INFECTION (page 76)

Prenatal Infections

Prenatal infections are common and varied; many cause placental changes. Infections may ascend from the vaginal-cervical canal breaching the protective cervical mucus plug (infecting the extraplacental membranes) or they may reach the placenta hematogenously through the maternal blood (infecting the placental maternal vascular space). Most infections cause gross and microscopic placental changes; others, like Coxsackie virus and Parvovirus cause few characteristic or specifically recognizable lesions. Examine the chorionic stroma and Wharton's jelly to rule out Toxoplasma. When viral infection is suspected, electron microscopy may be helpful. (Figure 8-4)

Etiology of placental infections


Infectious cervical or vaginal pathogens can infect the extraplacental membranes and amniotic fluid, resulting in chorioamnionitis, inflammation of the placental membranes. In up to 4% of term placentas and 25% of premature placentas, chorioamnionitis is an indication of amniotic fluid infection, usually of mixed flora.

Typically, delivery is premature, so the placenta lacks its normal blue sheen. The extraplacental and fetal surface membranes are gray-tan and opaque, obscuring the fetal surface vasculature, due to tissue infiltration by acute inflammatory cells (the myeloperoxidase from the polymorphonuclear cells). In cases of long standing inflammation, the surface becomes more yellow from accumulated leukocyte exudate and there may be mural thrombi in the chorionic vessels. The amnion may be roughened or may have lost its normal luster and the membranes are often friable. The decidua capsularis is frequently detached or hemorrhagic. A particular pathogen may liberate a recognizable odor.

Microscopically, acute (leukocytic, granulocytic) or chronic (monocytic, usually seen in association with acute) chorioamnionitis may be diagnosed. Most commonly, acute inflammation, principally polymorphonuclear, involves one or more of the follow: extraplacental membranes, chorionic plate and its under surface, or blood vessels in the chorionic plate and umbilical cord. Inflammation is most consistently found at the membrane point of rupture and the undersurface of the chorionic plate. The leukocytes emigrate from the intervillous space (maternal response) and from the fetal surface blood vessels (fetal response), always toward the amniotic cavity (the presumed antigenic source). Plasma cells are usually absent, but may be seen in some chronic infections. Inflammation may be absent in some microscopic sections of one or more of these areas; therefore sections should be submitted from all of these areas.

The ascending nature of chorioamnionitis is supported by the culture of intact sacs and three pathological findings: 1) severe, acute necrotizing deciduitis is usually associated with and often exceeds the degree of chorioamnionitis; 2) when the intrauterine position of twins is know, including the partition of their amniotic sacs, it is invariable the lower seated twin with chorioamnionitis or whose membranes are more severely inflamed; 3) when extraplacental membrane rolls include the point of spontaneous rupture on the inside, the degree of inflammation is most significant in the inner portion of the roll.

Meconium and Chorioamnionitis

It has been noted that meconium is often accompanied by chorioamnionitis. Particularly in term and postdates gestations, meconium may contribute to the severity of chorioamnionitis but it does not cause chorioamnionitis. A study of term pregnancies comparing meconium stained and clear amniotic fluid revealed a higher intrauterine infection rate in the meconium group. It was hypothesized that meconium alters the antimicrobial activity of amniotic fluid, creating an environment more favorable to infection, therefore carrying an increased risk for chorioamnionitis and its complications.