Tuberculosis and syphilis have also both been associated with poor fetal growth. Both extrapulmonary and pulmonary tuberculosis are linked with low birthweight (Chap. 51, p. 995). Sobhy (2017) analyzed 13 studies that included a total of3384 women with active tuberculosis. The odds ratio was 1.7 for low birthweight. The etiology is uncertain, however, the adverse efects on maternal health, compounded by efects of poor nutrition and poverty, are important Gana, 2012). Congenital syphilis is more common, and paradoxically, the placenta is almost always larger and heavier due to edema and perivascular inflammation (Chap. 65, p. 1237). Congenital syphilis is strongly linked with preterm birth and thus low-birthweight newborns (Sheield, 2002).
Toxoplasma gondii can also cause congenital infection, and Paquet and Yudin (2013) describe its classic association with fetal-growth restriction. Capobiango (2014) described 31 Brazilian pregnancies complicated by congenital toxoplasmosis. Only 13 percent were treated antepartum for toxoplasmosis, and low birthweight complicated nearly 40 percent of all the pregnancies. Congenital maaria also causes low birthweight and poor fetal growth. Briand and colleagues (2016) emphasize the importance of prophylaxis early in pregnancy for women at risk.
In a study of more than 13,000 fetuses with major structural anomalies, 22 percent had accompanying growth restriction (Khoury, 1988). In one study of 111 pregnancies complicated by fetal gastroschisis, a third had birthweights < 10th percentile (Nelson, 20 15a). As a general rule, the more severe the malformation, the more likely it is that the fetus will be SGA. This is especially evident in fetuses with chromosomal abnormalities or those with serious cardiovascular malformations.
Depending on which chromosome is redundant, fetuses with autosomal trisomies may display poor fetal growth. For example, in trisomy 21, fetal-growth restriction is generally mild. By contrast, fetal growth in trisomy 18 is virtually always significantly limited. he crown-rump length in fetuses with trisomy 18 and 13, unlike that with trisomy 21, is typically shorter than expected (Bahado-Singh, 1997; Schemmer, 1997). By the second trimester, long-bone measurements usually are below the 3rd percentile. In one group of 174 children with trisomy 13, the mean birthweight with trisomy 13 was 2500 g, and in 254 children with trisomy 18, it was 1800 g (Nelson, 2016).
Poor fetal growth also complicates Turner syndrome, and the severity correlates with increasing haploinsuiciency of the short arm of the X chromosome (Fiot, 2016). In contrast, poor growth is not characteristic of an increased number of X chromosomes (Ottesen, 2010; Wigby, 2016). As discussed in Chapter 13 (p. 263), aneuploidic patches in the placentaconined placental mosaicism (CPM)-is a recognized cause of fetal-growth restriction. Evidence suggests that aneuploidy afecting both the cytotrophoblast and mesenchymal core of the placenta, which is type 3 CPM, is associated with fetalgrowth restriction (Toutain, 2010).