover, A comparison of two passive agglutination procedures with enzyme-linked immunosorbent assay for rubella antibody status, Am. Grahame, Subclass distribution of IgG and IgA responses to rubella virus in man, J. Morgan-Capner, Specific IgG subclass antibody in rubella virus infections, Epidemiol. Oker-Blom, Maturation of IgG avidity to individual rubella virus structural proteins, J. Mansa, Rubella IgM antibodies in sera from infants born after maternal rubella later than the twelfth week of pregnancy, Scand. Pollock, Consequences of confirmed maternal rubella at successive stages of pregnancy, Lancet 2 (1982) 781. Peckham, Congenital rubella in the United Kingdom before 1970: the prevaccine era, Rev. Geme, Rubella virus reinfection during pregnancy leading to late-onset congenital rubella syndrome, J. Fogel, Clinical rubella with virus transmission to the fetus in a pregnant woman considered to be immune. Wolinsky, Characterization of immune complexes in progressive rubella panencephalitis, Ann. Nance, Congenital rubella syndrome and diabetes: a review of epidemiologic, genetic, and immunologic factors, Am. Banatvala, Studies on rubella virus strain variation by kinetic hemagglutination-inhibition tests, J. Kono, Antigenic structures of American and Japanese rubella virus strains and experimental vertical transmission of rubella virus in rabbits, Symp. Lennette, Rubella virus hemagglutination with a wide variety of erythrocyte species, Appl. Haukenes, Simplified rubella haemagglutination inhibition test not requiring removal of nonspecific inhibitors, Lancet 2 (1979) 196. Gee, Demonstration of rubella complement-fixing antigens of two distinct particle sizes by gel filtration on Sephadex G-200, Proc. Salmi, Gel precipitation reactions between alkaline extracted rubella antigens and human sera, Acta Pathol. Horstmann, Large-scale production of rubella precipitinogens and their use in the diagnostic laboratory, J. Vesikari, Small size rubella virus antigens and soluble immune complexes, analysis by the platelet aggregation technique, Arch.

It can be passaged for a limited number of replicative cycles with a generation time of 30 to 33 hours using rabbit epithelial cell monolayers under microaerobic conditions at 33 C to 35 C [10]. Such purified organisms retain their antigenicity, but not their motility or their virulence. This lack of a good animal model and the inability to culture and manipulate these organisms in vitro have prevented a detailed mechanistic understanding of virulence mechanisms or host-pathogen interactions in congenital syphilis [48,49]. The organism does not survive outside of its human host and is easily killed by heat, drying, soap, and water. Syphilis is not known to be spread through casual contact or through contact with fomites [50]. Horizontal transmission results primarily from sexual activity, although anecdotal reports cite kissing as a potential route as well [51]. Because sexual contact is the most common mode of transmission for acquired disease, the sites of inoculation usually are the genital organs, but lips, tongue, and abraded areas of the skin have been described as well. Such an entry point is identified as the site of the initial ulcerating sore, or chancre [51]. Health care providers or laboratory workers have apparently become infected with T. This transmission pattern may relate to maternal spirochetemia in early syphilis [70]. Among women with untreated primary or secondary early syphilis, the rate of transmission is 60% to 100% and slowly decreases with later stages of maternal infection to approximately 40% with early latent infection and 8% with late latent infection. In contrast, in women with early latent syphilis, 20% to 60% of their infants were healthy at birth, 20% were premature, and only 16% were stillborn; 4% died as neonates, and 40% of infants appearing healthy at birth developed the stigmata of congenital syphilis later in life. In the case of untreated late syphilis, about 70% of newborns appeared healthy, 10% were stillborn, and approximately 9% were premature; about 1% died as neonates, and about 10% of infants appearing healthy at birth developed signs of congenital syphilis later in life [68,69,71]. Potential interactions include acceleration of the natural history of either disease, alterations in the clinical or laboratory manifestations, increased risk for syphilitic complications, and diminished response to syphilis therapy [10,51,75,76]. Centuries ago, when it was more common for infants to be fed by a wet nurse, small epidemics of syphilis were caused by an infectious lesion on the nipple of a wet nurse, but no data indicate that breast milk itself is associated with mother-to-child transmission [66,67]. After major public health successes in the early 1990s, the incidence of acquired syphilis showed an alarming resurgence throughout the world. A dramatic decline in the number of cases did occur after the introduction of penicillin, with the incidence reaching a low point in the United States in the mid-1950s. When a disease approaches eradication, however, often the control program rather than the disease is eradicated. More resources were again committed to control efforts, and the incidence of syphilis promptly declined in the 1970s, only to increase dramatically again in the 1980s [85,86]. These trends did not continue, and the upward swing is becoming evident once more. It is an uncommon complication among sexually abused children, found in 1% or less in a case series from the United States. The frequency of syphilis transmission to sexually abused children may be higher, however, in regions with higher adult prevalence of the disease. The clinical manifestations may provide insight into the timing of acquisition of infection. This information may not always help to resolve the potential dilemma of whether the clinical findings are those of previously unrecognized congenital syphilis versus postnatally acquired syphilis. Also, some experts have postulated that antibiotics commonly prescribed for common childhood illnesses may partially treat congenital syphilis and alter the nature of late clinical manifestations.

