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Neutrophils have reached both aminions.

The migration of maternal inflammatory cells is unidirectional, originating in the intervillous space and maternal vessels of the decidua, migrating in the fibrin under the chorionic plate and finally reaching the chorion and amnion.1 The infection often elicits a fetal response in the form of acute funisitis -- however, this only occurs after 20 weeks gestation, when the fetal immune system has sufficiently matured.

Higher power shows multilobed neutrophils infiltrating the amniotic cell layer as well as the underlying chorion. Interestingly, the exuberance of the inflammatory exudate is not an indication of the clinical significance of the infection. For example, Group B Strep, an organism that may have devastating consequences, often elicits a minimal neutrophilic infiltrate.1

Here is a case of marked chorioamnionitis at 19 weeks resulting in PPROM (premature preterm rupture of membranes) and delivery.


Acute chorioamnionitis is defined as the presence of acute inflammatory cells (neutrophils in particular) in the fetal membranes. It is generally attributed to ascending infection from the vagina and endocervix. More infrequently it may result from hematogenous seeding of the placenta and membranes from a pre-existing maternal infection.

Acute chorioamnionitis is quite common, with an incidence of 20-24% of live births and up to 67% in preterm deliveries. Although premature rupture of membranes is often stated to be the predisposing factor to infection, recent data suggests that "it is the loss of membrane integrity resulting from inflammation that makes rupture a probability".1 Inflammatory mediators from ascending infection may initiate labor -- TNF (tumor necrosis factor) in particular may stimulate production of prostaglandins.1

Grossly, the placental membranes may be white, greenish and opaque. Microscopically, the defining feature is the robust presence of neutrophils. The presence of chronic inflammatory cells such as lymphocytes and plasma cells may indicate a subacute process.


Clinical detection of acute chorioamnionitis is not always possible as only a minority of women experience the classic symptoms of fever, leukocytosis and uterine tenderness. Alternatively, women with clinical symptoms of chorioamnionitis may not have corresponding pathology.


Once chorioamnionitis has been diagnosed, it is important to ensure the patient is proceeding towards delivery as expectant management is associated with poorer outcomes for both mother and fetus. Broad spectrum antibiotics are commonly employed. The preferred mode of delivery is vaginal if possible as hysterotomy may result in intra-abdominal spread of infection.


Infection typically resolves following delivery. Rarely in cases of longstanding infection a hysterectomy may be necessary. In addition women suffering from chorioamnionitis have higher rates of post-partum hemorrhage.


Placenta : Fusobacterium


1 Baergen RN. Manual of Benirschke and Kaufmann's Plathology of the Human Placenta. New York, NY: Springer; 2005: 280-5.

Last updated: 2010-10-26
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