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J. Sugut, M.A., M.D., Ph.D.

Clinical Director, University of North Carolina School of Medicine

The expected incidence of condylomata acuminata in women in the population studied by Cook and colleagues [12] was 1. Quick and coworkers [13] described a strong association between laryngeal papilloma in young children and maternal condylomata. Of the 31 patients with laryngeal papilloma they studied, 21 (68%) had been born to mothers who had had condylomata. Infection of the infant probably occurs by exposure to the virus at delivery, although papillomatosis has been described in infants delivered by cesarean section. Tang and associates [29] described an infant who was born with condylomata acuminata around the anal orifice. It is unknown whether this case reflects transplacental hematogenous spread or direct extension across intact membranes. Treatment of anogenital warts is not optimal, but podophyllum resin or podofilox is often used in older children and adults. Neither podophyllum resin nor podofilox has been tested for safety or efficacy in children, and both agents are contraindicated for use in pregnancy. Interferon has been used with some success for treatment of laryngeal papillomas [31]. Of these, only one woman had symptoms compatible with mononucleosis during pregnancy; she gave birth to a normal infant. One was stillborn, one had multiple congenital anomalies, and one was small for gestational age. The abnormal infants in this study did not have a characteristic syndrome, but instead had a variety of abnormalities. Brown and Stenchever [48] described an infant with multiple congenital anomalies who was born to a mother who had a positive monospot test result 4 weeks before conception and at 16 and 36 weeks of gestation. In addition to the anomalies, which involved many organs, the infant was small for gestational age. Goldberg and associates [49] described an infant born with hypotonia, micrognathia, bilateral cataracts, metaphyseal lucencies, and thrombocytopenia. In the second infant, permanent lymphoblastoid cell lines were established from the peripheral blood at birth and from postmortem heart blood at 3 days of age. The seroepidemiologic evidence and restriction enzyme analysis of paired virus isolates from mothers and their infants suggest that the usual route of transmission is perinatal or postnatal [69]. The average age at infection is about 2 years, and 75% of children are seropositive by 5 years of age. The primary mechanism of transmission is from contact with saliva of infected individuals. These investigators presented some evidence that women who had a history of having had influenza in the first trimester were more likely to give birth to infants who had congenital anomalies than women who had influenza later in the pregnancy. In a similar study conducted in Scotland, Doll and Hill [94] were unable to confirm that congenital anomalies occurred with a higher frequency in infants of women who had histories of influenza during pregnancy than in infants of women who did not. After reviewing the reported incidence of stillbirth related to anencephaly recorded by the Registrar General for Scotland, they concluded that there was a small increase in risk of anencephaly if the mother had had influenza during the first 2 months of pregnancy. In performing this analysis, certain assumptions were made because of the lack of precise data. An increase in congenital defects in infants of mothers who had influenza-like symptoms at 5 to 11 weeks of gestation was reported by Hakosalo and Saxen [97]. During the 1957 outbreak, Wilson and Stein [98] showed that 60% of pregnant women who denied symptoms of influenza had serologic evidence of having been recently infected. Conversely, 35% of women who stated that they had had influenza lacked serologic evidence of having been infected. Likewise, Hardy and coworkers [99] found that 24% of women who stated that they had had influenza lacked serologic evidence of past infection with the epidemic strain, and 39% of women with titers suggesting recent infection denied symptoms of influenza. MacKenzie and Houghton [100] summarized the reports implicating influenza virus as a cause of maternal morbidity and congenital anomalies and concluded that probably no association exists between maternal influenza infection and subsequent congenital malformations or neoplasms in childhood.