It has been estimated that colonization and infection of the neonate occur in only one third of instances in which the mother is infected [25]. This association was dramatically shown in one study in which premature rupture of membranes occurred in 6 (43%) of 14 women with untreated gonococcal infection during pregnancy compared with 4 (3%) of 144 women whose infection had been treated [29]. Screening and treatment programs for gonococcal infections during pregnancy are appropriate to reduce the risk of adverse pregnancy outcomes related to maternal infection. Finally, strains also are typed by coagulation testing after exposure to monoclonal antibodies made against the outer membrane protein I. Two major serogroups exist: 1A, which has 26 subgroups, and 1B, which has 32 subgroups [35]. The combination of auxotyping and serologic typing is now used in most epidemiologic studies to determine the linkages among infected persons [36]. When grown in anaerobic conditions, virulent strains express a lipoprotein called Pan 1. Its function is unknown, but it elicits an IgM antibody response in acute infection. Pinpoint colonies, classified as type 1 and type 2, usually are seen only on primary isolation. These colony types are distinguished from the large granular colonies classified as type 3 and type 4 by the presence of pili, which are thin bacterial appendages on the cell surface that are involved in attachment to mammalian cells. With repeated subculturing at 37 C, the genes are no longer expressed, and the pili disappear, resulting in colonialtype changes, with type 1 colonies shifting to type 4 and type 2 colonies shifting to type 3. Individual strains can also phase shift from forming opaque to forming clear colonies [33]. Different strains have differing stable auxotrophic requirements for amino acids, purines, pyrimidines, or vitamins. Additionally, enzyme-linked immunosorbent typing, based on differences in protein I, can be done. Several bacteria usually are found within each infected cell, but whether this represents invasion of the cell by multiple organisms or growth and multiplication of organisms within the infected cell is unknown. Gonococci possess a cytotoxic lipopolysaccharide and produce proteases, phospholipases, and elastases that ultimately destroy the infected cells. Some strains of gonococci seem to be relatively less susceptible to phagocytosis and are thought to be more capable of causing disseminated infection. Gonococci are found in the subepithelial connective tissue very quickly after infection. This dissemination may be due to the disruption of the integrity of the epidermal surface with cell death, or the gonococci may migrate into this area by moving between cells. Epithelial cell death triggers a vigorous inflammatory response, initially with neutrophils and then macrophages and lymphocytes in untreated patients. Human serum contains IgM antibody directed against lipopolysaccharide antigens on the gonococcus, which inhibits invasion. An IgG antibody against a surface protein antigen also is normally present on some gonococci that are classified as serum-resistant gonococci; this antibody blocks the bactericidal action of the antilipopolysaccharide IgM antibody [41,42]. These serum-resistant strains are the most common ones involved in systemic infections in adults and probably in neonates as well [43]. Because such infection does not occur frequently, additional protective factors must function to prevent it. This inactivation facilitates mucosal colonization and probably plays a role in the poor mucosal protection seen against subsequent gonococcal reinfection. Although symptomatic gonococcal infection stimulates a brisk inflammatory response, it does not produce a significant immunologic response [46]. There is very little immunologic memory; as a result, recurrent infections occur easily on reexposure.