Syndromes

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These have roughly the same morphology as that of the more central lesions, but they tend to be less significant as a cause of central visual loss unless they are accompanied by massive contractures of the overlying vitreous. The anterior uvea often is the site of intense inflammation, characterized by redness of the external eye, cells and protein in the anterior chamber, large keratic precipitates, posterior synechiae, nodules on the iris, and, occasionally, neovascular formations on the surface of the iris. This reaction may be accompanied by steep rises in intraocular pressure and by formation of cataracts. To be considered as a manifestation of toxoplasmosis, iritis should be preceded or at least accompanied by a posterior lesion. The same can be said of scleritis, which may be observed external to a focus of toxoplasmic chorioretinitis; it has no significance by itself as a sign of toxoplasmosis. Hogan and coworkers tabulated the data from 22 cases of chorioretinitis in infants 6 months of age or younger with congenital toxoplasmosis (in 81%, the lesions were bilateral) from the literature published through 1949 [407]. A precise determination of prevalence cannot be gleaned from these reports because for many of the infants, the data were incomplete-for example, in some, no description of the fundus was provided, but other features such as microphthalmia were described. Of those infants for whom sufficient information was available, seven had only healed retinal lesions, five had only acute lesions, and four had both acute and healed lesions. Macular involvement was seen in 5, and peripheral retinal involvement in 10; diffuse retinal involvement was present in 3. Twelve infants had microphthalmia, 5 had optic nerve atrophy, 3 had papilledema, 8 had strabismus, 7 had nystagmus, 10 had anterior segment involvement, and 2 had cataracts; in 10, parasites were noted in the retina at autopsy. Franceschetti and Bamatter reviewed the signs in 243 cases of congenital ocular toxoplasmosis and found the following percentages: bilateral involvement in 66%, unilateral involvement in 34%, microphthalmia in 23%, optic atrophy in 27%, nystagmus in 23%, strabismus in 28%, cataract in 8%, iritis and posterior synechiae in 8%, persistence of pupillary membrane in 4%, and vitreous changes in 11% [408]. For example, relatively normal visual acuity may occur in the presence of large macular scars either sparing or involving the fovea [279]. Synechiae and pupillary irregularities sometimes are present and reflect an especially severe intraocular inflammatory process. Intermittent occlusion (patching therapy) of the better-seeing eye may lead to substantial improvement in visual acuity even in the presence of large macular scars. In the first year of life, 134 of these 173 children had been treated with pyrimethamine, sulfadiazine, and leucovorin, while the remaining 39 were not treated. Locations of the cataracts included anterior polar (three eyes), anterior subcapsular (six eyes), nuclear (five eyes), posterior subcapsular (seven eyes), and unknown (six eyes). Patients with bilateral retinal detachment in whom the location of scars was not possible were excluded from the denominator. Twelve cataracts remained stable, 12 progressed, and progression was not known for 3. Choroidal neovascular membranes, which result in accumulation of fluid in the retina and can result in vision threatening bleeding into the retina, have been associated with toxoplasmic chorioretinitis [410]. The healed foci of toxoplasmic chorioretinitis may resemble a colobomatous defect. The associated ocular, systemic, and serologic changes make toxoplasmosis the most likely diagnosis. Abnormal retinal morphology has been described in one fetal eye [313], and similar findings have been described in a variety of animal models of the congenital infection. Intraocular hemorrhage may go unrecognized and may cause retinal damage with gliosis and fibrosis, potentially resulting in retinal detachment. The lesion usually is unilateral, associated cerebral damage is absent, and no serologic evidence is present to support a diagnosis of toxoplasmosis. Retinopathy of prematurity may occur in conjunction with toxoplasmic chorioretinitis. Congenital aneurysms and telangiectasia of retinal vessels may result in extensive retinal fibrosis, with pigmentation and detachment. The disease usually is unilateral and is not associated with cerebral involvement or other changes. Retinoblastoma rarely may have an appearance similar to that described for ocular toxoplasmosis. It most often is unilateral and is unassociated with visceral or cerebral damage unless an advanced stage has been reached. Pseudoglioma may be difficult to distinguish from a healed chorioretinitis lesion but usually is single and unilateral. Gliomas may be bilateral, progressing from a small nodule to a large polypoid mass protruding into the vitreous.

The subsequent spread of syphilis throughout the rest of the world was facilitated largely by wars with associated large troop and population movements and general social disarray [6,7]. Delineation of the characteristics of syphilis was hindered further by the confusion of its symptoms with symptoms of gonorrhea: In 1767, John Hunter, an English experimental biologist and physician, inoculated himself with urethral exudate from a patient with gonorrhea. The patient also had syphilis, however, and the subsequent symptoms experienced by Hunter convinced two generations of physicians of the unity of gonorrhea and syphilis. The separate nature of gonorrhea and syphilis was shown in 1838 by Ricord, who reported his observations on more than 2500 human inoculations. Recognition of the stages of syphilis followed, and in 1905, Schaudinn and Hoffman discovered the causative agent. The following year, Wassermann introduced the diagnostic blood test that bears his name [1]. Lopez and Fracastorius had already mentioned syphilis of the newborn, but they and others thought that infants became infected through contact at delivery or postpartum by ingestion of infected breast milk [2,5,8]. Because many mothers of infants with congenital syphilis had no obvious signs of infection, some investigators believed that congenital disease was transmitted by the father [1]. In 1858, Sir Jonathan Hutchinson described the famous triad of late congenital syphilis: notched incisor teeth, interstitial keratitis, and eighth cranial nerve deafness [9]. Myriad further presenting signs and symptoms have earned syphilis the title of "the great imitator" [10,11]. The horror syphilis causes is best encapsulated in its other old name lues, which means "plague" in Latin. This is still the most appropriate name because a staggering number of adults and newborn infants in developed and developing countries are suffering and dying as a consequence of infection with-MACROS-. The most shocking aspect of this plague is that hundreds of thousands are newly infected every year despite the availability of feasible, cost-effective interventions to detect, treat, and prevent syphilis [12,13]. The 2000 Report on Global Burden of Disease estimated that congenital syphilis is responsible for 1. Consequently, the elimination of congenital syphilis is an important global objective [12,15,16]. The name Treponema (Greek, meaning "turning thread") is based on its twisting motion, and pallidum (Latin) is derived from its pale, yellow color. Borrelia, Spirochaeta, Leptospira, and Cristispira are other genera of this order, grouped together primarily based on their morphologic characteristics. Several nonpathogenic treponemes also inhabit the oral cavity and intestinal tract of humans [28]. An outer membrane consisting of a lipid bilayer surrounds the endoflagella, cytoplasmic membrane, and protoplasmic cylinder. Genetic polymorphisms more recently identified at two loci have enabled strain typing of clinical isolates of-MACROS-. 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].

Although treatment of active tuberculosis during pregnancy is unquestioned, the treatment of a pregnant woman who has asymptomatic M. Some clinicians prefer to delay therapy until after delivery because pregnancy does not seem to increase the risk of developing active tuberculosis. Others believe that because recent infection can be accompanied by hematogenous spread to the placenta, it is preferable to treat without delay or to wait until the second trimester to start chemotherapy. The indications for treatment and the basic principles of management for the pregnant woman with tuberculosis disease are no different from those in nonpregnant patients. The recommendations for which drugs to use and how long to give them are slightly different, however, mostly because of possible effects of several of the drugs on the developing fetus. With any of the regimens, the drugs usually are given every day for the first 2 weeks to 2 months; then they can be given daily or intermittently (under directly observed therapy) for the remainder of therapy with equal effectiveness and rates of adverse reactions [209]. Although it crosses the placenta, it is not teratogenic even when given during the first 4 months of gestation [215]. The noted abnormalities included limb reductions, central nervous system abnormalities, and hypoprothrombinemia. The incidence of abnormalities in fetuses not exposed to antituberculosis medications ranges from 1% to 6%. One review of intravenous gentamicin and oral neomycin did not show teratogenicity, however, in a populationbased cohort of pregnant women in Hungary [227]. The central nervous system effects of cycloserine and the gastrointestinal effects of para-aminosalicylic acid in adults make their use in pregnancy undesirable. Fluoroquinolone use is not recommended for breast-feeding mothers [201]; however, there have been no reports of arthropathy in children under these conditions. After the first 2 weeks to 2 months of daily treatment, the drugs can be given twice a week under directly observed therapy, which is the preferred method of treatment by most experts. The treatment of any form of drug-resistant tuberculosis during pregnancy is extraordinarily difficult and should be handled by an expert with great experience with the disease [235]. Because treatment of tuberculosis in pregnant women often continues after delivery, there is concern as to whether it is safe for the mother to breast-feed her infant. Maternal mortality rates are higher for coinfected women than for women with either infection alone, and much of the excess mortality is due to tuberculosis [96,238]. All neonates and infants with tuberculosis should be treated by directly observed therapy. While receiving chemotherapy, patients should be seen monthly to encourage regular taking of the prescribed drugs and to check, by a few simple questions. Repeat chest radiographs probably should be obtained 1 to 2 months after the onset of chemotherapy to ascertain the maximal extent of disease before chemotherapy takes effect; thereafter, radiographs rarely are necessary. Chemotherapy has been so successful that follow-up beyond its termination is not usually necessary except for children with serious disease, such as congenital tuberculosis or meningitis, or children with extensive residual chest radiographic findings at the end of chemotherapy. The basic principles for treatment of other children and adults seem also to apply to the treatment of congenital tuberculosis [193,240]. Although the optimal duration of therapy has not been established, many experts treat infants with congenital or postnatally acquired tuberculosis for 9 to 12 months because of the decreased immunologic capability of the young infant. The results in survivors were good, but the follow-up was usually short [182,249]. In the modern era, mortality rates of 38% have been reported in some series [238].